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Cooper Medical College

No. /.'■ /A Shelf

aiKT OK

h£^&^

HANDBOOK

Practical Medicine

PB0FBS80R OF SPEOIAL PATHOLOOT AND THERAPEUTICS AKD DIRBOTOR OF THE

UNIYBRSITY MEDICAL CLINIC IN ZURICH

VOLUME III
DISEASES OF THE. NERVES, MUSCLES, AND SKIN

ONE HUNDRED AND FIFTY-SEVEN WOOD ENGRAVINGS

NEW YORK

WILLIAM WOOD & COMPANY

1886.
■?■

• ••
•• • •-

• • • • •

• • •

• •

• • •

• •• •

• •

• • •

COPTBZOBT BT

WILLIAM WOOD & COMPANY.

1888.

MCM OF

tTCTTiNUi, uMiMirr A ca,

Itl A 111 CKMBY CT.,
NKW VORK.

34a

Y.3
I 88(b

TABLE OF CONTENTS.

DISEASES OF THE NEBVES, MUSCLES, AND SKIN.

SECTION V.

DISEASES OF THE NERVES.

PART I.

Diseases of the Peripheral Nerves,
A. Diseases of the Motor Nerves,

a. Paralysis of the motor nerves. Akinesis,

1. Facial paralysis,

2. Motor trigeminus paralysis,
8. Spinal accessory paralysis, .

4. HypoKlossal paralysis, .

5. Radial paralysis,

6. Median paraljrsis,

7. Ulnar paralysis,

8. Musculo-cutaneous paralysis, .

9. Axillary paralysis, ....

10. Combined paralysis of the nerves of the arm,

11. Peripheral paralysis of the scapula and trunk

nerves, ......

a. Paralysis of serratus magnus,
&. Paralysis of pectorales,

c. Paralysis of rhomboids and levator angul

scapulas,

d. Paralysis of latissimus dorsi,

e. Paralysis of subscapularis and teres major,
/. Paralysis of infraspinatus and teres minor,
a. Paralysis of extensors of the back, .
A. Paralysis of abdominal muscles, . •

12. Phrenic paralysis. Paralysis Of the diaphragm,
18. Peripheral paralysis of nerves of lower limb,

a. Crural paralysis,
6. Obturator paralysis,

c. Gluteal paralysis,

d. Sciatic paralysis, ....
h. Spasm of the motor nerves. Hyperkinesis, .

1. Spasm of facial nerve, ....

a. Diffuse clonic facial spasm, .

&. Diffuse tonic facial spasm,

c. Partial tonic and clonic facial spasm,

2. Spasm of the motor trigeminal branches,
8. Spasm of hypoglossal nerve, .

4. Spasm of spinal accessory nerve, .

5. Spasm of muscles of neck, scapula, and arm,

PAOSB

1-77

1-46

1-86

1-18

18-14

14-16

16-18

18-22

22-28

28-25

26-27

27-80

27-28

80-81

81-86

81-88

88-84

84-86

86-45

86-40

87-89

89-40

40-41

41-42

42-48

itMox. iw cQirssaii.

II. bpttBDi tiT uitUiuur «i|iil

■4e-r>i
Ei-s:!

BB-jrr

in-se

*■ www iMUiMliwCH, -

1^ L^Mj^liwr ai^naJ hMnoniiagr.

■ ■ I ■■'■■ • flliit] ctnX,

77-IW

77-117
77-«»

77-78

98~M

, lOft-lSS

100-130

TABLB OF CONTENTS.

PAOK

1. Tabes doraalis 100-112

2. Spastic paralysis, ..... 112-114
8. Acute anterior poliomyelitis in infants, . 114-120
4. Acute, subacute, and chronic anterior poliomye-

litis in adults,
5. Spinal progressive muscular atrophy,
Combined system diseases of the cord,

1. Hereditary ataxia,

2. Secondary degeneration of the cord,

a. Descending secondary degeneration,
h. Ascending secondary degeneration,
c. Combined secondary degeneration,
8. Amyotrophic lateral sclerosis,
c. Traumatic diseases of the cord,

1. Unilateral lesion of the cord,

2. Acute injuries of the cord,
8. Concussion of the cord,
4. Slow compression of the cord,

B. Functional Diaecuea of the Cord, .

1. Spinal irritation,

2. Spinal neurasthenia,
8. Acute ascending spitial paralysis,
4. Reflex paralyses, .4
6. Psychical spinal paralysis,

6. Paralyses after acute diseases,

7. Toxic spinal paralyses, .

a. Lead paralysis,

b. Arsenic paralysis,

c. Phosphorus paralysis,

120-122
122-180
130-188

130
130-135
181-184

184
184-1 a5
185-188
138-147
183-141
141-143
148-144
144-147
147-162
147-148

148
149-150
150-151

151

151
151-155
151-154

154

154
d. Carbonic acid gas and bisulphide of carbon paralysis, 154

e. Ergot paralysis,
/. Alcoholic paralysis,

8. Writer's spasm,

9. Tetany, .....
id. Saltatory spasms,

11. Primary spinal muscular spasms,
C. Diseaaea of the Spinal Meninges, .

1. External spinal pachymeningitis,

2. Internal spinal pachymeningitis. .

a. Hypertrophic pachymeningitis,
6. Hemorrhagic pachymeningitis,
8. Acute spinal menin^tis,

4. Chronic spinal meningitis. .

5. Meningeal apoplexy,
7. Meningeal tumors, .

154
155

155-158
. 158-161

161-162
162

162-176
. 163-164

164-167
. 164-166

166-167
. 167-170

170-172
. 172-174

174-17^

PART m.

Diseases of the Medulla Oblongata, ....

1. Glosso-labio-laryngeal paralysis, . . . .

2. Hemorrhage into the meiulla oblongata,

8. Embolism and thrombosis of the m^ulla oblongata,

4. Acute bulbar myelitis, ......

5. Tumors of the medulla c blongata,

6. Injuries, acute and slow compression of medulla oblongata.

. 176-190
176-185

. 185-186

186-188

189

18a-180

. 189-198

PART IV.

Diseases of the Brain, ......

Diagnostic Preliminary Remarks,

a. Focal symptoms in diseases of the cortex,

b. Focal symptoms in diseases of the centrum ovale,

c. Focal symptoms in diseases of tho internal capsule,

190-301
190-191
191-196
196-197
197-199

TABLB OF CONTENTS.

8. Myositis ossificans progressiva,
4. Ischsdmic muscular paralysis,

PAOB

. 817-318
318

SECTION VII.

DISEASES OF THE SKIN.

PAET I.

Inflammations of the Skin. DBRMATrnDss,

A, Erythematous Injlammatiotia of the Skin,

1. Urticaria,

d. Erythema nodosum^

8. Erythema exsudativum multiforme,

4. Acrodynia, ....

6. Pellagra, . .

B, Ve9ide4ike Inflammations of the Skin, .

1. Eczema, ....

2. Miliaria, ....

C, Vesicular Inflammation of the Skin, .

Pemphigus, ....

D, Pustular InjjUimmations of the Skin,

1. Impetigo and ecthyma,

2. Acne vulgaris, .
8. Acne mentagra,
4. Acne rosacea,

E, Scaly Inflammations of the Skin^ .

1. PsoriasiR, ....

2. Pityriasis rubra,

F, Papular Inflammations of the Skin, .

1. Prurigo, ....

2. Lichen scrophulosorum,
8. Lichen ruber,

. 819-847

819-825
. 819- 8 il

822-828

. 828-824

824

. 824-825

825-881
. 8^5-880

880-881
. 881-888

881-888
. 888-840

888-885
. 835-886

886-888
. 838-840

840-844

. 840-844

844

. 844-847

844-346
846

846-847

PART n.

Sbcbbtobt Anomalues of the Skin,

A. Secretory Anomalies of the Sweat Olands,

1. Hyperhidrosis, ....

2. Anhidrosis, ....

8. Parhidrosis, ....

a. Osmhidrosis,

b, Chromhidrosis, .
c Urhidrosis. .

B. Secretory Anomalies of the Sebaceous Olands,

1. Seborrhoea, ....

2. Asteatosis, ....
8. Parasteatosis,

a. Comedo, . . . .

b. Milium,

848-858

848-850

848-349

849

849-850

849

850

350-858

350-352

352

352-353

852

858

PART in.

Hypebtrofht of the Skin. ....

A, Hypertrophy of the Cutaneous Pigment,

1. NSBVUS, .....

2. Chloasma, ....

B. Hypertrophy of the Epidermis. Keratosis, .

Ichthyosis, ....

C Hypertrophy of tJie Hair, Hirsuties,

858-860
853-355
853-354
854-355
855-356
355-856
856-357

vn.

TABLE OF O0XTE5TS.

//. iiM0vrUufiU^ iff the SqU*. OmifchauxU,
a. ifi^^tisrtrujpUy of the Comneeiwe Titaut,

S^krimH ajdultorum, .

AypnMt: Sckretna aponatorain.

857

857-859
869-880

PART IT.

Atk^/mr or tub 6kik.

A . Ain/pliy ^f ^^ CMianeous Pigment,
li Atr^de CftaugeM in the Hair^y

U. Alo|>9cU Bad atrichia, .

^J. Alroyfiif of tU Cutis Tistue,

I • • •

860-884

880-881

861-884

861

864
864

PART V.

• • •

. 864-865
864-866

PART VL

I'AUAhnUM or 1HK Hjcin,

A' Anininl PuraMileM, JMrmatozoonoseSf .
1. HcubittM, ....
ii. Acarustolliculorum,
B. Pddiculi

a. PttdiculuH capitis, .

h. PodiculuB viMtiioentorum,

t\ Pudioulutf pubis,
4. Kloiu, ....

(i. i'ulox irriUuti,

h. Pulux p4»ii»trHUs,
^. Itt^UmK. < Umax l«K}tul»riu8.
H, Filiii'iu iiiuiliuttiitflii,
7 ryiii.i(*uroi, .....
Vi. \'iy*'luljf i\iia»itt:»o/tfyiiSkin. Dermatomyooses,
1 rit^rittiiiii vtimioolor.
y. Kttvun, .....
t). H«rp«)ii tuimuriiu*, ....

. 865-888
865-375

. 865-873
873

. 873-874
873-878

. 878-874
874
874
874
874
874

. 874-875
875

. 875-883
875-877

. 877-879

HAISTDBOOK

PRACTICAL MEDICINE

SECTION Y.

DISEASES OF THE NERVES.

PART I.

DISEASES OF THE PERIPHERAL NERVES.

A. DISEASES OF THE MOTOR NERVES.

a. PARALYSIS (AKINESIS) OF THE MOTOR NERVES.

1. Paralysis of the Facial Nerve.
{Bell's Paralysis, Prosoplegia.)

I. Etiology. — Peripheral facial paralysis is that form of disease
whose causes are situated between tne peripheral terminations of the
nerve^ and the point at which the trunk of the nerve enters the sub-
stance of the central nervous system, at the posterior edge of the pedun-
cle of the pons. The paralysis also presents a peripheral character if
the central fibres of the nerve are injured before they enter the nucleus
in the floor of the fourth ventricle.

The peripheral course of the nerve may be divided into an intracra-
nial portion, the part contained in the Fallopian canal, and the purely
peripheral terminations.

Exposure occupies a prominent place among the causes of peripheral
facial paralysis (rheumatic form). The paralysis sometimes follows the
exposure at once, sometimes in a few hours or days.

The paralysis is often produced by riding in a car near an open window, look-
ing out of a window when the face is warm, standing at a windy corner of a

DI8BABB8 OF THE KOTOB NEBYES.

, etc., and especially on that tide which is exposed to the wind or cold air.
ing near a oold, damp wall is also sufficient to prodaoe the paralysis.

In other cusos traumatism is the cause of the paralysis.

This diseaso has be«n ohsenred as the resolt of a ship in the face, the blow of a
rapier, the ai>pUoatloii of the forceps during delivery. Tumors of the pelvis, and
a narrow pofvis nn« also said to produce facial paralysis in the new-bom. Blows,
stab-woundN, giitisliot wound^ may paralyze the nerve. The disease also results
not infriHitt<«titIy from surgical operations upon the parotid gland, and it has been
observed art«*r H(r«»iohlng of the nerve in convulsive tic. It is sometimes the re-
sult of fMvvnrA Injury to the skull, with subsequent fracture and hemorrhage,
since All AiHMtinulMtlon of blood in the Fallopian canal is apt to impair the func-
tion of ili(4 iM*rv»*.

t>\mM0n of the parotid gland, enlargement of the submaxillary lym-
phatio ghiuU, ahuceflnes in tne region of the lower jaw, or snppnration
of iubdronlar lymphatic glands, with subsequent formation of cica-
tric€*N« tuny alsi» give rise to the paralysis, eitner as the result of com-
preimUfU or (\\r^*X implication of the nerve in the morbid process. May
demriUm] hw\ik\ jwralysis in leukcemia from leukasmic infiltration of

the nf^rfp.

Thff lUt^n^^ in often the result of aural affections.

A/yi/^/llffK io Hmitf, the paralysis mav be caused by an accumulation of wax
Iff ihp tmt, affd mar ra^Hdly disai^peftr when the cerumen is removed. It has also
yimti ftmtiff*^^ ibat catarrhal inflammation of the cavitv of the tympanum may
ImnU^^ f^M* fa/ilal nm-vf*. Tlio connortion between tubercular processes in the
imtftifftni }ftfitm and fwft\n\ paralyMiM \n clearer, because the destructive process is
ftpi W #*«Mi/l l^t thu trunk nt thn rif*rvo. The paralysis is sometimes produced by
imti/himm ift fmtwftrhf^nfm in i\m Fallopian canal.

tfif^tf/nUt t^mmn \idrnf'.rtiu\ti\ (Umiumn are the causes of peripheral fa-
HiHi fmtftt^ff^n, Int i4<Arrfpl»< ntfiningifln changes, exostoses, tumors, an-
kHthiff*^ *^ ^'^'^* rM«4«|<i tii Mf^ liami of the bruin, etc.

*}hH )uhf^^hfim t)]fmniimn oftoflnlonnlly act as a cause (diphtheria, ery-
^iH^in*, ^'jfphff^^i f''V**tt tAr)olfi« Mul dysentery). Several cases have also
UhHi fi^^'t'f^^^ ^fh^t hft^fM 9^fmU^r» Vcripheral facial paralysis is not in-
UhHH^h^^ ^Uh pMtftiittt t^^iU\Ull» Tho lesion is sometimes intracranial
Ith^^^^^'^^- *fi^h'*hM^)f^ \ififmm*f^4 fvnoNiosoM; or gummata), sometimes it con-
mM^ //^ HU s^HnH^.)in \itiHi4im within tho Fallopian canal. French writeiis

Ji,^il ^ji^v^ ^^,>A ^y^^^l^#Nii//^NMimiiMo()nuri temporarily at the beginning
H^ *^^-^^i^hf) M.H^M (ft ^|(^h)ll«i particularly in females.

''^^.'A '|l/^.'*,w. ^ mfl ^Uh^h Uf*»**\ olsMirVMl in lead poisoning, and also after

'fly >; .AV/.A /.- «f^/ ^/^M^iMM^IIy trmiimd ono. It is observed more often

\f ^/^ »> 1 <. ' v^v**- ^ii^A^ f4in m*n» K^poMMtJ to the various causes, and is more

u/iy '' '**.' ^f.' '^^tU tiff- ink a «»lM*ilitr rMiWi)ii. Kulenburg observed a pa-

^/,V )fh'.' h'^i ^^l ^k^ 4}^H^ i wlMM oil tho right side, and three times on

If / .«/ 4v*ii/^4 ^ fiH}^ftM' -I llMVH had tho opportunity of making

mt.1 ij.'.ii. v/ ^^^f^\^i4^\tf^ nil ^,tiMant facial paralvsis, following tuber-

S^ V!. . w,. .// ilfi; iji4h^h>t |/oi'UoM of thtt temporal bpne. The changes

Iff^' i(/« "^" *'J >r'U/ ii^/y^' niiM^-yud ohortly after section of a nerve in an-

uJy- ^'■^.'■h'.''^'AiHH nf M^/^ HmU\\\M}/ MubMtauce into small fragments.

DISBABES OF TBV HOTOB HGBTES. 3

degtruotioQ of the axis oylinders, increase of the nuolei in the aheath
of Schwann, increase of the interstitial connective tissue and of its
nnclei (Fig. 1). ^Similar appearances were described bj Kaase in a oase
of six weeis' standing. In fliis case the frontal mnscle showed fatty de-
generation of the fibrilliB, increase of the interstitial connBctive tissue,
and an accumulation of fat within it.

These changes must always be expected when the lesions which hftTe
given rise to the facial paralysis have interrupted the continuity of the
nerve fibres. If the causes disappear, the anatomical changes may be
repaired. The restoration of the parts may remain absentQ the lesion
has lasted too long or if a large part of the nerve has been entirely
destroyed.

In mild, temporary paralyses, the lesions are probably less severe. In
not a few cases, they consist probably of inflammatory swelling and
changes in the connective-tissue portions of the nerve, which tempora-
rily compress the nerve fibres and impair conduction. As a matter of
course, such conditions will be more serious if situated within the Fallo-
pian canal, on account of its narrowness and unyielding character.

III. Stuptoms. — The symptoms of facial paralysis are not confined
to purely motor disturbances in all cases. According to some authors,
the facial nerve contains secretory fibres at its origin from the pons,
so that it is not surprising that disturbances in the secretion of saliva
may occur in facial paralysis. At the ganglion geniculatum, the facial
nerve receives gustatory nerve fibres from the trigeminus through the
agency of the petrosus 'supcrficialia major (but the gustatory fibres soon

4 DIBBA8B8 OF THK KOTOB HBBTXa.

leave the facial oerre with the chorda tympani), and hence the Bjmp-
toms of facial paralysis may inclade dieturDancee of taete. Filially,
fiince the faoiaF Derve innerrates the stapedius maacle through the
agen(^ of the Btapedias nerve, anditory disturbances may also be pro-
duced.

The symptoms of facial paralysis may occur suddenly or be preceded
by prodromata (pain in the ear and face, dizziness, etc.). In somecasea,
long-standing otorrhcaa and the signs of tuberculosis of the petrous por-
tion of the temporal bone prepare us for the possible onset of facial
paralysis.

The first B^ptoms are often noticed by the patient's family or acci-
dentally by himself on looking into a mirror. Sometimes the patient
complains merely of imperfect closure of the lid and epiphora, although
the paralysis most hare been present for several days. Some patients

Expresalon of tbe face, during the act of lanirtilUiIti a woman mffarlag from peripheral pantlr-

oomplain of a feeling of weight, stiffness, or coldness on one side of the
face, or of a sour, stSty, or metallic taste upon one-half of the tongue.

The motor disturbances are the most prominent symptoms. The
affected half of the face is destitute of folds, smooth, drawn towards the
healthy side, and remains motionless during laughter, crying, or talking
(Fig. i).

On accomit of paralysis of the frontal muscle, the forehead is some-
what higher on the aSected than on the healthy side; it is sinooth, and
remains so when the attempt is made to wrinkle it.

On account of paralysis of the corrugator snpercilii, the glabella on
the aSected side remains smooth when an attempt is made to wrinkle
the integument in- this region. The eyebrow is lower than on the
healthy side.

Faralyeis of the orbicularis palpebrarum causes the upper lid to

DISEASES OF THE MOTOB NERVES.

appear smaller than on the healthy side, and hence the palpebral fissure
to appear larger. The eyeball is sometimes more prominent. The

f>afient is unable to close the lid (lagophthalmus paralyticus), though
he palpebral fissure become^ somewhat narrower in the attempt.

Inasmuch as the eyeball is rolled upwards and inwards (more rarely
upwards and outwards) by associated movements, the sclera and the
lowermost segment of the iris make their appearance upon attempting
to close the paralyzed lid. All these movements are usually spasmodic
and irregular.

The explanations of the diminution in the size of the palpebral fissure during
the attempt to close the hd are unsatisfactory. Some assume an uneaual paraly-
sis of the various layers of the orbicularis. Henle believes that the levator pal-
Sebraa relaxes, contrary to the rule, during the attempt at closure, and thus ren-
era possible the phenomenon referred to.

The patients are very much annoyed by constant epiphora, the
result of paralysis of Homer's muscle, which changes the position of the
lachrymal points in such a way that the lachrymal fluid cannot enter
them freely. After a while, tfie paralysis may be associated with con-
junctivitis, ulceration of the cornea, or even deeper-seated diseases of
the eye. Marked ectropium paralyticum of the lower lid develops not
infrequently.

Tno tip of the nose is directed towards the healthy side. The nostril
on the affected side is smaller than that on the other side on account of
the paralysis of the muscles which move the alanasi. The patient often
complains of a peculiar feeling of dryness in the affected side of the
nose and diminished sense of smell, the result of dryness of the mucous
membrane on account of the imperfect flow of tears through the lachry-
mal canal, and of the diminished size of the nostril.

The naso-labial fold is lessened or abolished on the paralyzed side.
The angle of the mouth is depressed and drawn towards the healthy
side; this is also true of the chiu. The mouth is more or less open on
the paralyzed side, and often permits the escape of saliva and fluids.
For this reason, many patients, in drinking, throw the head backwards
and towards the healthy side. Articulation is interfered with on
account of the imperfect closure of the lips. This is most marked in
the enunciation of the labials, the paralyzed cheek flapping to and fro
in the attempt. Whistling, blowing, expectoration tire also interfered
with or rendered impossible, because the air escapes from the paralyzed
side of the mouth.

The movements of the tongue and of deglutition are undisturbed

J the stylohoid and biventer mandibulsB muscles are supplied by the
acial nerve, but are of such minor importance that their paralysis is
unnoticed).

The apparent deviation of the tongue when protruded is simply the result of
the drawing of the mouth towards the healthy side.

Although the movements of mastication are unaffected, this function
is interfered with to a certain extent by the paralysis of the buccinator
muscle. Food may accumulate between the gums and the cheek, and
must then be removed with the flngers or by pressure upon the cheek
from the outside.

Paralysis of the branches which supply the muscles of the concha is

nihfc:A«lfi6 OF THE MOTOB XEBVES.

,..k).i;. on iinii|M»«'tion. in those indiriduale who possesB the power
■ . * r! ,'w fill', or Uy 4'JectricttJ examinatiou of the muBcles.

•' M ■• V\\\\\ «>f ^*'*- i/jte;fument is almoest alwavB intact, with the
.1 ■\ \\w i'liru r.'iHes in which the cause of paralysis is situated so
. , .^\lv that th(.' iiiosculatiug peripheral ramifications of the

V M . ,^^\ »iii*liir*>"iiws are never observed. Berger reports one case

» I .'v \\i\\\ liiiiM-'d gray upon the paralyzed side.
;. li V \'.\ I it-^Hiii'iiH^'d movements are always absent in peripheral as

• '. uliiil fiH'iiil paralysis.

\ • - \ tliMliiihaiK^s are observed under certain circnmstances. If

\ I \\ \[\\Ui\ immiysis is the result of intracranial processes or tn-

. ,• ^'^^ i|illiiiiJ'»atury changes in the petrous portion of the tempo-

. I* '. • N\\/liiitin may \le impaired or abolished, either because the

• • *■ ■ •• I n> lit** J^''''^ '^^'^ injured or on account of the destruction of

•4 . I., -n (Ui|Hiiiitiis witliiu thetympanic cavity. On the other hand^

'.' -• ■>! L'MtHV'Ort i'i itself may be associated with increased power of

.1 •• .1. lU) jipitii'ii^itf; oxyokoia). Uitzig also mentions that some

, j.ih ..i 1 ii w n \ttw note upon voluntarv contraction of the frontal mus-

I,; ') }i ... |»|M'ii</nKMia are explained bv the fact that the stapedius

. ..1 t, . ] .tijijihi'l by the facial nerve. If this muscle is paralyz^, the

..- . ;,>ii|.i(iii uefciiimes the upper hand and produces the hyperacusis

, Ml ... . \.i 1 (•jicjandi hac$ not been satisfactorily explained).

!• ill ((..till Id of ta^te are possible, owing to the fact that the facial

I. . .(Ill 1^ 11 ^(t4Ltory fibres, at the ganglion geniculatum, through

III . ,1.1 jiiiroKiis superficialis major. Tnese fibres leave the facial

.1 >>• ilii; rhunJa tynipani. so that disturbance of taste will occur only

■I. I, ii... |r iiiin iei sitJiutiMJ between the ganglion geniculatum and the

; .1 '.I ill. i:iiiij-(Ju tyni|Miii. Tiie patients complain not infrequently of

iii«|> I II I. jM-ivrjxo biiiibutions of taste (salty, metallic, et<;.). In severe

i.-' .: Ill . |iiilji'iit8 lose the sense of taste entirelv (ageusis). or it is

li.-i... ill iiinjinitfiie<l or jj^^rvertt^d in the anterior two-thirds of the

I III. .,= .Ill lilt; jjuralyzt'd side (the posterior third is supplied by the

1.. :- i |.|iMi >Mfr«'ul nervi*).

Ill h liii/; (lie sense of t:i.st'3, the tongue should be protruded (the eyes
I. ... ' ■ I'-iiil), and its til) and edge brushed with various salty, sweet,
riui ,iii>l I. ilter solutions. The tongue should not be withdrawn into
I ti>. Ill .tiili during the txperimont. Taste may also be tested with the
Ml. ihti. I iijivjjt. A win? electrode, terminating in a small button,
l.".i( I jilt ruiployod (v'uUi Vol. I., Fig. 30), Theobject of the examina-
iii>i. i; iu ili'Unnine whether the first sensation of taste is produced on
11. ih I I. .1 l»v the same number of elements on touching the tongue with
ilii . I . iiinle, and whether the patient is able to discern that the anode
|ii<.(u 1.1 ii more intense gustatory sensation of a more metallic, sour
Ur i<' w liile the uetion of the catiiode U less intense, and the gustatory
iiMi ..iiMii more biting ami .salty. The indifferent electrode, 1. e., the one
vvlii' li is nut in eontaet witli the tongue, may be placed upon any indif-
iVkiiI .p(it» for example, the sternum. The test is begun with one ele-
lUfiit, iiihl the streii^rth of the eurront gradually increased, if necessary.
Till' |>ri<kling ben^atitui {U'Oilueod by the current must be distinguished
ffdiii ^Udtation.

The taeiile seuoihility of the tongue is not infrequently diminished
b^iuh the jiuralyzed dide.

DISEASES OF THE MOTOB NEBYES. 7

Many patients complain of diminished salivary secretion and a feel-
ing of dryness in the affected half of the bnccal cavity..

The connection of the ganglion genicnlatum with the spheno-palatine
ganglion, through the agency of the nervus petrosus saperficialis major,
also explains the possible occurrence of paralysis and changes in position
of the uvula and soft palate. The motor fibres in question pass from the
facial into the palatine nerve. On opening the mouth, the arch of the

{»a1ate is found depressed on the paralyzed side, and flutters to and fro on
orced respiration. The tip of the uvula almost always projects towards
the healthy side, but it must be remembered that deflections of the uvula
may occur in the healthy subject.

The electrical reactions of the paralyzed muscles are very important
with re^rd to diagnosis and proraosis. Facial paralysis may be divided
into mild, moderately severe, ana severe forms, according to the charac-
ter of the electrical reactions.

In the mild form, there are hardly any changes in the electrical irrita-
bility to the faradic and galvanic currents, the muscles reacting (both
directly and indirectly) as well as on the healthy side. In some cases,
indeed, th indirect electrical irritability is increased for a few days after
the paralysis, so that a milder current suffices to produce minimal
contractions of the paralyzed muscles. Paralvses which present such re-
actions until the seventh day offer a very favorable diagnosis. They
usually recover within two or three weeks without special treatment;

The moderateljT severe form of facial paralysis presents the partial
degeneration reaction. If electricity is applied to the nerve ^indirect
stimulation^, a slight increase of excitability may be noticeable lor a few
days after tne paralysis, but towards the end of the first week the faradic
and galvanic excitability diminishes more and more, as is shown by the
fact that the muscular contractions on the paralyzed side are less vigor-
ous than on the healthy side, although the minimal contractions often
are produced by the same current on the two sides. The electrical re-
actions on direct stimulation of the muscles are entirely different. They
S resent qualitative and quantitative changes which grow more profound
uring the second and tnird weeks of the disease. Towards the end of
the first week the faradic reaction gradually diminishes. The galvanic
excitability also diminishes somewhat during the first week, but it grows
more active during the second week. The mildest current is often suf-
ficient to produce muscular contractions on the paralyzed side. But
these contractions are slow, prolonged, and feeble, and are apt to become
tetanic, often during the entire duration of the passage of the current.
At the same time the law of normal contraction changes. If a healthy
muscle is stimulated with an increasing strength of current, the contrac-
tions will occur in the following order:

Cathodal closure contraction (CaClC).

Anodal closure contraction (AnClC).

Anodal opening contraction (AnOC).

Cathodal opening contraction (CaOO).

In peripheral paralysis, AnClO follows CaClO very rapidly at the be-
rinning, soon it appears with the same strength of current, and finally
AnOlO exceeds CaClO. This is also true of CaOO which soon becomes
equal to AnOC, though it rarely exceeds the latter.

The moderately severe form usually recovers in four to six weeks, at
the latest in eight to ten weeks. It disappears without leaving any

6 DI8EA8B8 OF THE MOTOB NEBYES.

recognizable, on inspection, in those individnals who possess the power
of moving the ear, or by electrical examination of the muscles.

The sensibility of the integument is almost always intact, with the
exception of the rare cases in which the cause of paralysis is situated so
far peripherally that the inosculating peripheral ramifications of the
trigeminus are also affected.

Vaso-motor disturbances are never observed. Berger reports one case
in which the hair turned gray upon the paralyzed side.

Reflex and associated movements are always absent in peripheral as*
opposed to central facial paralysis.

Auditory disturbances are observed under certain circumstances. If
a peripheral facial paralysis is the result of intracranial processes or tu-
bercular and inflammatory changes in the petrous portion of the tempo-
ral bone^ audition may be impaired or abolished^ either because the
acoustic nerve has also oeen injured or on account of the destruction of
the auditory apparatus within the tympanic cavity. On the other hand,
the facial paralysis in itself may be associated with increased power of
hearing (hyperacusis, oxyokoia). Hitzig also mentions that some
patients hear a low note upon voluntary contraction of the frontal mus-
cle. These phenomena are explained by the fact that the stapedius
muscle is supplied by the facial nerve. If this muscle is paralyzed, the
tensor tympani assumes the upper hand and produces the hyperacusis
(the modus operandi has not been satisfactorily explained).

Disturbances of taste are possible, owing to the fact that the facial
nerve receives gustatory fibres, at the ganglion geniculatum, through
the nervus petrosus superficialis major. These fibres leave the facial
nerve in the chorda tympani, so that disturbance of taste will occur only
when the lesion is situated between the ganglion geniculatum and the
exit of the chorda tympani. The patients complain not infrequently of
subjective perverse sensations of taste (salty, metallic, etc.). In severe
cases the patients lose the sense of taste entirely (ageusis), or it is
distinctly diminished or perverted in the anterior two-thirds of the
tongue on the paralyzed side (the posterior third is supplied by the
glosso-pharjrngeal nervp).

In testing the sense of taste, the tongue should be protruded (the eyes
being closed), and its tip and edge brushed with various salty, sweet,
sour, and bitter solutions. The tongue should not be withdrawn into
the mouth during the experiment. Taste may also be tested with the
galvanic current. A wire electrode, terminating in a small button,
should be employed (vide Vol. I., Fig. 30), The object of the examina-
tion is to determine whether the first sensation of taste is produced on
both sides by the same number of elements on touching the tongue with
the electrode, and whether the patient is able to discern that the anode
produces a more intense gustatory sensation of a more metallic, sour
taste, while the action of the cathode is less intense, and the gustatory
sensation more biting and salty. The indifferent electrode, i, e., the one
which is not in contact with the tongue, may be placed upon any indif-
ferent spot, for example, the sternum. The test is begun with one ele-
ment, and the strength of the current gradually increased, if necessary.
The prickling sensation produced by the current must be distinguished
from gustation.

The tactile sensibility of the tongue is not infrequently diminished
upon the paralyzed side.

DISEASES OF THE MOTOB KEBYES. 7

Many patients complain of diminished salivary secretion and a feel-
ing of dryness in the affected half of the buccal cavity..

The connection of the ganglion geniculatum with the spheno-palatine
ganglion, through the agency of the nervus petrosus superficialis major,
also explains the possible occurrence of paralysis and changes in position
of the uvula and soft palate. The motor fibres in question pass from the
facial into the palatine nerve. On opening the mouth, the arch of the
palate is found depressed on the paralyzed side, and flutters to and fro on
forced respiration. The tip of the uvula almost always projects towards
the healthy side, but it must be remembered that deflections of the uvula
may occur in the healthy subject.

The electrical reactions of the paralyzed muscles are very important
with regard to diagnosis and prognosis. Facial paralysis may be divided
into mild, moderately severe, ana severe forms, according to the charac-
ter of the electrical reactions.

The moderatel}r severe form of facial paralysis presents the partial
degeneration reaction. If electricity is applied to the nerve ^indirect
stimulation^, a slight increase of excitability may be noticeable lor a few
days after tne paralysis, but towards the end of the first week the faradic
and galvanic excitability diminishes more and more, as is shown by the
fact that the muscular contractions on the paralyzed side are less vigor-
ous than on the healthy side, although the minimal contractions often
are produced by the same current on the two sides. The electrical re-
actions on direct stimulation of the muscles are entirely different. They
S resent qualitative and quantitative changes which grow more profound
uring the second and tnird weeks of the disease. Towards the end of
the first week the faradic reaction gradually diminishes. The galvanic
excitability also diminishes somewhat during the first week, but it grows
more active during the second week. The mildest current is often suf-
ficient to produce muscular contractions on the paralyzed side. But
these contractions are slow, prolonged, and feeble, and are apt to become
tetanic, often during the entire duration of the passage of the current.
At the same time the law of normal contraction changes. If a healthy
muscle is stimulated with an increasing strength of current, the contrac-
tions will occur in the following order:

Oathodal closure contraction (CaClC).

Anodal closure contraction (AnClC^.

Anodal opening contraction (AnOCf).

Cathodal opening contraction (CaOO).

In peripheral paralysis, AnClO follows CaClO very rapidly at the be-
ginning, soon it appears with the same strength of current, and finally
AnGlO exceeds CaClO. This is also true of CaOO which soon becomes
equal to AnOO, though it rarely exceeds the latter.

The moderately severe form usually recovers in four to six weeks, at
the latest in eight to ten weeks. It disappears without leaving any

8 DISBAeXS OF THE HOTOB KBBTE8.

seqaelffi (twitchinga or contractures). Tolantaiy pover often rettorns
before the changes in the galranic excitability have disappeared.

In the severe form of the disease, complete degeneration reaction ia
observed. The excitability of the nerve to both cnrrents diminishes at
once or after a slight increase of excitability for one or two days. This
diminntion of excitability apreads from the central portiona of the nerve
to the periphery, and finally the electrical irritability disappears entirely.
It may remuin absent for weeks and months or, in incarable caaes, per-
manently. Direct stimulation of the mnsdes, on the other hand, reveals
the changes which we mentioned above in onr description of the moder-
ately severe form.

Uotor point! of the tadal nerre uiil the tteul miuolw mppUed by It.

In addition to an increase of galvanic excitability, the muscles also
manifest increased mechanical excitability.

In many cases of severe facial paralysis, a period of one to one and
one-half years elapses before recovery occurs. At all events, voluntary
contractions are nardly ever observed before the end of the second or
third month. Recovery is not infrequently incomplete; twitch ings and
contractures persist in the previously paralyzed muscles. Voluntary
power returns before the indirect electrical excitability, t. e., the nerve
fibres have become capable of conducting the stimulus of the will be-
fore they react to peripheral stimuli. In the incurable cases, the in-
creased excitability to the galvanic current gradually disappears, and
the mascles finally become altogether inexcitable.

DteBASES OF THE MOTOR NEBTK8. 9

The chaiuces ot electrical excitability which we have described depend upon
li definite aaatomical change in the nerves and muaclee. Experiments on animala
prove that when a peripneral nerve is cut, the medulla and axle cylinder of the
nbres in the peripheral portion undergo degeneration and become incapable of
conduction. The more the degeneration of the nerve progresses, the more its
electrical excitability diminiehee. Anatomical changes also appear in the mUH-
olea supplieil by the cut nerve. About the second week, the muscular fibres be-
come narrower, the transverse etriation less distinct, the muscle nuclei increase
in number, and the interstitial connective tissue proUreratee. E. Neumann
showed that muscles in this condition lose the power to rcaut to currents of short
duration (faradisml, but reaot to galvanic currents of sufficient duration in the
manner known as degenaration reaction.

After the degeneration of the nerve liaa lasted for some lime, a regeneration
of the fibres occurs, if the conditions are favorable. At first, the new fibres ore
destitute of medulla, and are unable to conduet peripheral impulses to the mus-

BlUtenil [BCl&I ponlf all. fWw la prattle. After Wrlcht.

Kides, although they conduct the will poiver. The electrical excitability appears

L to be dependent on the presence of the medulla.

In the mild form, there is probably no anatomical change in the nerve or mus-
cle; in the moderately severe form the anatomical disturbaoi'eB in the nerve are
only temporary, but the muscular tissue presents more marked lesions. In ii
curable cases the atrophy of the muscuistf fibres and increase of the con *"

^. ti»ne become so excessive that the electrical excitability is entirely lost.

Motor poititB are those places from which iv muscle can bo made to
act most rejulily to electrk^il stimulation, Tho motor points of the
Kial muscles arc shown in Fig. 3.

As a pule, peripheral facial paralyais is unilateral, and affects almost
J branches of the nerve.

Bilateral facial paralysis (diplegia facialis) is rare. It ia aometimiM

DISBASEB OF- THB XOTOB HBBVSe.

ind that, after exposnre, at first one norve is paralyzed, aod after a
r days the other lacial nervo is iilao paralyzed. ' Or bilateral paralysia
may be the result o( lesions of thcpetrousportionof both temporal bones,
or of intracranial processes. Maingauld desoribed diplegia facialis after
diphtheria. Sometimes the paralysis on one side is peripheral, oa the
other side it ia central in its origin.

Priraons suffering from diplegia facialis have entirely lost the power
of mimetic movementa. We may bear tho patients laugh or cry, but
their features remain rigid and set. There ia inability to close the lids,
the mouth is open, the upper lip often hanga down like a snout, saliva
dribbles from the mouth. Speech is indistinct and nasal. Deglutition
is impaired, and many patients are compelled to push the food, with the
fingers, back of the palate.

ezpreulon id bilaMnt CaclBl piir&l>*Ji Full tace After Wrlghl.

Various OBuses may give rise to incurability of the paralysis, via.,
tubercular prooeases iu the petrous portion of the temporal bone, opera-
tions, injuries, etc. In certain cases, recovery is incomplete. The
muscles remain paretic, and twitcbings and contractures are observed.
If the paralysis is permanent, the facial muscles and integument undergo
atrophy.

I\'. Diagnosis. — The recognition of facial paralysis aa auch is not
difficult, and, as a rule, it is also easy to difEerentiate the central from
the peripheral form.

It is characteristic of central facial paralysis that:

a. The movementa of tiio forehead and eyelid are usually unaffected,
except when the disease is the result of a lesion of the pons which affects
the courae of the facial nerve on the peripheral side of the facial nucleus.

DISEASES OF THE MOTOB NEBYES.

b. The electrical excitability is unchanged or is even increased for a
few days.

c. There is usually paralysis of the limbs on the same side^ except in
certain cases of pons lesion, in which the limbs are paralyzed on the
opposite side of the body,

d. According to Strauss, the secretion of perspiration after sub-
cutaneous injections of pilocarpin is unaffected on the paralyzed side
in central facial paralysis, but is delayed and diminished in peripheral
facial paralysis.

The following anatomical details must be considered with regard to
the situation of the paralysis (vide Fig. 6):

1. In paralysis whose causes are outside of the stylo-mastoid foramen,
the symptoms will consist simply of paralysis of the facial muscles
<yide Fig. 6, 1).

Fio. 6.

f0jm so'-

Schematic representation of the course of the facial nenre.
/c, tmnk of facial nerve; ac, trunk of acoustic nerve; naj, internal auditory foramen; Gf,
geniculate ranRlion;p«m, nervus petrosus superflcialis major; «<p, stapedius nerve: eht, chorda
tjmpani: fit, styloid foramen; nap, post, auricular nerve; bv and rth, nerves to the dicrastric and
i^lohyoia muscles; trg, trg', trg", trg"\ trunk and the three branches of the trigeminus; Otp^
sphenopalatine ganglion ; Ig, lingual nerve.

2. If the cause of paralysis is situated in the lower part of the Fal-
lopian canal, but below the point of departure of the chorda tympani,
the paralysis of the facial muscles is associated with paralysis of the
muscles of the ear and the occipitalis muscle, which are supplied by the
posterior auricular nerve (vide Fig. 6, 2).

3. If the lesion is situated within the canal between the origin of the
stapedius and chorda tympani nerves, we will find: paralysis of the
facial muscles, the muscles of the ear and occipitalis, disturbances of
taste and salivarv secretion (vide Fig. 6, 3).

4. If the lesion is situated between the ganglion geniculatum and

12 DISEASES OF THE MOTOB NEEYES.

the origin of the stapedius nerve, the symptoms produced are: paralysis
of the muscles of tne face, external ear, and the occipitalis, distiirb-
ances of taste, salivary secretion, and audition (vide Pig. 6, 4).

5. If the lesion is situated immediately above the nervus petrosus
superficialis major, or at the ^nglion geniculatum itself, paralysis of
the palate will l>e associated with the symptoms mentioned m the pre-
ceding section.

6. If the lesion is situated above the ganglion geniculatum and in the
intracranial portion of the nerve, disturbances of taste will be absent,
but paralysis of the facial muscles, occipitalis, external ear muscles, dis-
turbances of hearing and salivary secretion, and palatal paralysis will
remain. In this form of disease, the adjacent nerves are often paralyzed,
for example, the abducens, and particularly the acoustic.

V. Progkosis. — The prognosis depends in the first place upon the
cause. If the latter cannot be relieved, there is no hope of recovery of
the paralysis. Paralyses of the facial nerve which occur during delivery
recover spontaneously in one to two weeks, and rarely interfere with
nursing.

As a general thin^, the prognosis is more favorable in young persons*
Above all, however, it depends on the condition of the electrical excita-
bility (vide page 7).

VI. Treatment. — Causal treatment should first be instituted. For
example, syphilitic lesions must be treated with mercury and iodine.
Compressing tumors and abscesses must be treated according to surgical
principles. In rheumatic facial paralysis we may recommend hot baths
and iodide of potassium ( 3 iij. : z vij., one tablespoonful t. i. d.).

Local treatment must also be adopted. Not much can be expected
from applications of iodine, leeches, etc. Good results are said to have
been obtained from subcutaneous iniections of strychnine in certain forms
of paralysis, especially after diphtheria. But real benefit is obtained
from electrical treatment alone. However, our hopes must not be pitched
too high, since the anatomical changes in the nerve and muscles will run
their course despite all treatment. It appears possible to shorten the
duration of the disease only in so far as tne electrical treatment of the
nerves may hasten the removal of the products of infiammation, and
the direct stimulation of the muscles counteracts the atrophic changes.

If the paralysis is situated in the Fallopian canal or the intracranial
portion of the facial nerve, the galvanic current should be passed trans-
versely through the head, the anode being placed immediately in front
of the mastoid process on the affected side, the cathode on the correspond-
ing part on the opposite side. Each sitting should last two to five min-
utes, and be repeated three to four times a week. The current should
not be strong enouffh to produce pain or vertigo.

If the paralyzed muscles react to the faradic current, this should be
applied to each individual muscle, so that the latter undergoes several
successive contractions. The indifferent pole is applied to the sternum,
the other to the motor points of the muscles (vide Fig. 3). The electrode
applied to the motor points should be small, thoroughly moistened, and
firmly applied. Strong currents must be avoided, since they are apt to
give rise to electrical contracture of the muscles and serious deformity of
the face. The duration of the entire sitting should not be longer than
three or five minutes. Some physicians recommend the application of
the faradic current even if the paralyzed muscles have lost their faradic
excitability. In such cases we prefer the galvanic current. The indif-

DI8SABE8 OF THE MOTOB NEBYES. 13

ferent pole (preferably the anode) is applied to the sternnm, the cathode
is drawn across the individual muscles (so-called labile application). If
the faradic irritability of the muscles returns as the paralysis improves,
we may use the faradic and galvanic currents alternately.

In old cases of peripheral facial paralysis, Rosenthal recommended intra-buccal
galvanizatioQ, t. e., the anode is placed on the mucous membrane of the cheeb,
the cathode externally upon eacn individual muscle. Landois and Hosier em-
ployed the simultaneous application of the galvanic current to the nerve and the
faradic current to the muscles.

If contractures and spasmodic twitchings persist in the muscles after
peripheral facial paralysis, we may endeavor to relieve the contracture
oy the application of stabile constant currents (one pole on the mastoid
process, the other fixedly on the pes anserinus or the individual
muscles). Stretching or massage of tne contractured muscles may also
be recommended. Many patients attempt to relieve themselves by intro-
ducing small globes between the cheek and jaw. Myotomy and tenotomy
of the shortened muscles have been occasionally resorted to, or the attempt
has been made to compensate for the facial deiormity by producing vig-
orous faradip irritation and electrical contracture of thenealthy muscles.

2. Motor Trigeminus Paralysis.
{Paralysis of the Muscles of Mastication.)

1. The third branch of the trigeminus contains only motor fibres.
These form a separate nerve root at the point at which the trigeminus
emerges from the brain near the anterior border of the middle peduncle;
this root is smaller than the sensory trigeminus root, and is usually situ-
ated immediately in front of the latter. The inframaxillary branch
leaves the skull through the foramen ovale to pass to the muscles of
mastication — the temporal, masseter, external and internal pterygoids,
mylo-hyoid, anterior belly of the digastricus, tensor tympani, and spheno-
staphylinus.

JPeripheral paralyses in the distribution of the third branch of the
trigeminus are exceedingly rare. During its extracranial xjourse the
nerve is situati>d so deep that it is with difficulty accessible to refrigera-
tory (rheumatic) influences. Furthermore, tubercular, syphilitic, or
other diseases of the sphenoid bone are so uncommon that they are only
exceptional causes of paralysis. Tlie most frequent causes of peripheral
paralysis of this nerve are intracranial diseases — meningitis, syphilitic
changes, tumors, and aneurisms. At the same time, the first and second
branches of the nerve are often implicated, and the disease often extends
to adjacent cerebral nerves — for example, the facial or abducens.

2. In the disease under consideration there is loss of power in the
muscles of mastication. During this act, the projection of the temporal
and masseter regions remains absent, and upon applying the fingers we
miss the hard swelling which is usually felt over the contracting muscles.
On account of paralysis of the pterygoids, the jaw is defiected toward
the paralyzed side during each movement of mastication. The patients
are unable to move the jaw voluntarily towards the healthy side. They
attempt by the aid of the tongue to push the bolus of food between the
jaws on the unaffected side.

Changes in the position of the palate and auditory disturbances on

DISEASES OF THE MOTOR NEHTES.

account of the paralvBia of the spheno-staphylinus and tensor tympani
muscles are conceivable, but have not been recognized with certainty.
According to Lucae, paralysis of the tensor tympani is shown by the
fact that the patient hears a low murmur subjectively, but is unable to
recognize low notes objectively.

There are usually disturbances of sensation. These may be confined
to the third branch, or affect all branches of the trigeminus (vide article
on Aneesthesia of the Trigeminus).

The electrical reactions of the paralyzed ranscles correspond to those
observed in ordinary peripheral paralysis. Little Is known concerning
the reaction of the paralyzed nerve, on account of its deep situation.

Atrophy and contracture of the musclea may develop after paralysis
of long standing. The lower jaw is then drawn strongly upwards.

M. tetn^rElI&

fif the paralysis is bilateral, the lower jaw drops and is immovable.
This is often noticed during the final agony.
3. The treatment must be etiological and local. The former depends
Qpon the causation, the latter consists of electrical applications. If the
disease is the result of intracranial lesions, the constant current should
be passed transversely through the skull. In addition, applications
should be made directly to the paralyzed muscles. The motor points
are shown in Fig. 7,

3. Paralysis of the Spinal Accessory Nerve.
1. The spinal accessory nerve is composed of numerous nerve roots,
of which the lowermost may be followed into the spinal cord to the

DISSABBB OF THB HOTOB NSBVSS. lb

level of the sixth and eeyenth cervical Tertebr», while the uppermost
emerge from the medulla oblongata. After the roots hare anited into
the trunk of the nerve, they leave the skull through the jugular foramen.
The nerve then divides into an anterior, internal branch, and a pos-
terior, external branch. The former joins the pneumogastric, and passes
into the recurrent lairngeal, pharyngeal, and cardiac branches of the
vagus. The external branch snpphes motor fibres to the stemomastoid
and trapezius. These muscles also receive motor fibres from the cervical
plexus. According to Bernard, the external branch of the spinal ac-
cessory is composed chiefly of fibres of spinal origin.

The E^mptoms of paralysis of the nerve are most distiact when the

Motor polDta of the (tcrncmutold mad (rttpeiliu muaclea

external branch is alone aSected; that of the internal branch will not
be considered here.

The causes of peripheral paralysis of the estemal branch include:
cold, wounds, tumors, and abscesses in the nock, diseases of the cervical
vertebne, rarely intracranial lesions.

3. In unilateral paralysis of the stemomastoid muscle, the head is
held somewhat obliquely (caput obstipum paralyticum). The face looks
towards the paralyzed side; the chin is turned towards the same side,
and is directed slightly upwards (unopposed action of the healthy
muscle). Passive motion of the head from before backwards is possible,
bnt the active motion is performed only with the aid of auxiliary
muscles.

If the paralysis has lasted a long time, the muscle undergoes in-

16 DISEASES OF THE MOTOB NEBYES.

creasing atrophy. The healthy sternomastoid undergoes permanent
contraction, and caput obstipum spasticum gradually develops.

When both muscles are paralyzed, the head is held straight, but its
motion backwards and upwards is rendered yery difficult, and the pro-
jection of the muscle on each side of the neck remains absent.

in unilateral paralysis of the trapezius, the scapula is lower on the
paralyzed than on the healthy side. It is also farther removed from
the spine, the upper inner angle being farther remoyed than the lower
ang]e. The weight of the arm draws the upper outer angle of the
scapula forwards and downwards, and this effect is increased still more
by the contraction of the leyator anguli scapulsB and rhomboid muscles.
The supraclavicular fossa is unusually deep. The raising of the shoulder
is interfered with, and also the approximation of the scapula to the
spine. Eieyation of the arm above the horizontal is also interfered
with, because the scapula is imperfectly fixed upon the thorax.

In bilateral paralysis of the trapezii, the back appears unusually
broad and curvea. The head is usually inclined towards the chest.

In combined paralysis of the sternomastoid and trapezius, the symp-
toms include all those described aboye.

If the trunk of the nerye is paralyzed, the symptoms of paralysis of
the palate and of the recurrent laryngeal nerve are superadded (vide
Vol. I., page 196). Increased frequency of the pulse has been obsenred
in bilateral paralysis of the nerve (the cardiac branches of the yagus are
derived in part from the spinal accessory).

The electrical reactions of the paralyzed nerve and muscles corre-
spond to those described with regard to facial paralysis.

3. Treatment includes the removal of the cause, and the application
of electricity. If the disease is the result of intracranial causes, the
galvanic current should be passed transyersely through the skull; in ad-
dition, electricity should be applied to the paralyzed muscles. The
motor points and the superficial course of the nerve are shown in Pig.
8. Orthopeedic measures and myotomy are indicated in old cases, asso-
ciated with contracture.

4. Paralysis of the Hypoglossal Nerve.

( Olossoplegia, )

1. The hypoglossal nerye emerges from the grooye between the
olivary body and pyramid — the prolongation of the anterior lateral fur-
row of the spinal cord. After tne roots haye united into a trunk, the
latter passes through the anterior condyloid foramen, and is distributed
to the tongue muscles (hypoglossus, genioglossus, styloglossus, lingual^,
to the geniohyoid, omohyoid and sternohyoid, and to the sternothyroid
and hyothyroid muscles.

In unilateral paralysis of the hypoglossus, the tongue, when protruded,
deviates to the paralyzed side, on account of the unopposed action of
the normal genioglossus muscle. The paralyzed half of the tongue is
more deeply furrowed, and often presents lively fibrillary contractions ;
it often undergoes atrophy, after the paralysis has lasted for some time.

The disturbances in the movements of the tongue are especially
noticeable in mastication and talking. The formation of the Dolus is
imperfect, and particles of food often remain upon the paralyzed side.
On account of the diminished mobility of the bolus in the mouth, many

DISEASES OF THE MOTOB NERVES. 17

ipationts complain of diminished gustatory Bensation. The tongiie nor-
mally BBparatea the buccal from the pharyngeal cavity during dogluti-
tion. This is imperfectly effected in paralysis of the tongue, so that
food and drink regurgitate into the buccal cavity during deglutition.
For the same reason the patients experience difficulty in swallowing
saliva, and often expectorate it.

In some cases the chief symptom is difficulty in the articulation of
lingTials, /, «, sch, and also of k, g, ch, r. «, s, f. Ringing {the produc-
tion of high and falsettn notes) is also interfered with, hecanse those re-
quire associated movements of the tongue.

In bilateral hypoglossal paralysis, the tongue is motionless in the
buccal cavity, and the disturbances of speech and mastication become

U stemoiiyoidetii.
M. oraobyuiJsuB.

U. fitemoUtj-reaUetu.

iws almost uninterruptedly from

The electrical reactions are the same as in other peripiieral paralyses.

2, Peripheral paralysis of tho hypogloasus is rare. Gendrin reported
a case in wnich the nervo was compreased by hydatids within the condy-
loid foramen. Weir Mitchell observed it after a gunshot wound. It
has also been observed as the result of operations or the growth of
tumors.

3. 'i'reatment consistH in tho main of the application of electrioity.
The moior points of the musclBS are shown in Fig. 9; the peripheral
trunk of the nerve is found immediately above and behind the greater

licomu of tho Lyoid bono. In addition, electricity may be applied di-

18 DISEASES OF THE MOTOR NEBYES.

rectly to the tongue. The most suitable electrode for this purpose is
the one depicted in Vol. I., Fig. 50. In galvanization of the trunk of
the nerve, the cathode is applied to the point shown in Fig. 9, the anode
to the back of the neck.

6. Paralysis of the Radial Nerve.

I. Etiology. — Among the peripheral paralyses of the nerves of the-
arm, that of the radial nerve occurs most frequently. Its long and su-
perficial course makes it easily accessible to rheumatic and traumatic in-
fluences. The most frequent cause is traumatism; cold (rheumatic or
refrigeratory paralysis) is a rarer etiological factor. Isolated radial par-
alysis is observed not infrequently in hysteria and lead poisoning, but it is
not probable that this is the result of peripheral disturbances.

The disease also occurs after infectious diseases (typhus fever, acute
articular rheumatism). In rare cases it seems to be the result of over-
exertion of the muscles supplied by the nerve.

The most frequent form of peripheral radial paralysis is the so-called '* sleep ^
paralysis. It develops in individuals who, while drunk or worn out, have fallen
asleej) in a position in which thev pressed upon the outer surface of the arm and
with it the radial nerve, especially at the bend in its course. The patients some-
times fell asleep with the head resting on the arm, and the latter pressing upon
the sharp edge of the bed, etc. ; sometimes the arm was drawn alongside the
chest, and the protracted lateral decubitus and weight of the body produced the
compression; or the arm was drawn up under the head. The paralysis is more
frequent on the right side, because most people are accustomed to sleep upon the
right side of the TOdy. The more profound the sleep, the greater the danger of
paralysis. It rarely occurs after natural sleep at nignt, but usually in drunkards
or in laborers who take a short nap at noon. The paralysis is usually present on
awaking, in rarer cases the patients first complain of numbness and tingling in
the forearm, and this is followed in a few hours by paralysis. The triceps and
the cutaneous sensibility of the arm and forearm are unaffected, because the com-
pression generally takes place below the point at which the nerves to these parts
are given off. If the pressure has been produced upon the upper third of the
dorsal surface of the forearm, the supinator longus will not be pandyzed.

Crutch paralvsis is the term applied to that K>rm of the disease which results
from using poorly fitting crutches. It sometimes develops within a few hours after
first using the crutches, sometimes after the lapse of days and weeks. The radial
nerve is generally paralyzed on the side corresponding to the disease which ne-
cessitated the use of crutches. The paralysis sometimes occurs unexpectedly,
sometimes it is preceded by parsBsthesia. The ulnar and median nerves are often
also paialyzed to a less extent. The radial nerve is affected mainly or exclusively
because it is situated more posterially and inferiorly than the other nerves of the
brachial plexus and is thus especially accessible to the pressure of the crutch.

Prisoner's paralysis is the term applied by Brenner to cases in which prisoners,
whose arms are tied behind them, simer from compression and paralysis of the
radial nerves. Radial paralysis also occurs frequently in Russia in infants and
coachmen; in the former, on account of the custom of tying the arms firmly to
the chest and then laying the children on the side; in the latter, from the habit
of tying the reins tightly around the arm.

Water carrier's paralysis is produodd by carrying very heavy pails of water in
such a manner that the arms are placed under the handle, and the pail rests
upon the anterior surface of the chest and abdomen. The handle is, tnerefore,.
very apt to compress the radial nerve.

Traumatic radial paralyses also include cases which are the result of a blow,
fall, incised or gunshot wounds, fracture or dislocation of the humerus. In such
cases other nerves are also affected. In cases of fracture, the nerve may be di-
rectly injured by fragments of bone or by excessive growth of callus. This is
most apt to occur in fracture of the lower third of the humerus.

II. Anatomical Changes. -—We are justified in assuming the same

DISEASES OF THS UOTOB XSByES.

coDditious in the nerve and fiiueclea that have been described in the
section on facial paralyeis. Bernhardt reported a case, after typhus
fever, in which there was a nenritic swelling, three centimetrea in length,
in the course of the nerve. Above this point the nerve fibres were in-
tact, below thev were destroyed. The muscles innervated by the radial
nerve presented a considerable proliferation of nnclei and indistinctness
of the transverse striation.

III. Stuptoub. — Peripheral paralysis of the radial nerve may be
manifested by disturbances of motion and sensation. The former are
more striking and constant, the latter may be entirely absent.

a branch from the radial

nerve and also* from the nervus perforana Gasserii.

The posterior superior cutEuieous braoch BuppUes the poaterior auifaoe of
the arm as for as the elbow joint, the inferior poaterior cutaneous nerve
supplies tha extensor aapect of the forearm as far as the wrist. The terminal

■••«

- T.h -

• '

t* i*mr3b-.i-.

r*.*- ■

- -.; -»-r- r-- ii..- :.

r-:..:. zr '>}•

ji-«.;-'

•■».■-

91: . an. inrmiciKtMSA. Sneethe
r:r:7iHT d* the point of 4a«&

.^-t -

^Vi__ 1

••■ •>•;

iU^ ^

DIBEABB8 OF TUB HOTOK NEBTES. Si'

tnrbADoes may be absent, becanee other nerves act ricarioasly for those
in which conduction is interrupted.

Vaso-motor diBturbances, viz., diminution of temperature and livid
color of the akin, are occasionally observed.

Thickening of the joints of the fingers and hand, and nodnlar thick-
enings on Che extensor tendons (tenosjnitis hypertrophica of Gubler) may
also occnr, but their mode of origin is unknown. Atrophic changes de-
velop in the mtiBCles if the paralysis lasts a long time.

The electrical reactions of the nerve and muscles are the same, in
general, as in peripheral facial paralysis. In "sleep" paralysis, the elec-
trical irritability of the peripheral portion of the nerve is almost always
retained, and often increased. Irritation of the central end produces
no effect, so that the site of the lesion can thns be determined with
accnracy.

In one case Fischer noticed increased mechanical irritability of the
tnnscles.

The dnration of the disease varies extremely. Cmtch paralysis nsa-

is muulo nippUed br It.

MotorpoliiHottbenill&l nerreuid tk

ally recovers most rapidly. Sleep pamlyses generally require four to six
weeks before recovery is established.

IV. D1AONOBI8.— The peripheral character of the paralysis is nsually
evident from the fact that the radial nerve alone is paralyzed. But
Baynaud described a case in which a solitary tubercle in the fissare of
Kolando at the origin of the second frontal convolution gave rise to
isolated paralysis of the radial nerve. Apart from the rarity of such
cases, the penpherat nature of the cause iu this disease is usually evident
from the previous history, the objective changes, and electrical exami-
nation. Lead palsv of the radial is usually bilateral, the supinators are
almost always unaffected, and, as a rule, other symptoms of lead poison-
ing have been present. The situation of the lesion will be easily recog-
nized from the number and grouping of the paralyzed muscles, the
sensory disturbances, and particularly from the electrical examination of
the trunk of the nerve.

y. Proonosib and Tkeatuent. — The prognosis is usually good,
and the hope of recovery should not be abandoned even if the paralysis
has lasted a long time.

\ »

'. ... .

' \ I III II

•vxV V*t!* OK TUB MOTOB XEKVES.

: i viviit lu» ilinKJted toward the removal of the canse.

. 'v\UM* Mttiii^ crutches ehoiild ht? worn; diglocationa

l'w iu»i'\i» irt compressed bv c-illiis.the latter must be

I ■ \\» Hviul; if a ciciitrix has formed in the nerve as the

^. luu^t bo excised and the ends united with sutures^

i n. v«\»u«iidlH exclusively of electrical applications. The

V .)iK^\\ w \i\ Ki^. 13. Remak recommended the use of gal-

i.i.ls \\\Mi\\ the site of lesion, the anode tipon an indmer-

I . 1 iiuu\), iMirrent of moderate strength. The faradic cur-

, .i'*'i >i\ applii'utions to the muscles; three to four sittings

\ litm^ inrou to five minutes.

li. I'arnlystif of the Mediaii Xerve,

.4..i..i.i\ IVripheral paralysis of the median nerve is much
. I *> ki A (hn radial nerve. In the majority of cases it is trau-
\\» liniii^ injured, as a rule, in the forearm (not inf re-
in w I mIol.V above the wrist) by stab or incised wounds, ete,
II., . > ^. .1 mu-atiiniiaily after unskilful venesection at the bend of the
". ., ».i|ui\ li\ nieces of glass is relatively frequent.

\y)x ..n iiio pHmlyHis of this nerve is rare. The disease is observed

.. .llv uFliu- acute infectious diseases (variola, typhoid), and also as

>>■[ ii ii\iuritis.

1 1 .^xii'i\i\is AND DiAoyosrs, — If the lesion is situated imme-

!, .Ji..\o lilt' wrist, the paralysis is confined to the muscles

I I, ». ill i.|' I bo lliunil) (abductor, ilexor, and o]>ponens pollicis brevis);

. ». 4 i.ltii iiM iHiiiicis brevis esnn)es beciiusa it is supplied by the

I II. I u^ In atidition, there is paralysis of the first and second

. ,..,I.M. iloi. If the lesion is situated higher, there is also paralysis of

I. I... I t jiarl i»f llie volar muscles of the forearm, viz., pronator* teres,
.!i .1 ..u|ii ladialis, ))alniaris longus, the superficial and deep flexors

I I, ,1 „i It rri>o branches from the ulnar nerves), flexor longus pollicis
.t I I • u.^toi niiatlratus.

I'.M.Jv .11 ui I lie lloxor di^Mtorum sublimis causes inability to flex the

1. I i.Knlanui's; as the result of j)anilysis of the deep flexor, the termi-

. .1 ,.l..il.iu\ of Ihe soi'oihI, and often of the third linger cannot be flexed.

I I., in l |.halaiiges are flexed by the interossei, wliicL also extend the

. .1, I .indiiiinl phalanges (innervation from the ulnar nerve). Excessive

,. (i,.n III' the interossei sometimes i)roduces hyperextension of the

.1. I .iiid I bird phalanges, and a sort of subluxation. Volar flexion of
,1, ». Ml. I II inipaired;it is elTected by the ulnaris internus. If the forearm
. .1 iidod, pronation cannot be performed: when flexed, it can be pro-
n.i. I imjn rfoetlv by the aid of the su])inator longus.

|'..i,ih..is t>f tlie muscles i»f the ball of the thumb incapacitates the
ii,.,ii.i> h\iiii all delicate manipulations. Its phalanges cannot be flexed,
..III III » luuveineiit of opposition cannot be effected. The non-paralyzed
a. him iiii pollicis (supplievl by the ulnar nervel draws the thumo against
iKii iiulev Ungcr, and the extensors flex it srronglv towanls the dorsum.

•iiMioiv disturbances may Ive* entirely absent \>ecause the cutaneous
iii.iiH luH of the ulnar and radial nerves vieariously |>erform the function
..r IhiMiioilian. In otlier cases there is loss of sensation on the radial
\\^^^t of tho palm of the hand as far as the median lir.e of the f»>nrth
Uugoi. anil on the dorsal surface upon the terminal phalanges of the

DISBABBS or THE UUTOB KSBTBS.

thumb aud second and third fingers (vido Figs. 10 and 11). The auiea-
tbeaia is often moBt marked on the tij) of tlic Index linger.

Trophic dieturbances occur witli relative frequency. The affected
fingers have a peculiar smooth and shining appearance (glossy skin), and
the hairs arc uausuulty long and abundant; the nails become thickened
and distorted and exfoliate; pempbigua-like resiclesaad nlcoratious may
form upon the terminal phalanges.

Atropliy of the muscles often develops after the paralysis has lasted
a long time.

flexor (llKJt. commita. prafundu

I Flexor iiT^TL°eu.
Flexor pt

polllc. brei.
OpponenB polllcia.

The electrical exoitabilitv of the nerve and muscles oorresponda to
that uaaally observed in peripheral paralysis.

III. Peoososis Axn Treatmbxt are the same as in radial par-
I «Iysis.

7. Paralysis of Uie Ulnar Nerve.

. The most frequontcaufiu of peripheral ulnar paralysis is trauma-
; pressure of a crutch, fracture of the humerus and compressing

b gtmshot or incised wounds, etc. Compression paralysis
_ llopB after prolonged dorsal decubitus. DuchenneobserVed
Vltboare compelled to press the elbow for a long time against

OUAUS or THS MOICK XXSTB.

ft 8nn w p yort. Bbevmatic or nauitiic jttaljwnt xxl thon occttr rin g
after rafectwoj diMMn, are much rarer.

2. The ajmptoiM sre mdil; interpnted. Is pmljM at Um moades
(rf the bftil of the little fin^^er (sbdoctor, Beior bran^ oppooou), the
raorementi of the little finger are alauMt entirely aboUiked. PaiwljvtoS
"" ' i aod ihixi ftod fbarth Inmbricaki c

sbolttitm of the morements of addaction and abduction. In addition,
the first phalanges canDot be flexed, and the others cannot be extended
(paralrsie of the mteroasei). As the ulnar nerve supplies the ulnar por-
tion oi the flexor profundus digitorum, flexion of tl^ two or three outer
fingera is impaired. Paraljdaof the adductor pollicia prevents active ap-
*" " ' ' the index finger. Flexion and adduction

of the hand toward the ulnar side cannot be performed if the ulnaria in-
temuB faaa been paralyzed.

If cutaneous branches of the ninar nerve are affected, sensation will
be impaired upon the ulnar portion of the palm of the hand as farae the
median line of the fonrth finger. Upon the dorsal asnect cutaneous
SeneibUit; ia aSocted aa far as the median line of the midale finger (vide

DUXASKB OF THE MOTOR HEBTE3. 25-

Figs. 10 and 11). Sensory distarbances may be entirely absent on ac-
count of the Ticarioaa action of other nerves of the arm.

Trophic disturbances, on the whole, are rare. After long dnration
of the disease, muscular atrophy sets in, especially in the ball of the
little finger and the interosseous spaces. The hand not infrequently
aaanmes a peculiar shape, which is kno vn as the claw hand. On account-

in, ad sd Uld Mb InlflTOBHi.

Tbe MiBO Dorul surface al tbe Brm.

of the paralysis of the interosaei and Inmbrioales, the extensor digitomm
communis becomes oxceasiTsly contracted, and the first phalaneea are
flexed 80 strongly towards the dorsum that they become slightly
luxated. At the eame time, the aecond and third phalanges are strongly
fiexed by the action of the flexors, so that the tips of the fingers are im-
bedded in the palm of tbe hand (vide ligs. 16 and 16). These changes-

UUMUlO^CUtlUMIOl

Motor polnM o( the muaoul»ciiuuiBou( oerre >n J Uxi

are especially marked in the fourth and fifth fingers, because the first

and second lumbricales (aecond and third fingers) are supplied by ths

median nerve.

The electrical reactions are the same as in other peripheral paralyses,
3. The treatment ia the same as that of radial paralysis. The motor

points are shown in Figs. 17 and 18.

>il>

muKAfiEe OF TS£ MOTOB KEBTBL

I of ike Jluscuio-Cutatiwuk Siarve.

I ii'liiltit iii't'iplu-ral paralTsia of thie nerre is TStjiBra, md it £C)IH
'I--H. i.-i ii|iLi uvL'ii iu <x»nibmed paralyaiGof thenerreBof the arm. £rb
,, .j(. I rl jdi'lui'il ijurulviiu! of the nerre after extirpatios of a tanuv in
ji. . i,Mi,i> lukii.'ulur fowa. The motor distDrbaQces prodnoed are paraly-
1 . ,1 fill' liii I'jti-, oKwxibnicbialiE. aad brachialiE intemng: bat the latter
,.,., i> 1,1 iilixi bii^iijlitid by the radial oerve. The forearm can be flexed
I jliijii;il'u:Liy <tf not ut all upon the arm. Tbis is most marked in
. ..,F)fi,il|iiii Iff IIju forearm: iii prooatJon. the BDpinator longni aids in
^ V||i|j lli>i furuuriu. Any lu-rieory digtnrbances which majbe preaent
■'i, . l'iilHi>i upnii tlic' radial eurfitcc of the forearm (ride Figa. 10 and 11).

'J, I'aralyiif of Hu Azillari/ Xerve.

)'i:i puliui'ttl iMralyniii uf t)i« asiUarj nerve is most freqaentlj of tnui-
(•.■i|i<; fllKiUi but wwral caoeu of rbenmatic paialvms hare alto been de>

Bncbi^ pWiiu.

Nt>t itifretpiently it follows ludami
botau^U th« iudaiDQialiou oitond:

ttiou of the shoulder joint,
to the axillanr nerre and

{ivivt Tw lu utjuriiij-

'I'lm uu'tur diiiiubaucoi oouiist »iuplv of low of fiiuotion of the del-

i..il| iiiit^i;lv, a> that itua pattuut i* uuaW to lift th* arm to the hori-

DISEASES OF THE MOTOB NEBYES. 27

2ontal. The teres minor may be afFected, but no noticeable symptoms
are thereby produced. After paralysis of long standing, the deltoid
undergoes atrophv^ a deep horizontal furrow^ is felt and seen beneath the
acromial end oi the clavicle, and the head of the humerus is excessively
movable in its socket. Sensory disturbances may be found upon the
external and posterior surfaces of the arm (vide Figs. 10 and 11). The
motor point is shown in Fig. 20.

10. Combined Paralysis of the Nerves of the Arm.

Peripheral paralysis of several nerves of the arm occurs not infre-

Juently, but, as a rule, that of one nerve, particularly the radial, pre-
ominates. This form of disease is to be expectea if the cause of
paralysis is located in the brachial plexus. Seeligmueller claims that
paralysis of the plexus is often associated with disturbances of the sym-
pathetic, contraction of the palpebral fissure and pupil, and abnormal
redness of the skin. From the previous remarks on paralysis of the
individual nerves, we can readily determine what nerves are affected in
each case.

Traumatism is an unusually frequent cause of combined paralysis of
the nerves of the arm. This includes dislocation of the nead of the
humerus (especially subcoracoid dislocation), fracture of the humerus
or clavicle, a blow or fall on the shoulder, more rarely incised or gunshot
wounds in the lower part of the neck. The disease has also been ob-
served as the result of the use of crutches, and of tumors in the neck.

A special form of disease is that in which the paralvsis is confined to
the deltoid, biceps, brachialis anticus and supinator longus, and occa-
sionally involves the infraspinatus, supraspinatus, and supinator brevis.
Erb showed that these muscles can be made to contract oy placing one
electrode of a faradic current alongside the transverse process of the sixth
•cervical vertebra about two to three centimetres above the clavicle, and
a little behind the external border of the sterno-mastoid (vide Fig. 20^.
Hence the nerves supplying the muscles in question must be situated in
olose apposition at this locality (Erb's supraclavicular point)/ This
form of paralysis may be the result of rheumatic causes, tumors in the
neck, injury to the shoulder, and parturition.

Duchcnne applied the term parturition paralysis to those cases of
combined paralysis of the nerves of the arm occurring in the new-born
BA the result of difficult labor. The paralysis usually follows luxation or
fracture of the humerus, fracture of the clavicle or scapula, more rarely
direct compression of the plexus. These accidents may happen during
version, application of the forceps, application of the hook, etc. It is
doubtful whether the disease may occur during natural labor if the pel-
vis is narrow. The paralysis should not be mistaken for separation of
the epiphysis of the humerus.

Combined paralysis of the nerves of the arm may also be the result
of fractures and dislocations of the lower end of the humerus or radius,
the application of tight bandages, etc.

11. Peripheral Paralysis of the Nerves of the Scapula and Trunk.

a. Peripheral Paralysis of the Serrattis Magnus.

I. Etiology. — The serratus macnus is supplied by the long thoracic
nerve. On account of the long and superficial course of the nerve, the
muscle is frequently paralyzed.

28 DISEASES OF THE MOTOR IHEBVES.

Among the causes are rheumatic influences, and still more frequently
traumatism (fall, blow, incised wounds, surgical operations, carrying
heayy loads on the shoulder, etc.)* In not a few cases the disease is the
result of oyer-exertion of the muscle, for example, in sawing, mowing,
etc. Seeligmueller observed paralysis of the left serratus magnus in a
feeble nurse who over-exerted herself in carrying a heavy child. It some-
times develops after infectious diseases, particularly typhoid fever, but
also after dipntheria.

Tiie right serratus is more frequently affected. The disease is much
more frequent in males than in females ; it is rare uuder the age of
fifteen years.

II. Symptoms. — The symptoms consist chiefly of changes in the po-
sition of the scapula, which are noticeable during repose, but are much
more marked when the arm is raised. As a rule, tney develop slowly,
and are usually preceded by pains in the supraclavicular region and top
of the shoulder (implication of cutaneous branches of the brachiiu
plexus). After the paralysis appears, the primary neuralgia not infre-
quently gives way to cutaneous ansssthesia.

When the arm is dependent, the inner border of the scapula is more
closely approximated to the spine than on the healthy side, and the
lower angle of the bone is separated from the trunk to an unusual degree.
At the same time the lower angle is nearer the spine than the superior in-
ternal angle, and accordingly the superior external angle is abnormally de-
pressed. This is owing to the fact that, on account of the serratus par-
alysis, the trapezius, rhomboids, and levator anguli scapulsB assume the
upper hand, and draw the scapula towards the spine. In the same way,
the pectoris major, biceps, and coraco-brachialis lift the lower auRle
of the bone away from the trunk. The contracted rhomboids and le-
vator anguli scapulas are not infrequently visible beneath the skin as
more or less thick strands between tbe scapula and spinal column. If
these muscles are also paralyzed, the change in the position of the scap-
ula is lessened. Nor must it be forgotten that primary contracture of
these muscles may produce the same position of the scapula as is seen in
serratus paralysis, except that, in the latter, passive movements of the
scapula are readily performed.

The changes become more marked when the arm is raised in front.
The scapula then approaches the spine still more closely, and together
with the lower angle of the bone is separated very markedly from the
surface of the thorax (vide Fig. 21). The patients are unable to raise
the arm slowly and steadily above the horizontal, because this movement
requires rotation of the scapula by the serratus magnus. Elevation of
the arm to the vertical position becomes possible if the scapula is

S)ushed forwards passively, and its edges are pressed against the thorax.
$ome patients are able to raise the arm to the vertical by a swinging mo-
tion. The power of crossing the arm, or pushing it forwards, is also
lost, since these movements are effected by the serratus. The patients
are unable to offer any resistance to passive retraction of the scapula.

The electrical changes are similar to those observed in other periphe-
ral paralyses. The motor points are shown in Fig. 20. The nerve is
also readily reached in the axilla. If the muscle undergoes atrophy af-
ter paralysis of long standing, the digitations of the muscle, which are
readily seen on the healthy side when the arm is raised, disappear and
the lateral surface of the thorax is flattened.

J. Paralysis of the Pectoralis Major and Minor, — Both muscles are

DISEASES OT THE MOTOR SESVES.

8'jpplied by the anterior thoracic nerreB, They are very rarely paralysed
aloue. Such an isolated paralysis would be shown by the impairment or
abolition of abduction of the arm against the trunk, and- inability to
resist passive abduction of the arm. The patient is also unable to place
the hand of the paralyzed aide upon the opposite shoulder. If the mus-
cles undergo atrophy, the iufraclavicular region will be unusually flat.
The motor points are shown in Fig, 20.

c. Parah/siif of the Rhomboids and Levator AnguU Scapula}. — These
muscles are sup))!'^'^ '*? the dorsalis scapula nerve. Isolated paralysis of
the muaclcH will produce no special symptoms. If the trapezius is also

^^^onl

paralyzed (ride page 16), the paralysis of the rhomboids is shown by the
inability to approximate the scapula towards the spine, that of the leva-
tor anguli scapulae by inability to move the shoulder upwards.

d. Paralynit of Ihe Lati-simua Dorxt. — Isolated paralysis of this
muscle, which is supplied by the subsoapulurnerves, ia rare. In this dis-
ease adduction of tnearm against the trunk is diminished, the raised
arm can be drawn downwards with less force, and the band can with dif-

,lty be carried towards the buttocks. Rotation of the arm internally

80 DISEASES OF THE MOTOR KESYES.

is Tery little or not at all impaired, since the subscapular and teres major
muscles act vicariously in performing this movement.

e. Paralysis of the Subscapular and Teres Major {internal rotators
of the arm). — These muscles are also supplied by the subscapular nerves.
The predominance of the external rotators causes the arm to assume a
false position, the volar surface of the hand being directed anteriorly
and externally. Hence, manipulations of the hand upon the opposite
half of the head and body are rendered difficult or impossible, and the
patients are unable to rotate the arm internally.

f. Paralysis of the Infraspinatus and Teres Minor {external rotators
of the arm). — This form of paralysis is more frequent than that of the
internal rotators of the arm. The infraspinatus muscle is supplied by
the subscapular nerve, the teres minor by the axillary nerve. If the
arm is passively rotated internally, the patients are unable to ro-
tate it outwards. If there is atrophy of the infraspinatus, the infraspi-
nous fossa is abnormally flattened or depressed. The internal rotators
generally Lave the arm a false position, the ulna looking forwards. Paraly-
sis of the infraspinatus interferes with drawing, writing, and the use of
the needle, siuco these manipulations necessitate external rotation of the
arm.

g. Paralysis of the Extensors of the Back. — This disease is relatively
frequent after typhoid fever; it is sometimes the result of traumatic
or rheumatic causes.

In paralysis of the lumbar extensors, the chest of the patient, in
standing, is bent over backwards, while the lumbar spine presents lor-
dosis. While the patient is sitting, on the other hand, the lumbar spine
presents kyphosis, which disappears during dorsal decubitus. The
patient has a waddling gait. If he is sitting upon the floor, and
endeavors to assume an erect position, he first makes rotary movements
of the trunk, then grasps the thighs with the hands, and gradually, as
it were, climbs up his own thighs. If the muscles have undergone
atrophy, the loins are notably smaller.

In paralysis of the dorsal extensors,, the spine presents paralytic
kyphosis in the erect position, scoliosis if the paralysis is unilateral.
These changes disappear in dorsal decubitus.

h. Paralysis of the abdominal muscles is very rare. If it is unilate-
ral, the umbilicus will be drawn towards the healthy side during each
expiration. In bilateral paralysis, the patients walk with the body bent
over forwards ; in addition, there is lordosis of the lumbar spine.

Expiratory movements (coughing, sneezing, micturition, defecation,
etc.) are difficult or impossible. The abdomen appears distended.

riie treatment of the various forms of paralysis mentioned includes
the application of electricity, baths, massage, and gymnastic exercises.
In hopeless cases orthopaedic apparatus may be applied.

12. Paralysis of the Phrenic Nerve.

1. Paralysis of the diaphragm appears to be produced more fre-
quently by direct lesions of the muscle than by diseases of the phrenic
nerve. It is not uncommon in pleurisy and peritonitis, when the in-
flammatory process extends to the serous lining of the diaphragm. The
trunk of the phrenic nerve is affected most frequently by tumors and
abscesses in the neck. Eheumatic paralysis of the diaphragm has been
observed in a number of cases. Whether the paralysis occurring in

DISEA6BS OF THE MOTOfi NEBYE8. 31

lead poisoning and hysteria should be regarded as peripheral is more
than doubtfal. Oppolzer observed spontaneous paralysis of the dia-
phragm at the period of puberty.

In all these cases the paralysis sometimes affects the entire muscle^
sometimes it is unilateral or even more circumscribed.

2. The sjrmptoms are easily recognized, but it must be remembered
that the respiratory disturbances may be absent during quiet breathing.

Upon exposing the patient, it is found that the epigastrium and the
hypochondria are retracted during inspiration, and protrude during expi-
ration. If the hand is introduced beneath the thorax, it is not elevated
by the diaphragm during inspiration, and the lower border of the liver
is found to ascend during inspiration and descend during expiration.
Continued loud speaking or singing produces dyspnoea and exhaustion ;
pressing movements are also rendered difficult. The patients get out of
breath m walking, or going up-stairs, and the number of respirations
may be increased to fifty per minute. Bronchial and pulmonary inflam-
mations are extremely dangerous in this condition, because the power of
coughing is impaired, so that dangerous congestion of the lungs and
suffocation are apt to develop.

In one case Eulenbur^ noticed abolition of the reaction of the
phrenic nerve to the faradic current. Electrical examination must be
confined to the trunk of the nerve, which may be reached on the outer
side of the stemomastoid, immediately above the omohyoid muscle
(vide Fiff. 20).

3. The prognosis is always grave. Treatment consists mainly of appli-
cations of electricity, in addition to removal of the causes. Both currents
have been employed. One pole (cathode of constant current) is placed
on the trunk of the nerve, the other on an indifferent spot (sternum,
etc.), or on the hypochondrium. Contraction of the diapnragm i» .
shown by protrusion of the epigastrium, and entrance of air into the air
passages, accompanied by a movement of hiccough. Passage of the
current transversely through the diaphragm is not attended with much
success.

13. Peripheral Paralysis of the Nerves of the Lower Limbs.

Peripheral paralysis of the nerves of the lower limbs is rare; paralysis
in this locality is usually spinal or cerebral in its origin.

a. Peripheral paralysis of the crural nerve has been observed in dis-
eases and tumors of the lower part of the spine, hemorrhages near the
Cauda equina, inflammation of the psoas muscle and pelvic cellular tis-
sue, tumors of the pelvis, dislocations and fractures of the femur, in-
cised or gunshot wounds, after acute infectious diseases, etc. Paralysis
of the quadriceps femoris has been observed not infrequently in connec-
tion with inflammation of the knee-joint.

Paralysis of the crural nerve is shown by motor disturbances of the
iliopsoas, pectineus, sartorius, and quadriceps femoris. Paralysis otthe
iliopsoas muscle is shown by inability to flex the thigh upon the abdo-
men, that of the quadriceps femoris by inability to extend the flexed
thigh. These muscles are also important in walking and in passing
from the sitting to the erect position, so that these movements are
seriously interfered with when the parts are paralyzed,

Aiter paralysis of long standing, the muscles undergo atrophy, some-

VISEABZ8 OF THB MOTOB 1TBBVB8.

times to ench an extent that the anterior surface of the thigh seems to
be covered merely by the integument.

Sensory disturbanceB, when present, are found upon the anterior and
inner surface ot the thigh and the inner Burfaoe of tneleg (ride Fi^ 32
and 23). If the cause of paralysis is situated very high, other seneory
nerves may also be afiFected. In paralysis of the external cutaneous
nerve, sensation is diminished or abolished upon the outer surface of the
tliigh down to tbe region of the knee. Sensory disturbances on the
£orotum, lower part of the abdomen or loins must be attributed to

ftp

DlttrtbnttOD ot the eutueOUB n
Fig. K.— Anlerior mirfaco. 1, crur
nerre; S, eiteniBl cutuieous nerre; S, ill
inKUiud aerre; 4. lumbo-laiculak] nerre;
external spermatic Derve; S. posterior cuts
eous nerro; J.obturnior nerre; 8, mphen
major nerve; 9. comioiinlcBiui peroaeV '
■uperilcL&L perODeal nr-"*' *• '*"-" -*-'
nerre: is, co '--

M or the lower limbs. After E
Fig. S3.— Posterior si

B. obtunitor nerre; i. poacerlor median eu'
linrouanerye (peroneiw norre); S, oommunl-
cansperonel: fl, Mpbeniu major nerve (amni
nerre); ?, communicanB MUalla: S, nerrua
cutaneus planurli proprius (UbUlis); 9, pliui-
UrlBmed[u» (tibial nerre); 10, iiluibulltet*-
rails (tibial nerre).

implication of the ilio-hypogastric, ilio-inguinal, Inmbo-ingnioal, and
«ztemal spermatic nerves.

Tbe electrical reactions present no changes from the general mlee.

OIBBASBB OF THE UOTOB MBBVEB. 33

The nerve trunk can only be reached for a short distance immediately
beneath Poupart's ligament, but the masclea are more readily aocea^ible
to electrical exploration and treatment (vide Fig. Hi). In galvanic ap-
plicationa, the anode honld be applied to the loins, the catuode to the
«xit of the nervi immediately beneath Poupart's ligament.

b. Periphera- paralysis of the obturator nerve is even rarer than
that of the crunu nerre; sometimes both nerves are paralyzed. Iso-

Holor polDta ot tbe nerreg and muaclea ol Che loirei

lated paralysis of the obturator nerve has been observed after difficult
labor and in obtnrator hernia.

The motor paralysis affects all the adductors, the obturator extemne,
gracilis, and usually the pectineus, which is also supplied by the crural.
The patients are unable to move the thigh towards tne median line (par-
alysis of the adductors^. In sitting or lying, they are unable to cross the
affected leg over the nealthy one, or to turn over from the back upon
the belly, or vice versa. External rotation of the thigh is also inter-
fered witii.
3

84 DISEASES OF THE MOTOB KEBYES.

Sensory disturbances are noticed npon the inner surface of the thigh
as far down as the knee (vide Fig. 23).

c. Peripheral paralysis of the gluteal nerves is shown by motor dis-
turbances in the gluteal muscles, the obturator internus^ pynformis, and
tensor fasciae latse. There is impairment of internal and external rota-
tion, and abduction of the thigh. The patient cannot pass from a bent-
over forward position to an erect position of the body. Walking and
ascending stairs are interfered with, because it is the function of the ilio-
psoas and gluteus maximus to fix the trunk upon the thigh and main-
tain equilibrium, but on account of paralysis of the gluteus the iliopsoas
gains the upper hand and draws the trunk forward.

When atrophy of the muscles occurs, the buttock appears thin and
flattened. The motor points are shown in Figs. 24 and 25.

d. Peripheral paralysis of the sciatic nerve is the most frequent
form of paralysis of the nerves of the lower limbs. This is owing to the
long and superficial course of the nerve. According to the location of
the lesion, tne paralysis affects the entire nerve or individual branches,
particularly the peroneal or tibial nerves. The paralysis is sometimea
confined to a few of the muscles supplied by the peroneal nerve.

Diseases of the lumbar spine, hemorrhages near the cauda equina,*
fractures of the pelvis or sacrum, fractures and dislocations of the thigh
or leg, pelvic exudations and tumors, diflBcult labor, wounds, blows or
falls in the region of the buttocks, removal of tumors, tight-bandaginff,
etc., are the chief traumatic causes of sciatic paralysis, ft has been ob-
served in the new-born after attempts at extraction. Zenker and Both
have described compression-paralysis of the peroneal nerve in potato-
diggers who maintain a crouching or kneeling position for a long time.
Sciatica is sometimes followed by paralysis of the nerve. Rheumatic
paralysis is observed occasionally in individuals who are required to
stand in cold water. Neuritic and hysterical paralyses of the sciatic
have also been described.

The posterior muscles of the thigh supplied by the sciatic nerve are
least frequently paralyzed, and only when the lesion is situated very high.
The muscles in question are the obturator internus, gemelli, ouadratus,
semitendiuosus. semimembranosus, long head of the bicens (the short
head is supplied by the peroneal nerve). In paralysis of these muscles,
rotation and adduction of the thigh are impeded, and the patient is un-
able to draw the leg against the posterior surface of the thigh, or to re-
sist passive extension of the leg. The gastrocnemius (supplied by the
tibial nerve) is able to effect slight flexion of the leg. As a matter of
course, walking is interfered witn to a considerable extent.

Paralysis of the peroneal nerve, if complete, affects the tibialis anti-
cus, extensor nallucis longus, extensor communis longus, the peronei,
extensor digitorum brevis, and extensor hallucis brevis. The disease is
easily recognized. The foot assumes the varo-equinus position, and the
patient is unable to flex the foot or the first phalanges of the toes to-
wards the dorsal surface. During the attempt to walk, the foot hangs
downward so that the toes are dragged along the floor unless the
limb is unusually flexed at the hip joint. When the foot comes in con-
tact with the ground, it first touches with the tips of the toes and the
outer edge of the foot.

In isolated paralysis of the tibialis anticus, dorsal flexion and adduc-
tion of the foot are interfered with. Dorsal flexion is effected vica-
riously, in part by the extensor longus digitorum (the foot is abducted at

DISBASBS OF THE HOTOfi NEBTE8. S5

the same time); the extensor hallncis longas also aids the paralysed
muscle^ at the same time adducting the foot. But these muscles cannot
assume fully the function of the tibialis anticns, the calf-masoles acqjuire
the predominance, and the foot is drawn into pes equinus position.

In isolated paralysis of the extensor longus digitorum, dorsal flexion
and adduction of the foot are impeded. The first phalanx of the four
outer toes cannot be extended. The function of the paralyzed muscle is
performed vicariously by the tibialis anticus and extensor hallucis
longus, but eventually the flexors undergo antagonistic contraction and
the foot assumes pes varo-equinus position.

In isolated paralysis of the peroneus longus, adduction of the extended
foot is impossible. At the same time the arch on the inner side of the
foot is destroyed because the peroneus longus normally exerts traction on
the cuneiform and scaphoid bones. Pes planus paralyticus is thus pro-
duced. In walking, the patient first brings the outer edge of the foot
in contact with the floor; he complains of pain in the external malleolus^
and is quickly tired.

In isolated paralysis of the peroneus brevis, pure adduction of the foot
is impossible; this movement can only be effected if attended with dorsal
flexion (contraction of extensor longus), or plantar flexion (contraction,
of peroneus longus).

Peripheral paralysis of the tibial nerve affects the following muscles:
gastrocnemius, soleus, plantaris, popliteus, flexor longus digitorum, tibi-
alis posticus, flexor hallucis longus, flexor brevis digitorum, abductor hal-
lucis, flexor brevis hallucis, adductor hallucis, interossei, and lumbricales.
If all these muscles ure paralyzed, plantar flexion of the foot is almost
entirely abolished (effected slightly by the peroneus lon^s); plantar flex-
ion ana adduction of the toes are impossible. Predominance of the ex-
tensors gives rise to pes valgo-calcaneus.

In isolated paralysis of the gastrocnemius and soleus, plantar flexion
of the foot is markedly impaired; it is performed to a certain extent by
the peroneus longus and flexor longus digitorum.

The calf -muscles also adduct the foot, so that when they are paralyzed
the abductors also gain the upper hand. Hence pes calcaneus 'develops
with a tendency to pes valgus.

Paralysis of the tibialis posticus interferes with adduction of the foot
and elevation of its inner surface, t. e,, it favors the production of pes
valgus.

Paralysis of the flexor digitorum communis longus is shown by ina-
bility to flex the second and third phalanges of the four outer toes. Flex-
ion of the flrst phalanges is performed by the interossei, which also ex-
tend the second and third phalanges. In paralysis of the flexor hallucis
longus, there is loss of plantar flexion of the last phalanx of the great toe.
Paralysis of the interossei may give rise to the development of club-foot,
from predominance of the extensor communis and flexor digjitorum lonras.

The electrical reactions of the paralyzed muscles are similar to those
so often mentioned. More or less marked atrophy and contracture de-
velop after paralyses of long standing.

Sensory disturbances are observed not infrequently; their distribution
is shown in Pigs. 22 and 23.

Trophic changes have been described, particularly in paralysis of the
trunk of the sciatic nerve. They consist of coldness, cyanotic color of
the integument, rapidly developing decubitus over the malleoli, heels.

86 pmKABBa or thb hotob itkbtis.

ImttoekB, Bod trochanters, increased growth of hair, thiekening of the
nails, pemphigoid Tesicles, eto. ParsathesisB have alio been obBerred.

The diagnosis of paralysis of the sciatic nerve is not always easy; it
lunst be ba^ on sccnrate anatomical and physiological kno viedge, atrict
analvsis of the individual symptoms, and careful electrical exploration.

I'he prognosis is not always good; it depends on the causes of thedi^
ease and the resnlts of electrioaf exploration.

The treatment consists chiefly in the application of eleotrioiiy.

The motor points are shown in Fi^. 'Zi and 25. In hopeless cases, the

use of orthopaedic apparatus is indicated.

b. SPASM (nrPERKItfESIS) OF THE MOTOR KBRTES.

1. Spasm in the Distribution of the Facial Nerve.
{Mimic Facial Spasm. Prosospasmus.)

Spasms in the facial muscles are usually clonic, more rarely tonic.
- They may extend over the entire distribution of the facial nerve, or sfleot
only individual muscles.

DISEASES OF THE MOTOB NEBVBS. 37

a. Diffuse Clonic Facial Spasm, {Tic convulsif.)

I. Etiology. — The disease occurs more frequently in males than in
females, and is more common in advanced years than daring childhood.
It is sometimes the result of direct injuries to the facial nerve^ sometimes
it is a reflex effect of disturbances in other nerve tracts.

In certain cases, a cold has been mentioned as the immediate cause
of the disease.

Other patients attribute it to injury. A number of cases have been
reported in which the facial nerve was compressed or irritated by.
enlarged glands, diseases of the petrous portion of the temporal bone,
exostoses, tumors at the base of the skull, aneurism of cerebral ar-
teries, etc.

The reflex variety of facial spasm occurs most frequently in painful
diseases in the distribution of the trigeminus (diseases of the Uds and eye-
ball, painful dental affections, ulcerative processes in the nasal and
buccal mucous membrane, neuralgia, etc.).

Mimic facial spasm also develops not infrequently in diseases of the
genital apparatus, or irritation of the intestinal mucous membrane by
worms. Moreover, painful pressure points are sometimes found on the
spine, wrist-joints, and other parts of the body, treatment of which
occasionally exerts a magical effect upon the reflex facial spasm.

There is no doubt that in some cases heredity plays an etiological
part. But it must be remembered that the spasm is not always inherited
as such, but that there is often merely a general neuropathic taint,
manifested in the ancestors by hysteria, epilepsy, or other neuroses.

In some patients the nervous disposition is acquired, particularly
during the course of chlorosis.

Mimicry is occasionally an etiological factor. Frequent " making
faces ^' may flnally terminate in well-marked facial spasm.

In a large number of cases no cause can be discovered.

II. Anatomical Changes. — Nothing is known concerning the
anatomical changes in this disease. The cases examined have given
almost entirely negative results.

III. Symptoms. — Mimic facial spasm consists of involuntary grimaces
which occur in paroxysms. The patients suddenly wrinkle the brow,
wink the lids, snuffle with the nose, and distort the whole face. The
contractions are usually unilateral, rarely bilateral. They sometimes
occur spontaneously, sometimes after physical or mental exertion. As
a rule, they last only a few seconds; occasionally there are abortive
attacks, in which a quick contraction passes rapidly over one side of the
face. In some cases, only a few attacks occur daily; in others, twenty,
thirty, or even more, in a single hour, Eemissions and exacerbations
are noticed, and depend chiefly upon the mental and physical condition
of the patient. The twitchings generally cease during the night, but
this rule presents exceptions. Some patients can voluntarily moderate
the intensitv of the contractions, but the will is powerless in the majority
of cases. The palatal, digastric, and stylohyoid muscles are always, the
auricular muscles and platysma myoides are usually, unaffected. The
twitching may predominate in certain of the facial muscles, and this
may vary in dinerent attacks. In very violent and obstinate cases, the
spasm may extend to other groups of muscles, viz., to the tongue, neck,
and limbs.

The secretory and gustatory flbres of the facial nerve are unaffected.

38 DISEASES OF THE MOTOR NEBTE8.

In a number of cases, crackling, ringing, or roaring has been heard in
the ear during the spasms (spasm oi the stapedius?).

Pressure points should always be looked lor. These are points which
correspond to individual sensory nerves, and are very sensitive to pressure;
the latter may suddenly abolish, more rarely intensify, the spasmodic
attack. They may be found along the supra-orbital or infra-orbital nerve,
on the mucous membrane of the nose or mouth, transverse or spinous
processes of the cervical vertebras, sternum, or intercostal spaces, wrist-
goints, etc.

Tic convulsif is unattended with pain, but some patients complain
of a peculiar tired feeling in the affected muscles.

The electrical reactions of the nerve and muscles are unchanged.

The disease lasts months and years; in many cases for life.

lY. Diagnosis. — The recognition of the disease is easy, but it is often
difficult to ascertain its cause.

V. PttOGNOSis. — The disease is never dangerous to life. If the cause
can be removed, the prognosis is usually favorable; if not, the disease is
generally incurable.

VI. Treatment. — Causal treatment requires the most careful atten-
tion. In some cases, the extraction of a carious tooth has effected a
rapid and permanent cure. In nervous individuals, we order nervines
(potassium bromide, valerian, asafcetida, zinc, etc.); in chlorotic per-
sons, iron preparations. If the disease is the result of cold, resort should
be had to the use of baths, diaphoresis, alcoholic frictions, leeches be-
hind the ear, etc.

Pressure points should also be treated. Applications of the galyanio
current may oe made, the cathode being placed on an indifferent spot
(sternum, etc.), the anode upon the pressure point. The current should
not be too strong, and the sitting not prolonged be^rond five minutes.

The same treatment may be employed ii the tic is associated with
trigeminal neuralgia. If the latter is obstinate, neurotomy or neurec-
tomy of the nerve affected by neuralgia sometimes proves successful.

If there are no causal indications, narcotics may be injected subcu-
taneously (]ft Magendie's solution, ^^ syringeful; atropine, gr. J- : 3 iij.,
i syringeful; strychnine, gr. iss. : 3 iij., i syringeful; curare, gr. iss. :
3 iij., h^ syringeful).

As a rule, better results will be obtained from the use of electricity,
although great patience is requisite.

The preference is generally ^ven to the galvanic current. The anode is
placed on the trunk of the nerve immediately in front of or behind the ear, the
cathode upon an indifferent spot. The anode may also be applied stabile or labile
to the individual muscles. Benedikt favors frequent changes of polarity. In
diseases of the ear or base of the brain, the current may be passed transversely
through the mastoid processes. In some cases, Erb and JBerger advise the appli-
cation of a large anode (head electrode) to the parietal bone, particularly when
the disease is the result of central causes, in order to reach the cortical centre of
the facial nerve. Remak recommends galvanization of the cervical sympathetic,
the anode immediately behind the angle of the lower jaw to the outsicfe of the
carotid artery, the cathode on an indifferent ppot. The same author also obtained
good effects from descending currents, i. e., anode on the central, cathode on the
peripheral portion of the nerve.

Frommhold recommended faradization of the muscles with currents of gradu-
ally increasing strength.

Various surgical operations have been performed to relieve the dis-
ease. Thus, incision of the nerve and muscles has been performed.

DISEASES OF THE MOTOB NEBVE8. 39

Stretching of the nerve has been done with apparently good results^ but
Bernhardt showed that the effect is only temporary.

b. Diffuse Tonic Facial Spasm.

This disease is rare and is usually the result of previous facial paraly-
sis; less frequently it is an independent^ primary affection. The side of
the face is stiff and rigid, the lines and grooves are unusuallj deep, the
face appears drawn towards the affected side, the eyebrow is elevated;
rigidity of the cheek sometimes interferes with mastication. The disease
has been treated by galvanization of the contractured muscles, faradiza-
tion of the healthy facial muscles, introduction of wooden globes under
the cheek on the affected side.

c. Partial Tonic and Clonic Facial Spasm.

Contractions of individual facial muscles occur in many otherwise
Wealthy persons as soon us they become excited. In others contractions
occur during mental and physical rest, in the lips, aliB nasi, oorrugator
supercilii, frontalis, and even the auricular muscles. Contractions of the
zygomatic! cause a laughing expression (risus sardonicus). Bosenthal
noticed isolated contractions of tne palatal muscles.

Practical significance attaches to spasm of the orbicularis palpe-
brarum ; this is either tonic (blepharospasm) or clonic (nictitatmg
spasm). The causes of both varieties are almost identical. In the ma-
jority of cases they result from diseases of the eye (diseases of the con-
junctiva and cornea, foreign bodies, and other ocular affections attended
with pain). A bright light will sometimes produce blepharospasm in
otherwise healthy individuals. It may also occur in trigeminal neuralgia
and diseases of the nasal, buccal, and palatal mucous membrane, and
the teeth. As a matter of course, the spasm is the result in such cases
of reflex processes which are conveyed from the sensory branches of the
trigeminus to the facial nerve. The spasm may also be produced by
irritation in other sensory tracts, for example, the uterine, intestinal
nerves, etc. The causes of certain cases are unknown.

In blepharospasm the lids are suddenly and spasmodically closed; in
some cases there is narrowing of the palpebral fissure. The spasm is al-
most always bilateral, lasts several seconds or minutes, even nour<>, and
then ceases for a longer or shorter interval. In certain cases the spasm
continues for weeks and months, so that the patient is constantly unable
to see. The attacks often occur spontaneously, often as the result of
bodily or mental excitement or ocular irritation. Apart from the de-
formity, the patients suffer from the fact that they may be suddenly
rendered blind, in a mechanical manner, while walking the streets. The
vigor of the contractions is usually so great that the lids cannot be for-
cibly opened. Towards the close of the seizure, its duration may some-
times be shortened by forcible separation of the lids.

Pressure points are sometimes found, pressure on which causes sudden
cessation of the spasm. Graefe distinguishes primary and induced pres-
sure points; the former are present from the beginning of the disease,
the latter develop during its course.

These pressure points are observed most f reailently along the supra-
orbital, next along the infraorbital nerve, and also on the mucous mem-
brane of the nose, mouth, palatal arch, on the spine, wrist-joints, etc.

40 DISEASES OF THE MOTOR NEBVBS.

Blepharospasm sometimes dves rise to diffuse facial spasm, and even
to spasm of more remote muscles, for example, on the back of the neck.
Clonic spasm of the lids (nictitating spasm) is more frequent than ble-
pharospasm, and in many individu^s is merely a bad habit. It consists
merely of winking movements. The remarks made concerning blepharo-
spasm also hold good concerning this variety.

The prognosis of both affections is not always good; the disease is gen-
erally very obstinate, often incurable.

The treatment is the i^ame as that of diffuse clonic facial spasm.

2. Spasmodic Conditions of the Trigeminal Motor Branches.

{Spasm of the Muscles of Mastication.)

1. The changes in question affect the temporal, masseter, and ptery-
goid muscles. The spasm of these muscles is sometimes tonic, some-
times clonic. In the former event, the muscular contractions recur so
rapidly as to produce the impression of a permanent muscular contrac-
tion; m clonic spasm, the individual contractions can be distinctly dis-
tinguished from one another.

In the majority of cases, the spasms are the result of central changes,
not often of peripheral lesions. Exposure, injury to the nerve, and tri-
geminal neuralgia have been mentioned as causes. A relatively fre-
quent cause are diseases of the teeth (eruption of the molar and wisdom
teeth), inflammations of the periosteum of the inferior maxilla or
temporo-maxillary joint.

Reflex spasms occur in children suffering from worms, after peri-
pheral injury, and painful cicatrices.

2. Spasm of the muscles of mastication is almost always bUateral.
In tonic spasms, the contracted masseters and temporals protrude
beneath the skin, and feel as hard as a board. The patients have very
little or no power of drawing the lower jaw downwards, or from side to
side. As a rule, the mouth cannot be possibly opened by any amount of
force which can be used with safety. This condition is known as tris-
mus. Speech is difficult, and the patients are sometimes unable to take
even fluid food into the mouth. Such conditions may last days and
even weeks.

The best known form of clonic spasm of the muscles of mastication
is the chattering of the teeth, which occurs when the individual feels very
cold; the movements then occur from above downwards. In some cases,,
lateral movements are produced (grinding of the teeth). The tongue,.
gums, and mucous membrane of the mouth may be thereby injured.

3. Nothing is known concerning the anatomical changes.

4. The diagnosis is almost always easy. Tonic spasm is distinguished
from ankylosis of the temporo-maxillary joint bv the absence of the
hard contraction of the muscles; in addition, the history of the disease
is different. In doubtful cases, the patient may be anaesthetized with
chloroform, whereupon the muscular spasm will subside, while the
ankylosis persists.

5. The prognosis depends upon the etiology.

C. Treatment should first be directed towards the removal of the
causes. A subcutaneous injection of morphine into the cheek seems to
be the most reliable method of relieving the spasm. Chloroform may
be used in very violent and obstinate cases. Electricity may also be

DISSA8E8 OF THB MOTOB NEBYES. 41

employed — the galvanic current transversely through the masseters, at
first with feeble currents^ then gradually increased^ and as gradually
diminished. Benedikt recommends frequent changes of polarity.
Strong faradic currents, especially the wire brush, afford good results iii
some cases. In chronic cases, the attempt has been made to gradually
relieve the trismus by the introduction of wooden wedges of gradually
increasing size between the rows of teeth. It may be necessary to
nourish the patient by means of the oesophageal sound, through th&
nose, or by means of nutritive enemata.

3. Spasm in the Distribution of the Hypoglossal Nerve.

Spasmodic conditions in the hypoglossal tract are shown by abnormal
movements of the ton^e; they are rare, more frequently central than.

«eripheral, and usuafiy have a clonic, more rarely a tonic character.
7e must distinguish between masticatory and articulatory hypoglossal
spasms. The latter have been called aphthongia. This consists of
attacks in which the tongue is moved involuntarily in all directions. In
one of my cases, the tongue had been pushed against the teeth with such
force that losses of substance occurred on the surface of the tongue. As
a matter of course, speech and mastication are interfered with during^
the attacks. They occur in ansdmic, nervous, and hysterical individuals,
sometimes during trigeminal neuralgia or mimic facial spasm. The
hypoglossal spasm is sometimes primary, and the facial spasm develops,
later. Sensory disturbances have been observed upon the mucous mem-
brane of the tongue, lips, and mouth. The treatment is similar to that
of facial spasm.

4. Spasm in the Distributioti of the Spinal Accessory.

1. Spasm in the distribution of the spinal accessory affects the stemo-
mastoid and trapezius muscles. The spasm may be tonic or clonic, uni-
lateral or bilateral, and affect one or both of the muscles mentioned.

Some cases are undoubtedly rheumatic, others are traumatic in their
origin; they may arise from over-exertion or lifting heavy weights. It
is sometimes observed after infectious diseases (typhoid, puerpei*al
fever, etc.). Or it may be the result of diseases of the spine (tubercu-
losis, tumors, fractures, etc.). Reflex influences can sometimes be
demonstrated, for example, teething in childhood, helminthiasis, ute-
rine diseases, etc. It is not infrequently impossible to ascertain the
cause, and many cases of supposed peripheral diseases are undoubtedly
central in their origin. This is true of nervous and hysterical indi-
viduals in whom spasm of the spinal accessory may alternate with or be
followed by epilepsy, idiocy, or insanity. Central causes are directly
demonstrable m certain cases.

2. In unilateral clonic spasm of the stemomastoid, the head ia
turned at each muscular contraction in such a manner that the chin
looks toward the healthy side, and the mastoid process and lobe of the
ear on the affected siae are approximated to the clavicle. The con-
tracted, muscle is visible under tne skin as a tense strand.

If clonic spasm of the trapezius is present at the same time, the head
is drawn further backwards and the shoulder upwards, so that the occi-
put and shoulder are sometimes brought in contact. In certain cases,
the contraction is irregularly distributed in the trapezius, so that mor&

42 DISEASES OF THE MOTOR NERVES.

or less torsion of the scapula results. The contractions of the stemo-
mastoid and trapezius may alternate with one another, the vigor of one
may predominate over that of the other, or both may be synchronons
and equal in power.

In clonic spasm of both stemomastoids and trapezii, the Sjymptoms
vary according as the spasm occurs synchronously or alternately on the
two sides. In the former event, the head performs nodding movements,
but in the majority of such cases, other muscles of the neck are also
implicated. This form occurs almost exclusively in children from the
period of dentition to that of puberty. If the contractions occur alter-
nately on the two sides, the head is wagged to and fro. The spasm is
sometimes unilateral at first, and later spreads to the other side.

The attacks occur spontaneously, or they are produced by bodily or
mental excitement. Tney usually cease during sleep, but many patients
complain that they interfere with falling asleep. The number and
duration of the attacks are subject to great variation. Many patients
complain of a peculiar feeling of tension or exhaustion in the affected
muscles, whicn may become intensified into severe pain. Pressure
points are not frequent. Other groups of muscles often take part in the
spasm, for example, those of the eyes, face, throat, shoulder, limbs, and
in rare cases even general convulsions are produced. Romberg described
cedema and par»sthesia of the arms as the result of pressure on the
vessels and nerves in implication of the scaleni. The disease may last
weeks, months, years, even a lifetime.

Tonic spasms of the sternomastoid and trapezius muscles produce
permanent abnormal positions of the head (caput obstipum spasticum).
The position which will be assumed by the head, according as one or
both muscles are affected unilaterally or bilaterally, is evident from pre-
vious considerations.

The condition is sometimes congenital, or develops in early child-
hood, and thus often gives rise to secondary changes in the spinal
column. The spine presents a convex curve toward the healthy side,
the individual vertebrsB appear smaller on the diseased side, and even the
growth of the face may be retarded. The tonically contracted muscles
are often hypertrophied, their antagonists atrophied.

3. The rBOONOSis of tonic and clonic spasms of the spinal accessory
nerve is not always good. As a rule, there is no chance of recovery
unless the cause can be removed. Many patients have been driven to
suicide by their obstinate disease.

4. Treatment must first be directed to the removal of the cause of
the disease. The chief local method of treatment, apart from subcu-
taneous injections of morphine, curare, atropine, or strychnine, is the ap-
plication of electricity — constant stabile current, anode to the affected
nerve or muscle, fiusch obtained very rapid and successful results
from the use of the actual cautery. OrthopsBdic apparatus and gym-
nastic exercises may become requisite. Excision of the nerve and
myotomy of the muscles are hardly justifiable.

5. Spasm of the Neck, Scapula, and Arm.

These muscles are supplied by the cervical and brachial plexuses.
The spasms may be tonic or clonic, unilateral or bilateral, ana affect a
single muscle or various groups of muscles. We will refer to only a

DI8SABES OP THE UOTOB KBBVBS. 43

lew Tarietiea. The etiology, prognoeis, and treatment are the same as
in Bpasm of the spinal accessory nerve.

a. Spasm of the obUquus capitis inferior. — Contraction of this
muscle simply rotates the head in a horizontal line. In anilateral
clonic spasm there are constant rotatory moTements towards the afiFected
side ; in bilateral spasm there is rotation in both directions (rotatory
tic). In fixation of an object the patients must hold the head between
the hands in order to prevent the movements. In tonic spasm the
head assumes a constant abnormal position to one side.

b. Spasm of the aplenius capitis. — This muscle draws the head
backwards; at the same timu the face turns towards the contraotured
side, the chin is depressed and approaches the shoulder on the same
side. The contracted muscle projects beneath the anterior border of
the trapezius, the stemomastoia appears flaccid on the affected side, tense

ot the lisht iplenlua (mp[U< iniiiola.

npon the other side. Tonic spasm of the muscle is much more frequent
than the clonic form.

c. Spasm of the rhomboid has hitherto been observed only in the
tonic form. On contraction of this muscle, the lower angle of the
ecapula is elevated, its inner edge approaches the spine, and its direction
changed so that it runs from below internally, upwards externally. The
contracted muscle can be felt, and often seen in the interscapular space.
Elevation of the arm to the vertical position meets with resistance.

d. Spasm of the levator an^uli scapula produces elevation of the
scapula, especially its upper inner angle, and bends the head back*
wards. The contracted muscle is visible in the supraclavicular fossa.

6. Spasm of the Respiratory Muscles,
a. Clonic spasm of the diaphragm is called hiccough, singoltas.
Upon sudden contraction of the maphragm in this oonditioa, flie in-

44 DliSASXS OF THE MOTOR NEBYES.

«i>h4lMrr oitrront of air enters the air passages with a loud noiae. bat is
4iH)i|iMily olthr.k<i<l by closure of the rima glottidis. The ailment is more
fM^'itiMiiily imiirnl than peripheral in its origin, and is especiaUj fre-
i|Mi>tti )fi ttiirMliiiKN. In rare cases it is the result of irritation of the
hiMiti (if tho \tUrmUi twrve by mediastinal tumors, aneurisms, pericar-
tinu fitHl plmiriNV. Singultus sometimes occurs in diaphragmatic
l<ii.Mf )4v It <liiv<*fopM more frequently in a reflex manner, for example,
Im (iihtihi^Wtm iff tb<5 Htomach, ingestion of too hot or too cold food, oi^
h.«..i..) /if Mi<f l/it4?jctiri<}M or liver, biliary or renal calculi, uterine diseases
Mint ),htihiu\Utt, It in especially noteworthy that prostatic diseases giro
(.irth fiifl ihtttuiumiily to hiccough.

\i*inhf Mm( ti/ftntt fyfrxlucud bv central causes are included those
iihh\i* >'< n)iHtH**m iff ttiD brain and menint^eH, in hyHterical andameaiic individaa]8»
(i<otf'i^ ^¥ti0tt f||iMifiM«N, for example, after loesee of blood, cholera, djaenterj,
i.HUhhhm* t^i^m^Ui, ifuilarUi.

'ht'» <iU4/ib« rriity lie ho Hovoro that sixty to eighty contractions of the
\U*i^f^ttt4yih tHir.tir in it minute. The patients then suffer from dyspnoea,
IttiH'f'i^ '*'''^ «;itLinK (irn intt^rforod with, and pain is felt in the epigastrium
mtii i^fH^.MM/o of tli<i (liiij»liriigm. Pressure points are sometimes noticed
hf t ^ihtt\*i \h%rU, *V\\i^ fittaclcH may lust hours, days, weeks, even months,
f. iHih\i*ftti9 iilimmt uninterruptedly, Hometimes with free intervals. They
h'iu*4^^h ^'''^^< <^t ni^lit, but interfere with falling asleep.

yiit. tiimtiinii MoftHdinicH rcHiHts all methods oi treatment. We should
< «,'K#iVor Ui mniovo tho (*auHeH and divert the attention of the patient.
\it ^(.v«;/ul lit my iuim^H, nipid recjovery was produced by constantly count-
Hiti t4iffii*i ii^ iiiuiiforrri niteof rapidity. Vigorous straining, with closed
tUhff i(i'dMiif, pjufiiign of the (nsophap'al sound, or injection of cold
i'/^|>.A Ui^'t iUti <iiM<)ph(i^iiH until Huffocatiou threatens, have also been re-
' *iHim'^h^\^A. It u iMirtl. In employ narcotics subcutaneously in the region
',i Uti^ fiiu^fhnn/in. In it ('olleiigue, a*t. 7:3 years. I obtained rapid success
jlf'fftf li/' ii'fuiif iidifiiiiiNtnilion of U Potassium bromide, gr. viiss. ;
. ,./ h*.thtJi'fhhii', i/v, (. Vi^orouH cutaneous irritants — sinapisms or the
|i// »/');'. * iin*:h\ In Mm difi|)linigniati(^ region have also been tried. Be-
',,t f^ Uu*z \itMU tslff^rtud ill Home nineH by galvanic or faradic treatment
\ UfK ^fUniuh: m^rve. Kinally, the lower part of the thorax has been
. •///,^/>< ..KVi.d uifi Um) lidiul (Irmly proKHed against the chest a number of
\Htf' "J n^ 'yidi.j \m prodmtM vigorouH expinitory movements.

// Tiftilt: 6jiiiiiin lit tliii Uitiphnujm, as the result of peripheral causes,
\\tH '/'^^^ iAit^:iSiA iijUii' It mivnre cold or after intercostal neuralgia, mus-
, iJi/; ^n4 uiiu tiUi I'lMiumittiMin. Ah the result of central disturbancea
iif inni.ni^ihiu, il Una Imuiii olmnrved in tetanus, epilepsy, and hysteria.
jjn Jj.cM^c u c^iMiim^jy diiiignrouii. and will inevitably result in death

'J jii. t^tnii^'iihH uyti tiiMiilv rneognized. The lowermost part of the
||i>/<.jj uj^iycaia vtfiy dilatdili liiit tiikoH no part in the respiratory move-
lin fA^'. TJjc l<;wui' boi'dtir of tlio right lung, and occasionally the heart,
^u» J'/wci ihim Jioniial. 'I'lin epiguritriuni is very prominent, and the
^mnnal ic^j/iruh/jy iiiuvemeiitrt of the diapliragm cannot be felt on pal-
iifii iiiii uf iIjc Jj>|io<:hoiMlria. The upper part of the chest moves vigor-
(hi. J) 'i^i^: jmijciil, oompjiilim of dread of suffocation, has a cyanotic
)ii)^/i .uuiK «.; atiiHuUf liiinitid puUe, and is hardly able to talk in a loud
j/i/ii W lajiiil jcjit.f in not brought, death occurs from suffocation.

'J he iiXiiUncnl uiiJibitiLd of the application of strong cutaneous irri-

1 1 1 1 1

DISEASES OF THE MOTOR NEBYES. 45

tants — ^hot compresses to the region of the diaphragm, mustard poultices,
the faradic brush. We may give a subcutaneous injection of morphine
or chloroform by inhalation; m addition, faradization or galvanization
of the phrenic nerve.

Appendix.

Numerous other spasmodic conditions of the respiratory muscles have
been described, but their combinations ate so manifold that they cannot
be described from a general standpoint. This group includes spasms of
sneezing (ptarmus s. stemutatio convulsiva), of yawning, crying, laugh-
ing, shouting. As a rule, the causes are centml, as in hysteria and or-
ganic diseases of the nervous system, or the result of reflex irritation.

7. Spasm of the Abdominal Muscles.

Westphal reported a case of clonic spasm of the abdominal muscles,
which was relieved by the actual cautery. I observed a similar case in an
hysterical boy of nine years. Tonic spasms of central origin occur in
meningitis, tetanus, etc.

8. Spasm in the Muscles of the Lower Limbs.

Spasms rarely occur in the muscles of the lower limbs. They may
be tonic or clonic, and sometimes extend to all the muscles of the lower
limbs. We cannot enter into a detailed description, but, with regard to
the function of the various muscles, refer the reader to the section on
paralysis.

9. Cramp,

1. Cramp is a term applied to a tonic muscular spasm associated with
pain. It often lasts only a few seconds, and at all events, its duration is
yery brief.

The best known form is spasm of the calves of the legs. This is a
painful, tonic contraction of the muscles, which project with sharp con-
tours, and are very tender on pressure. Nevertheless, the muscles are
not contracted ad maximum. After the muscles are relaxed, at the end
of a few seconds or minutes, a peculiar feeling of tension and exhaustion
not infrequently is left over, and the muscles remain for a long time very
tender on pressure. Ecchymoses are sometimes formed during the cramp.
It is especially apt to occur at night, sometimes recurs very rapidly, dis-
turbs sleep, or produces such violent pain as to give rise to syncope.

Cramps also develop in other muscles, but particularly in the lower
limbs.

Schultz claims to have found increased electrical excitability of the
affected muscles.

2. Among the causes of such conditions may be mentioned: a. Over-
exertion of the muscles, for example, cramps" in the calves after long
walks, dancing, etc.; b. Nutritive disturbances, for example, in cholera,
as the result of losses of fluid (according to Erb, this also occurs in dia-
betes mellitus); c. Circulatory stasis, for example, the cramps in the
calves in varicose veins and pregnancy.

3. Treatment consists or rest on the back (although many persons
are relieved by hyperextension of the muscles), subcutaneous iniections
of morphine, friction or kneading of the muscles, inunctions of alcoholic
solutions.

DIBEA8E8 OF THE SENSOBT NSBVES.

B. DISEASES OF THE SEMSOBY NERVES.

a. NEL'UALC.IAS.

1. Trigeminal Neuralgia,
{Facial Neuralgia, Prosopalgia, Tic Douloureux.)

I. Etiology. — Among all the formB of neuralgia, that of the trigem-
inns IB the most frequently observed. This is owing to its long course,
the situation of many branches in narrow, bony cunala, and the super-
ficial position of its terminal ramifications.

It is most frequent in women, and from the twentieth to fiftieth years.
It is very rare in childhood, more frequent in old age. The proiiessea of
the period of involution, t. «., the fortieth year, on the average, in mates,
the menopause in female, favor the development of the disease. It is
said to he more frequent in cold than in warm climates. According to
some writers, individuals belonging to the well-to-do classes are predis-
posed to the affection. With regard to Goettingeu, I may state that it
la very common among the laboring classes.

The causes of the disease may Be divided into five groups, constitu-
tional, infectious, toxic, local, and reflex.

Eeredilai7 factora are active in many cases, Sometimee we observe families
in which several generations Iirvb suffered from trigeminal neuralgia, aometimes
there is an hereditary nervous taint, so that different members of the family
suffer from hysteria, epilepsy, psychopathies, or neuralgias. In some individuafs
^L- ^ disposition is acquired as the result of excesses, mental and bodily

^ _ t, such as occur after pro-

tractert dtarrhcea, rapidly tollowmg pregnancies, and excessive lactation.

Arni)ng the Infectious forms the most important are those which are the resuit
of malaria. In such cases the supraorbital nerve is almost always affected. The
neuralgic attacks generally occur daily at, the same time, more rarely they pre-
sent a tertian or quartan type. But we have seen many typical cases of inter-
mittent supraorbital neuralgia in indiriduals who were entirely free from
malaria. The disease may also occur in typhoid fever and recent syphilis. In
the majority of cases, however, syphilitic trigeminal neuralgia is the result of
exostoses, gummata, inflammation, etc., at the base of the skull or within the
bony canals.

Toxic trigeminal neuralgia has been observed in lead aJid mercurial poisoning.

The disease is very of leu the result of direct injury to the nerve, for example,
as the result of colci, injury, inflammation of the periosteum, unskilful extrac-
tion of the teeth, caries and exostoses of the teeth, eruption of the wisdiim teeth.
Gross has called attention to obstinate neuralgia in toothless old people in whom
the empty alveoli are gradually filled with bony substance, which irritates the
alveolar nerves.

Trigeminal neuralgia may be the result of diseases of the ear. inflammation of
the frontal sinuses with retention of secretion, and straining of the eyes.

The causes of the neuralgia must often be sought in the narrow bony canals
through which the branches of the nerve pass. Compression and irritation of
the nerve may be brought about by inflammation, thickening, and depoeits in
these [ocalitise, in many cases by simple distention of the blood-vessels. This
danger is so much greater the narrower the bony canal, and the more numerous
the blood-vessels situated within it,

The causes of neuralgia are sometimes found at the base of the skull, for
example, inflammations, exostoses, tumors or aneurisms nhich press upon the
trunk of the trigeminus.

Reflex trigeminal neuralgias include those which occur in uterine, ovarian,
and intestinal disc-Lses. The causal connection cannot be doubted in thoae cases

DISEASES OF THE SENSORY NERVES. 47

in which the neuralgia disappears as soon as the primary disease is relieved.
TrigemiDal neunUgia sometimes develops after injury of remote nerve tracts.

II. Anatomical Changes.— Little is known concerning the anatomical
changes in trigeminal neuralgia. Unusual redness and succulence of the
affected nerve branches have been observed in some cases; in others, prolifera-
tions or calcification of the neurilemma, fatty and atrophic changes in tne nerve-
fibres or cells of the Gku98erian ganglion. In Cruveilhier's celebrated case, nodulea
of carcinoma were found in the neurilemma of the peripheral branches of tha
facial nerve and the inoscidating trigeminal fibres.

III. Symptoms. — Trigeminal neuralgia is almost always unilateral
and, according to Canstatt, is more frequent on the right side (?). Bi-
lateral neuralgia is extremely rare, and occars only in the supraorbital
nerve. It is equally rare that the neuralgia affects first one, then the
other trigeminus. In a larger number of cases the disease spreads from
one branch to a second or third.

The ophthalmic nerve is affected most frequently, particularly the
supraorbital branch. Next in order of frequency is supramaxillary neur-
algia, that of the infraorbital nerve being the most frequent in this
class. The inframaxillary branch is least frequently affected; neuralgia
of the mental or alveolar branches is the most frequent.

The entire nerve is rarely affected, and then only when the neuralgia
is the result of intracranial causes, or of lesions affecting the trunk of
the nerve. It is also rare to find all the ramifications of a single branch
affected. The more the neuralgia is confined to the finer twigs, the
more we are justified in assuming peripheral causes. Some branches
exhibit very little tendency to neuralgia; this is particularly true of the
auriculo-temporal nerve.

The neuralgic attacks not infrequently develop suddenly, in other
cases they are preceded by prodromata. The latter almost always con-
sist of parsesthesiaB : a feeling of stiffness, pricking, formication in the
affected parts.

The neuralria itself is characterized by attacks of pain, which some-
times have a boring or burning, sometimes a lancinating character.
Some patients experience a sensation as if the nerve were being drawn
out slowly, or as if the bones were slowljr crushed. The pain is some-
times situated deeply, sometimes superficially. Some patients state that
the pains radiate from the centre towards the periphery; much more
rarely they pursue an opposite course. All patients agree that the
pains are atrocious, and render them incapable of doing anjrthing, so
that very few are able to keep on with their occupation. The pain al-
ways extends along certain tracts of the nerve. In some cases it radi-
ates into more remote parts, such as the back of the neck, and the ex-
tremities.

The attack usually lasts only a few seconds; in abortive attacks a
single, lightning- like spasm of pain is experienced.

The number of attacks within an hour may be very considerable. In
other cases attacks of variable duration occur at irregular intervals dur-
ing the day. In intermittent neuralgia the attack recurs at a definite
hour in the day, usually in the morning, or at noon, and disappears at
the end of a certain time. In very rare cases it begins with a chill and
ends in a sweat.

In many cases no immediate cause of the individual attacks can be
demonstrated. In others they occur after exposure to a draught, on
slight contact with the integument of the face, upon touching certain
dennite points, eating hard or cold articles of food, etc. Some patients

48 DISEASES OF THE 8EK80BT KKBYXB.

suffer after mental or physical excitement, if the eye is annoyed by a
bright light, or the ear by shrill tones, on yawning, sneezing, laughing,
often at the mere thought of an attack.

In the interparoxysmal period many patients feel entirely free from
pain, others are tormented by more or less Tiolent painful sensations.

Pressure points constitute a frequent, though by no means constant
symptom. These are points which are situated in the affected nerve
tracts, and are either the only parts which are painful on pressure or pain
more than other parts.. These points are sometimes present during the
attack alone, sometimes during the interparoxysmal period. Pressure
upon them may provoke a neuralgic paroxysm; stronj^ pressure some-
times relieves the pain, while gentle pressure increases it.

Trousseau showed that pressure noints are sometimes found upon the
spinous processes of the second ana third cervical vertebr®, or the ex-
ternal protuberance of the occipital bone.

Vaso motor disturbances are very often present during the attack. The
affected half of the face, or a circumscribed nerve tract is very red, the
arteries, especially the temporals, are unusually dilated and pulsate vig-
orously, and the cutaneous veins arc also dilated. The skin has a puffy,
peculiar shining appearance, is unusually warm, and covered witn per-
spiration. The beginning of the attack is preceded by anaemia of the
skin.

The conjunctiva is often injected, and this may even terminate in
csdema (chemosis). The lachrymal secretion is increased, the eyeball
seems to protrude from its socket.

The nasal mucous membrano secretes an increased amount of mucus,
which is sometimes tinged with blood. In rarer cases the secretion of
mucus is diminished.

There is sometimes an increased secretion of saliva, and the gums
may present swelling, aphthous excoriations, and hemorrhages. In rare
cases the patients complain of perverse gustatory sensations or auditory
disturbances.

The trophic changes are closely allied to the vaso-motor disturbances.
An excessive development of the panniculus adiposus sometimes forms
upon the affected side, and even the bones may undergo hyperplasia. In
other cases atrophic processes are observed, likewise herpes, acne, lichen,
and erysipelas on the affected parts. The hairs may become rough,
fractured, suddenly grow gray or fall out. In some cases we notice an
alternation of pigmented with white (unpigmented) hairs, the latter hav-
ing developed during the individual attacks of neuralgia. Among the
rarer phenomena are ophthalmia neuroparalytica, which has been at-
tributed to functional disturbances of certain trophic fibres in the tri-
geminus. Glaucoma and, according to Bull, iritis and chorioiditis have
also been observed after trigeminal neuralgia.

The sensibility of the integument of the affected nerves is not infre-
quently changed. It is generally heightened at the beginning of the
disease, later it is diminished. Sensory disturbances are sometimes no-
ticeable only during the attacks.

Involuntary contractions of the facial muscles are sometimes observed
during the seizures, so that tic douloureux is complicated with tic convul-
sif. In certain cases contractions occur in the muscles of the neck and
limbs; in Sinklar Holden^s case there were widespread tonic muscular
spasms.

The duration of the disease may vary from a few days to a number

DISEASES OF THE SENSOBY NEBVE8.

of years; it sometimes lasts a lifetime. It disappears occasionally during
intercurrent diseases, or alternates with neuralgia of other nerves.
Belapses are frequent, and sometimes recur after the lapse of years.

Some patients suffer from profound melancholy, and may even be
driven to commit suicide. Others become shy, because noisy surround-
ings provoke an attack. Still others lose strength from loss of sleep or
refusal to take food (because mastication gives rise to a paroxysm),

IV. Diagnosis. — The diagnosis is easy, if we bear in mind the par-
oxvsmal character of the pain, its distribution, and the presence of pain-
ful points.

1. Ophthalmic neuralgia. The pain is situated in the upper lid, the frontal re-
gion as far as the vertex, the eyeball and its socket, the base of the nose and its
integument as far as the tip, the anterior portion of the nasal cavity (vide Fig. 27).

Fia. 27.

Dlfltributlon of the tric^minus to the face.

a. Supraorbital neuralgia: pain in frontal region, upper lid, and root of
nose. Pressure points ; the most constant one at the supraorbital foramen or
notch, less constantl^r on the upper lid (palpebral point), the parietal eminence
(parietal point), the inner angle of the eye or cartilage of the nose; sometimes
tne entire nerve tract is sensitive.

b. Ciliary neuralgia. Most violent pain in the eyeball; a symptom of many
ocular diseases.

2. SupramaxiUary neuralgia. Pain situated in lower lid, cheek, upper lip,
lateral part of nose, region of malar bone, and anterior part of forehead, upper
row of teeth, gums, and nasal cavity.

a. Itifraorbital neuralgia. Situation of pain: lower lid, cheek, upper lip, lat-
eral part of nose; sometimes upper teeth, and mucous membrane of cheek; if
the nervus subcutaneus malaa is mvolved, in region of malar bone, and ante-
rior part of forehead. Pressure points : most constantly at infraorbital foramen,
more rarely on the upper lip (labial point), malar region (miliar point), alveolar
proQeeses of upper jaw (alveolar point), rarely on the gum.

60 DISEASES OF THE SENSOBT NEBVE8.

•

b. Alveolar neuralgia is con fined to the alveolar processes of the upper jaw.

3. InframaxiUary neuralgia. Situation of pain: region of chin and lower
jaw, mucous membrane of cheek, inferior alveolar process, tongue, external ear,
and forehead.

a. Mental neuralgia. Pain in the chin; pressure point at the mental fora-
men.

b. Lrngiuxl neuralgia (gloasalgia). Pain in one-half of the tongue; sometimeB
unilateral coating and increased thickness of the tongue. Painful point at the
side of the tongue; sometimes increased salivation, and involuntary movements
of the tong[ue.

c. Inferior alveolar neuralgia. Pain in lower alveolar processes.

d. AuriculO'temporal neuralgia (very rare). Pain in external auditory canal,
concha, and temple.

V. Prognosis. — This depends in great part nponthe etiological fac-
tors. Not all cases in which no cause can be ascertained present a
favorable prognosis. If heredity plays a part in the etiology, we must
expect great obstinacy and frequent relapses of the disease. The longer
the neuralgia has lasted, the slighter are the chances of recovery. The
prognosis of intermittent neuralgia is favorable.

VI. Tbeatmext. — The caustd treatment varies, of course, with the
etiology. In intermittent neuralgia we may give quinine (gr. xv., two
hours before the expected attack, for three days in succession); if qui-
nine is not tolerated, it is replaced by Powler^s solution (ten drops t. i.
d., after meals). If the disease is the result of exposure, we should or-
der diaphoretics, give salicylic acid internally (gr. vij. every hoiir, until
tinnitus aurium is produced), and cover the parts with wadding. Syphi-
litic cases are treated with iodine and mercury, anaemic cases with iron,
etc.

In the symptomatic treatment of trigeminal neuralgia we regard qui-
nine and arsenic as the most important internal remedies. Quinine
often does not act until given in very large doses (gr, Ixxv. or more).

Among other internal remedies may be mentioned: Aconit. (3 Aconi-
tin.,gr. }; ext. hyoscyam., gr. xv.; pulv. liq., q. s.. u. ft. pil. No. 50. D.
S. One to two pills morning and evening); Colcnicum (IJ Tinct. colchici,
3iij.; tinct. aconiti, 3 iss. M. D. S. Fifteen drops t. i. d.); Acid sali-
cylic, gr. XV. every hour; potassium iodide, gr. x. t.i. d.; 5 Argent,
nitrat., gr. xv., argill. albsB, q. s., f. cum aq. dest. q. s. pil. No. 100. D. S*
One pill t. i. d., after meals; ft Auro-natrium chloratum, gr. v.; ext. dul-
camar., gr. 1., f. pil. No. 50, D. S. One pill t. i. d; phosphorus, zinc,
mercurial and copper preparations; opium, belladonna, strychnia,
chloral hydrate, butylchloral ( ft Butylchloral hvdrat., gr. Ixxv. ; glycerin.,
3 v., aqu8B, | iv. M. D. S. One tablespooniul every five to ten min-
utes), potassium bromide ( 3 i.-iij. in a single dose), tinct. gelsemii (five
to twenty drops t. i. d.), amyl nitrite (five drops by inhalation until
the face is reddened), etc.

Among external remedies the most important is electricity, then fol-
lows the subcutaneous injection of narcotics.

As a rule, the galvanic current is indicated. Feeble currents should
be employed; its strength may be gradually increased during the
sitting; tne stabile application is preferable; the anode is placed upon
the affected parts, especially upon pressure points; the cathode, to the
back of the neck or indifferent part. The sitting should not last longer
than three to five minutes, but sometimes two to three sittings daily are
advisable. Some authors recommend descending currents, t. e., the
anode central, the cathode on the peripheral parts. In intra-cranial
disease, the current |s passed transversely through the skull.

DISEASES <)F THE SENSORY NEBYES. 51

• The faradic cnrrent may be employed with the wire-brush, but this
can rarely be applied to the face, on account of the severe pain produced
thereby. M. Meyer showed that it sometimes acts very well when ap-
plied to the back of the neck.

The remedies which may be employed subcutaneously are morphine
(gr. iss. : 1 i., 1 syringeful), atropine (gr. ss. : I i., i-4 syringeful),
strjrchnine (gr. iss. : 3 i., i-i syringeful), chloroform, and ether. The
patients themselves should not be allowed to make injections of mor-
phine, since they are apt to fall into the morphine habit. It is a note-
worthy fact that patients suffering from neuralgia often present a remark-
able tolerance to narcotics. For example. Trousseau recommended as
much as 3 iiss. of opium or 3 i* of morphine daily.

Among other external methods of treatment may be mentioned : aquapunc-
ture, inunctions of veratrine, belladonna, morphine, chloroform, ether, croton-oil
collodion — linear cauterization along the nerves — ^blisters, leeches, chloroform
poured on cotton and placed behind the ear, and compression of the nerves.

In desperate cases, surgical operations may be resorted to, such as
ligature or compression of the carotid, nerve stretching, neurotomy, and
neurectomy.

Compression of the carotid was successfully employed by Earle,
Gerhardl, and Seifert. Nussbaum and Patruban have had gooa results
from ligature of the arterjr. Nerve stretching is the mildest operation,
bat the most uncertain in its effects. Nor can neurotomv be regarded
as a radical operation. Neurectomy offers the greatest chances of suc-
cess, but relief can only be expected with certainty if the operation has
been performed on. the central side of the site of the neuralgia. Ex-
perience has shown, however, that the neuralgia is sometimes relieved
for a longer or shorter period, even if the affected part was not removed.

A, Wagner collated 134 cases of excision of the nerve in trigeminal
neuralgia, and found:

Eecovery for years 25 times (18.7ji).

" "months 18 " (ISA^).

Operation unsuccessful 9 " (6.6^).

~ (4.r

Death. 6 " (4.6^).

Result unknown 24 " (18.0^).

Eelapses. 62 " (38.8^).

2, CervicO' Occipital Neuralgia.
{Occipital Neuralgia.)

I. Etioloot. — Oervico-occipital neuralgia affects* branches of the
cervical plexus (four upper cervical nerves). The occipitalis major is
most frequently affected, in rarer cases the other sensory branches,
viz., occipitalis minor, auricularis magnus, subcutaneus colli inferior,
and supraclavicular.

Under unfavorable circumstances, accordingly, the pain may extend
over the back of the neck and occiput, the posterior surface of the ear, the
anterior and lateral parts of the neck, scapula, and upper part of the
chest.

The disease is more frequent in women, from the 20th to 50th years
of life* Heredity is rarely demonstrable; the affection is often found in
ansBmio, hysterical, and nervous individuals.

. • • • .1- ..■■ ' •' ■''■■■.■ ' u L".- - ^- .- f.»riiL • •'.-1^£J • .'liiil ' Jl

. "f-..~ • •-•. : \ i.fr".T 'lis- 'f "Lilt 'P't*TT'r:ir» 'T

■• V . ■•• • . •■ • -: ■ •■.:. 1' . Z'^U- > --• »*i:'L:? •: llir "r-^rir-Tt

• •

.. . T" ^ -1-
' . -.r I -Z. - . ..

■ I

r .

fc> ■«

:■■•■■■ ■.•■■- : ' : .•■■--• ^ii:. l :' iri-f iiei»i- j'Tvs?wr&

;.•«.-

■ •■ " ■

.. ..- - - u.v. : ■■ ?••:.. T.-rvrt :!- :ijr "L-rXEr'jr*- mc-r^e

• ■ .. . 11 • ■ • - . * *

••• •■ - • :•.-•.. • '-: -:.. ^ •.■'•.•.-'* r.*. ; rrt^ronain^ !:» ihe exit

.*. ' ■ • ■ — . v.- ■..'•:.*. :• ::.: iiTii.n ihe parieial emi-

.•. •■ •• ■ ■ ■• ■ ' ■ :■ -' *' ■-•■*; ■'■ -■ ---i o^ the spinouf pro-

• — ' : .. 1. -:•-». ''..J-: :.:.*: wi:h the painful points

f: • •...-■ "^ J .,::a.t.:. I:.-. L:-:.rf (X;arse of the nerve u

• ■ ■ ■ ■

1 ■ .."?•• :-.ir:- ..: -.::. -: ...wj. - :.\ :.■..- j?5:heiic at the beginning

\ ^-^ : : ' . -: • •..' 0= .^.rf- of:rn y ^?^cr.:, asd are probablj" prodnced
■ . -. • :i..v ' :, -.M. :i:r' ". ?::..• :'!.•.} :»r« :.•:■! iDfrequeni It associated
• .:•.; . ...-■• ' ..:.jr* Tiii-M- *vil; ".'II* L■u::^i^t ^.'f redness of one-half
:-.■ ?.. ■ • ::.. ■..:. .:.; :. ■:. rf :^v ■•:.;•.;:.. ::vd, «c*xnenmes lachrymal
:.:. ■ ..'.. ' \\" r- rv:.-!., :;:.'.;* .la', war!!.::, ar.ii ft^ling of increased heat

: ■ '. : : - ;•■:..? \*z\' LM.'.r.i..y !.urr..'ir. more rarelr dilated.
^ . ..: ■ ■ :- ::.;. ....:. -f .:.:M ..!:v .f r.iuriv.i: and rinxring in the ears.

.; :. '-;.'..•■ « \.\i\v 1 ••.•.:. r.i !•..>" lit >v Tiit-d. Bosenthal noticed

:. ' .... 1: ::.•• rj v'— . r\i : >!!..i'". sw..;::r,j:?, w hi ^^h developed upon the
: I..:. -J : '.». .»:::!■ W :i:. : i;:«<iv:v.irvi aftvr ::< cessation.

I:.. ..::.;i!. i.yv.r.x.z'.A :? ;i::i:..:v- i :.u: iLir^iJuenily with swelling of

li..:.*..i: \\^''.^\^ >k\:\\tk'>. www or /.o:::- :r.u>o:;Iar spasms may develop
.: !:;.i. ;.!i;i'-, ir ilirouiiho'.:: :h^ vv.v.rv l-Aiy. Violent Vomiting
v; :.;.:. J :.'.i :t:t:iK-k> has also Kvii v;o>:r:iK J.

I'.r liiiraiii'ii i»f iiiiMii*i'aM? vari^^fr- :r. a few weeks to several months
IT u-ait. lucux-ablc ca?cj arc much nkriT :iia'^ in rrigeminal neuralgia.

DISEASES OF THE SEKSOBY NEBYES. 53

I^euralgias of the other nerves belonging to the cervical plexus are readily rec-
ognized by the following symptoms:

Neurcdgia of the occipitalis minor gives rise to pain in the lateral p:irt of
th occiput as far as the ear; painful point behind the mastoid process at the exit
o/ the nerve beneath the skin (vide Fig. 27).

h. Neuralgia of the auricularis magnua causes pain on the posterior aspect of
the concha, above the mastoid process and over the parotid; painful point a little
above the middle of the neck, between the trapezius and sternomastoid, and also
upon the concha.

c. Neuralgia of the subcutaneua colli inferior : pain in the lower, middle, and
anterior parts of the neck; painful point, same as in neuralgia of auricularis.

d. Neuralgia of the aupradavicular : pain in the acromial region, shoulder,
and upper part of the chest.

III. DiAGKOSis. — The diagnosis is easy, but it must not be forgotten
that these neuralgias sometimes prece'de for years a latent affection of
the cervical yertebras and spinal cord. Hence these parts should be
carefully examined in obstinate cases.

IV. Pbognosis. — This is much more favorable, as a general thing,
than that of trigeminal neuralgia, but depends chiefly on the etiology.

V. Tbeatment. — The treatment, in general, must follow the prin-
ciples laid down in the consideration of trigeminal neuralgia. The
chief remedies are quinine internally, morphine subcutaneously, and t'le
galvanic (more rarely the faradic) current transversely through the
upper part of the nucha. In recent cases we may employ flying blisters
ana warm applications. In obstinate cases surgical intenerence may be
resorted to.

3. Phrenic Neuralgia,

1. The occufrence of neuralgia of the phrenic nerve has been reported a num-
ber of times by the older authors, and more recently bv French writers.

2. The disease is said to occur either as an independent affection or during the
course of diseases of the pleura, pericardium, myocardium, aorta, liver, spleen,
kidneys, stomach, intestines, and peritoneum. Under such circumstances it may
take a prominent part in the symptomatology, and, in angina pectoris, for example,
may be the cause of the overpowering pains. In addition, exposure, injury, hys-
teria, and epilepsy have been mentioned as causes.

3. The cnief symptom is pain, located chieflv at the base of the chest, but oc-
casionally running along the entire course of the nerve. The pains increase
paroxysmally, but not infrequently persist in a less degree; they may be unilateral
or bilateral. The pain often radiates into remote nerve tracts — into the ai ms,
neck, chin, nucha, out most constantly into the shoulders.

Pressure points are found in the followinK localities : a. anterior pointH of in-
sertion of the diaphragm, especially on the ninth rib; b, posterior pomts of inser-
tion of the diaphragm, especially the lowermost rib; c. lateral part of the neck
upon the scalenus anticus; d. on the sternum at the level of the second and third
intercostal spaces; e. over the spinous processes of the second and Hfth. rarely the
sixth cervical vertebrae.

We usually find disturbances of the respiratory movements: jerky, superficial,
painful inspiration, singultus, yawning, etc. Deglutition may also be interfered
with. Great terror and a feeling of impending dissolution are sometimes present.
Relapses may occur.

4. The diagnosis is difficult. The disease cannot always be distinguished
from an affection of the diaphragmatic pleura or the peritoneum.

5. Treatment: Mustard poultices, leeches, cups, blisters, injections of mor-
phine, electricity.

4. CervicO'Brachidl Neuralgia.

I. Etiology. — The brachial plexus is derived from the four lower
cervical and first dorsal nerves. Neuralgias of this plexus are not rare,
and occur somewhat more frequently in men than in women.

54 DISEASES OF THE SENSOBT NEBTES.

Some cases are the result of exposure, a much larger number are due
to injury.

The traumatic causes include fall, blow, incised or gunshot wounds, fracture or
dislocation, formation of callus, aneurism of the aorta or subclavian artery,
swollen glands in the axilla, neuromata or other tumors, tuberculosis or cancer
of the spine, phlebectomy, wounds, injuries to the little fingers, amputation-ueu-
romata. Allied to this form is that variety of neuralgia produced by over-exer-
tion of the muscles, as in playing piano, sewing, etc.

Brachial neuralgia sometimes follows articular affections of the elbow^
hand, or shoulder.

It is sometimes radiated from trigeminal or cervico-occipital neur-
algia, angina pectoris, diseases of the liver and spleen. According to
Salter, it may be a reflex effect of dental irritation,

ClUorosis, ansBmia, hysteria, malaria, and lead poisoning appear to be
the starting-point of the disease in some cases.

II. Symptoms. — The disease is almost always unilateral. Bilateral
neuralgia has been reported as the result of cancer of the spine and of
over-exertion in gymnastic exercises. The right arm seems to be
affected more frequently than the left.

As a rule, a Qumber of the cutaneous nerves are affected simultane-
ously, and motor disturbances are generally present.

The chief symptom is pain, which may be shooting, boring, burn-
ing, etc. Pains oi unusual intensity have been observea after ganshot
wounds of the nerves (causalgia). The patients are often unable to
localize the pains. They sometimes radiate into the neck, occiput, face,
or intercostal spaces. In many places the pains are constant, but pre-
sent paroxysmal exacerbations. The paroxysms are especially apt to
occur at night after going to bed, or after a careless movement of the
arm. Some patients experience relief from carrying the arm in a sling
or supporting it with the other hand; others are relieved by extension
of the limb.

The painful points vary according to the affected nerve tracts; they
are not constant, and sometimes entirely absent. In radial neuralgia,
the pressure points are: The point of flexion of the nerve in the arm,
and the dorsal surface of the forearm immediately above the wrist. In
ulnar neuralgia: A point between the internal condyle and olecranon,
and the anterior surface of the forearm immediately oelow the head of
the ulna. In median neuralgia, the painful points are: The bicipital
sulcus, the fold of the elbow, the radial side of the volar surface of the
forearm immediately over the head of the radius. Other pressure points
are: The supraclavicular and axillary fossae, lower angle of scapula, and
the points of exit of the various cutaneous nerves.

The more remote pressure points are the spinous processes of the
four lower cervical and two or three upper dorsal vertebrae.

Circulatory changes (pallor or redness of the skin) are not infre-
quent. There is sometimes an abnormally profuse formation of sweat.

Among the trophic changes may be mentioned herpes zoster, urti-
caria, eczema, pemphigus, increased growth of hair, changes in the
nails, glossy skin, etc. ; the muscles often undergo atrophy.

Motor disturbances are frequent, and consist of fibrillary twitchings,
a feeling of stiffness, paresis, paralysis, more rarely tonic and clonic spasms.
The patients often complain of a feeling of rigidity and stiffness in the
muscles, and the fingers are permanently extended like claws.

DISEASES OF THE SENSOBT NEBVES. 55

OroBS muscnlar power may be better retained than fine manipula-
tions, such as writing, sewing, etc.

ParsBsthesiae (feeling of coldness, formication) are frequently men-
tioned.

III. Diagnosis. — The diagnosis of brachial neuralgia is easy, but the
recognition of the etiology and site of the disease may be very difficult
or even impossible (vide Figs. 10 and 11).

IV. Pbognosis. — This depends almost entirely upon the etiology.
The neuralgia generally disappears if the cause is removed.

V. Tbeatment. — The treatment follows the same general principles
that have been laid down in the consideration of trigeminal neuralgia.
The local measures include: carrying the arm in a sling, absolute rest^
subcutaneous injections of morphine, and electricity. The galvanic cur-
rent is generally employed; stabile application, anode upon the painful
points or the aflected nerve trunks, or a descending current along the
nerves.

Nerve stretching is said to have been successful in some cases. Neur-
ectomy should not be performed, as a rule, because it gives rise to
paralysis.

6. Dorso-intercostal Neuralgia.

{Intercostal Neuralgia.)

I. Etiologt. — The intercostal nerves, after leaving the interverte-
bral foramina, divide into a posterior (dorsal) and anterior (intercostal)
branch. Neuralgia occurs most frequently in the latter, rarely in the
dorsal branches alone, somewhat more frequently in both.

The site of the pain is very extensive, since the dorsal branches sup-
ply the integument of the back down to the crest of the ilium, the inter-
costal branches supplv the lateral and anterior surfaces of the chest and
abdomen as far as the symphysis pubis. The first dorsal nerve also
passes into the brachial plexus, and supplies the inner surface of the
arm.

Intercostal neuralgia is more frequent in women than in men, and
from* the age of twenty to fifty years. Anaemia, chlorosis, and nervous-
ness possess a still greater etiological significance than in many other
neuralgias.

Exposure and traumatism are mentioned as frequent causes.

The traumata include: a fall, blow, fracture of the rib? and unfavorable de-
velopment of callus, tuberculosis of the ribs, neuromata and other tumors,
pressure of aneurisms on the spine; tuberculosis, cancer, periostitis, syphilis of
the vertebne or spinal meninges, etc. .

Intercostal neuralgia is sometimes the result of diseases of the respir-
atory organs, heart, i^omach, intestines, liver, or spleen.

' It is associated not infrequently with pleurisy and pulmonary phthisis, and
also with nervous affections of the heart; on the other hand, cardiac neuroses are
apt to develop after an attack of neuralgia. Intercostal neuralgia has also been
known to develop after gastralgia, or painful affections of the liver and spleen.

It sometimes develops during convalescence from severe diseases,
particularly typhoid fever. Malaria is a not infrequent cause.

Intercostal neuralgia may also appear as one of the effects of lead

66 D18BABE8 OF THE 8ESS0BT HBBVes.

poisoniag, as a reflex ajmptom of uterine oi' ovariau disease, ii
radiated Bymptom in trigeminal, occipital, and tervico-bracliial
algia.

II. Anatomical Chasges.— Very little is known in thia
Thickening and hypersemia of the neurilemma, ik'gtne ration i
nerve fibrea, and neuromata have been observed in a fpw cit^ea.
disease is not infrequently a true neurosis, vtiich does not pn^^'iib
anatomical changes.

III. Symptoms. — Intercostal neuralgia is commonly uniiaieral;
of bilateral disease are much rarer. It occurs mor.' fri'fjiieiitly oti ilie Wt
aide. This is attributed to the fact that the venous blood on the left aide
passes in a roundabout way through the vena hemiazygos to the inferior
vena cava, so that stasis and compression of adjacent structures are more
likely to happen on this side. As a rule, two or three adjacent intercos-
tal nerves are affected at the same time. The fifth to ninth intercostal
nerves are involved most frequently.

The pain may occur in paroxysms, or may persist constantly in a
milder degree. It may be so violent and obstinate as to deprive the
patient of sleep. The pain is described as burning, sticking, lancinat-
ing, etc. It sometimes extends half-way around the thorax, sometimes
is especially violent in circumscribed localities. It often radiates into
the arm. If the disease is bilateral, the patients experience the sens^
tion of a constrictine band around the thorax. Coughing, sneezing,
deep respirations, loud talking, etc, produce paroxysms of pain or inten-
sify existing pains. On this account the patients often speak in a low
tone, breathe superficially, and sometimes look like asthmatic individuals.
Slight pressure on the skin may intensify the pain; firm pressure not in-
frequently relieves it. The patients sometimes assume a bent positioa,
the spine usually presenting a convexity towards the healthy side.

'I^ere are three principal painful points: one immediately adjacent
to the spine, corresponding to the exit of the nerve from the interverte-
bral foramina (vertebral point), the other at the middle of the nerve
where the nervus perforans lateralis ramifies in the lateral part of the
thorax (lateral point), and a third along tiie edge of the sternum (ster-
nal point) or on the rectus abdominis, where the anterior perforating
nerve makes its exit. Pressure points are also found not imrequeatly
on the spinous processes of the dorsal vertebrffi.

Cutaneous hyperfesthesia is>often found in the distribution of the
affected nerve, sometimes diffusely, sometimes in circumscribed spots;
anEesthesia is observed more rarely, and usually in old cases.

Trophic disturbances are often present, herpes zoster being the most
frequent, 'f he neuralgia may precede or follow the zoster. If zoster
occurs without neuralgia (generally in children), it must be assumed that
only the trophic fibres are diseased, and that the sensory fibres have
escaped.

Woaker noticed foul-smelling perspiration daring the attacks.

The course and duration of the disease depend on the causes. In a
number of cases it is followed by hysteria or cardiac neuroses.

IV. Diagnosis. — The recognition of the disease is easy. In rheuma-
tism of the muscles of the chest, the muscles themselves are sensitive to
pressure, and the pain is constant. In pleurisy, other changes in the
respiratory apparatus are present. Inflammation of the ribs gives rise
to a visible swelling. In making a diagnosis, we should not be Batisfied,
until the etiology is established.

DieBASBa OF TUB SEMSOBT KEBTBb 57

koGNOSiS is unfavorable only when the disease ia produced by
I lesions.

iEATMEST. — The treatment is causal and local. The latter aa
luruleias : morphine eubcataneoualy, and the galvitnic, more
^ taradic, current. The current should be strong, stabile, the
I the painful points, or a descending current along the affected
in other respects the treatment is aimiiar to that of trigeminal
Nusabaum recently performed nerve stretching, but the re-
fere nut permanent.

Appendix.

Nmralffia of tkt Mammary Oland (Mastodynia) is a variety of intercoata)
neuralgia, slace the breast iHsupplJed bj the second to sixth intercostal aerves. ia
addition to the eupraclaivicular nerves. Neuralgic aSectioas of the breast occur
almost exclusively in women. It hardly ever develops before puberty, UBuutly
from the sixteentlito the thirtieth year, rarely later. Ansmia, chlorosis, hysteria,
and aervousneas not infre^uentlv form the basis of the disease. Id some cones it is
attributed to injury, uterine afEeciions, protracted lactation, and menstrual dis-
turbances. Nodular indurations are sometimes found in the gland, and often
disappear tvith the cessation of the neuralgia.

Mastodynia is otten bilateral; according tosome writers ft is more frequent on
the left Bide. The patients complain of a violent burning or lancinating pain
which increases paroxyanially and sometimes lauts several hours. Vomiting may
occur at the height of the paroxysms. The slightest contact with the skin in-
creases the pains, and their intensity is also increased, as a rule, shortly before
menstruation (congestion o( the breast?). The patients often experience a sensa-
tion o( tension and weight in the nipple. The pain is either diffused over the en-
tire gland or it is localized in certain points. It often radiates into the neck,
shoulders, arms, and back.

Pressure points are not constant or characteristic. The nipple ia generally
very sensitive to pressure, often also circumscribed parts of the gland. Painful
points are also found on the spinous processes of the lower cervical aad upper
dorsal (especially the second and fifth) verlebree.

A secretion of milk or a colostrum-like fluid has been observed in a few cases
after each paroxysm of pain. Altter observed herpes Eoster after mastodynia.

The disease may last many years and drive the patient to despair.

The diagnosis la usually easy. Inflammntory conditions are associated with
-' ' elevr'--' ' •'- ■-- — '-'

s changes and elevated temperature : malignant growths, which may
produce simitar pains, present a constant growth.

The prognosis is not always favorable.

Trkatuent, — The breast should bo kept elevated. Inunction with narcotic
ointments. Cooper recommended :

It Extract. Belladonna>,

Cerat. Cetacei aflSss.

M. D. a. Bztemally.

Subcutaneous injections of morphine, electricity. Due attention should be paid
to anemia or other predisposing conditions. As a last resort the breast may
be exttrjmted.

6. Litinbo-Abdominal Neuralgia.

Lumbo-abdominat neuralgia affects the short nerves of the crund plexus — ilio-
hypogastric, ilio-iuguinat. lumbo-inguinal, and external apermatic. a. The ilio-
hypogastric nerve is distributed to : the interment of the hip and upper part of
the hypogastrium. o. lUo-inguiual nerve : mtegument of the mons veneris and
tensor fusciffi latfe muscle, c. Lumbo-inguinal nerve: median part of the groin
and thigh half-way down, d. External spermatic nerve: scrotum or labium
majiis and inner surface of the thigh.

As a rule, several or all of these nerves ore affected at the same time. The
pain ia ^nerally felt in the integiiment of the loins as far as the buttocks, the hy-
pogastrium, mons veneris, scrotum (or labium inHJUN) and the ingmnnl region,
fe Among the causes mentioned are; exposure, dlseaaee of the spine and meninges.

58 DISEASES OF THE SENSORY NEBYES.

pelvic exudations or tumors, and flexions of the uterus. The neuralgia is moire
freouent on the left side.

The pains possess the ordinary neuralgic character. Pressure points are found
along the spine (lumbar point), in the middle of the crest of the ilium (iliac point),
on the scrotum, labium, occasionally on the cervix uteri. The neuralgia may be
associated with contraction of the cremaster musole, priapism, diaoharge of
49emen, ieucorrhoea, and vesical tenesmus.

The treatment is the same as in other neuralgias.

7. Crural Neuralgia.

1. Crural neuralgia is a rare affection. It is observed most frequently among
the laboring classes in males, in whom exposure and over-exertion are not infre-
quent causes. It may also be the result of injury : compression by exudations
iux>und the spine, psoas and pelvic organs, pressure of the uterus or swollen Ivm-
phatic glands in the pelvis and groins, aneurism of the crural artery, inffoinal her*
nia, luxation of the femur, stab and gunshot wounds, etc. SeeUgmudler claims
that sprain of the ankle joint often gives rise to neuralgia of the saphenus major
nerve. Cnural neuralgia sometimes follows sciatica,

2. The pains extend along the inner surface of the thigh to the knee, and fol-
lowing the course of the saphenus major nerve, may pass along the inner ear-
face of the leg to the great toe. The neuralgia is sometimes oonnned to a single
<;utaneous branch. The pains are increased on movement of the limb, and are
often more severe at night. They occasionally radiate into more remote regions,
particulu'ly into the loins. The pressure points are: a. Crural noint, below Poo-
part's ligament, corresponding to the exit of the crural nerve; o. Anterior thigh
point, at the exit of the saphenus minor throup^h the fascia lata; c Knee point,
inner surface of the knee loint; (i. Plantar pomt, immediately in front of the
ankle; e. Toe point, at the base of the big toe.

Hypersdsthesia is often, ansesthesia is rarely present. Some patients complain
of formication, coldness, and a feeling of stiffness. Vaso-motor or trophic distur-
bances are rare.

8. 'Hie treatment, apart from causal treatment, is the same as that of sciatica.

8. Obturator Neuralgia,

i Obturator neuralgia possesses more of a surgical interest, because it is an im-
portant sign of incarceration of herniad in the obturator foramen. Pains then
oevelop upon the inner surface of the thi^h as far as the knee, associated with
numbness, formication, and usually with inability to adduct the thigh (because
the motor fibres of the nerve have also been compressed). The treatment oonfifftf
in reposition of the hernia.

9. Neuralgia of the External Cutaneous Nerve.

The pains extend along the outer surface of the thigh as far as the knee. The
disease is generally associated with crural neuralgia, and rarely exists alone,

10. Sciatica,
{Ischialgia, Malum Cotunnii,)

I. Etiology. — Neuralgias of the sciatic nerve are very common.
They are more frequent in men than in women, exceptional in cliild-
hood, and develop, as a rule, between the ages of twenty and sixty
years.

Anasmia, chlorosis, and hysteria possess much less etiological import-
ance than in neuralgias of other nerves.

Exposure to cold and wet, and injury, on the other hand, are the
most frequent causes of the disease.

Traumata affecting the sciatic nerve include: tumors and infiamm^^/>y%|| of

DISEASES OF THE BENSOBT NEBYES. 69

the meninges, with compression of the sciatic nerve; tuberouloeis, cancer, gum-
ma, exostoses, and periostitis of the vertebrae, curvature of the spine, pelvic in-
flammations and tumors, flexions of the uterus, compression by the pregnant
uterus, difficult labor and compression by the child's head, distention of the rec-
tum with fasces or foreign bodies, dislocation or fracture of the femur, exostoses
on the bones of the lower limbs, sciatic hernia, fail or blow on the buttocks, con-
stant sitting and riding, heavy lifting; incised or gunshot wounds; neuromata
and other tumors with pressure on the nerve; aneurism of the abdominal aorta
and popliteal artery, etc.

Sciatica is sometimes associated with constitutional diseases, for ex-
ample, gout. It sometimes precedes diabetes mellitus and locomotor
ataxia^ probably as the result of central causes.

Certain cases are the result of infectious diseases^ viz.: malaria,
syphilis (without the formation of gummata), gonorrhoea, typhoid fever
(particularly during convalescence).

In rare instances it is the result of toxic influences, for example, in
lead and mercury poisoning.

Whether hemorrhoids and checked sweating of the feet give rise to
sciatica has not been determined with certainty.

Climatic and meteorological conditions are not devoid of influence in
this disease. Some English and German writers report an unusual fre-
quency of the disease in certain localities. It is known to every expe-
rienced physician that cases of the disease are more frequently observed
during cold seasons in which there are rapid changes of temperature.

II, Akatokical Changes. — These may be entirely absent, even if
the disease has lasted a long time. In other cases hyperasmia of the
nerve, yaricose dilatation of its blood-vessels, swelling and increase of
the connective tissue, atrophy and fatty degeneration of the nerve fibres
have been observed. Josset recently reported a case in which an obsti-
nate sciatica was cured by puncture of the nerve sheath and evacuation
of half an ounce of serum.

III. Symptoms. — As a rule, sciatica is unilateral, though Hasse main-
tained that it is not so infrequently bilateral as is generally believed,
but that the pain on one side may be comparatively slight, and therefore
overlooked. The disease sometimes begins on one side and then passes
to the other, sometimes it is bilateral from the start, particularly in dis-
eases of the meninges or spine.

The pain may affect the entire distribution of the nerve, or be con-
fined to individual branches (generally the posterior cutaneous, occa-
sionally the plantar nerve). In the former event the pain extends over the
buttocK, posterior surface of the thigh, the entire leg and foot, with the
exception of their inner surface (vide Figs. 22 and 23).

As a rule, the pains are constant, but their intensity increases in
paroxysms, which may assume an intermittent character, even when pro-
duced by organic lesions. They are described as burning, tearing, stick-
ing, bonng, etc. As a rule they run from above downwards, rarely in
the opposite direction. The paroxysms often develop spontaneously, in
other cases they are producea by an incautious movement of the limb,
slight pressure, laughing, sneezing, etc. In one of my patients unusu-
ally violent paroxysms occurred at the period of menstruation. As a
rule, the paroxysms subside so much more quickly the more quiet the
patient keeps. Some patients, on the other hand, are relieved while
walking about, or firmly compressing the sciatic nerve.

Vomiting sometimes occurs at the height of the paroxysm. Tonic
or clonic twitchings are noticed occasionally, and the heel may be drawn

60 DISEASES OF THE BEN80BY NEBYES.

agaiiijft the buttock. The pains radiate not infreqaently into the sacnl
region or the distribution of the crural nerve. Sciatica may atso be as-
iociated with intercostal neuralgia.

Pressure points may be entirely absent, in other cases they are incon-
Rtarit. The nerve is sometimes tender on pressure along its entire
course.

Among the most frequent painful points are : a, a point along the aacnun at
lh<! Uf¥«:i of the posterior superior spine of the ilium; &, lower border of glateua
fnAximus at the exit of the nerve from the 'sciatic foramen; c, immediately be-
hind the trochanter major; d, middle of the posterior surface of the thigh, cor-
ry^fK/oding to the exit of the posterior cutaneous nerve; e, bend of the knee
ittffud nerve); A immediately below the head of the fibula (peroneal nerve); g^
htthiwl the miulaoli; h, several points on dorsum of foot or the calf. The sacnil
pkxiM in sometimes found to be tender on pressure when examined per vagiiuuii
or factum.

Changes in the color of the skin and trophic disturbances are gener-
ally A^misnL In yery rare cases mention is made of abnormal redness of
th'; ifkin, increase^l heat and diaphoresis^ increased growth of hair, oat-
hrttsik of herfjes zoster and furuncles.

.Sensibility may l)e intact, but hypersBsthesia or anaesthesia has been
o\miryi'A in a number of instances. The patients complain not infre-
/|U^fntly of rmra$sthesia5: a feeling of coldness^ prickings burning, formi-
cation, stinness.

Kma^;iation of the muscles with secondary paretic symptoms is not
ixtirifimtni in chronic sciatica, and is often the result of disuse of the
limb. Hut marked atrophy sometimes develops very early and rapidly,
and has bcren attributed by Luiidouzy to neuritic changes m the sciatic

In one cawj fi raves observed hypertrophy of the muscles.

Th(; patellar tendon reflex was unchanged in all of my cases.

Tlic patients often asHuino a t)eculiar position. They generally lie
UfKni the healthy Hide, with the thigh drawn up and the knee bent, in
ordr;r to avoid stretching the nerve. They avoid walking altogether or
trefKi ui)on the floor very carefully, favoring the limb as much as possi-
ble. Many patients complain of violent pain while sitting, and are com-
pelled to asflume a recumbent position almost constantly.

Increased bodily temj)eraturo is sometimes observed at the beginning
of the disease. The patients often complain of constipation, associated
with increasing violence of the paroxysms of pain. Braun showed that
the urine not infrequently contains sugar.

Sciatica may run its course in two to six weeks, but is more often
chronic. Cases have been known to last more than thirty vears. In
rare cases spontaneous recovery ensues at the end of years. Tliere is al-
ways a great tendency to reldpses.

IV. Diagnosis. — The diagnosis is easy, inasmuch as the pains often
run along the exact anatomical course of the disease.

It maybe mistaken for: a, coxitis, which is excluded by the charac*>
teristic position of the body, pain on rotation of the limb or on com-
pression against the acetabulum; b, psoitis, in which a characteristic
position is also noticeable; c, muscular rheumatism, the pain is irregu-
larly distributed, and is produced particularly by pressure on the mus-
cles; dy hysterical joint affections, in which a diagnosis can often be
made only after prolonged observation.

V. Prognosis. — This varies according to the etiology of the disease.

VI. Treatment. — Apart from causal treatment, the leg should be

DISEA8B8 OF THE 8EN80BT NEBYES. 61

kept Quiet, the food should he easily digestihle^ and daily evacnation
irom tlie howels secured. The entire limb should be rubbed every morn-
ing and evening with Stokes' liniment:

5 01. terebinthin.,

Aq. communis aa 3 xiv.

Vitelli ovi 1.

01. lini 3 iss.

F. linimentum.

and the limb then wrapped in cotton batting; iodide of potassium
( 3 iij. : 5 vij., one tablespoonful t. i. d.) should be given internally.
This treatment will suffice in many cases.

I have seen good and permanent results in a number of cases from
change of air.

Electricity justly plays a prominent part in treatment, although I
have seen its application followed by an aggravation of the symptoms in
a number of fresh cases.

The galvanic current is usually preferred: large electrodes, a strong current,
anode stabile to the painful points, or a descending stabile current, or successive
galvanization of small, consecutive stretches of the nerve. Benedikt introduced
one pole into the rectum, and placed the other upon the sacrum. Ciniselli recom-
mended the constant application of zinc and copper plates, connected by a me-
tallic wire. Some authors recommend the use oi the faradic current, either as
the electric brush or moxa.

Great benefit may be derived from baths of all kinds.

Among other methods of treatment may be mentioned : a. Derivatives : cups,
blisters, moxa, actual cautery, aquapuncture, subcutaneous injection of nitrate
of silver, alcoholic inunctions, inunctions with veratrine or croton oil, etc.
b. Narcotics : morphine or atropine subcutaneously, belladonna in ointment or
endermically, chloroform and cnloral hydrate by enema, etc. c. Antirheumatics :
aconite, colchicum, potassium iodide, salicylic acid, etc. d. Specifics : turpen-
tine, arsenic, quinine. Tinct. gelsemii, 5-20 drops t. i. d., had a very rapid etfect
in several of my cases. Neuber recently recommended osmic acid subcutaneously
in all kinds of neuralgia. In my own hands, this remedy (gr. viij. : 3 iij. « a hali-
syringeful subcutaneously) gave no results in a large number of cases, and many
patients complained of severe, sometimes very protracted pain at the site of in-
jection.

Among the surgical remedies may be mentioned massage and nerve
stretching. Nerve stretching has recently been performed as a blood-
less operation, the limb being fiexed as strongly as possible upon the ab-
domen. In one case I obtained temporary good efiects from this plan.

11. Spermatic Neuralgia.

In spermatic neuralgia, attacks of pain occur in the testicles and epididymides,
and extend along the seminal duct to the loins. The testicles and epididymides
are tender on pressure, and are sometimes swollen. The pain may be so violent
that the patient is covered with cold sweat, and suffers from chattering of the
teeth, attacks of syncope, convulsions, and vomiting. The left testicle is most
freouently affected.

The disease often develops at the period of puberty. The patients are often
pale, nervous individuals, who have practised masturbation or indulged in
sexual excesses. In other cases, the disease has been attributed to sexual con-
tinenoe. Injury, exx>06ure, ana varicocele are also regarded as causes. Inter-

62 DisEAdxa or xhb sxaaoKr sxsm.

mittvnt n<»aralipm, which «liflappeus aftv the adminiHtrmtion of quinine, is some-
tifii^Hi i)b0erT«*4i.

Th*> majtiricv of Gh*rman wiitera beiieve thac the lii—iif is an afPectioa of sym-
pnth*>tii" tibrvH in thus tefKicles.

Th«* tr«atiu«*iic oomnsts of elevuaoa of the testicle bj means of a sospensorj,
iniiiv'ttun** with beHanionna ointmeac subcutaneous injections of morphine, lake-
warm >>ntlv«« i*(ectrtcitT, iron, i^uinioe. arsenic, or ponwinm bromide. Gastra-
tioii has tnwu performed in obstmate cases.

Appendix.

\ niimbiMr of other neuralgic affections, which cannot easfly be localized, may
(|«*v<*l<>p i*\ the esterual i^nitals and perineal region. They are usualljr the result
i*r 1*1 Wd. itijurr, onanism, and sexual excesses. We may briefly mention :

It. Ni*iinilKia of the ^tenis and K^ans penis: attacks of pain in the penis or
clnfin. fM«tnetTiu«*s associateil with priapinin. inroiuntary discharge of semen,
arid di-iinrhniMH^ of micturition.

h. NMiimlKia of the scrotum (or labia majora).

IV NiMinitKlii tif the urethra.

il Ari<* vimlotil ii«*unilt(m : spasm of the sphincters of the rectum and bladder,
wild hr^Htir>^th««<«lii (inon* mreiy ana»thesia) of the perineum.

ii, Aii(i.|Hirlniiul iiourulgia.

1 '^. Cocctfgndynia.

Thl4 l**tui U atiplled to attaoks of (viiu in the coccrgeal region, which incroaso
rm «}M)mi£. prmMiins walking, and iKxiily exertion. It almost always oocurs in
tvMrrf*ft. •«fMl In iiitnhtitetl to i\ fall, injury, dolivery. more rarely to a cold. La the
r/ifi)''f 11^ *»t «HUM«M, tho dirt(*)i.4t« !!« prol^bly not a neuralgia, but the result of organic
/•h'iffi!'*^ Ill Mmi (fo(M\vx. S<H«Ii};niueUor priniuced rapid recovery in an obstinate
f^ftnh h^ f h«* ii|fiillniition of tho fiirtuiio current. As a rule, surgical interference is
tt/*t'htmHtf ' «<iiMMiLiui<toiiM NoiNiPition of all t lie tendons and muscles inserted into
rffA f*f«t^ff^t I't I'uiiiovul uf tlio lH>no its^'lf.

\l\, Xruralt/ia of the Joints.

I 7 M4 tU^tthMh iHwiiifH Kitti««rall,v in tinteniic and hysterical women, more rarelj
tfi t'Jfifi^ U9*U '*\iUm\n or In iihmi. Kt|Hwurts injury.acute diseases, violent emo-
f\fiti^, /lM^«MiMi ftt IIm« i|iK««MlUo trma and genital apparatus are mentioned as

• (h^ ttff»*^IUt$t In nliiirii(^l4«riK<Mi by |Mir\>xysmAl|>ain in the joints. Thehipor
fv/kp'^ f/^/r^*< «##«» litihtttnWy, nilinr .i<»intj« an* rarely atTected; sometimes the small
f^t^f* ^*^^ ^^'^*ttftU\ of iliif niiutim lii'o alTiH'ttHi. As a rule, only one joint is involved.

h.'S ff*i**M fffU^h ii«lnhil iHtviiiid tho articular region proper. During the par-
,f/'f/f 'frA ^/^Ia^iiiim<m1. Mvtir Iho Joint niav pres^nit redness, heat, and swelling,
. V 'f.A"^^ nftoitl^tinit t^fMiornlly iliNtip|H*iir when tho pain subsides. The skin is
/ /, ">*/ liA^^nlllVH In NitKtil. prt*Hi<tii'«\ whilo vigi>rous pressure is often weU
. .? /^^^^ i t4*tm tilni IwltflilnKH iimv <KVur during the attack, or the patient pc
;<-// v4M>«^Mi«<iiiut iihiiMiniiti |Nmltlon of tho limK which is usually kept in
. ..' i '/^ <.#ii,Miil'iM (III Joliil liiMiiiiiinHllonM tho limb is usually flexed). *"
' t, */-*" ****- 9nnw\ i\n\. liififMiuiuillv o\rr tho joints.

}J -1'^ 'i,**.44€t^ Stkn^m II I'lMK liiito. tMiitliaotun« and atrophy of the muscles may

'ji' ^ ./ v.*A i4§H^ IaiI. fnt yitiit'4. In oam«ii of nmrkinl hysteria the prognosis is
,■ •' ' »j ¥f'.'f*^

, If' it^^ifffs^ii^ ttumi lilt iMitllv inonil ; wo must ondeavor to persuade the
. / ..■ . ,.A fh^ Ihnh III tMl<llllMM, wo iniiy onlor nervines, iron, quinine,
'7 m' . ./ • ''^^^ififtw *hh ffffiMllH immI cjilviiiilo oumMit, etc.

A, ,l/irr*.«//rf.«i'rr.

• t

i.^j.'i^/ f/fM4ifMM. AtiiPMlhoHia is tho term applied to
'hi ' j iV'-A*!*^'' Hi III'* MfMflory norvo tracts which give rise to

IHBBABBS 07 THE SBNSOBT NEBVSa. 63

diminiition or complete loaa of Beusation. This may occur in all kinds
of BODBory neryes (cutaneous, muacular, visceral, etc.), but we will here
discuss cutaneous ansesthesia alone.

The aenaory cutaneous nerves convey two priDcipal forma of sensa-
tions, viz.: tactile sensibility, and general aensationa. Tactile sensibility
includes:

a. Simple tactile sensibility, i. b., the pure sensation of contact.

b. The sense of presaure.

c. The sense of location.

d. The sense of temperature.

General sensation includes the sensatioD of pain aod electrical sensi-
bility, also the feeling of tickling, itching, and other sensory processes
which are coupled with pleasure or pain..

The methods of examination require skill and core, and tiie patient must po«-
M88 a certain amount of intelligeuoe and power of observation. It is best to
have the patient assume a comfortable, recumbent posture during the examina-
tion, ana to blindfold his eyes. He should bo clearly in- ir. »
formed as to the stages of the examination, "'*■ *^

To determine the simple sense of contact the skin is
slowly and carefully touched with the tip of the finger, or
the head of a pin, and the patient directed to say whether
he experiences a tactile sensation or not. The srticle em-
ployed should possess approximately the same temperature as
the skin, since otherwise a tactile sensation may bo mistaken
for one of temperature.

In addition, the skin is touched with smooth, rough, and
haracteijof whose surface must I

In elimination of the sense of preesure, the limb upon
which the examination is made should be placed on a firm
base, since otherwise the sense of pressure would be esti-
mated, not by the cutaneous nerves, but by the resistance over-
come by the muscles. The simplest method ia that of cover-
ine the interment with a disk of wood, and then placing
coina upon it at regular intervals. Eulenburg devised for
this purpose a banestheeiometer, which consists of a rod
movaola Df means o( a spring, and which at the same time
movea the index on a dial plate. The numbers on the dial

Elate indicate in grammes the amount of pressure requisite
> posh the index to the number in question (Fig. 38).
Kaumlerand Aubert found that the followuigwere the Tninimiim amounts
of pressure which could be felt :

Forehead,
Temple,

Dorsum of hand.
Forearm,
Fingers,

Dohm found that the smallest

Chin,
Abdomen,

Nose,
Finger Nails,

0.04-aOO gm.

if the origioal weight were one gm., we:

Third phalanx of the fingers, 0.4M gm.

Dorsum of the foot O.S "

Second phalanx of the finger.. 0.771 "
First " ■' " 0.83 "

Leg 1-0 "

lUm of hand 1.016 "

its of weight which could be detected,
e as follows :

Fold of the knee l.S gm.

Dorsumof the hand 1.168 "

Forearm l.M "

Sternum 8.0 "

Umbilical region S.S

Back..

..8.8

DI8BA6K8 OF THE BENBOBT KEBTE8.

TRTTS

Forehead, ) Phalanges of fingeiB,

Lips, Forearm,

Dorsum of tongue, > A-^Ai Hand,

Cheeks, Arm,

Temple, J

In examining the sense of locality, two factors must be considered, Tiz., the
proper l<x;alization of a stimulus, and the recognition of the tactile circle. To
determine the former, an irritant is applied to some part of the skin, and the
patient (with closed eyes) directed to describe the situation of the point of irrita-
tion. The measurement of the tactile circles is made by means of compassed or
Sieveking's assiliesiometer. The former is an ordinary pair of compaaaes with
blunt tips, the separation of which from one another may be read off in milli-
metres (vide Fig. 29). The a3sthesiometer is composed of a brass rod, divided
into millimetres, to one end of which is fixed a vertical arm, provided with a
sharp tip, while a second one may be moved to and fro. In using the instrument
(Fig. 30), both tips should be appliM at the same time, and with uniform pres-
sure. The peripheral boundaries of a tactile circle are found at those places
at which the tips of the cesthesiometer are no longer felt single, but double.
Their size depends upon the age of the individual, being less in childhood;
Landois furnishes the following table of measurements in an adult, and a boy of
twelve years.

Fio. S9.

Fxo. 80.

^wywttnmfrftifVfH^HinT JB^ tti tth rr?n rrm

SleveklDg's eeetheslometer.

Compasses.

Adult Boj.

Mm. Mm.

Tip of the tongue.... 1.1 1.1

Third phalanx of finger (volar). 2.3 1.7

Lips 4.5 3.9

Second phalanx of finger (volar) 4 5 3.9

Third *• •• «* (dorsum) C.8 4.5

Tip of nose 6.8 4.5

Head of metarcarpal bones (vo-
lar) 6.8 4.5

Dorsum of tongue ) q^ ^q

Metarcarpus of thumb J *'" ^'^

Great toe (plantar) 11.3 6.8

Second phalanx of finger (dorsal) 11.8 9.0

Cheek 11.8 9.0

Lids 11.8 9.0

Hard palate (middle) 13.5 11.3

Skin over malar bone (anteri-
orly) 16.8 11.3

Metastarsus of great toe (plan-
tar) 15.8 9.0

First phalanx of finger (dorsal) 15.8 9.0
Head of metarcarpal bones

(dorsal) 18.9 13.5

Inner surface of lips. , • 20.8 13.5

▲dolt.
Mm.

Skin of malar bone (pos-
teriorly) 22.6

Forehead (below) 22.6

Heel (behind) 22.6

Occiput (below) 27.1

Dorsum of hand.... ...81.6

Chin (below) 88.8

Vertex 88.8

Fold of knee 86.1

Sacrum I ja a

Glutfiei [*"•'*

Forearm I in a

Leg f*"-®

Dorsum pedis near the

toes 40.6

Sternum 45.1

Back of neck (high up). .54.1

Spine .64.1

Middle of neck 67.7

Arm

Thigh

Middle of back

Boj.

Mm.

15.8

lao

20.8
22.6
82.6
22.6
22.6
81.6

8S.8

[67.7J

96.1
88.8
86.1

Sl.e-40.6

DISEASES OF THE 8ENS0BT NEBYES.

In order to determine the temperature sense of the integument, Nothnagel em-
ployed round, vessels of wood, with a metallic bottom, and filled with water at
different temperatures. Eulenburg constructed a thermassthesiometer. This con-
sists of two thermometers, with large mercury bulbs, fastened to a stand upon
which they can be moved to and fro. The simplest method of examination is to
blow upon the skin, at the same time directing the patient to tell whether he no-
tices the difference. Or the same part of the skin is successively touched with
media at various temperatures, and the differences in sensibility noted. The abU.
ity to differentiate temperatures is most marked when the temperatures employed
range about that of the body. Nothnagel furnishes the following table of the
minimum of difference of temperature which can be detected in different parts
of the skin:

Forearm ••*•«•• } Ao«n

Arm ...f "-^ ^•

Dorsum of hand 0.3** '*

Cheek 0.4-0.2" "

Temple 0.4-0.8" *•

Chest (superiorly, exter-^J

naUy) I q go ..

Upper part of abdomen f

(laterally) J

Palm of hand ) ^ -^ a or*

Dorsum of foot [ 0.(>-0.4 U

Upper part of abdomen )

(middle) I 0.5' "

Thiflfh \

v-'alf ,1 Aft* <<

Sternum J ^'^

Leg (extensor side) 0.7* **

Back (laterally) 0.9** "

Back (middle) 1.2' "

To test the sense of pain, the skin may be pricked with a pin, pinched, the hairs
pulled, etc. Disturbances of the sense of touch and pain do not always go hand
m hand. Retention of tactile sensation and loss of the sense of pain are known as
analgesia.

Leyden and Munk also tested the electro-cutaneous sensibility. They employed
a pair of copper compasses with an insulated handle, which was connectea with
the secondary coil of an induction apparatus, and noted the position of the
cylinder when the patient expnerienced the first sensation, and also tiie first sensa-
tion of pain. Bernhardt furnishes the following table:

A. General Sensibility of the Skin to the Electrical Current.

Tip of tongue

Palate

Tip of nose

Laos

Gums

Dorsum of ton|^e. .
Vermilion of bps. . .

Cheeks

White of lips

Forehead

Acromion

Sternum

Cervical spine

Upper doraal spine.

Arm

Buttocks

Middle dorsal spine.

Occiput

Loins

17.5
16.7
15.7
15.2
15.2
15.2
15.1
14.8
14.5
14.4
18.7

18.0

cm.

n
n
It
(I
<(
«l
<<
<l
<f
<<

12.8

12.7

Neck at lower jaw

Arm

Vertex

Sacrum

Thigh

Dorsum of first phalanx. . . . )

Dorsum of foot )

Dorsum of second phalanx. . .
Dorsum of the metacarpus..

Dorsum of hand

Leg

Tip of finger (volar) )

Tip of finser (dorsal)

Volar surface of metacarpus. .

Tip of toes

Middle phalanx (volar)

Palm of hand

Thumb

First metatarsal bone (plantar)

13.7 cm,

12.6

12.5

12.85

12.3

12.0

11.75

11.6

11.5

11.8
10.9
10.6
10.5
10.6
10.5
10.2

<«

<<
<«
ii

4<
t»
«<
• «
<<
<<
«<

B. BlectrO' Cutaneous Sensibility to Pain.

Lids 14.2 cm

Palate 18.9 *

Tip of tongue 14.12

Gums )

•Kpof nose \ 18.0

White of lips )

Lower part of forehead 12.6 cm.

Vermilion of lips ) ^a «

Cheeks \ ^-^

Occiput 12.0

Throat below the jaw 11.8

Upper dorsal spine 11.7

I ,. M : '1 ' 711 fi'^Mum "-.i r.nr znsiuuu:

K'lr'arrr. .

I>'#r«itirfi .f --»*r^r:iniiii
*■•■■»-- 1-

Volar *iirf vj* .^ :wn jjuiuuiz:. .
MMl'II»">f -.r. .--..-. ., I

V'il;ir *'jrfA.-.i* :if i**r:>nj.

Till 'if |/,««.f

■ •

•

• t

■ (

: ]

J'»

J'l

i • I

)

I'l

'.»

•|

•»

• «

i.f'' "hfii; tiil.io.-: rfpr<<-.<'rir ^T-rVfc^ "vur.:! na- n—

. » .,,....•. ■■■ ■.l'li'.»i/ii ti -vnnfiitittr^ r^^ZfiSji'siiiic i..xzi -j^im

... I ii.-i-' ••• |«.iri--.iH of :i]\ rr. :•:■:;• :z 44*!iiii— .r

, . M.iM'ii I'M ''I -I'l'il ji i'»ii of iii'liv;; -.il iiii-r- .- — »i_

.. ;,',•. I.- 'ii > ■Mm '.iji iir»« "oriiotim^'-: ^.\*r^T^i*i. "^"ii

• ./ J- ii-l ' '" . '•" 'N-IIIlpI*'. tilt: piTlT-":- — I T -, -

.,.1 . .,M 1..-; <li Inn il\. Iiiit. Ilii'v muy iT.:sz^£r i.''.'±r, :::
. . ., I i.,.ii.li. .i II ; ii Mill I iiiiiv iiIko h*f folx, ;- :.i.:e*. : r

...J •.! .• |i»ii Mi.i\ lii t |ilni|||ci; ;i iiiolilt: 5*rI>siL.:: : Z.. l^.-
•fj,..iii '..ml Ii <'l \ril ill tllliJ'H a 'lou' .r =*T ii;Lr :i.

• ■ >.'■ ii.i I.I !• I ••iH' iiHiH' 1 1'\ rn*, as tlif; r*:i!*.;l: . "f i *_- ^"i
' ...- .il.i I nin\ii in wliir.h tin; |»ri';k of :i "rii: - *■-

■. ..ii'.M- i|i-.l\i- iluiiji). In julditior.. :r.f- r-er. •:

'I III' ■' n III mil liisiV Im- UMUSUullv I0X.Z • '^liT^-

'' i.' I.I ii- I ii« iim i'iiImmI or flifTnse. Ii i? s-::r.r-

I ■ 'ii. 1 1 iiiui MHi III i.iM« iir Mu»n' iicrve.s. In spizial ^:?i«~-
^. j.'.il, ili.i mIiiiI'-.I IiKp |»:ir{i|»lc'^ia (paraniteiLrsia.*.

I ' ; 1. ...... ii \ li. iiniliitcnil (iH'riiianwsthesia).

i! ■ M. •• ' • "I iHi I' 1 lii'.i.i :iri«sitnjit('(l inthe perH'iheral

• • , iM 1 \« ■. Ml I l»i» !• |ijirlH of the cerebral CO rrei

, ;.'..) .inmilii' I- iihinitIimI into HciiBution, OF in the

* . - .. I,' I ■ < I II llli> I W 11.

It , » I' ' !• n..\ II « 'Mil • I iiMi" ili'''Ji>i«'M of the peripheral ter-

» ■ ' .i.i.i-'.M.' .■•ii'iM\ iiiiM'.. h is true that Meissner

.- . i..iM.(i • Ml IIh- iiiriilf rurjiiisi'lcs ill (•erebral di^easo5,

I . II.' ii.ijn iiinl iiml .mm iiiiin'ly t'\t*hule(l from the fol-

... II' I I i liM'f MthMilion will be paid to dis-

I < >.■.. i.t ti III iIh- |»i<i i|iImi:iI nri'Ni' t ract.s.

/■' , ' I II.' .liii 'lijiiiMli \iM\ Minlorially upon the normal

■ I .. . i I. ' .1 Aii.i ; IJM'I li' .'N tiiplnins always develop in a part

' .... .1 ii.i.. Ik I II I NjHJji'.j li\ nu'aiis of an Esmarch ban-

I ■ .. .ii .1.1 1 ' liti.« III 1 11 |iiiiiliit'(Mi by iMMiipression of a vein.

Ill 'i. . II. 11I.1I..1 \ ill 1 III lijiiuTs as thi' result of morbid

I ' ... II. • . I. Ill \i iiiiu-< I lir(i!ti!)it>is, I'tc).

I '. I... ..I J- Miiiii(iiiii-t tlii'n'suli of thermic influences.

i> . .. ■ . . I I h. . I'Hi liv HH aiiH of eiluT retluoes the sensibility

DISEASES OF THE 8EKS0BT NESYES. 67

to such an extent that surgical operations may be performed in a painless
manner. Increased heat may act in a similar manner. In some cases,
probably, circulatory changes are produced chiefly or exclusively by the
action of temperature; in others, perhaps, there are direct effects on the
terminations of the sensory nerves.

Allied to thermal influences are the chemical noxa, which produce
anaesthesia if they act upon the skin. Thus, it is well known that work-
ing in lye, strong acids, or carbolic acid rapidly produces anaesthesia.

It is also claimed that the action of the electrical current upon the
skin influences the sensibility of the latter.

Toxic anaesthesia of the skin is that form which develops after the
use of narcotics, when employed subcutaneously or in tne form of
ointment. Thus, subcutaneous injections of morphine may diminish
cutaneous sensibility by direct action upon the terminations of the sen-
sory nerves. Anaesthesia has also been observed in poisoning with lead,
ergotin, or carbonic oxide, but this is perhaps the result of central causes.
Anaesthesia has also been observed after infectious diseases (typhoid
fever, diphtheria, syphilis, etc.).

In the majority of cases, however, morbid processes are found in the
peripheral nerves (rheumatic and traumatic influences, inflammations of
the nerves, compression by tumors, etc.)

III. Symptoms. — Cutaneous anaesthesia is easily recognized if the
methods of examination are carried out in intelligent patients. In &
thorough examination, all qualities of sensation should be submitted to
test. In addition, the anaesthetic district should be mapped out.

In partial anaesthesia, the symptoms may vary from time to time,
inasmuch as the individual qualities of sensation may disappear or reap-
pear at different times.

In some cases the patients call attention to the anaesthesia, because
they notice diminished sensation on touching objects, or feel as if they
were walking on felt or wool, etc.

If the hands are affected, the patient is apt to drop objects as soon as
the eye is turned in another direction.

Some patients also complain of paraesthesia (coldness, feeling of stiff-
ness or tension, prickling, formication).

In the simplest cases nothing is noticed beyond the objective signs of
anaesthesia. In other cases, there are a number of disturbances of inner-
vation, which depend upon an affection of other nerve tracts in addition
to the sensory fibres.

For example, the most violent neuralgic pains may be felt in the
affected nerve tract despite the absolute anaesthesia (anaesthesia dolorosa).
Thus, a tumor which compresses a nerve may interrupt conduction from
the skin to the tumor, t. e., produce anaesthesia. At the same time the
tumor may irritate the central end of the nerve in such a manner as to
produce in the central organ a sensation of pain which will be referred
xo the peripheral distribution of the compressed nerve.

Motor aisturbances will be present if mixed nerves are affected, and
may appear as paresis or paralysis, tonic or clonic spasms.

Beflex movements are always abolished in purely peripheral anaesthe-
sia, simply because the stimulus is not conveyed to the cord or brain.

Yaso-motor fibres are not infrequently affected at the same time as
the sensory fibres. The anaesthetic parts then present either unusual
pallor, or, more frequently, unusual redness and livid discoloration of
the skin; oedema and pufflness of the skin may also be noticed. This is

86 DIBBASE8 07 THB SENBOBT SSBVSB.

nsnal); aseooiated with changes in the cntaneons temperature (unusual
heat or cold),

Anteathegia may alao be associated with trophic changes, as the result
of an affection of trophic nerve fibres in the lesion. These changes
include abnormal growth of hair, escessiye formation and desqua-
mation of epidermis, marked thickening and gloss of the fingers,
inflammation of the nails, development of furuncles, herpes, pemphigus,
extravasations, etc.

IV. Diagnosis. — As a rule, the diagnosis of cutaneous anEesthesia is
not difficult. We should always endeavor to ascertain the cause and
situation of the anaesthesia. An important distinction betweeu peri-

{iheral and central aneBsthesia is the absence of reflex movements in the
atter. In addition, the concomitant symptoms and the distribution of
the cutuneoiis anaesthesia must bo considered in the diagnosis of the site
of the lesion.

V. Prognosis, — This depends entirely on the etiology of the disease,

VI. Treatment. — This should be first directed towards the removal
of the cause. In addition, we must rely on local measures, especially alco-
holic and irritating inunctions, and electricity. In employing galvan-
ism, the anode is placed ou an indifferent spot, the cathode is methodi-
cally stroked to and fro over the aniesthetic region (labile application),
The irritant effect is iuci-eosed if the wire brush ia connected with the
cathode. In faradic applications, the electrodes should not be too
moist, and should not be pressed too firmly upon the akin. The faradio
brush may also be applied in a labde manner.

As an illustration of aucestbesia of a special nerve, we will discuss:

Anesthesia of the Trigeminus Nerve.

Among the causeB mentioned are exposure and injury. In the former event,
individual branches are alone affected. Injuries to the nerve maj be of v&rious
kinds — atab and gunshot wounds, falls, htows, surgical operations, extraction of
teeth, ahacesaes, campressinK tumors, i aflat nmationn and other diseases of thwe
:b at the skull and face through whose foramina branches of the nerve take
their course; exostoses, tumors, etc., of the base of the skull, meningeal di»*

I II. Sthptoms. — As a rule, anaesthesia of the trigeminus is unilat-
eral. If the entire distribution of the nerve is involved, the motor
branch will also be affected, causing paralysis of the muscles of mastica-
tion on one side (vide iiage 13). In totJil trigeminal hemianesthesia,
there is loss of sensation in the face, the forehead as far as the vertex,
the external, upper part of the concha, and the mucous membrane of
the eye, nose, and buccal cavity. The patients suffer occasionally from
parfflsthesife or from neuralgic pains.

Circulatory and vaso-motor disturbances are not infrequent: redness
and swelbng of tfac integument of the face, changes in perspiration and
the temperature of the slcin.

Attention has long been attracted by certain trophic disturbances —
hemorrhages and ulcerations of the buccal mucous membrane, loosening
of the teeth, herpes, still more by inflammatory changes in the eye
' - ■ . In the latter oases, we find injection and

(ophthalmia neoroparalytica).

DISEASES OF THE NERVES OF SPECIAL SENSE. 69

swelling of the conjunctiva, opacity and acute destruction of the cornea,
followed by loss of the entire eyeball.

Meissner endeavored to shoi^ experimentally that ophthalmia neoroparalTtica
is due to the destructioa of certain trophic fibres situated in the median part of
the trunk of the trigeminus. Some authors maintained that the trophic fibres
do not reidly belong to the trigeminus. It was shown that the ocular changes
do not develop unless the nerve is injured at the Gkuserian ^nglion or on its
peripheral aspect, t. e., after sympathetic nerve fibres have joined the nerve.
Numerous observers claimed, on tne other hand, that the ocular affection is a
traumatic keratitis, the result of the fact that, on account of the ansssthesia of
the cornea, the eye is readily injured, and perhaps because, on account of inter-
ference with the movements of the lids, germs find a ready entrance into the
corneal tissue.

There is sometimes ansasthesia of the entire conjunctiva and cornea,
more rarely the sensibility of the cornea is retained. In the former
event, touching the cornea produces neither increased secretion of tears
nor winking, an important distinction from central ansssthesia. Wink-
ing will be producea if a bright light is allowed to fall upon the retina.

The application of stimuli to the nasal mucous membrane does not

? reduce any reflex effect (sneezing); this is also true of irritation of the
uccal mucous hiembrane. Gustatory disturbances have sometimes been
observed, even though the facial nerve was intact. Hence it seems that
the lingual branch of the trigeminus does not always receive all the
ffustatory fibres from the facial through the chorda tj^mpani, but that
tne trigeminus may contain such fibres from its origin. Unilateral
coating of the tongue has been described in some cases. Nothing is
known concerning disturbances of salivation or audition in this disease.

If the lesion is situated at the base of the skull, the adjacent cerebral
nerves, particularly the facial, acoustic, glosso-pharyngeus, and the nerves
of the ocular muscles, are often paralyzed.

The duration and course of the disease depend entirely upon its
causes.

III. Diagnosis, Prognosis and Treatment. — The recognition o£
the disease is easv. The more the individual branches of the nerve are
alone affected, the more peripherally is the lesion situated. In central
ansBsthesia the reflexes are always retained, if the lesion is situated on
the central side of the trigeminal nuclei.

The prognosis depends on the etiology.

The treatment is the same as that of cutaneous ansdsthesia in general.
If the eye is affected, it must be suitably protected. Some writers claim
to have obtained beneficial effects from the direct application of elec-
tricity to the eye.

G. DISEASES OF THE NERVES OF SPECIAL SENSE.

1. Diseases of the Olfactory Nerve.

{Hyperosmia, Anosmia, Parosmia,)

Very little is known concerning diaeaset of the olfactory nerve. Many indi-
viduals suffer from them for a long time until they are revealed by accident.

1. Hyperosmia or olfactory hypercesthesia is manifested by the fact that the
patients smell substances which normal individuals are unable to detect, or they
are so strongly affected by certain odors that they suffer in consequence from
syncope, vertigo, headache, and even general convulsions. Cases have "heem

70 DISEASES OF THE NEBYES OF SPECIAL SENSE.

known in which individuals educated the olfactory sense to such a def^ree tliat
they could trace objects like dogs or birds of prey. Uyperoemia R:enerally affects
hysterical, nervous, or psychopathic individuals, and is, therefore, more often
the result of central than of peripheral causes.

2. Anosmia or olfactory ancMthesia means the diminution or abolition of the
sense of smell. In examinations those substances should be avoided which, like
ammonia and acetic acid, irritate the nasal mucous membrane, and thus stimu-
late the trigeminus. Substances possessing a pleasant and thoah possessinic An
unpleasant odor should be employed, since the individual may be ansdsthetic to
one class and not to the other (partial anaesthesia). According to Althaos, irrita-
tion of the nasal mucous membrane with the constant current produced a smdl
like that of phosphorus (?).

Anosmic patients sometimes complain of subjective, usually unpleasant olfoo-
tory sensations; this corresponds to ansBsthesia aolorosa.

Many patients also complain of gustatory disturbances. This is only true of
those articlec of diet whose flavor depends chiefly on the olfactory sense, for ex-
ample, the bouquet of wines, the smell of cheese, meat, fruit, etc This only
occurs in bilateral anosmia.

The disease may be congenital or acquired. Cases have been reported in which
the olfactory nerve was absent. Anosmia is sometimes attributed to ooid, more
frequently to injury. According to Ogle, a blow on the occiput may, by oontre-
coup, tear the fibres passing through the ethmoidal foramina from the olfaotoiy
bulbs. It is sometimes the result of nasal affections (acute and chronic corysa,
polypi). Tumors, inflammations or exostoses Ht the base of the skull, etc., may
compress the olfactory nerve and impair its function. Anosmia is sometimes
associated with aphasU and right hemiplegia in disease of the {eft island of BeiL
According to Altnaus, olfactory neuritis, followed by anosmia, is a not verr rare
disease (?). Prevost attributes the anosmia of old age to atrophic changes in the
olfactorr bulbs. It has been observed occasionally after continued stimulation
of the olfactory nerve, or as the result of irritating nasal injections and doaches.
Raynaud observed intermittent anosmia; it has also been reported after aonte
infiectious diseases.

Ill certain cases the disturbance of olfaction is the result of disease ot the tri-
geminus or facial nerve. In trigeminal anaesthesia the sensibility of the nasal
mucous membrane for biting and irritating odors is impaired, and if the anaas-
thesia is peripheral, sne€*zing or other reflexes cannot be produced b^ tickiini^ the
mucous membrane. Olfaction proper may also be impaired by dimmution of the
lachrymal secretion, so that the nasal mucous membrane becomes dry and lest
sensitive to smells. Anosmia may also develop in facial paralysis, beoanss
paralysis of the lower lid impedes the flow of tears into the nose, and also
oecause the paralysis of the muscles of the ala nasi impede the entrance of iedr into
the nostril.

The prognosis is bad if the causes cannot be removed. In addition to caoaal
treatment, the galvanic or faradic current has been applied externally to the
nose or directly to the nasal mucous membrane by means of sound-shaped elec-
trodes; strychnine has lieen recommended subcutaneously, internally, or locally
to the nasal mucous membrane (strvchnine, gr. iss.; ol. amygdal., 3 uj.).

8. In parosmia there are unpleasant subjective sensations of smell, or the
patient perceives unpleasant odors as pleasant, and vice versa. This is observed
in hysterical and insane individuals, in epileptics as the so-called aura, sometimes
in anatomical lesions of the olfactory nerves or in central diseases, if the central
fibres of the olfactory nerves are affected. This group includes the predilection
for certain smells which are generally regarded as unpleasant, for ^^^ampl^
Schilier^s predilection for rotten apples.

2. Diseases of the Oustatory Nerves.

{Hypergeusia. Jgeusia. Parageusia. )

It is generally held at the present time that g^tation upon the anterior two>
thirds of the tongue is supphed by the lingual branch of the trigeminiu; upon
the posterior third of the tongue, soft palate, anterior palatal arch and pharynx.
by the glosso-pharyngeal.

Gustatory disturbances from diseases of the ^losso-pharvngeal nerve alone aie
unknown. We have previously shown that diseases of the facial nenre may be

DISEASES OF THE PEHIPHEEAI. NEETEH. "1

asBOciatedwith diBturbances of taste (vide page 6). If we pass from the peripheij
along the course of the gueia Lory fibres towariie the braiu, the aoterior two-thiriu
of the tongue are founa to be supplied by the Ungual branch of the trigeminiis.
The greater part of these gustatory Hbrea paas in the chorda t;mpaui to ilie tacial
nerve. They again leave the facial at the geniculate ganglion, paas through the
nervua petrosus superficialia major to the trigeminus, and through the spheno-
paiatino ganglion to the second branch of the trigeminus (vide Fig. 6). Some
authors believe that the gustatory fibres la the trigeminus are derived from the
gloRso-pha ry ngeiis.

The Bimple gustatory sensationa are: aour, sweet, bitter, and salty. Sour may
be tested by dilute vinegar, sweet by sugar in solution, bitter by aloes, oolooyuth,
strychnine, salty by sodiiun chloride, etc. Irritating and concentrated solutions
should be avoided. During the examination the patient should dose hia eyes, and
protrude the tongue, the surface of which is touched in various places with a
pieoe of rolled-0p blotting paper, dipped in the solutions previously mentioned.
A little brush or a glass rod may also be used, but the drops of Quid should not
be too large.

The patient should not withdraw the tongue until he has indicated that he
has ta«ted the subetance. Before experimenting with another substance the
mouth should be carefully rinsed with witter. It should be remembered that
bitter is perceived most distinctly by the root of the tongue, sweet by the tip. and
BOUT by the edges.

n. In giistatoi-T/ hyper CMtheaia or hypergeusia the patients can taste minimum
traces of a subsiance. or the gustatory seuaationB produce an unusual dM;ree of
pleasure ot disgust. This is observed in hysterical and nervous individuals.

b. O-uatalory anresthetia or ageusia is the diminution or abqiition of the si.^.
of taste. Only a few gustatory qualitiee may be abolished, or in addition 14 I
ageusia, the patient suffers from perversesitbjectjve sensations of taste. Thedia* I
ease may be oilateral, unilateral, or circumscribed. The conduction of the a "" '
sations is often delayed.

Ageusia is observed when the tongue is thickly coated, the buccal mucous
membrsue abnomially dry, and when too hot or cold substances are ingt^ted.
This is evidently the result of implication of the terminations of the lingual and
glosso-pharyngeat nerves, Ageusia also occurs in diseases of the lingual nerve,
and is a frequent symptom ot trigeminus anaesthesia and facial paralysis. The not
infrequent association of gustatory disturbances and diseases of the middle ear is
effecttfd through the chorda tympnni.

Treatment consists of galvanic applications to the tongue or Ungual nerve, to
the petrous portion of the temporal bone, or transversely through the head.

c, Pitrageaaia appears most frequently in hyatericaT and insane individuals.
The gustaiory sensations are generally nauseous and perverse, and may give rise
to special delusions in the insane. Wernich noticed a bitter taste in the mouth

t!r a subcutaneous injection of morphine, in feeble individuals, and in himself
a prolonged fasting. Parageusia is souiptimes associated with ageusia.
AN
1. Infiammation of the Nerves. Neuritis.
I. Anatomical Changes. — Inflammatory changes in the nerrea
may be located in the interstitial connGctivo tissue (perinearitigj or in
the nerve libree (parenchymatous nenritis). Tlie inflammation is some-
times confined to a circumscribed region (circumscribed neuritis) or it
sproade further and further (neuritis migrans) in a centripetal or centri-
fngal direction. The process may spread coiitinuoualy along the nerve,
cr it may overleap longer or eliarter stretches of the nerve (neuritis dis-

^^|L The anatomical changes in perineuritis vary according as the disease
^^^ncut« or chronic,

^^H In acnte perineuritis the nerve is UDUsnally congested, its vessels dis-
^^^fcded, and small extravasations of blood arc noticed here and ihore. ^

72 DI8EABB8 OF THE PEBIPHSBAL HXEVXB.

The surface of the nerve is less shining than nsaal, the inflamed part
is swollen and very succulent, and the macroscopic traosyerae striation
less distinct.

On microscopical examination the blood-vesaels in the nemilemma are f oond
unusually full, their walls are sometimes thickened and particolarlj ahining, and
the nuclei are occasionally increased in number.

Upon the outer surface of the vessels are found accumulations of round cells
which are especially profuse in places. Some of these white blood-i^obiilea con-
tain very fine granules of fat.

In some places the blood-vessels are torn, and red blood-globiilea are found
free in the cellular tissue.

The connective-tissue parts proper of the neurilemma axe awoUen, and their
cells increased.

If the neuritis is violent, the originally interstitial ohang:e8are oomplicated by
parenchymatous chan^gjes, evidently as the result of the circulatory dirturbanceiL
These chanees are similar to those observed in the peripheral parts of a nerve
after expenmentel section-regeneration and disappearance ca the medullaiy
matter, followed by destruction of the axis cylinder, and marked nuclear prolifer-
ation in the sheath of Schwann. This parenchymatous di^neration is genenlly
most marked near the perineurium.

If the acute neuritis recovers, the congestion disappears more and
more, the extravasations are absorbed, the emigrated white blood-glob-
ules undergo fatty degeneration and are absorbed, and the nerve gradu-
ally assumes its normal appearance. Recovery takes place muoli more
slowly if the interstitial process has been followed by parenchymatoua
changes. Very acute perineuritis may terminate in tne formation of
foci of pus, and these, if sufficiently large, may entirely destroy conduc-
tion in the nerve. This is most apt to occur ii the penneuritia jiaa be^
excited by suppuration in the vicinity of the nerve. Even gangrene has
been observea under such circumstances.

Acute perineuritis not infrequently becomes chronic, or the inflam-
mation may be chronic from the start. We then find proliferation and
increased consistence of the interstitial tissue, a grayish-red color of the
nerve, sometimes a grayish-black or graphite-like appearance, due to pig-
ment left over after previous hemorrhages. The increase of connective
tissue, shown by the abnormally-wide interstices, is especially distinct on
transverse section of hardened nerves. The individual fibres are some-
times constricted to such an extent that they undergo atrophy, and the
nerve may be converted finally into a solid band of fibrous tissue which
is destitute of nerve fibres (sclerotic neuritis). Corpora amylacea are
found occasionally at the site of inflammation. Chronic perineuritis
may develop in a single circumscribed spot, it may spread continuoudy
over a large tract, or it may skip over certain parts. In the latter event
the inflamed portions of the nerve not infrequently form nodular or
spindle-shaped prominences (neuritis nodosa). These thickenings may
follow one another in the shape of a rosary. The inflamed parts of the
nerve not infrequently present fibrous adhesions to surrounding parts.

Parenchvmatous neuritis is rarer than perineuritis, and stiU rarer aa
an independent affection. It occurs most purely if the continuity of tha
nerve has been interrupted in any part oi its course. The peripheral
portion of the nerve then presents a series of processes which are known
as degeneration, and which are partly infiammatory in their origin (nea-
ritis degenerativa) (vide Fig. 1).

II. jBtiolooy. — There can be no doubt that neuritis may develop aa

DTBEASBS OF THE PEEIPHEHAL WKKVE S.

the result of a cold, bat in a much larger number of cases it ie the result
of iujury.

Among the numeroux fonna of traumBtisro we ma^ mention incised and j^n-
ehot wounds, falla, blows, dislocations, fractures, compression bj tumors, lifting

rvy loads, etc, Neuritb sometimes develops in amputation stumps.
In some eases the inflammation extends from surrounding parts.

This is obeerved in pelvic abecesses. tubercular diseases of the spine, inflamma-
tion of the joints and sheaths of the tendons: after pleurisj, poeumonia, and
phthisis; in progressive muscular atrophy , according to Friedreicti; in cancer and
sarcoma, particularly of the vertebrsB. According to Leyden, many cases of
reflex paralysis are the result of the eztenaton of neuritis migrans to the spinal
cord.

Keuritis sometimes follows infectious diseases (typhoid and relapsing
fever, erysipelas, variola, diphtheria, syphilis, leprosy).

Toxic neuritis occurs moat fregnently in lead poisoning, but this form
still requires careful investigation. It also develops in phosphorus
poisoning.

No causes can be demonstrated in certain cases, and some authors
aesame a predispositioa to neuritis in certain individuals.

Hi. Pathological Significance of the Disease. — The eiperi-
iDAntat investigations of Tiesler, Feinberg, and Klemm have shown that
neuritis may extend to and implicate the meninges and snbstance of the
spinal cord, or that it may pass from the nerves of one side of the body-
to those of the other side without affecting the cord. Similar observa-
tions have been made in human beings.

It has been observed repeatedly in tetanus that nenritis disseminata,
starting from a peripheral wound, has extended to the spinal cord. It
is also assumed that migrating neuritis forms the connecting link in
reflex epilepsy, following cicatrices in which sensory nerves are imbedded.
Leydon suppoBcs— and not without reason — that certain complexes of
symptoms which have been attributed hitherto to anterior poliomyelitia
are really due to extensive neuritis.

A wide field of investigation is here opened, especially since the
results of experimental investigations have been disputed.

IV, Symptoms. — Among the symptoms, the local phenomena play an
important part from a diagnostic standpoint. They include increase in
the consistence of the nerve, nodular thickenings, and pain on pressure,
The pains are especially severe if the nerve is rolled to and fro between
the fingers. The pain may be confined to certain parts of the nerve, or
extend along its entire course. In some cases we notice a streaked or
more diffuse, erysipelatous redness along the course of the nerve, with
local diaphoresis and increased warmth.

The disturbances of innervation vary according as the nenritis affects
B motor, sensory, or mixed nerve.

In acute neuritis of sensory nerves, tactile sensation is generally di-
minished in the distribution of the nerve, while pain sensation is in-
creased (hyperalgesia). If the nerve fibres are destroyed, this is followed
by loss of pain-sensation (analgesia). The patients often complain of
paneathesiie, burning, pricking, formication, an abnormal feeling of
neat or cold. etc. Spontaneous pains are almost always present. They

generally constant, but are increased on pressure, or they in-

74 DISEASES OF THE PEBIPHSBAL NERVES.

crease epontaneonsl j in paroxysms. Intermittent paroxysms, like those
of neuralgia^ arc rarely observed. The }^ains often radiate into remote
nerve tracts. Trophic changes are not infrequent: herpes zoster, pem-
phigus, thickening and desquamation of the epidermis, glossy fingers,
changes in the nails, etc. Motor irritative symptoms (twitcnings, spasms,
contractures) sometimes develop as reflex symptoms.

Neuritis of motor nerves results in paresis, paralysis, tonic and
clonic spasms, and contractures. These changes may undergo rapid
resolution if they are the result of compression of the nerve fibres by
inflammatory swelling; they are more permanent if the nerve fibres them-
selves have taken part in the inflammation. In the latter event, trophic
changes in the muscles (diminution in the size of the individual bnndles
of muscular fibres, unusually distinct transverse striation, and increase
of the nuclei of the sarcolemma]) are apt to develop very rapidly.

At the outset, the electrical irritability is not infrequently increased,
but if the inflammation is severe, the symptoms of degeneration re-
action will develop ^vide page 7).

Acute neuritis of mixed nerves presents a mixture of the symptomi
mentioned above. Sensation is lost at an earlier period, and to a mora
marked degree than motion, but it returns earlier than the latter
recovery begins.

Chronic neuritis presents the same symptoms as the acate
except that they develop more slowly and run a milder course.

The disease sometimes lasts for months and years. Beoovery majlij^
complete, or permanent disturbances may be left over.

v. Diagnosis. — The diagnosis of neuritis is difficult if local chAiiMi
in the nerve are absent. It may be mistaken for a, neuralgia : in Ala
the pain is intermittent, and Valleix' pressure points constitute a mora

Srominent symptom; b, muscular rheumatism: pain is produced Inr
irect pressure upon the muscles; c, embolism or thrombosis of the vessM
of the limbs: circulatory disturbances (pulselessness, oedema, cyanosis)
are noticeable, 'd. The differentiation between neuritis nodosa and
neuroma is not always possible, even anatomically.

VI. Prognosis. — A favorable prognosis can only be given in those
cases in which the disease is the result of causes which can be readily
removed. But the possibility of the extension of the process to the
spinal cord should always be kept in 'mind.

VII. Treatment. — Apart from causal treatment, we must rely ex-
clusively on local measures : absolute rest, alcoholic inunctions, blue
ointment, potassium iodide ointment, tincture of iodine, local warm
baths, at times ice, leeches, cups, blisters, and, if the pain is venr se-
vere, subcutaneous injections of morphine. Electricity is one oi the
best remedies; stabile constant current, anode to the painful points,
cathode indifferent or on a central painful point. We prefer feeble
currents, others recommend strong currents. If the pain is very intense,
good results may bo obtained from the faradic brush or moxa.

In chronic neuritis we may resort to electricity, massage, nerve
stretching, various baths, and cauterization.

2. Multiple Neuritis.

{Progressive neuritis. Disseminated neuritis. Polyneuritis.)

I. Etiology. — Neuritis sometimes occurs as an independent affec-
tion in many peripheral nerves, and may run an acute, subacute, or
chronic course. Acute multiple neuritis may prove rapidly fatal.

DIBE^EB OP THE PUBIPHBBAI. SIEVES.

The snddeD onset, the rapid and febrile course of the disease raise the
suspicion that we hare to deal with an infeotiona process. Chronic
forms of the disease also appear to lie counecteil with infectious pro-
ccseea. For example, Scheiihe and Baels regard beriberi aa miasmatic
in its origin, and dejwndent on an extensive neuritis (paneuritis).

Traumatism has been mentioned as & cause of polyneuritiB.

The disease has also been observed after infectious diseases, such as
parotitis, acute articular rheumatism, and, according to Tjeyden. diph-
theria, typhoid and relapsing fever, erysipelas, syphilis, and phtliisis.

It generally occnrs between the ages of twenty-one and thirty years,
hut Webber reported a case in a child of nine years.

11. Stmptoms, — Acute multiple neuritis is not infrequentlv pre-
ceded by prodromata. in one of my cases, tiie patient suffered from
periodical chills, fever, and sweat. In other cases, there is merely a feel-
ing of general malaise.

The mauifest symptoms generally begin with pain and paia

The pain is described as burning, boring, lancinating, and may be very
intense; it may be superficial or deep.

A feeling of paresis and stiffness soon becomes noticeable in the dis-

.^bution of the nerve, and rapidly pasaoainto well-marked paralysis. In

ly case the paralysis occurred almost aa suddenly as a stroke of apoplexy.

The electrical irritability of the jiaralyzed muscles and nerves rapidly

Its, and degeneration reaction may be noticed within a tew days.

If the paralysis does not eoou recover, the muscles rapidly atrophy
and later undergo contracture.

The motor nerves are chiefly, sometimes almost exclusively affected.
Sensory disturbances are not infrequently present to a very slight de-
gree. Vaso-motor changes — ledema, cvanosis and diminished tempera-
ture of the skin — are often noticed. Secretory and trophic cutaneous
disturbances may also occur.

The tendon and catansous reflexes in the distribution ot the affected
'ea are lost.

OIBKASBS OF THE PEBTPHEBAL NBBVEB.

The affected nerves are not infrequently tender on ]
The situfttion becomes very dangerous when the disease exhibits a ten-
dency to spread. In a case under my obseryation, the symptoms began
in the left peroneal nerve, then spread from one nerve to "the other, from
the legs to the arms, finally to the optic and pneumog^astric nerves. Fie.
31 shows the temperature and date of the paralyses m this case. Impli-
cation of the vRgus (shown by acceleration and irregularity of the heart's
action, and by difficulty in breathing) is especially grave. Although the
disease generally spreads from below upwards, this does not always hold
good. It may cease at any time, and the paralysis may recover in part,
while atrophy and and contracture of the muscles occurs in other parts.
The bladder and rectum are usually unaffected. Albuminuria has
been observed a number of times; icterus has been deaoribed in two

TPBBtveree secdon ot ihc iBf t . _._...._..._

Tlslbla. wltb numeroiiH sltrsTuactona of blood, putlj nicliln tbem. psrtlr Id the surroundlBC
DonDectlve tlasue ipirr. peririeuriumi. Also Dumeroiu eitnvautloDB In tbe mora remoM
eplnmirtum, Fp. EolftrKBil SO Uiddb.

ThesymptomB of subacute and chronic multiple neuritis are similar
to those of tne acute form, but develop more slowly and less violently.

III. Anatomical Changes.— We have little to add to the remarks,
made concerning neuritis in general.

In acute multiple neuritis, the inflammation may bo chiefly intersti-
tial or chiefly parenchymatous. In my own case, the changes were
mainly interstitial. The periphei;al nerves were unusually red, opaque,
and succulent, and the microscope showed unusual distention of tne ves-
sels, and very numerous extravasations of blood in the insteretitial con-
nective tissue (vide Fig. 33),

On more detailed examination, the veaaela were found to be very tor-
tnous and dilated in places, tbe walls were streaked, vitreous, and thick-

DISEASES OF THE SPINAL OOSD. 77

ened, and contained numerous endothelial nuclei; outside of the ves-
sels were accumulations of round cells, mixed with granulo-fatty cells
in addition, swelling of the connective- tissue fibrillsB and proliferation o
the cellular elements of the interstitial tissue. Degenerated nerve iibre
and lively proliferation of nuclei within the sheath of Schwann were
found in tne nerve bundles, particularly near the extravasations of
blood. Mueller observed fatty changes and swelling of the paralyzed
museles.

The brain, spinal cord, and roots of the spinal nerves are intact.

IV. Diagnosis. — This is not always easy. Cases which run an
acute, ascending course remind us of acute ascending spinal paralysis,
but the latter presents no sensory disturbances or changes in electrical
irritability.

Multiple neuritis may also be mistaken for poliomyelitis; here, like-
wise, the presence of sensory disturbances is an important diagnostic
feature.

V. Prognosis. — The prognosis is always serious.. In acute multiple
neuritis there is danger of death when cerebral nerves, particularly the
vagus, become affected. The prognosis is also serious from the fact that
the paralysis often persists and cripples the patient.

VI. Treatment. — In the acute form salicylic acid (four to six doses
of fifteen grains every quarter-hour) should be given to combat the fever
and infection. Violent pains may be relieved by narcotic inunctions (for
example: chloroform, 3 iij. ; liniment, volatil., 3 iss. M. D. S. To be used
t. i. d.) or subcutaneous injections of morphine. After the acute svmp-
toms have subsided, the paralyzed muscles may be faradized and the
nerves treated with the galvanic current (anode labile, cathode indiffer-
ent). If the faradic irritability of the muscles is lost, they should be
treated by labile applications of the cathode of the galvanic current.
Potassium iodide may be given internally. Massage and indifferent ther-
mal waters have been employed in old cases.

PART II.

DISEASES OF THE SPINAL CORD.

A. DISEASES OF THE SUBSTANCE OF THE SPINAL CORD.

a. UNSYSTEMATIC (ATYPICAL) DISEASES OF THE CORD.

1. AncBmia of the Spinal Cord,

I. Etiolooy. — Our clinical knowledge of tliis disease is very scanty. Its
causes may be local or general. The former include: compression, embolism, or
thrombosis of the abdominal aorta, embohsm or thrombosis of fine vessels in the
spinal cord, and compression of the cord. The general causes include: profuse
losses of blood, chlorosiR, protracted suppuration, etc.

Brown-Sequard attributes reflex paralysis to spasm of the arteries in the
spinal cord.

In 1667, Stenson produced paralysis of the muscles, spliincters, and sensation
by compression of the abdommal aorta in animals (ansdmia of the spinal cord).
Panum produced embolism of spinal vessels by injecting substances into the
blood.

II. Anatomical Changes. — ^The substance of the spinal cord is pale, and the
g^y matter is depressed below the white matter. The latter is softened, more

7^ DI9£Ai£S OF THE dPDTAL COBD.

rarelv it3 consistence is increaaefi. Bed and veilijw «)fteiiin^ »
ohtiervetl as an ffxpreiuion at anaemic n^ftrpxais ot che cori. If Uie an^miA is chr
reauic of ci jmpr»r?-sii jr* .^r »*nibiji:.siii of ^nuill VHsjeeU in th»* cor!, che per.paery ot
Che ac«%mic fiN!iM will be markeii by uniuiiai oongescioa of the V^M^e&s ';u^i
extravadacitjos of btryxi. Leyden's obb**rvaci<ms inditrace chac mioroecijoical ex.
aailnacicjn k4 nei:e»9ar7 Co dececC tine edii^oU in che coni.

The m<::nini(eH are alacj anaemic, but th«^ vpqijiu plexuses in. che peridnra^ oe&lTx-
lax ti.^Hue .u''? 'jci:aiiitina.lly ilidcenileil wich bl<)«)ii.

Wi; mri.-c tie on our ;;^iard a;rainsc misraJcin^ these appearances f'jr '-"acaT^c
chan^'<- in rhe oupI. pjirtii:iilarly if m) caiLit-s i>f anamia are demoniitrable.

III. .*SVMPTOii.s. — If annF;miaof a Ian?e part of Che lumbar corl ^odii-^o I v x-
car, f'*r rxampit^. a^ cho ri^uic of i;mbolLdm of Che a)>ioaiinai aona» iz vLl b^
follow*^! i.>y mpiil paraly-i.4 'tt die Lower Limbs, loes of sensibilicj and. redex
irricahtilny. anil paraly-i-i of ch»f Ijladdor and ret!tum. Ac che same cime the poise
in che cnral artenrH disappears or becomes very ^mall, and the limbis onJer^j
g&nn^^n^T unleftH Che coLlar.»:rai circulation id quickly re-escabliahed.

EmViT^lL^m of smaller v^1^.nf•Aa ^f che conl may not jd^e ri:4e Co symptoms.

To -itpinal an;3F:mia -.ia eh»^ r*^uU of general anaemia hav»* been actriba'ed coo-
dicion.<« of lArt^'iA^ paraiv-tiH. cr»'mor. hypenesthesia. ana^schesia, and increased
redex «^zcitability hucli conditions may disappear as} aoonas che gpenezsl

in r*ril#-V*-fl.

IV. rJi.\ri.>yofltH. — Th« diai^oALs u not always easy: it depends
upon th»? • lemon -ftraCi* 111 of .iniHrniii as a cause of the coniiition.

V. pFtr^iSr>Hi:n — Thf- proi^oMiH is unfavorable if nutritive discuifaanoes occor
in the cord an«l ar»^ folltiwetl by lympDmis ot organic lesions.

VI. TrzaTXRNt. — Thi.^4 M >:hietly caused and sympcomatic. Brotrn-Seqaard
recommeniLf 'lor^al il»^.uUcua wich el^rvatei head anil limt>s. Bags of hoc sand
or Uot oirater may i-je appiinl to the back. Strychnine, opium, and axnyl niorice
ha7H; be»sn recrimmende«i. In och*»r renpects. purely sympcomatic treacnoent.

i . //y//" /"'^ //i if I 'j/ f h t^ Sp inal Co nL

I. A.'^ATriMrr.'.ir ('Mxyn »?>.,— TUk term con^jesii.m of the conl Ls often employed
by phviiMJinH who }iPT ;tr*x 1011.1 it* m^ik^; tine diagnoses, but our knowledge of tKi^
crjniiir.iori im nlmtMt ml.

On trinrtv*«r'-»e ^Ktion of r.h*? con;;^te<l cord, the white substance has a rosy
fftil a|if*»-firance. pr»^Ment.H niirnfrou.-i jl.iti of bf^od, unusually large and sinaoos
\eMH*riH, in plar:frH true *-xx.T:i...i.'.ii.U\tx\A. The gray matter has a red, sometimes
alnirjMt brownijih-rwl «:olor. 'W.k ':on«i.Htence of the cord may be increased or
diminished. The rfi*'r;iiifcf*-M a]-.o ap[i»r:ir congesteil. and the veins of the peri-
diirai ti.iHue ar*r Horuff.iiiu:^ -finuoiu and dilate* I. The spinal duid is not in£re>-
quently increaseil. .-^oml■tim^•M cloudy, f>cca."*i' inally tinge<l with blood.

CongHHtion and even hemorrhages of the nerve roots have been noticed in
some caaen.

Hyper;f:mia of the cord may have been present during life, although the
appearances have disapf^earerl in tlie dead-house. The reverse also holds good,
i. **., congestion of the conl may ap[iear to be present after death, either as the
re^tiilfc of prolonge^l (lO^ition on the buck, or cadaverous decomposition, etc.

If. F-rr* I Ujoy.— Active spinal congf'Mtion may be the result of cold, shock, in-
flamzuation, inferjtioii.^ di.-*efiriea, b*>« lily exertion, onanism, excessive coitus,
fK^i.-^r^nirig with car)'y>nic oxiile, atryr.-hnin. alcohol, prussic acid. It may also
d^'Velof* in congestive condition-* of certain abdominal organs, for example, in
nien.^tnjal and hemorrhoidal hemorrhag>rs, or in the absence of customary hem-
orrha:;»H of this character.

Pa^.MJvt; Hpinai congestion may hie the result of general disturbances in cardiac
and pulmonary diseas^'M. Or the causey of stasis may Ih? k>cai stasis uf the portal
vein, aVj< lorn inal tumors, pregnant uterus. Tliis also includes spasmodic condi-
tions repilefisy, tetanus, urrrsmia. agonal spasms, etc.) in which congestion and
hemorrhages .'particularly into the peridural tissue, often occur, and were often
falsely rej^arded as the can.ses of these diseases.

II f. SYMPTOM.S.— The symptom.s of active and passive spinal congestion are
alike; the lower limhis are generally affecte<l. Among the symptoms mentioned
are: a feeling of pressure, tension, and pain in the spine on external pressure, a cinc-
ture feeling arrMind the belly, pains in the limbs, hypersesthesia. paraesthesia,
rarely anaesthesia, twite hings" in some of the muscles, rarely complete paralysis,
increases I reflex excitability, and galvanic irritability. The bladder and x«ctam

DISEASES OF THE SPINAL OOBD. 79*

are rarely paralyzed. If the upper cervical cord is affected, there may be disturb*
ances of respiration and cardiac action. Cerebral congestion may also be pres<
ent, and its symptoms may occupy the foreground. According to Brown-Se-
quard, the symptoms increase in dorsal decubitus, decrease in abdominal decu-
bitus or in the standing position. Others maintain that the symptoms increase
in the erect posture. They often vary with remarkable rapidity.

IV. Treatmeni.— We may apply cups or leeches (ten to twenty) to the spine,
or apply leeches to the anus or cervix uteri, ice bags to the spine, foot or hand
mustard baths; internally ergotin or belladonna. The patient should assume ab-
dominal or lateral decuoitus, and the bowels should be thoroughly evacuated

daily.

3. Hemorrhage of the Spinal Cord.
{Spinal Apoplexy. Hcematomyelia.)

I. Etiology. — Primary hemorrhages into the cord are rare, and
Charcot and Hayem deny their occurrence. At all events secondary
hemorrhages are much more frequent, especially in connection with pre-
vious inflammation of the spinal cord (hsematomyelitis).

Among the causes of primary spinal hemorrhage are injuries, cold,
bodily strain, coitus, sexual excesses in general, stasis following cardiac,
pulmonary, and hepatic diseases. Previous disease of the spinal cord
or the immediate vicinity also favors the development of spinal hemor-^
rhaffe.

Males are affected more frequently than females.

II. Anatomical Changes. — Tne hemorrhagic focus in the cord
cannot infrequently be recognized beneath the pia mater, as soon as the
dura mater has been laid open. It often shows through the [)ia mater
as a bluish-black mass, and sometimes causes a prominence of the men-
inges. The pia mater may even be ruptured, and the blood escape into
the subariachnoid cavity.

The upper cervical or the dorsal portions of the cord are most fre-
quently affected. There is usually only one extravasation. It almost
always begins in the gray matter, particularly the anterior horns, and not
infrequently occupies the entire section of the cord. In rare cases the
blood extends along the length of the cord, following the longitudinal
fibres in the white matter, and attains a length of more than ten cm.

. Becent hemorrhages have a blackish-red, older ones a brownish-red,
rusty brown, even ochre-yellow color. In recent foci the blood is partly
coagulated, and the adjacent nerve tissue is generally in a condition of
red or yellow inflammatory softening. After a while a sort of fibrous
capsule may form around the hemorrhage, and the blood is replaced by
serous fluid (so-called apoplectic cysts). Smaller extravasations gener-
ally terminate in a sort of connective tissue, pigmented cicatrix. Spi-
nal hemorrhages may not alone be followed by meningeal hemorrhages,
but occasionally by fibrous and even purulent inflammations.

Among the complications and sequelae are inflammatory changes and
secondary degeneration of the cord (vide the section on secondary spinal
degenerations).

III. Symptoms. — The disease is characterized by the sudden (apoplec«
tiform) occurrence of paralytic symptoms, which vary according to the
situation and extent of the hemorrhage. The symptoms generally cor-
respond to those of complete section of the cord, sometimes to those of
a unilateral lesion. In other cases they indicate exclusive or chief
implication of the anterior, more rarely the posterior horns.

As a rule, the symptoms occur suddenly without prodromata, more

«0

DISBASES OF THE 8FISAL OOBD.

rarely they are preceded for a few hours or days bv morbid phenomeua,
which indicate congestion of the cord and meainges (|>aiu in the back,
fltiffness in the apioe, parjesihesis in the limbs, etc.).

Gonscionsuess is not impaired at the onset, unless the hemorrhage ia
situated high up m the cervical enlargement of the cord. In some cases
the symptomB of shock are manifested.

In the begiuniug, the bodily temperature is imchanged; in the next
few days there ia sometimes ii slight rise of temperature, High fever
develops in the later course of the disease if it becomes complicated
with cystitis, ammtniacal decomposition of the urine, and hed-sores.

The majority of patients complaiji at first of more or less violent
pain in tho spine, corresponding to the site of hemorrhage, but the pain
generally subsides in a few hours.

The pain is usually associated with paralysis, as a rule paraplegia,
more rarely spinal hemiplegia or monoplegia. The paralysis is often
complete from the beginning, in other cases it is incomplete at first, but
increases iu severity during the next few hours. It affects motion and een-
sation, the bladder and rectum. The reflexes are often abolished or en-
feebled, but, if the cord has been completely cut across, the reflex irri-
tability below the site of lesion will be increased at the end of a few
days. The reflexes will remain absent permanently if an extensive hem-
orrhage has taken place into the lumbar part of tne cord, or if the an-
terior or posterior nerve roots are affected (in the latter event the re-
flexes will be abolished merely in the distribution of the affected nerves).
Destruction of the anterior horus of gray matter or the anterior roots
is shown by rapid atrophy of the paralyzed muscles, and the develop-
ment of the degeneration reaction. Spontaneous twitchinga are eome-
timea observed in the paralyzed muscles, probably as the result of irrita-
tive conditions below the site of hemon-hage. Vaso-motor and trophic
disturbances in the paralyzed limbs have also been described. Haima-
tuna and albuminuria often develop in a short time.

Death may follow almost instantaneously if the hemorrhage is situated
^eo high as to involve the medulla oblongata and its respiratory centre.
In hemorrhages near the cervical enlargement, thesymptomsof paralyaiB
of the diaphragm may occur {affection of the phrenic nerve) and produce
fatal su ffocation. The disease may also he protracted for weeks, months,
and even a couple of years. In certain cases, acute decubitus or cystitis
and ammouiacal decomposition of the urine may give rise to septicaemic
symptoms, increasing exhaustion, and death.

rV. Diagnosis. — The chief interest attaches to two factors in diag-
nosis—to the andden occurrence of the symptoms, and to the predomin-
ance of paralytic phenomena. Although meningeal hemorrhage may
occur with equal suddenness, irritative symptoms, viz., pain, muscular
twitchings, etc., predominate in this disease. In hemorrhagic central
myelitis, extensive paralysis may likewise develop in a very sliort time,
but the spread of the process can usually be made out with distinctness.
Acute anterior poliomyelitis begins with fever, the paralytic symptoms
do not develop so Buddenly, and sensory disturbances, paralysis of the
bladder and rectum, and decubitus are absent. Cerebral hemorrhage is
readily excluded by the absence of paralysis of cerebral uer\-e8, particu-
larly of the facial nerve; in addition, the paralysis is generally hemi-
plegio.

The recognition of the site of hemorrhage is usually easy. It may
often be suspected from the location of the pains or cincture feeling, li

niSEABES OF THE 81-lNAL COftn.

thp Inm'bflr cord ia involved, we generally find paraplegia of the lower
iirabs, paralysis of the bladder and rectum, and loss of reflex irritability;
priapism is sometimea noticed. lu dorsal hemorrhage, the symptoms
remain the same, except that reflex movements reappear or are increased,
and tliat the abdominal muscles are paralyzed. Cervical hemorrhage
causes paraplegia of all the limbs, and somelimesparalysisof thephrenjo
nrrve. Bulbar symptoms (pupillary changes, slowness or acceleration
of the pulse, difficulty in deglutition, etc.) snpeiTene if the hemorrhage
is situated still higher.

V. Prognosis. — The prognosis is unfavorable, since permanent par&-
lyses are left over, even if the clot is sibsorbed.

Death may occur under different circum- ^°' **•

stance.^ witii varying rapidity.

VI. Theatmknt. — If there are symptoms

rapto
ichea

^^ibth

* nf tt

of spinal congestion, ten to twenty leeches or
cups should be applied to the spine, or five to '
ten leeches to the anus or cervix ntert. Daily
evacuations from the bowelssbouldbo seoured.
The patients should he kept as quiet as pos-
sible, upon a Chapman bag filled with tee
or ft water-bag. Potassium iodide (3iij. :
§iij,, one tablespoouful t. i. d.) should be
given internally, to facilitate absorption of
the extravasation. After the cessation of- the
acute symptoms (in six to ten weeks), the gal-
vanic cun-ent may be applied (at first the
anoilo. theu the cathode) stabile to the site of
disease, for five minutes three times :t
k, the indifferent electrode on the sternuTvi,

The Cliitpman rubbef'bag is oxtremelyimporUni
_. the treatiiient ol diaeaaes of the cord. It consists
of Ihrf* long rubber-baga, each of which is larger
than the one abuve it ivide Fig. 1(3), The bags are
filled with ice until the latter reaches to the lowereud
of the adjacent bag.

In order to prevent inflamination of theikin. a
piece of linen should aiwaja be interposed between
the rut)ber-bae and the integument. The bag should
be refilled as Bo6n as the ice has melted.

^^irmi

I Appkndk.

I Capillary {punctate) hemorrhagea of tlie »plnal
tord usually pussesa no clinical significance. Para-
lytic symptoms can only be expected when tliey are
very numerous and cloaely aggregated. The hemor-
rhages are found not infrequentTy on a transverse
section of the cord, either exclusively or chiefly in the gray matter. They are
rarely larger tban a fine dot. Unlike bleeding veaaels, they cannot be removed
by a stream of water or by the Augers. Tliey are situated in the lymphatic
sheaths of the vessels, which are sometimos ruptured, bo that the blood Is free In
the tissues.

The hemorrhages often constitute an agonal symptom, and are also found in
spasmodic diseases, in which they may be associated with meningeal hemor-
rhages. They are often fouud in infectious and severe constitutional diseases.

These hemorrhages have also been produced experimentally in animals which
ivere placed in rarefied air; they were so ounierouB as to give rise to paralytic
iptoms. Similar conditions have also been observed in men wlio worked for

dupman-i

82 IJSEASES OF TUE SPINAL OOBD.

B long time in compressc I air and then paased into the general atmosphere. In
these cases, however, hemorrhages were not found in the spinal cord. In a case
of this kind. Leyden found numerous cavities in the cord surrounded by large
cells, which he regards as altered white blood-globules. He explains the appear-
ances by Hoppe's experiments, according to which, in animals placed in rarefied
air, the gases partly escape from the blood and produce further serious changes.

4. Acufe Inflammation of the Spinal Cord.

Acute Myelitis,

I. Etiology. — Acute myelitis is one of the rarer diseases. It is rela*
tively frequent in middle life (fifteen to thirty years), and more frequent
in men than in women.

A predisposition to the disease is engendered by alcoholism, dissipa-
tion, overwork, living in damp rooms, etc. Under such circamstances
myelitis may be produced by very slight causes.

Myelitis may be primary or secondary. The former inclndes rheu-
matic, traumatic, ana toxic forms; it may also be the result of violent
mental excitement. Some claim that the disease may follow excesses in
venery, onanism, cessation of menstrual and hemorrhoidal hemorrhages,
but this is not beyond dispute.

There can be no doubt that a cold is a not infrequent cause of myelitis: it oc-
curs occasionally after a wetting, sleeping on the damp ground, etc.

Traumatic myelitis is still more frequent than the rheumatic form. It is ob-
served after wounds of the cord, fracture and dislocation of the vertebrsB, even
after violent concussion of the spine or of the entire body.

Toxic myelitis is better known experimentally than clinically. It has been
produceil in animals by |K)i8oiiing with phosphorus, arsenic, mercury, lead, ctr-
uonic oxide, and Hlcohol.

Secondary acute myelitis often follows diseases of the vertebneor
meninges (tuberculosis or cancer of the vertebrce, inflammations, hemor-
rhuges., and tuniorn of the meninges). It is sometimes aseqael of neu-
ritis migrans, occasioiuilly of previous diseases of the spinal cord itself.

It may also develop during or after certain acute and chronic infec-
tious diseases, viz , (liplitheria, pneumonia^ typhoid fever, articular

with changes in the interstitial tissue (vessels and neuroglia), and these
are immediately followed by an affection of the nervous tissue proper.
The (lorsjil cord is affected most frequently, next the lumbar and cemcfd
portionrs.

The first changes almost always occur in the ffray substance of the
cord (central myelitis), to which it may be confined; in other cases it ex-
tends to the white matter. Sometimes the entire transverse section of
tlie cord is iiifiamed (transverse myelitis), sometimes there is only a small
spot of infiammation (circumscribed myelitis), which is perhaps confined
to one-half of the cord. In certain cases there are numerous foci of
inflammation which may be so small as to be recognizable only nnderthe
microscope. In rare cases the inflammatory changes are confined to the
j)erii)liery, and are associated with meningeal changes (perimyelitiB or
myelo-meningitis).

When acute myelitis attains certain dimensions, the color and ooih

DISEASES OF THE SPINAL OOBD. 88

sistence of the parts are changed. Their consistence is diminished,
though softening of the cord may also be non-inflammatory in character.
Thus we sometimes find post-mortem softening of the cord, particularly
in the dorsal portion, in bodies which have lain on the back for a long
time during the summer months. Hence other changes must also be
present i n order to prove the inflammatory character of the softening.
Upon section, the softened parts project above the cut surface and form
a more or less soft pulp; in some cases they are entirely fluid. The nor-
mal markings are indistinct or entirely obliterated. According to the
duration of the inflammation, the softened parts present a different color
(red, yellow, gray softening).

In red inflammatory soitening of the cord, the parts have a bright-red,
brownish-red, or chocolate color. Numerous extravasations are often
found in the surrounding parts, sometimes in the inflamed parts them-
selves (hemorrhagic or apoplectiform myelitis).

Gradual absorption and transformation of the blood pigment and in-
creasing fatty degeneration of the constituents of the cord give rise to
yellow softening. Finally the pigment disappears in great part, the fatty
elements are absorbed, resulting m gray softening.

Microscopical examination should be made, partly on the fresh, partly on the
hardened cord. In the former method, scrapings from the knife-blade may be
examined in aone-half-per-cent solution of sodium chloride, or in diluted glycerin.
The cord may be hardened in potassium bichromate or ammonium chromate,
the dura mater having first been opened and the cord cut into sections three to
five cm. in length. TJhe cord is placed in a one-per-cent solution of the harden-
ing fluid for one week, and the strength of the fluid increased one per cent weekly
for a month. It becomes fit for making sections after it has been eight to twelve
weeks in the five-per-cent fluid.

The first microscopical changes in acute myelitis appear in the blood-vessels
and neuroglia. The vessels, especially the small veins, are unusually dilated,
sometimes very sinuous. Their walls are peculiarly thickened and shinmg, occa-
sionally fibriUated, and the nuclei increased in number. The lymph sheaths
are unusually wide, and contain red or white blood-globules. Extravasations
may also occur through these sheaths themselves, and appear upon their outer
surface.

At the same time, changes develop in the neuroglia; its cellular constituents
increase in size and number, and their nuclei also proliferate. Some of these
cells are perhaps emigrated leucocytes. The basement substance of the neuro-
glia is swollen.

These lesions are soon followed by changes in the nerve fibres and ganglion
cells. The medullary substance of the fibres coagulates, becomes finely granular,
takes carmine staining, and finally disappears entirely. At the same time the axis
cyUndera undergo striking changes in snape. In places they are enormously dis-
tended into a spindle-shape; several of these enlargements sometimes follow one
another, like a rosary. At the same time, the axis cylinder becomes homo^ne*
ous, vacuolse form in it, and nuclear proliferation has also been described.
Next it becomes granular, and later is absorbed.

The ganglion cells lose their granular and fibrillatod structure, and assume a
swollen, homogeneous, and vitreous appearance. They often contain vacuoles.
The prolongations are thickened and often separated from the cells. The nucleoli
become indistinct, but sometimes proliferate; the nucleus finally becomes more
and more indistinct. The cell substance becomes more granular and fatter, and is
absorbed; the affected cells often contain an abnormal amount of pigment.
Some of the ganglion cells do not disappear, but are converted into small round
bodies without prolongations which may remain for a longtime in that condition.
Foerster observed calcification of the ganglion cells.

An important phenomenon is the abundant development of granulo-fatty cells,
which are found not alone in inflammation, but also in necrotic processes. These
cells are round, composed of fine granules of fat, sometimes contain one or more
drops of myelin, and generally (fisclose a nucleus after staining with carmine.

84 DISEASES OF THE SPINAL OOSD.

In hardened preparations thej are detected most readilj after treatment with
potash.

These granulo-fatty cells are present in remarkable numbers. They are partly
free in the interstices, partly in the lymphatic sheaths of the vessels. In our
opinion, they play an important part in the absorption of the fatty masses which
result from degeneration of the nerve fibres and ganglion cells. To render the
absorption of tne fat possible, wandering cells are requisite, which will become
stuffed full with fat, and then make their way into the lymphatic sheaths of the
vessels.

In addition to the granulo-fatty cells, we also find laminated amyloid bodies,
whose origin and significance are linknown.

In some cases a sort of coagulated exudation is noticeable. It forms vitreous^
colloid clumps which are situated partly in the lymphatic sheaths, but in great
part upon the external wall of the blood-vessels, sometimes free in the interstices.

The extravasated red blood-globules are gradually destroved, their pigment ia
deposited in granules or crystalline form, or it is imbibed by the granulo-fatty
cells or by larger drops of fat.

If the inflammation is very intense, it may terminate in the forma-
tion of a circumscribed deposit of pus in the cord (abscess of the spinal
cord). This rare occurrence is observed most frequently when the mye-
litis is traumatic in origin, and foreign bodies have remained in the cord.

If the inflammatory process is protracted, it may terminate in the
formation of cysts. The softened parts of the spinal cord become more
and more fluid, forming at first an emulsion-like, then a milky, finally a
serous fluid. At the same time the surrounding neuroglia proliferates
so that a fibrous capsule forms around the fluid. The cyst is often
multilocular.

In some cases the originally softened spot in the cord undergoes
sclerosis, and the disease then usually becomes chronic. The indurated
tissue is composed chiefly of new-formed neuroglia which is rich in cells,
contains few nervous elements, granulo-fatty cells, and corpora amylacea.

Dujardin-Beaumetz has applied the term hyperplastic myelitis to a
certain anatomical form in which the interstitial inflammatory changes
are especially marked, and the inflamed parts are firm to the feel.

Tlie ascending and descending secondary degenerations will be dis-
cussed in a subsequent chapter.

As a rule, the meninges, particularly the pia mater, also take part in
the inflammation. The pia mater is reddened, succulent, occasionally
infiltrated with pus. According to Schultze, acute myelitis following
syphilis is characterized by marked affection of the meninges and vaeca-
lar apparatus.

Tlie nerve-roots have been found reddened and swollen, and some-
times present spindle-shaped enlargements; nuclear proliferation and
degeneration of the nervo-nbres may be seen under the microscope.

Degenerative changes have also been observed in the peripheral
nerves; increase of the nuclei, unusually distinct transverse striation,
more rarely fatty degeneration in the muscles, have been described.

Among other organic changes in acute myelitis may be mentioned : bed*
sores; inflammation, hemorrhage, ulceration and partial desquamation of the
mucous membrane of the urinary passages, particularly the bladder and pelvis
of the kidney; decomposed urine in the hladder; not infrequently moltipfe ab-
scesses in the kidneys; hemorrhages into the suprarenal capsules.

III. Symptoms. — The symptoms of acute myelitis may begin sud-
denly or may bo preceded by prodromata for a few hours or days. The
prodromata are often of a general, indefinite character: chilly sensa-

DISEASES OF THE SPINAL OOBD. 85

tions, elevation of temperature^ anorexia^ increased thirsty general mal-
aise^ etc. The symptomatology is sometimes like that of an acute infec-
tious disease; it begins with a chilly followed by hi^h temperature^ and
then the other manifest symptoms of myelitis develop rapidly and un-
mistakably. In children general convulsions may occur.

The suspicion of an acute spinal affection must be aroused if the
symptoms described are followed by disturbances of innervation, such
as formication in the limbs, a feeling of coldness, shooting pains, etc.
Retention of urine, more rarely incontinence of the bladder, is occasion-
ally one of the first symptoms.

Local changes soon oecome noticeable. The patients complain of

Sain in a circumscribed part of the spine, corresponding to the site of
isease. The pains are sometimes spontaneous, or they are provoked by
movement of the spine, pressure, etc. Many patients complain of a
constricting, band-nke feeling which extends from the painful spot
around the abdomen or thorax. Gardialgic symptoms sometimes appear
at an early period.

In the mean time, the disturbances of innervation have become more
distinct. Irritative symptoms (pain, hypers^sthesia, twitchings, and
contractures of the muscles) are temporary in character, and generally
present only at the beginning of the disease, while, as a rule, paralyses
constitute the chief feature of the symptomatology. The pains are
usually neuralgiform in character; they are sometimes localized in cer-
tain parts, for example, the joints. The pains are sometimes present
after the sensory and motor nerves are completely paralyzed (anaesthesia
dolorosa).

Paralysis of the muscles is one of the chief symptoms of acute myelitis.
It may be complete or incomplete, but the paralyzed parts are* always
flaccid. Transverse myelitis of the lumbar cord gives Vise to paraplegia
of the lower limbs, in addition to paralysis of the bladder ana rectum.
In a similar affection of the dorsal cord, the abdominal muscles are also
paralyzed, so that the patients cannot cough and strain. Under such
circumstances, even a mild bronchitis may be a source of danger. In
myelitis of the cervical enlargement, the arms and chest muscles are also
paralyzed. Hence inspiration is interfered with to such an extent that
diaphragmatic breathing becomes unusually vigorous. In cervical mye-
litis, the paralysis is sometimes confined to the arms, while the legs
oscape. Inflammation of the upper part of the cord is shown by implica-
tion of bulbar nerves: unilateral or bilateral myosis, slowness of the
pulse (twenty-eight beats in a minute in one case), disturbances of deglu-
tition, difficulty in articulation, etc. Redness and increased heat of the
face and neck indicate paralysis of the sympathetic. Descending^ optic
neuritis, with subsequent atrophy, has also been described. Painful
attacks of palpitation of the heart are sometimes observed. The chief
danger in cervical myelitis arises from paralysis of the phrenic nerve;
respiration is then impeded, and death takes place from asphyxia.

The nutrition of tne paralyzed muscles may be unimpaired for a long
time, until atrophy from disuse gradually develops. But in some cases
there is rapid emaciation, as the result of destruction of the large
(trophic) cells in the anterior horns of the gray matter, or of implication
of the nerve-roots in the morbid process.

In the latter event, the degeneration reaction is produced in the
paralyzed muscles. In atrophy from disease, the electrical irritability

te DneASBS <ff THE aPIHAL OOBO.

gn^oallT diminishes to a slight extent, &nd to ui equal degree to both
ciirTeDt&.

At first the cutaneous sensibility is occasionally diminished or ab-
olished only for certain modes of sensation; later, complete amesthesia
generally develops. In the former event, delayed condaction is some-
times noticeable. Certain patients experience a sensation of vibration
of the entire limb after the application of circumscribed Btimnli, for
example, the prick of a pin (dysesthesia).

Vaso-motor disturbances are almost always noticeable. The para-
Ivzed limbs are reddened or livid', warmer than normal, and do not sweat,
firieger found that the paralyzed parts remained dry even after dia-
phoresis was produced by injectioDB of pilocarpine. After the disease

Xcntf deeublcui in dona] mj-elltiL 1, KUtcreaaiu; i. eiyUienuious porUm. Alur duroot.

bae lasted for some time, the paralyzed parts become pale and cold.
(Edema of the skin and swelling of the joints are not infrequent.

Xor are trophic changes rare. They consist of active desquamation
of the epidermis, erythema, vesicular eruptions, and especially acute
decubitus. This develops most frequently over the sacrum, next over
the trochanters, malleoli, and heels. The skin reddens, then vesicular
elevations form, and finally the tissues undergo rapid gangrenous de-
struction. This often spreads with terrible rapidity, extends through
the spinal column, and invades the meninges and spinal cord. The
development of decubitus is favored by pressure on the parts, but it may
also develop independently, as the sole result of trophic disturbances.
It has been attributed to disease of the posterior horns and the adjacent
parts of the posterior columas of the cord.

DISEASES OF THE 8PINA.L OOBD. 87

Reflex irritability is affected in various ways. If the iuflammation
extends through the lumbar cord, reflex action in the lower limbs is
necessarily abolished. If the lesion is situated higher, the reflex irrita-
bility of the lower limbs may be diminished or abolished at first as the
result of the severe general disturbance of the cord, but later the reflex
irritability is increased and does not disappear again until the inflamma-
tion hap assumed larger proportions. The cutaneous and tendon reflexes
are affected in the same way.

Important changes in the urine very often develop at an early
period, and it has been assumed by some that these are the result of
trophic changes, not of simple stagnation of urine. The urine becomes
bloody, albuminous, cloudy, and ammoniacal, and the retention of urine
may give rise to septicsBmic and pysBmic conditions. Engelken ob-
served su^ar in the urine in dorsal myelitis.

The bladder and rectum are paralyzed from the beginning (in lum-
bar myelitis), or not until a later period of the disease. As a rule, there
is at first retention of urine (paralysis of the detrusor vesicsB). and
incontinence occurs at a later period (paralysis of the sphincter vesica).
Or paralysis of both muscles occurs simultaneously, L ^., there is a con-
stant flow of urine, although the bladder is not thoroughly emptied.
A similar condition obtains with regard to the rectum — at first obstinate
constipation, later involuntary evacuations. In cervical and dorsal
myelitis, priapism is not infrequent; the erection is generally flaccid,
but painful. Involuntary discharge of semen has also been described.

The paralysis sometimes begins suddenly at night, and within a few
hours or days spreads upwards or downwards, or in both directions, dis-
turbances of innervation on the part of the medulla set in, the tempera-
ture of the body often becomes hyperpyrexial, and finally death occurs
from the excessive rise of temperature or from suffocation. This is
especially apt to occur in hemorrhagic myelitis.

In other cases, the disease lasts one to three weeks; exhaustion, de-
cubitus, ammonisBmia, septicaemic and pysamic conditions, or a compli-
cating pneumonia put an end to life.

In still other cases, the disease runs a subacute course, and lasts
many weeks.

French writers apply the term recurrent myelitis to a form which is charac-
terized by relapses, the intervals sometimes lasting several months.

If the disease becomes chronic, certain paralyses disappear, others
remain permanent. Recovery of the paralysis is possible in those cases
in which certain parts of the cord are compressed by inflammatory
swelling or oedema, and this pressure is relieved. Muscular twitchings
and contractures, and exaggeration of the tendon reflexes indicate sec-
ondary degeneration in the cord.

Complete recovery can hardly be looked for.

IV. Diagnosis. — The recognition of acute myelitis is usually easy.
It is distinguished from acute spinal meningitis by the fact that in the
latter the irritative symptoms are more marked, the paralysis less
marked. In spinal and meningeal hemorrhage, the symptoms begin
more suddenly, and in the latter affection there are marked symptoms of
irritation; in addition, a greater degree of recovery is possible. Ascend-
ing myelitis may be mistaken for Landry^s ascending paralysis, but in
the latter, the electrical excitability is unchanged, and the course of the

88 DISEASES OF THE SPINAL CX)BD.

disease is usually more rapid. In multiple neuritis, the electrical irri-
tability of the paralyzed nerves and muscles rapidly diminishes. The
differentiation from hysterical paralysis is sometimes difficult, but this
disease generally affects women, and other symptoms of hysteria are
usually present.

We should also endeavor to ascertain the height of the morbid pro-
cess. We must therefore take into consideration the painful points on
the spine, the distribution of the motor paralysis, and particularly the
extent of the cutaneous anaesthesia. If the latter is tested from below
upwards, the boundary of the ansBsthetic region will be found a little
below the site of inflammation in the cord. In lumbar myelitis, the
anaesthesia usually extends about to the level of the umbilicus. In mye-
litis of the lower dorsal cord, the skin is ansBsthetic as far as the lower
end of the sternum. In myelitis of the upper part of the dorsal cord,
the anaesthetic zone extends to the axilla; in cervical myelitis it involves
the upper limbs.

The following statements may be made concerning the extension of
the inflammation over the transverse section of the cord. Motor paraly-
sis indicates an affection of the lateral columns, particularly the inner-
most parts and adjacent gray substance (pyramid tracts). If the motor
paralysis is followed by rapid atrophy and degeneration reaction in the

Earalyzed muscles and nerves, we may assume destruction of the anterior
oms (poliomyelitis) or interruption to conduction in the anterior roots.
The latter is more probable ir marked cincture feeling and pains are
noticed. Sensory disturbances indicate implication of the posterior
columns, posterior horns, or posterior roots.

V. Prognosis. — The prognosis is almost always unfavorable as re-
gards recovery. The greater the tendency to spread transversely or
along the cord, the more unfavorable is the prognosis. Decubitus,
alkaline decomposition of the urine, paralysis of the phrenic, and bulbar
symptoms are especially grave symptoms.

VI, Treatment. — Causal treatment should be adopted if the acute
myelitis is the result of syphilis. We may then order inunctions of
mercurial ointment (gr. Ixxv. daily) and potassium iodide internally
(gr. xij. t. i. d.). Some authors recommend the internal administration
oi calomel. Mercury has also been recommended as an active antiphlo-
gistic even in cases of non-syphilitic origin.

In the majority of cases, the treatment must be purely symptomatic.

The patient's bed should be perfectly smooth, in order to avoid
pressure and thus prevent bed-sores. He should lie upon the side or
abdomen as much as possible, and frequently change the position of the
body. In addition, the skin should be rubbed daQy with alcohol in
order to harden it. If the skin grows red or decubitus begins, the parts
should be covered with adhesive plaster which is renewed daily. In
addition, an air bag should be used. But if the bed-sore has already
spread widely, the oest services are rendered by the permanent water
bath (28^ to 30^ B.).

In retention of urine, the bladder should be catheterized three times
a day, care being taken to keep the catheter scrupulously clean by keep-
ing it constantly in a five-per-cent solution of carbolic acid. If the
urine is constantly dribbling away, a rubber urinal may be given to male
patients, while females may use a bed-pan encased in rubber. In our
opinion, the permanent introduction of a catheter into the bladder is

DISEASES OF THE SPINAL COED. 89

less advisable. We should always endeavor to avoid soiling the skin
with urine, since this is apt to result in decubitus.

If the urine has undergone decomposition, it may be caught in ves-
sels in which fifteen to seventy-five grains of naphthalin have been
placed to correct the urinous odor. We have also seen good results from
the internal administration of naphthalin (gr. vij. every two hours), but
the remedy must be discontinued in some patients because itproduces
intolerable burning in the urethra, and even albuminuria. We should
then order potassium chlorate, salicylic acid, etc., and wash the bladder
at regular intervals (vide Vol. II., page 12'^).

If the patients suffer from constipation, we may employ the remedies
recommended in Vol. II., page 334; if incontinence of fsBces occurs, a
bed-pan should be used at regular Intervals. The greatest care should
be taken to clean the patient at once, as soon as he has soiled himself.

The diet should be nutritious, but easily digestible. Tea, coffee, and
alcoholics must be avoided.

Local antiphlogosis is important. This is best effected by means of
Chapman^s ice-bag (vide Fig. 33), or by an ordinary ice-bag or water-bag
applied to the spine.

Derivatives ma^ also be applied in the neighborhood of the spine, the
best being alcoholic or other stimulating inunctions. But we object to
the employment of dry cups, leeches, blisters, tartar emetic ointment,
actual cautery, since they favor the development of decubitus. Applica-
tions of tincture of iodine to the spine must also be made with caution;
inunctions of potassium iodide or iodoform (1 : 16) ointment or iodoform
collodion are preferable.

Among internal remedies, potassium iodide (gr. xij., t. i. d.) is the
most highly esteemed, but too much should not be expected from it. In
ansBmic individuals, preference should be given to tne preparations of
iodide of iron.

Patients who complain of painful twitchings in the limbs or other
violent pains, require subcutaneous injections of morphine.

After the acute symptoms have subsided, we may employ the ner-
vines, concerning whose efficacy opinions vary greatly. We may mention
nitrate of silver, auro-natrium chloratum, strychnine, arsenic, phos-
phorus.

If irritative symptoms are absent, electrical treatment is much more
strongly indicated at this stage of the disease.

In electrical treatmADt of the site of disease, the galvanic current is alone
«mploved: current not too strong, sittings two to three times a week, not more
than five minutes at a time. If there is onlv one focus of disease, the anode and
cathode mav be used stabile alternately, witn large electrodes. Stabile ascending
and descenoing currents may be employed alternately if there are several foci of
disease.

Qalvanization of the cervical sympathetic has also been recommended: one
electrode on the sternum or last cervical vertebra, the other on the side of the
neck immediately below the angle of the lower jaw .

The faradic current may be applied to the paralyzed muscles to prevent
atrophy from disuse, and also in paralysis of the bladder and rectum.

After the patients begin to move their limbs, they must be warned
against over-exerting themselves. They must especially avoid sexual
intercourse.

Patients who are unable to travel may take baths during the summer,
especially chloride of sodium or thermic baths. Cold-water cures some-

90 DISEASES OF THE SPIN AX OORD.

times produce surprisingly good results. In ordering baths of any
kind, it should be remembered that they should not be too warm (not
above 28° R.), too frequent (not more than three to four times a week),
or too prolonged (ten to fifteen minutes).

5. Clironic Inflammation of the Spinal Cord,

Chronic Mi/elitis.

I. Etiology.— The causes of chronic myelitis are the same as those
of the iicute form, except that a congenital or acquired hereditary pre-
disposition is much more marked.

II. Anatomical Changes. — The cord may appear normal to the
naked eye, although the microscope reveals extensive changes.

In many cases macroscopic changes are noticeable. As a mle, the
cord is unusually firm at the affected parts. These parts are generally
diminished in size, and the cord appears depressed and flattened in cir-
cumscribed localities. These have a grav or gra^'ish-yellow color, appear
transparent, and sometimes shine through the pia mater. The meninges
over the affected parts are often thickened, adherent and congested, and
the pia mater can be removed with difficulty from the substance of the
cord.

In rarer cases, chronic myelitis appears as softening (myelomalacia).
After absorption of the inflammatory products, cavities may develop
(syringomyelia). The cavities, which are filled with serum, may attain
considerable size, or in other cases they impart to the cord a sieve-like
appearance (myelitis cribrosa).

Chronic myelitis affects the dorsal region most frequently, next the
cervical and lumbar enlargements.

The same conditions hold with regard to distribution and extent of
the inflammation as obtained in acute myelitis. If the gray matter is
chiefly or exclusively affected, the process is known as chronic central
myelitis.

Hallopeau has described a peri-ependymal sclerosis, which is confined,
in the main, to the connective tissue surrounding the central canal. In
chronic myelo-meningitis the peripheral portion of the white substance
is affected; this often follows a previous meningitis.

Chronic myelitis may also be circumscribed, transverse, and multiple
(disseminated, insular). The latter form must not be mistaken for sec-
ondary degeneration of the cord, which may follow a chronic inflamma-
tory process in the cord.

Among the microscopical changes in chronic myelitis, those in the interstitial
connective tissue are the most prominent, although a strict differentiation can-
not be made between interstitial and parenchymatous inflammatory processes.

The neuroglia presents increase of the interstitial tissue and the cellular ele-
ments. The spider cells are unusually abundant and distinct, often enlarged and
contain several nuclei. In addition, there are cells of a lower grade of develop-
ment, and even simple round cells. The intei*stitial tissue is gradually replaced by
distinctly flbrillated connective tissue. The blood-vessels are thickened, their nu-
clei increased, and their lymphatic sheaths unusually wide, and filled with fat,
granulo-fatty cells, pigment, or in places with white, more rarely red, blood-glob-
ules. The blood-vessels may be dilated in some parts, in others filled with dots.
Granulo-fatty cells may be entirely absent; at all events they are much rarer
than in acute myelitis. Amyloid bodies are more numerous.

The medullary sheaths of the nervous elements undf»rcro degeneration. The
axis cylinders may present numerous ppindle-sha()ed diiatAtions; the inflamroa-

DISEASES OF THE SPINAL COSD. 91

tory foci not infrequently contain numerous sclerosed, hypertrophiu axis cylin^
ders, without medullair sheaths. The ganglion cells are usualfy smaller, very
granular and pigmented, and often retracted into small round clumps. In other
places they contain vacuolsB.

Atrophic and sclerotic changes have been observed in the nerve
roots and even in the peripheral nerves, in some cases. Degenerative
atrophy of the muscles has also been seen.

Among other organic changes may be mentioned inflammation of the
bladder, urinary passages and kidneys, pneumonic, phthisical, hypo-
static changes in the lungs, decubitus, etc.

J If. Symptoms. — The symptoms begin not infrequently in an acute,
febrile manner, or several acute relapses follow one another before the
disease becomes chronic, while in other cases the development of the
disease is slow and dragging from the start. Apart from the gradual
onset of the affection, the symptoms are very similar to those of acute
myelitis.

It often begins with paraesthesiae, crawling, coldness, burning, etc.
These are often associated with neuralgiform pains which may be
very violent and are sometimes confined to defimte localities, for ex-
ample, the joints. Many patients complain of pains in the back and a
cincture feeling. Paralyses of motion and sensation gradually super-
vene. The first signs of weakness generally appear first in the lower
limbs, rarely in the upper limbs, somewhat more frequently in all the
limbs. Spinal hemiplegia or even paralysis of a single limb may occur
if the inflammatory focus in the cord is suflBciently circumscribed. The
paralysis sometimes begins in the lower limbs, and then gradually ex-
tends to the upper limbs and even to the bulbar nerves. Paralysis of
the bladder and rectum is sometimes an early symptom, and at all events
it appears sooner or later. Priapism, seminal ejaculations, and impo-
tence are also observed.

The same conditions obtain with regard to the reflexes, nutrition,
and electrical excitability as in acute myelitis (vide page 85). In the
later course of the disease we not infrequently notice tension and con-
tracture of the paralyzed muscles and increase of the tendon reflexes —
symptoms which are probably associated with secondary degeneration in
the lateral columns of the cord.

Acute pyrexial exacerbations sometimes occur and are almost always
followed by an aggravation of the symptoms, especially the paralysis.
Erb states that he has seen the symptoms improve after typhoid fever
and scarlatina.

The disease may last many years (ten to twenty); complete recovery
hardly ever occurs, and some of the symptoms will persist even in the
most favorable event. The disease sometimes takes an unexpected acute
turn, the symptoms of acute myelitis develop, rapidly extend upwards,
and prove latal from paralysis of the bulbar nerves. Other patients die
from ^adual exhaustion, or bed-sores and cystitis develop, followed by
pvaemic and septicsemic conditions. In some cases the clinical history
changes and merges into that of multiple cerebro-spinal sclerosis.

IV. — Diagnosis, Prognosis, and Treatment are the same as in
acute myelitis.

6. Multiple Cerebrospinal Sclerosis,

I. Etiology. — The disease is most frequent between the fifteenth
and thirty-fifth years, and is rare after the age of forty-flve. According

nniJ fKwiPrfor part ol

n, readily recogolied by [heir (Uri
-'- -• -,rfo™«IoonJ;/-l. lumbar

DISEASES OF THE BPTSAJ. COBO.

^H|d C'hiircot and Moric it is not very infreqnent in otiitdhood. Three con-

^"-genital caees {irithont autopsy) have been reportwl.

Heredity has been demonstrated in gome csaes. Many writers attri-
bute the disease to cold, exposure to wet, injury or mental excitement.
Pregnancy ie said to favor its deretopment. fit some cases it follows
acute infections diseases, such as typhoid ferer, variola, cholera, scarla-
tina, etc. According to some statementj multiple scleroeis may be pro<
diiced by hysteria (?).

n. AsATOjnCAL CHAS0E9. — Multiple sclerosis appears in the form
of inflammatory foci which are irregularly scattered throughout the
brain and cord. Their number and size vary exceedingly. Sometimes
there are more than a hundred foci, in other cases very few. Their size

Iraries from a barely visible Bpeck to a spot five to t«n centimetres in size.
Borne foci are so email M to be visible only under the microscope.

The superficial plaques are generally visible through the pia mater

with a grayish yellow, pearl-gray, or bluish-gray color. They eoraetimes

reject above tbe surrounding parts, sometimes they are depressed. .\a

Tjle. tbey are harder than the normal cord, more rarely tliey are gela-

loaa and soft. Transverse sections sometimes assume a light rosy-red

I when exi>oi«d to the iiir.

As a rule, a more or less abundant juice can be scraped from them
with the blaile of the knife. The plaque vary id shape, and usually
are sharply defined (vide Fips. 35 and 36). Under the microscope, how-

C' ey present gradual transitions into the normal tissues. The in-
t ptaqnea are sometimes connected with each other by a less
It ionamed portion, but this is not the rule, as is claimed by
Lid. Haoyoi the patches contain vellowdots and streaks (tatty,
ed vesBcb).

04 DISEASES OF THE SPINAL CORD.

The inflammatory foci are distributed in an entirely irre^lar man-
ner. In the cord the white substance is preferably affected; tne changes
are sometimes especially marked along certain columns. Secondary de-
generations are generally absent, even if the sclerotic patches are so ex-
tensive as to interrupt the paths of conduction. Schulze attributes this
to the fact that, on account of the long persistence of the axis cylinder,
a real destruction of the conducting paths rarely occurs.

The medulla oblongata and pons are very often affected; the floor of
the fourth ventricle presents a certain degree of predilection.

The cerebellum often escapes; if not, the sclerotic patches are al-
most always found in the white matter. This is also true of the cere-
brum, in whicli the most frequently affected parts are the walls of the
lateral ventricles, corpus callosum, centrum semiovale, corpus striatum,
and optic thalamus.

In addition to multiple sclerosis, diffuse sclerosis of the brain has also
been found.

The microscopical changes in multiple cerebro-epinal sclerosis are similar to
those of chronic mvelitis. The characteristic feature is proliferation of the con-
nective tissue, witn destruction of the nervous elements. In the most recent
patches, Deiter's cells are found enlarged, and their nuclei increased; in addition,
increase of the interstitial tissue. The neuroglia presents an unusual abundance
of cells and nuclei, partly the result of increase of the elements previously pres-
ent, partly of the emigration of white blood-globules from the vessels. Masses
of round cells are found in many places on the external wall of the vessels.
Finally, the interstitial tissue is converted into Arm flbrillated connective tissue.

At the same time, the blood-vessels are thickened, are dilated into a spindle
shape in places, their nuclei are increased; the lymphatic sheaths, which are di-
lat«d here and there, contain fat granules, granulo-fatty cells or larger accumula-
tions of fat. On the external wall of the vessels we sometimes find accumula-
tions of granulo-fatty cells, sometimes a larger or smaller number of fat crystals.

The number of granulo-fattv cells varies, but they disappear almost entirely
in older plaques. The amyloid bodies are more numerous.

The medullary sheaths of the nerve fibres degenerate and disappear, the axis
cylinders are dilated into a spindle shape, become firmer, and have a dull gloss.
They are very resistant, and often persist in very old plaques. The ganglion cells
often contain an unusual amount of yellow pigment, become granulur, lose their
prolongaMons, and are converted gradually into small round structures. Tlie
formation of vacuolse within them is also observed.

Many authors believe that the lesion begins in the nervous elements proper,
and that the proliferation of the neuroglia is a secondary process. Others re^urd
the blood-vessels as the starting-point of the disease. It is not impossible that
there are various modes of development. The blood-vessels have been regarded
^s the starting-point, particularly in those cases in which the process follows an
infectious disease.

The spinal meninges are sometimes unchanged. At other times they
are thickened, congested, and adherent over the sclerotic patches. Gray
sclerotic patches have also been found in the cerebral nerves and the
spinal nerve roots. Whether they also occur in the peripheral nerves
has not been positively settled. Degenerative atrophy and fatty deffen-
eration of the muscles have been observed at times, particularly when
the anterior horns of gray matter have been affected, Leyden discov-
ered sclerotic changes in the muscles.

Among the changes found in other organs may be mentioned: decu-
bitus, cvstitis, pyelonephritis, pneumonia, phthisis, bronchitis, and some-
times changes m the joints and bones.

III. Symptoms. — The symptoms of multiple sclerosis present an
unusually manifold character. Sometimes the cerebral, sometimes the

DISEASES OF THE SPINAL COSD. 95

spinal symptoms predominate. But, as a rule, certain characteristic
plienomena, viz.: volitional tremor, nystagmus, scanning speech, pa-
retic symptoms, and apoplectiform attacks, are always observed.

At the beginning of the disease, the symptoms often have a vague
character. Some patients complain of headache or vertigo, others of re-
peated attacks of vomiting and gastric pain (crises gastriques), still others
manifest spinal disturbances, particularly parsBsthesisB and neuralgiform
pains in the lower limbs.

The situation becomes more serious when paralytic symptoms develop.
The motor disturbances are more prominent; sensory paralysis is some-
times absent during the entire course of the disease. The patients are
easily tired in walking; the paresis gradually increases and extends to the
trunk and upper limbs.

Jt is especially characteristic that each volitional movement is attended
by violent tremoV (volitional tremor). If the patient rises from a seat
the trunk totters, generally from before backwards, and vice versa; when
directed to move the head this part wags to and fro. If the patient is
directed to place the fingers slowly upon the head of a pin, etc., theliml)
undergoes incessant zigzag, shaking movements. The more the patient's
hand approaches the desired object the more vigorous the movements be-
come. They cease, as a rule, during rest. This volitional tremor is so
characteristic of multiple sclerosis that great, perhaps insurmountable
obstacles will be encountered in diagnosis if the symptom is absent.

Charcot attributed the volitional tremor to the change in the axis cylinder
of the sclerotic patches and to its persistence, so that the impulse of the will
reaches the muscles in an intermittent manner. It is more probable that this
symptom is the result of an affection of certain parts of tne central nervous
system, perhaps the pons and more anterior portions of the brain.

Nystagmus is an equally important symptom. It almost always de-
velops when the patient is directed to look at an object steadily, or to
follow with the eyes an object that is moved about. The eyes are then
observed to twitch from one side to the other. Nystagmus is observed
in about half the cases, but its cause is unknown.

There may also be very peculiar changes in speech. The patients
speak slowly, scan the different syllables in a monotonous tone, often in
a very high pitch. At a later period speech often becomes indistinct if
paralysis and atrophy of the muscles of the tongue, palate, and lips be-
come more markea. The pronunciation of the consonants /, p, g, and t
is usually first affected.

Leube noticed, on laryngoscopic examination of a patient, that the
closure of the vocal cords during phonation was suddenly interrupted for
a short time; Lomikowski described trembling movements of the vocal
cords.

Apoplectiform attacks occur in many cases during the course of the
disease, sometimes at its onset, sometimes at a later period. The attacks

fenerally bejjin suddenly, are attended with disturbance of consciousness,
ut rarely with complete unconsciousness, and sometimes with epilepti-
form convulsions. The bodily temperature is often markedly elevated
(occasionally to 40^ or 42°), and hemiplegia is often left over, but gene-
rally disappears in a few days. The entire condition is very often im-
paired after recovery from these attacks. In addition to the chief symp-
toms already discussed, there are a number of other phenomena of spinal,
bulbar, or cerebral origin.

96 DISEASES OF THE SPINAL OOSD.

Sensory distnrbances may be entirely absent. In other cases^ certain
qualities of sensation may be abolished, but complete anadsthesia is rare
Paresis of the muscles is more frequent than complete paralysis.
Rigidity and muscular spasms, which may develop spontaneously or only
after purposive movements, are sometimes observed at a very early period.
Contractures gradually develop, particularly in the muscles of the back
of the neck and the aaductors of the thigh, at a later period in the flexor
muscles of the limbs, so that the patients become unable to walk. Pre-
vious to this the gait is awkward or stiff, like that of spastic spinal
paralysis. Distinct ataxia occasionally develops if the postenor columns,
particularly the bandelettes extemes, are affected in a marked degree.

Paralysis of the bladder and rectum sometimes occurs at a very early
period, but often disappears; at a later stage it remains persistent. This
opens the way for the development of cystitis, pyelonephritis, ammon-
semia, septicsBmia, and pyaemia. The sexual function is gradually abol-
ished.

Vasomotor disturbances (abnormal color of the skin, changes in tem-
perature and perspiration, gangrene and oedema of the skin) have been
observed in some cases.

Trophic changes may also occur, viz.: decubitus, herpes, bullous
eruptions, abnormal growth of hair, changes in the nails, swelling of the
joints, etc. Individual muscles may rapidly atrophy and lose their
faradic excitability; this takes place if the ganglion cells in the anterior
horns of gray matter are destroyed. Increased galvanic excitability has
sometimes been demonstrated in the contractured muscles.

Reflex excitability is markedly exaggerated in the majority of cases*
This is true not alone of the cutaneous, but also of the tendon reflexes.
Gentle tapping of the patellar tendon produces vigorous clonic contrac-
tions of the muscles of the corresponding limb, sometimes also in the
other limb. Rapid dorsal flexion of the foot causes trembling move-
ments of the whole limb, which often cease on sudden plantar flexion of
the great toe (reflex inhibition). Vigorous reflex contractions are also
produced by tapping the tendons of the biceps and triceps, etc.

If extensive changes occur in the medulla oblongata, symptoms de-
velop which are similar to those of bulbar paralysis. The tongue under-
goes atrophy and is moved with diflBculty; speech becomes so indistinct
as to terminate finally in a mere grunt; deglutition is impaired, closure
of the epiglottis and of the naso-pharyngeal cavity is impaired, and the
patients often swallow the wrong way; the lips atrophy, and can no
longer be closed. Attacks of palpitation and dyspnoea occasionally set
in, and may prove fatal (paralysis of the pneumogastric).

Other cerebral nerves may also be paralyzed, and this may give rise to
deafness, unilateral or bilateral ageusia, anosmia, ptosis, paralysis of one
or all the ocular muscles (in the latter event the eyeball is inamovable),
unilateral or bilateral myosis, or mydriasis. Many patients complain of
flashes of light before the eyes, and gradually become amblyopic. Amau-
rosis is rare. Ophthalmoscopic examination reveals atrophy of the
optic nerve, the papilla being abnormally white, and the retinal vessels
unusually narrow.

Uhlhoff found atrophy of the disc in 25% of the cases, marked optic neuritis
in 16^. Eulenburg recently described a case in which optic atrophy and com-
plete amaurosis preceded tlie first spinal symptoms for five years.

Vertigo is a very frequent spinal symptom. The patients may have

DISEASES OF THE SPINAL COBD. 97

the sensation either that objects are revolving around them or that they
themselves are revolving. The vertigo is sometimes not of central
origin^ but the result of ocular paralysis and diplopia. There is often a
remarkable variability of mood; the patients laugh and crj without
motive. They often become apathetic and dull, and the facial expres-
sion becomes apathetic. Mania, dementia, delusions of grandeur, etc.,
develop in some cases.

The disease may last twenty or even thirty years. Remissions and
exacerbations occur not infrequently. The former may be so pro-
nounced as to raise the vain hope of recovery.

Charcot recognizes three stages of the disease: the first stage, until
the development of contractures which compel the patient to keep con-
stantly in oed; the second stage, in which tne characteristic symptoms
of the disease are present, and which often lasts many years; the third
stiige, a period of increasing marasmus.

The aisease always terminates fatally. Death is the result of increas-
ing marasmus, sometimes accelerated by violent diarrhoea; of decubitus
afid vesical paralysis, with their sequelae; of an apoplectiform seizure;
of advancing bulbar symptoms, or finally of intercurrent diseases.

IV. Diagnosis. — In addition to nystagmus, disturbances of speech,
vertigo, and apoplectiform attacks, volitional tremor possesses a very
great diagnostic significance. The disease is not apt to be mistaken for
other affections which are associated with tremor.

In paralysis agitans, the tremor persists durin« repose, hardly ever affects the
head, and the patients are able to control it for a time by an effort of the will. In
addition, the motor symptoms are less marked, sensory disturbances and paralysis
of the bladder are absent, and the disease generally begins beyond the age of
forty years.

In chorea, the movements present greater excursions and persist during
repose; paralyses and sensory disturbances are absent.

Westphal recently described two cases in which the symptoms of
multiple sclerosis existed for years, but the autopsy revealed no lesion of
the nervous system. There is, therefore, a neurosis whose clinical
history is so like that of multiple sclerosis that it cannot be distinguished
from it with certainty. Optic nerve changes would be positive evidence
in favor of the diagnosis of sclerosis.

On the other hand, there may be extensive multiple sclerosis without
the typical clinical history of the disease. French writers have apj^ied
to this form the term sclerose en plaques fruste (atypical sclerosis). This
variety sometimes presents only cerebral symptoms (vertigo, headache,
apoplectiform or epileptiform attacks), although the autopsy shows ex-
tensive spinal sclerosis; other cases simulate the history of ordinary
myelitis, etc.

The history of multiple sclerosis may also be very similar to that of
locomotor ataxia. But in ataxia the patellar reflex is absent, and sen-
sory symptoms predominate, while the motor power of the muscles is
very little impaired. It may be very diflScult to distinguish multiple
sclerosis from progressive paralysis of the insane, since, apart from the
fact that both affections mav be combined, tremor, speech disturbances,
pupillary changes and apoplectiform attacks may be observed in uncom-
plicated progressive paralysis.

V. Prognosis. — The disease always terminates fatally, though life
may be prolonged for a long time.

98 DISEASES OF THE SPINAL GOBD.

VI. Treatment. — The treatment is the same as that of myelitis
(vide page 88).

7. Tumors of the Substance of the Spinal Cord.

I. Anatomical Changes. — ^Tumors rarely occur in the substance of the spinal
cord, and can hardly ever be diagnosed with certaii\ty during life.

llie most frequent form is glioma; next, pure sarcoma: myxosarcoma and
fibrosarcoma have also been observed. Tubercles and gummata will be consid*
ered in Vol. IV.

Qlioma affects mainly the enlargements of the cord, particularly the cervical
enlargement. According to Virchow, it starts from the neuroglia; according to
Klebs, from the nerve fibres and ganglion cells. It is sometimes unusually vas-
cular (telangiectatic glioma), ana is infiltrated with extravasations and blood
cysts. Mixed forms of glioma are also observed.

The size of the tumors varies from that of a hempseed to that of a hazelnut,
or even much larger. They are usually round, buc occasionally elongated, and
sometimes extend along the entire cord into the medulla oblongata. They are
often sharply circumscribed, occasionally surrounded by a fibrous capsule ; more
rarely they pass gradually into the substance of the cord.

The cord is often softened in the vicinity of the tumors, or secondary degen-
eration may result, etc.

II. Symptoms. — Despite their large size, tumors of the cord sometimes remain
entirely latent. In other cases, the most varied symptom complexes are ob-
served. In sudden hemorrhages into and rapid enlargement of a tumor, the
symptoms of haematomyelia are produced.- More or less acute signs of compres-
sion of the cord are most apt to aevelop. Or the signs of transverse ascending
and descending myelitis are produced. Tabetic or spastic symptoms are noticed,
according as the posterior or lateral columns are involved. The symptoms of
progressive muscular atrophv or the various forms of poliomyelitis have been
observed, if the ganglion cells of the anterior horns were affected. The symp-
toms of unilateral lesion of the cord have also been described. Or vague, mde-
finable spinal symptoms make their appearance. The dieease may last for many
years. Death results from intercurrent diseases or increasing marasmus.

III. Etiology.— Nothing is known concerning the etiology of the tumors.
Trauma, cold, pregnancy, mental excitement have been mentioned as causes.

IV. Diagnosis. — The dia^osis is generally impossible. As a rule, we must
be satisfied with the diagnosis of a spinal affection. We may suspect a neoplasm
if the svmptoms have b^n preceded by phthisis, scrofula, or sypnilis.

V. Prognosis. — With the exception of gummata, the prognosis is always bad.

VI. Treatment.— Gummata are treateti by antisypnilitic remedies. The
treatment of other forms of tumor is purely symptomatic.

8. Syringomyelia and Hydromyelia. Formation of Cavities ifi the

Spinal Cord.

1. Cavities in the cord may be congenital or acquired. They sometimes
extend the entire length of the cord, from the lower part of the fourth ventricle
to the conus terminiuis, somtimes they are very short. On transverse section,
they form narrow fissures or elongated, rounded, or irregular cavities; their size
often varies in different places. A number of cavities are sometimes closely
aggregated. They are generally most extensive in the cervical and dorsal por^
tions of the cord, so that these parts may form a fluctuating sac, which gener-
ally contains clear serous fluid. The fluid is rarely hemorrhagic or flocculent.

The wall of the cavity is often composed of firm connective tissue. ^ Under
the microscope, this is found to consist of branching cells, fibrillated intercel-
lular substance, a few granulo-fatty cells, and thickened blood-vessels. The
latter may be very brittle, and give rise to hemorrhages. In other cases, the
cavity is situated in a gray, gelatinous mass composed of intercellular snbstonce
and round cells. The inner surface of the cavity sometimes is covered with
cylindrical epithelium; sometimes this is absent.

The cavities are situated most frequently between the posterior columns of
the cord, but often change their position at different heights. Thev are often
independent of the central canal; in other cases they merge into it in places.

DISEASES OF THE SPINAL COBD.

Sclerosis, especially of the oolamns of Gk>ll or Bordach, acute and chronic mye-
litic foci, etc., are also often present.

2. Simon suggested that a distinction should be made between syringomyelia
and hydromyeBa, the latter term being applied to those cavities which result
from dilatation of the central canal. These dilatations, apart from congenital
cavities, may be the result of inflammatory proliferation and subsequent retrac-
tion of the connective tissue surrounding the central canal or of circulatory dis-
turbances in the cerebellar fossa as the result of tumors.

Simon and Westphal believe that softening of tumors and subsequent absorp-
tion may give rise to the formation of cavities in the cord, but Leyden claims
that these are apt to be mistaken for inflammatory new-formations or coagulation
at the periphery of . the cavities.

Hemorrhages and inflammatory softening; may also lead to the formation of
cavities, after absorption has taken place. Simon attributes some cases to men-
ingeal adhesions.

Fio. 87.

Fio. 88.

C t?

Two caaei of lyringoxnyelia without ■ymptoms during life, a-6, cexrlcal oord ; o-e, dorsal cord

Natural sise.

Eichhorst and Naunyn observed syringomyelia develop in new-bom dogs,
whose spinal cord had been strongly compressed at one spot soon after birth.

8. In a number of cases, very Targe cavities have been found which had given
rise to no symptoms during life, as is shown in two cases which came under our
own observation (Figs. 87 and 88). Spinal symptoms were absent in both cases,
although the cavities extended from the first cervical to the first lumbar nerves.
An attempt has been made recently to construct a symptom complex for certain
cases: slowly-progressing atrophy of the upper limbs, partial sensory disturb^
anoesv especially changes in temperature ana pain sensibilily, vaso-motor and
trophic onanges, absence of the tendon refiexes, rarely rigidity of the muscles
and contractures; bulbar symptoms often supervene at a later periodf

100 diseases of the spinal oobd.

h, system diseases of the spinal cord.

Simple System Diseases.

1. Gray Degeneration of the Posterior Columns, Tabes dorsalis.
{Sclerosis of the Posterior Columns. Progressive locomotor ataxia.)

I. Etiology. — Locomotor ataxia is the most frequent disease of
the spinal cord. It is much more common among men than among
uromen, and is chiefly a disease of middle life, particularly between the
ages of 30 and 40 years. It rarely begins after the age of 50 years or
during the period of childhood.

Among Its causes syphilis occupies a prominent part. Although our
experience corroborates that of Leyden and Westphal, who maintain
that Fournier and Erb have exaggerated the importance of this etiolo^-
cal factor, nevertheless it cannot be denied that a history of syphilis is
often obtained in this disease, and that an inunction treatment produces
surprising results in not a few cases.

From our present knowledge it would appear that ataxia is particolarlyapt to
follow syphilis if the symptoms of the latter were mild and were not thoroughly
treated. Tabes dorsalis is one of the late sequolse of syphilis ^usually five years,
often ten to twenty years, after infection). Some writers maintain that inrphiliB
merely causes a sort of weakness of the spinal cord, so that other hardly demon-
strable causes may give rise to tabes.

Cold is often mentioned as a cause, but it is probable that this will
act as an etiological factor only if there is an abnormally slight power of
resistance of the spinal cord, either congenital or acquired. Among
causes of a similar character may be mentioned : over-exertion, injury,
concussion of the spine, mental excitement, excessive lactation, sexual
excesses, etc.

The disease sometimes appears after acute infectious diseases, such
as pneumonia, typhoid fever, articular rheumatism, cholera, etc.

Tiiczek observed the symptoms of ataxia after chronic poisoning with
ergot, and Leyden makes ai similar statement with regard to pellagra.

Heredity plays a prominent pai-t in certain cases. Thus, Carr6 ob-
served the disease in the grandmother, mother, seven brothers and
sisters, and nine other relatives.

Westphal showed that the disease develops not infrequently during
the course of progressive paralysis of the insane.

II. Anatomical Changes. — In exceptional cases the spinal cord
appears normal to the naked eye, although the microscope reveals ad-
vanced changes.

The disease is often evident from the shape, color, and consistenoe
of the cord. The posterior surface appears flattened and narrowed, and
if the pia mater has remained transparent, a gray, pearl-gray, or yel-
lowish-gray tissue is seen in a position corresponding to the posterior
columns. As a rule, the consistence of this part is increluaed, rarely di-
minished. These appearances are often concealed by changes in the pia
mater, which is thickened and opaque over the affected parts of the cord,
contains numerous sinuous vessels, is occasionally markedljr pi^ented
and adherent to the arachnoid and dura mater. Opacities and cal-
careous p1at,es are often found on the arachnoid and dura mater.

SPIilAL OOSD.

_ On transverse section of the cord, the posterior

"liave a pearl-gray or yellowish-gray color. These
parent; they are aometimes unusually firm, in
gelatinous. The changes are generally most i
bar and lower dorsal portions of the cord (vide Fig,

"Tnmbar region they are often confined to
me colcmns of Burdach, in the cervical
Wgion to the columns of Goll. Even whera

■the changes are most marked, islets of the
posterior columns often remain intact. This
18 especially true, aa is shown in Fig, 40, of
the vicinity of the posterior gray commissure
and the part immediately adjacent to the
posterior horns. The changes may some-
times be followed to the medulla oblongata
into the funiculi graciles, aud gradually dis-
appear. In a few cases, changes have also
been found in the peripheral layers of the
pons and the corpora quadrigemiua,

(The posterior Spinal roots are atrophic
nd gray, and present changes similar to
(lose observed in the cord. These changes
ever extend beyond the intervertebral
anglia. The cauda equina contains thin,
ray strands which correspond exactly to the
trophic posterior spinal roots.
Gray degeneration of the cerebral nerves
Hs been observed in a number of cases, par-
ticularly in the optic nerve. It begins in the
immediate vicinity of the eveball and the
peripheral layers of the trunk of the nerve,
and may gi'adually extend along the ojitic
tract to the geniculate bodies. Similar
changes have been observed in some of the
iiervea of the ocular muscles, in the trigem-
inus, hypoglossus and pneum agastric . even
in the nuclei on the floor of the fourth ven-
tricle.

t The brain presents no change, unless the
Lxia is a complication of pi-ogressive paral-
B of the insane.
Friedreich first noticed atrophy of nerve
res, and increase of the interstitial tissue
in the peripheral nerves. Degenerative and
atrophic conditions have also oeen observed
ia the nerves of the muscles.

^ia th.

MiuroBcopical examination of tiie degenerated
of th« posterior columns shows disap-
I of the Dcrve fibres, and tlie presence
either o( arather lar^je-meshed eonaectivo tissue,
which is poor in cellii (vide Fig. 41) or at a. au
neotive tissue (vide Fig. i2). '
fibnllntpd.

iniilo-fftttv cells are ''nt

luvemeiit: c, upper: djinkldle;
B, lowsrilonil eord; / lumlMT
entsreement. The nleniUc

SirtlonH are Ueht In color.
■luTBlBiie. AtieT Lejitn.

„.-... .. - . -.8 delicately flbriilated eon-
lu some parts the connective tUeue is firmly

;!y absent in pluees, in others they are more or

DISEASES OF THE SPINAL OOBD.

conoective-tiMne changee aa eecondaiy, others coiuider the process a chionic pri-

.-_.. .-.;-i u^i^

e associated the disease with primarj changes in the btood-

AnarChucot,

vessels. Btill other writ«n
aold BB the primary lesion.
The posterior horns of gray

iphr or light snMTlor hon.

igard the infUmmation of the pia mater and arach-
usuoll^ take part in the process. They ap-

Qnj daBenentiod ot the bsndeleCtei exWniaa Id begliinlnK tkb<M>. After Charcot.
Pic. *t.—ltiM\a cerrlol nslon.
rU(.«.—Loir«rdar**l region; b<, bandeleiceaexunia.

pear small, their nerve flbrea are diminished in size or have disappeared, the
connective tissue is unusually abundant, and the ganglion cells are shrunken,
often filled with aa unusual amount of yellow pigment, and many of the cells
are destroyed.

104 DISEASES OF THE SPIXAL COBD.

Clarke's columiu in tbe doml cord often preaent a gnyuh diaoolontioD to
the naked eje. Under the micriMcope we find atruphj- ami ois^peannoe <^ tbe
nerve Hbiee and incroise of tbe connectiTe tiame, out the ganglion oelb are nsu-
allv intact.

The morbid process oft«n extends from the poBteiior colomna akniK the peri-
pberv to the lateral columns. Sometimes it extends only to the oovbeDar tracta,
m other cases it paaaes deeper into the laieiml oolomiw, oooasiotiallr it even ex-
tends to the anterior colnniiw. Finally, Charcot and Pietret found that, in rmrt
cases, the morbid proceea extends to the large ganglion cells of th« anterior
borns. Afterandergoingpigment degoieiation.thegaDglionodlsahiink anddb-
appear, and tbe corresponoing anterior bom appears atr^ihio (vide fig. 48), Thaos

processes correspond to atrophy of musclea, and degeneration reaction doling

Very little is known concerning the post-mortem appwranoee in the initial
stages of tabes. According to Chiut;ot, tbe primary site of dis«9ase is situated in
the internal root flbiea (bandelettes exlemes) in tbe lateral part of the coluntD of
Burdach near the posterior horti. All tbe other anatomical changes are said to
be spcoadary id character, particulnrly the affection of the columns of Ooll,
which is regarded merely aa au ascending secondary degeneration.

Stniempell has come to the following conclusioiu with re^fard to the distribn-
tion of the lesions:

In the luinbar cord, the cbangee begin symmetrically in the middle portiona

EkKiaalnK

of tbe posterior columns, and intact parts are left anteriorly betwewi them and
the posterior gray commiBuure and posteriorly between them and the outer
boundary of the posterior columns (vidB Fig. 48). As the disease progreoaea, the
process extends posteriorly, but a small oval or triangular Held, along the poste-
rior longitudinal sulcus, is generally left intact {vide Fig. 47), The most anterior
portions of the posterior columns always remain intact.

In the dotwd cord, the process begina in two lateral fields from which fibne
mainly radiate into the posterior horns. In addition, two median stripa, which

DISEASES OF THE SPINAL OOBD. 105-

are situated along the posterior longitudinal sulcus, are affected very early (vide '
Fig. 48). Later, the entire posterior column degenerates, but the posterior exter-
nal portion persists unchanged for an unusual length of time.

In the cervical cord, the change is first noticed in the columns of Goll, more
markedly posteriorly than anteriorly. Two anterior and two posterior external
fields remain intact for a long time (vide Fig. 49).

It would appear, accordingly, as if the total degeneration of the posterior
columns consists of the gradual affection of smaller systems of fibres which are
functionally similar.

In some cases, scattered sclerotic patches have also been found throughout
the cord.

III. Symptoms. — The most important and constant symptom of
tabes dorsalis is inco-ordination of voluntary movements, ataxia, with
unimpaired or slightly diminished muscular power.

Locomotor ataxia is an exquisitely chronic disease, which may last
more than thirty years.

Leyden distinguishes a neuralgic, ataxic, and paraplegic stage.

In the first (neuralgic) stage neuralgiform pains play a prominent
part. These may be associated with paraBsthesiaB, ocular paralyses,
pupillary changes, optic atrophy and amaurosis, loss of the patellar
tendon reflex, anassthesiaB, disturbances of the bladder and rectum, and
changes in the joints. This stage varies in duration from several weeks
to many years.

In the second (ataxic) stage, the symptoms of ataxia become more
prominent. These almost always appear first in the lower limbs, often
at a later period in the arms; they rarely begin in the upper limbs.
This stage may also last many years.

The third (paraplegic) stage be^ns when the patient is no longer
able to move the lower limbs, and is confined to bed. In some cases,
death is the result of bed-sores, paralysis of the bladder with alkaline
decomposition of the urine, ulceration and necrosis of the vesical mucous
membrane or pyelonephritis. Others die of pulmonary phthisis (a
frequent termination), or general marasmus, which is not infrequently
accelerated by profuse diarrhcea or by obstinate vomiting as the result of
so-called gastric crises, or intercurrent diseases. In several cases, Ley-
den observed acute delirium with coma, and a fatal termination.

We will now consider the individual symptoms somewhat more in
detail.

Neuralgiform pains are amon^ the most constant and earliest symp-
toms. As a rule, they are described as lightning-like, shooting, stick-
ing, boring, or crushing. They are often so violent that the patients
cry out aloud. They are almost always situated deeply, rarely in the
integument; the latter is often hypersBsthetic in the situation of the
pains. The pains sometimes appear along certain nerve tracts, some-
times as hemicrania, or chiefly in the joints, or they may not follow a
sharply defined anatomical course. They are often especially severe at
night.' Remissions and exacerbations are frequent, according to the
temperature and barometer; the exacerbations are most marked in
rainy, stormy weather, with a low barometer.

As a rule, the pains first appear in one, then in the other lower limb,
and are not infrequently rogaraed as sciatica. The pains usually appear
in the upper limbs at a later period, and are apt to extend along the dis-
tribution of the ulnar nerve.

The majority of the patients also complain of girdling pains (cincture
feeling) around the chest or abdomen.

106 DISEASES OF THE 8PINAX COBD.

Visceral neuralgias may also develop; violent gastralgia with vomit-
ing (gastric crises), violent burning in the urethra and rectum, associ-
ated with dysuria and tenesmus, occasionally with dysenteiy-form
stools, etc.

In rare cases, the pains are felt along the cerebral nerves, generally
along the occipital, next the trigeminal nerves.

The pains often continue during the further course of the disease.

ParaesthesiaB constitute a very constant sjrmptom, and, as a role,
develop at a very early period. The patients complain of a feeling of
coldness, burning, prickling, or formication. Many complain that tney
do not feel the floor in walking, that they have a sensation as if walking.
on felt, wool, or feathers, or on a bladder filled with water. The
paraBsthesise usually appear first in the lower limbs, and are generally
more marked in the feet and legs. At a later period, they extend to
the upper limbs, and even the trunk may be affected.

Uypersesthesia is not a very frequent symptom. It is sometimes as-
sociiited with the neuralgiform pains in the skin, and may rapidly change
its location.

Some patients do not experience pain on irritation of the skin unless the irri-
tant is very severe, but the pain is tnen unusually violent. Leyden has applied
to this phenomenon the term relative hyperaesthesia.

The patients rarely complain of pain in the back. M. Meyer has
called attention to the presence of pressure points on the spine, and has
had good results from treating them with electricity.

According to Leyden, anaesthesia occurs* in every case of tabes, but
careful examination is sometimes requisite in order to detect it. In
many cases there is partial anaesthesia, in more advanced cases it may be
complete. It is generally most marked in the feet and legs, but in the
beginning of the disease it is sometimes confined to circumscribed parts
of the integument, for example, the perineum, the lateral and posterior

f)art of the thigh, scrotum, etc. The sensation of tickling is generally
ost first, then the sensation to touch and pain, later the other modes of
sensation.

Delayed conduction is a not infrequent symptom. If the skin is
pricked with a pin, several seconds (up to five) mav elanse before the
sensation is perceived by the patient. Hertzberg and Nothnagel also ob-
served delayed conduction of* temperature impressions.

Naunyn recently described double sensation, t. e., the patient, after a single
prick of a pin, first experienced pain, and after an interval, a second, more in-
tense pain. E. Remak noticed in one patient tiiat the prick of a pin was first felt
as a simple touch, and after an interval as pain.

Fischer noticed polyaesthesia, t. e., one point was felt as several. In the early
stages of the disease, Berger noticed that feeble cutaneous irritants were perceived,
but strong ones were not perceived. £. Remak calls attention to the readiness with
which the sensory nerves are exhausted. If the skin is faradized, the patient,
after a while, states that he no longer feels anything. The current must then be
increased, but again a point arrives at which the sen-nation which was previously
pri'sent disappears. Mendelssohn showed that the electrical reaction of the sen-
sory cutaneous nerves is changed in tabes. There is often a prolonged after-een-
sation, so that rapidly following stimuli merge into one.

Leyden's investigations have shown that the anaBsthesia affects not
alone the skin, but also the fasciae, tendons, and muscles. The impair-
ment of muscular sense is especially important.

DISEASES OF THE SPINAL CORD. 107

If the patient's leg is slowlj and carefully raised while his ejes are closed, and
he is directed to raise the other leg to the same extent, gross mistakes are made.
If the lee is placed in a sling, and passive movements of the thigh, leg, or foot
are made, the patient is unable to tell the position of the limb. If one leg is
oarefuUj placed over the other he is unable to tell which leg is uppermost. If he
is directed, while the eyes are closed, to bring the fingers of tne two hands in
contact, he hunts for them in the air, etc.

The sense of effort, however, is retained, according to Leyden. This is tested
by placing a folded handkerchief upon tiie extended limb, after the latter has
been placed upon a support, and directing the patient, with the eyes closed, to
tell differences in weights placed upon the hanakerchief . Electro-muscular sen-
sibility may also be unchanged, but it is sometimes diminished.

The Brach-Bomberg symptom is generally attributed to changes in
the muscular sense. This is shown by the tottering movements of the
patient in the dark, or when the eyes are closed, it is evident that in
the light the eye is able, to a certain extent, to overcome the defect in
the muscular sense. The tottering is especially marked when the feet
are brought together.

The cutaneous reflexes present no characteristic changes. Thev may
be unchanged, diminished, increased, or delayed. When the prick of a
pin on the sole of the foot gives rise to reflex contractions of the leg, the
patient sometimes mistakes the perception of the muscular contractions
for that of the prick itself.

The condition of the patellar tendon reflex is an extremely important

Smptom. This is tested by directing the patient to cross one knee over
e other, and by tapping the tendon above the patella quickly with the
percussion hammer or the ulnar side of the hand. Or the patient allows
the limb to hang loosely over the ed^e of the bed, and the oatella tendon
is then tapped. Or the physician's hand is placed under tne knee-joint
of the patient, the limb is slightly elevated, and the tendon percussed.
In tabetic patients, the reflex (contraction of the quadriceps and pro-
pulsion of tne leg) remains absent in almost every case. This is one of
the earliest symptoms of ataxia. Its appearance indicates the existence
of foci of degeneration in the external portions of the posterior columns
in the upper lumbar region or its transition to the dorsal rerion.

Vaso-motor, secretory, and trophic changes may remain absent during
the entire course of the disease. In other cases there is a diminution in
the temperature of the skin of the affected limbs corresponding to a sen-
sation of coldness. Unilateral and local hyperidrosis and ptyalism have
been observed. Erythema, herpes, bullous and nodular eruptions may
appear, and acute decubitus with its sequelsa may also develop. Pooley
described unusual desquamation of the epidermis; Ballet ana Dutil ob-
served ichthyotic changes on parts of the skin which were anaesthetic,
hyperaesthetic, or the site of severe pains. Strauss described cutaneous
hemorrhages. Thickening, Assuring, and falling out of the nails have
been reported in a few cases. Falhng out of the teeth has also been
reportea, and according to Maveraudi^re, this is always preceded by
hypersBsthesia or anaesthesia at tde site of the tooth.

The panniculus adiposus and muscles may remain normal for a long
time, and emaciation does not occur, in many cases, until the patient
has been confined to bed for a long time. But rapid atrophy and de-
generation reaction (usually in the upper limbs) occur if tne ganglion
cells of the anterior horns are destroyed. According to Charcot, an im-
portant, early diagnostic sign of tabes is hemiatrophy of the tongue, gen-
erally associated with ocular paralysis.

108 DISEASES OF THE aPDTAI. COBD.

Charcot also includes among the trophic disturbances certain pecntlAr joint
changes, which oft«n occur very early, more raruij' in the later stages of tba
dieeme.

The knee-joint is more frequently affected, next the shoulder (eepeciuUv on
the right side), elbow, hip, and wrist. The disease is unattended with fever or
pain, but with marked swelling which sometimes extends orer a conaiderabls
part of the limb. The swelling, which generally (jonsists of an aocumulatlon ^
serum or sero-bloody fluid in llie joint, may disappear after weetm or months
without evil effei'ts. or it terminatea in erosion of tlie cartilages and enda <^ the
bones; the joints then creak on motion, and spontaneous dislocationa may de-
velop (vide Fig. SO). Suppuration and perforation of the joint are very rarely
observed.

Charcot has also noticed fragility of the boaes. terminaiing in spontaneous
fractures. The lower limbs aiv t;eneriilly affected, especially the tfiiKh^. Be-
covery is not infrequently iirtend<Ml ivitli mi .ibnorraal development of callua. In
such cases. Blancbard foiind ilisappearnnce o( the lime salts anil Rarefaction of the
osseous tissues in the nei'ghborhoood of the Haveiaian canals, moot markedly
near the medullary cavity.

These changes ore connected with the development of the tabetic foot. In

Fig. so.— Eroded head of bumenis In ubes Fig. SI.— .Somul head of hnoians. After
donallB. Cbsrcot.

this condition the scaphoid and internal cuneiform txines project strongly on the
inside, while the metatarsus falls back on the outside, so that a charBcteristio pro-
jection forms at tlie first tarso-ineta tarsal joint.

In one case Kroenig described spondylolisthesis. Among other secretory and
tropliic disturbances we may finally mention varicocele, swelling of the testicle,
and mal perforant du pied.

Motor disturbances play a prominent part in the symptomatology of
tabes. Paralysis is either altogether absent or occurs only at a late stage
of the disease as the simple result of prolonged disuse. Temporary
hemiplegic or paraplegic paralyses are observed occasionally, and are re-
garded by Leyden as eshaustion paralyses. But despite the fact that
the patients generally possess sufficient power, they present the signs of
motor inco-ordi nation or ataxia. In walking, tne legs are separated
widely, the heets are brought forcibly on the ground, and irregular move-
ments are performed in lifting the limbs. The gait becomes nncortain
and zipag. and the patients are unable to walk in a straight line. These
disturbances become especially marked on making sudden turns, walk>

DISEASES OF THE SPINAL COSD. 109

ing up-stairs, etc,, or on closing the eyes. The patient carefully follows
every movement with his eyes. As the symptom progresses, he is no
longer able to walk without assistance. Finally, tne feet make such
violent, irregular movements that he is confined permanently to the
chair or bed. Ataxic movements sometimes occur in the upper limbs,
so that the patient performs irregular, unnecessary movements in
threading a needle, etc. In advanced stages he is unable to write, eac,
or clothe himself, and becomes as helpless as a child. The electro-
muscular irritability remains unchanged.

According to Leaden, ataxia is merely the result of extensive anaesthesia (sen-
sory ataxia), including not alone cutaneous ansesthesia, but particularly diminu-
tion or abolition of the muscular sense. It has been contend!ed, in opposition to
this view, that ataxia may exist without disturbance of sensation, and also that
ansBstheaia occurs without ataxia. Friedreich explains ataxia by the paralysis of
definite co-ordinating nerve tracts (motor ataxia) which convev the co-ordinating
impulse from the centre in the brain through the posterior columns (or cerebellar
tracts?) to the periphery. It must be remembered, however, that no nerve tracts
of co-ordination have yet been discovered. Cvon believes that ataxia is the result
of an interruption of refiex paths in the spinal cord.

•

Muscular twitchings are rare and generally result from neuralgic
pains; contracture of the muscles is equally rare.

Disturbances of the bladder and rectum are frequent and often very
earljT symptoms. The patients often suffer from incontinence or from
inability to empty the bladder. In the later stages of the disease, com-
plete paralysis of the bladder may occur and result in stasis of urine, cysti-
tis, pyelitis, nephritis, pyaemia, and septicaemia. There may also be in-
voluntary evacuations from the bowels, or obstinate constipation.

Ocular symptoms are very often present and are extremely important
in diagnosis. Paralysis of ocular muscles is ^hown by ptosis, strabismus,
diplopia, and vertigo. The motor oculi is most frequently affected,
then the abducens, and then the trochlearis.

The pupils are often no larger than the head of a pin (spinal myosis).
They react very little or not at all to light, but change their dimensions
during accommodation. The pupils are sometimes unequal.

Amblyopia is often a very early symptom, and may terminate in
complete blindness. This is sometimes observed for years prior to the
first distinct signs of ataxia. The ophthalmoscope shows a very white
color of the disc, the lamina cribrosa is unusually distinct, the retinal
arteries narrowed.

The field of vision is more and more constricted, not concentrically, but by the
loss of sectors. There are also peculiar disturbances of color sense, viz., the
development of insensibility to certain colors; first for red and green; yellow,
and particularly blue, are retained longest.

Visceral crises is the term applied to peculiar attacks which affect
one or more of the viscera (stomach, larynx, pharynx, kidneys, urethra,
etc.).

Gastric crises are the best known among these symptoms. They
consist of attacks of violent gastric pain, associated with protracted
gagging and vomiting, at first of the gastric contents, later of mucus,
and then bilious fluid. These attacks sometimes last only a few hours,
sometimes several days. They produce great exhaustion, and even

110 DISEASES OF THE SPINAL CX)BD.

terminate fatally. Such conditions sometimes follow or are associated
with unusuallv violent neuralgiform pains. Diarrhoea and hemor-
rhages from the genitals {in women) have been observed dining the
attf^ks. James Russel noticed diminution of urine and urea, and albu-
minuria. Buzzard states that gastric crises occur particularly in pa-
tients who suffer from joint affections. They are sometimes an early
symptom (prior to the ataxia)^ but recur from time to time at a later
period.

Lupine also describes painless gastric crises^ characterized by profose
vomiting, which may be so obstinate as to endanger life.

Intestinal crises consist of attacks of diarrhoea associated with pain ;
they may be attended by salivation and hyperidrosis.

Laryngeal and pharyngeal crises are attacks of dyspnoea and suffoca-
tion and difficulty m deglutition, which may be associated with cyanosis
and temporary protrusio bulbi.

In renal crises there are violent attacks of pain, similar to renal colic;
the secretion of urine is diminished, but it contains no blood or pus.
The attacks may last a week.

Pitres has observed, in women, clitoris crises, i, e., attacks of volup-
tous sensations similar to those experienced during coitus. Priapistie
and spermatorrhoeic crises have been observed in men.

The development of the crises has been attributed in part to degene-
ration of the peripheral nerves, in part to degeneration of the nuclei of
the cerebral nerves.

Circulatory symptoms have been described in a number of cases.
The pulse is often very rapid, and attacks of palpitation, terror, and pain
in the heart (crises cardiaques) are also mentioned. Eulenburg noticed
very marked dicrotism oi the pulse. Berger and Rosenbach noted the
f reouent coincidence of tabes and aortic insufficiency.

Diseases of the cerebral nerves, apart from the optic and the nerves
distributed to the ocular muscles, occur quite rarely. Tinnitus aurium
and hardness of hearing have been described in a number of cases.
Trigeminus anaesthesia is sometimes observed ; likewise paralysis and
spasms in the distribution of the facial nerve.

Disturbances of the sexual functions are observed particularly in
males. At the onset of the disease there is often increased sexual desire,
and the semen is discharged very quickly ; pollutions occur very often.
These symptoms, however, gradually give way to impotence.

The psychical functions are often affected. The majority of writers
mention the cheerful disposition of the patients ; but, if closely watched,
this very disposition is often seen to be morbid. Well-marked insanity
occurred seventeen times in eighty-nine tabetic patients f Moeli). Bern-
hardt recently called attention to apoplectiform attacks, out these occur
much less frequently in tabes than in multiple sclerosis.

The following tables by Bernhardt (58 cases) and Erb {06 cases) show
the frequency of the individual symptoms in this disease :

DISEASES OF THE SPINAL COBD.

Ill

1. Absence of patellar tendon reflex. . .

2. Lancinating pains

8. Paresis of bladder

4. Paralysis of ocular muscles

5. Myosis

6. Rigiditj of pupils

7. Optic atropny

8. Sensory disturbances

9. Analgesia

10. Delayed conduction of pain

11. Bracn-Romberg symptom

12. Feeling of exhaustion ^

18. Ataxia

14. Sexual weakness

15. Joint affection

16. Crises gastriques

Demhardt.

Erb.

100.0

per cent

98.0

per

cent

79.5

92.5

74.1

81.0

89.6

88.7

27.2

54.0

48.4

( (

50.0

10.8

12.4

85.9

• •

81.6

69.0

84.4

89.5

90.2

88.5

92.0

97.9

94.1

100.0

48.7

78.5

9.6

• •

5.2

• •

IV. Diagnosis. — At the onset of the disease it may be mistaken for
rheumatism, hemicrania^ sciatica^ ^tric catarrh, hypochondria, and
hysteria. We must take into consideration the condition of the patel-
lar reflex, the reflex rigidity of the pupil, temporary ocular paralyses,
myosis, irregularity of the pupils, sensory disturbances, paralysis of the
bladder and rectum. The earliest symptoms, and one of the most im-
portant, is the absence of the patellar tendon reflex. This is occasion-
ally absent in healthy indiyiduals. It may be absent in indiyiduals who
belong to neuropathic families, in old age, and, according to Schreiber,
in chronic alcoholism.

With regard to the diagnostic significance of ataxia, it must be re-
membered that it may occur in diseases of the cerebellum (cerebellar
ataxia), and that it also appears occasionally after acute infectious dis-
eases (acute ataxia^. In the former eyent other cerebellar symptoms
will be present, sucn as constant yomiting, occipital pain, yertigo, etc.

D6j6rine has recently claimed that degenerative changes in the peripheral
nerves alone may produce the symptomatology of tabes dorsalis. He applies to
the disease the term neurotabes p^riph^rique.

V. Pbognosis. — The prognosis is always unfavorable. The hope of
improvement, rarely of complete recovery, can only be entertained if
the disease is the result of syphilis.

VI. Treatment. — If there is a suspicion of syphilis, we should order
mercurial inunctions, and give potassium iodide internally. The symp-
toms may grow worse for a few weeks after the inunctions are begun,
but their continued application sometimes produces remarkable results.

If the patient has not had syphilis, nothing remains except to treat
annoying symptoms. In general, the treatment employed in myelitis
may also be adopted in this disease. Great care should be exercised,
however, in the administration of ergotin, since Tuczek has shown that
chronic ergot poisoning may give rise to tabes. Moreover, sudden par-
alysis has been known to develop in these patients after the use of er-
gotin.

A certain amount of good may be derived from the use of electricity.
The galvanic current is cniefly employed; stabile or labile spinal current.

112 DISEASES OF THE SPINAL CORD.

ascending or descending; or a spinal cord-sympathetic current. If spi-
nal pressure points are present, they may be treated with the anoae.
Rumpf has recently recommended the faradic brush.

If the galvanic current is employed, it should not be verr strong, the sittingB
«h juld not last more than ten to fifteen minutes, nor be held oftener than once a
day. The electrodes should always be large in g^alvanization of the spinal cord.

In order to employ the spinal cord-sympathetic current, the cathode is placed
immediately below and behmd the angle of the lower jaw, upon the upper cervi-
cal ganglion of the sympathetic, while the anode is slowly paa^d, at snort inter-
vals, along the spine, at first on one side, then on the other.

In using the faradic brush, Rumpf employed a strong current ; the brush
<cathode) was applied a number of times to the trunk, back, and limbs until the
skin was thoroughly reddened. Duration of the sitting ten minutes, daily or
•every other day.

The administration of morphine and narcotics in general plays an
important part in the treatment of individual symptoms.

2. Spastic Spinal Paralysis,

(Lateral Sclerosis of the Cord. Tabes dorsalis spasmodica.)

I. Etiology. — In the majority of cases this disease is a complication
of various other affections of the spinal cord.

The primary form of the disease is more frequent in men than in
women, and particularly from the ages of thirty to fifty years. Cold,
injury, mental and bodily exhaustion, etc., are mentioned as causes.
Congenital predisposition and a neuropathic taint seem to play an impor-
tant part in etiology. The disease is not infrequent in childhood.
The marriage of relatives and congenital syphilis seem to be causal
factors.

The etiology of secondary or symptomatic spastic spinal paralysis is
the same as that of the primary disease (various forms of myelitis, syph-
ilitic spinal paralysis, spinal paralysis after acute diseases, hydromyelus,
internal hydrocephalus, lead poisoning, multiple sclerosis). Spastic
symptoms have even been observed in rare cases of locomotor ataxia.

II. Anatomical Changes. — From a theoretical standpoint, Erb at-
tributed primary spastic spinal paralysis to disease of the lateral col-
umns of tne cord. The autopsies of v. Stoffella, Morgan, Dreschfeld, and
Bramwell seem to confirm tnis view.

V. Stoffella's case presented grav degeneration of the lateral columns, most
marked in the lumbar and lower dorsal region, slightly marked in the cervical
cord. The disease affected the posterior part of the lateral columns, extended
internally to the posterior horns, externally to the pia mater. No microscopical
examination was made.

The appearances in BramwelPs case are shown in Fig. 53 ; it is evident that
the degeneration is confined to the pyramid tracts.

Westphal questions that the symptom-complex of spastic spinal puv
alysis is always the result of an affection of the lateral columns.

III. SYMPT03IS. — In uncomplicated cases the symptoms consist of
paresis, later of paralysis of the muscles, with rigidity and contracture,
exaggeration of tlie tendon reflexes, and spastic gait. Sensation and the
functions of the bladder and rectum are unaffected.

The symptoms, as a rule, begin in the lower limbs, and gradually ex-

DISEASES OF Tirii; SPtNAX OOBD.

tend to the trunk and upper limbs. They rarely travel in the opposite
direction. Still more rarely they are confined to one limb, or to the up-
per and lower limb of one eide.

Tho patients first complain of a feeling of weakness in walking;
this is soon followed by stiSness of the muscles during active and pas-
sive motion. Some patients complain of twitchinga in the muscles.
Gradnally, muscular contractures develop. These afCect the. extenfiora
and adductors of the thighg, the plantar flexors of the feet, the latter
giving riso to pes varo-equinus. In walking, the limbs are often held as
stiflly as two sticks. The patients are hardly, or not at all, able to lift
the feet from tho ground in walking, and therefore move the pelvis to
and fro; the trnnkis often bent over forward. At the same time the
thighs pass each other with difficulty, on account of the contracture of
the adductors. If the patient, in sitting down, brings the toes in con-
tact with the floor, the leg will undergo trembling movements, and a

nwell, Tbe Ufvai
1. Kaliugei] 10 tin

brt of hopping movement is sometimes noticed when the patient, in
ftlking, touches the floor with the tips of the toes (vide Figs. fi3 and 54).

The electrical irritability of the muscles is either unchanged or
slightly diminished. Tho muscular contractures may become so exces-
sive that the patient is confined to his bed. The flexor muacles may also
undergo contracture, and similar changes may appear in the muscles of
the trunk and upper limbs.

In uncomplicated cases, the cutaneous sensibility is unchanged.
Some patients suffer from jJariesthesifB or are very sensitive to cold.
There are no vaso-motor and trophic disturbances.

The cutaneous reflexes are unchanged or increased, but occasionally
diminished. The tendon reflexes are always increased. This is best
shown with regard to the patellar reflex. Foot clonus is also present, i.
t,, if the extended limb is raised, and dorsal flexion of the foot is sud*
nly performed by the physician, tho limb undergoes rapidly succeed-

114

DUBABES OF TG[B BFtKAI. COBD.

Dg trembllDg motions; these may be suddenly checked, in Bome cases,
hv plantar flexion of the ^reat toe. Reflex mnscular contrsctiona may
also be produced by tapping other tendons (tendo Achiilis, tendon of

Seronei, biceps of the arm and leg, triceps, supinators, eztensora and
ezors of the forearm, etc.).
The vesical, rectal, and sexual functions are unimpaired.
In the secondary forms of the disease, other symptoms, which de-
pend upon tlie primary affection, may also hp present.

The diaeaae mns an acnte (within a few weeks), subacute, or chronic
course (more than thirty years).

IV. Diagnosis. — The disease can hardly be mistaken for any other
U the cardinal symptoms are taken into consideration.

V. Pboqsosib. — In the secondary form of the disease the prognosis

Mode or staodiiig

depends upon the primair affection; in the primary form it is relatively
favorable, since recovery has been observed in a number of oases.

VI. Tbeathent. — In primary spastic paralysis the best effects are
obtained by the galvanic spinal current, as employed in tabes (vide page
112); in addition, warm baths (30° R.) and potassium iodide.

The treatment of the secordary form is the same as that of the dis-
ease which has given rise to it. Southam claims to have cured a case by
nerve stretching.

, Acuie Spinal Atrophic Infantile Paralysig.
Infantile Poliomyelitis.

Acute Anterior

I. Etiolooy. — This disease occurs chiefly in childhood, most fre-
queutly from the age of six months to four years. It is rare in mm-

DI8EASK8 OF THE SPINAL OOBD.

113

Fio. 5S.

lings before the period of dentition, though Duchenne, Jr., obserred two
cases in infants of twelve days and one month respectively. The disease
is also rare after the age of seven years.

Boys are affected more frequently than girls. As a rule, no direct
causes are demonstrable. It develops particularly during the summer ;
I have also seen several cases develop at the same time m adjacent lo-
calities. In fact the disease looks m many respects like an infectious
disease.

Whether heredity exerts an influence in
this malady is not known with certainty.
Several children in a family are sometimes
affected; occasionally, other children in the
family have died in eclampsia. It may also
occur in families in which insanity or other
nervous diseases have been observed in pre-
vious generations.

The etiological influence of dentition,
cold, injury, etc., has been grossly overesti-
mated. The disease develops not infre-
quently during or after infectious diseases,
viz., pneumonia, diphtheria, scarlatina,
acute gastro-enteritis, etc.

The attack often occurs during the night
without any demonstrable cause. The chil-
dren go to bed in perfect health and are
paralyzed during sleep. It is not true thac
rachitic and scrofulous children are predis-
posed to the disease.

II. Anatomical Changes. — This dis-
ease is an acute inflammation of the ^ray
matter of the spinal cord, which is locahzed
mainly or exclusively in the anterior horns,
and there gives rise to disappearance of the
large motor and trophic ganglion cells.

Leyden has recently called attention to the
fact that diseases which are clinically exactly
like atrophic infantile paralysis mav be the re-
sult of other lesions, particularly of inflamma-
tory processes, which are situated in the ;Qenin-
ges and the white matter of the cord, and extend,
secondarily, to the gray matter and its large gang-
lion cells. In the following remarks we refer only
to the typical form of the disease.

Distribution of the foci of diaease
in the gnu matter in acute spi-
nal, atrophic infantile paralygis.
After Roth.

a, Transverse section through the
conus meduUaris, 18 mm. above
the flium terminale; 6, trans-
verse section through the lumbar
enlargement, 10 mm. higher; c,
transverse section through the
middle of the lumbar enlarge-
ment, 7 mm. higher; d, trans-
verse section through upper part
of lumbar enlargement, 6 nun.
higher; «, lumbar cord near the
dorsal renon, 7 mm. above d.
Enlarged 8 times.

7he majority of anatomical observations
were made m patients who had had the dis-
ease for many years. In one case the disease had lasted only two
months.

In relativelv recent cases the anterior horns of the cord contain one
inflammatory focus, but more frequently there are several myelitic foci,
generally in the lumbar or cervical enlargements. The^ may be uni-
bteral or bilateral, microscopic in size or three to four cm. in dimensions.
The foci generally have a brownish-red or grayish-red color and dimin*
Uhed consistence.

116

DISEASES OF THE SPDtAL OORD.

Microeoopic exsml nation of the foci show« unusual folneaa of the lilnnil iiimhIh.
obanKeB in tneir walls, and increase oC Che neuroglia. The vessels preaent ajien-
rismaJ dilatations In pl&ces; their walls contain an unusnal number of nuclei and
are Chickened. The lymphatic sheaths contain fat gmnoles. granolo-fnttf cells,
white blood-globules, rareljr hsamatoidin. Oranulo-tattj cells are also found, in
greater ur lesser numbers, in the myelitic foot. They were entirely aheent inons
of Lieyden's cases, but were replaced by p^ecutiar epithelioidal cells whiph the
writer regarded as genetically identical with granulo-fatty cells. The oeurt^ia
is increased in amount and in the number of cellular elements. The gBngUon
i%I1b in the anterior horns are partly destroyed, some of them contain Tacnols.
The nerve fibres which enter the anterior horns also undergo degeneration.
Charcot regards the disease as a parenchymatous myelitis, others think the oon-
.nective tissue forms the starting-point (interstitial myelitis). At all events, we

n«niverM MCtloo throuKb

of ganglio

hom iB Atrgphled and

SnUrieil 10 tlnua. .

o some of the groups

In cases which hare lasted for Tears the myelitic foci are sclerosed.
At the same time the corresponding hom diminishes in size, and the
white matter often increases in consistence, and undergoes atrophy fvide
Fig. 57). The ganglion cells of the anterior horns have often disap-
peared in places, or those which remain contain yellow pigment, are
atrophied, or may present amyloid degeneration or sclerotic distention
(Rosenthal).

The poliomyelitic foci are sometimes converted into cystic spaoee,
which are traversed by a network of connective tissue.

Degenerative changes develop not infrequently in the lateral columns.

DISEASES OF THE SPINAL COBD.

IIT

occasionally even in the anterior columns. Clark's columns were af-
fected in some cases.

The posterior nerve roots are unchanged; the anterior roots corre-
sponding to the diseased portion of the cord undergo atrophic changes.
They appear thin and gray, and the microscope shows disappearance of
nerve ubres and increase of the interstitial tissue. Similar changes
are also found in the peripheral nerves.

The |)aralyzed muscles often have a strikingly pale-red color ; at a
later period this sometimes changes to a brownish-red. In the early
stages the microscope shows diminution in the size of the fibres and in-
crease of the nuclei of the sarcoleroma (Leyden found a few hypertrophic
fibres among the atrophic ones); in some fibres there are fissures resem-
bling those of Zenkers typhoid degeneration of the muscles. At a later
period the transverse stnation becomes obscured, and fat granules make
their appearance. The interstitial connective tissue increases in amount

Fig. BT.

^--i^u

Acute Bpinal atrophic infantile paralysis.
Transverse section through the cerrical cord. Rbtht antenor horn atrophic and sclerosed, the
white columns diminished in size on same side. ParalTsis of risrht arm during life. Death 50
years after the attack of paralysis. Enlarged 10 times. After Charcot.

and in the number of nuclei. The adipose tissue sometimes increases to
such an extent that the volume of the muscle seems to have enlarged.
Upon section, such muscles look like a mass of fat, in which are seen a
few pale streaks of relatively normal muscular tissue. In other cases the
muscles are converted into thin, connective-tissue, tendon-like strands.
In one case D6j6rine found complete atrophy of the intermuscular
nerves and nuclear proliferation in the sheath of Schwann.

The panniculus adiposus of the paralyzed limb, as a rule, is unusually
well developed; but the vessels, ligaments, fasciae, and bones underpfo
atrophy. The thickness of the bones, particularly of the compact sub-
stance, is diminished, and they are sometimes as flexible as in osteo-
malacia.

In one case, Sander described slight development of the central con-
volutions of the brain, but the disease was associated with idiocy.

11^ DI8EA6EB OF THE SPINAL COBD.

III. Symptoms. — The symptoms consist of the sudden occnrrence of
completely developed, non-progressive, flaccid paralysis, with rapid
atrophy of the paralyzed muscles, rapid development of degeneration
reaction in the paralyzed muscles and nerves, abolition of the cutaneous
and tendon retlexes, intact sensation, bladder, and rectum, and absence
of trophic changes in the skin.

The paralysis sometimes occurs unnoticed, sometimes it develops with
febrile and cerebral symptoms.

In some caaeB the paralysis is discoTered accidentally. The patients have per-
haps had some illness, and when they attempt tx> leave the bed, they are found to
be unable to walk. Or the child is brought to the physician because it learns to
walk very late, uses the hands awkwanily, etc., and the most superficial ex-
amination then shows severe paralyses and deformities. In many cases it is said
that the children have gone to bed well, and were found to be paralyzed on wak-
ing the next morning. In other cases, epileptiform convidsions occur, either
unexpectedly or after several days of general malaise, anorexia, restlessne^,
etc. The patients lose consciousness, become convulsed, are sometimes bathed
In perspiration, and have a high fever. The spasms may last one or more hours.
in rare oases recur at definite intervals, and are often looked upon as the result of
teething. When the convulsions disappear, the weakness or paralysis of the mus-
cles at once becomes noticeable. The fever mav last several days after the spasms
have ceased. It generally lasts two to three days, rarely more than a week ; it
ranges between 89-40' C.

The paralvsis aflfects the lower limbs much oftener than the upper
ones ; there is often paraplegia of the lower limbs. Occasionally the
arm and leg on the same side are paralyzed, or the arm on one side, the leg
on the other; in rare cases both upper limbs are paralyzed. The muscles
of the trunk, back, scapula?, more rarely the neck, may also be involved.
In very exceptional cases the facial muscles are attacked.

In many cases the disease at first attacks all the muscles of a limb, but
in the next few days or weeks tlie paralysis disappears in most of the
muscles, but persists in others. In very rare instances the paralysis
disappears entirely (temporary paralysis).

Careful observation shows that the muscles are very often affected in certain
definite groups. This indicates that certain parts of the cord are apt to be affected,
and that, on the other hand, spinal centres for definite groups of muscles are
situated in close proximity in such localities. E. Remak distinguishes two types
of the disease in the upper limbs : a, the arm type, involving the deltoid, biceps,
brachialis internus, and the supinators; 6, the forearm type, affecting chiefly the
extensors, and leaving the supinators intact. The centres for the extensors and
flexors of the forearm jirobably are relatively remote from one another, the former
in the middle of the cervical enlargement (fourth and fifth cervical nerve roots),
the latter lower (eighth cervical and first dorsal nerves). In paralysis of the dis-
tribution of the crural nerve, the sartorius generally escapes, while in paralysis
of the quadriceps femoris the tibialis anticus is not infrequently also affected : the
latter muscle generally escapes in spinal paralysis of the peroneal nerve. These
phenomena also indicate a peculiar arrangement of the muscle centres in the cord.
According to Elahler and Pick, the spinal centre of the calf muscles is situated
near the fourth and fifth dorsal roots.

The electrical reactions of the paralyzed muscles and nerves present
very important changes, viz., those of degeneration reaction (vide
page 8).

The electrical changes appear within a few days after the development of the

DISEASES OF THE SPINAL COBD. 119

The paralyzed muscles are often tender on pressure. • Cutaneous
hypersBstnesia is sometimes obsenred at the onset of the disease.

The paralyzed muscles rapidly undergo very marked atrophy. This
can sometimes be followed distinctly from week to week. The disappear-
ance of the muscles is sometimes marked by an abundant deposit of fat.
Fibrillary twitchings in the atrophic muscles have often been described.

The panniculus adiposus generally becomes unusually abundant, so
that it may be difficult to feel the thin bellies of the muscles. The skin
is generally very cool, bluish-red and marbled in appearance, sometimes
cedematous and fissured, or covered with cold perspiration. A tendency
to ulceration and the development of frost-bites is mentioned by some
writers.

The difference of temperature between the healthy and paralyzed limbs may
exceed 15° C. According to Tarti^re, the paralyzed limo, during the initial
febrile period, is 1-2*" C. warmer than the correeponding healthy linlb; later the
limb gradaally grows cooler.

If the paralysis is extensive, the cutaneous and tendon reflexes are
entirely abolished within the domain of the paralysis.

The bladder and rectum are unaffected; at the most, there is incon-
tinence at the beginning of the disease, rarely retention of urine and
constipation.

The atrophic changes extend to the bones, fasciae, tendons, etc. The
pulse of the paralyzed limbs has been known to become smaller. If the
disease has begun in early childhood, the paralyzed parts often remain
as mere rudiments. The difference in length of the corresponding
bones on the healthy and paralyzed sides may exceed twenty centimetres,
but, as a rule, it is mucn less. Seeligmueller has observed, in a few
<;ases, unusual length of the bones in the paralyzod limbs.

The disease terminates with the development of deformities. Several
factors concur in their production. In some cases they are the result of
contracture of the non-paralyzed muscles. In other cases, however, the
paralyzed muscles themselves undergo contracture, and the action of
gravity upon the limbs then aids in producing deformity.

In the foot we generally find pesequinus or varo-equinus, rarely pes valgo^ui-
nus or calcaneus. At the knee we not infrequently find genu recurvatum, t. e.,
the leg can be extended to a much larger angle than normally. (Contracture at
the hip-joint is a rarer seauel. Scoliosis, lordosis, rarely kyphosis, may result
from partial paralysis of the muscles of the back. Contracture of the pectoral
and latissimus dorsi sometimes impairs the mobility of the shoulder- joint. Or,
on account of paralysisjof the deltoid, the shoulder-joint becomes loose, inasmuch
as the weight of the arm draws it downwards ; the capsule of the joint is relaxed
and a deep furrow is often visible between the spine of the scapula and the head
of the humerus. Ck>ntracture at the elbow- joint is rare ; it is more frequent in
the hand and fingers.

The onset of atrophic infantile paralysis is almost always acute; in
rare cases it runs a subacute course, and the paralyses do not develop for
several days. Acute exacerbations followed by fresh paralyses are some-
times observed. Life is rarely, if ever, endangered.

IV. Diagnosis. — The differential diagnosis must take into consid-
eration :

a. Progressive muscular atrophy; this hardly ever occurs in childhood,
except in the hereditary form; it develops very slowly.

12() DI8EA6S8 OF THE SPDiAL CORD.

h, F'ftcm do-hypertrophy of the muscles; this develops very gradually,
tkU(\ miiHCiiIar atrophy remains absent.

n. SimHtic spinal paralysis; muscalar atrophy and degeneration are
not iiro<iticed, and the tendon reflexes are increased.

a. r»rtiirition paralyses; these are present from birth, labor has
awittlly \m*.n difHcuIt; sensory disturbances are generally noticeable.

e. \\\ m'ut(» (!ontral or transverse myelitis, in hsematomyelia and com-
pr^imiofi fiiY(^litiH, sensory disturbances are generally i^resent; there are
off^tn (JiHtitrbaiices of the bladder and rectum, trophic changes in the
fikin, ifKTouHod cutaneous reflexes, absence of degeneration reaction.

/*. Multiple degenerative neuritis is generally associated with sensory
diwfiirh'UK'OH.

V. Tuooxosis. — The prognosis is not especially favorable. As a
nilo, thorn m no danger to life, but we are unable to relieve the paralysis.

VI. TiiKATMENT. — During the period of the initial fever and spasms,
WM may order a warm bath (28° R.), lasting half an hour, with cold
(lonnlioH, and then an ice-bag to the head.

\^U^v the paralysis makes its appearance, the Chapman ice-bag may
b« iipidind to the supposed site of disease in the cora. Leeches, cups,
nfMl (Inrivativos of all kinds have also been applied. Potassium iodide
MMiy bn given internally to aid absorption of the inflammatory foci;
nrgotin and belladonna have also been given for the same purpose.

Aftor the most acute symptoms have subsided, we may attempt to
nid abHorption by the use of the galvanic current (large electrodes), at
ftrMt tlu^ anode (two to three minutes), then the cathode over the site of
dUiwiHo.

Thn paralyzed parts are treated with the galvanic or faradic current,
iJin luttor only when the muscles respond. The electrodes should be
llioroiighly moistened, and strong currents should be used in order to
piint«l rate the nkin and pauniculus adiposus. In a number of cases we
iiinph)yed. at l.he same tune, the galvanic spinal current and peripheral
fiinulic! Mt.ifnulation of the muscles.

(lyfiuniNtii^H, niasHage, tenotomy, and orthopaedic instruments may be
iiiM ployed to prevent and relievo deformities.

•i. Ariiti\ Sttharttfo, and Chronic Sptnal Atrophic Paralysis of Adults.

Arnfr, »utmcute, and chronic anterior poliomyelitis of adults.

Them^ nu)rl)id pro(M»Hse« art^ in i>art identical with, in part very closely
iillitMJ ((I, ueiitn atropine infantile paralysis.

a, .\rnf(* Hidnal atrophic paralysis of adults corresponds entirely tc
Ihti Hiiniliir diHoiiHo in ohildhood. ' Men are attacked more frequently
ihiiii wninon; it. j^emu'idly ooeurs befon^ the age of thirty years. Among
ihti I'lmmnt luhiuiMul are eohi, oveivxertion, and excesses in Baccho et
V uuere. It. hiw been olworved a numlH^r of times after infectious dis-
« .161 M It) winMtMj, parlieulnrlv after puerjH^ral fever. A certain etiological
htlliii'iiifi iMHiiinotiineH iiltriluited to hennlity, tuberculosis, and syphilis.
riii> ilit^i HMupiiiinrt luv tluwe of a giMienil febrile affection, but con-
vuLiLihti iiitt 111)1 piiuliuMMl. It n\ay N^giu with a violent chill, followed
liv hitih iniupiM'HtMro, head«oht\ lielirium, sometimes vomiting and
ili.iiihitii. iifioii ft»lli»\veil hv a tNphoid condition. Bramwell described
ii lupiiiui s uphatiia in i»iu» ea?<e. The fever gouorally lasts a week, some-

QIBBABE8 OP THB SPINA!. OORD. HI

times more than two weeks. The patients often complain of pain in the
back and limbs.

More or leBS extensive flaccid paralysis makes its appearance in a few
hours, occaaionallv in a single night, more rarely in the course of several
(lays. This mar be confined to a single group of rauscles. or an entire
timb; it sometimes appears as heraipleeia, paraplegia, or crossed paraly-
sis; it rarely attacks tne muscles of the neck, hardly ever those of the
face. In a few cases the respiratory muscles were affected, and the dis-
ease then ended fatally by producing suffocation.

In a few cases the paralysis gradually disappears iu a few weeks or
months (temporary paralysis); in others the paralysis disappears in some
muscles, but persists in others. The paralyzed muscles are often sensi-
tive ou pressure, and rapidly undergo atrophy; degeneration reaction is
also produced. As a matter of course, the growth of the bones is not
interfered with, as in children, but contractures of the muscle and, to a
leas extent, deformities are produced. The skin of the paralyzed parts
is cold, often bluish-red, and does not perspire; it is sometimes oedema-
tons. Sensibility is retained, but pareesthesite and cutaneous hyper-
eethesia are sometimes present at the outset. Reflex irritabilftv is
abolished in totul paralysis of a limb, otherwise it is diminished or
unchanged. The functions of the bladder and rectum remain normal,
though vesical paralysis is occasionally noticed at fhe outset. The sexual
powers are unaffected.

The prognosis ae regards life is generally favorable, although a fatal
termination is possible. The remarks made concerning the anatomical
changes, diagnosis, and treatment of this disease in children also hold
good in adults.

b. Subacute and chronic spinal atrophic paratugis of adults occurs at
a more advanced age {thirty to fifty years), nut Erb recently observed a
case in a child of six years. The causes are sometimes the same as those
of the acute form, sometimes no cause can be discovered. Remak showed
that lead poisoning may give rise to this disease.

It generally begins gradually without any severe impairment of the
general condition. Thepatients tire easily in walking, and. finally, well-
marked paralysis develops. As a rale, it begins in the lower limbs, and
then extends along the trunk to the upper limbs; more rarely the para-
lysis progresses in the opposite direction. It may also he confined to a
few groups of muscles. It begins most frequently in the extensors of
the legs; in the upper limbs, likewise, the extcitsors of the forearms are
first affected. The paralysis gradually extends from one group of mus-
cles to another. According as this occurs in the course of weeks or of
months and years, the disease is called subacute or chronic. The mus-
cles of the nock are not inf reouently affected. The disease may even
extend to the bulbar nuclei, bulbar symptoms then develop, and death
occurs from suffocation, etc. The characterof the paralysis (apart from
its progressive quality) is the same as that of acute atrophic paralysis,
i.e., the paralysis is always flaccid. It may entirely disappear in the
course of weeks or months, or it disappears only in part while other mus-
cles undergo nipid atrophy. This may be followed by contracture and a
hard tendinous condition of the muscles. The electrical irritability is
the same as in infantile pai'alyeis; in the beginning, the mechanical irri-
tability of the muscles may ho increased.

Improvement generally follows an opposite course to the paralysis,
i. e., first in the arm, then in the legs; the muscles supplied by the pero-

.>'. DISEASES OF THE SPINAL CORD.

• •

i^<*i iiti»t» v^fton remain paralyzed. Fibrillary contractions are often
o-i I » • •' ■ ■■^' piiriilyzed muscles.

viii»- -a'-tonts ooni plain of panesthesiaB, but the cutaneous sensibility
:, .».iA-. ^i^ unobanged. Disturbances of micturition are sometimes
\i,.» . \^^^l .4: tlio beginning of the disease, but they disappear at a later
.^...•xi. Iho joints and sheaths of the tendons are sometimes swollen.
\ M. u..i:uviu*i and tendon reflexes are abolished if a limb is complet<»ly
•»i. 4 > '.^ ti. othorwist^ they are diminished or unchanged. In progressive
.»..! .,\i.'aih iHVurs in one to four years.

V-ii ■»**''* «^r*» agreed that the lesion consists chiefly of destruction of
. 1. ;:iMj;liv»n colls of the anterior horns; atrophy of the cells of Clark's
, .;iri»»»s. iiiul of the anterior portions of the posterior horns, is also

l\w neuroglia may be unchanged or increased; there may also be
.i;x»:i'vnUu>n of the nuclei in the walls of the vessels, and atrophy of the
r.x',^ p,issing out of the anterior horns and of the anterior nerve roots.
: \ v-iuMativo changes have also been observed in the columns of the cord,
vtiNMVi»phoml nerves, and paralyzed muscles.

Tlio diaj^nosis is not always easy, especially in old cases. It is dis-
viMv-uulinl from progressive muscular atrophy by the following features:
k\w pai'tilvj<in precedes the atrophy, it is not fascicular, but affects the
uui^^'to** «•" //m.^.<»e; in progressive muscular atrophy, the reflexes are
lot.nnod, tlie disease is slower, but less unfavorable as regards the main-
^vu'Mu'o of life, recovery does not occur, and degeneration reaction
^s^MMrt 4»nl>' in those parts of the muscles which are affected with special

In amyotrophic lateral sclerosis, muscular rigidity and spasms, and
ouMva***'*! tendon reflexes are noticeable. Multiple degenerative neuritis
H ullondtMl with sensory disturbances.

riio prognosis is favorable as regards life, but less favorable as regards
^vnu'let** rr<!ovory.

'l^hii Iroiitment is the same as that of the acute form.

{

5. Prof/rrssire Spinal Muacular ^i trophy,

imifoff*itphi(t spinnh's prof/ressira. Polj/omf/elifis anterior chronica

disseminata,)

I. Mtfologt. — In spinal progressive muscular atrophy, there is a
.^nu^niMhivc (lisaj)i)earance of voluntary muscles, beginning in the upper
Itiiiii.i, and tirst affecting only ])arts of the muscles (fascicular), and un-
,ii tended with ))aralysis, apart from the loss of jmwer due to the dis-
j^mieiiniiK'e of tlie muscular flbrcs. There are no disturbances of sensa-
Hon, «'»' *>t" t^^^ functions of the bladder and rectum. All these changes
jH,i (lie H'sults of a primary chronic affection of the anterior columns of
\\\\\ enrd, particularly of tlie lar«re ganglion cells.

Art a III le, t lie disease oc(!urH between the ages of 30 and 50 years. Cases
\\\\\\^ iilf-o JKMMi reported in which the disease began in childhood— espe-
\udlv wlicn it is propagatA»d in families from one generation to another —
\\\\\ ihe belief is now growing that these cases are really due to a primar}*
^iJiielinn nf the nnisides. We shall, therefore, discuss them under the
\\\\\v\ «»f jiiv^'niU' muscular atrophy, or dystrophia musculorum progressiva.

lliTiMlitv is often mention<'d as a cause of ))rogressive muscular atro-
nh.Vi '"'*' ^^''"^ applies more pairticularly to the juvenile form.

DISEASES OF THE SPmAL OOBD. 125

The disease is often connected with overstrain of certsiu moscles
and groups of muscles.

!n other cases it is attribBted to injury, cold, onanism, and sexual

It has been claimed that the malady occurs after infectious diseases (measles,
scarlatina, small-pox, cholera, acute articular rheumatism, typhoid and puerperal
fever, syphiliB; according to Jackson and Clark, even after vaccination), V"' " *■--

ProgressiTe mnscuUr atrophy is more frequent in men than in women,
probab^becanse the former are more exposed to the etiolo^oal influences.

II. Sthftous. — Atrophy and, in connection with it, weakness of
the muscles develop very gradoally. As a rule, this begins in the inter-
OBsei and the muscles of the thenar and hypothenar emineQcea, bo that

R[Rht hftnd. Lrrt lUDd.

Donum of tutad with depranBd tuMmawoDi ipaces tn progreeilTe miueubtr Mropb)'. In > voman

the patients flrst complain of stiffness in the fingers and inability to per-
form delicate manipulations. These disturbances are increased by cold
and diminished by warmth.

According to Eulenburg, the flret interosseus is one of the very first
muscles affected. Atrophy of the interoseel is shown by the deep grooves
in the interosseous spaces (vide Figs. 58 and 59). The ball of the little
finger and thumb becomes flattened, and the subjacent bones can be
felt more distinctly (vide Figs. 60 and 61). In addition, the fingers
assume unusual positions. The muBcles first attacked in the ball of the
thumb are the adductor and opponens polUcis. On account of the pre-
dominance of the extensors and abductors of the thumb, the latter is
brought into a position of abduction and dorsal fiexion (ape-hand).
Atrophy of the interossei gives rise to the development of the so-called
claw-hand, as the result of the predominance of the Inmbricales; the
first phalanges are hyper-extended, the second and third phalanges
are strongly flexed. The claw-hand also develops in other Sections, lor

DISRUE8 OF TSB BPIKAI. OOBD.

example, in traumatic ulnar paralysia, but in this disease the midd]« ,|
and nng fingers are most markedly aflected (vide Figs, 63 and 63),

If tho liinibricales undergo atrophy the palm of the hand is flattened, I
but ihe estensor digitorum continues to extend the first phalanges. The 1

Rlsbtlund.
Palm ot hnncl witb BCroplir of Cbeiuir ».o<l hrpnthanu- nt

. rbe ume puidnt.

disease sometimea jumps from tho muBclea of the hand to the deltoid. In

this muscle it is especially evident thac the atrophy occurs in handler,
not en maaae. At first the posterior and middle thirds are chiefly

le result of Injury to thp ulnu- nerrs.

afTectcd. When the entire muscle has undergone atrophy, the shonlder
looks tittt and angular, and tho edges of the bones appear very distinctlT.
As a matter of conrFJ, the movements of the arm arc interfered with.anclt

DIBEABE3 OF TBE SPINAL CDBD.

125

if ttiG scapular muscles are also attacked, the arm hauga aloagaide tlie
trunk almost like an inert mass.

If the ligaments of the shoulder- joint are very flaccid, subluxation of
the head of the hnmorus may result.

In othur cases the discuae spreads from the finger masclea to those of
the forearm, especially the extensors. The supinators usually escape
unless the flexors become involved. The atrophy mav be so extensive
that the forearm consiHtB of hardly anything beyond skEn and bones, and
the interosseous space forms a deep groove (vide Figs. 64 and 65).

Among the muscles of the arm the triceps is the lost to be affected,
£0 that the arm is almoEit always extended.

I The right hand ia generally the first attacked, more rarely the left
I luwd or both at the same time. In the majoritvof caees, after themus-

clea of oue aide of the body have been attac"ked, the corresponding

ones on the other side are involved before the morbid process extends to

higher or lower groups of muscles.

If the disease is regarded as spinal in its origin, it must be assumed

that the process extends from one-half of the cord to the other before it

spreads in a longitudinal direction.

As a rule, the muscles of the scapula and trnnk are not attacked until
I tiio arms have undergone considerable emaciation. According to Du-

126

DIBBASE8 OP TBE BPDTAJ. OOBC

chenne, they are attacked in the folloving order: lower part of the
trapeziua, pectorals, latisaimus dorei, rhomDoid, scapalaris, ezteasors
and flesora of the head, deep muBciea of the back, abdomitml muscles,
finally the neck muscles and rotators of the head. Here, also, the dis-
ease often begins on one side, or is more marked on one side than on
the other. If the moBcles of the loins are affected, the spine is aniiBn-
ally curved anteriorly, bo that, in the vertical position, a vertical line
dropped from the shoulder falls behind the sacrnm (vide Pig. 66). If
the aodominal muscles are atrophied, a slight bronchitis may prove dan-
gerous, inasmuch as the energy ol coughing is interfered with, the bron-

chial secretion nay accumulate, and death oucur from suffocation. Fee-
bleness of the abdominal muscles also causes marked projection of the
spine anteriorly, liut a vertical line dropped from the shoulder passes
through the sacrum (vide Fig. 67). The diaphragm sometimes takes
part iu the atrophic process.

The lower limhs are usually attacked last. The flexors of the legs are
affected earliest and most markedly.

Fibrillary (more properly fasicular) muscular twitchings are an al-
most constant symptom of progressive muscular atrophy. They con-
sist of repeated brief contractions which always affect only individnal

DISEASES OF THE SPINAL OOBD. 127

Sarts of a muscle, now here, now there. They are especially active oa
isrobing, blowing on, tapping or faradizing the muscles. They some-
times appear in muscles which do not present any visible emaciation,
but may be entirely concealed hj a fat integument. In some cases
they are so vigorous as to cause involuntary twitchings of the fingers,
arm, or leg.

The electrical irritability of the paralyzed muscles corresponds, in

f general, to the degree of atrophy. The more the muscular substance is
ost, the more the electrical irritability of that muscle diminishes until
it is entirely abolished. Careful examination, however, shows that par-
tial, then complete degeneration reaction is manifested in parts of the
muscle.

If a small. anode is placed in the mastoid fossa or adjacent part of the neck,
and a large electrode between the scapulsa, more or less vigorous movements will
be produced in the arm on the aide opposite to the anode. This phenomenon, to
which the term diplegic contractions nas been appUed, is observed at times in
this disease, but is by no means characteristic.

If the muscles of a limb are extensively affected, the integument is
often bluish-red, marbled, and feels cold; its temperature has been found
markedly diminished (5° C). Some writers have observed an increase
of temperature (0.5° 0.) at the beginning of the disease. The skin pre-
sents a tendency to trophic changes: thickening, formation of scales,
diminished growth of hair, tendency to ulcerations, herpetic and pem-
phigoid eruptions, thickening of the nails, etc.

An abnormally abundant production of sweat has also been observed,
particularly in rapidly progressing or far advanced cases. Swelling of
the joints and phalanges is sometimes described.

Sensory cutaneous disturbances are almost always absent; at the most
the patients complain of a feeling of coldness in the limbs. The cuta-
neous and tendon reflexes disappear more and more with the extension
of the disease.

The functions of the bladder and rectum are unaffected.

Oculo-papillary changes were often noticed. The pupils were unusu-
alljr narrow on one or both sides, reacted slowly to lignt, and lost the
ability to dilate.

Laodouzy mentions changes in the ocular muscles in one case. Impaired
sight and flattening of the cornea were also mentioned in one case.

The general condition is very little affected; slight febrile movement
occurs occasionally, and is explained by Friedreich as absorption fever,
the result of the absorption of chemical products of the muscular de-
generation.

The disease advances very slowly and, as a rule, lasts many years.
The patient finally loses the use of his hands and arms, is unable to
move his legs, and becomes utterly helpless. The mental powers gen-^
erallv remain intact.

The condition becomes even more distressing when it is complicated
with bulbar symptoms; atrophy and paralysis of the muscles of the face,
tongue, pharynx, and larynx. In some cases the latter symptoms first
develop, and are followed by the symptoms of progressive muscular
atrophy.

Death occurs from intercurrent diseases or increasing marasmus, or

128

DISEASES OF TBS SPINAL OOBD.

bnlbar Bjmptoms give rise to difficulty in deglutition, ittaoitioD, " tm-
eign-hody " pneumonia, etc.

III. AxATOMiCAL CirANOEa, — According to Chsroot, pn^resnTe
muscular atrophy is dependent on a primary chronic destruction o( the
large ganglion cells in the anterior horns of the spinal cord. The
French writers attribute these changes to inflammatory lesioos of the
ganglion cells, which give rise to pigment degeneration and atrophy, or
to sclerotic atrophy and complete disappearance of the cells. Any
chnnn'^K which muv bo present in t!ie interstitial tissue (nuclear prolifer-
ation, dilatation, thickening, and fatty degeneration of the blood-reseels)
are Hiiid to be merely secoiidaiy. Others maintain that the process begins
in the iiiterstitia) tissue, or that both modes of origin are possible. If
the lesion is well marked, the corresponding anterior horn, and even
the ontirt! half of the cord are diminished in size (ride Fig. 66).
Degenerj'.tifin has also been noticed in the white columns; particular^
the lateral columns.

lallibtha e

_ '6 diAAppeared with tha fl2c«pU011 of ■ f«w o«lLi
Mrlor Bn«Le. Enlartced 10 Umea, AtMr Ch4roo[.

The anterior nerre roots are often thin, gray, and in a condition of
fatty degeneration and atrophy. Degenerative changes have also been
observed in the peripheral nerves.

Friedreich's examinations concerning the muscular changes hare fur-
nished the following results: They begin in the intermuscular connective
tissue (perimysium internum), with increase in amount and naclear
proliferation; this is followed directly by changes in the muscular sub-
stance; the nuclei of the saicolemma proliferate; there ia gradual
disappearance of the muscular substance proper; some fibres undergo
waxy degeneration, others cloudy swelling; some fibres are split longitu-
dinally, others in transverse sections; finidly, some of the fibres appear
split up into their elementary constituents. At the same time the mus-
cle substance gradually disappears, so that, in numerous places, the Bar-
oolemma contains nothing but nuclei. These obanges ortea occur only

DISEASES OF THE RPINAL CORD. 129

in certain parts of the muscle. The atrophic muscle appears pale, oc-
casionally orownish-red (unusual amount of pigment in the fibres).
Finally, it may be converted into a sort of tendinous structure (fibrous
defeneration). Fatty degeneration of the muscular fibres and accumu-
lation of fat in the interstitial connective tissue are rare, but are some-
times so extensive as to cause increased size of the muscle.

IV. Diagnosis. — The diagnosis is usually easy if we bear in mind
the beginning of the disease in the ball of the thumb and little finger,
and in the interossei, the absence of sensory disturbances, the develop-
ment of fascicular atrophy, and then of weakness of the muscles, the
fibrillary contractions, and the intact condition of the bladder and rec-
tum.

The disease may be mistaken for:

a. Juvenile progressive muscular atrophy ; this is often hereditary
and generally begins in childhood; it often oegins in the lower limbs.
Duchenne sometimes noticed a pecular impairment of motion of the
lower lip in the beginning of the disease. Moreover, the juvenile atro-
phy is much slower than the spinal form, fibrillary contractions are
usually absent, the atrophic muscles often increase in size from the inter-
stitial proliferation of fat, and the affected muscles do not present the
degeneration reaction.

i. Multiple* degenerative neuritis, when very extensive and slow in
its course, may also resemble progressive muscular atrophy. The differ-
ential points are: the occurrence of paralysis prior to the atrophy, the
occurrence of pain, paraesthesiaB and objective sensory disturbances of
the integument; the affected muscles and nerves are often tender on
pre^ure.

c. Acute, subacute, and chronic poliomyelitis are also characterized
by paralysis, muscula* atrophy, degeneration reaction, absence of sen-
sory disturbances ; but the process does not extend in .such a typical
manner aa in spinal progressive muscular atrophy, and, in addition, the
paralysis develops first, the atrophy later.

^ d. Muscular atrophy is sometimes secondary to other diseases of the
spinal cord, and occurs whenever myelitis, tabes, multiple sclerosis,
tumors, etc., affect the ganglion cells in the anterior columns of the
cord. The differential diagnosis depends upon the fact that the muscu-
lar atrophy is preceded by other signs of spinal disease.

V. rBOONOSis.— The prognosis is not favorable, since we are hanlly
able to restore the atrophied muscles to the normal condition and to pre-
vent the spread of the disease. The more extensive ^nd rapid the
atrophy the more gloomy the prognosis as regards danger to life. Bul-
bar symptoms generally accelerate the fatal termination. Under other
circumstances life may be prolonged for many years.

VI. Treatment. — Overstrain of muscles must be avoided and, if
the si^s of muscular atrophy make their appearance, the injurious oc-
cupation must bo abandoned forthwith.

The remedies recommended in myelitis (vide page 88) have been
employed in this disease, but very little can be expected from them.
The cautious employment of massage and rational gymnastics may be
recommended. Electricity remains our chief remedy. The most suit-
able mode of application is the galvanic spinal current (large elec-
trodes, the anoae for the first three to five minutes, then the cathode
over the site of disease, or the ascending and descending spinal cur-
rent). This may be followed by peripheral galvanization of the iudi-
9

180

DISEASES OF THE SPINAL CORD.

Fio. fifl.

Tidnal mnscles, the cathode labile to the mnscles, the anode on an indif-
ferent spot, or over the lumbar or cervical enlar^ment, according as
the application is made to the lower or upper limb. Galvanization of
the cervical sympathetic has also been recommended. The muscles may
be treated peripherally with a not too strong faradic current. Treatment
requires patience on the part of the physician as well as the patient.

COMBINED SYSTEM DISEASES OF THE SPINAL CORD. .

1. Hereditary Ataxia.
{Friedreich* s Disease.)

This disease is pre-eminently hereditary. For example, Friedreich

observed nine cases in three families;
Immermann and Ruetimeyer described
eleven cases in two families. Unlike
ordinary tabes, the female sex is more
often affected.

The first symptoms begin at the age
of 4 to 7 years, or at the period of pu-
berty. Ataxia is a prominent symptom
from the beginning, while sensory dis-
turbances remain absent 'or do not de-
velop until very late ; lancinating pains
are rare. The ataxia extends very rapid-
ly to the upper limbs, or it affects the
upper and lower limbs at the Fame time.
Ataxia of the ocular muscles (ataxic
nystagmus) and disturbances of articu-
lation (ataxia of the muscles of speech)
may also occur. The Brach-Bomberg
symptom was obeorved in a number of
cases. The ocular symptoms (ocular
paralyses, reflex rigidity of the pupils,
amaurosis), so common in ordinary
ataxia, are wanting. The vaso-motor
and secretory sjrmptoms observed are
)olyuria, salivation, and hyperidrosis.
To disturbance of the bladder, no b«i-
sores ; the patellar reflex absent. At a
later period, the muscles become para-
lyzed and contractured.

In a fatal case, degeneration was
found, not alone in the posterior col-
umns (most markedly in the cervical
cord), but also in the lateral columns
and, in the cervical portion, in the
anterior columns (vide Fig. 69).

The treatment is the same as that of
tabes dorsalis.

AnAtomlcal changes in the cord in Fried-
reich's heredltjury ataxia. The diseased
Sarts are shaded, a-c, cerricalcord : d,
orsal cord ; e-g^ lumhar cord. After
Friedreich.

2. Secondary Degeneration of the
Columns of the Spinal Cord.

We distinguish ascending, descends
ing, and combined secondary degeneration in the spinal cord.

a. Descending secondary degmeralion oftka columns of the gpinal cord
follows diaeasee of the brain, and occupioa the ilomatn of the pyramid
tracts. Hence the changes are fonnd in the posterior part of the lateral
colmniiB {the so-called lateral column-pyramid tract), and in the inner-
most parti of the anterior columns, next to the anterior longitudi-
nal fissure (vide Fig, 70, \pvs and 3ps&). Both fields contain nerve
tracts which convey the stimulus of the will from the brain to the peri-
phery.

Ab the cerebral lesion generally affects only one side of the brain, the
Regeneration in the cord is also fonnd only in one pyramid tract. But
unce the lateral column-pjrramid tract contains fibres which decussate in

ruuitli lumbar nerre.

the pyramids, while the pyramid-anterior column tract does not docuaaate,
the secondary degeneration in the former will be found on the side op-
posite to the cerebral lesion, in the latter on the same side.

It must not be forgotten that, according to Flecbsig's researches,
there are remarkably great individual differences in the proportion be-
tween the decussated and non-decussated fibres of the pyramid tracts.
The decussation is sometimes complete, go that no degeneration can occur
in the anterior columns. On the other hand, the degeneration in the
anterior column may be unuaually marked, because very slight decussa-

13« riM).nS.» .If -O iilSAL COBU.

tion h«*- ">*>''"■ '*'*'* " ■'" "■'^'"■■'^ E^;ws reports four cases in which
d.>efiii-iii"i ■> •■-■'! M'-'ii ''iiiiiiJi-ij'Tjiiiic :raou followed a unilateral

\\. , I- •.■T. ■■JIM, i-.i nl iiufitses of th-r brain are folloveil by
tw.;.'--'-- .ii;-: -:-'■■ ■■ ' ■'■■■ ''-■r'i. Thisuniyooc'^iri when the pyramid
— , ■- ■ ■'■-'■ ■ '^'■■■j-'.tii 11 "IV [lart ii( tlwir ourse. If these tracts

^- I. — '■■'11 iHT U-cu!j«tcioii, they will be found to pasa

..-..- : . iLailf ;uiii iiiftrior par:? of the peduQciilus

_,, > .' ■ ■ .: ■ ■•'sni'ur .livisioii »f the ir.;*mal eapsnle. and

. ■,.■■• •■1,-ii- ■( till' cerebral cortex 'asreriorand posterior

,,[ „ ■ ■ ■-; ''!<ta*'s 'if -ither parts of the ojrt*x or brain will

i_ ,. .■ 1 . . .n'i'ii:ir» ii^\^■u^;^atil■ln of the spinal oirtl.

.... '*.- s .uTi'tLHl in the cerebrum, :he secondary de-
^ . , . . «t.: 1 :iiv Jfiirinole, i«Mis. and the -xirresponding side

*■ . ,^ ...... .1 ;iu' aiiKiiilla (vidt' Fig. ;ii. The middle (more

,. ...i. . . ' s' . ■• :i :'■; -.ov.-.--''.^ arrears Cray, trans-
■ '■ ' , ■, ,, .... ^^■ .* l .v.-.vf .viV.; .i:r."-i{:: i vide Fie. 72, (7).

' ' . , . .,' , ■•.■•. .;:»:■ "^^irsre-i pyramid tract is

'" , ,..,.., ..- ^v ■• . ■,■■■■■, T>.;r, :: a'-wars gray and

. s. V. « ■ ■ : ■•■:*-■: s-i^ -P.si'.i.h. The

.. . ■ v.. •■>:,■.#.• :r.i: :=e o'JTary body 18

1 ' . . i .;■-* -. ::.; sv:"il .vrJ can be only

. , ,. , 1 ■■.-■. .■.irss ""■.:7>.^soop:ciiIrtamiua-

, > ,..■.■ ■■. ■ ;"•-■-■.:• sciiorbichromatcs,

. ., , I ,; ■ -■;".■■*- .■■:l-."r. b-E the yellow
>'■ . . ..- . ■-'- ■■■ :a'.^ The degenerated

, „ ,,. . i -. .'-- ■"■: .vl.T6.on account of
1 " . „ , ■ ; .■.,i-!V. .-f Tiirre-fibres.

.'. , , , . . , ■. - V- V. :--. -. :^. .> to A. The

' ' .... .-. :~s.-: ,l:=i:-ishes more and

'' > \.ij.ij . ~.' ■--■■.xr iii: of the lumbar

DISEASES OF 1

core] . The degeneration in the lateral column {on the opposite aide) is moat
extensive in the cervical cord, where it has a triangular or wedge-shape ;
in the dorsal cord it is less extensive und round. In the lumbar cord it
again becomes triangular, and gradually approaches the surface of the
cord until it is immediately beneath the pia mater. It terminates at the
level of the third and fourth sacral nerves (Fig, 70).

The flret changes in desccndinit degeneratian appear in the nerve fibres thera-
Ifrlve*. Knhler and Pickdetected them oa the eleventh dajr a(t«r on injury to the
brain, nnd perhaps they b«gln even earlier. Its rapid extension. And its restriijtioa
todellnite systems of libres. precludes the idea of a )>ropagatea iDflummution, and
juntifles the conclusion that we have to deal with a ilegeneratlve atrophy, the re-
mit of a separation of the nerve flhrea from their trophin centres.

The degetierateil fibres undergo toss of the medullary shealh and, finally, of th^

134 DISEASES OF THE SPINAL OOBD.

axis cylinders ; according to Henle, atrophy of the axis cylinders precedes disap-
pearance of the medullary sheaths. At a later period, the interstitial connective
tissue increases secondarily in amount, granulo-fatty cells and amyloid bodies
appear in it, the walls of the vessels become thickened, and their lymphatic
sneaths contain fat granules and gpranulo-fatty cells.

As a rule, the gray matter is unchanged. In rare cases, the anterior bom on
the side opposite to the cerebral lesion is diminished in size, and its ganglion cells
are atrophied, corresponding to atrophy of the paralyzed muscles during life.

If the changes have last^ a long time, proliferation of the interstitial connec-
tive tissue, and disappearance of the nerve fibres may take place in the periphe-
ral nerves of the limbs which have been paralyzed as the result of the cereoral
lesion, and the corresponding muscles may present diminished size, fat^ degen-
eration or proliferation of the nuclei of the saroolemma, and increase of tne inter-
stitial connective tissue, or proliferation of fat.

The contractures to which hemiplegias become subject, and the exag-
geration of the tendon reflexes, are attributed to the secondary degenera-
tion. The prognosis of this process is
Yio. T3. ^ unfavorable, because restitutio ad inte-

grum is impossible.

The treatment is the same as that of
the primary disease.

0. Ascending secondary degeneration

of the columns of the spinal cord occurs

as the result of disease of the posterior

nerve roots or spinal ganglia. Senger

produced it experimentally in dogs by

section of the posterior nerve roots ; in

man it is observed most distinctly in

^..^^^^ disease of the cauda equina. It is con-

^/CYjv^ y. /'filiN fined to the columns of Goll and to the

^ C/t\j f Vv^vV ^^^^^^^ cerebellar tracts (Fig. 73, a to

Distribution of ascending secondarr de- In the ColumnS of Ooll it may be

IS^^o1!d."8ite"of^o7nrr^,S^^^ ^^^^^ ^« ^^'^ »« *^^ rcstiform bodies of

at e; /, lumbar cord below the git« of the mcduUa, in the Cerebellar tracts it

d2S.Sion"*Na?SS?2S: ^~^^*°«^ extends to the cerebeUum. On account

of the primary affection, this degenera-
tion is usually bilateral. The degeneration of the columns of Goll is
assumed to occur when they are separated from their trophic centres —
the spinal ganglia. Some authors regard the columns of Clark as the
trophic centres of the cerebellar tracts, but whether these tracts contain
centripetal or centrifugal fibres is unknown. Ascending degeneration
gives rise to no clinical symptoms.

c. Combined secondary degeneration of the columns of the spinal cord
occurs when the continuity of the cord is interrupted entirely or in part.
In the former event, for example, in compression of the cord, the columns
of Goll and the cerebellar tracts degenerate above the primary disease
(ascending degeneration), the decussated and non-decussated pyramid
tracts degenerate below the focus of disease. But the cerebellar tracts
are only affected if the primary disease is situated in the dorsal or cervi-
cal region, since their supposed trophic centre, the column of Clark, be-
gins in the middle of the dorsal region. The secondary degeneration
does not begin in the immediate vicinity of the primary disease. The
latter generally presents a diffuse change of the entire section of the
cord, then follows, in an upward direction, degeneration of the entire
posterior columns and, finally, of the columns of Goll alone (Fig. 73, c

DISSi^ES OF THE Sl'KTAL COSD.

and d). As a matter of course, the degenei-ation i^ bilateral, unlesB one-
half of the cord alone is diseased. Secondary degenerations aometimea
follow circumscribed affections of the cord.

3. Amyotrophic Lateral Sclerosis,

I. EnOLOHT. — Charcot applied this term to a disease which is, to a
certain enteut, a combiusitiou of primary degeneration of the pyramid-
lateral tracts and of the large ganglion cells in the anterior horns and
in the nuclei of the medulla, particularly
the hypogloBBus, pneumogaetric, spinel
accessory, and facial.

Cold and exposure to wet are generally
mentioned us the causes of the disease.
It is most frequent from the ages of
twenty-five to fifty years ; women are
affected more often than men. Weir
Mitchell reported a case which was appar-
ently due to working in lead. Seelig-
mueller described four cases in brpthers
and sisters whose parents were cousins.
In these cases the disease began in iu-
fancy.

II. Anatomical CHANOEa. — Accord-
ing to Charcot, the disease begins in the
latoral columns of the cord (pyramid
tract). It ia most extensiye in trie cer-
vical cord, and gradually diminishes to-
wards the lumbar region (Fig, 7i). lu-
feriorly, the degenerated parts gradually
approach the pia mater ; superiorly, ■'

may be traced to the lower part of' the
pons (as far as the pyramitl tracts are
collected into a bundle), and even into

the foot of the peduncle. The iuternjil
capsule almost always escapes.

In some cases the undecuBsated portion of Q
the {lyratnid tract haa been found to be dis-

' According to Charcot, the disease is a obumeainamjo _

primary inflammation of the nerve fibres, *' wSS^S^mrt;' " d'o'^^^i^Sd;
which gives rise secondarily to an affec- iiimiwrDonL Tbs Ainnued put* uv
tionof the interstitUl connective tissue. ^'^' '^"^- w«»^«^-
The microscope reveals proliferation o!

the interstitial tissue, destruction of nenre fibres, thickening of the ves-
sels, granulo'fatty cells, and amyloid bodies. Perhaps it is more proper
to regard the disease as an atrophy of the nerve fibres and ganglion oeils.
'Ilirough the medium of the diseased nerve fibres, the disease is said
to extend secondarily to the gray matter of the anterior horns; the neur-
oglia then proliferates, the ganglion cells atrophy and disappear. These
enanges are most marked in the cervical region, gradually diminish in a

" 'award direction, and are generally absent in the lumbar cord.

136 DISKASEB OF THE 87INU. 09BD.

Raperiorly, they extend to the gacglion cells of the nuclei in the me-
dulla, particularly of the hypogloseue, pueumogastric, spinal tuxeeaorj,
and facial.

Atrophic and degenerative chafes are found in the anterior spinal
roots aou the peripheral nerves. Tne corresponding muscles are atro-
phic, the interetitial connective tisBtie is increased and often contains an
unusual amount of adipose tissue, so that the muscle may appear eren
larger than normal.

Leydea ehowed that the mode of development is not alwavB ag r^olar as in
the deacription just given, but that the diaease BOmetimea beginB in the grar
matter, and then extends to the nhite Bubstance. In addition, he showed th&t
the posterior columns are sometimes affected at the same time. - Fig. 75, which
is taken from Lejden's work, shows gray degeneration of the columns of UolL
Weiss reported a. case in which the ganglion cells of the posterior horns had un-
dergone atrophy, and attributes to this lesion the decubitus which developed upoo
the trochanters.

III. Sthftohs. — The clinical history is a combination of that of

spastic spinal paralysis and of progressive muecnlar atrophv and bulbar
paralysis. Seueatioii and the bladder and rectum are unafiected. The
scene generally opens with paralysis, rigidity, spasms and contractures
of the muscles, tiieii rapid emaciation. As a rule, the symptoms begin
in the upper limbs and extend downwards, but atrophic changes do
not occur in the lower limbs. Atrophy and paralysis follow in the dis-
tribution of the hypoglossus, vagus, spinal accessory, and facial.

n the lower limbs or in the distribution o(

The first symptoms in the upper limbs occur with or without pro-
dromata (formication and other parEesthesiie), The limbs feel weak and
well-marked paralysis gradually develops, followed by stiflncss, s2:asmK
and eontnictures. The arms are drawn against the trunk, and motion
at the shoulder- joint is attended with pain; the forearms are semi-flejed
aud at the same time pronated, and there is generally contracture at ihe

OISEASKS 07 THK SFINJU. OORD.

wrisi-joint iu a position of proimtioii> with the fingers drawu into tho
palm of the hand (Fig. 7C).

These Bymptoms are the result of diseafla of tho pyramid tracts.
The affection of the gray matter is shown by rapid atroph_y of tho mus-
L'les of tlie arms, affecting large masses at one time. Fibrillary contrac-
tions are observed during tho emaciation. The atrophic muscles are
tender on pressure, and generally show tho partial degeneration re-
action.

If the process extends to tho trunk and lover limbs, the patients
complain of stitlncss in the back, and aro hindered in sitting up, and
moving the bead ; they are compelled finally to keep to bed. Tho giiit
peculiar to spastic spinal paralysis is produced as the result of muscnlar
rigiditvand contracture, and the teudon reflexes are exaggerated. As a
r^e, tlio lowerlimbs do not undergo atrophy.

Bulbar symptoms begin with atrophy and fibrillary contractions in

Ponlcloa at the toreu-m uul battd In amfotn>phlc lUentl sderasla. After Chftrcol.

the tongue, and interference with articulation. Paralysis of the palate
then gives rise to difficulty in deglutition, and speech becomes indistinct
and nasal. The lips atrophy, the mouth is half opened, and continually
discharges saliva. The expression of the face is tearful, and, while the
forehead appears wrinkled, the lower half of the face is devoid of expres-
sion. This condition often leads to " foreign-body " pneumonia or at-
tacks of suffocation and death. Charcot regards the disease as absolutely,
fatal in one to three years, but Weir Mitchell observed recovery under
the use of potassium iodide and sulphur baths.

IV. Diagnosis, — The disease is distinguished from progressive mus-
cular atrophy bv the fact that in the latter the paralysis and atrophy go
hand in hand, tne atrophy is fascicular and generally begins in the in-
terossei, the thenar and hypothenar eminence; muscular rigidity does
not occur, and the tendon rellexes are lost.

It is distinguished from hypertrophic cervical pachymeningitis by tho
predominance, in the latter, of irritative symptoms at the outset, tno
development of severe sensory disturbances, uon-extonsion to the bulbar

138 TBAUMATIC AFFECTTIOKS OF THE SPINAL COSD.

nuclei, and the possibility of recoyery. The treatment is similar to thai
of spastic spinal paralysis.

C. TBAUMATIC AFFECTIONS OF THE SPINAL COED.

1. Unilateral Lesions of the Spinal Cord.

(BrowH'SiquarcPs Paralysis.)

I. Etiology. — Cases in which one-half the transyerse section of the
•cord is rendered incapable of function present characteristic clinical
symptoms, independent of the etiology of each indiyidual case.

It occurs most frecjuently as the result of wounds with a knife or
dagger, which haye injured only one-half the cord. This happens more
rarely in fractures, luxations, exostoses, or neoplasms of the vertebrae.
An unilateral lesion may also be produced by exudations, hemorrhages
or tumors of the meninges, myelitic foci, sclerosis, hemorrhages and
neoplasms of the cord. Kosenthal and Paoluzzi obsenred each a case
following a cold.

II. Symptoms. — The characteristic feature of the symptomatology of
an unilateral lesion of the cord is the occurrence of motor paralysis on
the same side and sensory paralysis on the opposite side. If the disease
is situated high up, we will find motor paralysis of the arm and leg on
the injured side, and loss of sensation on the opposite half of the body
exactly to the median line and to the level of the site of disease. If the
morbid. process affects the dorsal cord, motion is paralyzed in one lower
limb, sensation in the other lower limb.

These symptoms may develop suddenly as the result of injury, often
slowly as the result of other causes. They may lose in distinctness if the
spinal affection extends to the other side of the cord.

Upon the side of the body corresponding to the injured side of the
cord, there is complete or almost complete paralysis of all the muscles
whose nerves leave the cord below the site of injury. The thoracic and
abdominal muscles are affected, according to the level of the disease.

At the same time, hyperaesthesia is noticeable in the paralyzed parts.
As a rule, this affects all modes of sensation, more rarely the hypersBS-
thesia is partial, i, e., it affects only certain qualities of sensation. The
muscular sense is sometimes retained, sometimes absent.

The upper border of the hyperaesthetic region is formed by a narrow
anaesthetic zone (Fig. 77, b). This is the result of the direct injury of
the posterior nerve-roots. Above this is another hypersBsthetic zone
which extends beyond the median line to the other side of the body (Fig.
77, c and c').

The symptoms mentioned are associated with vaso-motor disturb-
ances, viz., redness and increased heat of the skin. If the injunr affectai
the cervical cord high up, there will be unilateral symptoms of paralysis
of the sympathetic on the same side: redness and increased heat of the
«ide of the face and concha of the ear, contraction of the pupil, narrow-
ing of the palpebral fissure, injection of the conjunctiva, increased fliow
of tears; hemicrania has also been noticed.

Trophic disturbances are often though not constantly observed; they
depend probably on implication of the nerve-roots. Acute decubitus
has been observed; sometimes the paralyzed muscles manifest loss of

TBA.t;itA.TIO AFFSCnONa OF TSS SPINAL OOBD.

lav

Qthfl

faradio excitabilit;. AleBBandrini mentions pain in the joints
paralyzed side, the result of eztraTasations of blood into the joints.

After a while, the paralyzed mnscles undergo atrophy from disuse,
associated with diminution of electrical irritability.

The cutaneous and tendon reflexes have been found increased in a
number of cases.

Paralysis of the bladder and rectum is frequently described. Fischer
observed erection of the penis; seznal power is generally abolished.

As a rule, there is complete, moie rarely partial, ameathesia on the
side of the body opposite to the site of the lesion; the muscular sense ia
alone retained. Motor power is almost always intact on this side, but

slight paresis is occasionally noticed. The reflexes are unchanged, and
vaso-motor disturbances are absent; in rare oases the temperature of this
side of the body is elevated.

Above the region of ansssthesia is a narrow zone of hypenesthesia,
Bontinuons with that on the opposite side of the body (Fij^. 77, e').

The patients often complain of a cincture feeling, which corresponds
to the level of the lesion. Fain and panesthesite may occur upon one or
the other side of the body.

If the cause permits, the symptoms are capable of recovery. In such

140

TRAiraUTIO AFFECnOIfa OF THE BFIHAJ. OOBD.

cases, according to Brown-Sfiqnard, the motor fonctiona recorer earlier
than the seusory functions, incontnidistinctionto what happens after thft
interruption oi conduction in peripljeral nerves. In other cases the
symptoms persist, or cystitis and decomposition of urine set in and thff
patients die, or finally the UKirbid process spreads and the symptoms of
a diSuse lesion of the cord make their appearance.

The symptoms of unilateral lesion of the cord are most sharply defined
if the dorsal cord is affected. In affections of the cervical eQlargen[ient,
the paralysis in the upper limbs is ofton confined to certaiD gronps of
muscles, because the iierve-tracte for the ind ividual muscles are relatirelr
far removed from one another in this locality. . The cutaneous nerves
are here given off in such a manner that the hyperaesthetic and anes-
thetic zones are oot circular but irregular in shape.

III. DiAOHOsis, Prognosis, and Tkeatment. — The diagnods is

easy, since in corebnil processes the paralysis and anaesthesia are always
on "the same side, and cerebral iiervea are also affected. In hysterioil
hemianiGsthcsia the special senses are also auiesthetic.

The prognosis and treatment depend on the primary disease.

IV, Patiinlogico-pltysiotogicalllemarka. The motor nerve-flbree pass from the
cerebral cortex to tbe internBl capsule and the foot of the cerebral peduncle,
tlience through the pons, and, after thedecuesation in the medulla oblongKta, paaa
in great p:trt into tua uppoeile side of the spinal cord. Here tliey pass along the
pcistfrior iiart of tlie laltral column (Fig. 70, Zmb), tli«n into the gray matter
iind Ihe anterior nerve room ot ibe Bame Birle. Hence n unilateral lesion of the
coril must produce paralysis of all the motor nerves on the same side which are'
situnle I l>elow the lesion.

TBAOMATTO ArPBOTIOSS OF THE 8PIKAI. COHD, 141

But it must be remembered that the decussation o( the motor tibres in the
medulla is not complete, » smnll portion remaining upon tiie same aide of the
cord. This is the pyramid -anterior column tract, which ia adjacent to the ante-
lior longitudinal Sasure (Fig. TO, 1 pve). Tliis tract decussitee within the spinal
curd, and paasea to the other side. Hence, a slight decree of motor paraijsis may
develop upon the side opposite to the spinal lesion. Flechsig has shown that, in
Mime cases, the undecussated pyramid tract may be the larger, so that, in excep-
t ioiial instances, the juiralysis may be aitualad on the side opposite to the apinal

The senaory fibrpe must lie assumed to decussate within the spinal cord, since
Ihia alone will explnin the crossed anaesthesia in unilateral lesion uf the cord
(vide Fix. 7S).

The tibres far muscular sense and the vaso-motor fibres do not decussate in
the cord, aince they are paralyzed on the side of the lesion.

Accordiug to Brown-S^uard. the decusaation of sensory fibres of the different
qualities of sensation occurs at different levels in the cord: goin^ from below up-
wards the fibres for tactile sensation first decussate, then those for tickling, pain,
and temperature.

The hTpereesthesia on the aide of the lesion is explained bv some aa the result
of irritation of the sensory nerve fibres by the wound, by others as the result of
paralysis of inhibitory mechanisms.

For an explanation of the narrow antesthetic zone on the paralyzed side, we
refer to Fig. 79.

3. Acute Injuries iif Ihe Spinal Cord.

I. Etiology. — As a rule, acute injurica of the spinal cord are asso-
ciated with external traumata. In Home cases, however, severe leeions of
the spinal cord are produced by an injury, although nothing ia noticeable
in the spine or soft parts. Moreover, sharp weapons may penetrate the
intervertebral spaces and injure the cord without injuring the bony parts
of the spine.

Aaite injuries of the cord are relatively frequent in fractures and dis-
locations of the vertebrie. Detached fragments of the bone may enter
the cord, or the dislocation narrows the spinal caual and compresses tue
cord. In certain cases this is preceded by disease of the vertebne, most
frequently tuherciilosis. In such an affection of the atlas and axis, a
sudden movement of the head may dislocate Ihe odontoid process and
compress the cord. Or the carious vertebra sink in and produce snch
marked flexion and narrowing of the spinal canal as to injure the cord.
Charcot observed rupture of the ord m the new-bora as the result of
excessive traction during delivery,

II. ANAXOMiciL Changes, — If death occurs soon after a simple in-
cised or stab wound, we will find a gaping wound in the cord which is
generally filled with blood clots. The substance of the cord soon under-
eoes swelling and softening at the cut ends, and the microscope shows
Fatty degeneration of the tissue elements. This terminates in tlie forma-
tion of a connective tissue which is rich in colls, which continues to
proliferate and thus restores the continuity of the cord by a sort of
cicatricial tissue. Whether the regeneration of nerve fibres occurs in
man is unknown, though clinical experience favors the belief in such an
occurrence.

The wound in the cord sometimes contains a part of the weapon, and
nnder such circumstances an abscess ia apt to develop.

If the patient survives the injurv for a long time, ascending and
descending secondary degeneration will develop.

In other cases, the cord undergoes contusion, hemorrhagic disintegra-
itioD, or rupture. Fatty degeneration, softening, and secondary degener-

142

TBACUATIO iTFECfnOXa OF TSB SPINAI. OIIBD.

atione follow. The meninges niay take part in the changea, or remain
entirely intact.

III. Syhptomb. — Aa a rale, there is paraplegia of motion and Benea-
tion, paralysis of the bladder and rectam, and changes of reflex excita-
bility. Vaso-motor symptoms (changes in the color and temperature o(
the akin, and in the formation of perspiration) have not infreqaentiv
been described. Priapism ia a frequent symptom; the penis is generally
semi-erect or flaccid. This is observed moat commonly in injury of the
cervical or doraal cord; it ia absent if the lesion is situated below the
third Inmbar vertebra. All these symptoms occur very soon after the
injury.

In injury of the cord above the cervical enlargement, death may
occur very rapidly. If life is spared, all the limbs are paralyzed aa re-
gards motion and sensation; reflex irritability is sometimes diminished
or abolished immediately after the injury, but is increased after the cord
has, to a certain extent, recovered its tone. Retention of urine and
fteces ia often observed at the startj but this disappears after a time, and
may be followed by paralysis of the bladder and rectum (cystitie, ammo-
niiemia, decubitus). Paralysis of the abdominal and thoracic muscles
interferes with respiration; if the diaphragm is panilyzeel, death from
suffocation will probably result in a short time. Implication of the
medulla oblongata will bo shown by diiEculty in deglutition, vomiting,
slowness of the pulse, pupillary changes. Abnormally high temperature
of the body has been observed in several cases. According to the esperi-
monta of Naunyn and Quincke, there are certain cerebro-spinal fibres
which inhibit tne production of animal heat.

Injury to the cervical enlargement is also followed by motor and sen-
sory paraplegia of all the limbs. The reflexes, the bladder, and rectum pre-
sent the same changes as have been described above. Respiration is im-
peded on account of paralysis of the thoracic and abdominal muscles.
The cerebral nerves are unaflSected, at the most there are pupillary
ohsngea (^cilio-spinal centre in the cervical cord).

In injury to the dorsal cord, the motor, eeusory. and vaso-motor dis-
turbances are confined to the lower limbs; bladder and rectum aa de-
scribed above. The situation of the injury can be determined by accu-
rately localizing the upper boundary of anfesthesia. The antesthetic
region is sometimes bounded by an apparently hyperasthetic zone. In
Nieden'a case of injury of the cord at the level of the first doraal verte-
bra, the temperature in the rectum, on the day of admission to the hos-
pital, was only 35.1° C, on the following day (day of death) only 27.5° C.

In injury to the lumbar cord, there is paraplegia of the lower limbs,
permanent paralysis of the bladder and rectum, and abolition of reflex
irritability. The paralyzed muscles often present rapid atrophy and loss
of faradic excitability.

The disease may last for weeks, months, or years. But, as a rale,
death soon occurs as a direct result of the spinal lesion. It often fol-
lows at a later period as the result of increasing marasmus, paralysis of
the bladder, and decubitus. Recovery is rarely observed, and only after
partial or comparatively slight injuries.

IV. Diagnosis, Prognosis, and Tbeatmejit.^— The diagnosis is
easy, when motor and sensory paraplegia follows an Injury to the spinal
column or its vicinity. The prognosis is almost alwaysunfavorable, and
recovery can hardly ever be expected.

The treatment depends upon the causal conditions. Opinions an

TRAUMATIO AFFEOTIOKS OF THE SPINAL OORD. 148

divided with regard to the advisability of trephining. In other respects
the treatment is purely symptomatic : absorbents (iodine, mercury), care-
ful attention to the bladder and rectum, prevention of bed sores, con-
stant current.

3. Concussion of the Spinal Cord,
{Railway Paralysis,)

I. Etiology. — Concussion of the spinal cord is the term applied to
those diseases of the cord which are the result of violent mechanical in-
jury of the entire body, or chieflv of the spinal column, without injury
to the vertebraB or meninges. This may occur after a fall or blow upon
the spine or buttocks, feet, or arms. Special attention has been paid
recently to concussion after railway accidents (railway spine), in which
the severity of the symptoms is often entirely disproportionate to the
antecedent lesion. Killer suggests that this is owing to the fact that
fright aids materially in producing the spinal symptoms. Locomotive
engineers and brakemen sometimes suffer from spinal symptoms, al-
though they have suffered no gross concussion as in railway accidents.

if. Akatomioal Ghanoes. — Anatomical changes may be wanting,
although death occurs shortly after the accident. This was observed by
Leyden, in a case which proved fatal in five days, and by Fischer in a
case which ended fatally in two davs. We must then assume purely
molecular changes in the substance of the cord.

In other cases hemorrhages are found in the cord and its meninges.
If they are numerous and extensive, they may be followed by inflamma-
tion and softening processes in the cord.

In still other cases, the symptoms of chronic meningitis, m^^elitis, or
myelo-meningitis gradually develop. In a case of this kind, in which
death occurred three years after a railway accident, Leyden found a
cheesy, tubercular inflammation in the peridural cellular tissue, and
acute myelitis in the cervical enlargement, with ascending and descend-
ing secondary defeneration. The inflammation had also passed through
the intervertebral foramina, into the left brachial plexus.

The development of tumors, especially gliomata, is also mentioned as
a sequel of spinal concussion.

111. Symptoms. — The symptoms are extremely variable. In one
series of cases the accident is immediately followed by the signs of shock
(small pulse, accelerated breathing, cool and cyanotic skin, paralyses,
involuntary evacuations, etc.) which terminates fatally in a few hours or
days.

In other cases, the symptoms of collapse are less marked and gradu-
ally disappear, the paralyses gradually improve, and complete recovery
occurs at the end or days or weeks.

In a third group of cases, recovery may be delayed for years, but
finally becomes complete.

Of great practical importance are those cases in which no morbid
phenomena are observed immediately after the accident, and the symp-
toms of a chronic affection of the cord or meninges do not develop
until after the lapse of weeks, oven of months.

Sometimes meningeal, t. e., irritative symptoms predominate, some-
times spinal symptoms, t. e,, paralvses. In some cases the symptoms
resemble those of multiple. spinal sclerosis (Westphal), sometimes those

144 TSAUMATIO AFFECTIOKB OF THE SPINAL OOBD.

of spastic spinal paralysis^ etc. Such cases., as a rule, terminate iq
deaths

If the brain has also suffered concussion^ the symptoms of the latter
generally obscure the spinal phenomena. In other patients, cerebral
symptoms (mania, progressive paralysis of the insane, etc.) develop at a
late period.

In four cases of railway spine, Wharton Jones observed amblyopia as the re
bult of Atrophy of the optic nerve.

IV. DiAOXOSis. — The diagnosis is easy if there is an undoubted
relation between the spinal symptoms and a previous concussion of the
body or spinal column. In guarding against simulation after railway acci-
dents, Schulz recommends attention to the tendon reflexes which, he
claims, are always changed, sometimes exaggerated, sometimes dimiu-
ished.

V. Prognosis. — The prognosis is always serious. The symptoms
sometimes grow unexpectedly worse, or they do not appear until a long
time after tne accident. The prognosis is especially grave when we are
justified in assuming serious changes in the substance of the cord.

VI. Treatment. — If the symptoms of shock predominate, we should
order stimulant measures: friction of the skin, coffee, brandy, camphor,
musk, ammonia, etc.

If the disease runs a chronic course, we may order absorbents, par-
ticularly potassium iodide, iodine and iron baths, and electricity.
In other respects, purely symptomatic treatment.

4. Slow Compression of the Spinal Cord,
{Compression Myelitis,)

I. Etiology. — The causes of compression sometimes enter the spinal
canal through the intervertebral foramina; they start from diseases of
the vertebrae themselves, from changes in the peridural cellular tissue
and meninges, or from diseases of the spinal cord itself.

Among lesions of the first class may be mentioned aneurisms of the
abdominal aorta, which have eroded the vertebrae, abdominal echino-
cocci, neoplasms and inflammations which have extended through the
intervertebral foramina into the spinal canal.

Among the diseases of the vertebrae, tuberculosis occupies a promi-
nent part. Of rarer occurrence is vertebral cancer, which is gen-
erally secondary, more rarely primary. In certain cases, the compres-
sion of the cord is the result of s^'philitic changes in the bones,
osteomata, exostoses, luxation or arthritic changes in the vertebrae, etc.
The compression is sometimes the result of thickening of the odontoid
process.

Diseases of the meninges and peridural tissue, which may give rise
to compression, include inflammatory changes, neoplasms, and parasites.
In some cases, the })rimary affection is situated in the vertebrae, but is
followed by changes in the meninges, which exercise pressure on the
cord.

Compression of the cora is rarely the result of the diseases of the
cord itself. This has been observed in tumors of the cord (glioma, sar-
coma, carcinoma, tubercle, gumma) and in cystic dilatation of the cen-
tral canal.

TBAUMATIU AFFKCTKUIS OF THK SPINAL CX>IU>.

145

_ The changes described above may not alone give rise to compression
of the cord, but also to infiammatory processes lu the meninges, nerve
roots, and the cord itself.

II. Anatomical Changes. — So far as regards the mechanical
results of compression, the cord will bs found flattened and thinned at
the site of compression. These appenrances are sometimes unilateral,
sometimes they extend around the entire circumfeionca of the cord.
The parts immediately above and below the site of compression are some-
times dilated into a spindle shape (vide Pigs. 80 aud 81).

These mechanical effoct-a are not the chief faotora in the clinical
symptoms, but the latter are the result of the inflammatory cliangea
which often affect the nerve roots, meninges, or the cord itself.

in the majority of caws, the cord is, indeed, thin and flattened, but
at the same time it is soft, diffluent, sometimes very pale and trans-
parent, B'jmetiraea injected, i. e., it presents the appearances of trans-
Terse myelitis. If the changes have existed for some timCj the affected

^Blds
^^Termi

UurliiR lite.

part of the cord not infrequently becomes very firm and sclerotic, and
ascending and descending secondary degeneration develops.

The lesione are chiefly of an interstitial character; the cellular elements of the
iroglia increase in number luid sixe, and the nuclei nleo increase in number;
„J6 basement substance becomes more abundant. The blood-veaseb present
thickening of their walls, increase of the nuclei, and fatty dej^eneration. The
medullary sheath nf the nerve fibrea underROes granular disinCein^tion and gradu-
ally disappears; the axis cylinders are swollen, and contain vacuolce: later they
deatroved. IMstention, increase of the nuclei and pigment, vacuole, and
ihangee have been observed in the ganglion cells.

The nerve roots and intervertebral ganglia also present inflammatory
1 atrophic changes, the former constituting the initial, the latter the
irminal stage.
Tlie meninges at the site of compresaion are either markedly con-
gested or unusually pale. They are often thicltened, opaque, and
adherent to one another. These changes may play a prominent part
^" the history of compression-myelitis. This is particularly true of the
10

146

TBATTMATIO AFFEOTTOHS OF THE SPINAL OOBD.

I
I

majority of cases following vertebral carioe, since compreBsion of the
oora is rarely the result of flexion of the spiual canal, but rather of
.inflammation and thickening of the outer surface of the dura mater
(external pachymeningitis). In rare cases of vertebral cariea, pus enters
the peridural space and compi'esses the spinal cord.

lii. Symptoms. — Compression-myelitis may liedivided into the pro-
dromal, irritative, and paralytic stagfs. The symptoms of the prodro-
mal stu^e depend upon the causes of the diseaEe in each individual case.
Theirntativo stage is characterized by symptoms which indicate irrita-
tion of the meninges, nerve roots, and cord. Tbe symptoms of the
paralytic stage depend upon compression and inflammation of the spinal
cord.

These stages are not always sharply defined. When the compression
is the result of intra-medullary diseases, the symptoms generally begin
withparalytic phenomena.

We cannot enter into a detailed description of the prodromal
phenomena; the chief ones are pain and tenderness in certain parts of
the spine, pain during movement, aud curvatures of the spine.

Inflammatory irritation, particularly in the nerve-roots, is shown by
neuralgiform pains. These radiate into the limbs, or pass around the
trunk (cincture feeling) ; they are sometimes localized in definite parts,
and may be especially severe at night. They are sometimes increased on
movement and concussion of the spine.

Hyperffisthesia and parcesthesiie are often noticed in the distribution
of the affected nerves. Charcot has also observed dysiBsthesia (vide
page 86). Trophic disturbances (herpes zoster, bullous eruptionSj
acute decubitus, joint changes, etc.) have been observed not infrequently.
The patients sometimes complain of twitchings aud contractures in the
muscles.

Paralysis slowly develops aud gradually occupies the foreground. It
occasionally develops very rapidly, almost in an apoplectiform manner.
In compression of the cervical cord, it sometimes happens that the arms
alone are paralyzed.

Previous hypertesthesia gradually gives way to increasing aniesthesia,
although complete anseathesia is rare. In many cases, sensation is very
little aSected, despite the severe motor symptoms. Delayed conduction
is sometimes noticeable. In addition to aniesthesia, the patient may
suffer from the most violent pains (antesthesia dolorosa), particularly in .
cancer of the vertebrte. If these symptoms are the result of compression
of individual nerve-roots, they will be confined to circumscribed areas,
and associated with loss of reflex excitability in the affected nerve-tracts.
The affected muscles then undergo rapid atrophy, aud degeneration
reaction develops. But if the symptoms result from compression of the
spinal cord itself, the motor and sensory disturbances almost always as-
sume a paraplegic character, and the cutaneous nnd tendon reflexes are
considerably increased. The signs of spinal hemiplegia occur in very
rare cases as the result of unilateral compression of the cord. Reflex
excitability is abolished if the lumbar cord is compressed, or if extensive
changes in the gray matter have extended from a focus situated higher
up. The paralyzed limbs sometimes present vaso-motor symptoms :
discoloration of the skin, elevation of temperature, and abnormahties in
the production of perspiration. Kahler and Pick described a case in
which the motor irritation began with ataxic symptoms. Disturbances

vxnscmosAL dissabes of the spinal cobd. 147

of the bladder and rectum occur from the start in diseases of the lumbar
cord. Under other conditions, they may remain long unaffected.

Complete or almost complete recovery may take place, even if the para*
lysis is very marked. Improvement often occurs with surprising rapidity.
1 know of a case of complete paraplegia of three or four years' duration,
following vertebral caries, in which, at the end of that time, improve-
ment occurred with such rapidity that the patient was able, at the end of
two weeks from the first signs oi recovery, to walk unaided to the dining,
room. In such cases, we may not assume acute regeneration of com-
pressed and destroyed nerve elements. It must be assumed that the few
intact nerve fibres at the site of compression suffice, when the compres-
sion ceases, to conduct impressions.

Some cases present repeated exacerbations and remissions. In others,
the disease progresses uninterruptedly. Increasing marasmus, decubi-
tus, cystitis, and amraoniaBmia, more rarely sudden bulbar paralyses,
cause the fatal termination.

Secondary degeneration is shown by the fact that the previously
flaccid paralyzed muscles become stiff, and twitchings and contractures
make tneir appearance. In the lower limbs, the extensors are at first
chiefly affected, but later the flexors becomes involved to a more marked
extent — the thighs are strongly flexed and drawn upwards, and the legs
are flexed so that the heels come in contact with the thighs. Secondary
degenerations may also give rise to recurrent paralyses, i. e,, paralysis
of the upper limbs becomes associated with paralysis of the lower limbs,
which resulted from a morbid process in the lumbar or dorsal cord*
This must be explained on the assumption that the secondary degenera-
tion has interrupted the paths of conauction to the upper limbs.

IV. Diagnosis. — While the diagnosis of compression of the cord is
usually easy, that of the cause of each individual case may be difficult.
This is especially true if no abnormality can be discovered in the spinal
column, and if the previous history furnishes no clue.

V. Prognosis. — This depends upon the etiology, and, as a matter of
course, it is unfavorable when the cause cannot be removed. Other-
wise, improvement and even complete recovery are not infrequent, par-
ticularly in vertebral caries.

VI. Treatmrnt. — This must first be directed towards the removal
of the cause. In other respects, the treatment is similar to that of acute
and chronic myelitis (see page 88).

B.— FUNCTIONAL DISEASES OF THE SPINAL CORD, OR SPINAL

NEUROSES.

1. Spinal Irritation.

1. The term spinal irritation is applied to a symptom-complex characterized b7
pain in the spine, associated with neuralgiform pains in the skin or viscera, vaso-
motor and secretory disturbances, motor weakness, functional cerebral changes,
etc., and not dependent on an anatomical lesion of the cord.

The condition has been attributed to spinal ansBmia or hypersemia, meningitio
irritation, or changes in the sympathetic. Some writers deny the very existence
of spinal irritation.

2. This condition is observed most frequently in women, and is often associated
with hysteria, chlorosis, and ansemia. Bodily and mental strain, exhausting dis-
eases, excesses in venery, abuse of alcohol or opium, and heredity have been men-
tioned as causes. It occurs generally from the age of 15 to 80 years.

148 FUNCTIONAL DISEASES OF THE HFINAJ. OOBD.

8. The most constant symptom is pain in the spinal column. It most flreqaently
affects the dorsal spine, but is aldo observed in other parts. It ocean spon-
taneously , but becomes especially severe on pressure upon the spinous processes,
and may be so violent as to give rit»e to syncope or epileptiform seizares. It also
becomes evident on passing over the spine a sponge dipped in hot water, or
the cathode of the galvanic current. The adjacent integument of the spine
is not ipfrequentlv very hypersBsthetic. Hammond also describes a deeper pain
which is produced by percussion of the spine.

In addition, there are eccentric symptoms of irritation which vary according
to the affected portion of the cord. In changes in the cervical cord, we notice
headache, vertigo, visual disturbances, tinnitus aurium, hyperssstliesia of the
face, depression, insomnia; in other cases, s>)mnolence, neuralgiform pains in the
face, neck, upper limbs: nausea and vomiting. The eccentric dorsal symptoms
of irritation include palpitation, asthmatic attacks, nervous cough, intercostal
neuralgia, gastralgia, vomiting, singultus, etc. Lumbar irritation is charac-
terized by pains in the back, lower limbs, bladder, rectum, uterus and ovaries,
strangury, polyuria, etc.

ParaBSthesise, muscular pareses, spasms, and vaso-motor changes are not un-
common.

The disease may last months and years, but hardly ever leads to more serious
affections.

4. The diagnosis is usually easy after prolonged observation.

5. The treatment consists of bodil;^ and mental rest, nutritious and abundant
food, the administration of quinine, iron, cod-liver oil, cold-water treatment, a
trip to the country, and the use of the galvanic spinal current (descending, not
too strong or prolonged, anode or cathode to unusually painful vertebras). The
faradic brush to the spine, or galvanization transversely through the skull, has
also proved useful. Strychnine, potassium bromide, zinc, arsenic, phospbonUv
and opium have also been recommended.

2. Functio7ial Weakness of the Spinal Cord, Spinal N'eurasthenia.

1. The etiology of spinal neurasthenia is the same as that of spinal irritation,
but the two conditions are not identical. Spinal neurasthenia is especially fre-
quent in men, particularly among the hi(2:her classes.

2. The symptoms consist of abnormal functional irritability and weakness of
the spinal cord. It is often associated with cerebral neurasthenia. It is dis-
tinguished from spinal irritation mainly by the fact that the motor disturbances
predominate, while sensory symptoms may be entirely absent.

The patients are easily tired on walking or standing. They often experience
that feeling of muscular exhaustion whicn is felt by healthy individuals only
after unusual exertion. This is often felt immediately after waking. The gait
is stiff, trembling, and uncertain. Similar symptoms may develop ui the upper
limbs (while writing, etc.).

Sleep is restless and disturbed by dreams. The patients become depressed,
irritable, and shy. Many complain of vertigo, a feeling of pressure in the head,
ringing in the ears ; in company, they suffer from a feeling of terror and palpita-
tion ; in theatre, they have a dread of fire. etc.

Sexual excitement is often noticeable, but its gratification is attended not in-
frequently with premature ejaculation of semen, and may be f oUowed by Sjmcope
(in one of my cases by palpitation and epileptiform seizures).

Anorexia, eructations, flatulence, and constipation are observed not infre-
quently.

Some patients complain of parsBsthesisB. vaso-motor disturbances (coldness of
the hands and feet), hypenesthesia of the back.

The disease is capable of recovery, often not until after the lapse of months and
•even years.

8. The treatment is similar to that of spinal irritation. Erb prefers the
ascending galvanic spinal currents. Good effects have been obtained from gencoral
faradization : the patient is placed in a bath-tub filled with lukewarm water, in
which is put the cathode of the secondary current, or the feet are placed upon a
large cathode, while a large anode is gradually passed over the different parts of
the body from above downwards. Or the physician takes the anode in one
moistened) hand, while the patient's body is stroked with the other (also rnds*
tened) hand. Duration of each sitting ten minutes, every two to three dajs.

FUNCTIONAL DISEASES OF THE SPINAL COSD. 149

3. Acute Ascendifig Spinal Paralysis,

{KussmauU Landry's Paralysis.)

I. Etiology. — The symptoms of this disease consist of progressive
paralysis from below upwards, with retention of electrical irritability
m the paralyzed muscles, absence of atrophy, of sensory and trophic dis-
turbances, of paralysis of bladder and rectum, and of anatomical changes
in the nervous system.

The disease is rare, but is much more common in men than in women,
and, as a rule, appears between the a^es of twenty and forty years.

The causes are often unknown, it has been attributed to cold, sup-
pression of menstruation, and mental excitement. Bablon observed it
after coitus in the standing position. Ic is relatively fre(][uent after
acute infectious diseases, and has also been attributed to syphilis.

II. Symptoms. — The paralysis develops unexpectedlv, or is preceded
by prodromata. The latter consist of chilliness, slight fever, pain ia the
bacK and limbs, formication, and other paraasthesise.

The motor paralytic symptoms do not always follow a strictly ascend-
inj^ course. They begin m one or both feet, then affect the legs, thighs,
loins, abdomen, chest, hands, forearms, and arms, then the neck, and
finally the bulbar nerves.

Westphal described a case in which bulbar paralyses were alone observed. In
rare cases the paralysis pursues a descending course.

The motor paralysis begins, as a rule, with paresis which gradually
deepens into complete paralysis; the limbs remain flaccid.

The patients first experience a tired feeling in the legs, and are soon
compelled to take to bed. If the dorsal muscles are affected, they are
unable to sit up, and paralysis of the abdominal muscles interferes with
defecation, couching, sneezing, i. e., with all expiratory processes.
Paralysis of the intercostal muscles impedes inspiration. Gradually the
movements of the hands, forearms, and arms are impaired, then the
movements of the head are interfered with. Phrenic paralysis will pro-
duce the most marked dyspnoea.

Then bulbar symptoms gradually make their appearance. Speech
becomes difficult on account of paralysis of the hypoglossus. Paralysis
of the palate and oesophagus makes the speech nasal, and produces diffi-
culty in deglutition. Tne pulse becomes very much accelerated, and
attacks of suffocation occur which terminate fatally. As a rule, the
cerebral nerves remain unaffected.

The paralyzed muscles retain their electrical irritability to the last,
and do not undergo atrophy.

Cutaneous sensibility is very little, if at all, affected. Anaesthesia
and hyperaesthesia have been observed in a few cases. Delayed conduc-
tion of the sensations of pain and temperature has also been reported.
Diminution of muscular sense has also been noticed.

Decubitus and other trophic disturbances do not occur.

The cutaneous and tendon reflexes are unchanged at first, but gradu-
ally they are diminished and finally abolished.

The bladder and rectum are not paralyzed, although temporary re-
tention of urine sometimes occurs at the outset.

The general condition may be unchanged. Febrile movement may

150 FUNCTIONAL DISEASES OF THE SPINAL OOBD.

or may not be present. Enlargement of the spleen and albuminnria
have been observed in some cases.

The disease runs an acute, progressive course. Death occurs gener-
ally in the middle of tlie second week of the disease, sometimes in two or
three days, at others in two or three weeks.

In rare cases recovery ensues even after bulbar symptoms have devel-
oped. Several months often elapse before the status quo ante is restored.
Bemissions and exacerbations, with a finally fatal termination, have aAso
been observed.

III. Anatomical Changes. — The nervous system presents no anatomical
changes in cases of this disease. But eniargemeot of the spleen and swelling of
the intestinal lympli follicles and mesenteric glands have been obseinred m a
number of cases, and this lends a certain degree of plausibility to Westphal's
suggestion that the disease is the result of some unknown infection.

IV. Diagnosis. — The disease is distinguished from ascending mve-
litis by the absence of fever, sensory disturbances, paralysis of the bladder
and rectum, decubitus, and changes in electrical excitability. Acute
anterior poliomyelitis does not possess a progressive character, and
results in rapid muscular atrophy and loss of electrical excitability. In
acute multiple neuritis, sensory disturbances predominate, and the elec-
trical irritability of the affected nerves and muscles rapidly diminishes.

V. Pbognosis. — The prognosis is always grave, although recovery is
not impossible. Tlie more acute the course, and the more prominent
the bulbar symptoms, tlie earlier will the fatal termination occur.

Vt. Treatment. — If the disease has been preceded by syphilis, anti-
syphilitic remedies must be administered.

Other measures recommended are: a. Externally — actual cautery,
cups, leeches, ice-bag, derivatives to the spine, cold compresses, b. In-
ternally — })ota8sium iodide, ergotine, atropine, etc. The galvanic spinal
current may also be employed.

4. Reflex Paralysis,

1. This term is based on the theory that diseases of the peripheral organs may
impair the function of the spinal cord to such an extent as to give rise to spinal
paralyses, which almost always appear as paraplegia. The disease is most fre-
quent as the result of affections of the genito-urinary apparatus and intestinal
tract; it has also been observed after injury, inflammations of joints, and cold.

Among the diseases of the urinary apparatus, we may mention cystitis, reten-
tion of urine, nephritis, and calculi. The morbid changes in the genital tract
include gonorrhoea, stricture, phimoses, hypertrophy of the prostate, hydrocele,
flexions and ulcerations of the uterus.

Reflex paralysis is also said to follow dysentery, more rarely simple diarrhcea,
improper administration of cathartics, constipation, colic, worms.

Paralyses of a spinal character have been observed after gunshot wounds which
did not directly involve the paralyzed limbs. They have also been reported as the
result of ulcers of the skin and of a cold.

2. Brown-Scquard believes that the paralysis is the result of spinal ansBmia due
to reflex spasm of the vessels, but it is hardly conceivable that such a spasm raay
last for years. Jaccoud believes that the peripheral irritation directly inhibits
and thus exhausts the functions of the spinal cord. In recent times, however, the
view is gaining ground that the majority of the cases are the result of anatomical
lesions. As a rule, we have to deal with inflammations which extend from the
primarily diseased organ along the peripheral nerves or blood-vessels to the con-
tents of the spinal canal, so that the affection is really the result of asoendinR or de-
scending degenerative neuritis, meningitic changes, or myelitic processes. But the

FUNCrlON.U, DISEASES OF THE SPIKAI. CORD, 151

poseibility of reflei paralysis in the strict sense must b« granted, partioularly
when the pamlyBis di9ap|)ears almoBt immediawly Oiller its cause is removed.

3, The symptomatology varies according as the disease is the result of Deuritis,
TneninEitis, or myelitis, The progooeis depends upon the etiology, and this is fjso
true of treatmeat.

6. Psi/cUical Spinal Paralt/nis.

(Fright Paralysis.)

Paraplegia is sometimes jiroduced by profound emotions. Kobts and Leyden
have referred recently to the great influence of fright in the development, not
alone of functional, but also of organic dieeasea of tlie spinal cord. Their observa-
tion is bEised on the abundant material furnished during the bombardment of Straa»-
burg. RuHsel Reynolds and Riegel have called attention to the fact that para-
plegia may result from the influence of the imagination, particularly in feeble,
exhauatea individuals. Sometimes there is complete parnlysis, in other case«
merely paresisj the bladder and rectum are generally intact, Pareestbeeiie and

anKsthesia are not infrequent. The treatment ia chiefly moral. Iron, quiotae,
Atrychnine, electricity, cold frictions, etc., may become necessary,

6. Paralyses after Acute Diseases,
{Infection Paralyses.)

1. These cases are obserred most frequently after acute infectious diseases,
particularly after certain epidemics. Ab a rule, the paralysis develops during
convalescence, but it baa also been observed at the outset.

The best-known form is that which occurs after diphtheria of the pharynx,
other mucous membranes, and skin. It generally occurs in the second or third
weeks after recovery, sometimee in the sixth and eighth weeks. It has also been
ofaeerved after catarrhal angina, and even after herpes pharyngia.

Paralyses sometimes occur after typhoid diseases, particularly after typhoid
fever; alBO after dysentery and cholera. Cases have also been reported after the
acute exanthemata (variola, scarlatina, measies, erysipelas, herpes zoster), after
erythema nodosum, urticaria febrilis, purpura, puerperal fever; also after pnen-
jnonia, whooping-cougli, articular rheumiitiiim. nleurisy, malaria.

a. In one series of cases tlie paralysis is confined to a single nerve, and occa-
aionally even to smaller groups of muscles. In other cases an entire limb is pora-
JyEed, find paraplegic conditions may develop, usually without implication of the
bladder and reetuiu. Or we find the symptoms of acute ataxia, multiple sclerosis,
progressive muscular atrophy, spinal atrophic paralysis, acute ascending paralysis,
etc. Cerebral hemiplegia with or without aphasia, or the latter affection alone,
may develop. It evident that all these conditions cannot be produced by the
same anatomical lesions.

The lesions which have been observed are: degen«rative neuritis, diffuse mye-
litis, or disseminated myelitic processes (found after variola by WestphalJ, multi-
ple Bcleroeis (also observed after variola), meningitic changes extending to the
anterior nerve-roots (in diphtherial, cerebral embolism or thrombosis, etc,
' It is now aHumed that the majority of cases of paralysis after acute infectious
diseases are the result of anatomical lesions, but in rarer coaes functional affec-
tions of the spinal cord are observed — for example, acute ascending paralysis
which presents no anatomical basis. In some instances of unusually rapid disap-
pearance of the paralysis, we muxt assume conditions of exhaustion of the spinal
cord (asthenic paralysis). The intermittent (wralysia of malaria must also be re-

garded as a functional affection. It is characterised by the development of a
"" ' ' ■ yiti, Qr without aniesthesia, and paraJvsis of the

^^^ garded a

^^^B Tisually pmi^ressive paralysis. i . ...

^^^H ^bladder, which disappears nt the end of a few hours after a sweat. The attacks

^^^H lecur at stated intervals, and are cured by anti-malarial remedies,

^H Kor

Toxic Spinal Paralyses.

i^lysis may bo produced b;
io, phoBphoruB, mercury, carbonic oiido, alcohol, tobacco, campbor.

Kore or ]ees aevere paralysis may bo produced by poisoning with lead,

152 FUNCnONAL DISEASES OF THE SPINAL CORD.

copaiba, ergot, absinthe, opium, belladonna, strychnine, etc. The par«
alyses may be confined to individnal groaps of muscles, may extend to
larger nerve-tracts or to entire limbs, or may be of a hemiplegic or fiara-
plegic cliaracter; they may be associated with ansBsthesia or hyperaBsthe*
sia, or sensation may he unaffected. We wiU here discuss a lew of the
most frequent forms of toxic paralysis.

a. Lead Paralysis.

1. Lead paralysis is one of the later symptoms of lead poisoning, and
is usually preceded by the formation of a blue line on the gums, more or
less frequent colic, and lead arthralgia. Tanquerel des Planches reports
one case in which the lead paralysis was produced a week after the {mtient
began working in lead. Usually a number of years elapse before the
paralysis is produced. Excessive use of alcohol and strain of certain
^oups of muscles are said to favor the development of lead paralysis.
It is unnecessary to enter here into the various ways- in which the system
may be poisonea with lead.

2. As a rule, the paralytic symptoms develop very gradually, but
more rarely they begin suddenly. Sometimes they follow immediately
upon an attack of lead colic.

In the majority of cases, the paralysis is confined to the upper limbs,
often only to those muscles which are supplied by the radial nerve. The
muscles of the lower limbs are rarely, those of the back still more rarely,
affected. Duchenne also observed lead paralysis of the intercostal mus-
cles and diaphragm.

The paralysis generally begins in the right arm (in left-handed per-
sons, in the left arm), but the corresponding muscles of the other arm
soon become affected.

The extensor digitorum communis is first affected, and there is difflcnlty in ez-
tenbion of the first phalanges of the second and third fingers. Then the extensor
digit, quint, propr. and extensor indie, propr. become affected; this is followed by
paralysis of the extensor carpi cad. et ulnar., next of the extensor polite, long, et
brev.; the abductf>r pollic lon^. resists for a long time, and is finally affected
with the muscles of the ball of the thumb. The interoesei. particularly the first,
also become involve<l.

It is characteristic that the supinator longus et brevis remain intact, unless
the biceps and brachialis iiiternus becomt* involved. Paralysis of the latter
group is generally f)receded by paralysis of the deltoid. The triceps is affected
very late or not at all.

in the lower liml>s the peronei are first affected, then the extensors of the leg»
but the tibialis anticus remains intact.

Degeneration reaction develops in the paralyzed muscles. The direct
and indirect faratlic irritability of the muscles is gradually abolished,
but the paralysis is sometimes more extensive than the disturbances of
faradic excitability. If the paralyzed muscles have not lost their faradic
irritability, their function is often restored after a few electrical sittings.
Direct galvanic stimulation of the muscles shows increased excitability,
slow contractions, and predominance of AnClC. The increased galTanic
excitability soon disappears, but AnClC remains predominant. Par-
tial degeneration reaction is observed in muscles which are not Tery
markedly affecteil. If the degeneration reaction is complete, the moscles
will not recover, if at all, until the end of three to four months.

The muscles often recover voluntary power, although they are still

FUNCnOKAL DISEASES OF THE SPINAL OORD. 153

inexcitable to the faradic current. Diplegic contractions have been ob-
served in a number of cases (vide page 127).

During the continuance of the degeneration reaction, the mechanical
excitability of the muscles is increased, and they sometimes present
fibrillary contractions. The paralysis is followed by atrophy of the mus-
cles, so tliat the interosseous spaces appear hollowed out. A deep groove
is seen on the dorsal surface of the lorearm^ the shoulder is flattened,
etc. Symptoms similar to those of progressive muscular atrophy have
been observed in some cases of lead poisoning.

The cutaneous and tendon reflexes are abolished in the regions in
which the muscles have lost their electrical excitability.

Trophic disturbances are sometimes noticed : enlargement of the
sheaths of the tendons (tenosynitis hypertrophica), enlargement of the
phalanges, etc.

The disease runs a chronic course. Belapses sometimes occur,
although the patient was not exposed anew to the influence of lead.

3. The anatomical changes in the muscles consist of narrowing of
the flbres, increase of the nuclei of the sarcolemma, gradual disappear-
ance of the muscle substance, proliferation of the interstitial tissue, and
sometimes of the adipose tissue. Some authors regard the muscular
changes as primary, the changes in the nervous system as secondary, t.
e.y as propagated from the muscles. Others maintain that changes in
the peripneral nerves are primary (degenerative atrophy). In one case
Westphal noticed changes in the radial nerve whicn he attributed to
regenerative processes (finest nerve fibres surrounded, in bundles, by a
common sheath).

The clinical symptoms point distinctly to an affection of the spinal
cord. They are so like those of subacute and chronic atrophic spinal
paralysis that it has been assumed that the lead poisoning first gives rise
to a functional disease of the large ganglion cells of the anterior horns
of the spinal cord, and this in turn to secondary changes in the periphe-
ral nerves and muscles.

4. The diagnosis is usually easy, not alone from the etiology, but also
from the characteristic distribution of the paralysis (radial nerve with
intact supinators). In peripheral radial paralysis, the supinators are af-
fected, as a rule, sensory disturbances are present, and peripheral causes
are demonstrable. The differential diagnosis from s{)inal atrophic para-
lysis may be difficult in the absence of a previous history ana of other
symptoms of lead poisoning.

5. The prognosis is not favorable, as a rule, because the patients
generally suffer from relapses unless they give up their occupation.
Belapses may also occur without the intervention of renewed poisoning.

In individual cases, the prognosis depends chiefly on the extent of
the paralysis and the electrical irritability of the paralyzed muscles.
Cases which approach generalized lead paralysis offer a more serious
prognosis. In muscles which have lost their faradic excitability, re-
covery cannot be expected before the end of three or four months, if
at all.

6. Prophylaxis is an important feature in treatment, and chiefly
involves the proper construction of factories. After the paralysis has
developed, potasisium iodide (gr. xij. t. i. d.) may be given internally.
Annuschat nas recently shown that this facilitates the excretion of lead
from the body. In audition, warm baths, particularly sulphur baths
(30^ B., fifteen to thirty minutes' duration). We may also apply th&

154 FUNOTIONAL DISEASES OF THE SPINAL OOBD.

galvanic spinal current (large electrodes, vigorous current, at first the
anode for two to three minutes, then the cathode to the cervical en-
largement). Also the galvanic current labile, the anode being placed in
the cervical enlargement, the cathode stroked methodically over the
individual muscles. The faradic current may be employed if the mus-
cles retain their faradic excitability. Galvanization of the Sjrmpathetic
has also been recommended.

b. Arsenic Paralysis.

1. Arsenic paralynis is more often the result of acute than of chronic poiaoii-
ing, and may aevelop in a few days. It is distinguished from lead paralysis by
affecting chiefly the lower limbs, by the more rapid atrophy of the paralyzed
muscles, and the prominence of sensory disturbances.

2. As a rule, there is paraple^a of the lower limbs, more rarely of all the
limbs or the upper limbs alone. The paralysis and atrophy of the muscles are
often preceded by violent pains; and numbness, formication, and analgeaia are
noticed not infrequently. The electrical irritability, the cutaneous and tendon
reflexes present the same changes as in lead paralysis. In one case, Seeligmueller
observed marked tabetic symptoms.

8. In pieces of the muscle, which had been removed from the patient by har-
pooning, Da Ck>sta noticed narrowness of the muscular fibres, increase of the
nuclei of the sarcolemma, in other parts waxy degeneration, slight fatty degen*
eration, increase of the interstitial connective tissue, and accumulation of fiit in
it. Nevertheless, Da Costa assumes a spinal origin of the paralysis. In their
experimental investigations, Mierzejewski and Popof observed poliomyelitis, bat
the process often extended into the white matter.

4. The treatment is the same as in lead paralysis.

c. Phosphorus Poisoning.

Acute and chronic phosphorus poisoning may also give rise to paralyses, in
the form of partial paralysis, monoplegia, and paraplegia. Pains, parsosthesiad,
and objective sensory disturbances have also been observed in the paralysed
parts. The situation of the lesion is not known with certainty. Degeneration
of the peripheral nerves has been observed, and likewise changes in the spinal
cord. Danillo and Vulpian have recently made experiments on doss. In acute
poisoning, they found hypersBmia and an accumulation of pigment in the vessels
of the anterior horns, and swelling and the development of vaouolsd in the
ganglion cells themselves; in chronic poisoning, the white matter also took part
in the process.

(h Carbonic Oxide Oas and Bisulphide of Carbon Paralysis.

Paralyses have been described after a number of cases of carbonic oxide
poisoning. These paralvses may he peripheral, spinal or cerebral in orinn, and are
probably the result of hemorrhages with secondary inflammatory and degenersr
tive changes.

These remarks hold good concerning paralysis after poisoning with bisulphide
of carbon, to which workmen in India-rubber factories are especially liable.

e. Paralysis after Ergot Poisoning. Ergotism.
{Raphania. Morbus Cerealis.)

Paralyses after ergot poisoning are almost always spinal in character. In
three cases (in one family) under my observation, marked atrophy and contrac-
tures of the muscles had developed. Little is known concerning the site of the
disease. Tuczek recently described very marked changes m the posterior
columns; the knee jerk was absent in these cases during Ufe, and the Brach-
Romberg symptom and ataxia had also been observed in some cases. Treatment
according to general principles.

Pellagra and ergotism are probably identical.

FUirOTIOKAL DISEASES OF THE SPINAL OOBD. 155

/. Alcohol Paralysis,

Spinal paralytic symptoms may develop in acute, more f rejiuently in chronic,
alcoholism. It is well known that some individuals, when intoxicated, keep a
clear head, while the feet become *' groggy." Certain alcoholic drinks have a
special -power of affecting the legs.

Paraplegia, ataxia, and cutaneous hyperaasthesia have been observed in
chronic alcoholism. The latter are perha^ associated with meningitic changes.
The condition of the tendon reflexes is indicated on page 111. The symptoma-
tologv may be very similar to that of tabes (pseudo-taoes). The treatment oon-
aists in gradually weaning the patients from their bad habits.

8. Writer's Spasm, Mogigraphia,
( Graphospasm . Cheirospasm. )

I. Etiology. — Writer's spasm is most freouent from the twentieth
to fortieth years; it never occurs in childhooa^ and is rare in old age.
The disease almost always attacks men.

The causes are variable. In some patients there is a congenital
nervous disposition, inasmuch as epilepsy, hysteria, and other neuroses
are observea among the relatives, and perhaps the patient himself was
nervous since youth.

In other cases acquired nervousness constitutes the predisposition to
writer's spasm, for example, in masturbators and those who indulge in
excesses in Baccho et Venere.

Strong mental excitement may produce or intensify the disease.

Some patients attribute their complaints to cold or injury, for ex-
ample, a wound of the finger, running a needle into it, wearing tight
gloves, etc.

In rare cases an inflammation of some of the nerves of the brachial
plexus has acted as the cause of the disease. Bunge describes a case
which resulted from periostitis of the arm.

The most frequent cause, however, is strain or a bad position of the
hand in writing.

It is stated not infrequently by the patients that the flrst symptoms appeared
while making the balance sheet at the end of the year. The disease has abo been
attributed to the use of steel pens, but tins cannot be the sole cause since it was
observed before their introduction.

II. Symptoms. — As a rule, the symptoms develop very gradually.
There are sometimes certain prodomata, such as a feeling of pressure in
the head, depression, excitement, poor sleep, nervous dyspepsia, etc.
The manifest symptoms begin as more or less impediment to the act of
writing, but after a time (sometimes not until the lapse of months and
years^ writing becomes impossible.

The first muscles affected are those employed in writing, yiz., the
interossoi and lumbricales, the muscles of the ball of the thumb, and the
extensors and flexors of the forearm. The spasm may also extend to
the muscles of the arm, shoulder, and even the neck. Sometimes only
a few, in other cases many groups of muscles are affected.

Benedikt distinguishes spastic, tremulous, and paralytic writer's
spasm.

The spastic form is the most frequent, the paralytic variety the rarest. One
form is sometimes complicated by another.

( X KL'KCnONAL DISEASES OF THE SPINAL OOBI>.

•V'^^:' I'' wriutr'H Kpa.sm consists of tonic, more rarely clonic muscolar
t\^.'ff,f, wUif'.U impair or prevent the sure manipulation of the pen.

It, «/fffi<i r.nm*H thorn U flexion spn^m of the thumb, so that, on attempting to
vf,h ihii ltiuiii>> in ili':i>vii H|)aHin«KlicHlly into the palm of the hand. In other
' M-w.i iiiiiMi iri H|»aHitio4li(; tlexioii or extension of the index finger. If theextenson
n9 itii: iliiiiiiii liinl iii(U*x tliiger are affected at the same time, the pen will drop
luim lliM hiiiul. Tit<« M|):iMiii somecimeH affects tho extensors or the abductor
.ffi'l ii|i|Mihi«iiH (li^iti minimi, and is associatefl with such distressing pain that it
l«iii.i#Mii»» iiii|ioitHiblii to continue writinf;. Spasm of the flexors of the w^rist joint
|.: M'li iiitivqiiiiiit. If it (Mvurrt in the flt^xor and extensor carpi ulnaris, the hand
i.i iti'iwii fiiicitilv ui'n>rts tho i>aper. Various other combinations of spasm may

iil.Wf liti iihbiil \inl.

'riiiiniiltiiirt writor'ri 8p*ism is characterized by trembling movements
^Jiit h ot'i'ur onlv ilurin^ writing.

I'urulvtu' writor*rt si>asm is really writer's paralysis. It is shown by
ii fi nliii^ (if liiort'H.Hin>; oxhaustion and tension which develops during the
•t> I tif writing, and Uvoines so severe that the hand is held quiet on the
)iii|M-.r

'VU^^ iliahirbaiuvs of oo-onlination in question sometimes occur at
i.iirh tiiliiiupt to writi\ in other cases only after prolonged writing.
Mi.iiiul nw^iiMUi'tit oxoivisos u marked influence upon the disease.

Tim ^roaa powor of iho mus\.*les affecteil by spasm is in no wise im-
|iuiuul Many juitiouts oau also i)erform. without difficultv. other deli-
liiiii mHin|iula(u>us« such as tlirv^adiug a needle, sewing, playing piano,

111 mlduu^n u> \vritor*s s^asnu the patient may also suffer from spasm
nt »iilii'i xiuMips v»f niusclcs : wz.. strabismus, stuttering, pharyngeal
i'jui'iu. :|M-.m 111 I ho miisolos X-: tho back of the neck, also tremor and

Tho ;»!looiovl iv.us<'*os i>:^ somt^tisies tender on pressure.

r»»iin»Luia IS '.::.i-lv r. : :r.f>?i; :o:::'.y of •jansjsthesia?: a feeling of cold-
no.' i. imiuiui:, fv^r:::i:;i:::::. rZ-:. Sr/.-: Autiiors have noticed vaso-motor
tli.uuh.Mioo'i vj^^'- " - --- --f""> ir. i .5. rVeli-^i: as if they were dead) at

lh»i hi'i^nuiiiii: v^f :hv ?; iszi. T-ir yatiVtss*^ me times complain of neur-
iili'Koiiu p:iiv.s, ir.v^s: frv/i-rL-.'.y in :>.; •.■.>:r.:u::on of the ulnar nerve,
hi'vc m ilia I of t'.'.o iv.^iijkr. r.rrvv, T •■; -.jrvos <?t the arm are occasion-
M\ loudoi o!\ prx\<^*.;rv, iul -r-:i:;: > v; *.".•.:— < iave sometimes been ob-

M'l\v'vl \lPv'l\ thotVi.

l\kiui;i'» rrx^ss/.re iv.v.tii a:v >:n::::"us :;::v..l on certain parts of tho
hoUv"» x^: ;!.o a-':t: or ov. s-.^iuo of :..:: .^r*. .:a1 si'.ual rrooesses.

V[w oUv.riooi'. .rr.:;i. ;.::> ;: :>.: ,i:?-\:cv. ru-.iscles is ^nerally un
ih.iHi^ovi; '.: ',s s.^:v,o:.:v;*< sli^rV.:.; ,v:v.. .>.:;v:. more rarely increased.
lu>\\,'. N o.v'so' 'v< ,i.v''::;v. . : :;•: r> —,.:>*>■ v. Ar A::d electro-cutaneous
>o I Ks . b . . ■: \ K .;■ ••.'.;' >; ' i .^, s .' .' <v ■ ■ :» i. ■ .: :i. : :.i : : *. i .* liac^s in the electrical
i 1 1 u .1 1 ' . I \ x^ ; ', ' '• v.o . X v's >■ ■« . . . * ,: : ; i^; o : ;:\l rv,: scles ^predominance

lio xi >Oviv/ AVI ;.'...;.> :.^ ^7. ^ *.?>?<* v.v.iSci tjit? :>acients are able to

I : u' I II o I \* i ■>. s* x^. ^o.i >v' v ■. \-^v XA' >. -. . ,• "-•. / -V : >,•; vriiien characters are
I h.iuo.o.l . ..o \^ . *; o .. *. .\ v> is .:' ^ ":::o" *rv ^ Serinner, or while
n» 1 i I u; »» \ .", .» . \' ,L »; >, '. v^i • . .i . . i. , v ,4. . ! ,\j: V '. -: :>. ir*,* rer? can no longer be

ih.4«U

NI.I..X j^ ..,> :> o ...... NT, ^,> A. >: V'. -is.u^ thick penholders or

vjvo.M i\ >x :< x^ - . . ,' M V. , .^;^.^^i ." v.t.\ .'Ji^iT.^!^ position of thd

FUNOTIONAL DI8EASBS OF THE SPINAL OOBD. 157

wristjoint and fingers. Others learn to write with the left hand. But,
unfortunately, the same symptoms develop not infrequently in the left
arm, or writing with the left nand causes very annoying spasmodic con-
ditions in the right arm.

III. Pathogenesis. — The disease is probably the result of purely functional dis-
turbances. These are evidently situated in the spinal cord, because the act of
writing requires the delicate co-ordination of adjacent groups of muscles, and
the co-ordinating centres of these muscles are situated in the cervical enlarge-
ment of the cord. Abnormal irritability, ready exhaustion, and irregular stimu-
lation of these centres suffice to explain the symptoms of writer's spasm. In
some cases, however, the primary o«sturbance is situated in the brain, as is
shown by the feeling of pressure in the head, vertigo, mental depression, etc.
In otheV cases the starting-point is at the periphery (neuritis, periostitis, etc.).

IV. Diagnosis. — The diagnosis is easily made. We must always
endeavor to determine the variety of the disease, and for this purpose
must carefully study the disturbances during the act of writing. We
should also search carefully for pressure points.

V. Prognosis. — The prognosis is not very favorable. Eecovery is
rare unless the patient abstains permanently from writing.

VI. Treatment. — Writing must be strictly prohibited for many
months. If hereditary factors or an acquired nervous disposition enter
into the etiology, we should prescribe potassium bromide, iron, quinine,
cold-water cures, a stay in the country, and careful massage of the
muscles. Injurious haoits must be given up, and peripheral lesions
(injury, periostitis, neuritis) treated in the ordinary way. If pressure
points are present on the sninal column, the anode of the galvanic cur-
rent should be applied to tnem (cathode to the sternum, daily sitting for
live minutes, current not too strong).

Treatment with the galvanic current likewise offers the best hopes of
success under other circumstances. If cerebral symptoms are prominent,
feeble currents should be passed transversely and ooliquely tnrough the
skull. A spinal current may also be applied to the cervical cord. Peri-
pheral galvanization may be applied to the aflfected muscles and nerves —
the labile current in the tremulous and paralytic varieties, the stabile
current in the tonic form (according to Eulenburg the anode is prefer-
able). Galvanization of the cervical sympathetic has also been recom-
mended. M. Meyer obtained good results from faradization of the indi-
vidual muscles, but this must be avoided in the spastic variety. Erb
applied permanently a simple galvanic element (copper and zinc plates
connected by a wire and placed over a nerve trunk of the arm upon a
moist piece of linen). The treatment must be continued for a long time
in all cases.

Good results have been obtained recently from massage of the affected
muscles and gymnastics, but it is advisable to have the treatment carried
out by a skilled specialist.

Numerous other measures have been employed in this disease: a, alcoholic
and narcotic inunctions, douches, blisters, cups, derivatives of all kinds, ice-bag,
ether irrigation of the spine; 6, narcotics and nervines; c, meclianical apparatus
(thick, cork penholders, rings to fasten the penholders, bandages to the wrist-
joint); d, nerve stretching.

Appendix.— Similar disturbances may occur in other fine manipulations
which necessitate the co-ordinated action of groups of muscles. The gross power
of the muscles is unchanged, but their power of co-ordinated action is lost (co-or-
dinating professional neuroses).

158 FUNOTIONAL DISEASES OF THE SPINAL OOBD.

Most closely allied to writer*s spasm is telegrapher's spasm. Pianist's spasm
occurs particularly in young ladies, and usually in the right hand. Violinist's
spasm may afifect either hand. Tailor's and shoemaker's spasm is manifested in
the muscles of the hand and arm, and renders impossible tne use of the scissors,
needle, etc. Similar conditions are observed in smiths, masons, sawyera, weavers,
watchmakers, printers, etc., and also in the lower limbs, in turners, sewing machine
operators, dancerp, etc.

Spasm of the laxynz has been described in players on the clarionet.

9. Tetany.

I. Etiology. — Tetany manifests itself by the occnrrence of tonic
muscular spasms, which come and go in paroxysms, affect certain groups
of muscles, and are associated with increased electrical and mechaniod
excitability of the corresponding motor nerves.

The disease occurs most frequently at a youthful age. It is not in-
frequent in teething children, later it occurs particularly at the period
of puberty (thirteenth to thirtieth years). It is rare in fater life.

Rachitic, pale, and feeble individuals exhibit a predisposition to the
disease.

Some authors attribute a certain desrree of influence to heredity.
Murdoch observed tetany in several brothers and sisters, and Bouchut
states that it is particularly frequent in children whose parents are ner-
vous and suffer from neuroses.

Among the not infrequent direct causes are colds, particularly from
sleeping in damp rooms, camping out, etc. The influence of rheumatic
causes also ap}K»ars to be shown bv the fact that tetany is often associated
with swelling of the joints, and tliat it is especially frequent in the cool
months.

It often appears to be the reflex effect of peripheral irritation (teeth-
ing, worms, overloading of the stomacli ana intestines, suppression of
the menses, pregnancy, lactation, ojH^ration for goitre).

Tetany sometimes follows acute infectious diseases or exhausting dis-
eases. These conditions probably proiluce. in many cases, merely a pre-
disposition, and otht-r influences are necessary to produce the disease
itself.

It is s<.^metimes the result of violent excitement. A number of cases
have been reporteil in which tetany occured as an epidemic in schools
and similar institutions.

II. Symptoms. — The attacks of spasm are almost always preceded by
certain i>rLKlrv.^mata: dragging and tearing j»ains in the limbs, a feeling'
of coldness, formication, etc. The pnxlromata may last for days and
week?. In nire cas<.*s cerebral symptoms occur: vertigo, ringing in the
ears, a f-.vliiig of confusion.

Tht* :«.':iic muscular spasms s<-">metimes follow the prodromata sponta-
neous'y, a::l in certain patients are apt to occur at night, or they appear
after bodily strain or nu-:ital excitement.

In typical cases thoy are condned to the ilexors of the Anders and
wrists: thev are almost alwavs bilateral, excer'tionailv unilateral. Thev
often extend to the tiexors of the forearm and th-* adductors of the arm.
In except i>nal cases the spasm affects the extens«>rs of the fingers and
wrist, or both the dt-xors and extensors.

The muscles of the lower limbs are sometimes affected, sometimes
only the plantar flexors of the toes, or the calf muscles, occasionally
even the extensors and adductors of the thigh.

FUKOTXONAL DISEASES OF THE SPINAL OOBD. 159^

The spasm extends more rarely to the muscles of the back^ abdomen^
and chest, to the muscles of the pelvis and diaphragm. Indeed, the
spasm finally may become general, and affect the muscles of the face,
larynx, pharynx, tongue, oesophagus, and detrusor of the bladder.

In typical cases, the position of the affected fingers and hands is so
characteristic that it almost suffices to warrant a diagnosis. Trousseau
compares it to the position assumed by the obstetrician when he attempts
to introduce the hand into the vagina.

The thumb is strongly adducted and bent into the palm of the hand;
the other fingers, particularly the fourth and fifth, are strongly flexed
in the metacarpo-phalangeal joint, and extended in the phalangeal
joints; the palm of the hand is deeply hollowed, and the entire hand is
strongly flexed towards the ulnar side. If the flexors of the forearm are
affected, the forearm appears semi-flexed; in spasm of the adductors of
the arm, the arms may oe so strongly drawn against the thorax that the
flexed forearms cross each other over the epigastrium.

In spasm of the flexors of the toes, the great toe is drawn under the adjacent
toes; spasm of the calf muscles is shown by pes equinus, pes varo-equinus, more
rarely bv pes valgo-equinus. In the knee-joints, the lower limbs are usually
extended, and the thighs are adducted against one another. In tonic spasm of
the muscles of the back, the spinal column appears strongly curved anteriorly.
Spasm of the thoracic muscles and diaphragm may give rise to threatening
symptoms of suffocation. Spasm of the muscles of the neck and throat causes
cyanosis of the face and protrusion of the eyeballs as the result of venous stasis.

The contours of the muscles often stand out sharply beneath the
skin. Fibrillary contractions are sometimes visible during the spasm.
The muscles are firm, and more or less tender on pressure.

The contractures can usually be overcome after a certain degree of
effort, but the limb returns to its former position as soon as it is released^

The spasmodic attacks vary in duration from a minute to one or
more hours, and even three days. The contractures persist, though less
vigorously, during sleep.

The number of attacks also varies greatly. Sometimes single attacka
occur at intervals of days, weeks, and months, and occasionally the dis-
ease terminates with one paroxysm. In other cases, numerous seizures
recur in the course of a single day.

During the attack, the majority of patients suffer from annoying
sensations: a feeling of coldness, prickling, formication, etc. Some
complain of a painful feeling of tension in the contracted muscles,
others of neuralgiform pains, which may be confined to certain nerve
tracts; central symptoms may also be noticed (vertigo, pressure in the
head, ringing in the ears, etc.).

Great diagnostic significance attaches to three other symptoms, viz..
Trousseau's phenomenon, the increase of the electrical and of the
mechanical irritability of the motor nerves.

Trousseau'd phenomenon is the ability to produce a^seizure of tetany by
pressure upon the nerve trunks or arteries of the arm. Tne attack occurs after
the pressure has been exercised one to two minutes, and disappears when the
pressure is discontinued. In some oases, pressure on the arte^ alone produces
an attack, while compression of the nerve is useless. This symptom is very
rarely absent, and so long as it can be produced, we must be prepared for the
recurrence of spontaneous attacks of tetany.

A few cases have been reported in which pressure on other parts of the body
also produced attacks, for example, compression of the cervical sympathetic and

160 FUNOnONAL DI8SABE8 OF THE SPQTAL OUSD.

carotid, pressure and faradic irritation of painful points on the spine, or proagu ie
oil the muscles of the wrist joint and on the radial artery. Czerny observed a*i
attaclc follow elevation of the arm. The symptom is produced with luore diffi-
culty in the lower limbs by pressure on the crural artery or sciatic nerve.

The electrical irritability of the motor nerves is increased. A faradic current
of very slight strength, when applied to the nerve, suffices to produce muscular
contractions. On the application of the galvanic current (to the uerve) CaCIC
and AnOC occur very early, CaClTe and AnClTe soon follow, and it is a |>eculiar
fact that AnOTe is produced without difficulty. Chvostek claims to hare
observed CaOTe in two cases. These reninrks hold good concerning the nerves
alone, not concerning the muscles ^uppheil by them. The facial nerve, as a rule,
remains unaffected.

So long as these electrical changes iiersist, the attacks of tetany may relapse.

The mechanical irritability of the Kiotor nerves is increased paK poMU with
the electrical irritability, so that gentle tapping on the nerve wul produce con-
tractions in the corresponding muscles. As a rule, the facial nerve iB not
affected.

The appearance of the parts affected with tetany is often unaltered,
in some cases swelling of tlie joints with redness and CBdema has been
observed.

The cutaneous sensibility is generally changed, but sometimes very
slightly. Manouvriez observed partial anaesthesia even in the intenrafs
between the attacks.

Uasse states that the more marked the anaesthesia the more severe
the attacks of spasm will be. lie also observed abolition of the muscu-
lar sense, so that the patients could only hold objects by the aid of the
sense of sight. Painful pressure points on the spine are reported in a
number of cases.

Tlie general condition is often unaffected. Some patients complain
of dyspepsia and drowsiness, or, on the otlier hand, of excitement. The
heiglit of the attack is sometimes accompanied by profuse perspiration
or fever, or both.

As a rule, the disease terminates in recovery, though slight contrac-
tures and pareses may persist for a long time. Kussmaul observed
retinitis as a sequel. In cliiidren, tlie height of the disease may be
attended with fatal eclampsia. Death may also result from increasing
exhaustion and persistent diarrhoea.

III. Anatomical Changes and Pathooenesis.— Nothing is known concern-
ing the anatomical changes in tetany. Hemorrhages into the spinal meninges,
increase and sanguinolent color of the spinal fluid, softening and sclerosis of the
cord, minutQ hemorrhages into the cord, and thickening of the vessels, have
been observed in a number of cases; but these are either accidental complicatiooB,
or the secondary effects of the tetany.

It is now generally conceded that the disease is neuropathic in its origin, but
it is questionable whether the starting-point is in the nerves, spinal cord, brain,
or Hy mpathetic. The cerebral theory is opposed by the fact that, in the majority
of cases, cerebral symptoms are absent, and the cerebral nerves are usually un-
affected. The increased electrical and mechanical excitability of the motor
nerves seems to point to itH peripheral origin, but this may also be a secondary
effect of spinal changes. If we take into consideration that the disease is often
produced m a reflex manner (necessarily through the medium of the spinal cord),
and that pressure points are found on the spine, it seems plausible to assume a
spinvl origin of the disease, and to explain it by increased irritability of the
ganglion cells of the anterior horns, upon which depend the secondary changes in
the peripheral nerves. N. Weiss thinks that the sympathetic is the starting-point
of tne disease, and that its irritation gives rise to the circulatory changes in ttM
cord.

IV. Diagnosis. — The diagnosis is easy if we bear in mind the cardi-

nal gymptoms: intermittent tonic spsfimB in certain gmupe of moacles,
Troufiseau's phenomenon, and increased electrical and mechanical ex-
citability of the nerves.

The disease is distlnguishHi from tetanus bjtbe fact that the latter first mani-
fe«t« itaelf b; trieiiiuH. In li.vattrical H)>a8ine iind the co-ordinating professional
neuroBes, the mechaniCB.! and electrical irritability of the nerves is not increased.
Some coses of flpaamotlio ergotism pimsess very great similarity to tetany, but
are distitiguiahed from the latter by the etiology.

V. Prognosis. — The diseasa almost always terminates in recovery,
although months may elapse before it disappears entirely. The patient
cannot be regarded as completely cured until Trousseau's phenomenon
and the increused excitability of the motor nerves have disappeiired.
TrouBsean recognized three degrees of severity of the disease: in the
mildest, it is conSned to the muscles of the limbs and general symptoms
are absent; in the second grade, the muscles of the trunk are affected,
the attacks are more frequent and violent; in the third, there are dis-
turbances of the general condition.

VI. Treatment. — Our attention must first be directed to the re-
moval of the cause. In rheumatic cases, we order potassium iodide, sali-
cylic acid, and sweat bathe; in suppressio mensium, warm foot baths and
leeches to the cervis uteri, etc,

Narcotics and nervines have been recommended against the disease
itself, but no single remedy is especially cfficaeions.

We may mention; potassium bromide, chloral hydrate, opium, belladonna,
curare, chloroform, ether, vaierioo, arsenic, etc. Tlie remedies may be admin-
iatared iu various ways.

Cups, blisters, ice-bags to the spine, Inkewarm baths, cold-water

'es, etc., have also been recommended.

Good results have been obtained from the use of electricity, hot no

igle method of application seems to be especially useful.

^^^r If there are painful spinal points, the anode of a constant galvanic current
^^^Wt too strong) may bu applied to them, the cathode to the sternum; each
Bitting two to four minutes, irivery other day. The anode may also be applied to
the cervical or the lumbar enlarEement. Or the peripheral nerves are galvanized
labile with the anode, which is slowly stroked towards the nerve plexus, Anodol
AppUcationB may also prove effective during the spasmodic seizures. If the fara*
"* ~ current Is employed at oU, it should be appliea as a feeble current to the spine
' nervB trunks.

10. Saltatory Spasms.

Seven coses Of this disease have been reported. It occurred portloulBTly
in nervous and hysterical individuals with a neuropathic hereditary taint.
Upon bringing the toot to the ground, and i a standing and walking, clonic mus-
ciilsr contractions occur ot such a vigorous character that the entire body under-
Roes a hopping, dancing movement. The spasms were confined to the lower
limbs, or they also involved tbe up[>er limbs and the muscles of the trunk and
back of the neck. They were accompanied by drawing pains, and in two cases
occurred in paroiystus and were accompanied by a sort of aura. No paralysis,
anaesthesia, or other severe spinal symptoms. Some patients complained of

Kinal tenderness, and Outtmann could produce attacks by pressure on the spine,
lere is evidently increased reflex excitability of the pmglion cells of Ibe anterior
boms in this afFeciion. Frey attributes it to a definitely localized myelitis; Erb

■Inclined to regard some of the cases as spastic spinal paralysis. Spontaneoua

162 DISEASES OF THE 8PISAL MESOTOBB.

improTement occurred in some cases, while oChen were incnnble. Warm >^>^ff ^
ice and wet cups to the spine, narcotics, nerrines, and electricity have been eoi-
ployed in treatment.

11. Primary Spinal Muscular Spasms.

(Thomsen's Disease,)

L £}noi/X}T.~In this disease, tonic spasm of the muscles oocosb daring volim-
tary movements, and either delay or entirely ahoiish the execution of the intended
movement. Ihe disease i& also known as mvotonia congenita, tonic g^Mwif jn
Toluntarily moved muscles, and hypertrophic'spastic spinal paralyaia.

Heredity plays a very important part in the etiology. InThomaen's familT
the disease occurred in five generations. Schoenfeld observed the development
of the disease as the result of fright. Other causes areu unknown.

II. Symptoms.— The symptoms are confined chiefly to the voluntary muscles,
but Seeligmueller observed in one case formication and a feeling of coldness in
the limbs, in another case absence of the tendon reflexes. The Gladder and rec-
tum were always unaffected.

The muscles of the lower limbs were most affected, next those of the upper
limbs. In some cases the muscles of the tongue, face and eyes, and of mastica-
tion were also involved.

In this disease, voluntary movements cannot be carried out immediately be-
cause tonic spasm develops in the muscles which aro to be moved. If the patients
wish to rise and walk, they feel a disagreeable feeling of tension; some time
elapses before the resistance'is overcome. The spasms may be so violent ^y^»% the
patients fall and roll involuntarily about the floor. If they have grasped an ob-
ject with the fingers, they are unable to let it drop at once. Affection of the
tongue is shown by hesitating speech and awkwardness in mastication.

Kesistance is also experienced during passive iftovements.

The muscles are often unusually large, generally feel very firm, and, on
mechanical and faradic irritation, form thick ridges which persist for a long time.
The faradic and galvanic excitability is unchanged. Fibrillary contractions are
sometimes observed in the muscles.

Continued movement and warmth diminish the spasms, mental excitement
and cold intensify tbem.

The first oymptoms are often noticeable in the cradle. During childhood the

Satients attract attention by their a\vkward manner; in rare cases the symptoms
o not begin until the twentieth year or later.
The disease continues for life, but remissions and exacerbations have been
descriljed.

III. Anatomical Ciianoes.— In one case, examination of a piece of excised
muscle showed nothing beyond somewhat unusual width of the fibrillsB. The
disease is generally regarded as spinal in its origin, but nothing further is known
of its nature.

IV. Diaonosib.— The diagnosis is easy. It is distinguished from muscular
hypertrophy by the absence of changes of electrical excitability and the presence
or spasms.

V. TREATME!n* is of no avaiL Some relief is said to have been obtained by
gymnastic exercises. Trial should be made of batlis and electricity.

C. DISEASES OF THE SPINAL MENINGES.

1. Inflammation of ihe External Surface of the Dura Mater.

External Spinal Pachymeningitis,

{^Peripachymeningitis. Perimeningitis Spinalis.)

I. Anatohical Chanobs. —The inflammatory process in question is situated
on the outer surface of tlie dura mater in the loose, fatty connective tissue which
separates the dura mater from the inner surface of the spinal canaL In the
majority of cases tho inflammation is circumscribed, hardly occupying more

DISEA&AS OF THE SPINAL UEXINGES.

163

than tbe height of one to three Tertebrae; tuore ext«n6ive inOamniations are
rare. In some cases there are several separate foci of infiammation.

The inflammation is moat marked on the posterior a iir face, cliiefly because the
connective tissue is most abundant in that locality, perhaps in part on account
of the influence of tlie force of gravity. It rarely eitends beyond the cervical
region, because the extradural cellular tissue gradually diminiBhea in tbe upper
part of the cord.

In a series of cases the inflammatory products constitute a thickening and
cellular inflammation on tlie outer surface of the dura mater and in the peridural
cellular tiwae. This may be associated witli more or leas swelling and redness at

Eztarnal aptiiBl pachymiTiiiiEltliatthi' 1.
8piii«J can) Been from behind. Hum

polntofUie iMlon In n lijtht-ilded cheiiar pivucis)', wl
[„„„„[„^ 1^ .1 ._., 1

the eite of diaeoee. In other cases the outer surface of the dura mater is covered
with a thick, callus-like membrane, which is almost fibrinous in appearance.
Well-marked abacesses are found in some casee. Dry. cheeey, tuberculous masses
of conKJderable Biie may also be pro-luced (vide Fift. 82). In clironic cases fibrous
tbiokeoinKS and adheaiona to the outer surface of the dura mater are found.
The Inflammation extends not infrequently to the inner surface of the dura

164 DISEASES OF THE SPINAL MENINGES.

mater, giving rise to swelling, redness, infiltration, abeoeBs, or cheesr tubercu-
lous processes. Even the arachnoid and pia mater may take part in the inflam-
mation.

In a series of cases the process results in simple compreesion of the oord and
nerve roots, in others it gives rise to compression myelitis (vide page 145).

II. Etiology.— Externa] spinal pachymeningitis is almost always a seoondarj
condition, indeed it is questionable whether it is ever primary. The primair
morbid process is generally situated near the spine, whence the inflammation
extends through the intervertebral foramina to the peridural space. It has
been observed after tuberculosis or inflammation of the vertebrsa, pleuritis, peri-
pleuritis, syphilitic ulcers of the pharynx, suppuration of the cellular tissue of
the neck, psoas abscess, and deep spreading decubitus It may also be prodaced
by other conditions, particularly suppurations in the thorax, peritoneum and
pelvis, and in migrating neuritis. Syphilis must also be mentioned as a cause.

III. Symptoms.— -The symptoms are very similar to those of spinal meninj^tis.
Most patients complain of stiffness in the back, which is especially noticeabk

while sitting or standmg, or on rotating the spine.

The spine is tender on pressure over parts corresponding to the inflammation.
A blow on the head or shoulders, the passage of a sponge dipped in hot water, or
the slow labile application of the cathode of a galvanic current causes pain ex-
clusively or chiefly in these localities.

Visible or palpable changes in the spine (swelling, redness, fluctuating tumors,
etc.) are noticeable if the affeotion is secondary to disease of the spinal column.

The patients often complain of a cincture feeling around the trunk, corre-
sponding to the approximate site of disease.

Violent pains — usually in paroxysms — are experienced, either along the spine
or radiating into the extremities. Hyperaesthesia, hyperalgesia, and parassthesis
are often observed. In addition, there may be tonic or clonic twitchings and con-
tractures in the muscles of the extremities. Paralysis and anaesthesia may be
looked for, if pressure on the nerve roots has interfered with conduction. The
reflex irritability is then destroyed, and the paralyzed muscles underigo atrophy.
The electrical irritability of the paralyzed muscles is the same as in peripheral
paralysis (vide page 7).

If the cord is compressed, motor and sensory paraplegia will develop below
the site of compression, with para^sthesia, increased reflex excitability, vesical
disturbances (at first retention, later incontinence), perhaps incontinence of fsBces
and decubitus (vide page 146). The disease generally runs a subacute or chronic
course. Fever is occasionally noticeable, often as the result of the primary dis-
ease itself.

IV. DiAaNOSis.— The diagnosis is not easy. The chief points to be considered
are the etiology and the irritative symptoms mentioned above. It is distinguished
from spinal meningitis by the absence of rigidity of the neck, since the cervical
region is almost always unaffected.

V. Prognosis.— The prognosis is always grave. The majority of cases termi-
nate fatally, but Leyden has shown that recovery is possible.

VI. Treatment. — Treatment must first be directed towards the removal of
the CHunes. In other respects it is the same as that of spinal meningitis (vide
page 170).

2. Inflammation of the Inner Surface of the Sjpinal Dura Mater,

Internal Spinal Pachymeningitis.

Internal spinal pachymeningitis generally runs a chronic course, and occurs
as the hypertrophic or hemorrhagic varieties.

a. Jaypertrophic internal spinal pachymeningitis consists of inflammatory
proliferations and fibrous thickenings on the inner surface of the dura nutter. In
the majority of cases similar changes have developed upon the arachnoid and pia
mater, so that the spinal cord is constricted by a ring of connective tissue which
sometimes attains a thickness of one cm., often presents concentric lamellsB, and
contains numerous interstitial spaces (vide Fig. 88). The proliferation is generally
most marked posteriorly, where there are usually extradural adhesions to the pos-
terior ligament. The changes are generally circumscribed, the lower half of the
cervical enlargement being most frequently affected (pachymeningitis oenricalit
hypertrophica).

The daDgers of the disease consist in the constriction of the nerve roots and

Sinai cord. The ByraptomB of cnmpreesioci ot the cord are grRdually followed by
oae ot compression-myelitia. The gray matter will be atTected with cuecial
leverity, and it is perforated by new.form^ canals (vide Fig. 83), The latter are
found chiefly in tne gray commiBsure, ai-e lined with a meiubTaDe, and c

It has been attributed to colds, and living in damp

; B. Del

The disease
places.

Symptoms will not be produced unleBu the nerve roota are G0m|)reB9e<l and
later paralyzed, or the cord itself underRoea compression. Charcot disliURTjiahes
a staKe of irritation (lasting two to three months), and a. stage of paraJjals and
fttropny.

In the stage of iiritation, the patients complain of pains in the upper part of
the spine, the occiput, betweeu the shoulden, and in the arms (particularly in the
Urce joints). Pressure on the spine does not give rise to pain. The inajoriLy of
the patienta complain of BtifTnfiBs in the back of the neck, and a feeling ot ron-
■triction in the upper part ot tlie chest. The paina appear in paroxyama or in-

166 DI8EA8E8 OF THE BPIMAL UZSISQES.

crease periodically In intenrity.

are noticeable in the upper limbL. ._ ,

and rouf;hnew of the epidermis may alao mitke their appenranoe. The mnacln
not infrequently present tonic or clonic contrsctiona, rigidity, and contr a ct a w.
These eyinptome are evidently the result of irritation of the nerve roola whkh
paas through the hyperplastic portions of the dura mat«r.

Tlie second aCagts is characterized hy paralvais of muscle* in the upper Umbt,
fihritlary contractions and atrophy of the par^yzed muscles, changes in electrical
irritability (such as occur in peripheral paralysis), and anEeetheBia. As a mle, the
ulnar and niodian nerves are paralyzed, the intact extensora of the forearm
acquire the predominance and produce permanent dorsal flexion of the hand,
while the fingers are flexed at the second and third joints (vide Fig- 84). If the
morbid process is situated very high, the radial nerve will be paralTZMl, and the
hand will permanently assume a flexed position (ride Fig. 86). All these symp-
toms are the result of compression and complete interruption to oonduction U
the spinal roots.

If the spinal cord itself becomes compresaed, paretic and paralytic symptOffit
will develop in the lower limbs. The muscles undergo atrophy merely aa the re-
sult of disuse, and their electrical irritability is unchanged. We frill find En-
cresaed reflex excitability, diminished sensibility, disturnuices of the t' "
decubitus, etc.

The disease often lasts for many years, but recovery is possible. The compli-
cation with pulmonary phthisis is relatively frequent.

The diagnosis is not very difficult. The second stage may be mistaken tor

eo^ressive muscular atropliy. but the latter is not preceded by an irritative stage,
gins generally in the iiiterossei, the thenar and hypothenar eminences, and
sometimes extends to the nerve-nuclei in the medulla, and gives riae to bulbar
paralysis; hypertrophic pachymeningitis hardly ever extends to the medulla
oblongata, and although it cnunes paralysisof the lower limbe, the muscles do not
undergo rapid atrophy or changes in electrical excitability.

In amyotrophic lateral ftclerosis there is no stage of irritation, sensory disturb-
ances are absent, the diseaoe runs a more rapid course, affects the upper and
lower limbe in a uniform manner, and almost always proves fatal by extensioii
to the medulla oblongata.

The differential diagnosis must also be made from tuherculoeis of the spine,
tumors of the spine and meninges, and external spinal pachymeningitis; the
chief points to be considered are pain and deformity in the spine, tuberouloois of
the lymphatic glands and lungs, and tuniora in other organs.

Thetr---

IT to that of spinni meningitis.
b. Hemorrhagic internal pachymeningitis corresponds exactly to hmmatoma
of the cerebral dura mater. The inner surface of the dura mater la covered with
more or less extensive, extremely vascular membrnnee. These may often be
separated into several layers, between which is situated partly fluid, pu^
olotl«d blood. Under the microscope we And hEsmatoidin crystals and red nlooa-

DISEASES OF THE SPISAL MEItI»OE9. 167

fclobul«8 in varioaa stngea of destruction. The extravaflationi may bo bo large as
tu compresB the nerve-rooM aatl spinal cord. Tlie pia maMr aomeCtmes takea
part in the hemorrhage, and the spinal fluid is tinged with blood. In some cases
the change extends along tlie entire length of the oord, in others it is confined to
ainall. scattered foci.

tiimilar changes are generally found on the cerebral dura mater, because both
condiiioDs are the results ot the same cauBes. They are observed in the insane
and in drunkards; Lejden reports one case after injury.

In many cases the disease remains Intent, in otherti it produces the symptoms
of irritation or paralysis of the nerve-roots or spinal cord. These syrnptoras may
beattributedlohemorrhagicpachymeninglljsif the etiological factotsare present.
Sudden signs of meningeal hemorrhage may develop if vessels in the new mem-
branes rupture and pn^uce an extensive hemorrhage.

The treatment is similar to that of spinal meningitis.

3. Acute Spinal Mejiinijitia.

I. Etiology. — Inflamroationa of the arachnoid (arachnitia) and pia
mater (piitia) are alnioBt always asaociatBcl with one another, and are
known B» spinal moniugitU or bptomeiiingitis. They are sometimes
confined to tlie cord or to parts of jt, aometimos they extend to the cere-
bral meninges or vice versa (cerebro-apinal meningitis). We will here
discuss spinal meningitis alone.

Golds (sleepinj; on the damp ground, working in water, etc.) and
injuries are mentioned not infrequently as causes. Spinal meningitis is
sometimes the result of simple concussion or lifting heavy weights, in
other eases it is produced by fracture or dislocation of the vertebrte, stab
or gunshot wounds, etc.

Secondary inflammations are more frequent. In Cmveilhier's case a
pulmonary cavity perforated the spinal canal and set up spinal meningi-
tis. It may also be the result of any of the etiological factors which give
rise to external spinal pachymeningitis (vide page 164).

Spinal meningitis occurs occasionally in connection with infections
diseases: pneumonia, typhoid fever, cholera, dysentery, etc. Hasse ob-
served several cases after articular and muscular rhenmatism.

It is more frequent in the male sex, particularly in childhood and
middle age.

II. Anatohical Chanqes.— Theeo are divided into the stage of
hyperemia and beginning exudation, that of the completed exudation,
and that of resolution.

la exceptional cases death occurs in the first stage. The pia mater
and arachnoid tissue are unusually red, swollen, and succulent. The
redness is diffuse and uniform, or depends upon unusually distended,
finer blood-vessels. Here and there are more or less numerous and ex-
tensive extravasations. The larger vessels are sinuous and distended to
the point of bursting. The surface of the pia mater and arachnoid
tissues looks loosened and velvety. The epjnal fluid is cloudy and con-
tains flocculi.

The second stage begins with the deposit of purulent or fibro-punilent
flakes. Those continue to increase, aud finally cover the surface of the
pia mater, the arachnoid tissue, and even the inner surface of the dura
mater with purulent or fibrinous deposits, which are often dotted with
blood. These changes are circumscribed or diffuse, aonording to the
etiological factors. They are most marked on the posterior surface (in-
fluence of the force of gravity), and diminish towards the medulla ob-

1
I

ti'.s inSEASES OF THE SPINAL KEIONOEB.

I'lii^^titpi. KvtMi if ivrebral meningitis is also present, the medulla often
i-r^ iipiii I'liiiivlv, or almi)6t entirely.

til III.* thif«l 4ta^^', the purulent masses are gradually absorbed^ but
I lit. ii.'iiMi;^H .iiiii iilMiormal adhesions of the menmges usually remain as

|»i<i iii.iMritl U-rUillUi.

V4 I !ii!i\ t!io iMi!:inunationi3noteonfinedtothepia mater and arach-
ii.iiil itc.iii\ Uiii :htt;wlws important ailjacent structures. Unimportant
u«.iiM<«.. .i:«) i!io iiitUmmutory processes which are of ten seen on the
iiiiM^i 4 111} Mfor riurfMoo of the dura mater, and the hemorrhages in the
|it<t i.l'i- i! .'t'iluuir tisst:o. Much more important are the changes in the
III I V*' 'o*'.x .riii s(MiiaI cord.

I 'k' Mi:iti"»v»*»jH.* siiows hyper;^mia of the nenre roots, infiltration of
iiki> -iiu^su: ,:ii liv^uo with round cells, and degeneration of the nefve*

I'. . ;ioi iistotiishtng that the spinal cord should take part in the iu-
il.dutit.itioM. siiKV the pia mater sends innumerable prolongations into
till' luuM iv»r of the con.]. In many cases, the cord, on transverse section,
.i|i)^.(i» ditnucnt, aniomatous, and injected in places, in other parts ex-
ii»<iu>I\ |»;ili\ In not a few cases, changes are only observed upon
iiiii uKMopio examination of sections of the hardened cord. They are
MMiii'itiiii'A very slight, and are partly parenchymatous, partly interstitial
III t li.ii.u'tiT. In phioes, the axis cylinders are found swollen and un-
ii.u.iltv l.nxo; in addition, the meilullary sheaths may be degenerated,
III.. Hi liio^liji inort\Hsctl in places, and its nuclei proliferated. The pro-
i..iin.iii*mMi»i' tlic pia mater into the cord present distention of the vessels,
. iiii,^ iaii(>u of white MiHxl-clobules. and increaseof the cellular elements.
Ill I lit- 1 1, IN manor the s^voiuiary changes are less marked than in the
^1 liiif lu.iHoi. Init tV.o piiiiilioii ceils arv nc>i infre«3uentlv swollen.

Ui.«|«ti\ and doi^^norativ'^ of the cord, parricuiarly in the posterior
... 1 1 1 II I II . 1 1 .1 \ \» a ! so Iw r. obsc-rve^: .

Ill :.\ mtu^mn. The iria:.:fe5: symptoms are not infrequently pre-
.. I'.i ii\ t'ii»*lix»u\:»:a, s'.'.vh as ar.orexia. c hi'. ly sensations, general mal-
.1 . I. I li,' :.x ov.o :s s*^:v.<:::n:vs otnr.eviby a sir.zle severe chill, followed
I . I. I. I «ii uo |vr. i-.v-.'/.ar :y:v. wr.ioh may attain a considerable height

I h. Muiii,Miv» ,;.-."b;::aV'; t;- t:.o monir.i-ltis itself are relatively

h 1,1 \ . ti.,' y % :v. ^., ' •> \.Ty r::'.-. -r. v.orvesrwe may attribute to in-

il .i...u.oi.>ii »«i »'■> •■ s':v.. r:i*./ ::-.i Vsvir.s a::i stiffness in the spinal

Im.mm wUxs u I.-, N .X- . •' -.•/\,r/.:v.:/ R-.::. as a rule, these pains are not

. . . .M\ |MN . . \' . ' . •/ sv ..;\ :/.: vsisctiice of the cathode of a gal-

ttiiiiii «-\

\n . .J,. . X.M.. .--x * V ; ^* -.<,:';> :i :rr:tat:-"^n or paralysis of the

• • • ^

• III .\i 1^. ■ .. .... «>. .^.x...ft. ««*N 4>.

\i.. . . I ,' '.' s ' .•: -s' ;-.>:. -J :\i:v.> :'u the limbs, chest, or

I . .!. », ,' ',•....:.,>:;-'. r v.orre roots. The same

, V ,\ .: Ar." /.:..: the thorax or abdomen.

Ii . •.^,. » . : . : .V-: ->A ^":" the skin, so that very

,. ,x.. .. ^ .- \: .*:vr:kir.s: the integument.

•v,v. ^:-^ ii^.iitly: the patients cry out
-. 7;>^^\ xriroen the fingers.

\ I , I

\\ \ , ,ss . N N , 7^:- Art-* sometimes reflex, as

I. , , ^ . >.;:*.- .',: ,^f rr^^sure on the mus-

. . ,., X, , ...» :;.:c X ir:"viV:?nily spontaneous.

DISEASES OF THE 8P1KAL UEmiTOES. IStf

Stiffness of the muscles or contractures are observed not infrequently,
the latter involving chiefly the extensors.

If the process extends to the t;errical cord, the musclea of the back of
the ueck undergo tonic contracture (rigidity of the neck). The head la
drawn more or less backwards, and the occiput is bored deep into the
pillow. Active and passive movements of the head anteriorly, and aome-
timcs rotatory movements, are impeded or entirely prevented. The
entire body can often be lifted by the occiput like a rigid piece of wood.

Contracture of the muscles of the back ia shown by the unusual an-
terior convexity of the spine, so that the trunk tonch'es the bed only at
the occiput and sacrum,

Contracture of the chest muscle? interferes with inspiration; con-
tracture of the abdominai muscles produces retraction of the abdomen.

Ketention of urine and faeces is a common symptom, and isattributed
to spasm of the vesical and rectal sphincters. The urine is generally
scanty, dark in color, and contains a sediment.

Not infrequently there are changes in the pupils {contraction or in-
equality) as the result of disturbed innervation of the cilio-spinal centre.

Other symptoms, such as acceleration of the pulse and respiration,
etc., depend upon the fever, rather than upon the meningitis.

Tiie symptoms described must be regarded as irritative phenomena,
and form the first stage of the disease. Recovery may occur, or the dis-
ease may progress to t"he second or paralytic stage. ITie transitioaisnot
sharply defined, and irritative and paralytic symptoms are often present,
at the same time. Paralytic symptoms must be looked for when the
nerve roots are changed to such an extent as to rander conduction im-
possible. Antesthesia and analgesia take the place of hyperesthesia and
nyperalgesia. The muscles become paretic, then paralyzed, and show
the signs of degeneration reaction, They undergo degenerative atropliy
after the disease has lasted for some time. Reflex irritability ia abol-
ished. The function of the bladder is disturbed — at first retention,
later incontinence. The urine ia often unusually watery, pale, and
abundant; it sometimes contains sugar.

These symptoms may also disappear. Indeed, recovery mayoccur in
a comparatively short time, if the paralysis is the result of pressure, rather
than of parenchymatous changes in the nerves. In many cases, per-
manent paralysis and atrophy of certain muscles are left over, or the signa
of a chronic spinal affection make their appearance.

Great dangers may arise if the inflammatory process extends upwards
and attacks the medulla oblongata. Thiaisshownbydifficultyinspeech
and deglutition, frequent vomiting, irregular respirations, which some-
times assume the Cheyne-Stokes type; the pulse, at first slow, becomes
ao rapid that it can no longer be counted, and the temperature often
becomes hyperpyrexia!. Death may result from suffocation, paralysia
of the heart, or excessive rise of temperature.

The disease sometimes lasts only a few days, occasionally weeks and
months: seqiielie may persist for life.

IV. DiAososis, — The diagnosis ia neually easy. It ia diatinguished
from rheumatism of the muscles of the back by the facts that, in the lai-
^^tM affection, severe and febrile conatitutional symptoms are gener-
^^■BjT absent, that the muscles are tender on pressure, and that there
^^Bb no muecnlar twitchinga. sensory disturbances in remote parts or vea-
^^■il symptoms. Meningitis with extensive, long-continued muscular
^^^Witcnings may simulate tetanus, but the latter presents no sensory

170 DISEASES OF THE SPINAL MENINGES.

changes and bladder symptoms, the muscles of mastication ^nerallt
take part in the tonic contractions, and the contractions are increased
by peripheral irritations. Finally, acute meningitis may be mistaken
for acute myelitis. In myelitis the irritative symptoms are less promi-
nent, while paralysis generally develops early. In myelitis the pams in
the back are less and hypcrsesthesia is generally absent, while anaesthe-
sia develops very early; vesical paralysis and ammoniacal decomposition
of the urine are soon produced; fever is slight or absent; trophic cuta-
neous changes are more frequent than in meningitis.

V. Prognosis. — The prognosis is always grave. The more promi-
nent the paralytic symptoms the more dangerous is the situation. If
symptoms of implication of the m.edulla oblongata or brain make their
appearance, recovery is exceptional. It must also be remembered that
permanent paralyses and atrophies are left over not inf requently, or that
the signs of a chronic spinal affection finally develop.

VI. Tbeatmekt. — This is similar to that of acute myelitis (vide
page 88).

4. Chronic Spinal Meningitis.

I. Etiology. — Chronic spinal meningitis or leptomeningitis either
develops as such from the start, or it forms the terminal stage of an acute
attack. The latter is ai)t to occur if there are repeated exacerbations of
the inflammation in rapid succession, or if injunous influences exercise
their effect during the stage of convalescence.

The etiology is, in part, the same as that of acute meningitis, but
certain etiological peculiarities must be taken into consideration. Thus,
there can be no doubt that certain cases are produced by alcoholic ex-
ces8es. Chronic meningitis also occurs in syphilis and leprosy. Ac-
cording to Koehler, chronic diseases of the lungs, heart, or liver predis-
pose to the disease by producing circulatory stasis. Finally, it often,
indeed almost constantly, accompanies many chronic diseases of the cord;
for example, tabes dorsalis, multiple sclerosis, etc. Most authors regard
the meningitis, under such circumstances, as a sequel and complication
of the chronic spinal affection, while others consider the meningitis pri-
mary, the spinal disease secondary.

II. Anatomical Changes.— The lesions rarely extend over the
entire length of the cord, but are generally confined to more or less ex-
tensive, often multiple foci. The lower portions are most frequently,
the upper cervical region rarely, affected. The changes are usually more
marked on the posterior surface.

Chronic meningitis is characterized by thickening and fibrous opaci-
ties of the pia mater and araclinoid. The new-formed connective tissue
may attain a thickness of several millimetres, and feel as hard as carti-
lage. Calcification and ossification also occur, particularly in the arach-
noid tissue.

In many cases the inflamed parts are unusually filled with blood,
particularly in the veins and capillaries. There may also be an abnormal
production of pigment, resulting in brownish-red or black patches (secon-
aary to previous nemorrhages). It must be remembered that pigmenta-
tion of the meninges, particularly in the cervical region, occurs in nealthy
individuals in old age.

There are numerous, sometimes very extensive adhesions to the dura
mater. The spinal fiuid is often excessive in amount, and is not infre-

quently cloudy and mixed with flocciUi,
more purulent character.

Oil niakiu^ a transverse section of the cord, it ie sometimeB seen that
the prolongatious of the pia mater into the Bubstaiice of the spinal cord
are unusually broad. The pia mater becomes so adherent to the cord
that it cannot be detached from the latter without producing losses of
substance.

The dura mate r presents thickening, calcification, and adhesions, and
its inner snrface ia often nodular and granular. The microscope reveals
connective-tissue proliferations which contain chalky concretions.

The nerve roots are often flat and atrophic, the result of compression
by the connective-tissue new-formations. Internally they present in-
flammatory processes, and the microscope not infrequently shows degen-
erative changes in the nerve fibres.

The spinal cord may contain macroscopic or microscopic foci of dis-
ease—annular sclerosis, ascending and descending secondary degenera-
tion, destruction of nerve fibres, interstitial proliferation of connective
tissue in spots, etc.

III. SvuiTosis. — The symptoms are similariu many respects to those
of acute meningitis, but they are less violent, more often present remis-
sions and exacerbations, and are unattended with fever, unless accompa-
nied by some febrile complication. We will merely point out that the
symptoms are irritative or paralytic, or a combination of the two.

There are frequent complaints of pain and stiffness in the spine, and
of rigidity of the oack of the neck, if the disease is situated sufficiently
high. Toe pains increase on motion, but not on pressure upon the
spme. Complaint is often made of a cincture feeling and radiating
pains in the limbs. Uyperssthesia and parfesthesire are often noticed
m the beginning, and are followed ata later period by anoesthesia, which
is usually incomplete. Q. Fischer observed polysestheaia in a number
of casc^. Tonic orclonic muscular twitcliings or contractures occur very
commonly, aud micturition ami defecation are often delayed. If the
compression of the nerve roots increases or their nerve fibres degenerate,
paralytic symptoms will become prominent. They appear more fre-
quently as paresis than paralysis, and often inorease in doreal decubitus,
in other cases during the erect position. They are followed by degener-
ative atrophy of the paralyzed muscles, degeneration reaction, and aboli-
tion of reflex Irritability. Paralysis of the bladder and rectum, and
decubitus will ensue if the lower spinal nerves or the cord itself areimpli.
cated.

The disease sometimes lasts for years. It may terminate in recovery,
or permanent paralyses and atrophy remain, or acute fatal exacerbations
develop, or the process extends to the medulla oblongata, or death is tha
result of decubitus, or of cystitis aod ammoniacal decomposition of
urine. Chvostck claims thfLt the calcareous plates mentioned above (bat
whose inflammatory origin is not always certain) may be the source of
verv obstinate pains.

IV. D1AON06IS. — The diagnosis is sometimes very difficult, and if it
is associated with an affection of the cord itself, it will be almost im-
possible to differentiate the symptoms of both diseases. In general, tho
principles laid down in the differential diagnosis of myelitis hold good
iiere. The onset of the malady may be mistaken for tabes, but the lat-
ter presents no paralytic symptoms, pupillary changes are generally no-

, ticed, the aueesthesia is more murkud, tho patellar reflex disappears early,

i'i

Pfc/y.s'/^ii. — Tee f r'vzTiwJ d«pecij tui tb* aun-t Actors « :iiit
>: iU.uu ni«:ilii2iiii, ki^j thu U tlA^ true o' t

5. .If?niii^«4/ Ap^/plcry,

( IIiBmotorrhach it. )

I. AxaTomical Cba^coes. — Meningeal hemoirfaages acmr mae^-f^r-
'jij'-fitiv itiff ttm liy.nte pcri'lurul cellular tisnie which sepArazcs the jui
Hiiil<:r fr'f ru tb^ ton v Hpinitl oinal. They Gil the epidnnd sp«ce i Fx-

id iptD*) cord (>clM*inaUc1.
ad. smchnidd ; Av, poMartw ■■■"
root ; 1 rpr, ^>idai»l mpaCB : t air.

I r/ir), mill urn kiinwii an c))i(1ural apoplexy. A second site is the
luml N|iin(i (Ii'ifr. ml, a sdr). Imtwocn thcdu'raaQd arachnoid (sobdn-
It- iii'iu'luiiiiilnl ii|io]ili'xy). FiTiiilly, hemorrhages may occur in the
inl tiNHiii' liotwi'iiii |.tii> uriM^luioiil iiml \>m mater, the ■aubarachnoid
•• (i''i(;. nn. ,i mir), iiiii] urn kimwii iia suuiirachuoid apoplexy.

II i>|)iilurul ii|ii)|ilt'Kv, tliK lii'iuiirrliHgo rarely extends along the entire
. Iiiit iiiilv over II fi'tv vt'rii'brn'. or occll^D in Bevenil scattered focL

!ii'iiMn'liiii;o iH Hiitiii'tiiiii'H cnuliiu'il to tho posterior sarface, or also
iiil.t 111 lh« hitU's; il. nirt'ly iuv«lvi>» tiie entire circumference of the
'I'lin IiIihhI iji'iii'nilly riirmn dark-Rnl, loose clots, whicll may bew
iisi\,. urt III |.iish ihf liiiru inwnnU mid compress the cord. The
1 ilsolf. in- iiH iHiiiT Hiirriu'i'. may jtrcsent bloody suffusions, and ex-
iisiiiiH lu-o iiisn nSs;irvi'.l in tlu' tiorvi- roots. The vessels of the dura
i-r atv nfU'ii a';i;;i>;.ifit. Sivi'inlury clmnRes are slight or entirely ab-

'»l :

Tll.t>.|

tuilii'j

L< that these lesions are capable of re*

DISEASES OF THE SPINAL MENINGES. 17C

covery. The blood-clots are probably absorbed as in other organs, and
deposits of pigment and adhesions are ge lerally left over. In especially
unfavorable cases there may be irreparable atrophy of some of the nerve
roots and grave changes in the substance of the spinal cord.

The changes in subdural apoplexy are the same as in internal hemor-
rhagic pachymeningitis (vide page 166).

In subarachnoid apoplexy, the amount of blood may be very consider-
able. It is sometimes derived from hemorrhages within the skull, and
may extend along the entire length of the cord. The spinal cord and
nerve roots are not infrequently compressed.

II. Etiology. — Meningeal apoplexy is one of the rarer diseases, and
is more common in men than in women. In some cases no cause can be
discovered. Not infrequently it is attributed to injury (incised and gun-
shot wounds, fall, blow or violent concussion of the spine, lifting heavy
loads, instrumental extraction of the new-bom).

In some cases the hemorrhage is associated with diseases of adjacent
organs (tuberculosis or cancer of the spine, rupture of aortic aneurism
into the spinal canal, acute inflammations of the cord and its menin-
ges).

It is sometimes the result of excessive active or passive congestion of
the meninges. This occurs in suppressio mensium, or suppressed hem-
orrhoidal hemorrhages, in cardiac hypertrophy, violent excitement; in
those who have died of tetanus, eclampsia, epilepsy, chorea, hydropho-
bia or asphyxia; in toxic spasms; in chronic diseases of the heart, lungs
and liver.

Meningeal hemorrhages sometimes occur in infectious diseases, as
the result of so-called blood dissolution or the hemorrhagic diathesis.

Finally, they may be derived from a cerebral hemorrhage which has
flown into the spinal canal, or from rupture of the vertebral or spinal
artery.

It is not known whether the hemorrhage is ever the result of pri-
mary affections of the vessels.

III. Symptoms. — The symptoms are characterizd by their sudden
onset and apyrexial course. Prodromata are rare and result from conges-
tion of the cerebral and spinal meninges (slight pains in the back, a feel-
ing of heaviness, etc.). blight febrile movement sometimes occurs on
the second or third day as the result of reactive inflammation.

Consciousness almost always remains intact, unless the hemorrhage
is situated very high, or is very large in amount.

The patients suddenly complain of pain in a certain part of the spine.
The pains often extend along the entire spine, shoot into the arms, cnest,
abdomen, or legs, according to the site of the hemorrhage, and give rise
to a cincture feeling around the chest or belly. The spine is not tender,
but there is a feeling of stiffness, and even rigidity of the back of the neck
if the hemorrhage is situated high up. These symptoms result in part
from irritation of the meninges, in part from irritation o^the nerve
roots.

Irritative and paralytic symptoms may be closely connected in the
further course of the disease. The former include hypersesthesia of the
skin, parsesthesia, tonic and clonic muscular twitchmgs and contrac-
tures; the latter include partial, rarely complete, anaesthesia and motor
paralysis. The paralyses are often slight at first, but increase at the end
of a few hours. In other cases, the paralysis improves very rapidly.
Atrophy of the muscles, degeneration reaction, and abolition of reflex

174 DISEASES OF THE SPINAL MENINGES.

excitability may be expected if the nerve roots are compressed for a long
time. If the substance of the spinal cord is affected, paralysis of the
bladder and rectum^ cystitis, and decubitus may develop.

As a rule^ the disease lasts from two to eight weeks, but in not a few
cases the duration is much longer. Death sometimes occurs, with symp-
toms of shock, very soon after the beginning of the hemorrhage. In
other cases, the hemorrhage is situated so high that death results from
disturbances of innervation in the medulla oblongata. The disease is
sometimes complicated with meningitis, and the extension of the latter
to the medulla oblongata causes the fatal termination. Recovery is often
incomplete, and permanent paralysis and atrophy of groups of muscles
are left over.

IV. Diagnosis. — The diagnosis is generally easy; special import-
ance must be attached to the apoplectiform beginning of the symptoms,
and their apyrexial course. In acute spinal meningitis, there is febrile
movement, tne irritative symptoms are more intense, and the symptoms
develop more gradually. In acute myelitis and in hemorrhage into the
cord, the pains are slight or absent, paralytic symptoms predominate,
and there is a rapid development of trophic disturbances, decubitus,
paralysis of the bladder, and decomposition of the urine. In concussion
of the spine, also, the irritative symptoms are less marked, paralytic
symptoms are prominent from the beginning.

The localization of the hemorrhage is not diflBcult. If the lumbar
cord is affected, the symptoms refer chiefly to the lower limbs, bladder,
and perineal region, and priapism is occasionally observed; hemorrhages
into the dorsal region are attended by a cincture feeling around the ab-
domen or thorax; cervical hemorrhages are attended by irritative and
paralytic symptoms in the upper limbs; hemorrhages in still higher
regions are followed by bulbar symptoms. In addition, the localization
of the pain in the spine must be taken into consideration. Whether
the hemorrhage is epidural, subdural, or subarachnoidal depends par-
ticularly on the etiology.

V. Prognosis. — A relatively large number of cases terminate in com-
plete, or almost complete, recovery. The situation is so much more
serious the nearer the hemorrhage is to the medulla oblongata, the larger
it is, and the more the nerve roots and cord are compressed.*

VI. Treatment. — This is similar to that of hemorrhages into the
substance of the spinal cord (vide page 81).

6. Tumors of the Spi)ial Meninges,

I. Anatomical Changes. — These tumors may be epidural, subdural, or sub-
arachnoidal, but clinically their symptoms depend merely on irritation of the
meninges and of the substance of the cord or paralysis of these parts by exces-
sive compression. Tumors which measure more than ten centimetres in length
or four to five centimetres in thickness are exceedingly rare. Further g^wth is
only possible by proliferation through the intervertebral foramina and continued
growth outside of the spinal canal, or by implication of the bodies of the verte-
brae in the neoplastic process.

Meningeal tumors start most frequently from the dura mater, and are situ-
ated either upon its outer surface or project from its inner surface into the
subdural space; they start less frequently from the pia mater or arachnoid tissue.
The meninges in the vicinity are often inflamed. The growths are generally
round or oval in shape, and often bore a hole into the substance of the cord (vide
Figs. 87 and 88). They are almost always single, rarely multiple. In some cases,
tumors are found only on the spinal meninges, in others they are also present in
the cranial cavity, the spine, adjacent organs, or remote parts of the body.

DI8KASEB OF TBB SPINAL MSmNOSB.

Fibroma, lipoma, myxoma. Barcoma, psammoma, melanoma.
tubercle, (pimma. enchoniiroma, osteoma, and carciaonia are
meningeal tumors which bavi^ bi?en described.

Cancer of the meninges is rarely primary, but usually extends from adjacent
parts or epreoda by metaataflie. Closely allied to neoplasms are the animaT para-
sites, VIE,, echinococci and cyaticercua cellutoss [in one case reported by
Westphal).

Circumscribed foci of inflammation and hemorrhage of the meninges are co-
ordinate with tumors from a clinical stamlpoint.

After the neoplasmuhaveattained a certain sife. they compress the nerve coots
and spinal cord. At flrst the nerve roots are swollen, succulent, and reddened;
later they become gray and atrophic. Cumpression of the cord rarely gives rise
to simple circular atrophy, but, as a general tiling, to cr>mpreBsion myeJilirt which
ia especially apt to progress below tJie site of compression, and not infrequently
gives rise to secondary degeneration. In rare cases, there is purulent liquetactiou
of the lower portion of the cord.

II, Etioloot.— Meningeal tumors occur most frequently in males in rhiddle
lite. Their causes are generally unknown. They are Bometimes attributed to
injury and cold. According to soma authors, the tumors are apt to dev
^ rapidly during pregnancy and the puerperal condition. Leydi

Turn.

t po;Uible

Tumors are

sidera mental excitement, especially fright, i
hereditary in some families.

Ill, Syhftous. — As a rule, symptoms do not appear until the nerve roots or
spinal cord are affected, They are sometimes preceded for years by peculiar
painful sensations in certain parts of the spine, which may increase on making
certain movements, and are probably the result of local imtatioik by the tumor.
Some portions of the spine may he tender on pressure.

The irritative symptoms increase in eevetity when the tumor begins to grow.
The patients complain of a cincture feeling, and suHer from radiating pains in
the limbs, cutaneous hypersBstbesia and partesthesiee; tonic and clonic muscular
twilchinga and oontractures make tlieir appearance.

The stago of irritation passes more or less suddenly into that of paralysis,
characterized by aniesthesia, and paresis or paralysis of the muscles. If these
symptoms depeiLd on compression and subsequent degeneration of the nerve
routs, atrophy of the muBcles, degeneration reaction, and loss of reflex excita-
bility will soon make tlieir api>earunce.

In other casea. the paratytio symptoms indicate implication of the cord. If
the tumor starts from the anterior surface of the meninges, muscular paralysis
will occur very early; if it starts from the posterior surface, aenaorydisturbanoea
1 'irill be more prominent.

176 DISEASES OF THE MEDdLLA OBLONGATA.

In Bome cases, the compression is confined to one-half of the cord, and the
symptoms of a unilateral i^ion are produced, i. e,, paralysis and hypernethesia
on the Bide of the compression, ansesthesia on the other side (vide page 188).

If the tumor simply interrupts conduction in a transverse section of the cord,
paraplegia. ansBSthesia, paralysis of the bladder and rectum, increase of the
tendon reflexes and of reflex excitability are noticeable.

If simple compression is followed by compression myelitis which extends deep
into the lumbar cord, reflex irritability becomes lost, the paralyzed muscles
atrophy, and lose their electrical excitability.

Descending degeneration of the pyramid tracts may be suspected if muscular
contracture and twitchings set in and the tendon reflexes are markedly
increased.

As a matter of course, the clinical aistory may vary from time to time.

As a rule, the disease progresses uninterruptedly to an unfavorable termina-
tion. Recovery is only possible in the case of inflammatory and syphilitic pro-
ducts. The disease may last months or years. Death is sometimes the result of
marasmus, or is l>rouf2;ht about by the primary tumor in other orKanf». In
some cases, it results from decubitus or cystitis and ammoniac^ decomposition
of the urine. Acute meningitis sometimes develops and proves fataL . If the
tumors are situated very nigh, oulbar symptoms may be prcxluced and terminate
in death.

IV. DiAQNOSis.-^No single symptom is positive evidence of a meningeal
tumor. The same symptoms also occur in other conditions. We infer that
they are produced by tumors when the presence of new growths may be demon-
strated in other organs or in the vicinity of the spinal column, or when the patient
is scrofulous, phthisical, or sypliilitic. If these diagnostic aids are wanting, we
must suspect a meningeal tumor if there are symptoms of increasing compres-
sion of the cord, which start in a circumscribed region.

The diagnosis of the level of the tumor is usually easy. Sometimes it is evi-
dent from visible changes in the spine: in other cases the patients feel pain in
this spot, or the spine is tender over certain parts. In addition, we are aided by
the situation of the cincture feeling, and the distribution of the eccentric pains,
sensory disturbances, and paralyses.

In tumors of the cauda equina, the patients complain of the most violent
pains in the sacral region, ansBsthesia develops, with paralysis and atrophy of
the muscles, abolition of electrical and reflex excitability, and the bladder and
rectum are often paralyzed. True spinal symptoms (motor and sensory para-
plegia) are absent, and the symptoms occur only in the distribution of certain
peripheral nerves.

V. Prognosis.— Recovery is possible in those tumors alone which are the
result of syphilis.

VI. Treatment. — The treatment is similar to that of intramedullary tumors.

PART III.
DISEASES OF THE MEDULLA OBLONGATA.

1. Progressive Bulbar Paralysis. Olosso-labio-laryngeal Paralysis,

I. Etiology. — Progressive bulbar paralysis depends on disappear-
ance of the large ganglion cells of the nerve nuclei situated in the floor
of the fourth ventricle. These cells correspond in function and anato-
mical arrangement to the large ganglion cells in the anterior horns of
the spinal cord.

The disease is not very frequent, nor is it exceedingly rare. It is
more common in men than in women, and from the age of lorty to sixty
years; it is also somewhat more frequent among the better classes.

Colds and injuries of all kinds are often mentioned as direct causes.
Stein described a case as the result of strain from protracted blowing of
wind instruments. It has also been attributed to mental excitement.

DI8KASKS OF THE HEDCLLA OBI.ONOATA.

The influence of hereditjr liiu not been proven witli certaintj. Sypbilis ia
* montionHd as a cause iu a number of cases. The first aymptoma sometimea
develop during conToieacence from infectious diaenees.

ProgresBive bulbar paralysis may be primary or aecondary. The
former variety develops independently, not infrequently extends sec-
ondarily to the spinal cord, and gives rise to the symptoms of spinal
progressive muscular- atrophy. The secondary form ioIIowb progressive
muscular atrophy or amyotrophic lateral sclerosis.

II. SiMPTOiie. — As a rule, the disease begins gradually, and its
further progress is also slow but uninterrupted. In very rare ca«es, it
has a sort of apoplectiform beginning, as in Kaaamaul's patient, who
suddenly noticed difficulty in speech wliilo preaching. The prodromata
generally consist of tearing pains in the back of the neck and occiput,
a feeling of constriction in tlie throat, and dizziness. In one of Leyaen'a
cases the disease began with attacks of dyspncea.

The Urst manifest symptom is difficulty in the movement of the
ton^o, shown bj^ subjective and objective changes in speech and masti-
catiou. The patients quickly grow tired from talking nr chewing, and
articulation becomes indistinct.

Difficulty in movement and visible atrophy of the li]>a (paralysis and
atrophy oC the orhicnlaris oris) gradually develop. Then symptoms
occur which must be attributed to paralysis of the muscles of the palate,
pharynx, and larynit.

All the symptoms are bilateral. Bamberger has recently reported
a case, however, in which the affection appeared to bo unilateral, but no
autopsy could bo obtained.

Ill rare cases, the disease begins in the lips. It almost always
advances uninterruptedly, though slig'ht remissions and exacerbations
sometimes occur. In one of his patients, Kussmaul noticed the exacer-
bations at the period of menstruation.

The paralysis of tbe tongue begins as mere impairment of motion, but gradu-

: ._. liysis. The tong^ue tben can no loDger be moved in

floor of the mouth like a lifelega niasB; the baclc-
1 sometimes retain conaiderikbls vigor.
i undergoes atrophy. Its surface is furrowed and

.._ .__ iiniHhe<l, and, on attempting to protrude it, active

libriltary controotions become visible.

At tneeante time, the difficulties in speaking and eating become more marked,
and increase still more when the other groups of muscles mentioned above
l>econie paralyied. Among the vowels, the articulation of i is affected most (re-
qiiE^ntly. because this requires the approximation of the dorsum of tlie tcmgue to
the hard palate. Among the consonants b and sch are the ones wliich are flrst
lost, then g, t, k, g, t in succession, and l^iioUy d and n. All these disturbances
are purely mechanical (anarthria or paralytic alalia).

The parulj^slB of the tongue also mtf rttres with the formation of a bolus and
with deglutition. The tongue cannot form the food into a bolus or remove par-
ticles which have pasni'd between the gums and cheek. The patient is often
compelled, by the aid of the finger or a 8)>oon, to bring the food back into the
buccal cavity. Since the tongue, by its apposition against the hard palate, must
force the bolus backwards, paralysis o( the tongue itself sufficed to produce dio-
turbanoea of deglutition. Some patients push the bolus backwards with the
fingere, etc., or bend the head strongly backwards so that the bolus may fall
bacRwarda from the action of gravity.

If the orbicularis oris become paralysed, the difScuItiea in articulation and
mastication increase. Among the vowels, the prouunciation of o and u is first
tendereil impossible because it necessitates the puckering of the mouth; later i
' e disappear, while a is retained so long as pronation is at nil possible. Th9

ally passes into complete paralysis. The tong^ue then can no longer be moved
uiiy direction, and lies on the floor of the mouth like a lifeless mass; the baclc-
w;ir'l movements of the organ sometimes retain conaiderabls vigor.

In man^ cases the tongue undergoes atrophy. Its surface is furrowed and

■riiikled, its volume is dim

wul

DISEASES OF THE MEDCLLLA OBW)!IGATA.

eauBouuits are aSecl«d in the ToUoiviiig order: at first, p and/, then it and iii,
flnaUjip.

As a result of the paralysis of the lips, the mouth is constantly kept more or
less open, so tliat flitid or solid food ia apt to regurgitate in part from the mouth.

This paralysis ie also one ot the causes of the salivation from which the
patients suffer almost constantlj. In part, however, this B;rmptom is the result
of the di'sturbancB of deglutition. The salivation generaUy ceases spontaneously
at night, when the patients assume the dorsal decuhitus, and the aaCva may eiow
backwards. In some cases, the amount of Balira has been found to be increiued.
probablv as the result of irritation of Ilie centres of soHvary secretion eituated in
the medulla oblongata. Some authors regard the salivation as paralytio in jB
origin— it occurs alter section ot the chorda tympani nerve — but the ■' —

I EipreHsion in progreaHire bulbar jjuraljals. Att«r Lerdan.

It of saliva Is sometimes too large to be explained in this
man? patients, the saliva flows almost incessautlv out of both angles of the
mouth, and this may give rise to erythema of the chin.

Atrophy of the paralyzed lips is often evident upon feeling them between the
thumb and index linger. The patients are unable to pucker the lips in order to
kiss, blow, etc. Tlie mouth appears to be widened ; the entire expression of the
face is chanced, particularly if other facial muscles have undergone atrophy
(levator anguli oris, quadratus menti, buccinator, etc.). The frontal branches at
the faciaJ nerve are usually unaffected, so that the mobile forehead contrasts
very strongly with the mask-like, lower half of the (ace with its tearful expres-
sion. The face also manifests an expression of astonishment (vide Fig, 89).

Paralysis of the palatal muscles increawa the disturbances in articulation and
deglutition. Speech becomes n,i<ial, :tii<l the enunciation of b and^ Iwcomes im-

DISEASES OF THE MEDULLA OBLOKOATA. Il9

possible if a sufficiently large cnrrent of air maj escape through the noBS, on ac-
count of imperfect closure uf tlie naso-pharyngeal cavity. B and p then sound
like me, we, or/e. but resume their normnl acoustic character if boui postrils are
closed, nith the Qngers and the escape of air tlirough t)ie nose is thus i>r«Ten.ted.
The patients often swallow the wrong wav. On inspection, the palatal arch ap-
pears to Iw flaccid, sometimes more dependent on oneside than on the other, movee
very little or not at all during phonation, and flutters to and fro during vigorous
respiratory movements.

Speech gradually degenerates into an unintelligible grunting, so that tlie pa-
tients must express themselves in writing or, if the arms are paralyzed, by making
signs with the eyes or nicvements of tlie head. On account of paralysis uf the
vocal cords and patency of the glottis during phonation, the latter act requires
the expenditure of a lar^e amount of air and vigorous action of the abdominal
musi^les, so that the patients rapidly grow tired.

Paralysis of the organs ot deglutition is shown by the increasing disturlunces
during the act of deglutition. The bolus often remainsin the pharynx or letiopba-
gUB, and puts the patient in danger of suffocation. After a while, the food ac-
cumulates, during deglutition, between the anterior surface of the epiglottis and
base of the tongue in the pyriform sinunefi, and distends them tosuch an extent as
to interfere with respiration. Many patients must l>e nourished entirely with the
cesophageal sound.

Paralysis of the muscles of the larynx interferes with deglutition, inasmuch
as the food may enter the larynx, on account of its imperfect closure. This may
be the source of foreign-body pneumonia. If closure of the larynx is impaired,
on account of paralvsis of the depressor epiglottidis, bits of sulid food are espe-
cially apt to enter tne larynx. A second formof closure of the larynx is produced
during d^lutition by the approximation of the aryttenoid cartilages and srv-
epiglottic folds. If this is impaired, fluids are particularly apt to enter the

The laryneoscope often shows impaired mobility and diminished tension of
the vocal cords, or even complete paralysis of the recurrent laryngeals.

Paralysis ot the muscular roat of tlie bronchi is also said to occur, and to be
manifested by difficulty in yawning, coughing, hawking, etc.

The paralyses described above occur in the distribution of the hypo-
glossal, (tIosso- pharyngeal, piieumogaetric, spinal accessory, and facial
nerves. Other cerebral nerves are rarely affected. In one case, Ilerard
described paralysis of the abducena nerve. Paralysis of the motor
branches of the trigeminus has also boeii reported.

The muscles of tho back of the neck are often atrophied, so that the

Pliead siiika over forwards and can be rotated very sligutly or nut at all.
The muscles of the thenar and hypothenar cminencea, and the interosaei
often undergo atrophy and paralysis, and this may be followed by the
fisteiisive spread of the diseaso as in spina! progressive muscular atrophy.
Finally tho patients may become entirely helpless and incapable of
motion. Mental disturbances have not been observed hitherto. At the
most, the mood is tearful or laughing without reason.

The paralyzed muscles and nerves present partial degeneration re-
action, as in progressive muscular atrophy (vide page 127).

The mechanical excitability of the muscles has also been found in-
creased. The occurrence of diplegic contractions possesses no special
signi Seance.

Oulunoous Bensibility is always nncbanged. t^omo patients complain
of pains in the neck and occiput, and also in the back and limbs if pro-
gressive muscular atrophy develops.

tThe reflex irritability of the mucouB membrane of the mouth,
pharynx, and larynx is often abolished or greatly diminished. Krishaber
noticed this as one of the first symptoms in two cases.
The rliseaso runs a chronic course, the average duration being one to
throe y»;ari. In one of Leydeu'acases it lasted seven years. Death may

JtLA OBLOSQATA.

be the reanlt of increasing marasmas from defective nutrition, of " fo(^
eign-body" pneumouia, of attacks of dvspu(£u or sudden lieart failare
from (laralyais of the pneuniogastric and spinal accessory. In B!umen-
tbal's case the dangerous dyepua>a did not anbaido until trachootomy had
been performed.

Fatal attacks of syncope also develop in some cases. We most not
forget to mention that paralysis of the pneumogastric and B|>iiut! occea-
sory is also shown by the constant or parosysmal increase in the fre-
quency of the pulse (to one hundred and fifty per minute). Thta is
sometimes preceded by retardation of the pulse.

Ill, Anatomical Ohanoes, — The anatomical changes affect the
nerve nuclei of the floor of the fourth ventricle, and the corresponding
nerves and muscles. The sympathetic and the spinal ganglia have been
found intact.

The changes in the bulbar nuclei are exactly like those found in the

anterior horns of the cord in spinal progressivo muscular atrophy. The
laree ganglion cells atro|)hy and disappear, generally as the result of
yellow pigment degeneration. The cells are filled more and more witli
golden yellow, granular pigment, the nuclei are at first concealed and then
disappear, the cells become smaller and smaller, lose their processes, and
finally form small round clumps of pigment, which may also undergo
absorption (vide Figs. 90 and 01).

Whether the process is a simple degenerative atrophy or a primari-
inflammatory change in the ganglion cells, or whether the ganglion cell's
are affected secondarily to inmLmmatory interstitial processes, is etitl
unsettled. In our opimon th^fHan, like progreu|l|dUBOular atrophy,
is a primary degenerative ata^H^Hjtfie ganglio^^^^HK

Macroscopically, the me^^^^^Hjj^war in^^^^^^Bdi flattening,
narrowing, and changes ii^^^^^^^^B|pe of ^^^^^^^1(8 also been
described. It may al

DISEASES OF THE HEDITLLA OBLOmiATA,

in chromic acid or cliromates. Although extensive cliaDgea i
uncJer the microscope.

The emerging nerve roots are also atrophied and degenerated, so that,
on transverse section through the medulla oblongata, their fibres are
found atrophied or have disappeared (vide Fig. 92).

The process affects adjacent nerve nuclei. It begins almost always
in the nuulei of the hypoglossal nerve, which are situated in the lower
half of the medulla, nest to the median line (Fig. 93. 4 hk). The nuclei
of the spinal accessory and pneumogastric are immediately adjacent (Fig.
93. 6 t'k. and 7 aeek), and are soon involved in the process. But the
nucleus of the acoustic nerve (Fig. 03. 5 ak) almost always escapes, so
that auditory disturbances constitute very rare Bymptoms. The facial is
inTolved very early, although its nucleus is situated in the upper half of

rousb Uis mmlullB obloneaca lo proenwatm bulbnr pBrKlTilB ; hji, hyv"-

IIU illwiiiwarance otilie minKlInn wlls; tw. atroplilsJ^reniBJnHDf tbe roix

FB i)[ lliH hrpoglatHus -, yn, pyratuld trscl i ov, oUtary body. Eolsrsed 6 times. AJCer

the modnlla (Pig. 9-3, 2 fa). Acconling to many writers, however, there
IB also another facial nucleus in tbe lower half of the medulla, about at
the level of the nuclei of the hypoglossua and spinal accessory nerves.
Tho implication of the glogso-pharyugeal nerve is not astonishing, since
its nucleus is situated deep in the medulla, immediately adjacent to that
of the pneuraogastric. The nucleus of the trigeminus, corresponding to

tthe locus cceruleus (Fig. 93, 1 k'), is so far from the main site of the
morbid process that it usually escapes, and hence disturbances in masti-
«ation are rare in this diseaso. Implication of the abducens mav be
expected more frequently, since its nucleus is very close to the root dbrds

182 msBAflsa op the mkdulla obloitoata.

of the facial nerve aod, immediately adjacent to the knee of the facial
fibres, corresponds to the eminentia teres (Fig. 93, 3 et).

Fig. 94 shows a transTene section of the medulla oblongata, ocnreaponding to
about the middle ot the olivary bodies; Fig. 95 shows the poEiUs of exit of the
different nerves.

The changes within the medulla oblongata are not alwaye oonflned to the
nerve nuclei and the correeponding nerves. The surrounding parts present in.
crease of the interstitial oonneotfve tissue, accumulatloti of granulo-fattf ceils
and amyloid bodies, andde^enerativeatrophy of the nerve fibres. IntbeiraUBof
the blood-vessels, we eometimss noticed thicKeuing, nuclear proUfetation, fatty
degeneration, and accumulation of fat granules, ^ranulo-fatty cells and roand
oeUs in the lymphatic sheaths. Disease of the formatio reticularis and olivary
bodies lias lieen deeoribed, but particularly ctumges in the pyramid tracts. In one
case, Leyden found changes in the latter extending upwards Into the poiia and
downwards into the decussated and nonnleouasated pyramid tracts in tbe oord.
The restiform bodies always remain intact.

The nervee in question (hypogloBaus, spinal acoeasory, paeamo-

PoMerlor mrfacaof Che medulla obloi
I Ic, locug ccemleiu (nucleus of
eiDinBiitl« lerBB (knee of the lacia

inta. shoirlDg tbe fourth venCrfole sad the nuelsl oi

the trtntnlnusl: 2 fa. lovea aatarior itaclsl ducIc
1 uerrey ; 4 hk, liTpoElossal uuoleu* : S ak. medlkn i

iplaalscc«eear7 ; t

. corpora quadrUcei

I ; pc. pedunculua oerebellj

cerebelll ad corpom
i(m, BtrltB acuKke ;

fastric, facial, glosso- pharyngeal, sometimes tbe abdnoens and motor
ranch of the trigeminus) are thin, flattened, gray, and transparent.
Under the microscope, some of them are found to consist diieflr of con-
nective tissue, while the nerve fibres have disappeared more or leas com-
pletely (degenerative atrophy).

The muscles of the tongue and face also present degenerative
changes : diminution in the size of the fibres, increase of the nuclei, dis-
appearance of the muscular substance, proliferation of the interstitial
connective tissue and its nnclei. The development of fat is sometimes
BO abundant that the muscles seem to have increased in size. Waxy de-
generation has also been observed. Despite all these changes, tbe mus-

DISEASES OF THE MEDULLA. OBLOSOATA.

cles may appear unchanged to the naked eye. In advanced cases, they
bare a light-yellow to butter-yelloi

color.

If balbar paralysis ia coraplicated with progressive muscular atrophy
or vice versa, atrophy of the large gaoglion cells of the anterior horns of
the cord will also be noticed. If bulbar paralysis complicates aniyo-
trophic lateral sclerosis, we will find a bilateral aJfection of the pyramid
tracts, degenerative atrophy of the ganglion cells iu the anterior honis
of the spinal cord, and bulbar changes (vide page 136),

IV. Diagnosis. — The diagnosis is easy. As a matter of course,
bulbar symptoms may develop, in an acute or chronic manner, in all pos-
sible diseases of the medulla oblongata, but their mode of development
will then be different. It will also be easy, as a general thine, to differen-
tiate between primary or secondary progressive bulbar paralysis.

The disease must Dedifferentiated from: «, Hemorrhages, thrombosis,
and emi/olism in the medulla oblongata; the latter generally begin sud-
denly, Ihe paralysis is often' mainly or exclusively unilateral, sensory

uoglimus : 3 Ak):. poiwrlar
iillraiT bod; : Spy, pynuald.

disturbances are frequent, there is aliseuce "i atrophy tuid f>f changes in
electrical excitability.

b. Trimors ti'/iich compress the medulla oblongata and emerging

nerves; these often produce unilateral, or mainly unilateral paralytic

(symptoms, often aftoct tbo trigeminus and acoustic nerves, profiuco

twitchings in the facial muscles and tongue, and complete degeneration

r lesctioQ in the paralyzed muscles; convulsions, vomiting, vertigo, choked

r disc, and amaurosis are frequent svmptoms.

I c. Legions of certain parts of the cerebrum sometimes give rise to
Lbnlbar symptoms, but they are then unequal on the two sides; the eleo-
Etrical irritability is retained, the muscles do not undergo atrophy, and
f iflie limbs are paralyzed,

d. Jolly described a case of mitltiph rrrmro-spinal sclerosis with

DISSiL8E9 OF THB UEDCXI^ OBLOttOATA.

marked symptoms of bulbar paralysis, but in which the medolla ob-l
longata appeared to be iutact, on autopsy, Iii cawa of this kioil, otbcir I
eymptoma are present in addition to the bulbar Bvmptoms. I

e. The disease will be mistaken for diplegia jarialis of periphe- I
ral origin only ou snpertlcial examination. In such onses, all the I
branches of the facial nerve are {)aralyzed, and there is complete de-J
generation reaction. The muecles of the tongue, palate, and larynx an J
not naralyzed. 1

V. FxOQNOSls. — The prognosis is unfavorable, since tho diseaae ad-f

? THE VEDVU^ 0BL0BrOA.TA. 185

pure air, nutritioiia food, avoidance of stimulating food aad drink, later
careful feeding with the cesophageal sound.

At the beginning of the disease, derivatives may be applied high up
on the back of the neck.

Not much can be expected from internal remedies (potassium iodide,
nitrate of silver, arsenic, strychnine, etc.).

Electricity may also be employed. The following methods have
been reeortea to: a. Galvanization, either transversely through the
mastoid proceaaes, or longitudinally through the skull; or galvamzation
of the cervical sympathetic, the anode in the neck, the cathode below
and behind the angle of the lower jiiw. i. Faradization of the paralyzed
muscles, c. Production of reflex movements of deglutition by the agency
of the galvanic current, the anode being placed on the back of the neck,
the cathode stroked rapidly and at snort intervals over the sides of
the larynx {feeble currents).

Special symptoms must sometimes he-treated. Thus, Kayser treated
salivation by subcutaneous injections of atropine (gr, ^ : 3ii8s.,:i— ^
syringeful) in the region of the chetk, and Pauvel relieved dangerous
attacks of suSocation by means of tracheotomy,

2. Hemorrhage into tko Medulla Oblongata,

1. Very little is known concerninK hemorrhages into the medulla oblongata,
on account at their extreme rarity. They are associated somewhat more fre-
quently with hemorrhages Into the pons. Under such circumstancee the aymp-
toma may be ideDlical with those of pons hemorrhage.

3. The causes are the same as in cerebral hemorrhage. The chief factoris the
rupture of so-called miliary aneurisms ; their rupture is favored by permanent
" — ease of blood pressure (left ventricular hypertrophy) or its temporary increase
iitement, drinking). Secondary hemorrhage mav occur in inflammation, Kitt-
uiiing, or compreBsion of the iiiednlla oblongata, ^estplial produced it in guinea
pigs by filigbt blows on the head.

The hemorrhage may be extremely minute (capillary), or it may l>e so exten-
sive that the medulla oblongata is almost completely destroyed.

3. Uemorrhagee of a certain extent give rise to sudden or very rapid death.
The patients, with a cry, fall lifelesa to the floor, or they become unconscious;
epileptiform spasms develop not infrequently, the breathnig becomee stertorous
or assunieii the Cheyne^tokes type, the pulse is accelerated and irregular, hyper-
pyretic temperature sets in, and ueatli occurs in a few minutes or hours.

Heraorrhaeea of smaller dimensions produce manifold symptoms. They gen-
erally begin lilce a stroke of apoplexy, tlie patients suddenly lose conscious u ess
and do not regain it until after a certain length of time. Epileptiform consul-
siona are not infrequent, but appear to be due to irritation of the adjacent pons.
Paralysis ia produced in the limbs, but particularly in the bulbar nerves (acuteor
apoplectiform bulbar paralysis). Gut, on theone hand, acute bulbar paralysis may
be entirely abeeut and, on Che other hand, it may occur in thrombotic or embolic
softening, acute inflammation, ur compreasion of the medulla oblongata.

The motor paralysis not infrequently affects aU the limlis. In other caaee, it is

heniiplegiti in ita distribution or, if the hemorrhage is very amall. produces only

monoplegia. Hemorrhage at the decussation may give rise to crossed paralysis,

i, <., paralysis of the arm on one side, of the leg on the opposite aide of the body.

_ The paralyzed limbs present eensory disturbances if sensory fibres are also

Mflected by the hemorrhage.

E Paralysis of the bulbar nerves is associated with paralysis of the limbs if the
oemorrhage affects the nuclei on the floor of the fourth ventricle, the nerve bun-
dles in their intramedullary course, or the bulbar nerves at their points of exit.
The facial, hypoglossus, glosso-pharyngeal, vagus, spinal accessory, st'oustic, ab-
dacens, and trigeminus may be affected in varying oombinations, unilaterally or
bilaterally. The corresponding clinical symptoms are : pamlyata of the face,
ir, palate, paralytic disturbance of artioulalion (anarthria), Interference with

^^_(Ongu<

186 DISEASES OF THE MEDULLA OBLONGATA.

mastication and deglutition, dyspnoea, acceleration and irregularity of the pulse;
singultus, Tomiting, deafness, strabismus, and sensory disturbances in the face.

The hemorrhage may be situated in such a locaut^ as to cause hemiplegia
alternans, i, e., paralysis of the limbs on the side^oppoeite to the hemorrhage, par-
alysis of the bulbar nerves on the same side. The hemorrhage has evidently af-
fected the bulbar nerves after their (more central) decussation, while the pyramid
tracts are affected before their decussation.

In some cases, the cerebral nerves are not paralyzed, but manifest evidences ol
irritation, particularly in the trigeminal distribution (trismus).

4. The diagnosis is only possible to one who possesses a thorough knowledge of
the anatomy and physiology of the medulla. Even then, iu the migority of
casest, the intactness of the pons Varolii cannot be ascertained with certainty, nor
can embolism or thrombosis of the arteries of the medulla be poeitively ex*
eluded.

The prognosis is very gprave; the treatment is similar to that of cerebral hem-
orrhage.

3. Embolism and Thrombosis of the Arteries of the Medulla Oblongata.

1. The etiology and anatomical changes are the same as in cerebral embolism
and thrombosis. Thrombosis is the result of compression, and of arterio-mdeiotic
and endarteritic changes (the latter often depend on syphilis); embolism usually
follows endocardial chan^ in the left heart.

Thrombosis or embolism is followed by necrotic softening (red, vellow, or
white) in the district in which the circulation of blood has been abolished. In
some cases, only the finest arteries are affected, and fine, almost punctate infarc-
tions are then found, particularly on the floor of the fourth ventricle. They are
distinctly wedge-shaped, the base being directed upwards, the apex downwards.

Thrombotic and embolic softening of the medulla is sometimes associated
with a similar condition in other parts of the brain.

2. Embolism and thrombosis in the medulla oblongata give rise to acute or
apoplectiform bulbar paralysis. The symptoms vary, however, according to the
vascular district in which the circulation has been abolished.

The medulla oblongata is supplied with blood bv the vertebral and basilar
arteries. The vertebral arteries supply direct vessels to the nerve roots alone,
while the substance of the medulla is supplied by two main branches of the ver-
tebral arteries, viz., the anterior spinal artery and the posterior inferior cere>
bellar arteries (vide Fig. 96, 12, chip, 15, spp).

The branches of the anterior spinal artery pass at a right angle to the median
fissure of the medulla, and their terminal arteries pass to the floor of the fourth
ventricle, where they surround with a capillary network the nuclei of the
hypoglossus, spinal accessory, and the supposed lower facial nucleus.

The inferior cerebellar arter^r supplies the pyramids, olivary bodies, and cho-
roid plexus of the fourth ventricle, either directly or by means of the posterior
spinal artery which springs from it.

Hence, the symptomatology will vary according as the thrombosis or embo-
lism affects the anterior spinal artery or the posterior inferior cerebellar artery;
the former is followed by paralysis of the hypoglossus, spinal accessory, and
facial nerve, the latter by motor aisturbances in the limbs. If the entire trunk
of one of the vertebral arteries is occluded, the symptomatology will consist of
paralysis of the bulbar nerves and the limbs. The left vertebral artery is plugged
more frequently than the right, because it leaves the subclavian artery on the
cardiac side of the arch, so that the current of blood runs more nearly in a
straight line from the right subclavian.

The anterior spinal artery is not infrequently present on one side alone, and
then is generally derived from the left vertebral. In such cases, the occlusion of
one vertebral artery may possibly give rise to the symptoms of bilateral bulbar
paralysis.

The basilar artery, by means of branches from its lower half, supplies the
nuclei of the pneumogastric, glosso-pharyngeus, and acoustic, while the upper
half sends branches to the nuclei of the facial (upper nucleus), abducens, ociuo-
motor, and trochlearis. Extensive bulbar paralysis is to he particularly looked
for when the vertebral and basilar arteries are both affected. Plug^ng of the
I'^wer part of the basilar artery is especially dangerous, since vagus paitdysismay
pivt? !i.>«' to j-uddon death.

It is true that these consi derations are Bchemfttio. but their proper under-
standing' is necessary in order not to lose the thread in the labyriDtb of innu*
merable variations which may be presented in different cases.

3. Sudden death may occur in tliromboais or emboiism of the medulla ob-
longattk, as in extensive hemorrhages into tliis locality.

In other oaaes, the ayraptonia are those of an attacK of apoplexy, with loss of
consciousness and occasionally with convulsions. The apoplectic onset may he
absent if small veiiaels alone are affected or the thrombus forms slowly. Some
patient* suffer from dizziness and vomiting, or they complain of increasing weak-
ness wliich. in a few hours, advances to complete paralysis.

The paralysis may be confined to the limbs (distribution of the inferior cere-
bellar artery) or to the bulbar nerves (anterior spinal and basilar arteries), or it
affects t>i>lh. It is sometimes unilateral, sometiraes alternating, sometimes
I bilateral, Bilateral paralysis is sometimes the result of a unilateral lesion.

Distribution of the arteries at the ba«e o( Om bralo. ACMr Henlo.
r c«rebral artery : •!. coa, siiterlor cammualcaCIng artarj' ; S. cm, mtddle oerobrkl

. .. rt,iDtanial earacid srlery : S. cA. choroid ortei? i a.eop, pomerlor oaDiinuDic*tlu«

, tntrr ; 7, epe. poHerior oerebnl •rtery ; 8. cfti, suparJor □erabeUu' artery : 9. efcio, Kilorlor
■MoramMlar artery; 10, aud.Auditcry artery: ll.ba, txulUr artery ; is. ebip. potterlor
I •-'--■— eeraMUfartsry : IS. v. right TnrMbral arterr ; It. ipa, anlvrtor tplnal artery: 19, (pp.
* ninal artary ; L Of. olfedory ner»a i II. Op, optlo nerT* ; III. ocm, oculo-moior

V.trg, trtKemlnus aerv^ : VI. nb. abduaeai cervs ; TO. fae, facial nsrve -. vm. ae,

Bcouitio nervB ; IX. pi, KloBao-ptuuyDeeui nerve.

The paralysis of the bulbar nerves produces effects similar to those described in
the article on hemorrhage into tlio medulla. Sensory disturbances may he
present or absent. Senator reported a case of thrombiwia of tlie left vertebral
artery with softening in the external, posterior, inferior portion of the left half
of the medulla in which there was alternate paralysis of sensation, i. e., ancestlie-
sia of the left aide of the face and the rieht limbs.

Tbe paralysea may disappear gradually if the circulatory disturbances subside.

n the medulla

188 DISEASES OF THS HXDULLA. 0BLOIIOA.TA.

In other cum ooiuiderable improTemeat ooonn. OraeocnMUrr dcgsnenUoD
<leTelapB in the pynmid tracts, and is shown b7 contractures aod increaae of tbs
tendon reflexes in the affected extremities. The dtaoBse mar then iTsriiitJr
ainTotropluc lateral sclerosis, but is distingaished from it bj tba sadden onset
and the absence of marked atrophy,

4. ThediSerentialdiaffnOBisfromhemorrhsgeisnot alwajrsposeible. Haifced
improvement of the parairrsis, the existence of aortic or mitral lesions, prerkMU
svphilis, advanced age, and anerio-eclerosia of peripheral arterie* favor Uie
diaKnoBis of emboliam and thromboeia.

Griesinger states that if both vertebrals or the basilar artery are occln^d,
oompreeaion ot both carotids will produce epileptiform conrulsiona as the reeolt
of cerebral anfemia, but Levden called att«Dtion to the danger asaociated with
this experiment and to the fact that oompressicHi of the carotids may produce
-onrulsions although the basilar is not occluded.

5. The prognoMs is grave. The treatment is the same as that of cerebnl

_mbolism and thrombosis. If there i« •—■- -' -'—•■-'="— '--' ■ '-

introduced through the cesophageal sou

4. Acute Inflammation of the Medulla Oblongata.
{Bulbar Myelitis.)

by Leyden prove that acute inflammatory im o c* —
oblongata as in the niinal cord. We wul not dov
consider the seconoary inflammations following
thrombosis, embolism, hemorrhage, andoomprenon
of the nieduUa, or wlilcli extend to this organ bua
the spinal cord.

2. The disease occurred in irregularly scattered,
usually small foci which were occasionally Tfiilik
only f^ter microscopical examination. These fod
were in a condition of red softening. The walls ef
the veseeta were thickened, their nuclei Increased,
the lymphatic eiieaths were filled with cellolar ele-
ments; there were perivascular hemorrhsKes, gnn-
ulo-fatty cells, and swelling of the axis-cylindera.

8. The causes of the disease are unknown. One

Tnnivena netlon itirousb tbe of Leyden's casen occurred in a drunkard, the two
medulla oblonnta^ with nu- others had suffered from articular rheumatism.
??!r?^!!fJ?°'r9f*?=,'?.?f.'2- 4. The symptoms are those of an acute, apoplec-

tiform bulbar paralyHis, with or without mriuyiil
"hili^"" '"" "" """'■' of the limbs. Different nerves are aflectea aocord-
"^ ing to the number, situation, and size of the inflam-

matory foci. There is slight eievation of tem-
perature. The disease always terminates fatally, with increasing difSculty ot
respiration. Duration of the disease, four to ten days.

S, The differentiation of the disease from hemorrhnge, embolism, softening,
or compression is facilitated by the following featuree: the absence of an apoplec-
tic onset and convulsions, tlie presence of sUght fever, and increase of the symp-
toms until the fatal termination.

0. The disease is always fatal. The treatment is the same as that of acute
myelitis (vide page 88).

5. Tumors of the Medulla Oblongata.

2. Solitary tubercles constitute the most frequent variety. One to three ate
founJ, in the shape of yellow, cheesy nodules, which may attain the siae of a
walnut. Next in frequency are the gliomata. R. Schulti reports a case iu which
a glioma was found at the oottom of a cyst filled with brown fluid (previous soft-
eninc ':}. Mosler and Yirchow have described a gliosarconta. Fibroma, myxoma,
papilloiua. and carcinoma are also mentioned. The possibility of the der^op
Tnent of gummata mu<<t also be taken into consideration. The tumors may Uwl
the siee of a pigeon's egg.

DISEASES OF THE MEDULLA, 0BL0SaA.1i.

paralytic phenomena on the part of the bulbar

i;<jiibres hmu uurvtfs.

Tlie gtinerat eymptoma include headache (particularly in the back of the neck
and occiput, and often increasing into paroxysms), freiiuent vomiting, dizzineaa,
stnggeniiK gait, ohoked disc, impairment of viaion, and epileptiform oonvuUionB.

Itie chief local symptoms are irritation and paralysis of the bulbar nerves and
nuclei (strabismus, paraly-iia of the face, tongue, pharynx, palate, vocal cords,

L, iuii) impairment of hearing, respiratory disturbances, and slow-
ness of (he pulse and obeli Ma[« singultus). Paralysis of the limbs and sensory dis-
turbancps may also aroif ; ataxic movements have been described. Polyuria and
mellituria are indicative of implication of the fourth ventricle. Quioc observed
forced deviatiua of tlie head und eyes to the right in a case of tumor of the left-
half of the medulla.

AmoiiK eighteen cases Bernbardt found;

Headaclie, in more tlian half the cases.

Vomiting^, in more than half the coses.

Dizziness, six tiiiie«.

Epileptiform cimvul-ioris, one time.

Diplojiia, three times.

Imimirriient of sight, live times. ■

Dii.ilatl'in of the pupils, five times.

P^iralyaia of ocular musclett. in more thao half the cases.

Audiliiry disturbiinctw, four times.

Speifcli disturbances, four times.

DirHi'ulty in deglutition, one time.

Singultus, two tiinen.

Hetardation of the pulse, two times. *

Difficulty in briiiithinK, two times.

Changes in the urinary secretion, three times.

In some coses, however, the tumors give rise to no syRiptotna. They are
■ometim'vt found accidentally, or may give rise tosudden death, Scbultz recently
^epo^tl:^l u cast; which ha<i prnsented nil the symptoms of spastic spinal paralysis.

Tlie mental condition is often alfected; inalmosthalf the cases reported by
Bernliiinlt, mention is made of impairment of memory, confusion of ideas, diu-
ness, and itomnolence.

4. The diagnosis presents numerous difficulties and is often entirely impo»-
sibti>. Aa a rule, it cau bo made only with a certain degree of probability. The
diagnoeiit ia pasie^t when the general and local symptoms are present in their com-
plete'ie»a. It is distinguishea from progresaive bulbar paralysis by the fact that
no general symptoms are noticeable in the latter disease.

5. The prognosis is relatively favorable in aypbilis; otherwiae it is unfavor-
able. The treaimwnt ia purely symptomatic.

G. Injuries, Acute or Slow Compression of the Medulla Oblongata.

1. Injuries to the medulla are produced by stab and gunshot wounds and
blows. . Ad a rule, death takes place at once. The patients fall lifeless to the
ground, with or without a cry and epileptiform convulsions.

2. Injuries some times give rise to the symptoms of acute compression. This
ia observed in trocturea and dialucationa of the upper oervical vertebrae, particu-
larly the atlas and axis (as the result of a fallorblow, or of tuberculous processes).
Dislocation of the odontoid process occurs with relative frequency, and the
bone then presses backwards on the medulla. It is a noteworthy fact that tuber-
cu]nrpi'i>ce««B mav develop in the vertebrae in n latent manner, and give rise
unexpectedly to a fatal termination. Sudden liemorrhage, for example, from A
ruptureil aneurism of the basilar artery, may produce rapid death, with symptoms
of acute compression of the medulla. It the injury ia slight, the maintenance
of life ia conceivable 1 the acute developmentof bulbar symptoms vrould indicate
a lesion of the me<lulla,

S. SlowcompreMionof the medulla often depends upon thickenings or *o-
cuniulatioDS of pus at the occiput or upper cervic^ vertebrse, such as occur not
iiifiequently in tuberculosis. Thickening of the odontoid process (sometimea,

erhaim, the result of rachitis) occasionally gives rise to compression ; or this may
pi-iHlnwd liy iin abnormal condition of the occiput or posterior arch of the

190 DISEASES OF THE BRAIN.

atlas and odontoid process. The compression is occasionally the result of deform-
ing arthritis of the joints between the occiput, atlas, and odontoid process, par-
ticularly if the latter has undergone thickening. The same mechanical effects
will be produced by tumors growing from adjacent parts, and bv aneurisms.

Compression of the medulla nut alone exercises a mechanical effect, but also
gives rise to a compression myelitis.

The clinical history consists of bulbar irritative and paralytic phenomena, the
former appearing at the onset, the latter at the close. The symptomatologT
varies according to the site of compression. Paralysis sometimes appears in the
limbs earlier than in the bulbar nerves. Spastic spinal paralysis has been ob-
served when the pyramid tracts were chiefly affected. The diagnosis may be im-
possible. Prognosis usually unfavorable. Treatment symptomatic.

PART IV.
DISEASES OF THE BRAIN.

Diagnostic Preliminary Remarks.

Since the time of Griesinger, we distinguish between diffuse cerebral
symptoms and focal symptoms in diseases within the cranial cavity.

The diffuse cerebral symptoms are of a general nature, and merely
indicate that the brain has been affected in some way. They are the
resul^ of changes of pressure within the cranium, of circulatorv dis-
turbances, of so-called general shock, or of a number of factors, these
symptoms include: vertigo, clouded consciousness, impairment of intelli-
gence, flashes of light before the eyes, ringing in the ears, vomiting,
changes in the frequency and rhythm of the pulse, irregularity in re-
spiration, epileptiiorm convulsions, etc. Certain diseases witnin the
skull produce diffuse symptoms alone, for example, affections of the
meninges.

The focal symptoms, on the other hand, possess a special diagnostic
significance because they indicate a definite site of disease in the brain.
They are divided into two groups, viz. : irritative and paralytic sjrmp-
toms. Like the diffuse symptoms, the focal symptoms may exist as such
from the start, but as a general thing they may be looked for only when
the lesion develops slowly, is small in extent, and does not possess those
properties which would give rise to the development of diffuse cerebral
symptoms.

Diffuse and local symptoms are often associated with one another.
The former are often present at the start, but the more they subside the
more distinct the focal symptoms become. This is well illustrated in
cerebral hemorrhage. On the other hand, focal symptoms may open the
scene, and are followed by diffuse symptoms, the more the lesion in-
creases in extent.

The focal symptoms may be direct or indirect, temporary or perma-
nent.

The indirect focal symptoms are the result of a sort of action at a
distance. The lesion is perhaps remote from the part towards which the
symptoms point, but it acts upon the latter from a distance in such a
manner as if the part in question were directly injured. Almost all cere-
bral lesions possess the peculiarity of exercising a more or less distinct
remote action, and of impairing the cerebral functions beyond their
proper boundaries. In many of them the remote effects disappear after
a time (temporary focal symptoms). The symptoms which remain permA-

DI8XASB8 OF THE BBAIN.

191

nently, becatise the lesion has produced irreparable changes in the par--
encbyma of the brain, constitateB the permanent focal symptoms,

A distinct line cannot always bo drawn between focal and diffuse
symptome, or between the different varieties of focal symptoms. Vomit-
inf^, for example, is often a diffuse symptom, bat sometimes attains the
dignity of a focal symptom.

a. Focal Symptoms in Diseases of the Cerebral Cortex.
The motor fanctions of the brain are confined almost exclusively to
the anterior and posterior central convolations and the paracentral
lobule.

X/fi

Coovolutli

of, niparioT (flnt) trooUl cor

bnior (third) Iroi — " '■

MDirolutlOQ ; 4 (lew. aatorf or oenCnl oonTOlutlon : B JiciB, posterior central
(uptrlcr perietal lobule ; 7 up", Intertor [MrtetiJ lobule: S ol', nipertor
DluUoa ; A mt", middle (iscodJ) teiapoiml conrolutloa ; 10 uf". Inferior

horlionlal r&miu

; 13 vo"', iofeiior (Lhlrd) ooolplul conTolutlon ; 14 op. operou-
I : Ifl u^. inferior frontiU flnure i IT/t. flHuraof Srlriiu,
j< .1.- ,-ft gijg . ig ^_ eanun or Rolando;

tl if, superior (flrit) uid In

oad) temporal Oiiiuea ;

IBy-.d! _

0] fpft, parleto-ooolpltal flvun
Bl ipc, pnecentral flaure.

This region ia easily found on the surfaiM of the brain. The chief landmark
is the fisBure of Rolando, which b^ins near the median border of the hemi-
sphere and runs obliquel; forwards and dowDwards (Fig. W, 18 ef). Its lower «x-
^mit^ ia situated between the two rami of the Sylvian fissure, of which the
poatenor is known as the horizontal ramus, the anterior as the asoending ramus.
Anteriorly the liasiire of Bolando is bounded by the anterior central convolution

192

DISEASES OF THE BBAIN,

> ig. 08, 4 vcw), posteriorly by the posterior central conyolution (Fig. 06, 5 hcnf^
jtn merKO into one another above and below the fissure of Rolando. The para-
central lobule IB visible on the median aspect of the hemisphere (Fig. 99, 1 tprtU
and is the direct continuation of the central convolutions. It is bound poeterioriy
by the calloso-mar^nal fissure which separates it from the prsBcanens (Fig. 99.
6pc), and its anterior boundary is formed by a prolongation of the calloeo-raai^
ginal fissure (Fig. 99, 4 acm), to which Schwalbe applies the term paracentral fis-
sure (Fig. 99, 2 aprc).

The symptoms of an affection of the motor regions of the cortex will
vary according as the brain substance is destroyed or irritated. In the
former event paralysis, in the latter spasm of the muscles will be pro-
duced. But Doth symptoms are often associated with one another, and
this very feature is, to a certain extent, pathognomonic of cortical
lesions.

The distribution of the paralytic and spasmodic phenomena depends

Fio. 99.

Median aspect of die surface of the brain. After Ecker.
1 Iprc, paracentral lobule Qefc centre) ; 9 aprc^ paracentral fissure ; 8 tc, end of the fiasiire of Ro-
lando ; 4 acm, calloso-margrinal fissure ; 5pc, prsscuneus ; 6 cu, cuneus : 7 cc, corpus caUosnm ;
8 sru, gyrus uncinatus ; 9 gh^ gjrrus hippocampi ; 10 /po, parieto-ocoipltal fiasure ; 11 /oo, cal-
carine fissure.

■

upon the extent of the lesion. It is characteristic of circumscribed
cortical affections that they not infrequently produce monoplegias of the
face, arm, leg, or even of small nerve tracts, with the character of a
central paralysis in regard to the electrical current (no degeneration
reaction).

If the entire motor region of the cortex is destroyed, the symptoms
of ordinary cerebral hemiplegia are produced, i, e., the arm and leg are
paralyzed on the side opposite to the lesion, and also the facial nerve so
lar as regards the lirancnes to the mouth and cheeks, while the frontal
branch is unaffected, and the patient retains the power of wrinkling the
forehead and closing the lid. In uncomplicated cases, sensory and vaso-
motor disturbances are absent, but ptosis (paralysis of the oculo-motor
nerve) has been observed in some cases. The paralysis is exaoUj like
that produced by destruction ol the inUin&l eai^^ale^ or certain portions

DISEASES OF THE BBAIN. 198

of the centrnm ovale which coutaiTi the radiating fibres from the inter-
nal capsule. At times the cortical origin of the paralysis can be inferred
from ttie etiology alone. This includes particularly injuries to the skull
and embolism or thrombosis of cortical arteries. Tne two latter pro-
cesaes generally involve the middle cerebral artery, which supplies the
motor cortical region.

But as this artery also supplies the third frontal convoltition and
island of Reil, those parts are often affected in addition to the motor
region proper, and aphasia will result if the lesion is situated on the
left side. In diffuse cortical paralysis, ae in that produced by lesion of
the internal capsule, improvement la generally more marked m the leg
than in the arm; after a while contractures, spasms, and increase of the
tendon reflexes make their appearance, the result of secondary degener-
ation of the pyramid tracts from the cerebral cortex to the spinal cord.

SchemaUo reprewnt

The more circumscribed the cortical lesion, the more the paralysis
will he confined to the distribution of individual nerves (nerves of the
arm or leg, facial, hypoglossal, and motor oculi nerves).

So far as known at present, the motor cortical centres are located as
follows:

a. Centre for the leg in the upper third of the anterior central con-
volution and the paracentral lobule, and in the upper two-tfairda of the
posterior central convolution.

d. Centre for the arms in the middle third of the anterior (perhaps
also the posterior) central convolution.

c. Centre for tho facial nerve in the lower third of the anterior cen-
tral convolution.

rf. Centre for the hypoglossal nerve, in the lower part of the an-
terior central convolution (vide Fig. 100).
13

194 DI8EABB8 OF THE BRAIN.

Hence, if the lesion extends in circumference, the paralysis may
spread from one motor tract to an adjacent one. For example, if tint
lesion began in the arm centre and spread upwards, it will be foUowed
by paralysis of the leg; if it spread downwards, by paralysis of the
facial nerve. Cortical paralysis of the leg and face alone is hardly con-
ceiyable, since the lesion must then have jumped over the motor tract
of the arm. The gradual conversion of a monople^ into an incom-
plete and finally, perhaps, a complete hemiplegia is characteristic of
cortical disease.

Disease of the motor part of the cortex may also produce muscular
spasms and epileptiform convulsions, whose distribution varies accord-
ing to the extent of the irritating lesion. But an unilateral cortical
lesion may also ^ve rise to general convulsions. Consciousness may or
may not be retained during the attacks. In the latter eyent they may
be mistaken for ordinary epilepsy, but in cortical (Jacksonian) epilepsy
the convulsions always began m a certain limb, or are confined to that
part.

The not infrequent combination of paralysis and epileptiform twitch-
in^s is especially characteristic of disease of the cortex. As a general
thing, the twitcnin^ follow the paralysis.

The following data favor the diagnosis of an affection of the motor
cortical centres:

a. Monoplegias of a central quality as regards the electrical current
(no degeneration reaction).

b. Hemiplegias with implication of the motor oculi nerve (ptosis),
later contracture and increased tendon reflexes as the result of secondary
degeneration of the pyramid tracts.

c. Development of liemiplegias from the combination of circumscribed
paralyses ; owing to the gradual spread of the lesion to adjacent cortical
motor centres.

d. Epileptiform convulsions in individual nerve tracts, or general
epileptiform convulsions, which always begin in the same limb, and are
often attended with loss of consciousness ( Jacksonian or cortical epi-
lepsy).

e. A combination of spasms and paralysis in individual nerve tracts,
or in a hemiplegic form.

We will now consider the lesions of other portions of the cortex.

Diseases of the cortex of the frontal lobe are related to certain dis-
turbances of speech, known as aphasia, which will be discussed in detail
at a later period. It will here suffice to remark that motor or ataxic
aphasia is associated with lesions of the pars opercularis of the third
frontal convolutions (Fig. 98, 3 mf"). The larger part of the frontal cor-
tex is probably associated with purely psychical processes; it has been
found to be markedly atrophied in dementia paralytica and idiocy.

Diseases of the cortex of the temporal lobe are related, nnaer cer-
tain circumstances, to auditory disturbances and, as a consequence, to
sensory aphasia (word-deafness). According to Wernicke, this form of
aphasia occurs only when the lesion is situated in the first (superior)
temporal convolution. The occurrence of deafness in such cases has
not been positively proven. For further details, vide page 206,

The relation of diseases of the cortex of the basal portion of the temporal
lobe to disturbances of the olfactory sense requires further investigation.

Deatmction of the 'cortex of the parietal lobe, in which, aooording

DISli:AeK8 OF THE BHADf.

19S

to Flechaig, the sensory tracts of the skiu termiuate, is said to produce
lose of muaoular bcdbh. The patients are no longer able, when the
eyes are cloaed, to tell the position of the limbs. This symptom may bo
ussociated with paralysis, if the motor portions of the cortes are also
implicated.

Lesion of the cortex of the occipital lobe is associated with visaal
disturbances (hemianopsia or hemiopia).

In order to understand this symptom, we must bear in mind that a
partial decussation of the optic fibres takes place in the optic chiasm,
and that in both optic nerves the lateral portions remain upon the same
aide, while the median portions decussate (vide Fig. 101). Hence tha

left optic nerve, for example, supplies not alone the temporal side of the
left eye, hut also the nasal portion of the right eye. If we now asaume
that each optic nerve terminates centrally in the occipital cortex of the
same side, it follows that lesions of the left occipital lobe will give rise
to an affection of both eyes, the left eye becoming blind upon the tem-
poral half, the right eye upon the nasal half of the retina. In other
words, the right half of the field of vision in each eye is lost, i. e., there
is right hemianopsia. Lesions of the right occipital lobe will produce
left nemianopsia.

Id Bome cases the hemianopaifi is not complete, and affects in unequal degrees
Ibe senses ot light, color, and apace.

Fuerstner noticed that insane patients, who suffered from diseBses of the 00-
cipilal lobe, were able to see objects, hut did not rerognize them, so thattheop-
tical images appeared to have been lost (psychical blindness).

196

DISEASES OF THE BKAIN.

h. Focal Symptoms in Diseases of the Centrum Ovale.

The centrum semioyale is the mass of white fibres which is sitnated
between the cerebral cortex and the basal ganglia. It is formed of fibres
which differ very much in function. Some connect different parts of the
cortex of the same hemisphere (association system). The symptoms pro-
duced by their destruction are unknown. Other fibres belong to the system
of the corpus callosum^ i. e., through the medium of the latter they con-
nect parts of the cortex of one hemisphere with identical parts in the other
hemisphere (commissural system). Concerning the effects of their destrao-
tion we are also in the dark. Of special importance is the radiation of the

Fig. 108.

gcc

2 9^0

Horizontal section at the level of the surface of the corpus caUosom.
1 Z90^ centrum semiovale ; 2 «pc, splenium corporis callosi ; 3 ycc, genu oorpoiis *^'«^

middle portion of the cms cerebri, which first enters the internal cap-
sule and then passes into the cortex (Fig. 103) (corona radiata). Since
this part is the means of conduction oetween the cerebral cortex and the
periphery of the body, interruption of conduction will produce, as a
matter of course, the same symptoms as a lesion of the cortex itseU, and
during life we are unable to distinguish between the two processes. The
distinction is often difficult anatomically, and we cannot always decide
with certainty whether the lesion is situated in the cortex alone, or also
implicates the immediately adjacent portion of the corona radiata. In
diseases of the corona radiata, the symptoms vary according to the
bundles of fibres which are aftected. li tlioee fibres whioh pass to the

DISEASES OF TEE BBAHT.

central convolutions are aflected, small, oircnmBCribed leaiona will pro-
duce monoplegia of this or that part; extensive leBJoOB eive rise to hemi-
plegia of the other half of the body. DeBtruction of the fi"

nviDCal «ectlon
three dlTJilo-
ee. Gorpiu mil

to the Upper temporal lobo produces word-deafness, to the occipital lobe
hemianopsia, etc.

c. I'ocal Symptoms in Diseases of the Internal Oapsuh.

The internal capsule is that mass of fibres which ia bounded inter-
nally by the optic tnalamua and caudate nucleus, extemaUy by tho lenti-
cular nucleus (vide Figs. 103 and 104). It presents an anterior and
{loslerior division, the former situated between the caudate nucleus and
enticnlar nucleus, the latter between tho optic thalamus and lenticular
nacleuB. Both divisions meet at the knee of the internal capsule (vide
Fig. 104).

The internal capsule receives the motor and sensory fibres passing
from the cortex to the crua cerebri. Heuce its destruction is attended
with motor and sensory paralysia.

The motor tracts are situated in the posterior division of the internal
capsule, about at tho posterior end of its middle third, the paths of con-
duction for the facial nerve being situated iu front of those for thelimba.
Tho sensory tracts for the skin, musclea, and cerebral nerves are situated
in the posterior third of tho posterior division (vide Fig. 104). The
symptoms produced by lesions of other parte of the internal capsule ate
□nknowQ,

Ltarior dlTfsIon, ht, pos- |

the cortex. The frontal branch of the facial nerve, which innerratos
the frontalis, corrugator BuperciHi, and orbicularia paipebramm, remain*
anaSected, bo tfjat the patienla ivre able to wriukle the brow and does

DISEASES Of THE BBAllT.

the oves. The hypoglossal nerre also is often paralyzed. If the para-
lyais has lasted for some time, secondary degcneratioo is often produced;
it extends on the peripheral side of the lesion through the pyramid tract
of the corresponding ems (middle third) and pons Varolii, then through
the decussation of the pyramids into the lateral col umb- pyramid tract of
the opposite aide of the cord, and the anterior column-pyramid tract
of tlie eamo side.

Lesions which Are confined to the motor portion of the internal cap-
sule are rather exceptional, and it is particularly noticeable in cerebral
hemorrhages that the corpus gtriatum is also affected. This is owing to
the fact that the distribution of cerebral lesions depends upon the dis-
tribution of the blood-vessels, and the internal capsule and corpus stri-
atum are supplied by the same vessels. The usually simultaneous affec-
tion of the internal capsule and corpus etriatum long led to the erroneona
notion that cerebi'al hemiplegia depended on destruction of the latter.
At the present time the motor tracts of the internal capsule are held re-
sponsible for the symptoms, and it ia not known whether the lesion of
the corpus striatum produces anv change in the clinical history.

Lesions of the posterior third of tho posterior division of the internal
capsule are followed by cerebral hero i anesthesia. On the opposite half
of the body the patients suffer from complete cutaneous aniesthesia,
which terminates abruptly at the median line. The raucous membranes
of the lips, mouth, nose, conjunctiva, external auditory meatus, penis,
vagina, and rectum are also antesthetic. The eye, ear, nose, and tongue
are often, but not constantly, hem iau (Bathetic. Thediseaee is often asso-
ciated with vaso-motor disturbances, viz., reduess of the skin, elevation
of temperature, and diaphoresis.

Lesions which affect the middle and posterior thirds of the posterior
division of the internal capsule are followed by hemiplegia and hemian-
ffisthesia.

Some authors attribute prsehemiplegio and posthemiplegic chorea and athe.
tosia to disease of the hindmost portions nt the posterior diviHion of the internal
capsule, but this theory has not been sulBciently well established.

(I. Fiiral Sifinptoms in Diseases of Ike Basal Ganglia

The term basal ganglia is applied to tho lenticular nucleus (Figs. 108
and 104, 2 H^) and caudate nucleus (Figs, 103 and 104. 3 ?tc). Lesions
may be present in both ganglia, withont giving rise to permanent motor
disturbances. Transitory paralyses are obaei'ved more frequently, but
are probably the result of pressure on the adjacent internal capsule.

e. Focal St/mptoins in Diseases of Ihe Crura Cerebri.

The characteristic symptom of diseases of the cms cerebri ooasiste of
alternate hemiplegia with regard to the motor oculi nerve, i. e., the
upper and lower limbs, generally the facial and hypoglossal nerves, even
the trigeminus, are paralyzed upon the side of the body opposite to the
lesion; tho motor oculi is paralyzed on the same side. This strikio^
feature is readily understood. I'ig. 95 III. ocin shows the intimate re*
lation of this norve to the crus cerebri, and this is shown still more dis-
tinctly on a transverse section through tho cms (vide Fig. 105). It
contains two stnita, the lower one or foot of the peduncle being more
important clinically, because it contains in its middle portion the pyiEk*

900 DIBBASBS or THB BBUB.

mid tract, which passes from the central convolationH through the
iDternal capBnle and the peduncle of the pons, medalla, and pyramid
tracts in the cord. The npper stratum of the cms is knoint as the teg-
mentum. Both strata are separated by a narrow zoneof blackish-brown
substance (substantia nigra) which results from marked pigmentation of
the ganglion cells in this locality. Paralysis of the limbs is produced
by lesions of the crus only when the pyramid tract is injured. The
paralysis occurs almost always upon tne side opposite to the lesiim,
because the larger part of the pyramid tract decussates in the pyramids.
PantlysiB of the limbs on the same side as the lesion is only conceivable
if there is no decussation. The root fibres of the motor oonli nerve paa
to the median portion of the substantia nigra, pass through it, and ex-
tend upwards to their nucleus (Fig. 105, 1 ocm and 2 tocm), which,
atnated alongside the raphe, occupies the space between the pos-

TmuTeiM Kctian ot tbe cerebral peduncle, comepoodfaK to the pottarior put of the ulterior
corpora qiudrigemlna. EnluKed 8 limes, 1 ocm. omilD-molor nflrre ; » Ihkih, noeleus o( ihe
ooulo-mouir aerr* ; S py, p^nJiild tract ; 4 m, lubeMntln nisra ; G rk, red noeletu ; S u. aqua-
dact ol Bf Mua.

terior commissure and the border of the anterior and posterior corpora
quadrigemina. Hence it ia evident that the paralysis of the motor ocnU
nerve will not be crossed like that of the limbs, since the fibres of the
nerve decussate on the central aspect of the nucleus, and, therefore, of
a lesion of the cms. Moreover, this nerve may not be paralyzed in
lesions of the crus, if the median portion of the cms remains unaffected
or if the lesion is situated, not in the neighborhood of the pons, i, e.,
near the point of entrance of the nerve, but in the anterior Half of the
crus. Under the latter circumstances an hemiplegia is produced which
cannot be distinguished from that occurring in lesions of the internal
capsule. Lesions of very small extent, if they are situated in the ex-
ternal portion of the peduncle, may be lacking in symptoms, since the
pyramid tract is situated in the middle portion (Fig. 71).

Paralysis of the motor ocuU nerve is easily recogniied. On account

DISEASES or THE BBAQT. 901

ei paralysis of the levator palpebrtc saperioris, the tipper lid droops npon
the paralyzed side (ptosis) and canuot be drawn up volantarily; internal
rotation of the eye is impossible on account of paralysis of the internal
rectus, and the eye is drawn permanently outwards on account of the
preponderance of the external rectus which is applied by the abducens.
MovemeDts of the eye upwards and downwards are also abolished, and
impaired on account of paralysis of the superior and inferior recti and
inferior oblique muscles. The patients compluin of double vision, the
pupil is dilated (mydriasis), and does uot react to light.

Hemiplegia with alternate parnlyaia of the motor oculi may also occur if an
ordinary hemiplegia la Bssooiated with b basal process which paralyzea tlie nerve
on the siiie of the lesion in the cerebrum, and a differential diagnosis is not

'ays possible under auch circumstances.

The tegmentum of the cms contains sensory tracts, which pass to
le posterior third of the internal capsule, and 'thenc« to the cerebral
cortex (vide Fig. 104, Se?iii). Although it is very probable that lesions
of the tegmentum will give rise to sensory disturbances, nothing is known
positively in this regard.

^Mlwi

/. Focal Symptoms in Diseases of the Pons Varolii.

Although slight lesions sometimes produce rapid death, morbid pro-
eases in tbis region may be entirely latent. This is sometimes true of

Pio. IDS.

TTZij* rr.ahk nil', a

le wction or the [wiu Tarolil ibout i
.. ..-J, ueendlDKlrlirenilniw r<«l: VI. a.
fc. fut-lnl nene ; VlT.ft. fcM niioloi.n ;
Aw^lnn ; VIII. aCy anl«iior uwiutlo roo
pXramld tnct.

die at cne fourth veatiiule. E^nlarged 3 UmM.
1, abauceaa nerve t VI'. abk, &bducen> nualeus : VIL
VII". /c, InMnnedlata portion of fMlal on mnnene I
t ; VIU'. ae, uucleui ot ulterior aooustlc rogt ; py, '

tubercles of the pons, probably because they alowly separate, but do not
destroy the nerve fibres.

A characteristic feature of diseaaee of the pons is alternate hemi-

T THE BBAET.

plegia, in which the facial nerre is paralyzed on one side of the body
(the Bame aide as the lesion), the limbs upon the opposite side. At tM
aame time, nil the branches of the facial nerve are paralyzed as in peri-
pheral pantlyaifi. Furthermore, degeneration reaction acTelops id the
paralyzed facial muscles.

Alternate hemiplegia is not, however, a necessary result of nnilatenl

{ions lesions. It will only oocnr if the lesion is situated in the medal-
ary (lower) half of the pons, since it is the result of interruption to
conduction in the facial nerve on the peripheral aspect of its decusaa-
tioii (which takes place in the upper part of the pone)i while the fibitt

■■•fiba, niperior

which pass to the limbs (pyramid tract) i
side of their decussation.

e interrupted ou the central

If the leaioD is situated ia the upper (peduncular) portion of the pons, th«
facial nerve and the pyramid tract are injured above their decussation, bo that the
face and litnbH are paralyzed on the opposite side of the body. At the Bame time.
the frontal branch of the facial nerve rertiains unaHected, as It does in cerebral
beuiplogia. and degeneration reaction is not produced. Under such circum-
stances, the diagnosis may be very difficult unless other pons symptoms ate
present. The latter must be present in a certain combination in onler to render
the diagnosis certain. The pons symptoms include: a, paralj'Sis of otiier cere-
bral nerves, especially the tngeminuB, abducens, acoustic, hypoglossus, occasion-
ally the vagus, spinal accessory, and glosao-pharTngeus (the two latter as Ih*
result of pressure on the inp'diilla), and the motor oculi, if the peduncle is
affected; b, disturbances in articulation (anarthria); c. disturbances of deglutitiaD

(dTspba^a); d, marked contraction of the pupils; e, a tendency to epileptiform
convii iBionB. The motor paralfBiH of liie limba is associated not infrequently
with aoEeetheeia; according to aome writers, ttiia only occurs in leeiona of the
lateral third of the pons (cide Fig. 106).

The diagnosis is tepecially uifficiilt when indiTidiial Hjstems of fibres are
alone affected by the leeion. If tile pyramid tracts are alone aETected (Fig. 107,
1 pji), the limbs will be paralyzed on the opposite aide of the body if the lesion la
unilateral, indeed monoplegia is occasionally produced. Lesions near the floor
of llie fourth ventricle will give rise to paralysis of the cerebral nerves in differ-
ent combinations, according to the distribution of the lesion. The nerves may
be paralysed on the side of the lesion, or on the opposite side, according as they
are injured above the decussation (paralysis on the opposite aide) or below it
(pamlyeis on the same aide).

Lesions near the median line may give rise to paraplegic symptoms, either
because the conduction is interrupted on both sides, or because tue unilateral
lesion produces ptessure-effecta upon the opposite side. If the compression dis-
appears, the symptoms dependent on it will aUo subeida. The symptomatology
is extremely varied, because sometimes the limbs are paraplegic, while the cerebral
i paralyzed in an heiniplegio manner, or vice versa, or the cerebral

ApPEtfDII.

The diagnoeia of diaeoses of the optic thalamus is generally impossible. At alt
events, they are not associated with motor paralysis. DestmctjoD of the poetRrior
thirdof the thalamus gives rise to visual diaturbances similar to those produced by
lesions of the occipital cortex (homonymous or lateral hemianopsia). HemiaiiSM-
thesia and hemichorea, which have also been attributed to lesions of the posterior
part of the thalamus, are probably the result of pressure on the senaory tracts in
the internal capsule,

Lesions of tlie external capsule or claustrum (vide Figs. 103 and 104, 8 aek, 7 d)
cannot be diagnosed during life. They may exist without symptoms.

The symptonts of disease of the cornu Ammonia are unknown.

Lesions of the corpora quadrigemina have been associated with disturbances
of sight, paralysis of the ocular muscles, and disturbances of equilibrium, but the
number of authentic cases is small. There ia reason for believing that the ante-
rior and posterior corpora quadrigemina possess different functions, E>estruction
of the anterior pair may w aasumed to produce amblyopia or amaurosis, with
negative ophthalmoscopic appearances and absence of reaction in the pupils.
Hemianopsia may be expect^ if the lesion is unilHteral. Paralysis of branches
of the motor oculi nerve (sometlinea bilateral despite a unilateral lesion) has been
observed in injury to the posterior pair. Symptoms of cerebral ataxia have also
been attributea to tliis lesion.

Hitherto no characteristic symptoms of cerebellar diseases have been discov-
ered. The cerebellar hemispheres may undergo extensive destruction without
producing morbid symptoms during life. Nothnagel believes that diseases of
the vermis are associated with staggering gait, cerebellar ataxia, and vertigo, but
this view is contradicted by recent reports oj cases.

Diseases of the cerebellar peduncfes may run an entirely latent course. This
Is true of the anterior and posterior cerebellar peduncles, also known as the crura
oerebelliad corpora quHdrJKemlnaet medullam oblongatam. Lesions in the crura
oereltelli ad pontem may give rise to symptoms if the connection with the cere-
bellum is not entirely mlernipted and irritative effects are produced, Such lesions
result in certain forced movements in whioh the body occasionally turns com.
pletely around its vertical axte, sometimes towards the side of the lesion, sometimes
towards the opposite side. In Nouet's cose, the eves were immovable, the right
eye being directed downwards and exIernBlly, tne left eye upwards and inter-
nally. Simple lateral position of the body, una rotation of the head and eyes in
the same direction (conjugate deviation; also occur in lesions of many other
puts of the brain.

DtSitUBB OF THB BOAXS.

g. Focal Symplonu in Diseases of the Base of the Urnia.

Morbid processea at tho base of tbe brain arc characterized partira-
riv by implication of the cerebral nerves {compression paroljsis).
These paralyses generally affect ail the branches of the nerres, aol

™rve ; VII. /c. (aoial nt _

' ' Id Mterjr i fl. bypopbyali ; " "~

have the electrical characteristics of peripheral paralyaia. They are not
infrequently bilateral. If the morbid process is located in the anterior
fosBa, tba changes may be confined to tho olfactory nerves, and i
fested by loss of smell or perverse olfactory sensations (vide Fig. 108).

DIBBA5E3 OF THE BBA». 305

If the middle fossa is affected, the optic, ocnlo-motor, trochlearis, tri-
geminus, and abducena nerves are involved (Fig. 108, V., VI.); in dis-
eases of tlie posterior fossa, the facial, acoustic, glosso-pharyngens,
vagus, spinal accessory, and hypo^lossus are implicated (Fig. lOS, VII.,
Xfl.). Under the latt«r conditions, the symptomatology may be very
similar to that of progressive bulbar paralysis. The morbid process
spreads occasionally from one fossa to another, bo that very remote
nerves may become affected, In diseases of the posterior fossa, the

Eans and medulla are often aSected. and this resulta in paralysis of the
mbs. Implication of the cerebellum may give rise to tbe symptoms of
cerebellar ataxia.

th. TKe Aphasic Symptom-Complex.
{Aphasia, Agraphia, Alexia, Amimia, Apraxia, Asymbolla.)

1. The term aphasia is applied only to disturbances of speech, but
these are often associated with disturbances in the ability to write
(agraphia), to read (alexia), or to express ideas by means of gestures
(amimia), so that the patient may have lost the power of communicating
ideas to his fellow-man or of uuderetanding those of others. The pa-
tients have lost the facultaa siguntris (Kant), they suffer from asymbolia
(Finkelnburg) or aseniia (Steinthal),

There are various forms of aphasia, agraphia, alexia, and amimia,
and various combinations of the individual forms.

2. In aphasia, the most important and striking symptom is the use of
wrong words by the patient. Wernicke first showed that there are two
principal varieties of aphasia, according as there are disturbaucea in the
mechanism of speech or in the perceptive part of the faculty of speech.
The former ia known as motor or ataxic aphasia, the latter as sensory
aphasia.

The child learns to speak by hearing words and attempting to imitate
them, without associating the words, at first, with any definite idea.
The acoustic nerve of the child receives the woi-d, spoken by others, con-
ducts it to its centre in the cerebral cortex (acoustic centre), whence
other conducting paths convey it to the centre of the speech musclea,
and thence, after a while, it gives rise to volitional or co-ordinated
movements of the speech muscles innervated by the speech centre. This
process is shown schematically in Fig. 109.

The child gradually emerges from the stage of an automatic speak-
ing-machine to that of ideational speech. It learns to associate with the
word a certain idea, and in this way becomes able to understand others
and to make its own thoughts understood by others. In addition to
the cortical centres for the acoustic and the speech muscles, there also
develotia an ideational centre which converts the speech image conveyed
from toe acoustic nerve to the cortical acoustic centre into a conception,
and furthermore, by its connection with the cortical speech centre, con-
verts ideas into words. This process is shown schematically in Fig. 110.

a. In cases in which the cortical speech centre is disturbed, the pa-
tients understand everything that is said to them. They protnide the
tongue when directed to do so, point to this or that object as required—
in other words, present no disturbances in the perceptive or ideational
part ot speech. A different state of affairs is manifested when they are
hfiirected to repeat words or to clothe their own ideas va\Kn.^«i?j'6. "^^st-

206

DIHEA8E8 OF THE JSRAJN.

tnrbances then make their appearance, because the muscles of speech,
as the result of changes in their cortical centre^ have lost the power of
obeying the will and of acting together in a co-ordinated manner. In
advanced cases^ the patient is unable to repeat or to utter roluntarilj
a spoken word. Sometimes his entire vocabulary is lost, with the excep-
tion of a few words or syllables or incoherent sentences, which are con-
stantly repeated on attempting to speak. Cases of this kind are known
as motor or ataxic aphasia.

b. In disturbances of the cortical acoustic centre, the patient hean
the spoken word as an element of sound, and is by no means deaf, but
the word-image is lost, and he is, therefore, unable to understand the
spoken language of others. He does not perform any required action,

Fio. no.

ing« lot.

Association

between
theacoustio
and speech-
muscle centre

Speech-muscle tract.

▲oouBtic tract.

Speech-muscle tract.

Schematic representation of the
carried on in learning to speak.

processes Schematic representation of the .

carried on in the fully deyeloped power to
speaJc.

because he is unable to comprehend the spoken request. In examining
the patient, care must be taken to avoid the use of gestures, since he may
then perform the required action without comprehending the spoken
request. Since the connection between the acoustic tract and the cor-
tical speech centre is also interrupted, the patient is unable to repeat
a spoken word. On the other hand, he is able to express his own thoughts
in language. Kussmaul applied to this form of disease the term word-
deafness. It is a variety of sensory aphasia.

c. When the functions of the cortical speech-muscle centre and of the
acoustic centre are both impaired, total aphasia is produced. The pa-
tients are then unable to understand spoken words, to repeat them, or
to speak voluntarily without hindrance.

THBEA8E9 OF THE, BKADf.

SOT

Aa a matter of cotirse, aphaaic disturbances will be produced, not
"alone by diseasea of tbe cortical speech- muscle and acoustic centres, but
also by iuterraption of the conducting patba between tbeae centres.
Tbese forma are known as conduction -aphasia.

d. In interruption to tbe conducting paths between the cortical
Bpeech-mnscle centre and the ideational centre (vide Fig. 110, 1 S— 3 B)
the patient understands spoken words, is able to follow our directions
and can repeat spoken words, but is unable to find words wherewith to
express his own thoughts. Oases of this kind are known aa amnesic
aphasia.

e. In interruption to the conducting paths between the cortical
acoufltic centre and the centre of ideation (Vide Fig, 110, 3 Ac — 3 B),
tbe patient can repeat spoken words aud can also speak voluntarily, but
he fails to understand the words which he hears.

/. In destruction of the conducting paths between the cortical
acoustic and speech-muscle centres, the patient understands spoken
words and can speak Toluntarily, but tbe power of repeating words is in-
terfered with. The intact condition of the centre of ideation may
eliminate this defect, and paraphasia is then generally produced, t. «.,
the patients often use the wrong words in voluntary speech.

g. Interruptiona in the speecb-mnscle tract which emanate from the
cortical apeech-muacle centre will produce, so far as purely aphasio
disturbances are concerned, the same symptoms as an affection of the
the muscle centre itself, t. e., the patients understand spoken words, hut
are unable to repeat them, and cannot speak voluntarily without bin-
drancc. Since those paths must be looked for in the white matter odiacent
to the cortical speech-musclo centres, it appears to bi^impoasible durine
life to distinguish purely apbaaic disturbances produced by a corticu
leeion from those produced by a lesion in tbe adjacent white matter.
■ A. Disturbances in tho tract of the aconstic nerve w\\\ "^i^^i.-aae-a.^^^'na.-

sic symptoms similar to those resulting from dcetrtiction of thocorticd
acoustic centre itself, viz., inability to understand language, inability \»
repeat spoken words, but intactiiess of voluntary speech. The differ-
ential diagnosis between lesions in the cortical acoustic centre and ihi
adjacent white mutter is impossible.

3. Our present knowledge justifies the conclusioR that the inferior
(third) frontal convolution ib affected in motor or ataxic aphakia. ih»
Buperior (first) temporal convolation in word-deafness and. in all proba-
bility, also in amuesic aphakia; while the white matter adjacent to [be
island of Reil may be regarded as paths of association between the cor-
tical epeech centres of the inferior frontal and superior temporal codto-
lations. Aphaeio symptoms occur only in lesions of the left side of tha

4. We have remarked on a previous occasion that the distribution of

cerebral diaeasea, unlike tliose of tlie spinal cord, depends on the distri-
bution of the blood-vessels. Hencechangea in the cortical speech tracts
are aeaociated genemllj^ with diseases of the middle cerebral artery.
Embolism or tbromboBis of this vessel is the most frequent cause of
aphasia. The peripheral branches of tlie artery are rarely affected, more
frequently the main trunk of the vessel. Since this supplies not alone
the third frontal convolution, first temporal convolution, and the island
of Reil, but also the central convolutions (Fig. 112), aphasia is often
associated with right hemiplegia, and the majority of cases are mixed
forms.

Aphasia will also develop if the cortical speech centres are injured
independently of the hlood-vesaeh, for example, by direct injury,
tumors, and mflammatory products of the meninges or bones. Congen-
ital aphasia haa also been observed (four cases in boys. )

As a rule, aphasia is a permanent condition which is capable of
improvement or recovery only when other portions of the cortex become
able, as the result of practice, to take part in the ability to generate
speech,

Aphasic symptoms sometimes disappear gradually if they are not
the result of destruction of the cortical speech centres, but of functional
interference with them as the result of congestion, cedema, etc.

in addition, very brief aphasia haa been observed in hysteria, chorea,
catalepsy, after epileptic seizures, in helminthiasis and coprostasis.
In such cases we must assume temporary circulatory disturbances with-
out permanent anatomical lesions.

The prognosis and treatment depend on the primary disease^ The
aphasia itself may be treated by speech exercises which, if carried out
persisteotly, sometimes produce rapid and marked success. Aphasic
patients have been known to have the power of speech suddenly restored
as the result of violent emotions.

5. Diseases of the cerebral cortex and adjacent white matter may
also interfere with the ability to read, write, or to express ideas by means
of gestures. It is not astonishing that aphasia should often be associated
with agraphia and alexia. It is evident that writing from dictation is
only possible when the cortical acoustic centre isintact, since otherwise the
word-image could not be formed. Hence destruction of the cortical
acoustic centre will also cause inability to write according to dictation.
In disturbances of the visual centre the patients become unable to copy
printed words. The muscles employed in writing, like the speech mus-
cles, can be stimulated to co-ordinated activity from a certain centre;
if this is destroyed, the patient sulfers from motor or ataxic agraphia. If
the paths of association between the ideational centre and the cortical
centre of the muscles of writing are destroyed, the patient is unable to
write voluntarily, he suffers from amnesic agraphia.

With regard to alexia it is known that the occipital lobes contain the
cortical terminations of the optic nerve. It they are destroyed, the pa-
tients suffer from a form of alexia which corresponds to word-deafness.
They are sble to see the written characters, but the sign images are lost,
the patients have become psychically blind. It is evident that this cor-
tical centre of the optic nerve is connected by fibres of association with
the cortical speech-muscle centre, else it would be impossible to read
written characters aloud. Hence, in destruction of the cortical speech-
tscle centre, motor alexia is present in addition to motor aQhB&\»., «(A
14

^^^1

210 DISEASES OF THE BRAIN.

the patients are unable to read aloud, although they understand what

Psychical blindness does not always afiPect written characters alone. Caan
are known in which the patients looked upon objects in every-day use as thingi
unknown. When the patients were disrobed and the articles of clothing wen
then returned, they didf not know to what usee to put thero. This condition has
been termed apraxia.

Finally, the patient may lose the ability to express himself by means
of gestures (amimia). Sometimes they do not understand the gestures
of others^ sometimes they are unable to express their own ideas by means
of gestures, either because the cortical centre for the co-ordinated acti?itj
of the mimic muscles is destroyed, or because the connection between
the cortical centre of conceptions or ideas and the cortical centre of
mimic movements is interrupted.

In all these conditions, the intelligence may be unimpaired, so that
some patients carry on business in an intelligent manner, aespite the ex-
istence of marked aphasia.

A. Diseases of the Substance of the Bbaxn.

1. Ancemta of the Brain. "

I, Akatomioal Changes. — Ansemia of the brain can hardly be sepa-
rated from ansemia of the meninges. This is particularly true of anie-
mia of the brain and pia mater; tlie latter, as is well known, conveying
blood-vessels to the brain. We distinguish between general and parti^
or circumscribed cerebral anaemia.

The condition is characterized anatomically by unusual pallor of the
brain substance. The white substance has lost its pale rose-colored ap-

?iearance and has assumed a dull white, occasionally bluish-white color
especially in children). The puncta vasculosa are absent or present in
small numbers. The cortex has a pale-gray color, and the boundary be-
tween it and the subjacent white matter is often indistinct. The consist-
ence of the brain varies; it is sometimes abnormally firm and dry, some-
times unusually succulent. This depends chiefly on the etiology, the
former condition being observed when the anaemia is the result of exten-
sive losses of blood, the latter when it follows oedema of the brain. The
sulci on the surface of the brain are sometimes unusually broad.

Gk>lgi claims to have found distention and unusual filling of the perivascular
lymph spaces — perhaps a vicarious dilatation, to take the place of the Darrow ves*

sels.

The cerebro-spinal fluid is not infrequently increased in the subar-
achnoid tissue and the cerebral ventricles. The meninges are generally
pale, and the sinuses sometimes contain very little blood. In some cases
the meningeal vessels are markedly distended, compared with the pale
cerebral parenchyma.

II. Etiology. — Cerebral anaamiais the result of changes in the blood
itself or in the blood-vessels. The former include acute and chronic di-
minution of the amount of blood. Acute diminution occurs not infre-
quently after profuse losses of blood in any part of the body. In all
such cases, other organs ^Iso take part in the anaemic condition.

DISEASES OF THE BRAIN. 211

Acute general anaemia of the brain sometimes develops on account of
the vigorous efflux of blood to other parts of the body. For example,
this has been observed after the puncture of ascites, ovarian tumors, or
pleurisy. This may also occur after delivery when the uterus, freed of
its contents, becomes engorged with blood. According to H. Fischer, the
symptoms of shock are also the result of cerebral ansemisj this writer
claims that in shock there is paralj^sis of the abdominal sympathetic, and
therefore distention of the abdominal vessels supplied by it. Symptoms
of cerebral anaemia also occur at times in individuals, especially old peo-
ple, when an evacuation from the bowels takes place after long-protracted
constipation.

Somewhat similar conditions are produced by affections which dimin-
ish the ntfmber of red blood-globules in the blood, or change their char-
acter in such a manner that the final effect is equivalent to that of anae-
mia. As a rule, the symptoms of cerebral anaemia run a chronic
course in such cases. They include chlorosis, progressive pernicious
anaemia, leukaemia, cachexia, suppuration, vital losses of all kinds.

Cerebral anaemia includes the symptom-complex known as hydrooephaloid,
which is observed not infrequently in children, particularly nurslinp^, after ex-
hausting diarrhoea. Signs of cerebral anaemia are observed not mfrequently
in cancer of the oesophagus or stomach; also after typhoid fever, relapsing fever,

Eneumonia, and other febrile infectious diseases, if umnition has been produced
y fever and imperfect nutrition.

Cerebral anaemia from changes in the blood-vessels occurs in embolism
and thrombosis of the cerebral arteries, but these conditions are usually
followed very rapidly by the signs of necrotic (anaemic) softening of the
brain. They will be discussed in a subsequent section.

Stenosis or even occlusion of the vessels is sometimes produced by
compression from the outside, for example, by meningeal hemorrhages,
exudations, tumors, or oedema of the brain. The compression is some-
times produced from within, for example, in dropsy of the ventricles.
Tumors, aneurisms, exudations, arterio-sclerotic and endarteritic changes
outside the skull may also give rise to compression of the vessels.

Cerebral anaemia is sometimes the result of weakness of the heart,
for example, in fatty heart, pericarditis, and aortic stenosis.

Finally, stenosis of the cerebral vessels may be produced by vaso-
motor spasm, as the result of mental emotion or pam. Certain toxic
agents may produce spasm of the cerebral arteries, but, as a rule, they
also give rise to other symptoms which complicate the symptomatology.

III. Symptoms. — It is not astonishing that the substance of the
brain should react to anaemio conditions with functional disturbances.
But the purely anaemic symptoms are often complicated by another set
of phenomena. It has been shown by experiments that anaemia of the
brain in animals lowers the pressure within the skull. It is true that
the increased flow of cerebro-spinal fluid to the brain and the greater
distention of the perivascular lymph spaces counteract the diminution of
the cerebral pressure, but this can take place onl^ to a certain extent^
beyond which diminution of cerebral pressure with its sequelae must
ensue.

Sudden cerebral anaemia as the result of mental emotions, i. e,, from
spasm of the cerebral arteries, is attended by the following symptoms:
tne patients experience a sensation of oppression and anxiety m the
chest, especially in the praecordial region, and occasionally there is tern*

^12 DISEASES OF THE BRADf.

porary palpitation of the heart. The patients yawn inTolnntarilj, feel
chilly^ have a goose-skin^ and look pale. There is impaimient of' hear-
ing and ringing in the ears; sight is impaired until complete amauroeii
develops; vertigo and nausea set in; consciousness becomes more and
more clouded, and finallv the patients fall with a low cry or twitchings
in the face and limbs. This condition is known as fainting or syncope.
Complete recovery occurs at the end of a few seconds or minutes. In
some cases, however, syncope is followed by immediate death.

If cercbitil anaemia is the result of acute losses of blood, the symp-
toms are verv like those produced in animals by liratare of both carotid
and vertebral arteries. The symptoms mentionea above are then asso-
ciated with epileptiform convulsions, which remain absent only in indi-
viduals who are verv much reduced.

According to Marshall Hall, the symptoms of hjdrocephaloid are
divided into two stages: In the first stage, that of irritation, the face is
reddened, the eyes glistening and staring, the patient restless and fret-
ful, sleep poor and disturbed; older children are delirious. In the second
stage, that of torpor, the face is pale and pinched, the skin cool, fonta-
nelles depressed, the lids half closed, the i)upils wide, and their reaction
slow or abolished, the back of the neck is rigid; the patients are in a
condition of apathy, and suffer from convulsions. If no improvement
occurs, the coma deepens, the pulse becomes imperceptible, the respira-
tions irregular and feeble, and finally death ensues.

The symptoms of cerebral anaemia consist of irritative and paralytic
phenomena which are often associated with each other.

The psychical functions are very often disturbed, probably as the re-
sult of anaemia of the cerebral cortex. Delirium often develops, some-
times very suddenly, and not infrequently assumes a violent and maniacal
character. It may subside very rapidly, or it may last for days, or even
weeks. Delusions may arise and in rare cases persist permanently.
Some patients often suffer from obstinate insomnia (agrjrpnia), others
from apathy, somnolence, or coma.

Disturbances of special sense are often observed; ringing in the
ears, difficulty of hearing, flashes of light, impairment of vision, even
amaurosis.

The patients often complain of headache, which has been attributed
to anaemia of the dura mater; it is either unilateral or bilateral. Not
infrequently there is violent vertigo. Complaint is sometimes made of
paraesthesiae.

Spasms and paralyses are frequent symptoms of cerebral anaemia.

The respirations are not infrequently irregular, unusually profound
or superficial; there is often subjective and even objective dyspnoea

Tne pulse may be irregular, accelerated, or retarded. Nausea and
vomiting are frequent symptoms. The integument is generally pale and
feels cold, and is covered occasionally with cold perspiration. Chilly
sensations and chattering of the teeth are often observed.

It is noteworthy that the symptoms may only be present or, at least,
are increased when the patient assumes the upright position.

IV. Diagnosis. — Since some of the symptoms are the same as those
of cerebral hyperaemia, the diagnosis can only be made with certainty
when the etiological factors are taken into consideration.

V. Prognosis. — The prognosis depends upon the etiology and the in-
tensity of the cerebral anaemia. It sometimes acts as the immediate
cause of death. Eussmaul attributes prognostic importance to the con-

DISEASES' OF THE BRAIN. 213

dition of the pupils. Immediately after the occurrence of acute cere-
bral anaemia tne pupils contract^ and this is soon followed by dilatation
and loss of reaction. The return of the pupils to the normal condition
is a favorable indication.

VI. Treatment. — Brilliant results may be attained by prophylaxis.
This includes nutritious diet and tonic treatment in febrile and wasting
conditions, avoidance or rapid checking of hemorrhages, rapid relief of
infantile diarrhoea, etc. In addition, the attendants should be directed
to prevent feeble patients from assuming the upright position. The use
of the night vess^ instead of a bed-pan may be especially dangerous to
such individuals.

If the si^s of acute cerebral anaamia have developed, the patient's
head should oe kept as low as possible. If syncope occurs, the fore-
head should be ruboed with eau do Cologne, irritating substances fam-
monia, eau de Cologne) inhaled, the nasal mucous membrane tickled
with a feather, the face and chest douched with cold water, the soles of
the feet rubbed, the faradic brush applied to the skin, or, if necessary,
artificial respiration performed, for example, by faradization of the
phrenic nerve (vide page 31).

The medicinal agents include stimulants and tonics: wine, soups,
eggs, ethereal tincture of valerian (ten drops given a few times at inter-
vals of fifteen minutes), sulphuric ether (five drops on sugar, or one-
half to one syringeful subcutaneously), camphor (gr. xv.; ol. amygdalar.^
3iii., one syringeful subcutaneously), etc.

Morphine (gr. i), paraldehyde (gr. 75), or chloral hydrate (gr. xxx.),
often produce remarkably rapid results in cases of great mental excite-
ment and insomnia.

The danger arising from profuse hemorrhage must sometimes be met
by the transfusion of physiolo^cal sodium chloride solution.

In chronic cases the galvanic current has been recommended, either
a longitudinal current through the skull, the anode hi^h up on the
back of the neck (vaso-motor centre), or galvanization oi the cervical
sympathetic.

2, Hypermmia of the Brain.

I. Etiology. — Hypersemia of the substance of the brain is always
associated with a similar condition of the meninges. Cerebral conges-
tion may be acute or chronic, general (in the majority of cases) or pad^ial
(circumscribed). It may be the result of an abnormal supply of arterial
blood (active hypersemia, fluxion, congestion), or of impeded outflow of
venous blood (passive or stasis hypersBmia).

Active cerebral hypersBmia may be produced by unusually vigorous
contractions of the heart, such as occur in excessive bodily activity
(running, lifting, etc.). It may also be the result of emotional excite-
ment which stimulates the heart to increased action. As a matter of
course, its occurrence is favored by left ventricular hypertrophy, partic-
ularly the so-called idiopathic hypertrophy. The symptoms of cerebral
congestion may also appear in cardiac nypertrophy, following cirrhosis
of the kidneys, more rarely in the hypertrophy which is secondary to
valvular lesions. This is more apt to occur in aortic insufSciency, be-
cause the cardiac hypertrophy then corresponds, as a rule, to the severity
of the valvular lesion, and both lesions compensate one another. In all
these cases the cerebral hypersemia will be general.

214 DISEASES OF THis BRAIK.

This is also true of those conditions in which congestion of the bnun
is owing to the fact that large vascular areas are excluded more or less
completely from the arterial circulation. This is observed in stenosis of
the isthmus aortse^ in enlargements of the liver or extensive abdominal
tumors which compress the abdominal aorta, and thus increase the arte-
rial flow to the brain. Obstinate constipation and distention of the in*
testines with fsBces and gases may act in the same manner. After liga-
ture of one carotid the half of the brain on the other side will be
congested.

Cerebral congestion sometimes takes the place of suppressed hemor-
rhages (suppression of the menses or hemorrhoidal fluxes).

Dilatation of the cerebral vessels may be the result of vaso-motor
paralysis (starting from the cervical sympathetic), which may occur
spontaneously, or from mental or physical exertion, or the action of cer-
tain poisons (alcohol, amyl nitrite).

General cerebral hypersemia may also occur as a collateral arterial
fluxion, for example, in facial erysipelas, diphtheria, parotitis, abscises
on the outer surface of the skull, etc.

Circumscribed arterial congestion of the brain often follows other
diseases of the brain or meninges (meningitis, meningeal or cerebral
hemorrhage, tumors, abscesses, etc.).

The causes of venous congestion of the brain may be located in the
skull, the large veins, or the heart.

Thus, it occurs in thrombosis of the cerebral sinuses; in obstruction
to the escape of blood from the brain owing to compression of the in-
ternal jugular or innominate veins by inflammation in the neck or medi-
astinum, tumors in these localities, aneurism of the aorta, etc.

The outflow of venous blood is often interfered with by valvular
lesions of the heart, particularly mitral stenosis and insuflSciency and
tricuspid insufficiency; also by diseases of the heart muscle (fatty degen-
eration, development of cicatrices), and by pericarditis (from pressure
on the vena cava or implication of the heart muscle).

Venous congestion of tlie brain is also observed not infrequently in
diseases of the respiratory organs (emphysema, interstitial pneumonia,
pleurisy, chronic bronchitis, etc.). It is rare in phthisis, because this
disease runs a very slow course, and is attended by a considerable dimi-
nution in the amount of blood.

Passive cerebral congestion may be produced voluntarily by continued
straining. It is observed accordingly in diseases attended with cough,
stenosis of the air passages, lifting heavy loads, straining at stool, suffo-
cation, etc.

II. Anatomical Changes. — The anatomical changes are not always
easily recognized. They may be mistaken for post-mortem hypostasis,
but this condition is confined to the most dependent portions of the
brain. On the other hand, the symptoms of cerebral congestion may
have been present during life, but nothing is found at the autopsy. In
experiments en animals, Ackermann found that anaemia of the brain is
present in suffocation, but Jolly showed that this occurs only at the
moment of death, and that congestion of the brain is really present
during life.

Cerebral congestion is shown by the increased amount of blood and
the changed color of the brain. iJpon removing the calvarium, numer-
ous drops of blood exude from torn vessels on the outer surface of the
dura mater and the inner surface of the skull. The Pacchionian

DISEASES OF THE BRAIN. 215

foodies are unusually well supplied with bloody and^ in chronic cases^ are
often very large and numerous. The sinuses of the dura mater are
often distended with blood, and contain loose, dark clots, rarely amber-
colored or grayish-yellow clots. When the dura mater is cut hori-
zontally, the brain often protrudes through the incision as if it had been
cramped for room. Upon throwing back the halves of the dura mater,
the large veins of the pia mater (in venous congestion) are found en-
larged and distended, often sinuous; in some cases they are said to have
presented varicose dilatations. The surface of the brain often appears
flattened, the convolutions are flat and broad, the sulci narrow; the sur-
face is often very dry. Opacities and thickenings are often visible on
the arachnoid.

On section of the brain, the changed color of the parenchjrma is
particularly noticeable. The cortex is dark-red or brownish-red in ap^

?earance, while the white substance has a rosy red or hortensia color,
'he latter color is often especially marked in patches. !N'umerous dots
of blood are present in the Drain; in some cases small extravasations are
found. The pigment in the latter may undergo changes, so that yellow-
ish or rusty-brown patches result. The choroid plexuses are often dis-
tended with blood, and this is recognized mainly by the sinuosity of their
vessels. The unusual congestion is also noticeable in the ventricles.
The cut section of the brain is often unusually moist (oedema).

On microscopical examination an accumulation of red blood-globules is found
not infrequently in the adventitious Ivmph sheaths of the blood-vessels.

In some places, the walls of the blood-Tessels contain rents through which
the red blood-globules have passed into the lymph sheath, and have distended
the latter into an ampuUa-ehaped dissecting aneurism. If the congestion has
lasted a long time, the red globules undergo gradual degeneration and metamor-
phosis of their coloring matter, so that the lymph sheaths are found filled with
yeUow pigment graniues. These are especially abundant at the bifurcation of
the vessels, because the adventitious lymph sheaths in that locality are very
loose and present a larger space.

Gk>gli states that the perivascular lymph sheaths are narrow and emptv.
This indicates that an increase in the amount of blood within the skuU is only
possible if the lymphatic spaces in the brain have emptied their contents into the
spinal cord and peripheral lymphatics. This also includes the displacement of
the cerebro-spinal fiuid into the spinal canal. Some authors state that chronic
cerebral congestion results in overfilling of the p^nglion cells with yeUow pig-
ment and increase of the neuroglia in the immediate vicinity of the blood-ves^als.

Atrophy of the brain is regarded as a sequel of chronic cerebral hy-
persBmia, but in some cases the former condition is primary, the latter
secondary. Durand-Fardel also attributes the so-called 6tat cribl6 to
cerebral congestion. It consists of dilatation of the perivascular lymph
spaces, so that the blood-vessels are surrounded by gaping openings^
whose size may exceed the dimensions of the head of a pin.

III. Symptoms. — The symptoms of cerebral hvperaemia depend not
alone on the changed nutritive conditions, but also upon changes of
pressure. Jolly showed experimentally that the cerebral pressure is in-
creased in venous hypersemia as the result of ligature of the veins.

The symptoms of cerebral congestion are very similar to those of
ansBmia, and the diagnosis can sometimes be made only by taking the
etiology into consideration. Irritative and paralytic conditions of the
brain are produced in both cases.

The conditions differ according as the congestion is arterial or ve-
nous. In the former event, there is an increased su^^l^ oi \sst\*T>JcN;:^^

216 DISEASES OF THE BEAIN.

material; in the latter^ there is also poisoning with carbonic acid«
Symptoms of irritation predominate in arterial congestion, symptoms of
depression in venous congestion.

Disturbances of the psychical functions are ver^ tre^aent, manifested
by an irritable^ whimsical mood and unusual excitability, or by an apa-
thetic condition. The patients are unable to think clearly, they appear
forgetful, and are often tortured by the fear of approaching insanity.

Delirium occurs not infrequently, and illusions, hallucinations, and
maniacal attacks are also observed. If such symptoms last for a long
time or recur at short intervals^ the condition will lead to well-marked
psychopathy.

Sleep is often disturbed and interrupted by frightful dreams; other
patients are somnolent and dull. Many suffer from diaiziness; at times
from attacks of heat and rush of blood to the head, during which all the
other symptoms increase in severity. Such attacks may terminate in
complete unconsciousness.

Frequent complaint is made of headache. The pain is j^enerally dull
and diffuse, more rarely it is unilateral or confined to circumscribed
parts of the skull.

The nerves of special sense, particularly of the eye and ear, are often
unduly excitable, so that the patients are annoyed to an' unusual degree
by bright light, noises, etc. In other cases, they complaim of flashes of
light before the eyes, dimness of sight, ringing in the ears, etc.

Some patients complain of parsesthesise: deling of deadness in the
skin, formication, etc. These sensations may be unilatend, confined to
one limb or to parts of a limb.

Muscular twitchings are not infrequent; they may be confined to a
few muscles of the face or limb, or they may spread to an entire limb,
to one side of the body, or become geueral; they are often associated
with disturbances of consciousness and assume an epileptiform character.
The differential diagnosis between epilepsy and cerebral hypersmia not
infrequently is very difficult.

Some patients complain of a dead feeling in the muscles, and pareses
and paralyses may be present. As a rule, these are ephemeral and dis-
appear as soon as the circulatory disturbance is relieved.

It has always been held that puffy, short-necked individuals, who
live well, take little exercise, t. e., plethoric individuals, have a special
tendency to cerebral congestion; but lean, slender individuals may also
suffer from this affection.

During the attacks, the face is often very red, in passive congestion it
is intensely cyanotic. The heart's action is not infrequently accelerated,
stronger, occasionally irregular; the patients often complain of palpitation
and an anxious feeling of oppression in the praBCordial region. In active
cerebral hyperaemia, the pulse feels full and nard, in the passiye form it
grows small, even imperceptible. The carotids pulsate vigorously, and
pulsations are sometimes visible in the smaller arteries. These changes
may be associated with irregular respirations. During apoplectiform
and comatose attacks, the breathing becomes stertorous and may even
assume the Gheyne-Stokes type. Slight rise of temperature is not un-
usual.

Vomiting must be regarded as a symptom of cerebral irritation. In-
voluntary evacuations sometimes occur during comatose conditions.

The symptoms mentioned above may appear in various degrees of in-
tensity, combination, and duration. They sometimes last only a few

DISSASE8 or TBE BBAIX.

seconds, sometimes hours, days, weeks, even mouthe. Rclapaea occur in

very many cases.

We distinguish four characteristic groups of aymptoms.

a. Cepluilulyio form. The headache, f&ellDg of coafuaion in the head, and
hyperEcsihefiia to liKht and sound predoniiaate. In addition, palpitation of the
heart, rush of blood to llie head, etu.

b. Psychical form. The patients are excited and sleepless, suffer from illa-
dona and hallucinations, become maniacal in unfavorable oases, and may become
permanently insane.

c. Convulsive form. This is observed most frequently in children. It is
characterized by twitchings and epileptiform attacks, often by tetanic Htiffness of
the muscles of uie back of the neck. Itniaybe,mistaken for epilepsy, meningitis,
or tetanus.

d. ApopUetic form. Attacks of unconsciousness occur in this form as in
cerebral hemorrhage. With or without prodromata, the patients fall uncon-
ecious to the ground, remain comatose for a longer or shorter period; and on
coming to, present pareses and paralyses which soon disappear. Experience
teaches that these symptoms not infrequently precede cerebral tiemorrhage.

IV. Diagnosis. — The diagnoaia ia generally easy if we take into con-
BideratioD, not alone the symptoms, but also the causes of tiie affection.
Aa a rule, the latter will also determine whether the hyperaemia is nctivo
or pasaive.

V. Prognosis. — The prognosis ia often serioua or unfavorable on
account of the primary affection. If the causes can be removed, the
prognosis is generally good, although death may occur during a convnl-
aive or apoplectiform attack.

IV. Treatment. — Causal treatment varies according to the primary
affection — digitalis in heart disease; restricted diet, exercise, etc., in
plethora, etc.

In active cerebral congestion, the upper part of the bodv should be kept
elevated, from eight to sixteen ounces of blood removed, by venesection
(in children four to six leeches to the mastoid processes), an ice-bag or
cold applications applied to the head, and the bowels thoroughly opened.
Uot foot-baths or mustard hand-bathe may be employed to produce a
rapid derivative effect. The food ahould be fluid, the room should be
large and airy and a little darkened; absolute hodily and mental rest. Nar-
cotics should not be given it the patient suffers from insomnia; potaa-
Mum bromide {3i.-iiaB, at night) alone may be recommended. The
after-treatment may consist of a cold-water cure or a trip to the moun-
tains or sea-shore. Chronic congestion has been treated with the gal-
vanic current (longitudinal current through the skull, anode upon the
forehead, cathodo on the back of the neck near the vaao-motor centre).

3. (Edema of the Brain.

In cerebral rsdema, the cut surface of the substance of the brain appears unu- I
aually moiat. Its consistence is generally diminished and sometimes described aa
almost diffluent, but such cases are often the result of post-mortem maceration.
In many instances, tlie brain substanco is unusually palei its volume may be in-
creased and the surface appear flattened. Not infrequently there is increase of
the cerebro-spinal fluid in the ventricles and subarachnoid space, and also osde-
matoue swelhng of the subarachnoid meshed lirnue.

The microsoope is said to shoiv dilatation and overfilling of the perivascular
iTrnpli spaces,

Cerebral cedema is so much more apt to interfere nith the functions of the
brain the more rapid and diffuse tlie development of the oedema. It produces
the symptoms of increased cerebral preseure, so that in indi»vd\ia!i tajKaSS.^**-

218 DISEASES OF THE BSAIN.

mains for us to ascertain the causes of the condition (henEioniimge»
tumor, etc.). In many cases cerebral oedema is an agonal phenomenon.'

The difficulty of arriving at a correct conclusion conoeming oedema of the
brain is evident from the differences of opinion conoeming its rriatioiis to
urromia.

The causes of cerebral oedema are the same as those of oedema in other orgm
— circulatory disturbances and changes in the constitution of the blood, with nc-
oudary increased permeability of the walls of the TeeselB.

•

4. Cerebral Hemorrhage.

{Encephalorrhagia, )

I. Etiology. — Primary or spontaneous cerebral hemorrhage, whidi
will alone be considered, generally occurs beyond the age of 40 years,
though cases are also observed in childhood. Its relative freqaencr in-
creases with each decade beyond the age of 40 years.

it is more frequent in men than in women. Hereditary infiaenca
are sometimes demonstrable.

Experience teaches that it is more frequent daring the winter
months.

The development of cerebral hemorrhage depends on three poasibilitiee : exoes*
sive blood pressure in the arteries, disease and diminished resistanoe of the cere-
bral vessels, and, finally, cerebral changes in the immediate vicinity of the blood-
vessels (softening and atrophic disappearance).

It is not probable that the mere increase of arterial presBore will give rin
to a hemorrhage into the brain. It has been proven, experimental! j, that rapture
of the cerebral arteries requires a pressure which is so enormous that it can
hardly ever be produced during life.

The opinion is constantly growing stronger that changes in the blood-
vessels (with diminished resistance) are always the cause of cerebral hem-
orrhage, and the theory that rupture of the vessels maj result from soft-
ening or atrophv of the surrounding brain substance is now uniyersallT
abandoned. The latter event is perhaps possible^ but at all eyents it u
exceptional.

The changes in the vessels, which consist generally of the formation of
miliary aneurisms in the smaller cerebral arteries, produce, per se, the
tendency to rupture. But the latter will be apt to occur so much sooner
if the arterial blood pressure is also increased. In some cases, the
hemorrhage occurs during sleep; in others, immediately after some event
which increases the arterial pressure (anger, mental excitement, bodilv
exertion, a heavy meal, etc.). Special mention should be made of the
fact tliat hypertrophy of the left ventricle with secondary increase of the
blood pressure in the aortic system is a frequent exciting cause of cere-
bral hemorrliage. This is less true of hypertrophy following valvular
lesions— the hypertrophy then merely compensates the valvular lesions—
but rather of the hypertrophy following cirrhosis of the kidneys and arte-
rio-sclerosis. It was also mentioned in the paragraph on congenital steno-
sis of the isthmus aortas that an unusually large proportion of the
patients die of cerebral hemorrhage (vide Vol. I, page 170).

Stasis in the venous system sometimes acts as an exciting cause of
Iiemorrhage of the brain, for example, as the result of violent straining
at stool, lifting a heavy load, violent coughing, sneezing, laughing, in
jare cases from straining during delivery, etc.

II. Anatomical Changes. — If the hemorrhage has attained certain

DISEASES OF THE BBAIN. 219

dimensions, its location can sometimes be recognized after removal of the
dura mater. The brain projects more markedly on the affected side, the
gyri are flattened, the sulci flat, the brain is often anaemic from com-
pression of the vessels. In some cases, the falx cerebri is pushed over
strongly towards the unaflfected side. At times the hemorrhage is not
confined to the parenchyma, but passes into the ventricles or breaks
through the cortex and pia mater, and may enter the subarachiioid space
in both directions. It then spreads to a considerable extent over the
surface of the brain, and may even surround the larger part of the cir-
cumference of the brain like a sort of bloody cap. The blood may pass
likewise into the subarachnoid cavity of the spinal cord, and extend far
down the spinal canal. It is generally coagulated, and may be removed
readily from the subjacent parts.

The size of the hemorrhage is extremely variable; it sometimes occu-
pies an entire hemisphere. In some cases, more than twelve ounces are
extravasated. The nemorrhage may be round, elongated, or irregular in
shape. As a rule, hemorrhages in the white matter are less extensive
and more elongated, because the white matter ofllers greater resistance
to the extravasated blood than the gray matter. If the hemorrhage
affects both parts at the same time, it is generally more extensive in the
gray matter.

In the majority of cases, it takes place into one hemisphere alone,
more rarely it is bilateral. Hemorrhages in the vicinity of the median
line of the pons are apt to involve both halves of that organ. A number
of hemorrhagic foci, varying in age, are found not infrequently.

In recent cases, the hemorrhagic focus forms a soft mass which con-
sists of extravasated blood and d6bris of brain tissue. At the periphery
of the hemorrhage the brain forms a ragged, floating fringe, from which
coils of vessels sometimes pass into the extravasation. The parts around
the latter are often innltrated with punctate hemorrhages, appear
swollen, moist, yellow (citron- colored oedema).

Next the blood coagulates, and then the red blood-globules gradually
degenerate, and their blood pigment becomes changed and crystallizes.
The color of the clot changes from chocolate to rusty brown, finally to
ochre yellow, the extravasated blood is gradually absorbed and is replaced
by serous fluid. In the mean time, reactive inflammation has occurred
in the adjacent layer of brain tissue, the principal part being played by
the neuroglia. CTonnective tissue is produced and encysts the hemor-
rhagic focus (apoplectic cyst).

The contents of an apoplectic cyst are not always clear and serous.
In some cases they form a milky, emulsive fluid, on account of the abun-
dant mixture of fat drops ana granulo-fatty cells. Blood crystals, in
the shape of a brick-red or brownish-red precipitate, are especially apt
to be found on the inner surface of the cyst-wall. In rare cases the cyst
exceeds the size of a walnut, and may even attain the dimensions of an
apple.

The reactive hiflammation around the hemorrhagic focus is sometimes so
active as to give rise to extensive encephalitis. Under such circumstances the
cysts may have purulent contents. In rare cases, non-encapsulated cysts are
found.

The cavity of the cyst is sometimes traversed by fine threads, which
consist in part of persistent blood-vessels, in part are newly formed.
Their number may be so considerable as to form a mTiltvlc^\)XA2t) T^^'c^t^^^-

Dia&ASBS OF TEE BRAIK.

meshed cavity whose chambers are filled iritb fluid. It Ib sopposed thit
the cyats may disappear, from gradual absorption of the flaid and tfaa
approximation of their walls, so that finally nothing is left but a |Hg-
mented, apoplectic cicatrix. Apoplectic c^sts and cicatrices may pro-
duce torsion npon adjacent parts of the brain.

la hemorrhages into the cortex, the pia mater becomea thickoied

BunaUuteTTliithelaQtlculsrnucleiii. KilarK«d»'

above the site of hemorrha^. Beneath it is found a aerooa, apoplecda
cyst or a depressed apoplectic cicatrix.

HicrOBCopic ezaminationof recflnthemorrha^ofooireveala red blood -^otiiil^
dibrie of nerve tissue, amoeboid oelle and graaulo-fatt7 oella. Theia *i« ottan i
TuiaUe number of cells containing blood-Klobolee (Ingeatlon 1^ amosboid wJ^
Next the red globules uadei^o shrinkinE and granular disintegration, and ta
number of granulo-tattjr cella mcreasea. The tree pigment ataina the other itniB-

'TMKUona faito thead*«Mi-

Uouilrmph epMces. AtCer Cornll kod B&uner. XiUttrgvd tt tlmea.

tures yellow, in part it ia depoeited free or in the cells in the form of gnmofa,
netMlleH, or tablets; it is particularly abundant upon the inner Hurface of the CTst-
'wall. The remains of the vessels are very fatty, and heematoidin grannlM or
crystals are fouod not infrequently in their lympli sheaths or on Uielr outer lor-

The changes in the blood-vessela are best detected by removing the hemor-
rhagic focus, in addition to tlie adjacent brain aubstanoe, placing it in water,
carefully renewing the water during tha next few days, and then cantloaly
pouring a otream of water over the bmin substance, until nothing is left bot Ibt
vessels. The latter are then removed with forceps and placed upon a glav lUda

The TBSotilar ohanKes, Bo^jalled miJiarf aneurisms, affect only the smaller vessels,
and are often viaiWa to the uaked eye. Tiiey may be one millimelre in aize (vide
Fig, 113), or rerngdizable only with the microscope. They are apt to develop at
the point of the bifurcation of the arteries, and are often present in large
numbers. .

At the aneuriBDi, the muscular coat of the vessel lias disappeared, and the
intinia and adventitious lymph eheath approach one another until they oorae in
contact. In aome places, the aneurism is found ruptured, and the blood eitra-
vasuted into the adruutitious lymph sheath (vide Fig. 114, bk). In otiiers, the
latter contains a rent through which blood has passed into the surrounding
parenchyma.

Bouchard and Charcot regard the aneurism as the result of periarteritis,
which conBiBts of increase of the nuclei in the adventitious lymph sheathe and
thickening of the latter, and disappearance of the muscular coat, Zenker attri-
butes the lesion to arterio-eclerosis. Plnallj. Roth maintains that the aneurism
is the result of a primary affection of the muscular coat, which first undergoes
hypertrophy, and causes <ySuse cylindrical dilatation of the arteries; later, the
muscular coat undergoes Tatty and vraxy degeneration. At the same time, the
artery suffers aneuriamal dilatation, which antagonizes the thickening of the
adventitious lymph sheath or tunioa imima. Although the aneurisms manifast
a tendency to rupture. Roth believeB that there is sometimes an attempt at
recovery in the Bhape of tliickening of the iutima. which may advance to com-
plete ohlit«rstion.

Miliary aneurisms are observed almost aonstantly in cerebral hemorrhage.
Although the possibility of cerebral hemorrhage from fatt^ degeneration and
eimple atheromatous changes of the vessels cannot be denied, atill this is un-
doubtedly exceptional.

Miliary aneurisms are particularly apt to be found in advanced life. They are
most frequent in the optic thalamus and corpus striatum, next in the cerebral
convolutions and the pia mater, then in the pons, medulla oblongata, and gray
matter of the cerebellum. Cerebral hemorrhages are found most frequently in
the optic thalamus and corpus striatum; then follow the other parts of thecero-
brum, then the cerebellum, pons, and cerebral peduncle; next the medulla ob-
longata and corpora quadrigemina; the cornu ammonis, corpus callosum, and
fornix almost always escape.

Hemorrhages into the ventriclee are generally derived from foci which hava
broken through the thalamus, corpus striatum, or tlie pons. Rupture of a vessel
in the wall of the ventricle ocouih much more rarely,

IndividualB who die booh after the occnrrenco of a cerebral hemor-
rhage, Bometimea present hemorrhages ia internal orgaas, for example,
the bronchial mucoca membrane, lungs, or kidneys, gastro-intestmal
mucous membrane; it the organs are two in number, in the one opposite
to the side of the cerebral hemorrhage. Thia has been attributed to
vaso-motor disturbances.

In three cases, Lepine noticed that the paralyzed limbs grew cold
more rapidlj after death than the healthy limbs.

Lionville detected miliary anenriams in the arteries of the retina.

After the hemorrhagic foci have existed for a long time, they are fol-
lowed by secondary degeneration in certain systems of fibres in the cen-
tral nervous apparatus (vide page 131J.

Unilateral atrophy of the brain also occurs as a result of cerebral
hemorrhage, especially into the cortex.

The peripheral nerves and muscles remain nnchanged. But a few
doubtful cases have been reported in which there was an increase of the
interstitial tissue iu the peripheral nerves. Meissner mentions degen-
erative changes in the tactile corpuscles, but this ia contradicted by
Langerhans. Debove mentions dilatation of the medullary spaces and
Haversian canals of the bones on the hemiplegic side.

IV. SXKFXOUS. — In typical cases, cerebral hemorrhage presents five

222 DISEASES OF THE BRAIN.

stages, the prodromata, the apoplectic attack, the inflammatory reaction,
the permaneat symptoms, and the secondary changes.

The prodromata generally consist of the symptoms of cerebral con-
gestion, viz., rush of blood to the head, vertigo, slight confusion, flashes
of light before the eyes, ringing in the ears, a feeling of anxiety and
oppression. The patient generally grows excitable and whimsical, and
complains of restless sleep, interrupted by bad dreams. He often suf-
fers from headache, which occurs either spontaneously or after bodUj or
mental exertion; the pain may be diffused or circumscribed. The pa-
tient feels incapable of mental work, the memory is impaired. In some
cases there is occasional loss of words, more rarely articalation ii
impeded and the speech thick.

These symptoms may precede the apoplectic attack for months,
weeks, days, or hours. ^

In six cases, Foerster obsenred small hemorrhages into the conjunctiTa and
retina of individuals who died several years afterwards of cerebral hemorrhage.

The symptoms become more serious when complicated with uni-
lateral disturbances of motion or sensation: formication, prickling,
weakness of the limbs, dragging of one leg in walking, etc. These
symptoms are confined not infrequently to one limb, and may dis-
appear at the end of a few hours or days. These are probably the result
of small hemorrhages, which are capable of rapid reparation.

The apoplectic attack is either preceded for a longer or shorter period
by the prodromata just mentioned, or it develops suddenly and unex-
pectedly. In the severest cases, the patients fall as if struck down; they
are completely unconscious, do not react to irritation, pass urine and
faeces involuntarily. Death mav take place almost immediately after the
onset of the apoplectic seizure (apoplexia fulminans s. attonita).

When the patient is profoundly comatose, it may be difficult to reGog-
nize the existence of a hemiplegia. The limbs are completely flaccid,
and if raised fall like dead masses. Hence, the condition may be mis-
taken for drunkenness and opium poisoning. But drunken individuals
will generally smell of alcohol, and in opium poisoning the pupils are
contracted to pin-point dimensions.

As a result of the unilateral paralysis, changes are often noticed on
one side of the face: flattening or abolition of the naso-labial fold, to
and fro movement of the flaccid cheek during inspiration and expiration,
flow of saliva from the open angle of the mouth, depression of one-half
of the palatal arch, and deflection of the uvula (the latter is physiologi-
cal in some individuals), sometimes towards the healthy, sometimes
towards the paralyzed side.

Pinching or pricking the skin produces no reflex movements in pro-
foundly comatose patients. Less comatose individuals contract the non-
paralyzed side of the face, or groan and moan. In still slighter grades
of coma, the limbs on the unaffected side are moved, those on the other
side remain motionless. If the limbs are raised, those on the paralysed
side fall as if dead, those on the opposite drop slowly. Passive move-
ments of the paralyzed side may sometimes be performed without
resistance.

In profound coma, attention must also be paid to the presence or
absence of certain cutaneous reflexes (reflexes of the testicle, of the
muscles of the abdomen, loins, and buttocks, and of the nipple).

DISEASES OF THE BBAIN. 22S

If the finger or other hard body is rubbed across the integnment of
the upper and inner part of the thigh, or if the saphenus maior nerve is
compressed about a hand's breath above the internal conayle of the
femur in the space between the sartorius and vastus internus^ the testicle
on the side corresponding to the irritation will be elevated by the con-
traction of tho cremaster muscle. Bapid stroking over the abdomen,
buttocks, or loins will produce reflex muscular contraction upon the irri-
tated side. Stroking of the nipple will give rise to erection of this part
and to wrinkling of the pigmented areola.

In hemiplegics, on tne other hand, these reflex movements remain
absent on the paralyzed side, in recent cases as well as during the status
apoplecticus. This symptom is so much more important because these
reflexes are rarely absent in healthy individuals. In the further course
of the disease, the reflexes gradually return, but are distinctly weaker^
BO long as the paralytic symptoms persist.

In some cases hemiplegia does not occur, but in its stead appear epi*
leptiform, general or unilaterel convulsions, or unilateral contractures.
Tnis is especially true of cortical or pons hemorrhages, or those which
have ruptured into the ventricles.

Some patients assume forced positions. The head and eyes are
turned constantly to one side, sometimes the trunk is also turned in the
same direction. If the patient is moved out of the forced position, he
will gradually return to it. The rotation sometimes occurs towards the
side of the paralysis, sometimes in the opposite direction.

During the apoplectic seizure, the face is often red and con^ested^
the carotids throo violently, and there are often vigorous pulsations in
the temporal arteries. The pulse is tense, slow, normal or accelerated,
and not infrequently irregular. In some cases the patient is pale, the
heart sounds feeble, and the pulse small. The respirations are often
arhythmical, or Cheyne-Stokes oreathing is observed. The respirationa
are often snoring and stertorous, and at each inspiration it is found that
the paralyzed ala nasi closes the nostril and prevents the entrance of air.
Tracheal rAles will be heard if the saliva and mucus accumulate in tho
upper air passages. The pupils may be narrow or irregularly dilated,
and destitute of reaction; the latter is a bad prognostic sign. In a case
of apoplexy which developed under my observation, I noticed that the
pupil upon the side opposite to the hemorrhage dilated, and assumed the
shape of a cat's pupil.

The patient comes out of the apoplectic attack either quite suddenly,
for example, after venesection, or days and weeks elapse during which
consciousness gradually returns. If the disease terminates fatally, life
is gradually extinguisned after increasing disturbances of respiration^
tracheal r&les, cyanosis, and increasing general collapse.

Boumeville states that, in a quarter hour to a half-hour after the beginning of
the attack, the bodily temperature sinks below the normal. If the case ter-
minates favorably, the temperature returns to the normal after the diffuse cere«
bral symptoms have subeided, and the focal symptoms have become more distinct.
A fatal termination is preceded for seTeral days oy a considerable rise of tempera-
ture. In apoplexia fulminans, the temperature continues to sink until the
moment of death.

Ollivier makes the following statement with regard to the urinary excretion.
Immediately (half-hoiu:) after the hemorrhage, there is an increased secretion of
urine, so that in one case two thousand cuoio centimetres were passed in two
hours. The urine is very pale and its specific gravity very low (1.004). It con-
'■'' — but little urea, some albumin, and later sugar. The albummuria is &t fLsKLtk

224; DISEASES OF THE BRAIS.

sliglit aod then increaRes gradually, but all these changes disappear in twelre to
twenty-four hours. The urinary changes are so much more marked the man
profuse the hemorrhage, t. 6., the more violent the shock to the medulla obko-
gata, to which Ollivier attributes these symptoms. Sudden inciease in the
amount of urea excreted is an unfavorable prognostic event.

In some cases^ the coma, at the period at the apoplectic seizure, is not
suflBciently profonnd to prevent movements of tne limbs or manifesta-
tions of pam upon irritating the skin. The patients sometimes come
out of an apoplectic attack and remain in excellent condition for days;
then follows another seizure, perhaps more severe than the first, and the
patient succumbs.

The apoplectic seizure is sometimes the third stage of the disease, in-
asmuch as it is preceded by paralytic symptoms. Some time ago I had
under- observation a man set. 60 years, who suddenly fell, whilenunting,
on account of paralysis of the right leg. 1 saw him two honrs later; con-
sciousness was perfectly clear, but the right arm and leg could not be
moved. Somnolence developed thirty hours afterwards, and deepened
into coma of several days' duration.

In some cases, there is a so-called abortive form of apoplexy: vertigo,
vomiting, slight syncope, etc.

The chief cause of the apoplectic seizure is the sudden elevation of brain pre»-
sure produced by the extravasation. The second factor is the purely mechanictl
effect, the concussion or shock to the brain, whose intensity likewise depends on
the profuseness and rapidity of the hemorrhage. Another factor is the ansemia
of the brain resulting from the compression. Finally, it must not be forgottoi
that the site of the hemorrhage also influences the development and mode of on*
set of tlie apoplectic seizure.

The symptoms of reaction are manifested by an increase of tempera-
ture ^more tiiat 2° C), delirium, and renewed somnolence, often by slight
twitcnings and contractures in the paralyzed limbs, occasionally by pam.
They generally begin from the second to the fourth day after the seizure,
and are the result of the inflammatory changes in the Ticinity of the
extravasation.

Permanent focal symptoms develop so much more distinctly the
more the symptoms of the apoplectic attack and of reactive inflamma-
tion subside. In the majority of cases, they present a striking similarity
because the majority of hemorrhages affect the internal capsule in addi-
tion to the adjacent corpus striatum (and optic thalamus). We will con-
fine our remarks to the consideration of this principal type.

Hemorrhages present a predilection for the region in question for two
first, because miliary aneurisms are especially frequent in this locality; seoondly,
on account of the relations of the blood pressure. The arteries supplyiDg the
basal ganglia are given off directly from the anterior and middle cerebral
arteries and are therefore subject to the changes in blood pressure in the domain
of the internal carotid which would otherwise be enfeebled if there "were nu-
merous arterial branches.

In hemorrhages into the internal capsule (and adjacent corpus stria-
tum) the chief symptom is motor paralysis of one side (cerebral hemi-
plegia).

Unlike peripheral and pons paralyses, the facial nerve is not afil!ected
in all its branches. The frontal branch escapes, so that the forehead can
be wrinkled and the eye closed. The cheek and region of the chin on
the paralyzed side are motionless.

DIBKASES OF THE BRAIS, 2S5

n ezplnnation of the uon-paraljaie of the frontal branch of the facial nerve,
e asHume two diatinct centrad hdiI separate central paths for the two parts of
the facial iit>rve. others believe that both frontal brancbeB are innervated by one
cerebral hemisphere, so tliat in a nnilatei^ leaion tlie other hemisphere acta vi-
carioual;.

The hypogloasna is more or less paralyzed. This is shown by im-
paired mobility of the tongue in mastication and 8]>eakiDg: the speech ia
slow and thiok. The tongue, when protruded, deviates toward the para-
lyzed side {predominance of the non-paralyzed genioglossus muscle). In
tlie further course of the disease, the hypoglossal paralysis disappears
in part, but, as a rule, not entirely.

The paralysis of the arm is more marked than that of the leg. and it
has been supposed that the prognosis is unfavorable if the reverse holds
go oil.

The muscles of the thorax and abdomen also take part in the par-
alysis, so that the movements of respiration and straining are less vigorous
on the paralyzed side. Paralysis of the trapezius is shown by the sinking
of the shoulder.

In a number of cases T have found, with the laryngoscope, impaired
mobility of the vocal cord on the paralyzed side.

The following phenomena have been observed in the paralyzed limbs: a. Eu-
]eDl>erg noticed that the pulse upon the paralyzed side ia smaller and presents
a more marked elevation of recoil; b. According to Brictiuebeck and Charcot, the
blood taken from a vein on the paralyzed side looks redder than that taken from
the opposite aide; c. Lupine and Briuquebeck noticed that tbe paralyzed limbs are
cooli'd more rapidly in cold water than the healthy ones; d. According to Char-
cot, the tempemture of the paralyzed limbs increases a few hours after the sei-
zure (sometimes as much as 9'). In some cases this rise subsides very i^uickly, or
it may remain entirely absent; e, Cyanotio color, (edema, and perspiration are
sometimes noticed on the paralyzed limbs (imphcation of the vaso-raotor norvesj.
According to Nothnaj^el, some cases manifest symptoms of paralysis of the cervi-
cal ey III pathetic: uDiiBteral redness and sweating of the face, narrowing of the
palpebral liaaure, dilatation of the pupil, and increase of the salivary, lachrymal,
ana nasal secretions.

Ab a rule, all the paralytic fljymptoms are moat marked immediately
after the attack. Very gradually some of them begin to subside. The
first signs of returning power appear iu the legs, next in the arms, bat
the latter rarely recover to the same extent aa the former, Theparalysia
of the face often disappears almost entirely. Complete restoration of

Cower is possible, but only when the motor tracts are merely comproaeed
y the extravasation.
Associated movements constitute a peculiar phenomenon. While the
patients are unable to perform voluntary movements of the paralyzed
side, these occur involuntarily during laughing, crying, or sneezing. If
the eye is blinded by a brignt light, or tlie nasal mucous membrane or
face is tickled, the patients not infrequently make reflex movements o(
repulsion with the paralyzed arm. If they are directed to make vigorous
pressure with the healthy hand, involuntary pressure will be made with
the other hand. Sometimes in attempting to move tbe paralyzed limbB>
^^aToluntary movements ocour in tbe bealtby limbs.

236 DISEASES OP THE BBAJK.

In the f onn of hemorrhage under consideration, Bensibility is Dtun-
pured. AnssBthesia is f reqaent, immediately after the apoplectic attuk,
Bat is merely the result of pressure on remote parts and gradually dis-
appears. If the sensor? tracts are irritated, hyperasthesia and p«n»-
t£esia are produced. Partial anaesthesia has also been described.

The reflex moTements mav be diminished or anaffected; when sec-
ondary degeneration aete in, they may be increased.

Poallioii of the arm and kg Id a mao let. S3 jeare, attacked by bamiplSKla ilz mtniUu prerlooil;.

The paralyzed muscles maintain their normal volume for a long time;
slight emaciation occurs at a Into period as the result of disaae. The
taradic and galvanic excitability of the nerves and muscles is retained,
indeed it is said to be increased at times, during the first few days.

Trophic changes are sometimes noticed, such as abnormal develop-
ment of hair on the paralyzed limbs, thickening and fissures of the naiu,
desquamatioQ of the epidermis. The joints and sheaths of the tendoni

DI8X&8H OF THE BKAIN. 227

are sometimes aSectod. The diaeoBe of the joints ia shown by riolent
paius wliich generally begin one to three months after the paralysis. The
affected limb is generally warmer and moister than the other. The
shoulder joint is most frequently attacked, next the wrist, knee, elbow,
and metacarpo- phalangeal joints. On antopsy, Charcot found injection
and villous swelling of the synovial membrane, and in one case serous
exudation. In seven cases, Uitzig noticed subluxation of the head of
the humerus.

Oubler and FourniS noticed painful inflammatory swellings of the
sheaths of the tendons which developed one to three weeks after the
apoplectic seizure, and recovered in one to three months. Nodular
thickenings of the peripheral nerves (neuritis nodosa) are sometimes ob-
served .

The nerves of special sense are affected very slightly or not all. Oo-
CAsional mention is made of disturbances of taste.

The vegetative functions may be unchanged. The most important
phenomena in the stage of secondary changes are: Contractures of the
paralyzed Limbs, twitcuinga, increase of the tendon reflexes, which have
been attributed to secondary degeneration of the pyramid tracts.

The contractures are more marked in the upper than in the lower
limbs. The flexors are chiefly affected, so that the fingers, band, and
forearm are flexed. The arm is generally adducted against the thorax.
In the leg, the extensors predominate over the peroneal muscles. The
contractures diminish after prolonged rest, especially after sleep, and are
Increased on attempting to move the limbs. If they have lasted a long
time, they give rise to changes in the joints which favor malposition oi
the limbs and increase the difficulty of movement.

The secondary changes also inelnde the fre<|^nent impairment of the
mental faculties. The patients are unnsually irritable and whimsical,
thev laugh and cry without reason, become forgetful, and finally im<
becile. According to Carpani, the intelligence is more impaired in
right than in left nemiplegia.

The duration and course of this disease vary greatly; death eo me times
occurs almost immediately; in other cases, life is prolonged ten to twenty
years.

Cerebral hemorrhage presents a great tendency to relapses, after an
interval varying from a few hours to months or even years.

If death does not occcur during the apoplectic seizure, it is generally
the result of increasing marasmus or intercurrent diseases (pneumonia,
bronchitis, etc.).

IV. Diagnosis. — The diagnosis is generally easy. We have previ-
ously referred to the possibility of mistaking the apoplectic seisnre (or
drunkenness or opium poisoning. Apoplectiform attacks may also occur
in circulatory disturbances and oedema of the brain, but these are not
followed by permanent paralvaia. It ie not always easy to distinguish
cerebral hemorrhage from emiioltam or thrombosis of the cerebral arte-
ries. Special importance must be attached to the existence of valvular
lesions aa a source of emboli. Apoplectiform attacks are also observed
in cerobro-spinal sclerosis, rarely m epilepsy and tabes dorsalis, but thcso
attacky are not followed by permanent hemiplegia, and, in addition,
other sym p to ms of the diseases in question are noticeable. Finally, such
attacks also occur in progressive paralysis of the insane, bnt the mental
disturbances and affection of speech predominate in this disease.
-The localization of the hemorrhage is determined according to the

228 DISEASES OF THE BRAIN.

rules laid down in the preliminary remarks on the localization of cere-
bral diseases. The hemorrhage and paralysis are very rarely on tk
same side of the body. Such an occurrence can only be explained bj the
absence of decussation of the pyramid tracts.

Secondary degeneration of the pyramid tracts may be inferred from
the presence of contractures, increased tendon reflexes^ and twitchings
in the paralyzed limbs.

V. rROGNOSis. — The prognosis is always grave, since immediate
death may ensue or irreparable injury is left over. The most dangerooi
hemorrhages are those into the pons and medulla, because these parts
are the site of important centres. Kise of temperature and the develop-
ment of trophic changes at the period of the apoplectic seizure have as
especially unfavorable prognostic significance.

VI. Treatment. — Prophylactic measures must be adopted in those
who have suffered from a previous attack of hemorrhage. Such indi-
viduals must avoid mental and bodily excitement, take non-irritating
but nourishing food, avoid tea, coffee, and alcoholics, and secure a ddlj
evacuation from the bowels.

During the apoplectic seizure, venesection is indicated if the pulse ii
hard, the carotids ttirob vigorously, the action of the heart excited, and
the face congested. Under such circumstauces the patients, after the
venesection, not infrequently come out of the most profound coma uid
remain conscious. Venesection is contra-indicated ii the pnlse is small,
the heart-sounds feeble, and the face pale. In the former event the head
should be kept high, in the latter we may order irritants (injection of
camphor, enema of vinegar, mustard draughts to calves, chest, etc),
and attempt to check the hemorrhage by injection of ergotin in the
region of the forehead or ear, and the application of an ice-bag to the
head on the side of the hemorrhage.

After the symptoms of the apoplectic attack have subsided, the diet
should consist mainly of milk, soup, and soft-boiled e^gs; wine maybe
administered cautiously to aujeniic individuals. The bowels should be
evacuated by a mild laxative. About the middle of the second week we
may attempt to aid the absorption of the extravasation. Potassiam
iodide (gr. xij. t. i. d.), iodide of iron, and mercurial inunctions have
been largely employed for this purpose without any very brilliant re-
sults.

In our opinion, the electrical current is a powerful therapeutic agent
We do not employ the galvanic current until all irritative symptoms
have subsided, as a rule, not before the close of the sixth week. The
current is applied as follows: a large electrode on the skull over the sup-
posed site or hemorrhage, a small one immediately below and behind the
angle of the lower jaw upon the upper cervical ganglion of the sympa-
thetic, feeble ourrent (six to eight elements), the cathode applied to the
skull for three minutes, then the anode for the same period, three to
four sittings a week.

The development of muscular contractures may be limited and al-
most prevented, if the position'of the paralyzed limbs is changed several
times daily, massage applied to the muscles, and the hand and fingen
fastened to splints at night. The stabile galvanic current may be em-
ployed to relieve existing contractures.

The paralysis as such may be treated by faradism or by the labile
galvanic current, the cathode on the paralyzed muscles, the anode on
the back of the neck or over the focus m the brain.

Indiflerent thermal springa and cold-water cures are also i
mended, bat ehould not be employed until the irritativo ejinptonK
subsided.

_ ..._ __ _fi singly, Bometimes in very large nutubere. They are

sometimes bo numerous and tto cloeel<r aggregated that their effect ia the xame att
that of a hemorrhage en masse. The surrounding parts ot the brain are often
softened and infiltrated with bloody serum.

On microscopical examination, a blood-vessel ia found to form the centre of
the capillary hemorrhageti. If it is isolated by means ot needles, the udventitioua
lympli Bheatb of the vessel 13 found dilated into an aneurism, and filled witli red
blood-globules. A rent can be detected at times in the wnlls of the vexsel ilself.
Fatty deKeneration and nuclear proliferation of the walls of the vessela are fre-
quently found, but often are merely secondary to the hemorrhage.

In many places the adventitious lymph sbeaths are also ruptured, so that the
red blood-globules escape into the adjacent parenchyma, and extend more or less
deeply between the nerve elements. Destruction of the nerve tissue often takes
place, and granulo-fatty cells are tJien associated with the red blood -globu lea.

After punctate hemorrhages have lasted for some time, the red blood-globules
degenerate, their pigment chanices, and the foci assume a brownish, tater an
ocore-yellow color. Remains of the blood pigment are found in the adventitious
lymph BiMcea, tlie perivascular lymph spaces, and the brain tissue (either free or
Inclosed in round cells in tiie form of yellow and brown granules, needier, or
tablets). It has been supposed oy some writers that the absorption of the blood
and destroyed nerve tissue may give rise to the development of cystic cavities
filled with serous fluid.

Punctate hemorrhaees are most frequent in the course of infectious diseases
and cacliectic conditions (small-poz, splenic fever, pyramla, puerperal fever,
acute articular rheumatism, all diseases associated with dissolution of the blood,
et«.).

The immediate causes of these hemorrhages are not a1<vays alike. In the
majority of cases, it is probably the result of morbid permeability of the vcsels
and abnormally abundant diapedeeia of red blood -globules, produced by moriild
constitution of the blood and defective nutrition of the vessels: in other condi-
tions— pyaemia and leukEemia— it Is probably the result of embolic and throm-
botic processes in tJie cerehral vessels. Finally, many authors renfard fatty
degeneration and fragility ot the walls of the vessels as the cause of capillary
oerebral hemorrhages.

5. Embolism and Thromhosis of the Cerebral Arteries. Embolic and
TJtrombotic Cerehral Softening.

(Necrotic Softening of Ike Brain.)

I. Etiology. — Stenosis or occlusion of cerebral arteries ia produced
either by obstructions to the oircuiatioa which have formed in situ
(thrombi) or by those which have been carried into the veasela by the
current uf blood (emboli).

The most frequetit causes of embolism are affections of the left heart,
especially valvular lesions; inflammatory deposits or particles of the val-
vular tiBBue being carried off by the current of blood.

Among 207 cases of valvular disease of the left heart, embolism occurred 74
times, and in 15 cases affected tlie brain. Mitral lesions appear to be followed
most frequently by cerebral embolism. The lesion may be the result of acute or
chronic changes in the endocardium. In acute septic endocarditis, the emboli
are generally very small, and obstruct only the capillaries: in chronic endooar-
ditis, larger piece's ore dislodged and occlude vessels of considerable alu.

230 DISEASES OF THE BRAIN.

Emboli are sometimes secondary to cardiac thrombosis^ which mm-
fests a predilection for the left auncular appendix.

Next follow tumors (gumma, cancer), echinococci, abscesses, ui
aneurism of the heart muscle; these rupture into the caTities of the left
heart or carry into them the clots which have formed in an aneurism.

In some cases, tlie emboli are derived from lesions of the aorta or
carotid (ruptured atheromatous abscesses, coagula from aortic aneurisms,
dilatation of the carotid and dislodgment of clots, tumors near the
large vessels which have penetrated into their lumen, etc.).

Diseases in the distribution of the pulmonary veins may give rise to
embolic changes in the brain. This may occur in ulcerating phthisiol
cavities, pulmonary abscess, cancer and gangrene, putrid bronchitis, thi
washing out of the pleural cavity after the operation for empyems
(vide vol. I., page 372).

Changes in the right heart cannot produce emboli of the aortic sts-
tem (on account of the intervention of the narrow capillary system'^
the lungs) unless the foramen ovale is patent, so that emboli can pia
directly from the right auricle into the left side of the heart.

Fat and pigment emboli are special forms of cerebral emboli, and
usually affect the smaller vessels or the cerebral cortex.

Fat emboli generally follow fractures of the bones, and result from
the entrance into the veins of the fat which has made its exit from the
medullary cavities. H. Mueller also observed it after fatty degeneratioD
of inflamed kidneys.

Pigment embolism is a sequel of grave intermittent fever. Thii
leads to the development of black pigment in the blood which some-
times enters the vessels of the brain.

Cerebral thrombosis is generally the result of changes in the vessek
These sometimes develop after severe diseases (marantic thrombosis),
such as pneumonia, typhoid fever, etc. It is probable that the cachee-
tic condition gives rise to fatty degeneration of the endothelium of the
intima, and that this affords opportunity for the accumulation of white
blood globules in such localities, and the formation of white thrombi.

Thrombi are more often the result of endarteritic changes. These
sometimes develop as senile changes; sometimes they develop at an early
period as the result of syphilis or alcoholism. They are sometimes so
extensive as to produce almost complete occlusion of the arteries.

In syphilis, Baumgarten observ^ed gummata in the adventitia and muscular
it of the cerebral arteries; these gi
endarteritis obliterans, are apt to give

coat of the cerebral arteries; these growths, particularly wheu associated with

:ive rise to thrombosis.

In some cases, the thrombosis is the result of compression of the
arteries, for example, bv a tumor (compression thrombosis) or by
inflammation in the vicinity, for example, meningitis (inflammatory
thrombosis).

Thrombi in the cerebral arteries sometimes originate from thrombi
of the carotid or vertebral arteries, but the continued deposit of purely
thrombotic material finally causes them to extend to the cerebral vessels

From the previous considerations it is evident that embolism and
thrombosis will be associated with acute articular rheumatism, syphilis,
alcoholism, cachexia, and old age. Embolism occurs more frequently in
earlier years, thrombosis beyond the ago of forty years.

II. Anatomical Changes. — Cerebral embolism and thrombosis

mSBASBS OP THE BRAIS,

affoct most frequently the left middle cerebral artery, and, accordingly,
tho clinical history is found to possess a certain uniformity manifested
by right hemiplegia and aphasia.

The predilection of emboli for the left middle cerebral artery is
attributed to the fact that the left carotid la not given off from the aortic
arch at such a eharp angle as the right carotid, and that the left middle
cerebral artery is, in a certain measure, its direct terminal ramiRcation.

If a cerebral artery is occluded by an embolus or thrombus, the
effects will vary according as the occluded Tcssel may be supplied by
adjacent and communicating vessels, or collateral circulation cannot be
effected. In the former erent, the disturbance of circulation snbaiJes
almost completely; in the latter, it gives rise directly to necrosis or to
hemorrhagic infarction.

In the brain, the conditions vary according as the affected vessels be-
long to the circle of WiUia and to the cortex, or to the arteries which
fasa from the circle of Willis into the basal portion of the cerebrum.
n the former event, the effects of occlusion of the vessels are readily
eliminated because the vessels communicate freely with one another. Lt
the communicating branches in the circle of WiDis are well developed,
the brain may tolerate very marked lesions, as, for example, in Kusa-
maul's case, in which both subclavians and one carotid were occluded.

The conditions are entirely changed in occlusion of the arteriea which
originate from the circle of Willis and paaa into the cerebrum at the base
of the brain. These so-called terminal arteries do not communicate
with adjacent vessels, so that their occlusion is necessarily followed by
necrosis or hemorrhagic infarction.

Necrotic changes in the brain are known as softening ^encephalo-
malacia); according to their appearance they are called white or gray,
red or yellow softening. Cerebral softening is the resnlt, not alone of
embolism and thrombosis, but also of inflammation of the parenchyma
of the brain f encephalitis). A distinction must be made, therefore, be-
tween necrotic and inflammatory encephalomalacia. Macroscopically,
they are almost identical. Microscopiuallj, the inflammatory form pre-
sents processes of proliferation in the cellular structures, but these may
be concealed by the predominance of fatty elements, so that the discov-
ery of an embolus or thrombus would be the sole factor to provo the
necrotic character of the softening. In some cases, however, emboli or
thrombi are gradually absorbed, and bave behind only their sequel, viz.,
encephalomalacia. tJndor such circumstances search must be made for
embolic material in remote parts, or for eudarteritic changes in the
cerebral vessels (the latter would arouse the suspicion of previous
thrombosis). Nevertheless the explanation of the cose may remain im-
possible.

In white or gray sottonine of the brain, the affected part forma a
white or gray, soft, occasionally almost diffluent mass, which often can
be washed away by a streom of water, and leaves a cavity with jagged
walls.

Microscopical examination of the necrotic tissues shows more or less advaoi^ed
fatty de|;eneration of the nervous elements. The nerve fibres are the earliest to
be (UTected, tlie ganglion cells are more reslataut. Wengler has observed calcifl-
oation ol tlie ganglion cells. How loof; the nerve flbres may be deprived of blood
without undergoing tmatomicul channeH is not Icnown with certainty, but there
is no doubt that tliey will develop, at the latest, at the end of forty *ight hotirs.
^ - The medullary sheath coagulates and breaks up into smaller and smaller

232 DISEASES OF THE BBAIN.

pieces, the axis cylinder also undergoes de^neration, next the cellular elemeini
of the neuroglia and the vessels. Finally, nothing remains but fat granubs,
granulo-fatty cells, and empty, fatty remains of the blood-vesaels.

The more the fatty degeneration progresses the more the gray w I
white color changes to yellow (yellow softening). This generally re-
quires four to six weeks.

Tlie absorbed fatty elements are sometimes replaced by a serous fluiil.
which is either clear or milky. This softening cyst may or may not be
encapsulated. Tlie cystic cavity is traversed occasionally by a networi
whose meshes contain fluid. The meshes consist in part of the remains
of obliterated vessels, in part of newly formed bands of connective tissae.
It is sometimes impossible to distinguish them from apople^ctic cysts.

Red softening of the brain corresponds to the wedge-shapwi hemor-
rhagic infarctions of other organs; in the brain, however, it is usually
elongated and elliptiical in shajje. It is not a necessary result of embo-
lism. The affected part appears red and soft, its periphery contaios
punctate hemorrhages. The microscope shows more or less changed red
blood-globules and fatty detritus. The red blood-globules contmue to
degenerate and their pigment crystallizes. The part then assumes a
brownish-red, chocolate, or ochre-yellow appearance, finally the characicr
of yellow softening. We must avoid mistaking it for a hemorrhage
(demonstration of nn embolus).

The size of the softened spot sometimes exceeds that of an apple. A
number of such spots are occasionally observed in various stages of de-
velopment.

The emboli will possess infectious properties if they are derived from infec-
tious foci, for example, putrid pulmonary processes, septic endocarditis, etc.
They may then give rise to inflammation and abscess of the brain, indeed even to
ichorous processes, if they are derived from gangrenous foci.

Little need be said concerning the changes in the vessels themselves.
Emboli are often recognized as such by the mere fact that they are situ-
ated at the points of bifurcation of the arteries. The artery is not in-
frequentlv dilated into a spindle shape at the site of obstruction. In a
case in which the embolus was derived from the lung, Boettcher detected
pulmonary pigment in it. In thrombosis, the vessel is found thickened
in j)la(!e8, calcareous, yellow, and hard, and gaping on transverse section.
The thrombus may entirely occlude the vessel, it may be peripheral,
or i)ropagated from more remote parts. It inay undergo absorption,
canalization, fibrous metamorphosis, and calcification.

ill. Symptoms. — Cerebral thrombosis often develops slowly, embo-
lism suddenly. Thrombosis is preceded not infrequently by prodromata,
such as headache, dizziness, nausea, vomiting, disturbances of sight
and hearing, irritability, impairment of memory, temporary aphakia,
para'Kthesm, temporary paresis or paralysis. These are evidently the re-
sult of narrowing of the lumen of the vessel; but it appears as if the
brain can accommodate itself to a certain diminution in the supplv of
hlood and produces functional disturbances only when the minimum
boumiary is passed. This mav occur as suddenly as in embolism.
««,! fi f>'"^P^^^"^.» i^re then exactly like those of an apoplectic attack,
b i. ^^^"VI"'*'^^*!"^'^'"^ "^^^ identical. It has been thought that em-
{ .;l i"^"- thrombosis are associated more frequently with general or
feren&n !''''^ ?"\>'^^>pl^^^ic convulsions, but this does not justify a dif-
Itrtntial diagnosis between hemorrhage and emboUsm or thrombosis.

DISEASES OF THE BSAIN. 233

lu many cases, the stage of apoplectic coma is followed, as in cerebral
hemorrhage, by a stage of inflammatory reaction.

This is followed by the stage of focal symptoms, which vary accord-
ing to the portion of the brain aflfected. Since embolic and thrombotic
processes occur most frequently in the left middle cerebral artery, the
symptoms usually consist of right hemiplegia and aphasia.

Embolic hemorrhages into the retina are sometimes observed as prodromal
symptoms.

The secondary changes after embolism or thrombosis are the same as
in cerebral hemorrhage (vide page 227).

The symptoms sometftnes subside very rapidly, for example, if an
embolus is broken up and the particles are driven into small, unimpor-
tant arteries. Relapses are not infrequent.

IV. Diagnosis. — The recognition of embolism and thrombosis of
the cerebral arteries is one of the most difficult diagnostic problems.
They may hardly ever be diflferentiated with certainty from cerebral
hemorrhage. If the patient is young and has a demonstrable valvular
lesion, if embolic phenomena have been noticed in other organs (haema-
turia, enlargement of the spleen, pulselessness in certain parts, etc.), if
changes can be demonstrated in the aorta or carotids (aneurism) or em-
bolic changes in the e^es, the diagnosis of embolism is more probable.

The differential diagnosis between cerebral hemorrhage and throm-
bosis is much more difficult. The latter is more probable if arterio-
sclerotic changes can be demonstrated in the peripheral arteries, if the
middle cerebral artery is attacked, or if syphilis constitutes a probable
etiological factor. But the diagnosis never can be made with more than
a certain degree of probability.

The same factors must be taken into cousideration in attempting to
make a differential diagnosis between embolism and thrombosis of the
cerebral arteries.

V. Prognosis. — The prognosis is also grave, because the disease may
prove immediately dangerous to life; the foci of softeniug and the symp-
toms dependent thereon cannot be made to disappear, and relapses are
frequent and cannot be prevented. Becovery is possible only in embo*
lism of the cortical vessels.

VI. Treatment. — The treatment is similar to that of cerebral hem-
orrhage, except that stimulants, and not venesection, are indicated during-
the apoplectic seizure. In syphilitic cases, inunctions of mercurial oint-
ment ( 3 !• daily) and potassium iodide internally (gr. xij. t. i. d.).

6. Inflammation and Abscess of the Brain.

Cerebral Encephalitis.

I. Etiology. — Encephalitis and its termination in abscess are rare
occurrences.

One of the most frequent causes is traumatism. As a matter of
course, it occurs particularly after injuries to the skull. These include
simple concussion, fractures and fissures, impaction of fragments of bone
in tne brain, entrance of foreign bodies.

The cerebral lesion is sometimes found at the site of injury, some*
times on the opposite side of the brain (contrecoup).

234 DIShlASES OF THE BBAIN.

In some cases the inflammation is propagated from adjacent parts.

A promiuent part is placed by ear diseases. Taberculosis or ordinary suppu-
ration of the petrous portion of the temporal bone or the mastoid process is a
not infrequent cause of encephalitis and cerebral abscess. In some cases the pas
makes its way to the meninges and brain substance, and directly inflames them;
or it creeps along the sheaths of the facial and acoustic nerves to the brain; or
the blood-vessels and lymphatics convey the inflammation-produoera to the brain,
ao that encephalitis or cerebral abscess (with or without thrombosis of thesinusf^)
is produced, despite the fact that the bones and nerve sheaths are intact. Dis-
eases in other external cavities of the skull may aiso give rise to encephalitis, in-
asmuch as the inflammation is propagated directly to the brain.

This category includes tumors of the antrum of Highmore, of the naso-
pharyngeal cavity, and the orbits. True inflammations, for example, ozasna or
orbital inflammations, are even more apt to exteifd to the brain. It is hardly
necessary to say that ulcerating, tuberculous, and syphilitio changes in the skoU
are apt to attack the meninges and brain.

Embolic and metastatic processes sometimes play an important part
the etiology.

In the previous section we have called attention to the fact that cerebral em-
boli sometimes possess infectious and inflammation-producing properties (septU)
endocarditis, pulmonary abscess and gangrene, putria bronchitis, bronchiectans,
empyema, suppurations at the periphery of the body and in the abdominal cavity,
infectious diseases, and inflammations of the soft parts of the skull, etc.).

A fourth group of cases includes those in which a nrevious disease of
the brain is followed by secondary inflammation. Thus, hemorrhages,
necrotic softening, tumors, and parasites may setup inflammation in the
surrounding parenchyma.

A series of cases remains in which no cause can be demonstrated
(spontaneous cerebral abscess). The number of such cases diminishes
with increasing care in post-mortem examinations, and many modem
authors deny their occurence.

Men are attacked more frequently than women, because they are more
subject to injuries.

II. Anatomical Changes. — The inflammatory changes of encepha-
litis t)ccur either as inflammatory softening or abscess. We distinguish
red and yellow inflammatory softening. Necrotic and inflammatory sof-
tening may look exactly ahke and often can be differentiated only by
taking into consideration the previous history and other pathological
appearances (embolus, thrombus, trauma).

In red softening, the affected spot exhibits a diminished consistence
and a blood-red, in older cases brownish-red to chocolate color. At the
centre, the color is uniform; at the periphery, we find patchy redness and
punctate extravasations. On account of serous infiltration, the morbid
focus occupies a greater space than that originally occupied by the in-
flamed portion of the brain. It projects, therefore, upon the cut sur-
face or presses upon the entire hemisphere, as shown by flattening of the
convolutions, dryness and anaemia of the surface of the brain. In some
cases, the changes are confined chiefly to the immediate vicinity of the
lesion, and are manifested by anaemia or inflammatory oedema, or both.

A distinction cannot be made between parenchymatous and interstitial en-
cephalitiSf since both parts of the parenchyma take part in the inflammation.

The neuroglia presents swelling of its cellular elements and the intercellular
tissue, proliferation of the nuclei and development of myeloplaxes, cloudy swell-
ing terminating in fatty degeneration. In the ganglion cells, swelling, nuclear

DISEABK8 OF THE BBADT.

proliferation, vesicular traasformation of the nuclei, cloudy swelliog, Rnallj'
latlT degeneration and iJeBtruction have been described. Destruction of the
raeuuilary sheaths of the nerve fibres, spindle-ahaped distention, and later fattj
defeneration of the axis cylinders, have lieen observed. Among the changes
mentioned are extravasations of blood, so tliat tree blood-globules are found
eingly or in groups between the nervous elements of the brain. The blood-
vessels are dilated in places, their nuclei swollen and increased in number; here
and there the adventitious lymph sheaths are diliLted anipulln-Iike, and filled
with extravasated red blood-globules. In some places, the vessels are sur-
rounded bjr emigrated white blood-globuleH.

The transition from red to yellow isoftening takes place gradnallj, as

: result of destruction of the extrarosated red blood-globulea and coa-
irsion of their pigment, but especially of the increasing fatty degeuera*
iion in the inflamed parts. As the final result of the former process,
we And, aa the remains of previous hemorrhages, hsematoidin in the
form of gratmles, needles, and tablets, partly free, partly inclosed in
cells. Some of the ganglion cells are stuffed full of yellow pigment
(so-called pigment dogenenition ). Calcification of the ganglion cells
baa also been observed. The main mass of the spot of softening is
formed of granules of fat and grannlo-fatty cells. Tne latter may result
from fatty degeneration of the neuroglia cells, the nuclei of the vessels,
and the ganglion cells, but in part they are fat-containing um<Bboiii
cells which transport the fat to the lymphatic and vascular channels.
Hence the adventitious lymph sheaths of the blood-vessels are also litled
with fat granules and grannlo-fatty cells. The blood-vessels in part are
obliterated.

If a stream of water is allowed to flow over the site of disease, the
^jftened mass will be washed away, and leave an irregular cavity with
jagged walls.

The fatty mass may be entirely absorbed and replaced by a firm,
sclerotic cicatrix, which is pigmented particnlarly at its centre. As a
matter of course, the nerve elements which have "been destroyed do not
undergo regeneration. It the cicatrix has formed in the cortex, it
results in a more or less marked depression, over which tlie pia mater is
thickened, and firmly adherent to the surface of the brain. This termi-
nation is similar to that of many hemorrhages, and indeed it is often
impossible to determine whether the cicatrix is hemorrhagic or inflam-
matory in its origin. In other cases, the attempts at recovery lead to
the formation of cysts. The fatty mass ia gradually absorbed, and re-
placed by serous or clondy fluid. The latter is encapsulated, the capsule
"ling often traversed by connective-tissue septa, formed partly of new

med connective tissue, partly of obliterated vessels.

The number, size, and situation of the encephalitic foci are subjeot
lo great variation. In the majority of cases, there is only one focus, nut
under certain circumstances, for example, in pyjemia, there may be ten
or twenty. They are usually so much larger the smaller their number.
Pymmicfoci are often no larger than the head of a pin; solitary ones
may attain the size of an apple or fist, or occupy almost an entire hemi-
flphere. The cortex and basal ganglia are the moat frequent sites of the

^_1vi

the t
^^elace

^■leine

^^■sTmi
^■tOgri

^^^It

Under certain circumstances, the inflammation terminates in the
development o( pus (cerebral abscess). Abscess of the brain may be dif-
fuse or encapsulated.

In diffuse cerebral abscess, the collection of pus is directly in contact
rith the parenchyma of tho brain. It exhibits a decided tendency to

236 DI8SABE8 OF THE BRAIN.

spread more and more^ and finally maj lead to perforation into the yen-
tricles^ towards the base of the bram (with secondary menin^tis), or
upwards through the cortex. If there are openings m the skulls for
example^ as the result of injury or ulcerative processes in the bones, the
pus may make its way externally. Diffase cerebral abscess is often
irregularly elongated. It may be situated in the cortex or deep in the
substance of the brain.

In encapsulated cerebral abscess, the collection of pus is surrounded
by a fibrous capsule. This may attain a thickness of several millimetres,
and be very firm and resistant; it passes gradually into the surrounding
parenchyma. The encapsulation of an abscess does not appear to put
an end to its further growth. It may exceed the dimensions of an
apple.

There may be transitional forms between the two varieties of abscess,
i, e., only a part of the abscess may possess a cyst- wall.

The formation of pus in the brain may occur very lapidly^ and in
some cases it has been found five days after injury. Emcapsulation
occurs, on the average, from the seventh to twelfth weeks; in Lalle-
mand's case, it was found on the fifteenth day.

The pus in a cerebral abscess is generally acid, has a rancid odor,
and not infrequently presents a consistence like that of synovial fluid or
mucus. Goagula form on the addition of acetic acid. The pus may
become putrid if it communicates with the air through an opening in
the skull, or if it is produced by ichorous inflammation of surrounding
parts, or by ichorous emboli.

Pramients of bone or foreign bodies — the results of previous injury
to the skull — are sometimes found in the pus.

On microscopical examination the pus is found to consist, in great part, of pus-
corpuscles, which have been dencribed as multinuclear (perhaps the result of pro-
longed maceration). In addition, drops and granules of fat, needles of margario
acid, and, according to some writrers, corpora amylacea.

The cyst-wall is composed of firm, fibrillated connective tissue, ivith spindle-
shaped ceils scattered here and there. Rows of fat and pigment granules also are
found in places between the fibies. The abscess- wall is poor in hlood-veftsels. It
is probably produced chiefly by the adjacent neuroglia, a certain part being
played bv emigrated white blood-globules which are converted into connective-
ossue cells.

Thickening, caseation, and calcification cf the pus have been de-
scribed among the secondary changes in abscesses of the brain. It is
said that the pus may undergo gradual absorption, and the cyst-walls
become adherent to one another.

III. Symptoms. — Encephalitis and cerebral abscess may remain
latent during life, and be found accidentally in individuals who have
died from an intercurrent disease.

In other cases, an apoplectiform attack occurs, and proves more or
less rapidly fatal. The fatal event is occasionally preceded by a series
of apoplectiform attacks.

In a third series of cases, gradual exhaustion takes place, but the
causes remain latent during life. The most prominent symptoms are
anorexia, emaciation, sallow complexion, and increasing feebleness;
death results from exhaustion, and the autopsy reveals an abscess of the
brain.

In still other cases, peculiar febrile movement is noticeable (chills,
followed by high fever, and terminating in sweat). These attacks may

DISEASES OF THE BBAHT. 937

occur at sncii regular interrals as to rouse the gnspicion of iDterniittont
fever, particularly if the liver and spleen are enlarged. The fever ia
attended by emaciation and a cachectic appearance.

Two of my cases ran their course with gastro-enteritic and typhoid
fiymptoms: gradual onset, continued fever, frequent Tomiting, coated
tongue, abdominal tenderness, obstinate diarrhcea, and ileo-csecal gur-
gling, roseola, and slight enlargement of the epleen,

A auspicion of cerebral disease will only be aroused if difluse or focal
cerebral symptoms make their appearance. Even then the diagnosis
will remain doubtful, unless an injury to the skull, ear diseases, or pu-
trid urocesaes in the organs of respiration point to a cerebral absceaa.

'1 he symptoms sometimes affect almost exclusively the mental sphere.
The patients suffer from impairment of memory, gradually become im-
becile or maniacal, etc.

In others, convulsive phenomena occupy the foreground; epilepti-
form attacks occur, at first rarelj', then more and more frequently, and
finally terminate in death.

Headache is one of the most constant of the diffuse symptoms. . It
may be constant, or present only at times, or increases in parosyems.
^^ Its intensity varies from a feeling of dull pressure to pain of intolerable
^^L Tiolence.

^H Some patients complain of a disagreeable sensation of a rolling or
^^piDOving body within the skull; this is often felt only in ceitaiu positions.
^^ Vomiting is sometimes very obstinate, in other cases it is almost en-
tirely absent. Vertigo, insomnia, and irregularity of the pulse may also
be mentioned among the diffuse cerebral symptoms.

Some patients complain of pain and parffisthesieB in the limbs, in one
limb, or in hemiplegic or paraplegic distribution.

The changes in the fundus of the eye constitute, to a certain extent,
the transition from the diffuse to the focal symptoms. The fundus
often, though not constantly, presents the signs of choked disk, retini-
tis, and neuro-retinitia, which terminate in optic atrophy, after they
have lasted a long time. The changes arc sometimes more marked in
one eye (on the side of the abscess). Retinal hemorrhages have also
been observed.

The focal symptoms include paralyses, spasms, and contractures, the
distribution of which depends upon the sitnation of the inflammatory
focus in the brain.

To;nbee showed that diseasea of the external auditory canal are followed
most frequently by ahecefls of the cerebeUuin, thoBi- of Ihe tympanic cavity by
abecess of tbe cerebrum, those of the tabyiintli by abscess of the medulla
oblongata.

Among the unusual symptoms is escape of the pna externally. If the
abscess ruptures into the ventricles, deatli generally occurs very rapidly,
preceded by epileptiform convulsions. Perforation beneath or through
the pia mater also gives rise to general convulsions, apoplectiform sei-
zures, meningitic symptoms, and speedv death.

The duration and course of encephalitis and cerebral abscess vary

I extremely. In Haertlin's case, the absoeas ran an entirely latent course
for twenty-six years. In other cases, death occurs in a few hours or
A prolonged latent course often is interrupted suddenly by violent
((fluptoma which subside, perhaps reappear, etc.

238 DISEA8B8 OF THE BRAIN.

IV. Diagnosis. — It is evident from the preyious remarks that the
detection of encephalitis and cerebral abscess is often impossible.
The diagnosis includes the recognition of the presence of an abscess and
its location. The first point is determined by the etiologr, the second
is based on the principles laid down in the preliminary diagnostic re-
marks.

V. Prognosis. — The prognosis is always grave, almost always fatal
After suppuration has taken place, recovery cannot be looked, for unless
the pus 18 removed artificially by operation.

VI. Treatment. — Prophylactic measures (concerning which we
refer the reader to special treatises), must be adopted in injuries to the
skull and diseases of the auditory apparatus. If there is reason to as-
sume the existence of encephalitis, we should order an ice-bag to the
head, local abstraction of blood, inunctions of mercurial ointment, and
mild laxatives, or, if the boweU are regular, potassium iodide. After
pus has formed, the treatment consists of trephining and evacuation of
the pus, if the abscess can be localized. OtherwisCj purely symptomatic
treatment.

Appendix.

a. Congenital encephcUitia, Virchow has shown that encephalitis may some-
times be congenital. He observed it in still-bom children and in ne^v'-bom, whose
mothers had suffered from small-pox or syphilis. Birch-Hirschfeld oboerved it
in children suffering from jaundice and suppuration of the umbilicus. But not
every discoloration of the brain and accumulation of fpranulo-fatty ceUs may be
regarded as an inflamnuitory product, since Jastrowitz has shown that the de-
velopment of the medullary sheaths in the foetal brain is attended with the fornuu
tion of gran ulo-fatty cells. While the diffuse occurrence of granulo-fatty odls
is physiological, their aggregation in foci is the result of an inflammatory process;
in addition, proliferation of round cells and hemorrhages are often present.

b. Acute cerebral, atrophic infantile paralysis. Acute infantile p(h
lio-encephalitis. This disease generally attacks children between the a^es
of one to three years. As a rule, no cause can be demonstrated; an in-
fectious influence appears very plausible.

As a rule, the disease begins acute and suddenly. The children are
attacked with fever, vomit, become stupid, and are seized with epilepti-
form spasms. They generally recover consciousness in one or two days;
hemiplegia is then noticeable. In the majority of cases, the limbs alone
are affected, but more rarely the facial or other cerebral nerves are par-
alyzed. Monoplegia is sometimes observed.

The paralysis occasionally disappears in certain parts. The perma-
nently paralyzed muscles soon undergo atrophy, and the growth of the
paralyzed limbs is retarded. The panniculus adiposus is increased in
thickness, the skin is cold, and has a blue, marbled appearance. Sen-
sibility is generally unchanged, the tendon reflexes exaggerated. There
is sometimes a marked tendency to profuse perspiration.

The paralyzed muscles gradually become rigid, and muscular con-
tractures may develop. Motor irritative symptoms set in not infre-
quently in the form of hemichorea, hemiathetosis, or associated move-
ments. At a subsequent period, the children often suffer from epilepsy
or become idiotic.

Tlie clinical history is very like that of acute poliomyelitis (vide
page 118). and probably it is the result of corresponding anatomical le-
sions. Tnere is no doubt that acute polioencephalitis is an acute iuflam-
mation of the motor cortical centres.

DISEASES OF THE BRAIK. 239

Autopsies have been made hitherto in old cases alone; the lesions
found were atrophy of the cortex, the formation of cysts, thickening and
adhesions of the pia mater. In rare cases, the disease is the result, per-
haps, of cortical hemorrhage or embolism.

The prognosis and treatment are the same as in acute poliomyelitis
(vide page 120).

7. Tumors within the Cranial Cavity.

I. Etiology. — Intracranial tumors may grow from the brain sub-
stance, the meninges, or the bones of the skull. Extracranial tumors
sometimes j)roliferate into the cranial cavity through openings in the
skull. This may happen in the case of orbital tumors which pass
through the optic foramen into the cranial cavity; or tumors of the nasal
cavity, the antrum of Highmore, the spheno-palatine fossa, or the
petrous portion of the temporal bone, after eroding the bones which
cover them, may also proliferate into the brain. On the other hand,
tumors within the cranial cavity sometimes perforate the bones of the
skull and grow outside.

Very little, if anything, is known concerning the real cause of develop-
ment 01 intracranial tumors. We are satisfied of the influence exerted
by traumatism, although this was strenuously denied by Cohnheim.

Intracranial tumors may be the result of chronic infectious diseases,
particularly tuberculosis and syphilis (solitary tubercles and gummata),
out these will not be considered here.

Metastatic growths are sometimes found, following neoplasms (cancer
and sarcoma) in other organs.

Some writers attach importance to hereditary influences. The
development of intracranial tumors is also attributed to excessive
mental strain, excesses in Baccho et Venere, and exposure to the sun.

They are more frequent in men than in women, probably from the
greater liability of the former to suffer injuries, to indulge in alcoholio
excesses, and to the greater demands upon their mental activity.

Cerebral tumors occur at every age (Hasse found a cancer of tho
brain in a new-born babe). Tubercles are more common in children
^usually beyond the age of 2 or 3 years), while cancer is observed more
irequently at an advanced age.

II. Anatomical Changes. — Two factors must be taken into con-
sideration — the structure of the tumor, and its effects upon the brain.

The following are the varieties of tumors (intheir order of frequency)
found in the cranial cavity: glioma, sarcoma, psammoma, myxoma,
carcinoma, melanoma, cholesteatoma. Very rare are: papilloma, fibroma,
lipoma, enchondroma, osteoma, dermoid cysts, cysts, and angioma.

Allied to tumors are the cases of heterotopia of the ^ray matter.
This term is applied to an accumulation of gray matter m abnormal
positions, occasionally in the form of small nodules, which sometimes
project like a tumor into the ventricles.

Among the tumors should also be included hyperplasia of the pineal
gland and struma pituitaria.

Gliomata generallv occur singly and start from the white matter ; if they ex-
tend to the surface of the brain, they form no adhesions to the meninges ; they
develop with striking frequency as the result of injury, grow very slowly, and
sometimes attain almost the size of a fist. Their color often differs very little from
that of normal g^y matter, so that smidl tumors are readily overlooked ; in other

240 DISEASES OF THE BRAIN.

cases, they have a more or less bright red color, according to their Tucnlant^.
Tlie latter is often very great, thus affording the possibility of rapid changes in
size, and clinically of rapidly alternating symptoms of irritation and paralysis:
furthermore, of extravasations of blood. The latter mar resemble ordinaiy
cerebral hemorrhages, and the diagnosis often cannot be made until tumor maasei
are discovered at the peripheral zones of the hemorrhage. Virchow also statei
that fatty degeneration of a glioma is apt to be mistaken for yellow softening of
the brain. Small gliomata may simulate sclerotic foci, but the latter are gener-
ally multiple. These tumors start from the neuroglia, so that they are indis-
tinctly separated from the adjacent parenchyma of the brain. There may be
transitions between glioma and myxoma or sarcoma (myxo-^lioma and sarco-
glioma). The former are soft and gelatinous on account of the mucoid character
of the basement substance ; the latter are rich in cells, tougher and firmer.

Sarcoma of the brain is generally primary, more rarely metafitatic, or the ex-
pression of general sarcomatosis. Melanosarcoma has a special tendency to the
lormation of metastatic growths in the cranial cavity.

As a general thing, only one sarcoma is found in the cranial cavity, more
rarely there are several. They may start from thn meninges or substance of the
brain. Sarcoma of the dura mater is relatively frequent at the base of the skull,
and is especially apt to grow from the sella turcica and petrous portion of the
temporal Done.

Sarcomata of the substance of the brain generally possess a vascular membrane
around them, so that they can readily be peeled out of the brain. The tumon
may be firm or soft, whitish in color, or vascular. In the latter event they ex-
hibit a tendency to hemorrhage. They are distinguished from gliomata by their
more rapid growth. The cells of sarcoma are very delicate, so that in fresh,
teased preparations we find chiefly free nuclei.

Psammoma is characterized by the occurrence of chalky concretiona in iti
tissues. The latter are often visible to the naked eye as yellowish granules, icrale
under the knife, and are composed of laminated masses of carbonate of linia
The chief mass of the tumor is fibrous. It exhibits a predilection for the dors
mater, particularly of the convexity of the brain. The tumors are generally sin-
gle, rarely multiple, and do not often exceed the size of a walnut. They are
sometimes found in the brain substance itself.

Carcinoma rarely develops in the cranial cavity. In the majority of cases the
tumor is primary and usually single. Multiple cancers are sometimes situated in
symmetrical localities. Cruveilhier counted over one hundred tumors in one
case. Their shape is round, nodular, lobulated, more rarely they are diffusely in-
filtrated. Tliey may start from the dura mater, pia mater, or substance of the
brain, and occasionally grow into the cranial cavity from the outside. On the
other hand, tumors which start from the outer surface of the dura mater some-
times perforate the skull and appear beneath the scalp. They sometimes attain
the size of a flst. Medullary cancer is frequent, scirrnus is rar^. According to
Rindfleisch, all cancers of the brain start from the pia mater, although their con-
nection with the latter may become indistinct. The^ often possess a capsular
membrane. Fatty degeneratien, caseation, calcification, and ossification have
been described as secondary changes.

Myxomata and melanomata are rare growths; the latter develop from the
pigment cells of the pia mater.

Cholesteatomata are Arm, epithelioidal tumors, with a mother-of-pearl gloss,
and sometimes attain the size of a walnut.

Intracranial tumors may injure the brain temporarily and perma-
nently — temporarily by changes in volume as the result of varying vas-
cularity, permanently by increasing growth, compression, and irritation.
If the tumor starts from the bones or meninges, the surface of the brain
beneath is flattened, the gyri and sulci are effaced, the surface often dry
and unusually anaBmic. Tumors at the base of the skull often exert
pressure on the cerebral nerves and cause them to undergo atrophy.

In tumors of the substance of the brain, the affected side often ap-
pears more prominent; when the dura mater is thrown back, the surface
IS flattened, dry, and ansBmic. The falx cerebri and the brain itself are
sometimes pushed towards the opposite side (vide Fig. 116).

DIBBABES OF 1'HB BRAIK.

The vicinity of the tumor may undergo important changes: Buppu-
ration, eofteniug, hemorrhage, and aniemia. New growths are followed
occasioiiallv by meningitio symptoms, more frequently by hydrocephalic
changes as the result of pressure on the vena Oaleni.

ifl. Symptoms. — Intracranial tumors sometimes run an entirely
latent course, and are discovered accidentally at the autopsy. This may
be true of relatively large neoplasms, while, on the other hand, very
small ones may produce the most violent eymptoms. Tbia depends upon
the localization and rapidity of development.

Among the diffuse eymptoms of intracranial tumors, headache occu-

pies a prominent part, and it is so couEtant that lis absence contra-indi-
cates the diagnosis of tumor in a doubtful case. The pain may be
constant or intermittent, occasionallv it is fett chiefly at night. It is
provoked or intensified by bodily and mental excitement, and excesses
in Kaccho et Vonere, lis intensity may become so extreme that
the patients grow wild with paio. In other cases it consists merely of a
feeling of dull pressure within the skull. The patients are often unable
to localize the pain accurately. As a general thing, its distribution does ,
not throw muca light on the location of the tumor. But if the pain is
referred constantly to the occiput and nape of the neck, the tumor may be
asBnmed to be situated in the posterior fossa (occii)ital lobes, moro fre-
IG

qnently the cerebellum). Tho pain is probably the result oC dra^ib;
upon tne meninges, which are rich in nerve fibres.

The skull is aomelimes very tender on percasaion. If the toD<ienie»
is confined to ft circuniBcribed gpot, it muv be assumed to be connected
with the situation of tJie tumor; but thia la a rare occurrence.

Very many patients complain of vertigo. It ie sometimes so ooo-
stant iind severe that the patients are unable to move about tinsuppoitel.
They often exhibit a tendency to tali in a definite dircctioQ, bsck-
wards or forwards, to the right or left. This Bvmptom is apt (o be
especially well marked in tumors of the posterior fossa.

Psychical disturbances are of frei^ueut occurrence. The putiejita fw-

Cboked dlik In cerebr&l Cumor. titter HaicnuB.

come moody, irritable, apathetic^ somnolent, the memory ia impaired:
delirium, maniacal attacks and well-marked psychopathies set in, and
sometimes obscure the real cause of the disease. The mental distorban-
oes also present remissions and exacerbations.

Conditions of somnoienco and coma occur with remarkable f reqn^cyj
they may last hours, days, or even weeks.

Apoplectiform and epileptiform attacks are by no means infrequent.
The former may be the result of hemorrhages into the tumor or its
vicinity, or, like tlio epileptiform seizures, they are the result of irri-
tation produced by sudden increaso of cerebral pressure. Henoe tb^
are followed, according to circumstances, by ■^ — * '

DISEASES OF THK BBilX. 2i3

rparalvsos. The epileptiform apasma n-re general, unilateral, confined to
one limb or to groups of muacios. In somo cages, consciousneas is re-
tained. Epileptiform twitchinga in the distribntion of a single nerve, or
recurring epaama in one limb alone, must arouse the suspicion of irri-
tation of parts of the motor region of the cortex.

Choreiform movements sometimes appear in individual limbs. Tliia
symptom has been attributed to a lesion of the posterior ]>art of the in-
ternal capsule, but it has also been observed in diseases of other parts,
for example, tho pons Varolii.

Many patients complain of vague, peripheral, rheumatoid pains, and
occasionally of intoleraule itching of the skin.

Changes in the fundus of the eye and in vision constitute some of the
most important diagnostic symptoms. The most important is the so-
called choked disk (papillitis), which is recognized by swelling of tha
optic nerve, distention of the retinal veins, and narrowing of tho arteries
(vide Fig. 117). Reich found that among eighty-eight cases of tnmor of
the brain, choked disk vas present in 95.1::£. Sight is impaired in
many cases; amblyopia is produced and even complete amaurosis. It
musi'borememherGd, however, that the most marked evidences of choked
disk may be present, although vision remains intact.

I Asa rule, choked disk ia bilateral, although otio eye may be more afTected
~ than the other. The leaion ia Che result of thu increased intracranial pressure, iu
consequence of which cerebro-epinat fluid is forced from the subarachnoid apace
between the external and internal uptic sheaths ( inter vaginal space). The dropsy
of the optiusheath compreasea the retinal veins, produces venoua congestion, and,
at the same time, swelling of the optic papilla. Tlie changes in question subside
at times, |«o that mere traces remain. In other cases, they are followed by
retinitis, neuro-retinitis, aud atrophy of the optic nerve, but the latter may also
be the result of direct pressure of the tumor on the chiasm or optic tract.

Choked disk is also found in hydrocephalus, abscess, and menigitis, in short,
in increased intracrauial pressure from whatever cause, but 'it is most constant
and marked in cerebral tumors.

Tumors of the brain are sometimes attended by retinal hemorrhages and
by yellow patches, as in Bright's disease.

With regard to narrowing of the Held of vision and disturbances of the color
sense, we refer the reader to text-books on ophthalmology. Some patients com-
plain of subjective sensations of light. Sudden bUndoeas (apoplectiform amau-
rosis) occurs occasionally; it may be unilateral or bilateral, disappear and return,
liie ophthalmoscope ahows no striking changes, and the symptom is probably tha
result of temporary increase of intracranial pressure.

■ Distnrbanccs of the olfactory and acoustic nerves are sometimes
^^beerved, as the result of direct pressure on the nerve trunks, of neuritis,
lor of increased intracranial pressure, which ia propagated to the sheathe
of the nerves as in choked disk.

The general nutrition may be undisturbed, indeed there ia some-
times an unusual development of the panniculus adiposua. Other
patients are very pale and present an appearance like those euftering
from Bright's disease. Cachexia develops rapidly if tha tumor is can-

The appetite is often lost, but in two cases wo noticed insatiable
boulimia. Increased thirst is often noticeable, particularly if the patients
BuiTer much from vomiting. The urine may contain angar if the
tumor is situated in the floor of the fourth ventricle; Schultze found
inoeit in two cases of this kind. The bowels are usually constipated;
■^volautary evacuations may occur during comatose and apoplectiform

244 DISEASES OF THE BRAJSi.

conditions. Sexual desire is increased in some patients^ in others it is
lost. During comatose and somnolent conditions, the patients often
play with their genitals, but some writers regard these moyements as
purely mechanical and automatic*

Irregularity in breathing, Gheyne-Stokes respiration, and retardation
of the pulse are frequent symptoms, which occur solely or chiefly during
comatose conditions. Fever sometimes appears as a terminal symptom.

The focal symptoms consist of irritative and paralytic phenomena
(spasms and contractures, pareses and paralyfres). The previous remarks
on the local diagnosis of brain diseases hold good here. Special import-
ance attaches to paralyses of cerebral nerves of a peripheral character,
because they are generally the result of compression oy tumors at the
base of the brain. The paralyses retain the peripheral character even
when the nuclei of the nerves are destroyed by the tumor. Paralyses of
central character only develop when the nerve-tracts are injured on the
central aspect of the nuclei.

The sensory nerves quite often present the signs of ansesthesia dolo-
rosa, because the tumor compresses the nerve and prevents conduction
from the periphery, while it irritates the central end, and thus produces
pain which is referred to the periphery.

The duration of intracranial tumors varies; calculations are not re-
liable, because it is very difficult to determine the beginning of the dis-
ease. Some years ago I saw a case of glioma of the brain which had
lasted at least twelve years (v. Graefe had made the diagnosis from the
presence of choked disk twelve years before death). Andral reports a
case which lasted fifteen years. But, as a rule, they run their course in
one to two years, sometimes in a shorter time.

Death may occur suddenly in an apoplectiform or epileptiform
seizure, after a longer or shorter period oi coma, or after bodily or
mental exertion, for example, coitus or a drinking bout. The nital
termination is sometimes preceded by meningitic symptoms. If the
tumor perforates externally, the scalp grows prominent and red, the hairs
fall out, the tumor often exhibits a sort of fluctuation and respiratory
movements; dulness, vertigo, and convulsions are produced if the tumor
is j^ushed back. In rare cases, the patient is relieved by this manipu-
lation. The edges of the opening in the skull are sometimes everted,
and furnish a sensation of crepitation. If the integument is also per-
forated, the tumor ulcerates and often becomes gangrenous.

IV. Diagnosis. — The recognition of cerebral tumors is occasionally
impossible. Choked disk is the most important symptom. The disease
may be mistaken for: a. Cerebral hemorrhage ; the advanced age and
sudden onset of the symptoms deserve special consideration, b. Cere-
bral thrombosis and embolism; the diagnosis of embolism is favored by
the existence of valvular disease of the heart; in thrombosis the etiology
must be considered; the latter is of still greater importance in the differ-
ential diagnosis from c. cerebral abscess (traumatism, suppuration of
bone), d. Patients who are found in a comatose condition may arouse
the suspicion of tircemia, but this will be decided by examination of the
urine, e. The differentiation from epilepsy and psychopathy, without
material changes in the brain, is hardly possible if the ophthalmoscopio
appearances are negative. /. Hysteria is sometimes simulated if the
patients present only ill-denned focal symntoms. g. In a q^we which I
saw in consultation, and in which choked aisk alone pointed to the real
diagnoBis (which was confirmed on autopsy)) the pallor of the patieot

mSEASEs ov THi: Bails'. 94S

led the attending phyBicion to make the diagnosis of progressive perni'
cious aniernia.

V. PROGSOSIS, — The prognosis is nnfavorable. The disease gener-
ally progresses uninterruptedly to a fatal termination.

\I. Treatment. — The treatmeut is purely symptoinatic. The
patient should oat easily digesteti, nutritious food, secure a daily evacu-
ation from the bowels, and avoid bodily and mental exertion. Coitua
and alcoholic stimulants must be interdicted. Morphine may be given
Bubciitaneonsly to relieve headache and vomiting, potassium bromide
{ 3 iisa.-v. at a dose) may he used in conditioua of great excitement.

Godlee recently eoucleated n gUomsk. whicli waa situated below the ri)(ht
anterior central convolution, After temporary i ni prove me nt. the patient died in
the fourth week from menJngitia.

8. Animal Parasites in (he Cranial Caoity.

Cjitlcercus racemoaui. Aner Harchand.

a. Cyaticercua cellulost^. Cj-Bticerci of the brain are not very rare. They may
start from the meaiuKea. from the parenchyma of the bi-aiii (geufitillj- groy mat-
ter), the BuhurachnoUl Kpace, or they may be free in the veniriulen. Tiiose that
■tart In the meninges grow geuerolly from the pia mater, rarely from the inner
nirface of the dura mater. They press upon the surface of the brain, aud bore
depressions into it. In many ciises there is only one vesicle, in others there may
be several hunJred, so that the surface of the brain and tlio meninges are strewn
with tliem. The larger ones attain the aixe of a walnut, in exceptional oases
that of a lien's egg or apple. The wall of the cyst is usually surrounded by a
fibrous capsule, with onion-like lamellee. The contents of the cyst are fluid. At
a certain part, which is generally recognizable externally by a depression and
thickening, is situated a prominence to which the neck and head of the worm
are attached. The head is darkly pigmented at its apex, and the microscope
shows a row of hooka and four suction disks. The cysticerci are said to live
tilree to six years. After death of the parasite, the cysts nnderEO thickening,
caseation, and calcification, and might be mistaken for degenerated tubercles and
gummata, were it not for the persistence of the hooks.

The Imniediat* vicinity of the cysticerci is sometimes entirely unchanged,
In other case*, we notice interstitial proliferation of connective tissue or antemia,
bvperfemia. punctate extravasations, softening, inflammation, and suppuration.
I f^drocephalu-i is ni>t infrequent.

246 DISEASES OF THE BRAIN.

Cysticercus racemosus exhibits a special mode of growth. The cjst formi
inverBions, acquires daughter vesicles, like echinococci, and nuLV form amnltiloo-
ular structure (vide Fign. 118 and 119). This peculiar mode of ae^elopment is at-
tributed to the favorable conditions for growth, such as are fouod particularly in
the subarachnoid cavity at the base of the brain.

Cysticercus racemosus should not be mistaken for free cysticerci which have
become adherent to the wall of a vessel (vide Fig. 120). This variety is also rel-
atively frequent at the base of the brain.

The paths followed by the ))ara8ite8 in their passage from the gastro-intestina]
tract to the brain are not known with certainty. The parasites are more
frequent in men, and develop, as a rule, beyond the age of twenty years.

The cysticerci sometimes run an entirely latent course, in others they give
rise to weU-marked insanity. In ntill others, the symptoms of a cerebral 'tmnor
become noticeable, especially irritative phenomena: headache, vertigo, vomitiog,
neuralgia, epileptiform attacks; paretic or paralytic symptoms are rare.

The diagnosis is often uncertain. Cerebral symptoms may be attributed, with
great probability, to intracranial cysticerci only when the parasites are also
found in the sublcutaneous cellular tissue, the intermuscular connective tissue, or
the fundus of the eye.

The prognosis is unfavorable, nince there is no means at our command of kill-
ing the parasite. The treatment is purely symptomatic.

b. Echinococci are generally found in the brain as single vesicles, noiore rardy
they are multiple. They vary in size, but occasionally attain the dimensions of

a cerebral hemisphere. Morgan described one vesicle as
Fio 120 lar^e as a cocoanut, and weighing eighteen ounces. The

vesicles sometimes perforate the skull and dischai^ge their
contents externally; spontaneous recovery may occur in this
manner. Perforation through the nose and ear has also been
described.

The cysts often contain daughter vesicles, but not in-
frequently they are sterile and contain no scolicea. The
cyst- wall is generally surrounded by a fibrous capsule. The
adjacent parenchyma may be anssmic or hypersemic. con-
tains extravasations, or in rare cases is entirely normal.
Intracranial echinococci often develop in young indivi-
Free cysticercus upon duals. The s}rmptoms are those of a brain tumor with pre-
an artery at the base dominant irritative symptoms, particularly epileptiform
of the brain. Natu- convulsions. Exophthalmus and oedema or the hds may
rai size. After Heuer. y^ produced when perforation is about to occur. In
Westphal's case, more than ninety vesicles were spontaneously discluurged ex-
ternally. Perforation externally may be followed by cure or merely by temporary
relief. Death is sometimes apoplectiform.

The diagnosis is often impossible. The prognosis is very g^ve, since treat-
ment could only prove successful by surgicsu removal of the parasites.

9. Aneurism of the Cerebral Arteries.

1. The causes of the development of aneurisms of the cerebral arteries are
often unknown. Among those mentioned are: injuries to the head, abuse of alco-
hol, and syphilis. The remainder of the vascular system is often intact, in other
cases aortic aneurism is also present. A combination with valvular endocarditis
has often been noticed, and some English writers believe that cerebral aneur-
isms are, in part, of embolic origin.

They are more frequent in men than in women, and not infrequently occur
at an early age. Among fifty-seven cases collected by Lebert,

18 (24%) occurred from 0-19 years.
22(SS%) *♦ " 20-89 **

22(38jt) *' •* 40-60 **

Among seventy-nine cases collected by Coats, forty-two occurred between the
ages of ten to forty years, thirty-seven from the age of forty to eighty years.

2. In almost all cases, we have to deal with true aneurisms, t. e., all the coats
of the vessel are involved. Their size varies from that of a pea to that of a wal-
nut, or in rare cases even larger. They are sometimes fiUea more or less com-
pletely with old clots. The adjacent nerves often suffer compression and atrophy,
the parenchyma of the brain is softened. In three-fourths of the cases, the

DISEASES OF THE BRAIN. 247

aneurism ruptures, giving rise to profuse mening^l (particularly subarachnoid)
hemorrhage, occasionally to destruction of the adjacent substance of the brain.

The aneurisms are found most frequently in the circle of Willis and its per-
ipheral branches, more rarelj[ in the internal carotid or vertebrals. Gairdner de-
scribed an aneurism of the middle meningeal artery.

The most frequently affected vessel is the middle cerebral artery, next the
basilar. Left-sided aneurisms are more frequent than those on the right side,
occasionally they are multiple.

8. Aneurisms of the cereorul arteries may be entirely latent during life. In
some cttses, insanity or epilepsy develops; in others, there are diffuse and focal
cerebral symptoms: headache, vertigo, vomiting, neuralgia, blindness, optic
atrophy, twitchings, and paralyses in certain nerve tracts. Of course, these
symptoms depend on the situation of the aneurism. Paralysis of the motor
ocuh nerve is especially frequent. Rupture of the aneurism is followed by an
apoplectic attack, which, as a rule, is very rapidly fatal. Some patients com-
plain of a subjective auditory sensation of roarine. and vascular murmurs have
sometimes been heard on auscultation of the skull.

The following case may serve as an illustration of the history of the disease.
A servant, set. 23 years, who had suffered several weeks from vertigo, nausea,
rush of blood to the head, and insomnia, noticed for several days a weakness of
the right limbs. On admission to the hospital, there was pare^ of aU the
branches of the facial nerve, and of the right arm and leg; in addition, paralvsis
of the left motor oculi nerve. Hence a diagnosis of disease of the left cerebral
peduncle. A few days later, the patient had an apopletic attack, and died thirty-
sL:: houra later. It was found that an aneurism of tne left posterior cerebnd artery,
which had pressed on the cerebral peduncle, had undergone rupture.

4. The diagnosis is very difficult, almost always uncertain. The prognosis is
unfavorable on account of the tendency to rupture; treatment purely sympto-
matic.

10. Hydrocephalus,

Hydrocephalus is the term applied to a collection of serous transu-
dation, either between the meninges or into the cerebral ventricles. The
former is known as external hydrocephalus, the latter as internal hydro-
cephalus.

In external hydrocephalus, the fluid may be situated in the subdural
cavity, or in the subarachinoid meshwork. It is now believed that the
latter variety is much more frequent than the former.

I ntermeninffeal and ventricular hydrocephalus are not entirely distinct,
since, as is well known, the subarachnoid space communicates with the
cavity of the ventricles. Moreover, observation teaches that effusions
may be present at the same time in both localities.

Hydrocephalus may be diffused or circumscribed. The former is
much more common than the latter. In the second variety, the accu-
mulation of fluid is confined to circumscribed parts of various cavities.
In this manner, cystic spaces develop between the meninges, or certain
portions of the ventricles are dilated and fllled with fluid.

In order that a large amount of fluid may enter the skull, the bones
must yield to the pressure of the fluid and undergo distention, or the
brain substance must be compressed. Distention of the skull can only
occur during childhood. It is apt to be especially marked before the
closure of the sutures and fontanelles. In adults, the fluid exercises
its chief effect in producing compression of the brain, though not infre-
quently the cranial bones also present chans^es. They are unusually
tnin, the diplog is remarkabl}r atrophied, in places the external and in-
ternal tables arc in contact with one another, and ^he inner surface of
the latter is often rough and uneven.

Hydrocephalus may be acute or chronic. In the former the fluid
sometimes accumulates in a few hours, to an extent incompatible miK

248 DISEASES OF THE BRAIN.

life; in the latter the disease may last months and yeans. Finallj,
hydrocephalus may be acquired or congenital.

a. Acquired Hydrocephalus.

I. Etiology. — ^The causes of acquired hydrocephalas include all
those conditions which give rise to oedema in other parts. It oocurs also
in inflammations as inflammatory oedema.

Hydrocephalus is an almost constant element of purulent and tubercular
meningitis. It may also occur in chronic inflammations. In such cases, yantri-
cular hydrocephalus is generally associated with changes in the choroid plexoft
and the ependyma. Hydrooepkialus occasionally deyelops after, not daring the
meningitis.

In some cases this oondition is the result of stasis of blood.

The causes of stasis may be situated inside or outside of the skull. They in-
clude: tumors and inflammatory products which compress the vena GWeni or
the sinus rectus of the dura mater; cardiac and pulmonary affections, and db>
eases in the mediastinum and neck, when associated with obetmction to the cur-
rent of blood in the internal jugular vein; whooping-cough, in whicti the Tioleiit
spasms of cough give rise to stasis.

In some cases hydrocephalus depends on cachectic and hydrsemic con-
ditions (cancer^ phthisis, JBright^s disease, etc.).

A special form is that known as hydrocephalus ex vacuo, which i&
found chiefly in old people who suffer from senile atrophy of the brain.

In a considerable number of cases, no causes can be found, or, at
least, their si^iflcance remains doubtful. Alcoholism, syphilis, mental
strain, and the effects of high temperature on the head ixave been re-
garded as causes of the disease.

There is no doubt that rachitis is associated with remarkable fre-
quency with hydrocephalus.

The age of childhood appears to present a predisposition to the
disease.

II. Anatomical Changes. — Hydroceohalus is manifested in many
cases, particularly in children, by the peculiar shape of the head. The
head is unusually large, the frontal bones ascend straight upwards and
forwards, the orbital cavities appear flattened, the fontanelles are un-
usually large, so that the largo one extends to the region of the glabella,
and the bones are separated by abnormally wide sutures. If ossification
of the sutures takes place, it often occurs from the development of
numerous supernumerary bones in the sutures. The hair of the scalp is
generally thin, dry, and scanty. Dilated and sinuous veins are often
noticeable on the forehead, temples, and vertex. The face appears un-
usually small, and is often triangular, with the base directed upwards,
the apex at the chin.

The bones of the skull are sometimes remarkably thin, so that they
appear transparent when a light is held behind them.

The remainder of the skeleton often presents evidences of rachitis;
enlargement of the epiphyses, deformities in the limbs and thorax, ir-
regular development and poor formation of the teeth.

In adults, and in children past the age of seven, the changes in the
skull remain absent, indeed, the skull is sometimes very small, for ex-
ample^ in cretins.

DISEASES OF THE BRAIN.

249

In external hydrocephalus, the surface of the brain is often flattened
and anasmic. In internal hydrocephalus, the brain is pushed outwards,
but the convexity also appears flattened and anasmic. The ventricles are
found to be distended and filled with serous, more rarely flocculent,
cloudy, or bloody fluid. The flocculi are generally composed of desqua-
mated epithelium cells, occasionally also of softened portions of the
parenchyma. The walls of the ventricles, particularly the basal ganglia,
appear flattened. They are occasionally softened and somewhat aeli-
quescent, the result in great part of post-mortem changes fso-called
white or hydrocephalic softening). The brain is sometimes so aistended
and thin that it resembles a vesicle. It may undergo rupture, almost
always upon the convexity. The ependvma of the ventricle is often
thickened and granular, particularly m chronic hydrocephalus, and its.
blood-vessels are sometimes dilated and sinuous. The choroid plexuses
may present thickenings, sometimes cystic formations.

These changes appear earliest, and are the most marked in the lateral
ventricles, next in the third, least frequently in the fourth ventricle.
The foramen of Munro is not infrequently largely dilated, and forms a
wide communication between the lateral and third ventricles. The
white commissures in the latter are often macerated and distended.

Sometimes only a small part of the ventricles is affected, for exam-
ple, a horn of the lateral ventricle, the aditus infundibuli, the space be-
tween the septum pellucidum, etc. In such cases the fluid is often en-
capsulated and resembles a cyst. As a matter of course, there may be
symptoms of local compression of adjacent structures.

We give the following analyses of the fluid in three cases of chronic
hydrocephalus.

Hilger (1867;.

Tidy (1W9).
A child.

Neuh*ufi(1874). A

child, nt. 18

monthR.

Water

. 98.775
1.225
0.246

0.762
0.897
0.082
0.082
0124

0.096

1006.

98.492
0.518
0.098
0.010
0.068

0.214
0.060

0.002
0.008
1007.6

99.049

Solid matters

0.951

Albumin

0.181

Fate

Alcoholic extracte

0.004

Ashes .

Sodium chloride

Potassium cliloride

0.82

Potassium sulpliHte

Potassium Dhosohate

Sodium phosphate

liiTne phosphate

0.02
0.01

Other phosphates

Sodium caroonate

0.41

Sodium sulphate . .

Specific jcravity

1007.

Reaction alkaline.

Hilgeralso found mucin, fibrin, urea, succinic acid, cholestearin, and a leudn-
like substance. He also obtained 0.164 of a reducing substance which did not
ferment, while Tidy obtained 0.068 sugar. Bock discovered sugar in other cede-
matous fluids. Hoppe-Seyler found sugar which fermented, and deflected polar-
ized light to the rignt, only after the hydrocephalus had been punctured several
times.

Huguenin assumes that more than twenty-five per cent albumin in the fluid
of acute hydrocephalus indicates ito inflammatory origin.

.250 DISEASES OF THE BBAIN.

III. Symptoms. — The most striking external phenomena are ob-
serred in children^ especially in chronic hydroceplialus. Acate hydio-
cephalus runs its course so rapidly that sufficient time does not ela{^ for
marked distention of the skull (macrocephaly). Characteristic symp-
toms are not infrequently absent in acute h^drocephalas, on account of
the prominence of the symptoms of the primary disease, especially if
the latter gires rise to increase of intracramal pressure.

In chronic hydrocephalus the increase in the size of the skull pro-
duces groat deformity. In the upright position the head often totters to
and fro^ or from one side to the other^ so that the patients mast support
it with the hands.

The mental faculties are often affected. The patients become d^
mented^ do not learn to speak^ or speech is indistinguishable, they pan
urine and fsBces in the clothes, and must be fed by others.

In addition, we notice epileptiform attacks, contractures, twitchings
in individual muscles, pareses, more rarely paralyses, and often spastic
symptoms.

If enlargement of the skull is wanting, the symptoms may simulate
those of tumor of the brain, and even choked disK may be present.

In some cases optic nerve atrophy and blindness are present from the
beginning.

The disease may kill in a few months, but in other cases it continues
from childhood until the age of fifty years. Death may occur after an apo-
plectiform or epileptiform attack, or after coma. Spontaneous discharge
of the fluid is occasionally observed, generally through the nose, but
also through the mouth, ear, or orbit. Leber described a case in which
for five years the fluid trickled constantly from the nose, the amount
varying from four to twenty-two centimetres in an hour. This is some-
times followed by spontaneous recovery; in other cases the fluid again
accumulates, general and local symptoms of increased cerebral pressure
reappear, and finally death occurs.

iV. Diagnosis. — The diagnosis is easj if the size of the skull is
increased; if not, it is hardly possible to distinguish the condition from
tumor of the brain.

V. The Pboqnosis is unfavorable, although slight effusions mav
undergo absorption. ^

VI. Tbeatment. — Our attention should first be directed to the

of congenital hydrocephalus.

b. Congenital Hydrocephalus.

I. Anatomical Changes. — This condition almost alwajrs occurs as
internal hydrocephalus. The amount of fluid may be very large, and it
is said that even more than twenty pounds have been found. It is
almost always clear and serous in character.

In the fluid withdrawn by puncture, SchloBsberger found:

Water, ...... 99.07

Solid constituents, . . . . .0.98

Albumin, ..... 0.80

Extractive matters, • . . .0.08

Salts. ...... 0.00

DISEASES OF THE BBAIN. 251

The following was the result of the analysis in Bostock's case:

Water, . • # • • • • ®8-86

Solid constituents, . . . . 1.74 .

Albumin, ...... 0.6

Sodium chloride, . . . 0.7

Urea, ....... 0.8

Soda, ...... 0.14

As a matter of course^ large accumulations of fluid must give rise to.
serious changes in the skull and brain. The ventricles are enormously
dilated, the basal ganglia flattened, the commissures distended, or even
torn, etc. The brain often forms a flabby vesicle, whose walls are only
a few millimetres in thickness, and in which the gray and white matter
are hardly distinguishable. The skull often attains remarkable dimen-
sions, the fontanelles and sutures are widely separated, although later
they may undergo ossification.

Con^nital hydrocephalus is often associated with other malformations, such
as meningocele, encephalocele, hydroenoephalocele, hare-Up, club-foot, etc.

II. Etiology. — In the majority of cases no cause is discoverable.
Among those mentioned are drunkenness and syphilis of the parents,
injury during pregnancy, and congenital rachitis. Several cnildren,
suffering from congenital hydrocephalus, are sometimes born in succes-
sion, so that heredity seems to play a part. Some authors attribute it to
ulceration of the os uteri during pregnancy, which is said to interfere
with the circulation of blood in tne foetal skull. In very rare cases, it is
the result of congenital intracranial tumors, with pressure on the blood-
vessels.

III. Symptoms. — In some cases the children are bom with an hydro-
cephalic skull, and this may constitute a great obstacle to delivery. The
infants are sometimes born prematurely.

In other cases, the external signs of hydrocephalus are very slight, or
entirely absent at birth, but after the lapse of davs or weeks the growth
of the skull is almost visible from day to day. The symptoms are iden-
tical with those of the acquired form. Amaurosis from congenital
atrophy of the optic nerve has been observed in a few cases.

IV. The Diagnosis is usually easy; the Phognosis is unfavoroble,
although life is sometimes prolonged to the age of fifty years. Treat-
ment includes the use of diuretics, drastics, derivatives, compression of
the head by means of strips of adhesive plaster, and puncture. As a
general thing, we must remain satisfied with general treatment.

11. Hypertrophy of the Brain.

I. E2TI0L0GY. — ^This condition is most frequent during childhood, and then is
generally congenital. It is either well advanced at birth, or it develops gradually
after birth. Cases belonging to the latter variety are apt to be regarded as
acquired.

Similar changes are sometimes observed in the parents and children, so that
heredity seems to play a part. Rachitis has also been regarded as an etiological
factor.

In adults, alcoholism, mental strain and excitement, epilepsy and idiocy, even
injury, are regarded as occasional causes of this condition.

II. Anatomical Changes.— The changes affect chiefly or exclusively the
cerebrum, more rarely the cerebellum. They are almost always bilateral, though
sometimes only one hemisphere is affected, or only the pons^ meduUB^^ <2ft ^«c\3bxs^

252 DI8EASBS OF THE BBATN*.

of the basal ganglia. It affects the white matter alone, and Is the remit of
increase of the neuroglia.

When the calTarium and dura mater are removed, the brain p r oiPOB o ufinb
as if it had not had sufficient room within the skull. The meningeB are airan>
ally^ thin and ansBmic, and there is no cerebro-spinal fluid. The snrfue of the
brain is flattened, the brain-substance is anssmic, and the boundary between thi
white and gray matter is often indistinct. The consistence of uiebtainisiiir
creased and is like that of coagulated albumen, cheese, or tooghRum. In torn
cases, the brain could be stretched like gum without tearing^, upon tnntnm
section of the brain, we are struck with the enormous development of the wUli
matter, the narrowness of the Tentricles, and the absence of ▼eatr i culT fluid.

If the hypertrophy develops at or immediately after birth, the skull ahoii-
creases in size, and may even attain the dimensions of the hydrocephalie ikni.
In children in whom the sutures have united, the pressure of the h ju er tiop Mc
brain may again cause separation of the cranial nones. Sooie of ue cniiil
bones are occasionally perforated, particularly the roof of the orbit and the i
noid. In adults, the skull is not distended, but the bones are thinned.

Hyperplasia of the lymphatic glands, thyroid, and thymus glands hss
described in several cases of congenital hypertrophy of the brain.

III. SYHFTOMS.^The condition sometimes remains latent. Oertsin
were marked by premature and very marked mental development; in otfaeni the
chief symptom was enlargement of the skull, which gave rise in children l»
uncertain gait. Epileptiform convulsions are frequent, and many patients co»
plain of headache, dizziness, and vomiting. Paralyses, contractures, men
rarely sensory disturbances, are also observed. Irregularitry of the reqiinitian
and retardation of the pulse mav develop as the intracranial preasure incream.
Disturbances of sight have also been mentioned.

The mental faculties are often affected, and apathy, flnally denientia» gndt-
ally develop.

The svmptoms sometimes develop suddenly, and quickly terminate in daA^
80 that the condition has been called acute hypertrophy of the brain, althougli it
had evidently lasted a long time, and the acute symptoms were the rsmt of
rapid increase of intracranial pressure. The disease generally lasts many yesni
Death occurs after oonvulsions, meningitic symptoms, coma, or apoplectifom
attacks.

IV. DiAONOSis. — ^The diagnosis is hardly possible if the skull is not enlarged.
In the latter event, it must be distinguished from hydrocephalus. If the akiul ii
translucent, we have to deal with hydrocephalus. In the latter condition,
furthermore, the greater fontanelle is convex externally and pulsates leas diK
tinctly than in hypertrophy of the brain, in which the fontanelle is flat.

v. The PRoaNOSis is unfavorable, the Treatment purely symptomatic.

12. Atrophy of the Brain.

I. Etioloot. — Atrophic changes may be congenital or acquired; they affect
the entire brain, one-half, or small parts of the organ.

Congenital atrophy of the brain is sometimes the result of imperfect develop-
ment, sometimes it is owing to involution of parts already developed. Among
the causes mentioned are foetal inflammation of the meninges and ependyma (h
the ventricles, abnormal distribution of the vessels, premature ossification of
the sutures, traumata during pregnancy, and uterine diseases with secondary
circulatory changes in the foetus.

A relatively frequent form is unilateral atrophy of the brain in children,
which may be congenital or develops soon after birth. One cerebral hemisphere,
generally the left, may alone be affected, or the cerebellum is also involvM (not
infrequently upon the side opposite to the cerebral atrophy), or individual lobes
of the cerebrum are chiefly attacked.

General atrophy of the brain is not infrequent in old age {senile atrophy of Ae
brain). It must hie remembered, however, that this is not a necessary- sequence
of old age. Closely allied to this variety is the marantic form which develops
after protracted diseases (phthisis, cancer, syphilis, Bright's disease).

The atrophy is sometimes the result of diseases of the brain, meninges, or
bones of the skull (cerebral hemorrhage, embolism, thrombosis, abscess, tumon^
hydrocephalus, meningitis). This variety of atrophy may be confined to the
immediate vicinity of the morbid pxocess, ot \t vcvoly «^tend over a greater area.

DISEASES OF TOE CEEEBKAL MENraOKB,

Peripheral diseaseB eometimes result ia seconJa^ry atrophj of their central
terminal etationa in the brain. For example, atrophy of the corpora quadri-
gemina has been observed in phthisis bulbi, and secoadary atrophy of the bnun
£a8 aim beea known to follon' amputatioDs.

Toxic cerebral atrophy is a epenial form which haa been observed aa the
result of abuse of alcohol, working in lead, and the opium habit.

It is also said that li^ture of one carotid may produce unilateral atrophy of
the brain, particularly if there are abnormalities in the communications of the
idrcle of Willis.

II. AkatOUICai. Chanobs. — In general atrophy, the brain does not fill the
akull-cap; the c^^rebro-spiual fluid in the subarachnoid space and ventricles is
considerably inoreosed. The convolutions are unusually unrrow, the sulci deep
and broad. The consistence of the brain ia generslly increased, the cortex baa
a deep grayish-red color, the white Hubstauce ia yellowish.

Within the brain, wide spaces are often found around the vessels (6tat
oribleet, particularly in the basal ganglia; occasionally we find new-formed
cystic spaces filled with serum. The ventricles are rery narrow (sometimes the
reverse), and the basal ganglia are unusually small. The ependyma of the
-ventricles in occasionally tliickened and covered with warty granulations.

In unilateral atrophy of the brain in children, the liemisphere is sometimes
converted into a thin covering, which contains more fibrous than nervous con-
Btituents. There may be merely indications -jf the convolulioaa. There is oft^
asymmetry of the skull and diminution in size upon the atrophied side, with
thickening of the bones. The atropliy is sometimes followed by secondary
degeneration, which extends into the spinal cord and even into the nerve roots.

III. Symptoms and Diaonosib.— In unilateral atrophy of the brain of child-
hood, the mental anil bodily powers rarely remain intact. As a rule, the chil-
dren are imbecile or idiotic. There are often paralysis and atrophy of the limbs
and even the face upon the side opposite to the atropliy; contractures are very
often present. The paralysis is less marked in the leg than in the arm. The
contractures generally Increase on attempting to execute a movenient. The
atrophy aSects chiefly the muscles and bones, and the limbs retain the dimen-
sions ot those of a cliild even after tlie patient has arrived at adult life. The
ekin sometimes presents an unusual development of the panniculus adipoeus.
Sensibility is often very little a&ected, but tliere arc sometimes disturI»inceB of
special senae. Epileptiform convulsions occur frequently. The patients have
Blight powers of resistance, and readily succumb to intercurrent diaeaaes, or die
in an epileptiform, apoplectiform, or comatose attack.

Senile cerebral atrophy is regarded as the cause ot the feebleness of memory,
cbildisbneas, tremor of the limbs, etc., which are peculiar to old age.

Some authors attribute the Hymptomatoloey of lead encephalopathy to satur-
nine atrophy, The tremor, weak memory, andparesis ot clrunkards are attributed
to alcohnlio atrophy of the brain.

IV. PhoososiS and Treatment.— The prognosis is unfavorable, the treatment
purelj; symptomatic. In unilateral cerebral atrophy of childhood, good results
are said to have been obtained from faradism of the paralysed muscles and gym*
naelic exercises.

B. Diseases of thb Mekinoes.

1. Internal Bemorrhagic Pachymeningitis, Infiammafory Hemorrhagic
Changes on the Inner Surface of the Dura Mater.

AlfATOMlcAL Chanqeb. — This is not a rare condition. Id the initial
stage, it appears as more or less recent extravasations upon the inner sur-
facti of the dura mater, which can readily be removed. In more advanced
cases, it forms thin, wob-liko deposits, which are infiltrated with extra-
Tasations and are organicaUy united to the dura mater, Bometimca by
means of vessels. Older extravasations have a ruaty brown color, or im-
part a diffuse yellow color to the new membrane. *

In many cases the process exhibits a progressive character. This ia
owing to the numerous blood-vessels contained in the new meTO.h«sia»

25^ DISEASES OF THE CEREBRAL MENXSTOSS.

and which give rise to fresh extrayasatioas upon the inner enrfacewM
is directed towards the cortex of the brain. These eztrarasatioiu i»
converted gradually into new membranes. In this manner layer is d6>
posited upon layer^ sometimes to the number of twenty or more.

In not a few cases, large extravasations take place between the indi-
vidual lamellae (hsematoma dursB matris). They may attain the sin of
a fist or more, and compress the brain over a wide extent. The bnii
sometimes contains a deep depression in which the haBinatonia is sitntted,
or if the hsematoma is unilateral^ the falx cerebri is pushed into tin
other half of the cranial cavity. The amount of extrayasated blood
sometimes exceeds sixteen ounces.

On section through the sac of blood, it is often evident that betwea
the different lamellae are collections of blood of varying age^ some flnid
and bright red, others coagulated, brownish-red, or rust colored. Tk
walls of these cystic spaces are sometimes smooth and look like a serou
membrane, sometimes they are jagged, in some cases their contenti
are serous, rarely purulent or calcareous.

The new membranes may be adherent to the arachnoid. The Iftar
and the pia mater are occasionally opaque and thickened. The com-
pressed portions of the brain present yellow softening', and the brain k
almost always anaemic. The blood sometimes breaks through the li-
mellae and destroys the brain tissue.

The changes in question are generally bilateral, and are apt to be
located at the top of the parietal region near the falx cerebri, tnen over
the forehead, less frequently near the occiput. They are much rarer it
the base of the skull. They are sometimes so extensive as to surroimd
half, sometimes even the entire surface of the brain.

The older physicians believed that the hemorrhages upon the inner surfaoe tf
the dura mater were primary, and that later they become or^^anized and con-
verted into new membranes. Then Virchow attempted to show that the primaiT
process was an inflammation upon the inner surface of the dura mater, tnat this
results in the formation of a vascular tissue, the rupture of whose Teasels pio>
duces the hemorrhages.

Recently there has been a return to the older doctrine. Sperling^ showed, in ex*
periments on rabbits, that the injection of blood under the dura mater termi-
nates, at the end of two to three weeks, in the formation of new membrane^
which are exactly similar to those of internal hemorrhagic pachymeningitis in
man. Irritation of the dura mater resulted in inflammation^ sometiines in
suppuration, but never in hemorrhage.

According to Huguenin, the primary hemorrhage takes place from the vete
which pass from the convexity of the brain to the longitudmal sinus. Fbrhapt
it also occurs from the veins in the Pacchionian bodies. In some cases, degeneri-
tion of the vessels, rupture, and thrombosis have been found. It must be ad-
mitted that the theory of the organization of primary hranorrhages in hemor-
rhagic pachymeningitis is verv plausible, since it often occurs under oonditiooi
which favor the pn^uction of small hemorrhages in other localities.

So long as free coagula alone are found on tne inner surface of the dura, thej
contain nothing but red and white blood-globules, imbedded in a fine netwatkA
fibrin. In places the white blood-globules are collected into clumps. The epi-
thelium of the adjacent dura and arachnoid is unchanged. The red blood-glMh
ules gradually degenerate and disappear, while the white globules aie converted
into connective-tissue corpuscles. Tne tissue in which they lie becomes changed
BO that it grows cloudy on the addition of acetic acid. The cosffulum then as-
sumes gradually the characters of a membrane. In manjr places tne white Uood-
g lobules are arranged in rows and result in the formation of capillaries. The
itter have an unusually large lumen, possess numerous ramifications and com-
munications with one another, and have unusually thin walls. They often present
ampulla-like or rosary-like dilatations. These vessels are supplied from thediin^
in places from the arachnoid, from which, vessiels enter the new^formed

DISEASES OP THE CEREBEAL MEJOSOES,

brane. The tendency to liemorrhsgea arises Tery rarly. According to Eind~
fleiacli, this is ex^laiaet) by the retrcictioii of the newly formed connective tissue,
whicli oiMludea a. portion al the capillaiiea, and thus increases the blood pressure
ill the remaining open ones. Hemorrhages are recognizable for along time as
patches of pigment (hcematoidin). iThiob appears as granules, rhombic tablets and
needles, or as a diffusa imbibition. Perls found tiiat they furnished an irou reac-
tion. When the blood-vessels and dura or arachnoid penetrate into the new-
membranes, there ia an intimate connection between the structures, hut even
then the endothelium of the meninges is intact over large surfaces, eo that u dif-
fuse organic union ia absent for a long time.

II, Etiology, — The diaeaso ia more frequent in men {in 77.4;» ac-
cording to Duritad-Fardcl). It is chiefly a disease of advanced life,
particularly beyond the age of fifty years. Gases rarely occur in child-
hood (they have been observed at tne age of fonr, six, seven, and nine
montliBj. Among the direct causes may be mentioned:

rt. Tratimitta; the period between the injury and the firat manifest
symptomB may last several (three) years.

b. Inflammations conveyed from the vicinity, for example, in tuber-
culosis of the petrous portion of the temporal bone, and bones of the
skull in general.

c. Abuse of alcohol.

(/. Diseases of the brain: tumors, softening, particularly atrophy;.
insanity, almost constantly in dementia paralytica.

e. Infections diseases: pleuropneumonia, typhoid and typhus fever,
relapsing fever, acute articular rheumatism, small-pox, scarlatina,
whooping-cough, pyromia, puerperal fever.

/, Diseases of the respiratory and circulatory organs: phthisis, pleu-
risy, pneumothorax, pericarditis, valvular lesions, atrophy of the neart.
muscle.

g. Marasmus and conditions of blood dissolunoii: cancer, Bright's
disease, progressive pernicious ancemia, leukiemia, hemophilia, and.
scurvy.

h. Congenital and acquired syphilis has been mentioned among the
CBUses.

In not a few cases no causo can be discovered.

Until recently it was generally believed that pachv meningitis was the result
of conditions of arterial fluxion, especially in the middle meningeal art«ry. But
Huguenin attaches chief weight to changes in the blood-vessels which predispose
to abnormal brittleness or permeabihty. In many cases, in addition, there isi
stasis (cough, heart diseaaea). but in the majority there is diminution in the
volume of the brain which favors the occurrence of hemorrhages.

III. STMPTOMa AND DiAHNosis.— Morbid symptoms are absent in-
many cases of internal hemorrhagic pachymeningitis. The extravasated
blood and new membranes take up so little room that they produce no
noteworthy compression. It is very probable that, in many cases, they
give rise to headache, but a diagnosis cannot be based on such n vague
symptom alone. Fnerstner has recently called attention to constantly
recnrring. apparently purposive grasping movements, which are oftou
observed in somnolent individuals, for example, in phthisical individuals
during the agony, and in wliom the autopsy discloses intei-nal pachy-
meningitis. The patients arc constantly pulling the beard, genitals, bed
covering, etc. Fuerstner regards these symptoms as the result of irri-
tation of the motor cortical centres by the hemorrhage.

^M More marked symptoms generally appear as evidences of. %'cA.\'sck.'\ap

250 DISEASES OF THE CEBEBSAL MENINGES.

crease of pressure in the cranial cavity^ and generally affect the conTeihT
of the brain to the most marked degree. Such symptoms occur only
after larger extravasations of blood.

As a rule^ an apoplectic seizure develops. The patients fall nncon-
scious^ remain comatose for hours^ days^ and even weeks, or death
occurs in coma at the end of a longer or shorter period. The coma is
followed not infrequently by a dream-like condition. The patients
sleep a good deal, pass urine and faeces in bed, must be aroused to eat
and drink, do not Know where they are, and stagger in walking. The
pupils are narrow. Later, they become moderately dilated, but are
rigid, and not very sensitive to light. The pupils are sometimes nu-
equal, the wider one being generallv on the side opposite to the ledon
In three cases Fuerstuer observed clicked disk,* as tne result of entrana
of blood into the optic sheath; he also observed unilateral nystagmnf.
Paralysis of ocular muscles is almost always absent. Paralyses are fr^
quent symptoms. All the limbs are often paretic, one side more mari[-
edly than the other, and the facial and hjrpo^lossus nerves may also
be implicated. Occasionally there are irritative symptoms, such as
convulsions and contractures of certain limbs. Porcea moTementfiot
the eyes, head, and bodv are sometimes noticed. Among the mo^
frequent symptoms are slowness and irregularity of the pulse. Fuerst-
ner mentions profuse diaphoresis. Considerable rise of temperature has
also been described (41° C.).

The symptoms may gradually subside, if the extravasated blood is
partly absorbed, and the brain accommodates itself to the increand
pressure.

Per 86 the symptoms described are not indicative of hemorrhagic
pachymeningitis, since they are merely evidences of sudden increase of
intracranial pressure. But the matter is different if the etiolo^v favors
the view of the development of an haematoma, and if such attacks recur
from time to time. In all cases, however, the diagnosis is diflScult, and
often very doubtful.

In psychopathic conditions, hsematomata may develop without giv-
ing rise to the symptoms mentioned above. They are o^n noticeable
only from the peculiar change in the psychical condition, beginning
with excitement and then passing into coma.

IV. Prognosis and Treatment. — The prognosis is always serious,
and so much the more the more pronounced the symptoms of compres-
sion. Nor are we able to prevent the occurrence or return of the hemor-
rhages.

During the apoplectic attacks, venesection sometimes relieves the
coma with great rapidity, but it should not be performed in feeble in-
dividuals. An ice-bag should be applied to the head, and laxatives ad-
ministered, for example: IJInf. sennsB comp., 3vi.; sodii sulph., 3vi
M. D. S. One tablespoonful three or four times a day. Later we may
order absorbents, particularly potassium iodide (gr. xij. t. i. d.). The
galvanic current may also be employed. During tne acute period, some
physicians order leeches, blisters, irritating ointments to the foreheadi
mastoid processes, or nape of the neck.

2. Thrombosis and Inflammation of the Cerebral Sinuses.

I. Etiology. — These conditions are found not infrequently. Bat
however close their relations to one another, they must be strictly aep*

DTSSAjKB OF THE CBBEBBAL HENDTOES.

arated anatoEnically and cHnically. Inflammation of the cerebral sinuses
is almost always followed by secondary ihromboaiH, arid hence the clinical
symptoms will be identical in so far as thej depend on disturbances of
Tenons circulation.

Pure (non- inflammatory) tlirombosia is generally of marantic origin.
The cerebral sinuses are particularly adapted to the formation of thrombi,
because their walls are fixed, and adapt themselves with difficulty to
variations in the amount of blood; their lumen is oftenaugnlar, and they
are often traversed by threads and excrescences (Hyrti). Marantic
thrombi are found most frequently in the superior longitudinal and trans-
Terse sinuses. They occur often in children who are enfeebled by chronic
diarrhcea, suppuration, chronic pnlmonary diseases, etc. Under similar
conditions the thrombi may also form m adults.

Oompression thrombi are observed much more rarely. The causes of
compression may be situated in the cranial cavity (brain and meningeal
tnmora), or they are extracranial. In the latter event, they affect mainly
the internal jugular vein, more rarely the superior vena cava (lymphatic
glands or mediastinal tumors). The thrombi in the latter vessels then
epread upwards to the transverse sinus, more rarely to the inferior
petrosal emus.

Whether thrombosis of the sinuses may develop as the resnit of mere
stasis of blood and slow circulation is not known with certainty.

Inflammation of the cerebral sinuses with secondary (inflammatory)
thrombosis is moat frequently the result of inflammation near the dura
mater. It is observed most commonly in tuberculous processes in the
petrous portion of the temporal bone, which gradually extend tlirough
the bone to the dura mater. Purulent inflammations of the meninges
and brain substance also extend occasionally to the cerebral sinuses. In
some cases t!ic primary site of inflammation is far removed, and the
sinuses are affected, either aa the result of thrombo-phlebitio processes
which extend from extracranial veins into the sinuses, or the blood carries
infectious and inflammation-producing particles into the sinuses. To
this category belong wounds of the skull and face, which may be very
trilling at the start, until suddenly the symptoms of thrombosis of the
sinuses give evidence of great danger. Oases have been observed after
abscess of the gums, facial erysipelas, diphtheria, abscesses in the deep
muscles of the neck, orbital inflammations.

In very rare cases, it is the result of direct traumatic inflammation.
Among one hundred and fifty-one cases of thrombosis and inflammation
of the sinuses collecteil bv Wreden, one was the reaultof the entrance of
a foreign body through tne spheno-orbital Assure.

II. Anatomical Chanqes. — In simple thrombosis, the sinus con-
tains a brownish-red, rusty brown, or grayish-red clot which is notably
Arm. It is generally adherent to the wall of the sinus, to which it is some-
times organically united. On transverse section, it not infrequently
S resents distinct lamination. Upon the primary thrombus arc sometimes
eposited others, whose increasing age ia shown by the greater discolora-
tion and consistence. The primary thrombi sometimes occlude the
vessel entirely, or they are situated only upon its walls. They may fill the
entire sinus and even extend into the adjacent sinuses and veins. Thus
in thrombosis of the superior longitudinal siuns the clots sometimes ex-
tend into the veins which pass into the sinns from the convexity of the
brain. Thrombosis of tlie tranitverse or inferior petrosal sinus often
extends to the internal jugular vein and gives rise,duriii?,WftA'^i^'K?«^

858 DIHEA8E8 OF THE OEREBSAL MSNINOSB.

of the external jagnlar on the same side (Oerhardt). In other cmses, the
thrombosis affects only a small part of the sinus, or the latter contains
several thrombi.

The changes described are associated with yenous stasis on the p^-
phoral side of all the vascular tracts which supply blood to the affected
sinus. These symptoms of stasis will be most marked in bilateral com-
plete occlusion of the transverse and inferior petrosal sinuses, with con-
tinuation of the thrombus into the internal jugulars. They are mani-
fested by marked venous congestion and hemorrhages into the brain and
meninges, followed by cerebral softening, by increase and sometimei
bloody discoloration of the cerebro-spinal fluid, and by hydrocephalni
yentriculorum.

Particles of a thrombus are sometimes dislodged and enter the right
auricle, ventricle, and pulmonary artery, and are thus conyeyed to the
lungs, where they constitute pulmonary emboli (hemorrhagic, wedge-
shaped infarctions).

Some authors maintain that thrombi may undergo organization and
be partly absorbed, or at least become permeable and permit the passage
of blooa. This is denied by others.

In inflammation of the cerebral sinuses with secondary thrombosis,
the effects upon the venous circulation are the same as in simple throm-
bosis. In addition, there is a tendency to suppuration and gangrene.
The thrombi are not infrequently soft, purulent, ichorous, and fonl
smelling. The wall of the sinus is inflltrated, brittle, sometimes on the
point of rupture. There may be inflammation of the dura mater and
other meninges, also abscess of the brain. Pulmonary emboli give
rise to secondary inflammation and metastatic abscesses, and these may
rupture into the pleural cavity. The primary affection may also have
given rise to pyaemic foci of pus in the spleen, liver, and kidneys.

III. Symptoms and Diagnosis. — The recognition of thrombosis of
the sinuses is very difficult, and often impossible.

In not a few cases no symptoms are observed. This is especially true
if previous disease has enfeebled the circulation and dimicisned the irri-
tability of the brain to such an extent that the increment of circulatory
disturbances produces no noteworthy effects.

Bouchut maintains that many cases of convulsions in children, oc-
curring just before death, depend upon thrombosis of the sinuses, but
this symptom is too vague to warrant even a probable diagnosis.

A third series of cases is attended with clouded conscioasness. in-
equality of the pupils, strabismus, nystagmus, rigidity of the back of the
neck, vomiting, convulsions, paralyses, and contractures. But these
symptoms and the primary disease are more apt to arouse the suspicion
of purulent meningitis, and, indeed, this lesion is generally present
while the thrombosis remains unreco^ized.

Disturbances of central innervation are sometimes absent and all
else is masked by the symptomatology of the pyasraic condition.

A probable diagnosis may be made if tlie symptoms of pulmonary
infarctions or metastatic abscesses make their appearance, while, at the
same time, diseases are present which, as a matter of experience, are
known to give rise to thrombosis of the sinuses, and other causes of pul-
monary embolism are absent.

The diagnosis grows more positive if there are evidences of stasis in
the external veins of the face, scalp, and neck.

In thrombosis of the superior longitudinal sinus, there is unusual dis-

DISEASES OF THE CEBEBKAL MENINGES. 359'

tention and sinuosity of the veins which are situated between the greater
fontanelle and the temporo-auricular region. This iBeapecially distinct
in children in whom thtiemmissariaSantorini are very large, and the hair
on the scalp is scanty. In a girl, cet. 3 years, under mj observation, the
distention of the veins was so marked as to ^ve rise to gross deformity.
According to Gerhardt, there is also cyanosis in the dirtribution o( the
ftnterior facial veins, v. Diisch observed epistaxis as the result of stasis
in the communications between the veinB of the nose and the superior
longitudinal sinus, hut Staeger observed the same symptoms in throm-
bosis of tlie cavernous sinus. An important feature in children is the
condition of the fontanelle. The greater fontanelle is depressed at first
ao that one parietal bone is sometimes pushed over the other. Later,
the fontanelle becomes more extensive and tense than it was originally,
if the cerebro- spinal fluid increases as the result of occlusion of the
sinus.

In thrombosis of a transverse sinus, the corresponding external jugu-
lar vein is sometimes emptier than the one on the healthy side, beoanse
it empties its blood more readily into the loss distended internal jugular.
This symptom will be so much more marked the more vigorous the cir-
culation, and the further the thrombus extends into the beginning of
the jugular vein (which receives the inferior petrosal sinus), or if the
superior and inferior petrosal sinuses are both occluded.

If a thrombus of tne transverse sinuaextends to the posterior auricu-
lar veins, tedema (hard and tender) develops behind the ear and mastoid
process.

If both transverse sinuses are occluded, the symptoms of thrombo-
sis of the superior longitudinal sinus may be produced.

In thromnosis of the cavernous sinus, the chief symptom is fltaais in
the orbit, since this sinus receives the blood of the ophthalmic vein
(cedemaof the lids and conjunctiva, acute exophthalmus from disten-
tion of the retrobulbar veins, occasionally cedema of an entii-e half of
the face (stasis in the communications between the ophthalmic and
facial veins), venous congestion of the retina (sinuositv and distention
of the veins and narrowing of the arteries), redemaof the retina, choked
disk, amblyopia or amaurosis), Boucbut described thrombosis of the
retinal veins.

Another important symptom of thrombosis of the cavernous sinua
consists of disturbances of innervation of the trigeminus (first branch),
trochlear, oculomotor, and abducena nerves, which pass between the
sinuses, and are apt to be irritated or paralyzed by fltasis-mdema of the
snrrounding connective tissue (trigeminal neuralgia, ocular paralysis,
trophic changes in the eye).

Similar symptoms may be looked for, if both inferior and transverse
petrosal sinuses are obstructed.

Thrombosis of the sinuses generally runs an acute course ; death
often occurs in u few days. The average duration is one to four weeks.
Recovery is of rare occurrence. There are sometimes striking remis-
sions and exacerbations, but the former should not induce us to make a
premature favorable prognosis. Elevation of temperature occurs ia
simple thrombosis, remittent and intermittent fever in purulent throm-
bosis. Death is the result of increasing exhaustion or excessive depres-
sion of the central nervous system,

IV, pROONOSifl AND Tbbatmbnt. — The prognosis is almost always
anfavorable. The treatment is purely symptomatic.

260 DISEAflES OF THE CEBEBBAL HEITINOBS.

3. Meningeal Hemorrhages.

I. AXATOuiCAli Changes. — Hemorrhaj^es ma; be aitnated betreen
the mcQinges or in the tissues of the iudividual meningea.

According to their Bituation we diatingnish epidural, anbdnral, sob-
arachnoid al, and snbpial hemorrhages; Bereral forms are often combined.

Fig. 131 furnisbee a Kbematio representation of the topographical relatioBtol
the meniDKes. The dura mater is intimately adherent to the inner anrfaceoftbe
bonea of the ekull (endocranium). HemorrhaKea between the ^ull and the ai-
' It out. ' • ■■ • ^- -> -■• . .

>nIyo

Between the dura mater and arachnoid is fonnd a capillary space (snbdmil
space, 2. sdr), correeponding to the arachnoid cavity of older ■vn\iet%. HenKr
rha^es into this cavity are called subdural hemorrhages.

Between the arachnoid and pia mater is a meshed tissuo (Fig. 121, S. Mir)!!
which the cerebro-apinal fluid ia aituated. It also contains the large oerebnl
arteries and vtins. Hemorrhagee in this locality are nailed eubarachnoid bemtc-

LoDgltudlaikl sectlau (hroUKb the bonec. meslaEea. lu
epidural ppoce ; ^. AJr. subdural spac'e iiLrachnoJdi

hrmJD (•cbematic). I. tpt.

rbagea. Finally, intracerebral hemorrhagea which extend to the surface beneath
the pia mater constitute aubpial hemorrhages. The pia is often ruptured, and Um
blood then pasaea into the subarachnoid space.

Meningeal hemorrhages Tary in extent and number. Thej m«be
multiple, many of them attaining barely the size of a pin's head, or
there may be a single large extravasation. The latter is sometimes so
considerable as to surround the entire brain, fill the ventricles, and es-
temi along the spinal canal to the filum terminale; in other cases, it is
confined chiefly to one-lialf of tlie brain, or to the convexity or base.
The appearance of the hlood varies according to the age of the hemor-
rhage. If it is followed very rapidly by death, the blood is fluid or
forms loose, dark-red clots; in other cases it is brownish-red, mst
colored, and firmer in consistence. When the hemorrhage occurs in
repeated relai)8ea, a sort of lamination is produced, the older brownish
masses being situated externaily, the more recent, red ones internally.
Hemorrhag'es of slight extent seem to be capable of undergoing absorp-
tion, and to this are attributed the pigmentations, thickenings, and ad-
hesions of the meninges to each other and to the surface of the bi&iii
(sequelffi of inflammatory reaction).

As a matter of course, hemorrhages of a certain extent must com-
press the cranial contents. The surface of the brain beneath the extrt-

DISEABE3 OP THE CEKEBRAL MESCTGES.

Taaation ia flattened, and the cortex, on section, is pale, and ite consist-
ence is increased. If the hemorrhage ha.3 lasted for some time, the
surface of the hrain ia generally cedematous. There is often destmctiin
of brain tisaue, as the result of" the primary injury.

U. Etiology. — The causes of meningeal hemorrhages are trauma-
tism, circulatory diaturbanoea, and changes in the constitution of the
blood.

Traumata include a blow, fall or cut upon the head, or severe concussion of
the entire body. The hemoirhagea may occur on the side of the injury, or on
the opposite side, And may or may not be associated with injury to the soft parts
and bones.

Traumatic meningeal hemorrhages are not infretjuent in the new-born, as the
result of too rapid or too protracted labor, applicatjon of the forceps or narrow
peWia. These hemorrhages are the result of marked displacement of the meujn.
ges upon the boues of the skull.

t'irciitatorj disturbances act as a source of meningeal hemorrhages, for ex-
ample, in thrombosis of the sinuses, rupture of aneurisms of the cerebral arteries
at the base of the brain (most frequently tlie basilar or middle cerebral artery).
Id rare cases meningeal hemorrhages occur as the result of stasis in cardiac and
pulmonary diseases, often in spasmodic conditions (tetanus, triamus, epilepsy),
but m the latter event, it is often doubtful whether the hemorrhage is primary or
secondary.

Meningeal hemorrhages aa the result of changed constitution of the blood are
found not infrequently in infectious diaeaaes, leiiksmia. scurvy, htemophilia,
progressive peraicious anceniia, grave jaundice, etc.

III. Symptoms asd DiAoyosia. — Slight meningeal hemorrhages
may present no symj^toms and may be discovered accidentally on autopsy.
Large hemorrhages in the new-born often run n latent course, Gerhardt
believes that this is owing to the imperfect development of the motor
cortical centres.

In some cases, particularly in children, the hemorrhage producea
epileptiform and tetanic spusnis; but, as a rule, the diagnosis cannot be
made.

In the new-bom, meningeal hemorrhages are sometimes the cause of
asphyxia neonatorum. The little ones breathe very poorly or not at all
after delivery, have a cyanotic or leadeti-grav appearance, are somnolent,
and die in a few minntea, hours, or days. Their condition occasionally
is tolerably good immediately after birth, but in a few days the above-
mentioned symptoms make their appearance, and the patients perish.
The aymptoma are explained in part by renewed and more estensive
hemorrhages.

Meningeal hemorrhage often oo-exista with intracerebral hemor-
rhage, but we are unable to determine during life whether the latter
exists alone or in combination with the former.

The symptoms occur in their purest form when the hemorrhage is
the result of rupture of an aneurism. They consist chieSy of the evi-
dences of acute increase of intracranial pressure, such as we described in
the discussion of internal hemorrhagic pacliy meningitis. The patients
fall unconscious, either suddenly or after various prodromata (dizziness,
headache, vomiting), the respirations are irregular, the pulse slow, the
pupils narrow, and usually react slowly or not at all, urine and feces oru
passed involuntarily; there is generally paralysis or rigid contracture of
all the limbs. Death occurs very rapidly (within the first ten hours in
Boventeon out of forty-eight cases collected by Irfbert), or the patients
conaciousneas, are paralyzed, ami die in a few days, after

S62 FXTNOnONAL DISEASES OF THE BBAISr.

increasing symptoms of cerebral paralysis. Well-defined hemipl^ is
rare, even ii the hemorrhage is nnilateral.

Recovery can be looked for only after small hemorrhages.

IV. Treatment. — The treatment is purely symptomatic: ice-bag
to the head^ stimulants; in asphyctic new-bom infants^ stimulation d
respiration by cutaneous irritants and faradization of the phrenic nerre,
administration of milk and wine; later, absorbents.

C. Functional Diseases of the B&AX£r«
(Gebebbal Neijboses.)

1. Epilepsy,

I. Etiology. — Epilepsy is a chronic disease, the typical form d
which appears as attacks oi unconsciousness and clonic conyalsions.

The disease is very frequent; according to different authorities, there
are one to six epileptics to one thousand individuals. It was formerlv
supposed to be more frequent among males, but this has been denied
The disease generally begins between the ages of seven to twenty years.
But cases of congenital epilepsy have been reported, and in rare
instances it begins at a very advanced age (seventy years).

Epilepsy may be primary or idiopathic, and secondary or ^ympto-
matio. The former is an independent affection and chronic neurosis of
the brain, the latter is excited by changes in various parts of the body.

Heredity plays a prominent part among the causes of primary
epilepsy.

In some families, it is hereditary; in others, hysteria, insanity, neuralgia, etc,
alternate in different generations. In some cases, certain gOQerations escape the
neuropathic taint. Ic has been maintained that epilepsy is more apt to be in-
herited from the mother. Phthisis has also been looked upon as the c^use of
epilepsy in the offspring (?).

In certain cases, it is not so much nervous heredity which comes
into play, but other injurious factors in tlie parents afford the basis for
epilepsy in the offspring. This is particularly true of drunkenness.

Epilepsy is sometimes the result of excessive mental excitement
(fright, sorrow, excessive joy). This is also true of mental strain.

In rare cases, individuals become epileptic as the result of so-called
imitation, i, e,, after seeing an epileptic attack in another individual.
It is also stated that the disease may develop in persons who have simu-
lated epilepsy for a longer or shorter period.

Bodily strain is also regarded as an occasional cause of the disease.

It sometimes occurs after infectious diseases, particularly syphilis.
Indeed, it has been held that this cause should be suspected in all ca^es
of epilepsy which develop after the ago of thirty years. It may also
follow pleurisy, pneumonia, measles, scarlatina, variola, acute articnlar
rheumatism, and scrofula.

Constitutional changes, such as rickets, are also said to play a ]Virt
in the etiology.

Of great importance are the development of puberty and various
other processes in the sexual life. Many become epileptic at the period
of first menstruation, others during the first act of coitus. Some women
fire first attacked during pregnancy. It is also stated that congenital

phimosiB is frequent in opileptics, and there is uo doubt that onanism
laTors the development of the disease. This haa also been asserted with
regard to BPxaal continence.

The epilepev of drunkards must be regarded, to & certain extent, as a
toiic form of the diaease.

The disease ia sometimes the result of injuries which produce diffuse
concussion and molecular changes in the central nervous system (full,
blow, etc., upon the skull and spinal column).

Injnries may also give rise to epilepsy in another way, and this leads
ne to the consideration of rellex epilepsy, and thus of secondary epilepsy.

The term reflex epilepsy is applied to those cast's in which the disease
is produced by morbid changes situated in regions which are sometimes
far distant. For example, cicatrices which mclose nerves, and tumors
which compress nerves, may produce Buch a condition of increased irri-
tability of the central nervous system by their constant irritation as to
resnlt in epilepsy. This has also been observed as the effect of an accu-
mulation of wax in the ear, foreign bodies or inflammation of the ear,
polypi of the vocal cords and naso-pharyngeal space, by^ierplasia of the
nasal mucous membrane, intestinal worms, coprostaais, distention of the
intestines bv imiigeatible substances, and genital diseases. The epilepsy
sometimes disappears after the removal of the reflex exciting cause.

Epilepsy is occasionally the result of lesions of the cranial cavity,
fluch as fracture of the bones and impaction of particles in the brain,
tumors, softening, abscesses, and cysticerci in the brain. Many of these
cases are the result of direct irritation of the cortical motor centres (cor-
tical epilepsy).

The causes of the morbid predisposition and of the individual at-
tacks must be kept separate. Both often remain unknown; in other
cases, the individual attacks are produced by bodily or mental exertion,
excesses iu Venere et Baccho, suddenly increased irritation, for exam-
ple, coitus, etc.

n. Akatomical Chanobs.— The anatomical changes which give rise topri-
iDaiT epilepBj are unkuown. Some of Che aBsuiued anatomical leaions are un-
doubtedly accidental. The following changes have been found :

Asymmetry of the skuJl, thickening and Hcteroais of the bones of the skull, ex-
oslofies, thickening, calciH cation, oeaiiloation, and pigmentation of the meningee,
punctat« and larger extravasations in the meninges, brain, and epjoal cold, if
death occurred during an epileptic attack <the reeultof stasis in the circulation);
Blenoses of tlie occipital and carotid foramina, Htenoses and abnormal commu-
niimtions in the circle of Willis, interstitial and parenchymatous changes in va-
rious parts of the central nervous ay stem with indammatory changes in the blood-
vessels, atrophy of the cornu AmmoniB, hyperemia, proliferation of interstitial
connective tissue and degeueralioa of the ganglion cells of the sympathetic, etc

III, Symptoms. — Wedivide epilepayinto two principftl forms, severe

I mild, according to the intensity and significance of the symptoms.

Severe epilepsy (epilepsia gravis) ia recognized most readily when it
occurs under the typical history of well-developed epileptic attacks. These
may occur suddenly or are preceded by certain prodromata.

The prodromata are either remote or immediate. The former pre-
cede the attack for hours or days, the latter often last only a fev
seconds.

The remote prodromata generally consist of psychical changes. The
patients grow moody, irritable, sleepless or somnolent, forgetful and
-""'.hetio— symptoms which disappear after the epileptic attack.

^^1

264 FUNCnONAL DISEASES OF THE BRAIN.

The immediate prodromata are also known as aara epileptica, becsw
some patients state they can recognize the onset of a fit by a sensational
if a current of air were blowing upon them. But this form of annii
very rare.

According to the region affected, wo distinguish a sensitiye, motor,
sensory y and yaso-motor aura.

The sensitive aura consists of parsBsthesisB of various kinds: prickling,
sensation of cold, drawing pains, feeling of oppression in the prsecordii,
eructations, distention oi tne abdomen, etc. The sensations sometimes
recur before each attack, sometimes different ones.

The motor aura consists of a feeling of numbness^ paralysis, or twitch-
ings in the muscles of the limbs or face. The symptoms sometime!
pass from one limb to the others in regular order, untu the epileptic fit
appears.

The sensory aura manifests itself not infrequently in abnormal
special-sense impressions. The patients complain of peculiar sensations
of taste or smell, or they hear ringing or roaring in the ears^ or see bright
flaming colors (often red). Sometimes there are hallucinations, partic-
ularly the appearance of frightful shapes, or delirium develops. ]& raie
cases there is a sensation of unspeakable well-being.

The vaso-motor aura appears as pallor, coldness, later as a cyanotie
color of the skin, associated with a feeling of falling asleep.' The phe-
nomena often begin in one limb and then spread to all the others. The
majority of patients state that the phenomena extend from the peripheiy
towards the centre, but they are evidently the result of previously ex-
isting disturbances of central innervation.

The aura generally lasts a few seconds or minutes, but its duration
may vary considerably in the same individual. In many patients the
epileptic attacks sometimes occur with, sometimes without an aura. The
latter sometimes occurs without being followed by an epileptic seizure.

The presence or absence of an aura has no noticeable effect upon the
number and character of the epileptic seizures. In some cases, the sei-
zure may be prevented by vigorous counter-irritation at the onset of the
aura (rapidly strapping tllio limb from which the aum starts, swallowing
a teaspoonful of salt, etc.). But many patients maintain that the arti-
ficial prevention of an attack is not infrequently followed for a long
time by a feeling of great exhaustion and mental depression, while they
feel relieved and refreshed after an attack.

The epileptic attack proper begins, in many patients, with a shrilly
heart-rending cry, which is the result of sudden tonic spasm of the
muscles of inspiration or expiration. Almost at the same time the
patients fall unconscious, and thus often sustain severe injuries. Scars
upon the skull or other parts of the body are rarely al>sent in those who
have had numerous attacks. The unconsciousness is complete. Indi-
viduals who have fallen into the fire during the attack have been known
to be burnt to the bone without experiencing the slightest sensation. At
first, the color of the face and skin is pale, and the entire muscular system
undergoes tonic spasm. The eyes are turned fixedly upwards and in-
wards, the features are distorted, the head is drawn strongly backwards,
the muscles of the back and limbs are rigidly contracted. The stage of
tonic spasm generally does not last more than ten to fifteen seconds.
This is followed by tfie stage of clonic muscular spasms; shortly before
the pale color of the skin has generally given place to cyanosis. During
the clonic convulsions, rapidly changing contortions and grimaces ap-

FUNCTIONAL DISEASES OF THE BBAIN. 265

pear in the face. The eyes roll to and fro, the tongue is' protruded be-
tween the teeth and retracted, and the organ may be bitten. The
cicatrices left over may be important in diagnosis. The muscles of the
pharynx and larynx also tate part in the clonic convulsions. The
saliva cannot be swallowed, and appears externallv as a white, frothy,
sometimes sanguinolent mass. Spasm of the muscles of the neck com-
presses the jugular veins, which appear under the skin as cords almost of
the thickness of the little finger. The stasis is often so great that more
or less extensive hemorrhages appear beneath the conjunctiva and the in-
tegument of the forehead and face. This may also occur in other parts
of the body. These subscutaneous hemorrhages are especially impor-
tant in the diagnosis of epileptic attacks which have occurred during
sleep. The stasis of blood also gives rise to protrusion of the eye-
balls. The fingers are generally contracted spasmodically, and the
thumb drawn forcibly into the palm of the hand. The patient con-
stantly works convulsively with the arms and leg, and may fall out of
bed. The respirations are rendered irregular by the spasm of the re-
spiratory muscles, sighing and gurgling sounds are produced, and the
cyanosis increases.

The condition ot the pupils varies. As a general thing they are
markedly dilated and they never react to light. The latter characteris-
tic is important in excluding simulation. Kefiex action is abolished, as
a rule, but in some cases the lids are closed upon touching the cornea,
and muscular twitchings occur upon sprinkling the body witn cold water.
There is sometimes involuntary evacuation of urine and fasces; priapism
and evacuation of semen may also occur.

The bodily temperature is almost always unchanged, at the most it
rises a few tenths of a degree. The pulse is sometimes irregular and
small; if the convulsions are very violent, it may be imperceptible.

The clonic convulsions are often equally vigorous on both sides of the
body, sometimes they are stronger on one side. The vigor of the con-
tractions may be very considerable. They may result in fracture of the
teeth, dislocations and fractures of bones. Shortes reports a case of rup-
ture of the heart, probably as the result of the enormous stasis.

The stage of clonic spasm lasts from half a minute to five minutes,
rarely longer. Towards the end of the attack the skin is often covered
with profuse, usually clammy, cool perspiration, rumbling in the abdo-
men and eructations often make their appearance, the twitchings be-
come less violent and frequent, and gradually cease. In rare cases the
spasms cease abruptly.

This sta^e is followed by a series of phenomena which are called the
post-epileptic stage.

The cyanosis gradually disappears, but the patients remain asleep for
a certain period. Many awaken with a deep sigh, unaware of what has
happened. For hours, even for days, they remain stupid, forgetful, irri-
table, and a feeling of well-being and relief appears only graaually. In
others delirium sets in. Or there may be maniacal attacks and acts of
violence (biting, destructive acts, homicidal attacks) of which the pa-
tients have no recollection when they recover complete consciousness.
Transitory paralyses are sometimes left over. I recently had under ob-
servation an epileptic who suffered, after an attack, from complete right
hemiplegia and aphasia. At the end of a week the symptoms rapidly
disappeared. In another case the paralysis persisted three weeks.
Sometimes there is paresis or paralysis of a single limb.

"266 FuiicrnoNAL diseases of the bbaht.

Huppert clidms that transitory albuminuria is a constant post-epUqitic sjn^
torn, and that hyaline casts and spermatozoa are Bometimes f ouna in Uie mine.
This is by no means true of all cases i in twenty cases examined by Efastebt al-
buminuria was not found in a single one. Polyuria is sometinies observed.

lu some patients^ epileptic attacks occnr only in the day (dinml
epilepsy)^ in others only at night (nocturnal epilepsy). Not in-
frequently they appear at different times in the day. Noctur-
nal attacks arc recognized by the production of extrayasations ani
wounds of the tongue, or the soiling of the bed with urine and !«»»
or by the fact that the patients feel remarkably exhausted on awaking.
Attacks may occur after intervals of months and even years, of afewdiji
or hours, or even less. In one of Delasiauve's patients 2,500 attacks oc-
curred in a single month. There are not infrequently periods in which
the attacks recur at short intervals, then longer or shorter periods in
which they remain entirely absent. The attacKS often cease ouringtlie
course of acute infectious diseases, and may even disappear permi*
nently.

The patients are sometimes seized by a new attack before they hiis
entirel}[ recovered from the preceding one. The constant repetition d
such seizures for days is known as the status epilepticus. As a rule, this
is accompanied by great elevation of temperature, which may reach 42*
G. or even more, and may prove fatal. Bemissions and exacerbations
are noticed in some cases, and recovery may occur, but is rarer than the
fatal termination. The excessive rise of temperature appears to be the
result of central disturbances of innervation.

The scquelsB of the epileptic attack are divided into the immediite
and mediate. The former give rise to death or other injury directly as
the result of the seizure. Death may occur from suffocation as the re-
sult of tonic and clonic spasm of the respiratory muscles, or suffocation
results accidentally from the falling of the patient on his mouth and nose
so that the air passages are occluded, or from the occurrence of the
attack while eating and the entrance of food into the larynx. The
serious disturbances of circulation sometimes give rise to pnlmoniuy
oedema or cerebral hemorrhage ; rupture of the heart is also a possible
sequel. The disturbances of less signiticance include cutaneous wounds
and excoriations, fractures and dislocations.

Persons who have long suffered from epileptic attacks often presents
change in their bodily and mental characteristics. The features become
dull, stupid, occasionally animal, the eyes are prominent and staring,
the lips are thickened, etc. Dilatation of the retinal veins as the resmt
of stasis is sometimes observed. The changes in the mental sphere are
shown by the irritability, diminished power of memory and judgment
Children are no longer able to make their way in school, dementia or
some other form of insanity makes its appearance, and not a few
patients end their lives in lunatic asylums. In some cases the mental
powers are unaffected, and some of the most celebrated men have suf-
fered from this disease.

Mild epilepsy appears in various forms. In some cases the symptoms
are confined to temporary disturbances of consciousness (absentia epilep-
tica). The patients suddenly grow pale, have a staring, glassy look,
stop suddenly in the middle of a sentence, or in walking, playing on the
piano, or any other occupation in which they may be engaged. At the
end of a few minutes the pallor of the face disappears, the patients sigh
deeply, or yawn several times in succession, and then continue the oo-

FUNirnONAI. DISBA^es OP TUB BB&DT.

cnpation which had been interrupted. In some cases the aeizure is fol-
lowed at once by confusion of ideas and delirium, and some time elapses
before the patient comes to himself. It may also happen that they per-
form unconscious automatic actions during the attack. Such conditions
often remain unknown to the patient himself for a long time. Very
many seizures Eometimea occur during the course of an hour, in others
they appear at long intervals,

in some patients there is not complete loss of consciousness, but
merely temporary confusion and vertigo (epileptic vertigo). They are
generally forced to hold on to some support or to sit down, more rarely
they fall to the ground.

In certain cases of mild epilepsy, typical oonytilsions occur, but they
are very brief and slightly developed. Twitohinga occur in only a few
groups of muscles, sometimes only tonic, sometimes so slightly clonic as
to resemble tremor, rather than a clonic muscular spasm. It is also
said that the attack may consist merely of muscular spasm without
loee of consciousness, but we have never seen attacks of this character.

Some patients suffer only from attacks of mild epilepsy. In others,
the disease begins in the mild form, later it merges into the severe
Tariety. The reverse condition may also obtain. Mild and severe at-
tacks may also alternate irregularly with one another.

In addition to typical epilepsy (mild and severe forms), there is also
an atypical form of epilepsy, whose epileptoid character is often rec-
ognized with difficulty. This includes the morbid states to which
Griesinger applied the term epileptoid conditione. The symptoms are
often purely psychical. The patients have temporary hallucinations
and delirium, talk obscenely, act iu a strange manner, or become
violent. These symptoms occur in paroxysms, and are not remembered
by the patient. They are particularly important from a medico-legal
standpoint, since to them homicide and other acts of violence may owe
their origin. They often appear suddenly; in other cases, they are pre-
ceded by prodromata, so that the patients warn those around them of
the approaching danger. In some instances, the symptoms assume
more of a motor character; the patients suddenly beirin to run forwards
or to revolve in a circle, without being conscious of their action. In
others, there arc sudden outbreaks of perspiration, etc.

IV. Pathooenesis. — In a disease which consists of brief, temporary
attacks, the causes must be assumed to be transitory, abnormal condi-
tions of the brain, such as temporary circulatory disturbances. These
are now generally regarded as anmmic in character.

The epileptic attack undoubtedly starts from the motor regions in
the central convolutions of the brain. Hitzig succeeded in making dogs
epileptic by extirpation of the motor centres in the cerebral cortex, and
the experiments of Uuverricht and F. Bosenbach point in the same
direction.

It was fortneily held that the site of epilepsy is located in the medulla oblon-
galH.

Nothnogel located the so-^allnj conTuleive centre iu the pOtiB: and expUined
. the occurrifuce of the epileptic attack in the following manner : irritation of the
vaeo'iuotor i.-entre in the medulla oblongata; spasm of the cerebral arteries;
aniBoiin of the brain; tosa of Runsoiousn^s; in addition, irritation of the convul-
sive centre, general con vul si oils.

Brown-Sequard found that ^inea pigs became epileptic after section of the
sciatic, or herai-»ection ot the itpinal cord. Weatphal produced epilepsy in
guinea pigs by making quick strokes with the hamioer upon the head. At the

268 FUNCTIONAL DI8SASB8 OF THE BRATET.

autopsies, small extravasations of blood were found in the mednllm oMongifi «d
upper part of the cervical cord. Both authors noticed that the epileptic atttcb
dia not begin until some time after the experiment, that the individual attach
may be produced by irritation of definite parts of the skin (eo^^salled epUeptogoie
zone), and that the disease is transmitted to the offsprinR, Unverricht and
Rosenbach have recently produced epileptic attacks in dogs by irritAtian of the
cerebral cortex.

V. Diagnosis. — The diapiosis of the typical forms of epilepsy is
generally easy^ while a long time may elapse before the true natnre of
atypical epilepsy is recognized.

Not every epileptiform spasmodic seizure may at once be called epi-
lepsy; it must be remembered that epilepsy is a chronic disease, charac-
terized by the recurrence of the attacks, and that gross, particolailj
acute, anatomical changes are not discoverable.

In the differential diagnosis between epilepsy and hystero-epilepsj,
the chief element is the fact that in the latter consciousness is retained
or at least not entirely abolished. In addition, other hysterical symp-
toms are generally present.

Epilepsy is not infrequently simulated. But in malingerers no
wounds or cicatrices are found upon the ton^e or skin, the pupils react
to light during the attack, reflex irritability is retained, and the thumbs,
if extended, are at once restored to the flexed position. In spite of dl,
great tact is sometimes necessary to discover the deception.

If the diagnosis of epilepsy is rendered certain, we must endeavor t<^
ascertain whether the disease is primary or secondary. The diagnosiBof
a direct affection of the cerebral cortex — cortical or Jacksonian epi-
lepsy — is favored by the fact that the spasmodic seizure is always con-
finea to one limb.

VI. Prognosis. — The prognosis is decidedly grave. Recovery is
the exception, rather than the rule. Years may elapse in which do
attack occurs, and the disease is regarded as cured, when a relapse
proves our error. The hereditary forms of the disease are especially ob-
stinate. It is readily understood tliat the prognosis is grave in tho»
cases in whicji the attacks recur with great frequency, are severe and
protracted, and associated with mental disturbances.

VII. Treatment. — Prophylaxis is indicated with regard to the
children of epileptic parents. A mother, who is epileptic or comes of
an epileptic or neuropathic family, should not nurse her own child.
The children should be nourished with special care, and should avoid
bodily and mental strain and sudden mental excitement.

The regimen constitutes an important part of the treatment of
epilepsy. Stimulating drinks (alcoholics, tea, and coffee) and articles
of food which are difficult of digestion should be interdicted, a daily
evacuation from the bowels should be secured, and plethoric individuals
may take a cure at Carlsbad, Kissingen, Marienbad, etc. Excesses in
Baccho and Venere must be strenuously avoided. Cold baths mast be
used with caution, since they sometimes prove too stimulating; hatha
should never be taken except in the company of another individual.
Benefit may be derived from lukewarm baths at a temperature of 26° B.
(for a half-hour every other day).

Causal conditions must first be taken into consideration as re^rds
treatment — mercury and potassium iodide in syphilis, antihelmmtics
in helminthiasis, excision of cicatrices with inclosed nerves, removal of

FTNCnONAL DISEASES OF THE BRAIN.

269

tumors, treatment of ear diseases, scrofula, rickets, trepanation in cases
of foreign bodies between the skull and brain.

The treatment of epilepsy as such must be separated from that of the
individual attacks.

Among the numerous remedies recommended, the most reliable, in
our opinion, are potassium bromide and radix artemisiaB. Potassium
must oe given in large doses in a large amount of water, and for a long
time:

]J Potass, bromid 3 xiv.

Aq. destil ^ q. s. ad | x.

M. D. S. One tablespoonful t. i. d.

In some of our cases, we feel convinced that the action of the bro-
mide was increased by the addition of artemisia: .

I^ Rad. ArtemisiaB § ss.

Coque cum Aa. dest q. s. ad colatnr f viij.

Potass, bromid • 3 xiv.

M. D. S. One tablespoonful t. i. d.

Other bromide salts are also recommended, particularly sodium,
ammonium, and lithium bromide; the latter is said to be tolerated much
bettor than the other salts. Erlenmeyer extols the combination of
sodium and ammonium bromide in equal proportions. If the dru^ is
given in too large doses or for too long a time, symptoms of poisoning
set in — acne, feebleness, mental sloth, weakness of memory, uncertain
and tremulous movements, somnolence, and feebleness oi the heart.
The drug must then be discontinued for a time. P. Bosenbach has
shown experimentally, in dogs, that potassium bromide diminishes the
irritability of the motor cortical centres.

We have rarely seen any good effects from the use of valerian, bella-
donna, nitrate of silver, zinc, copper, or gold. According to Albertoni
and Unverricht, atropine increases the excitability of the cerebral cortex
in animals.

We may make mention of the following remedies, which have been employed
in this disease: a. Venesection, leeches, cups, b, Seton in the neck, issues,
derivatives of all kinds, e. cold-water cures, salt-water and fresh- water baths.
d, narcotics: opium, chloroform, chloral hydrate, hyoscyamus, curare, stramo-
niam, strychnine, digitalis, e. nervines: asafoetida, castoreum, arsenic, phos-
phorus, perosmio acid. /. Electricity (salvanio current transversely or obliquely
through the cerebrum, to the medulla oblongata, or the sympathetic) has secured
no positive results hitherto, g, Alexander claims to have cured cases by ligature
of tne vertebral artery.

In the treatment of an epileptic seizure, it is doubtful whether it is
advisable to check the attack on the appearance of an aura, since many
patients state that they then feel worse than before, and that the next
attack is more severe. As a general thing, our treatment during an
attack must be confined to placing the patient in a good position, to
guarding him against injury, and to prevent acts of violence when he
awakens.

Compression of the carotids is irrational, and chloroform narcosis is not devoid
of dangler; the most rational measure appears to be the inhalation of nitrite of
amyl, since this dilates the vessels, and will relieve cerebral anaemia.

270 FUNOnONAL DI8EASBS OF THE BSAIK.

Inhalations of chloroform, ether, and nitrite of amyl have been reooBk
mended in the treatment of status epilepticus.

2. Eclampsia.

I. Etiology. — The term eclampsia is applied to acute attacks of
epileptiform spasms, which have toe same genesis as true epileptic
attacks, and are produced by irritation of the motor cortical centres of
the brain. It may be the result of various causes, such as toxic influ-
ences (uraemia and lead poisoning), diseases of the brain and its men-
inges.

Childhood is especially predisposed to eclamptsia, probably on acconnt
of the slighter development of the reflex inhibitory apparatus (Solt-
mann), and in the following remarks we will consider eclampsia in-
fantum alone.

The disease is observed chiefly in nursling ffifth to twentieth
months), and is much rarer in the new-bom and m cnildren beyond the
age of two years.

Heredity exercises a certain amount of influence, since eclampoft
occurs particularly in children whoso parents or other relatives are
neurotic. Under such circumstances, the exciting cause may be of sudk
a trifling nature that the attack appears to develop spontaneously.

Eclampsia is sometimes the result of violent mental emotion (joT»
fright, anger, etc.).

It occurs most frequently in a reflex manner, as the result of periph-
eral irritations (painful wounds of the skin, eruption of the teeth, in-
flammations of the buccal cavity, foreign bodies and inflammations of
the ear, violent gastric and intestinal catarrh, faecal stasis, worms, renal
and vesical calculi, etc.). Eclampsia is much rarer, under such cir-
cumstances, in adults than in children.

It also occurs not infrequently in febrile conditions and infections
diseases in children.

Eclampsia sometimes occurs idiopathically without any demonstrable
cause. Rachitic children are attacked not infrequently, perhaps as the
result of pressure on the brain by the yielding skull.

II. Anatomical Changes of a causal character have not been disooTered
hitherto. Tlie secondary changes which have been observed are hemorrhaces
into the meninges, brain, and spinal cord, increase of the cerebro-spiiial fluid,
etc.

III. Symptoms.— The symptoms develop suddenly, for example,
immediately after a fright, or they are preceded by prodromata. The
latter consist of changed disposition (restlessness, terror, a tendency to
cry), restless sleep, tlisturbances of appetite and digestion. Shght
twitchings in individual groups of muscles often occur during sleep; the
children lie with half-closed eyes, grit the teeth now and then, langh in
their sleep, pass urine and faeces m bed, contrary to their usual habit,
etc.

The eclamptic seizure itself is exactly like an epileptic attack. It
may last from a few minutes to several hours. A status eclampticns
sometimes develops, /. e , the child does not recover consciousness com-
pletely before another attack begins. In such cases the bodily tempera*
lure may rise very high, while it is unchanged in shorter attacks.

Sometimes a single attack alone occurs, in other cases the attacks .

FUNCrnONAL DIBBASBS OF THE BSAIN. 271

recur at longer or shorter intervals, or with each eruption of a new
tooth.

A fatal termination may result from suffocation in consequence of
closure of the vocal cords, or disturbances of the respiratory apparatus,
or collapse. Or complete recovery takes place. Slight pareses may be
left over for some time; permanentparalyses must be attnbuted to hem-
orrhage and lesions of the brain. Fractures and dislocations and break-
ing of the teeth have been observed as the result of the violence of the
muscular contractions. Eclampsia is sometimes followed by epilepsy.

IV. Diagnosis, Prognosis, Tkkatment. — The diagnosis is easy;
the prognosis is always serious.

Children must be protected against sudden mental excitement, and
must not be nursed by mothers wno come of neuropathic families.

In combating the individual attack, the child must be relieved of all
tight clothing, and placed in a large, slightly darkened, airy room, with
the head low; it should be given a lukewarm bath (28° B.), with cold
douche to the head, and an enema of vinegar or salt given. A mustard
draught may also be applied to the breast or calves. In status eclamp-
ticus, we may employ inhalations of chloroform, or amyl nitrite and
enemata of chloral. After the attack has subsided, causal treatment
must be inaugurated, or, if there are no causal indications, we may order
potassium bromide or other bromides, in order to diminish the irritabil-
ity of the cerebral cortex.

3. Tetanus,

I. Etiology. — Tetanus manifests itself bj tonic muscular spasms:
which are interrupted now and then by clonic twitchings, and oy in-
creased reflex excitability, consciousness remaining entirely intact.

It is divided into four varieties, viz. ; idiopathic, traumatic, rheumatic,
and toxic tetanus.

The traumatic form is the most frequent. It may be the result of
operation wounds or accidental injuries. Among the latter, the most
dangerous are contused and torn wounds, wounds containing foreign
bodies, and injuries of nerves and tendons. Experience also teaches
that tetanus is apt to arise from wounds of the fingers, toes, palms of the
hands, and soles of feet. In some cases, it does not develop until pysB-
mic symptoms have made their appearance.

Tetanus may follow a wound at once. Thus, it has been observed
immediately after ligature of the crural nerve in amputation of the thigh.
In other cases, it develops after the lapse of days and weeks.

In some patients, certain auxiliary factors seem to further the development of
the disease. It has been noticed in several campaigns that the vanquished were
attacked more frequently than the vidtors, so ttiat a psychical influence may be
suspected. Irritating treatment of wounds and colds also favor its development,
and occasionally epidemic influences seem to play a part.

Even the most insigniflcant wound (piercing the ear, extraction of a tooth,
sting of a bee, etc.) may give rise to the disease. Nor is it necessary that the
wound be open. Concussion of the spine and head may act as a cause.

It is sometimes the result of internal wounds. Thus, tetanus sometimes fol-
lows an abortion, or even a natural delivery (generally from the third to seventh
day after delivery). It occurs occasionally during pregnancy. It has also been
known to follow tne spontaneous removal of an uterine fibroma, rectal ulcera-
tions, etc.

Tetanus neonatorum cor^titutes a special group. It begins, as a-

272 FUNcrnoNAL diseases of thb brain.

rule, between the fifth and twelfth days of life, and in the majority of
cases is the result of disease of the umbilicus. In other cases, it foUowj
puerperal infection of the new-born, sometimes faecal stasis. Smith
maintains that the majority of cases are the result of the strong back-
ward pressure of the occiput and the mechanical irritation of the
medulla oblongata (convulsive centre).

Rheumatic tetanus was formerly regarded as extremely frequent, not
it is considered to be a rare disease. According to recent views it i*
doubtful whether a cold, as such, is capable of producing tetanus, or
whether the action of certain lower organisms does not constitute the
real cause of disease.

Toxic tetanus is that form which follows thermal or chemical noia.
The former includes certain cases which occurred in the new-born as the
result of the use of hot baths by midwives wno were accustomed to
measure the temperature of the water with the hand^ and whose tem-
perature sense was impaired as the result of disease.

Tetanus following poisoning with strychnine, brucine, or pierotoxine
is regarded as the prototype oi toxic tetanus, but it must be noted that
in this form clonic muscular twitchings are much more prominent than
in other forms of tetanus.

The term idiopathic tetanus is applied to those cases in which no
cause can be discovered.

Leaving tetanus neonatorum out of consideration, the disease is
most frequent in middle life, because there is then more liabilitvto trau-
matism, which is the most common cause of the disease. For this rea-
son, likewise, tetanus is more frequent in the male sex. It is said that
individuals of full-blooded constitutions are attacked more frequently bv
tetanus, but this is not in accordance with our own experience. In' the
tropics negroes are affected much more often than the whites, but some
authors maintain that this is not owing to race })eculiarities, but rather
to the facts that the negroes are loss cleanly and live under less favor-
able surroundings. Climate exercises a notable effect. The disease is
very frequent and sometimes epidemic, in the tropics, particularly during
hot spells, or when hot days are followed by cold nights. General hy-
gienic conditions are also important. In poorly ventilated and uncleaniv
maternity hospitals, particularly in former times, terrible epidemics o^
tetanus neonatorum have been observed, which ceased as soon as rules of
cleanliness were enforced. Similar conditions may also prove destructive
in the community at large.

11. Symptoms. — The disease is generally preceded by prodromata.
In traumatic tetanus the patients complain of pain in the wound, and
the latter sometimes assumes a bad color. The pains sometimes run
along the course of a large adjacent nerve, but this does not justify the
conclusion that there is an inflammation of the nerve in question. "

Many patients are peculiarly restless, excited, sleepless, and anxious.
Pain and stiffness soon supervene in the jaws and muscles of the pharynx
and back of the neck, finally muscular spasms make their appearance.

In the new-bom, the occurrence of tetanus is preceded not infre-
quently by inflammation of the umbilicus. The children cry often dur-
ing sleep, are restless, and not infrequently present disturbances of di-
gestion.

The first manifest signs appear in the face, then in the muscles of
mastication and of the pharynx, the muscles of the back of the neck,
and finally the tetanic symptoms appear in the muscles of the back and

FDNOriONAI. DISUSES OF TBB JOUJS. iftS

limbs. In general, therefore, the liiaease spreads from above down-
wards.

In some cases, tetanus of the jaw muscles is especially prominent
(trismus), so that the slighter implication of the muscles of the buck of
the neck is overlooked. But our experience is corroborative of that of
those author's who deny the existence of trismus pure and simple.

The muscles of the extremities are not infrequently almost entirely
unalfected. This is particularly true of tho tetanus of adults,

Tetanus of tho facia! muscles gives rise very early to a peculiar
change of facial expression, which by soma writers is regarded erro-

neously as a prodromal symptom. The forohead is drawn Into horiaon-
tal and, near the glabella, into longitudinal folds, the contours of the
massetora appear distinctly under the integument, the alse nasi are
drawn outward and upward, the mouth is widened, the angles of the
mouth are drawn downwards and Bend out diverging folds of skin, the
teeth become visible, etc. The features express the most antagonistic
feelings. While the upper half of the face has a cheerful though tired
expression (diminution in size of the palpebral fissure), the lower part is
Bad, and the mouth has the expression of one who is sobbing. On ac-
count of the uncovering of the teeth, the expression has been compared
to that of langhing, risus sardoDioua (vide Fig. 132).
L 1^

274 FUNCTIONAL DISKA8K8 OF THE BRAIK.

The patients are able to open the mouth very little or not at all, be-
cause the masseters draw the jaws very firmly against one another. In-
fants are unable to retain the nipple between the jaws ; tbey often applj
the lips greedily to the nipple, but quickly let go with a loud cry. Tht
jaws oppose such a resistance to passive motion that it wonid appear u
if the lower jaw would be dislocated or fractured rather than tlie spasm
be overcome. The nutrition suffers on account of this condition, and if
the disease lasts a long time threatens inanition.

This danger is increased still further by tetanus of the phaijnx,
which generally appears very early and is often very marked. The w-
tients often suffer the tortures of Tantalus on account of their inabiUtj
to satisfy their hunger and thirst.

The muscles of the nape are aknost always in a state of tetanic contrac-
tion, so that the head is arawn forcibly backwards. The bellies of the
contracted muscles stand out distinctly beneath the interment, par-
ticularly at the sides. Rotatory movements and increased flexion of the
head backwards may sometimes be performed with surprising faciUtv.

Among the muscles of the back, the lon^ extensors generally acqaiie
the predominance. The back, and with it the entire body, is so stiff that
the patient can be lifted up in ioto by the back of the head. In derail
decubitus, the spine is unusually curved anteriorly, so that the fist may
often be passed between the back and bed (opisthotonos).

Much rarer are tetanic curvature anteriorly (emprosthotonos), or to one side
(pleurothotoQoe) ; the body is rarely held perfectly straight (orthotonoe).

If the muscles of the thorax and diaphragm are affected, the respira-
tory movements are interfered with, and the patient falls into a condi-
tion of extreme dyspnoea. He becomes cyanotic, breathes irregularlr
and with difficulty; finally, carbonic-oxide narcosis sets in, and death
from suffocation. These dangers increase when, as is not infrequent, the
muscles of the larynx undergo tetanic spasms. Disturbances of speech
are associated with tetanus of the muscles of the tongue.

Tetanus of the abdominal muscles is shown by retraction of the ab-
domen^ which is sometimes boat-shaped.

The older re{)ort8 mention priapism and involuntary discharge of semen. In
the case shown in Fig. 122, the penis was permanently in a semi^rect conditioii
(tetanus of the ischio-cavernosus and bulbo-cavernosus muscles ?;.

In tetanus of the muscles of the limbs, the latter are rigid and per-
manently flexed or extended, and the tense bellies of the muscles appear
prominently under the skin.

In very rare cases is there tetanus of cerebral nerves other than the
facial, trigeminus, and glosso-pharyngeus, but strabismus has been de-
scribed in a number of cases, generally as an ominous sign of approaching
death.

The character of the tonic contractions is not always alike. In a
series of cases, they persist with almost unchanged intensity for hours,
days, and even weeks. They disappear only during sleep or chloroform
and chloral narcosis, and reappear very quickly on awaking. In
other patients, the tetanic contractions occur only in paroxysms. Such
attacks generally begin with clonic twitchings, which often produce
violent convulsion of the entire body. They may be product oy very
slight irritants, so that it is evident that tetanus is the result of incieased

FUNCmONAL DISEASES OF THE BBAIN. 276

reflex excitability. Gently touching or blowing on the skin, a bright
light, the slamming of a door, or even the mere idea of an a{)proachmg
attack may excite the contractions. The number and duration of the
attacks also depend on the severity of the disease. Rapid fibrillary
twitchings are sometimes seen to run across the tetanically contracted
muscles. The vigor of the contractions may be very considerable, and
they sometimes result in fracture or dislocation of the bones or breaking
of the teeth.

The sensorinm is always unaffected, except that delirium sets in not
infrequently towards the end of life.

The patients almost always complain of pain in the contracted mus-
cles, and of obstinate insomnia. The majority experience a sensation of
unspeakable terror.

The bodily temperature may be unchanged. In other cases, it is
subnormal or there are slight, irregular elevations of temperature.
There is sometimes a prsemortal, hyperpyrexia! elevation of temperature
(44.7° 0. in Wunderlich's case).

It has been shown in criminals that the bodUy temperature rises when general
tetanic spasms are produced by strychnine-poisoning or faradization of the
spinal coid. Nevertheless, the elevation of temperature does not appear to depend
on the muscular contractions alone. It is more probable that tnis is the result
of central influences and of the extension of the nervous disturbances to the
heat-moderating centres.

The pulse is generally accelerated, sometimes irregular.

The skin is often covered with profuse sweat, probably as the result
of disturbances of innervation of the sweat centre m the medulla oblon-
gata. The cutaneous sensibility is generally unchanged; Demme claims
to have found diminution of sensibility to temperature and touch. The
cutaneous reflexes are often increased. In a case recently under treat-
ment, the patellar reflex was diminished; it is sometimes lound to be in-
creased.

There is generally difficulty in the evacuation of urine and faeces.
The urine is generally scanty, highly colored, and of slightly increased
specific gravity; it often deposits a sediment of urates. It sometimes
contains albumin, occasionally sugar; Griesinger discovered casts and
an increased amount of indican.

According to Senator, the urea is unchanged or diminished in amount; krea-
tioin is diminished. In one of my cases, the amount of urea was diminished, that
of kreatinin distinctly increased. The albuminuria may be the result of nephritis
(produced by rheumatic influences), or of stasis in consequence of the muscular
spasms, or of disturbances of central or peripheral innervation of the renal
nerves.

Bronchitis, pneumonia, and acute nephritis are described as compli-
cations of tetanus.

The duration and course of the disease are extremely variable.
Bobinson reported a case in which death occurred, in a ne^ro, fifteen
minutes after the receipt of the injury. In other cases, the disease lasts
days, weeks, even months, and m favorable cases a long time often
elapses before the last traces disappear. The patients often complain
for a long time of stiffness, weakness, and drawing pains. Pareses and
even paralyses have been mentioned as sequelsB.

A fatal termination may be the result of exhaustion, suffocation, or
excessive rise of temperature.

276 FUNcrnoNAL dissabes of the bsain.

The term head tetanus (tetanus hydrophobicns) is applied to a apecial formtf
tetanus, eft which seventeen cases have been hitherto reported. Hie disease mm
in injuries to the head, often of a very trifling character. This is followed bj
trismus and paralysis of all the branches of the facial nerve upon the side of die
injury. The facial paralysis either precedes or follows the trismas. The electii-
cal irritability of the nerve remains normal. The paralyased mnscles are not
infrequentlv in a condition of contracture. At a later period, spasms of deglnti-
tition and then general tonic spasms make their i^pearance. The disease geo-
erally terminates fatally. Macrosoopically, the facuil nerve appears to be intact

III. Anatomical Ghakges. — Bieor mortis generally sets in Terr
rapidly, and is very marked in the bodies of those dead of tetanus, fi
death was precedea by a rise of temperature^ the latter sometimes con-
tinues to increase after death. This has been attributed to the coagula-
tion of myosin and the consequent production of heat.

The muscles are often unusually pale. In places, they contain
extravasations of blood, and the microscope shows rupture of the mus-
cular tissue in these parts. In traumatic tetanus, the nerve trunks in
the neighborhood oi the wound are not infrequently reddened and
swollen. In some cases, it is said that these changes extend along the
nerves to the spinal cord. Froriep described, in two casesy nodular
swellings of the nerves (neuritis nodosa) extending as far as the spinal
cord. U mbilical arteritis and phlebitis have been observed in sevenl
cases of tetanus neonatorum.

Rigid contraction of the heart muscle has been noticed in a few
thai describes extravasations and rupture of fibres in the heart muscle. Marked
contraction of the oesophagus and injection of its mucous membrane are alio
mentioned.

Meningeal hemorrhages are often found and, as in other spasmodic
conditions, are the result of circulatory stasis. These insignificant
hemorrhages do not constitute the essence of the disease. If they are
more extensive, the cerebro-spinal fluid becomes sanguinolent, and is
often increased in quantity, probably a post-mortem change. The sub-
stance of the brain and spinal cord may present ansBmia, hypersemia, or
small extravasations of blood, or all combined. Various microscopical
changes in the nervous tissues have been described^ but the observations
are not reliable.

In our opinion, tetanus is an infectious disease, produced hy the action of
definite lower organisms, the nature of which is still unknown. Fluegge and
Nikolaier have recently cultivated bacteria which, when injected subcutaneouslj
in animals, gave rise to tetanus-like symptoms. As a matter of course, infec-
tious tetanus does not include the toxic form which is the result of purely chenu-
cal influences. It is an interesting fact that, in the decomposition of organic
matters, substances are produced which possess strychnine-hke cuffects, and the
q^uestion arises whether the supposed bacteria do not produce tetanus by fonning
similar chemical agents during their development.

IV. DiAGKOSis. — The recognition of tetanus and its etiology is gen-
erally easy, it is distinguished from spinal meningitis by the fact tliat,
in the latter, trismus is absent and irritative phenomena predominate.
In simple masticatory facial spasm the muscles of the back of the ne^
are unaffected. I recently saw a case of violent, acute muscular rheu-
matism of the muscles of the back, which gave rise to persistent, severe
opisthotonos, but the muscles of mastication and deglutition were en*
tirely intact.

V, Pboqsosis. — Tlie prognosia is always grave, bnt the cases rnn s
very variable course, bo that aoine observers lose nearly 100^ of iheir
cases, others not more than 50^. It must bo remembered that an ap-
parently favorable case sometimes takes a ra|iidly unfavorable turn.

Unfavorable signs are elevation of temperature, oontinaed insomnia,
delirium, and strabismus. The longer the disease lasts and the more the
temperature remains within normal limits, the more favorable are the
chances.

As a general thing, idiopathic tetanus presents a more favorable
prognosis than the traumatic variety; in the latter, the prognosis im-
proves the greater the interval between the injury and the first symp-
toms.

VI. Teeatmekt. — The causal indications must first be taken into
consideration. These include cleanliness and careful treatment of
wounds, laj-iug open wounds to remove pus or foreign bodies, removal of
ligatures from nerves, etc. Nerves have also been incised in the hope
of preventing the spread of an infiammatory process along the nerve to
the spinal cord.

The following plan appears to be the simplest and most reliable in
the treatment oi tetanus per se: milk diet, 1( necessary the administra*
tion of nourishment by means of the cesophageal sound or nutritive ene-
mata; if there is constipation, calomel and jalap, aa. gr. v., and chloral
hydrate gr. xxx.-lxxv, daily.

We will Bimpty mention the foUowiDg anions the methods of treatment rec-
ommended iu tliia disease: a. Derivatives to tbe spine; leeches, cups, alcoholic
inuDCtiuns, etiier spraj. b. Antlplilogietica: ice bag to the spine, mercury inter-
nallj and by munction, potassium iodide, c. Narcotics: opium, paraldebyd,
strychnine, belladonna, atropine, eserine, curare, couiiiie, hyoscyaoiine, polas-
eium bromide, amyl nitrite, tobacco enemata. Morphine and opium should be
avoided, since they are capable of producing t«tanuB. Nor does curare exercise
any good effects agaiost tetanus itseIC; in tlie most favorable event it merely
checks the spasmodio phenomena by parBlyi:ing the terminal nervous apparatus.
In addition to chloral hydrate, reliHncemay bo placed upon large dopes ot the bro-
mides, since they diminish the reflex irriiafaiiity of the central nervous systom.
Paraldebyd ( I i-ij. daily) may also be employed, d. Nervines, e. Electricity:
constant descending current on the spine, feeble current, one to two hours' dura-
tion, two to three times daily, or the anode labile on the individual tetanic mus-
cles, cathode on an iodlSerent spot, /. Nerve stretching bas also been tried.

4. SI. Vilus' Dance. Chorea.

(Cliorea Minor.)

I, Etioloqt, — Chorea is a neurosis which is located, in all proba-
bility, in the brain. The disease manifests itself by muscular restless-
ness and in co-ordinated movements, which ocuur spontaneously or aa
associated movements in volnntary muscular actions, and by changes i
the < ■ ' '

psychical sphere.
It occur

It occurs chiefly in childhood, particularly at the period of second
dentition (sixth and seventh years) aud puberty (eleventh to fifteenth

fears). It is rare In adults, relatively most frequent from the fifteenth to
he twenty-fourth years. In some cases it occurs iu old age (chorea
sooilif), mainly as the resuit of violent mental emotions.

D said that chorea

S7B vusunoSAi, diseabes or the bbadt.

Heredity playa an important part in tlie etiology of chorea. In a
number of my cases the children, parenta, and other relatives bad suf-
fered from the- disease. In other families, there are isolated cases of
chorea, while other members suffer from hysteria, epilepsy, psycho-
pathy, and nervousness.

In some cases the predispoBJtiou to chorea is acquired. Excessive ap-
plication in school, excitement following the reading of obscene bool^,
malnutrition, onanism, and ancemia may give rise to such a predisposi-
tion, BO that alight exciting canaea are apt to produce the disease.

Among the direct exciting causes may be mentioned : joy, grief, and
partionlariy fright.

In rarer cases it is attributed to injury, for example, a blow on the
head or back. etc.

Chorea is sometimes the result of reflex causes.

Borelli reported a case which recovered after the removal of (. ._
from one of the nerves of the nrm. Attention hae been called recently __ _.._

SresencB of painful points on peripheml aerves, the treatment of which pro-
uced rapid improvement. Wood observed heniichora after amputation of the
leg. FtEcal BtasiH and intestinal worm h sometimes give rise to chorea in chil-
dren. This U also true of dentition and defective condition of the teeth. Chorea
sometimeB disappears rapid!}' after the relief of phimosis.

This category probably includes the chorea of pregnancy, in which
the irritation starts from the inner surface of the uterus. It occurs
generally in primiparffi, particularly if they have suffered previously from
ansemia, nervousness, or chorea. As a general thing, it does not appear
before the end of the second mouth, but it is not rare iu the second half
of pregnancy. As a rule, the symptoms are very violent, terminate not
infrequently in death, give rise to abortion, and do not cease nntil deliv-
ery, The disease may then terminate quite suddenly. Occasionally the
BUDsequent pregnancies are accompanied by chorea. Lawson Tait re-
ports the case of a woman who suffered from chorea in four suooessive
pregnancies, and died in the fourth pregnancy despite the occurrence of
abortion.

Some of the older writers explain the frequent combination of chorea
and heart disease as the result of mechanical irritation of the phrenic
nerve by the enlarged heart. Others regard capillary emboli of the
cerebral arteries as the connecting link between the two conditions.

Numerous ]ier9onal observations confirm the frequent connection of chorea
-with heart diseases, (larticularlj valvular lesions (usuallj'' mitral iiisufflciencj).
more rarely pericardilia and diseases of the heatt muscle. French authors have
overestimated the frequency of this connection, inasmuch as they attribule
every By Btolic murmur, which occuni so frequently in the antemic patients, to
mitral insufficiency. We confess that, in our o|iinion, the previously mentioned
theory of the refiex origin of chorea iu heart disease seems to be very plausible In
many cases.

Chorea sometimes follows infectious diseases, viz., pneumonia,
typhoid fever, cholera, diphtheria, variola, morbilU, scarlatina, and,
above all, acute articular rheutnatism. It also occurs, in very rare

ea, with the outbreak of the so-called secondary symptoms of syphilis.

The connection of chorea with infectious diseases is entirely obscure.

In children, it sometimes develojis as the result of imitation, t. t..
when brought into close contact with choreic patients, the children aim

FUNCTIONAL DI8EA8B8 OF THE BBAIN. 279

begin gradually to perform choreic movements. This explains its en-
demic occurrence in boarding-schools and convents.

The disease appears occasionally as an epidemic. Steiner renorts an
epidemic in Prague, which lasted two months (February and March).
This is perhaps the result of climatic influences. At all events, many
writers agree that chorea is most frequent in the autumn and winter,
particularly if there are sudden changes of temperature.

Oirls are affected more frequently than boys (in the proportion of
two to one).

II. Symptoms. — The symptoms rarely begin suddenly; this is most
apt to happen after fright and emotional excitement. As a rule, the
disease is preceded for days and weeks by prodromata, consisting of un-
usual irritability, depression, apathy, disinclination to mental and bodily
work, impairment of memory, anorexia, restlessness, pallor, pains in the
spine, limbs, joints, headache, etc.

Gradually the patients atti*act attention by their awkwardness. The
^n^ers do not obe^ promptly in sewing or playing piano, food is spilt in
eating and drinking, there is inability to stand still, etc. So long as
the motor disturbances are not verj marked, they are often regarded as
the result of bad habits or ill-behavior. But soon the symptoms become
unmistakable.

Involuntary pronation and supination, flexion and extension of the
fingers, and twitchings of the shoulders are observed in the upper limbs.
If the patient is directed to slowly grasp an object or thread a needle,
etc., all sorts of zigzag movements are performed, and prevent the con-
summation of the desired action (insanity of muscles, folic musculaire,
muscle delirium).. In advanced cases, the arms are thrown violently to
and fro, and the patients are incapable of dressing themselves, or attend-
ing to the ordinary duties of life. It is notable that even in advanced
cases the ability to write is sometimes very little affected.

Corresponding movements are often noticeable in the lower limbs.
They may be so violent that the patient is unable to stand, and, if asso-
ciated with similar twitchings in the muscles of the trunk, he is placed
in danger of being thrown out of bed.

If the muscles of the thorax are markedly affected, considerable
dyspnoea may develop, the patients have a cyanotic appearance, and are
in aanger of suffocation.

Orimaces are observed in the face. The patients wrinkle the fore-
head involuntarily, roll the eyes, distort the cheeks, and move the tongue
restlessly, so that speech, deglutition, and mastication are interfered
with. Speech is often entirely indistinguishable. The movements of
the jaw muscles may be so violent as to break the teeth, and the tongue
and mucous membrane of the cheeks are not infrequently injured.

The laryngoscope often discloses choreic movements of the vocal
cords.

The bladder, rectum, and heart are always unaffected; it is true that
many writers speak of chorea of the heart, but the existence of this '
symptom is justly doubted.

The patients rarely experience a feeling of exhaustion, despite the
fact that the muscular contractions are kept up almost uninterruptedly.
They cease during sleep, but interfere with ttie act of falling asleep.
The patients often complain that sleep is interrupted by brief, disagreeable
dreams. The muscles also remain quiet during the artificial sleep pro-
duced by chloroform and chloral hydrate.

S80

rVKJnOHAL DISBASEa OP THS BRAJIf.

The electrical irriUbilitv ot the nerves is generally unch«Dged. bit
is said to be increased occasionally jti recent esses.

The movemente gencraUv du not begin at the gamo timo in sll t^
muHclea. They ofteu begin In ud« limb, generally un arm, tbenextti^
to the oorrestioudiug [orearni. to the Itmbs on the other side, and al» U
the face. Thvjr are sometimes confined to one limb, or to the limbt/
one side (hemi-chorca). very rarely they appear in a crossed form. Tbt
left aide of the body presents a deoidea predisposition, and eren in m-
eral chorea the movemeuts are sometimes mure intense on the left alt

The movements are often intensified by mental and bodily excitemraL
According to Watson, they diminish, and even cease during deepin^in-
tions. Tneir intensity Bometimes presents a lively contrast in the atlu;;
and reonmbent positions.

Sensory diaturbanoee are entirely absent in many cases. Ormt im-

I
i

durlug [lie period of neovarj.

portance was formerly attached to painful points on the peripheral
nerves, the spinous and transverse processes of the vertebne, eapoL-ially
of thecervical region, but this symptom is of rare occurrence. Bosen-
bach and SeiHert found painful points on the peripheral nerves io
examination with the electrical current; their electrical treatment was
followed by rapidly favorable results.

The mental condition is affected in almost all cases. There is nut
alone impairment of memory, bad temper, and irritability, but the
majority of patients manifest more serious psychical changes, especiallr
causeless laughing and cn'ing and stupid demeanor. In some, imbec)^
ity and mania develop, t^ertous psychopathic conditions are more apt to
occur in adults.

The patients often become rapidly pale andemiiciated. The Iwnit
dediable is heard over the jugulars, and accidental systoUo mnrmnrs are

heard more or lees distinctly over tlie heart valves. There ia aometimes
slight dilatation oT the right ventricle (increased cardiac dulnesa to the
outside of the right border of the sternum), and if the action of the
heart ia excited, the second pulmonary BOimd is intensified.

There is often a sort of pseudo-irregulai-ity of the pulse, because it
cannot be felt distinctly on the occurrence of choreic movements. The

fnlse curve in Fig, 123 was tnken at the height of the disease, that in
'ig. 124 after complete recovery. Dnringthe disease the curve is lower
and the arterial pressure diminished (more marked elevatioa of recoil
and diminished elevation of elasticity).

The bodily temperature remaius unchanged ; iu hemichorea there is
sometimes a slight elevation of temperature upon the affected side.

Chorea may be attended with not a few complications. There is
sometimes paiufnl swelling of the joints, which begins subsequent to the
onset of the chorea. Haddon described three casesof right hemichorea
with aphasia. Transitory paralyses have also been reported.

The combination of chorea and Basedow's disease has been repeat-
edly observed. The pupils are oft^n very wide and react slowly to light,
E. Remak noticed dilatation of the pupil on the affected side in hemi-
chorea. Stevens mentions the frequent occurrence of hyperraetropia,
but this ia denied by Bull.

SeifTert found diminution of the chlorides in the urine, de Casserea did not
yerity this obeervatioa. According to the latter, the phosphoric acid is generallj
diminished, the sulphuric acid usually unchan^l. Tait found sugar in one case,
Leube and RuebbI report albuminuria in several cases.

Under favorable circnmstances the disease lasts from four to twelve
weeks. Cases of shorter duration are rare; more frequently they last
longer. The symptoms sometimes disappear during •nte re urrent, acute
infectious diseases (measles, scarlatina, diphtheria, pneumonia), but they
may reappear after recovery from the latter. The morbid phenomena
generally subside gradually, but a sudden termination is sometimes ob-
served if the exciting cause is rapidly removed.

The disease exhibits a decided tendency to relapses. According to
See, this danger is so much greater if the disease lasts more than sixty-
nine days.

In almost all cases it runs a spontaneously favorable course. A fatal
termination is rare, and generally occurs quite suddenly after increased
intensity of the choreic movements. In rare cases the disease beoomea
chronic and lasts for life. Paralysis and atrophy have been mentioned
as aeqiielie. In a few cases the patients remain permanently insane.

in. Anatomical CsAh'OES.— The anatomical changes of chorea are
unknown. Even the site of the disease is uncertain, and the assump*
tion of certain authors that it is located in the corpus striatum or optic
thalamus is unfounded.

]

JV. DiAONoais. — Tho recognition of the disease ia easy, althongli
ireiform movements also occur as the result of irritation of the mo-

zt-^ : M- --^.^izi "^ :::^r:.Tr'=a^ n>&ryle&, hemorrhage, soft-
i.z -• - -i.--=- - --^:i.:- -=^~': :!•:«*». The latter conditioL!

■ -— n: z_- :i-.i.--- .^ Ti:7« =irhr*:is lesions of thecentnl
r - ---T.. _i .------a --ir^^ ilaj 1.3:- cwoHr Tioleiit choreifom

. -- r- :-^— • 3.?^ -."■-: T-m la^ i:r::itioii5 and disturbanoesd

=?:: w - --A iL-i-r:- li TTaC-^L-jr^jlr^c chorea the choreic

i.^ Ti-i. :»:-- ': a.\.r: =:- -.It n-'i^-r-ia apc regular and con-

ii - -r ^ *-> r-^iTTw" - :rr- r-TLT : rcL* :f an organic nerroiudii-

-i^ : r .." ■-.:"?:=■ ::!':.> ^ ir^-nr^r c-n Tolnntary movement.

■* ri •• • T^.- =• 4.-r.- < a^^i-i> ri-rn^l-f. In children it is better
-Li^z 1 i ::-■>. -"'* ri^^k.:.-: nai.Ln:!.:* ^ iz. rrfaTorable prognostic rign.

'."1 -"::.. "i :.*T —jLi^:; .a^ni ~_i^ lif iiseaae will run its conne
■L.-:. :.: .Ti.^-- . - -r*::a:zi-: : -. ?ur ji ..ir .cczi:^ the disease will termi-
^u:.- T. r»: *i . .. L.- .:.- -.--r z ■^- t-j:^ sitl* rliT of treatment:

.iisa. -^^K-:*:--:- n :ic i.%r :v Mi:'r=-i. f>r example, treatment of
-r ."T.-. :=•-:»* <js^-^ ;-:■:,'.- T-r:^ r>' T^gLS. neuromata, etc. Thu
A->. ..i..t;-- ":•: *r •:.». Ti^^inn-rz: .c'ra^zf^ joints with the galTsnie
jv:--^-:. 1: " :■: .:«..-*r:i :... t? -ici-raciiai. we mav order saliorlk
Al\:. -«. :aa*;i.Ti •.»;•:---. t.- .:- ah.::. .■•\:!i:'. •:!=.. or aconite.

Arr." ::t .taisa-. zL.'AT.:r.< za'i :»:t3 zi-K. we shonld order light,
zirrr... ;? :.•:»:. ^'.vl^ i :^'; r-jviar: - fr::! :he bowels, avoid bcwilj
AZ'i zi-.zzL izm^r.. i^ i £7-7 :^e ran-rz: ^ q^et as possible. Ereij
^-.n^zj, izi -i-^^z-zs ^T ?^' :-i r^^ i '.:iiewir=i hath (28° B,) lasting
rr-T- t:_- :~rs. izl :" .. v.-.; ": - it lesfcsc JLilf ir hour of repose. Inlw-

-^^ xzi ^' . i-'i." ... ..•••••■•••••• sa 3 ^^*

M 1 S. y ^ :-. - : : ir.-- -i:^^; :h.e daily amount to bein-
-.- L-. -. :■-..-; i:-*... Li ?. :::.. :<■- ir^rps are taken t. i. d.

^•:.". . s'-z:.:.:l.- ?<;: :. :/.-.- i.-stz_:-' rniv be ^Iven subcutaneon^&lT
r::. zzz .:" vii;.-. j-.-iMr:! :■: :-r-iidLi syringeful, oncea

■ ~~^'t ^t-t

A liTT? zimSfr :•: :c2er r«r::e»iir?s i^t^ >ws -eaplopsd. of which the following
aTT :r-»r irji'.iza* ;r:»-»; z vi-ltci :-'•'•*. "^v-'ich. ihxvniin^ to the older writers.
9t*jf2i'i alwaj's c^ r.^^r. i: :i^f '>;^*=-:i:^ .*£ :2« iiiwckw: 6. deriTatives and ether
■^p raj to ^-r ipLn-e: ?. ::erv—»*j; V' »^*»«J'-:-=i ?r:nt:ie. strychnine, curare, calabar
oraii. -rtser-ze. :ij.>«cvxii:n»-. ii*-.'. .■• L"L>:r. SLlv-r. c-nd. etc.: tf, narcotics: opium.
rr.crpciZf?. zt'lL^Ijcza, :i- :r.z:r2i» yr..:rx. zy irize. amjl nitrite; e, aniline ml-
lA..i.r-r ^. ii'.' ZT *.; in li.l : . T'li :. :. :. . .'. :rc rr^parations: jy, electricitv. pa^
ti .; .ir.v tr..r ^v-ici-: ■.•■";rr"t:: :rA2.>ver!w!y .^r ."oii-^'ielr throo^ the skull, bthen
f-^.'.rrtT-iend'nitfie ^scunfi.z^ *^lzmC .-'sirr^i::: ''.. ^zuaakic exerctaes: 1, cold-water

CUT'S*.

.3. Pr :Wi :*>;.; .:'t ; ^^ 'fi''"4":V;iV (.^Aorrti,

• to > to

Thi.1 fsrm U aprii<?<i to choreiform move axe nts which either precede or follow
A hetriipleifia pr'jiiiiceti by cerebral dLseade. ^eueralLy hemorrha^. The former is
rar*:r oji'i ii-i -izniri':an':e more serious. The «:hon?Lform movements are alwat^
urjiUt«:ral, corr*:spon'iing to the distribution ot the paralrsia. and vary greatly in
irit*fn.-jity.

In |ir%hemipl*;gir: chorea, the symptoms generally appear a few days before
th*r *}<:*:tirrHTif:h of the a[j'>ple«:tic attack. Liiid cease a^ ^vn as the paralysis makes
itt apj/^ann'Te. P'jsthMmiple:iic chorea <.i' vs ii>c begin, on the ouxer hand, until
thr; pr»'Viriij.^ty f^ralvz^l limbs have reigned a certain amount of motor power.
The affected lim^js are oftifn contracted and not infrequently anaaathetic« Even

FITNCnONAL DISEASES OP THE BB&^tN.

if special sense may take part in the hetoianajathesia. It ia probable,
. , — refore, that the lesion ia located in that part of the cerebrum at which certain
r nbres of the pyramid tract in the ioterniO capsule pass between the lenticular nn-
vleus and optic thalamus to the oocipital lobe (vide Fig. 104), At times, however,
Bimilar sjmptotnB eeem to be produced bj lesions in other parts, tor example, the
pons and spinal cord, but. at all eventB, uritntion of some portion of the pTramid
tract seems to be neoessarj.

The treatment is the same as that of the primary disease.

C. Athetosis.

The majority of authors look upon athetosis as identical with posthemipl^c
chorea, or at least aa a modiSed form of that disease. The aymptuma almost al-
ways follow an attack of hemiplegia (hemiathetosis). but in some cases ihey occur
In spinal diseases (infantile paralysis, tati^s). Bilateral athetosis has been ob-
served in epileptics, insane, and idiots. It is sometimes observed as an indepen-
dent neurosis; in rare cases itia congenital.

The characteristic symptoms appear in the lingers and toes. The fingers are
generally in slow, more rarely in rapid, almost tremulous motion, and are etjccea-
Bively Hexed, extended, abducted, abducEed. The patients are unable to repress
the movements entirely, and tliey continue during sleep. They are sometimes
inhibited by firmly grasping thi) wrist with the fingers of the other hand, or by
raising the arm erect. The thumb, index, and little fingers generally are most
alTected, and the external and InU^rnal interossei are chiefly involved. The wrist
may also be afCected, and not infrequently performs movements opposed to those
of the fingers. During sleep the movements, diminish or subside almost entirely;
thev often increase on excitement. Subluxation of the phalangeal joints and
inaltKNiition of the fingers and hands may develop after protracted duration of Che
disease. The paralyzed limbs may undergo contracture. Ihe muscles of the
affected forearm sometimes undergo hypertrophy, but they may also be un-
changed in volume or even atrophi^. EemianEestiiesiais occasionally observed.
The electrical excitability ia unchanged.

Similar symptoms niay be manifested by the toes and feet and by the muscles
of the face and back of the neck.

The prognosis is unfavorable as regards recovery, but Giowers reported one
successful case. Improvement is said to be obtained at times by descending
Bpino-moMular currents, potassium bromide, and nrsenic.

7. Slinking Palgy. Parah/sis Agitans.
{Parkinson's Disease. )

I. Etiology. — Puralyeis agitans, which is characterized by trembling
movements of the limbs, diminiahed muscular power, muscular rigidity,
slowness of mnscular contraction, peculiar position of the body, changed
facial expression, and forced movements, is not a frequent diseaae.

The causes mentioned are: colds, injury, fright and mental escite-
ment, heredity, infectious diseases, alcoholic excesses, gout, excesses in
veuery, particularly coitus in the standing position. In some oases no
canee is demonstrable.

The influence of a cold cannot be denied, because it is sometimes followed at
once by the symptoms of the disease. Among traumata, injuries of the nervea
are especially to be dreaded. 8. Martin recently described a case in which' the
diseaae followed an injury of the radial nerve. Weetphal saw a case following
simple cutaneous burn of the second degree. In not a small number of casea
the disease developed immediately after severe fright. The importance of hered-
ity has only been recognieedof late years. In some cases, the disease is con-
veyed as such to the descendants; \a others, it alternates with epilepsy, hysteria,
and allied conditions. Romberg observed a case after intermittent fever, and a
few cases have been known to follow typhoid fever and acute articular rheuma-
tism.

£H

rrvcnosAL dbkasb of ths i

Sex does not ^pear to tmsbms much inflnnioe on the freqaener 4
the iisetst. It b mon oommon at sn idruiccd age (forty to ait;
jeaisi, ^ni is rerr niv before the ag« of tvenly jvftrs.

Among fix ihoonnd cues of nerroiu du o M ca , Beyer obseired panl;*
sis aeitasi ihirtr-seTea limee (0.6 per cent).

II. Stxptoxs. — The vrmptoms Boraetiraea derelop mddenlj; ii
other CAie<, ther appear bo gndnally that we are unable to determiiK
the befinning of the diieaae. A Eodden oiuet is especially apt to ocoii
after frighL

Prodromata are sometimes experienced, such as neuralgiform paini,
parsethesis, a feeling of dalnes, rertigo, etc

The first manifest ermptom ia the tremor. Aa a rule, it first afieca
the miuclea of the fingers and hand, and later extends to the arms ud
lower limba. It begins generallT in the right arm, then the right li^
then the left arm, and fiaallr the left I^, In some rnorrr, it is confined
to one limb or is distribnted in a hemip^gic manner, or affects the im
on one side, the I^ on the other, or it may appear in paraplegic distti-

WritlDEPOsl^oooC

p*ra]T>I> aglluu. After OrdaoaUlii.

bntion. The muscles of the head and face are generally, though not
always, unaffected; in eome caaea even the maacles of the tongne take

Eart. Oscillating movements may be conveyed from the limbs to the
ead.
The trembling movements generally continue umformly during re-
pose and motion; at all events, they do not in creaae daring TolnotaiJ
movements. On the contrary, the patients are often able to inhibit
them voluntarily for a short time. They often increase in intensitj
during excitement. At first, they cease during sleep, but if the diseaw
has. ludtcd for a long time, they continue, though with diminished in-
tensity, during sleep. The majority of patients complain that the
tremor interferes with falling asleep.

At first tlio muscular eicuraious are often very slight, but they gradn*
ally increase, and often pass from mere tremor into violent shaking.
Under such circumatances, the floor, chair, and bed may be Tigorously
shaken. Writing and other delicate manipulations are interfered witn,
and tlnully rendered impossible; indeed some of the patients must be

TDNCTIONAL DISEASES OP THE BHAHT. 886

clothed and fed for years. The tremor aometimea presents remieeioiis
and eiacerbations.

Charoot has shown that in rare cases this important eymptom is absent while
all the otherB may be present. Moreover. t1ie diseaae may begin with muscular
paresis, and the tremor may not develop until a later period.

The trembling movementa are soon followod by a peculiar poaition of
tbe timb», trunk, and head as the result of paresis and rigidity of cer-
tain muscles.

^Sfi

a of tba flngara Id paralfgis atf tana. BimUar to tlut

The diminution of muscular power has been shown by the dynamo-
meter iu a number of cases. In others, the muscles retain their normal
power, but rapidly become exhausted. In the arms, the oxtenaors are
affected earliest and most markedly, while the dexors are more apt to
suffer from rigidity and spasraa. This gives rise to very peculiar
changes in the position of the fingers and hands. In many cases tbe
thumb and fingers are simply approximated, and assume the writiug
position (vide Fig. 125), This position, together with the constant
movements of the thumb and Jndox finger, produces an appearance oa
if the patient were continually rolling a ball between tbe thumb and
' iger. In other casesj the poeition of the fingers resembles that of

artfaritis deformana (vide Figs. 13G and Vil), i. e., the first phaltDjR
are flexed, the middle oaea iiyperciteiided, and the termiiuil pb&las^
flexed. The foreArni ist generally flexed on the arm, the elbow is maif I
what removed from the thorax. Id exceptional cases, the amu hof 1
down aloiigside the thorax.

The knees are aometimes approximated eo closely that thej cm
each other in walking. The uoDstant friction of the knees mar ^n
rise to erythema, ulceration, and gangrene. The feet are in pes nui^
eqninus poaitioU) and the toci< present deformities siniilar to those Botiad
in the fingera.

rorwftnk) In P"^ysls Kgituia. After CluuioiM.

Asa rule, the head ia bent over forwards, more rarely baokvsrdi.
On acconnt of the muscular rigidity, it offers resistance to paniT*
motion.

The trunk is also hent over forward, as if the patient were in con-
stant danger of tumbling head over heels (vide Fig. 138).

The affected limbs generally present no change in color or Tolame.
In rare cases they ai-e emaciated, and in one case hypertrophy of ihe
muscles has been described. In one of my cases in which tho tremor
was confined to the right npper limb, the arm was conatautlv reddened,
and was 2,5° to 3.5° C. warmer than the opposite limb. 6rasaet and
Apoliuari observed elevation of the cutaucoua temperature amouuting tx>

FUNCTIONAL DISEASES OF THE BBAIN. 287

3.2° C, while voluntary moyements of the limb in healthy persons pro-
duced a rise of temperature of only 1° to 2° C.

The electrical excitability in the affected limbs is unchanged.

Cutaneous sensibility is almost always intact. Hadden recently de-
scribed increase of all the tendon reflexes.

Painful pressure points are sometimes found on remote parts: the
skull, spine, shoulder, and perif)heral nerves.

A very important symptom is the change of facial expression. The
features become peculiarly stiff, lifeless, mask-like; the play of expres-
sion ceases, and the patient acquires a stupid expression. Speech be-
comes slow and monotonous, and is often high pitched, almost tearful.
If the muscles of the lips and tongue take part in the trembling move-
ments, speech is also interfered with mechanically. Many patients keep
the mouth open constantly, and the saliva often dribbles uninterruptedly.
Even when the mouth is kept closed, the buccal cavity often contains
very large amounts of saliva. Whether this is the result of increase of
the salivary secretion is doubtful, since it may depend upon the difficulty
in deglutition, which increases more and more in many patients.

Debove reoentiy caUed attention to peculiar disturbances of vision. To a cer-
tain extent, the patients have lost power over the movements of the eyes. In
reading, they are unable to pass quickly from the end of one line to the begin-
ning of the next, and if the reading matter consists of adjacent columns, the eve
passes from one column to the next one on the same line. The ocular muscles
do not take part in the oscillating movements.

The patients walk bent over forward, the gait is festinating, becomes

Quicker and quicker (propulsion); there is inability to stand still sud-
enly, t. e,, the patients perform a sort of forced movement, and often
fall to the ground, if not assisted. It is also very difficult for the pa-
tient to turn around suddenly. Some patients, if their garments are
pulled backwards, begin to walk backwards, the movements become
more and more rapid, and finally they fall (retropulsion).

The causes of these forced movements are unknown. They have been attrib-
uted to the changed position of the body and the consequent dislocation of the
centre of gravity of the body, so that the patients are forced, so to speak, to run
after their centre of gravity. This explanation is unsatisfactory.

The temperature and pulse are unchanged, but many patients experi-
ence a subjective sensation of increased heat.

The sensorium is often undisturbed during the entire course of the
disease. But many patients complain of an annoying feeling of restless-
ness, and in some cases apathy, imbecility, and well-marked forms of
insanity appear towards the end of life.

The bladder and rectum are unaffected, except that incontinence of
urine and fsBces may occur towards the end of life as the result of in-
creasing marasmus. Obstinate constipation has been noticed in a
number of coses.

The disease generally lasts many years, sometimes even more than
thirty. It exhibits a constant tendency to giow worse, and intermissions
or remissions are rare. Apoplectiform attacks (without anatomical
basis) sometimes occur as in multiple sclerosis or, in rarer cases, in loco-
motor ataxia. Death is the result of intercurrent diseases, particularly
bronchitis and pneumonia, or of increasing exhaustion. Severe bed-sores

2SS FTNCnOXAL DISEASES OF THS BBAIX.

and their sequelae are sometimea observed. Tlie tremor may sateide
completely for a few dav$ before death.

III. Anatomical Ohaxges. — Anatomical changes in paralysis igi-
tans are unknown, so that the disease must be regarded as lunctionaL

Atrophy, accumulation of pigment in the ganglion cells, and

changes have been found in the brain and spinal cord, but these appearmooes an
the result of senile processes. Even small patches of sclerosis in old peopk IR
devoid of significance. The older writers often mistook paralysis afittns fdi
multiple sclerosis. Luys claims recently to have disco verea h ypertr ophy of tk
ganglion cells in the pons Varolii, and explains the disease as a *' hype i secrcfa
of motor impulse " (!),

The disease is located by some in the corpora quadrigeminav by othen in tk
pons and medulla oblongata. R. Remak distinguishes a cerebral and tpinal
form; the disturbances in walking are said to be characteristic of the former.

IV. Diaoxosis. — The diagnosis is easy if we take into considentioi
the entire complex of svmptoms. It is distinguished from simple trenw
by the facts tiiat in the latter the oscillating movements are slighter, thit
other symptoms are absent, and that, in mercurial, lead, and alcohoKe
tremor/ evident injurious factors are demonstrable. It cannot be mis-
taken for multiple sclerosis if we remember that in the latter tremor
occurs only on voluntary motion, nystagmus is present, and the symp-
toms almost always begin in the lower limbs. In chorea, the movements
are irregular, cease at times, become greater during voluntary moT^
ments, and the excursions are larger but slower.

V. Prognosis. — It is impossible to check the constant advance of
the disease. Life is not put in immediate danger by the disease, and
many patients live for years after its inception.

VI. Treatment.— Treatment must be confined, in general, to con-
stitutional measures. Trial may be made of Fowler's solution (one part
to two of water, one-quarter to one-half syringeful subcutaneoosly), bat
this has produced very little effect in our cases.

Various authors have recommended narcotics, nervines, iron, baths, cold-
water cures, electricity ^fj^enerally the jz^alvanic current to the head, cerrical
cord, cervical sympathetic or limbe, according to circumstances), and nerve
stretching.

8. Tremor.

I. Symptoms. — Tremor is manifested by brief, rapidly following
oscillatory muscular movements, which are independent of the will or
volitional movement. In some cases, it is confined to individual mus-
cles or groups of muscles; in others, it affects a whole limb, or is dis-
tributed in an hemiplegic or paraplegic fashion, or extends to almost
the entire muscular svstem.

The muscles of the fingers and hands are affected most frequently,
sometimes more markedlvon the right side. In other cases, the mus-
cles of the head and neclc are chiefly affected, so that the head is con-
stantly wagging to and fro. In the face, the muscles supplied by the
facial nerve are most apt to be affected, sometimes the muscles of the
tongue, so that articulation is interfered with, rarely the ocular muscles
(nystagmus). It there is violent tremor of the lower linibs> the knees
may bo rubbed so vigorously against one another as to give rise to in-
flammations of the skm, excoriations, and even pngrene.

The tremor often subsides if the tremulous hmbs are efficiently sup-

FTTNCTIONAL DISEASES OF THE BRAIN. 289

ported, and it also ceases during sleep. It may be repressed temporarily
by an effort of the will by many, though not by all patients. It is in-
creased, in some cases, on attempting to execute a movement.

Tremor does not give rise to any danger, but is attended with manj
annoyances, and interferes with various occupations. The condition is
usually very obstinate.

II. Etiology. — The causes of tremor are manifold. It may be the
result of mental excitement, such as anger, ioy, sorrow, or fright. In
other cases, it follows bodily strain, such as lifting heavv loads, standing
on the tips of the toes, efcc. It is sometimes the result of toxic influ-
ences, such as excessive use of coffee, tea, tobacco, working in lead or
mercury, alcoholic excesses, chronic opium eating. Closely related to,
often perhaps identical with the toxic forms of tremor, is that form
which follows conditions of exhaustion (nervous and neurasthenic indi-
viduals, vital losses, onanism, prolonged lactation, convalescence from
tserious diseases, etc.). According to Charcot, tremor is a constant
symptom of Basedow^s disease. A well-known form is senile tremor.
The symptom may also be produced by thermal influences and by
injury.

The genesis of tremor evidently varies according to the causation. In some
cases, it depends, as was shown by FrensberK's experiments, upon changes in the
circulatory apparatus, such as are produced by psychical and tnermal influences.
In other cases, it is a phenomenon of exhaustion, in still others of disturbances
of co-ordination between certain groups of muscles and their antagonists. The
finer processe9in the nervous system upon which tremor depends are unknown.

III. Treatmekt. — As a matter of course, the first desideratum is to
remove the cause. In the next place, benefit may be expected in many
cases from the application of electricity; if the causes are central, gal-
vanization of the Drain or cord, otherwise galvanization of the peripheral
nerves and faradization of individual muscles. Good results nave been
obtained from gymnastic exercises, or the application of orthoptedic ap-
paratus.

In conditions of weakness, we may order iron, quinine, nourishing
diet, cold-water cures, a trip to the country; in nervousness and neuras-
thenia, valerian, strychnine, veratrine, potassium bromide, and other
nervines.

Eulenberg regards Fowler's solution as, in a certain sense, specific,
and Oulmont obtained good effects from hyoscyamine (gr. ^V ^^ i daily).
Gn6neau de Mussy succeeded in curing mercurial tremor very rapidly
with zinc phosphide (gr. -^ t. i. d. in pul form).

9. Dizziness. Vertigo,

1. Dizziness is the term applied to an interference with the con-
sciousness of the eauilibrium of the bodv in space. The sensation of
dizziness has been located in the cerebellum, but this is not strictly
proven. The retention of the equilibrium of the body is influenced to a
great extent by various sensory impressions, so that, when che latter are
disturbed, dizziness often makes its appearance.

2. Dizziness is a symptom of various conditions. In rare cases, it is^
to a certain extent, an independent condition, such as oconrs in old age^
probably as the result of vascular changes in the brain. Perhaps such

2*>» 7rrSCn\^S\L DEEA^ES OF THE BR\rX.

:ii:i:i:r*s ^."'^ r.i*? :•> "►^rri:;') :a :Iie niainrlrv of (:ades. The .svinpior. ii
rur ■ ".u -iii^iLliuiMi.

1: a t'-.'ii ::ii* r^^au!: jl iacnwranial ciian^re.-?. such as meiiin;jiii£,
!i'-'Lr')i'L»pi::u:ii. r::ii' rs. •?a<t?i.uiaiorr:i:i;j:i:i. encephaiitLs. hyperaemia.
aiKem.a." "?:j. TIil* tv-u^^T'iu la ^pc :•» "ji* •-'aueouiiiv- severe if the lesion a
■;i::m: '•: in ":ie ^I'arer.i-r :"*5a ':»':ir r.ie ■;er:fbeLium.

I: -.i if:o!i ::iv.* r»?snl: oc r^dct -•aii.-res. suoh as gustric affections (ver-
ri:!') 1 :«r.^iii;h':i«> !iP><^ . .'oiM-jsra^is. f-n-'iiTTi bodies, worms, or digital ei-
Lini-na::-ia -t :.ie mis. I: s*)nier::iiHS follows the ing'estioa of certaia
:irti'\os t^c : '•^«i. Erie:imov.*r r*.Mj«)r'ol j. •.•use wliiijli was eu"^?d by t tie
reiief •?£* .la m:^-:!!.-!! ^rr:L'rur»e. S)Lrinann observeti ic ia a boy as the re-
3ui.c of r'Toa'i'Mi ■ r -.il* :i?<r:-.»ie a. :'.ie injniniil oaaaL Vertigo is abo
i^bjserv'.vi in lii^a:"*: i>.»uses. mz riiis is 0^)01401^ the result of anaemia or
hvTjer-enuLi of :iie 'jnua.. L liar-'oc 'iesoribeii vertiir»> following: Jise:i3e of
:iie iarvai.

Dizziness mav be A!»4)i.'iato*i w.:!! iiseases of the organs of special
^enst*. I: ".s x v_»ry ot'mruoa sympc.rii :n p^irdlysisof the ocular muscles,
anii :s e«:"M.-;* :T^;nea: ::i v:ir:oi;c? >i. senses of the ear (foreitm b«)«Hes in
::ie e:^:** lal a.i-iiicrv ait.'-.i::;-. ii'«";ni:!:i:iori of wax. inflammations of
all kin-Ls'. *^«=iue :n.:i''-.«:.ials ^ii."f'r ir'-m violent vertigo when air is
blown ir.:o :he E.istaoii.an :n"v. D'iseases of the labyrinth, particulark
the semj-irr-'ii ar Mzials. arv acoomyanietl by very intense attacks of ver-
tigo J Men.:er*>*s 'i.^ease .

" V^r'iZ''' 'ia s*-cier:nit?s ass«:i.':are«i wirli jrenertl ansmia or plethora. It
may al.?*) be tii'f r'*s;;L: : :ov.»j indieii-'es (al 1:0 hoi. opium, nicotine.
erii^^r. e*.:. v »."".''s<f".y ali.-.L ■? :i:a: : ■mi wni-^h is ■ r.e result of an infee-
:[.•:: tc vt.ini-.U'^. S "v. r-.- :« ■;' ••: "-v^ ^'asos u* intermittent vertigo
wl:: -1 T-r-.- .••. ■'-♦: ':/ :.:■■■ i»i:L:.:::i:7'i:L. :i ■ f 'raiiiine.

Vrr.j) :::.i ■ .iL-' ;«.» ;:-:: *«L ::■■.• t.I'* a :^:>L::a: ion of electrical cur-
re".:.^ "•> :..} *\ : i: ::: tu.i . " :: 1. ■r'ar-? ?v«n w::en the electrical current
ii i.--'.i:f«i ir a i.-Mii •■ :r •: rli-j siv'.:!.. :■.': exacii'le, in the neck.

I" Li *. : ::::". -ft. •:.::-;.- :/. r-.-?;:!: ■■:' in:;\iiroil ahilitv of do terminini:
or.'-*'! y- '•.::■: :".: ?::;h;»:. T": ;.'?. jiizi-.j: at a dowin^" stream, turning
a:- ::r.i .n a :'j".-. -vi-^j:';-.:. jo:!:::^. oiinibing high mountains and
t«j'ver=, '■'. .. ni.f." rr-'ii ::»:» v-irriji^.

W-r'.j . r.i.i." .ils*> ■'» :i:L'as:::ir«l '^y a :':?yo:iopathy, for example, in
" f:-ar •■: ; .a- -.

3. Di.:\:.:.:-.r r^ay vxi?: al-:-.:'- r mav *>».» fj'i!-^we*l by other funcrional
vliiturba:: ■«;- '.t t'.ic •■;ai:.: v-.::: ;:■::::. .L;'?t:.:r::-a::oes of special serijie. loss fif
0'i:-..T.;iy;<.:>i. ST-asn:-. -:.:. r.::- :iia:-.'»ri:v ...f oatieurs are dizzv ilurins
t:ie 'lay. T-ari-^iiariv i:: :':e ■-':•■": i'«vs:"io:i: more rarely the seni^ati-.'n
O'.ivirs o::iy «!;ri:.j:-ir-:'an:? :.■;■'■•■.-'■.. li v-rij-^ . or is increased in thehori-
Ziv.'al p*»-i*i-r.. >"ri>::::n-^ :...' r;r: ::" i'.i'nsr/.: appears t«^ rev.»lve.
aorn-v^im-T .-:irro'i:"."ii::i: •■■■:-:-'*s a- ■ ».ar r-^ r'-v ''.vo ar-.nirul the i»atio!it.
T'u*i movv-m-iit may st-'i-ni :.» i't.- r-:.i:.w. ■•..•■i-iz.vitLil or vertical. In son^e
in livi'lual.-i riie 'lizzir. »=•■•."= .^•i?-;r-j "r.ly in tiie m'»rninL: when the stomach
\A »*mprv, wiii.M in .itliers r iiuf'/a.-i^-^ after meals. The >vmptom is very
annoying, makes the patient anxious, aiil interferes witii freeilom of
action.

4. In making a diagnosis, the «.-ause should always be sought for,
since upon this depend the prognosis and treatment.

FtTNOnOSAL MBEABES OF TnE BKAtS.

less complete loaa ot con-
atain any position wtiich
another position, iii whica

10. Catalepsy.

. Catalepay is oliaraotariBed by attacks o( more
Qsness, during which the limbs permnnentl)' n
__Uj l>e iissuoied, but may be passively brought int
ihey will theu remain.

Ttie symptoms sometimes develop suddenly, but a
prodromata: changed mood, feeling of proasiire in the
of the heart, yawning, eructations, etc.

When the attack occurs, the patient remains as if petrified in the position ut
which he happened to be at the time. The eyes are nxed. the features are un-
changed; if tliearm has been raised, it remains in that position, etc. The patient
is unable to cliange his position, when asked, even it he understands the request.
The muacles appear tense, but passive movements may be performed with very
little force, and the limbs may thus l>e brought into the strangest positions. Tlte
readiness with which the limba may be brought into any position desired, and llie

Bsrsistency with which they remain in such positions, are known ae waxy flexi-
ilttv of the muscles.

This condition generally extendi over the entire muscular system, sometimes
it begins in one limb, and then spreadj to the rest of the body. Rosenthal found
increase of the direct and indirect electrical excitability of the muscles during the
attacks. Benedikt, on the other hand, observed increase of indirect galvanic ex-
citability, diminution of direct and indirect faradio excitability. Ouimus states
that muscular contractions are produced more readily by the direct than by
the indirect application of galvanism. '

The involuntary movements remain unchanged- While the patients are often
unable to swallow voluntarily, deglutition is unobstructed it the bolus is placed
behind the root of the tongud. Reapiratiou and the action of the heart are un-
changed or. at tlie most, slowed.

Consciousness may be entirely abolished, or only more or less impaired. In
the former event, the patients remain ignorant ot what happened during the
attack. They keep the eyes closed, and awake — often with a loua sigh— at the end
of the attack as if from a deep sleep.

In some cases, reflex excitability is entirely abolished, the pupils are dilated,
and do not react to light. In milder cases, rejlex movements may be produced,
but the patients ott«n state that they did not feel the cutaneous irritants.

The skin is sometimes very pale and its temperature very low, but the move,
ments of the heart remain audible, thus distinguishing the condition from

An attack may last from a few minutes to hours and even days. In some
cases, only a single attack develops; in others, they recur for months and years.

If the condition is protracted, there is danger of inanition, so that the admin-
istration of nourishment through the cesophageal sound becomes necessary,

3, Catalepsy is one of the rarer diseases. In some cases, it is a complication
of other neuroses, such as hysteria, chorea, melancholia, and various other forms
of insanity. It haaalso beeuobeervedinmeningitis, encephalitis, and encephalo-
malacia, It is sometimes the result of great mental excitement, particularly
fright, and of religious sentimentality. Some patients mention injury as a cause,
for example, a slap in the face. It has been observed in typhoid and intermit-
tent fever — in the latter affection as periodical attacks. Cataleptic attacks may
also occur under the inlluonce ot chloroform or ether.

All of my patients were in a condition of profound uneemia. The disease oo-
cura even In childhood, and is most frequent during the period of pulrarty: in
women it is sometimes observed at the tieginning of pregnancy.

3. Tliediagnosis iseasy: the prognosis depends on the primary affection. The
treatment must badlrected chiefly sitainst the general condition of the patienti
since very little, except the applicalion of cutaneous irritants, can be done to re-
lieve the individual ailack.

4. The pathogenesis is entirely unknown.

11. Hysteria.

Etioloot. — Hysteria is tho torm appllod to a central nearosis in
ih tho bruin, cord, and Bym|mthetic may take piirt, and which ia char-

9«3

TVSCmOSAL DIBBABSB OF THE BHAIff.

iicterized chiefly b^ increased excitability of these parU. Conditions of
intensified or dimmisiied function alternate or eoexist in manifold nerre
tracts.

Tlie disease occurs almost exclusively in women, and is rare in men.

The symptoms generally become prominent at the period of paberty
(fifteenth to twenty-fifth vear), but in the mujority of cases distinct
prodromata are noticeable during childhood. Indtcd, in my experience,
we II -developed hysteria is not at all nncoramon in children.

Like almost all neuroses, hysteria is an exquisitely hereditary disease,
which ia either transmitted directly or alternates with epilepsy, insanity,
and allied conditions. The hereifltary influence of the mother is espe-
cially marked; but fathers who are themselves free from nervonsness, bat
who come of a neurotic family, may convey hysteria to their female oS-
Bpring.

In some cases, hysteria is not hereditary, but the result of a congeni-
tal predisposition. Thus it is said that hysteria is especially apt to de-
velop in those children whose parents married late m life, or suffered
from phthisis, or were weak and feeble at the time of concejition.

There may also be an acquired predisposition to hysteria. This is
observed in individuals who, since childhood, have been improperly edu-
cated, mentally and physically. We refer to improper diet, insufficient
exercise, exciting and obscene stories and books, stimulation of false
pride, want of intercourse with other childrpn, too early entrance into
society, etc.

The tendency to hysteria may also be acquired by adults. Thia may
develop after severe and protracted diseases, for example, typhoid fever,
phthisis, excessive lactation, losses of blood, chlorosis.

Mental excitement, resulting from worry, care, disappointed hopes,
exercises a great influence on the development of hysteria,

A remarkably large number of cases are reflex in their origin, the re-
sult of diseases of the peripheral organs. Some writers believe that this
form constitutes almost the only form of the disease. The peripheral
irritation often starts from diseases of the female sexual apparatus, es-
pecially the uterus. I have seen a number of cases in individuals suf-
fering "from floating kidney. This is also true of gastric affections, par-
ticularly painful cicatrices or round ulcers and other chronic organic
diseases.

Certain diseases of the female aeatual organs are particularly apt to be aasoci-
at«d with hjBteria. Among Ihe diseaaes of the uterus may be mentioned liei-
iuiiB, veraitiiiB, and ulceratiooa, while tumors rarely gLve rise to hysterical BTtnp-
to[u£. Uysteria is bIso rare in liirge cystoid degeneratiouB of the ovnriee, but is
much more frequent in dermoid cysts, and acute and chronic iuflammatory con-
ditions of the ovatiee.

Hysteria is not infrequently a disease of married life. Women become hys-

_, ■.. .!__:_ v.__i. — J ^ impotent, it the marria^ is unhappy, if they remain

-'- Sexual comiDeace is also said to act as a

terical if their husbands ai

Imitation plays an important part in some cases. In repeated in-
stances, the disease has developed in a previously healthy individual as
the result of witnessing an hysterical attack. This explains the epidemic
and endemic occurrence of hysteria in schools, convents, etc.

In the majority of cases, several causes combine to give rise to the

FUNCrriONAL DISEASES OP THE BRAIN. 293

II. Anatomical Chanoes. — Death rarely occurs immediately after an hys-
terical attack, BO that few autopsies have been obtained. No lesions have been
discovered hitherto, so that the disease must be regarded as the result of molec-
ular chanf^es.

III. Symptoms. — The symptoms rarely begin suddenly; they gener-
ally begin with slight manifestations, and gradually grow more and
more intense. Motor, sensory, vaso-motor, trophic, secretory, and
psychical disturbances make their appearance, ana often alternate with
one another, or local diseases of individual organs are produced. On
account of the Protean character of the clinical history, we must confine
ourselves to an enumeration of the individual possible symptoms.

Among the motor disturbances, paralyses are remarkably frequent.
They are confined to individual groups of muscles, or appear as mono-
plegia, paraplegia, or hemiplegia. Cfrossed paralysis or paralysis of all
the limbs is rarer. Hystencal hemiplegia is associated not infrequently
with hemianaesthesia of the paralyzed side — a fact which should at once
arouse the suspicion of hysteria, especially if the face and tongue are not
paralyzed. The hysterical origin of the paralysis is often evident from
the fact that the paralysis varies very greatly within a short period.
The paralysis sometimes disappears as suddenly as if blown away, and
then again it may reappear as unexpectedly. Violent mental excitement
or hystero-epileptic seizures sometimes give rise to paralysis, sometimes
they cause its disappearance. Nothing definite can be predicted con-
cerning the duration of tlie paralysis. It may last a day, sometimes it
continues for months, years, even for a lifetime.

Paralyses of individual groups of muscles and monoplegias are more
frequent in the upper than in the lower limbs, while paraplegia is more
frequent in the latter. Hemiplegias are more common on the left side.

£jven after the paralysis has lasted for a long time, it is not followed
by atrophy or changes in electrical excitability. At the most, there is
slight atrophy from disuse and trifling diminution of electrical excita-
bility.

The facial and hypoglossal nerves possess a certain degree of immu-
nity. Hysterical paralyses of the ocular muscles are also rare; ptosis is
relatively frequent.

If the muscular tissue of the pharynx and oesophagus is paralyzed,
disturbances of deglutition are produced which may give rise to danger
of inanition, unless nourishment is introduced through the oesophageal
soand. The unobstructed introduction of the sound is evidence that we
have to deal with a paralytic condition.

Not infrequently there is paralysis of some of the laryngeal muscles,

Generally the internal thyro-arytaenoid and posterior crico-arytaenoid.
^he patients are hoarse and aphonic, and, in paralysis of the last-men-
tioned muscles, suffer from inspiratory dyspnoea, which may reach a
dangerous height, and render tracheotomy necessary. Hysterical
paralyses of the laryngeal muscles often enable us to observe the effects
of unusual stimuli and of moral suasion on hysterical phenomena.
Patients who are ignorant of the action of the faradic current may be
cured at once upon touching them with the electrode, and the laryngo-
scope may also show that the paralysis has disappeared. In the majority
of cases, such results are not permanent.

Muscular contractures also are often observed in hysteria. They may
develop gradually or suddenly, may or may not be preceded by paralysis,
may be of short duration, or last for years. They are most frequently

294 FUNcno:!9AL diseases of the bbaxet.

the results of mental excitement and hystero-epileptic attacks, more
rarely of injury, or appear to develop spontaneously. By means of cer
tain manipulations, Cnarcot was able to produce contractarcs at will in
hypnotized hysterical individuals. Contractures in the arms are usnaUj
in the flexed position, those in the lower limbs in extension or hyper-
extension. They grow less intense, but do not disappear during sleep;
they may subside entirely during chloroform narcosis. If contracture
has lasted for a long time, the affected muscles undergo atrophy. Joint
deformities may also be produced as the result of pressure, so that the
use of the limb may be impaired even after relief of the contractnre.
Charcot believes that the contracture may provoke sclerotic changes in
the lateral columns of the cord, and that this explains the exaggeration
of the tendon reflexes which is sometimes observed. Great mental ex-
citement and unusual impressions of all kinds may cause rapid disap-
pearance of the contracture, but relapses are the rule rather than the
exception.

Many hysterical patients present obstinate tremor, but it is often
difficult to decide whether this is the effect of hysteria or of co-existing
anaemia and weakness.

Tonic and clonic muscular spasms form an important symptom.
They may appear as tic convulsif or as paroxysmal twitchings in indi-
vidual groups of muscles in tho limbs. Almost all of the muscles of the
body sometimes take part in the spasm, but consciousness is often
retained. Cases also occur with a distinct epileptic character (hystero-
epilepsy). The patients often experience a sort of aura, a sensation of
something rising in the abdomen, oesophageal spasm, pallor, occasionally
hallucinations, and delirium.

Charcot divides hystero-epileptic attacks into distinct periods. They begin
with epileptiform symptonis Then follow peculiar distortions and changes of*
position in the trunk and limbs (clownism), marked opisthotonos, liftinj^ of some
of the limbs, statuesque poses, etc. Then follows the stage of passionate attitudes,
in which the features express fright, joy, or lust; the patients often make use of
cynical and erotic expressions. In si>me cases, the attack ceases abruptly; in oth-
ers, it gradually subsides. The patients know nothing of what has happened.
They often fall into a profound sleep lasting several hours, from which they
awaken greatly refreshed.

These hysterical convulsions may occur spontaneously or are pro-
voked by mental emotions. Imitation also plays an important part in
this i)articular. In many patients, convulsions may be j) reduced by
pressure on certain hyperaBsthetic points in different parts of the body.
According to Charcot, they are especially apt to occur after pressure on
the ovarian region, particularly on the left side. In other cases, pressure
on such points diminishes the severity of the attack or inhibits it alto-
gether.

The attacks sometimes return in such rapid succession as to give rise
to a sort of status hystero-epilepticus. Under such circumstances,
Wunderlich observed increase of the temperature of the body to 43° C,
and death.

Ilystero-epilepsy is closely allied to the laughing, crying, and shout-
ing spasms, from which tliese patients suffer not infrequently. Cata-
lei)sv may also occur in hysterical individuals.

►Sensory disturbances are as common as motor symptoms, and may or
may not be associated with the latter. Anaesthesia, parsesthesia, and hy-

FUNCTIONAL DI8EA8B8 OF THE BRAIN. 295

persesthesia alternate with one another or are present at the same time.
Hensory disturbances are probably the result of hysteria, if they vary con-
siderably within a short period and if their distribution does not follow
definite neiTe tracts.

Profound anaesthesia is most fre<][uent on the soles of the feet and
palms of the hand. In other cases, it inyolves a certain nerve, a limb,
one-half or the entire body. Hysterical hemiansBsthesia is often associ-
ated with hemiplegia; this is supposed to be occasioned by a functional
disturbance of the posterior part of the internal capsule (Fig. 104,
Sens,),

All the modes of sensation or only individual ones maybe diminished
or abolished. In hemiansBsthesia, there is not infrequently complete
anaesthesia, which involves the skin, fasciae, joints, muscles, and organs
of special sense. The mucous membranes may also be anaesthetic.

The anaesthetic parts are often pale and cold, and discharge an ex-
tremely small amount of blood when pricked with a pin (complication
with vaso-motor disturbances).

Amon^ the symptoms of hyperaesthesia, neuralgias are especially fre-
<iuent and distressing. They affect the trigeminal or occipital nerves, the
intercostal or lumbar nerves, or they appear as mastodynia and coccvgo-
djnia. Their location sometimes changes in a comparatively short
time.

Many hysterical individuals complain of headache, which may be
diffuse or unilateral. In two of my cases, the headache was followed by
pronounced aphasia, which disappeared in a few hours. Complaint is
often made of a boring pain hiffh up on the vertex (clavus hystericus),
others experience a sensation oi the application of a cold body (ovum
hystericum). Symptoms of spinal irritation are not uncommon.

Special attention is merited by the painful or hysterical pressure

Eoints. They are found upon the skull, spine, ribs, certain parts of the
mbs, or other localities. French authors emphasize the frequency of
ovarian tenderness (situated immediately above Poupart^s ligament).
Left ovarian tenderness (ovarialgia) is especially frequent. It is said
that this tenderness is found on that side of the body on which other
unilateral hysterical svmptoms are found, and that pressure upon the
ovary will produce such symptoms or cause them to disappear. German
writers do not admit the frequency of ovarialgia, and in many cases it is
doubtful whether it is the result of an affection of the ovary, since-pain-
ful points are found not infrequently upon the abdominal walls, and
mav give rise to error. Such painful points are sometimes very extensive,
and may arouse the suspicion of peritonitis.

Articular neuroses may also be noticed (vide page 62). In many
patients, increased irritability of the smooth muscular fibres of the skin
IS shown by the almost constant goose skin (cutis anserina hysterica).

The patients often complain of paraesthesiae: a feeling of cold or
heat, pnckling, etc. These symptoms sometimes occur in attacks of
short duration, in other cases they continue for a long time. They may
or may not be associated with vaso-motor changes (pallor of the skin,
lower cutaneous temperature, diminished turgor of the skin). Among the
vaso-motor and secretory changes may be mentioned cutaneous hemor-
rhages and sweats (local, unilateral), etc.

Ocular symptoms are often noticeable in hysteria. Ptosis and other
forms of ocular paralyses have been previously mentioned. Galezowsky
lias observed hysterical contracture of the ocular muscles with secondary

296 FUNCTIONAL DISEASES OF THE BRAIN.

diplopia. Foerster applied the term copiopia hysterica to a not infre-
quent CToup of symptoms, produced by hyperadsthesia of the optic nene
and orbital branch of the n£th nerve, Tne patients complain of paim
around the globe, which often cease at night, and reappear in the da?;
they are increased by reading, sewing, and straining the eyes. As i
rule, no change in the eye is noticeable on inspection, except that in ex-
ceptional cases the pupil is destitute of reaction; visual power is gener-
ally unimpaired.

Many patients complain of unusual sensitiveness of the retina, and
are distressed to an unusual degree by bright light, especially by red.

Amblyopia and amaurosis are sometimes observed, either on^one or
both sides; in the former event, hemiansesthesia is often present. This
is associated with diminution of the field of vision and distorbances of
the color sense. According to Galezowsky, hemianopsia also occurs, bnt
Leber does not consider his cases convincing. Ophthalmoscopic appear-
ances are generally negative, but it is said tnat hysteria sometimes gires
rise to inflammation and atrophy of the optic nerve.

Many patients complain oi spots before the eyes, flashes of light, etc
During hysterical attacks, there may be visual hallucination** in which
rats, snakes, and small animals play an important part.

Some patients enjoy unusual powers of hearing. They hear sounds
which are inaudible to healthy individuals, or are annoy^ to an anosnal
extent by ordinary sounds. In other cases, there is partial or complete
loss of hearing on one or both sides — the former generally in hemianses-
thesia. Under such circumstances, there is abolition of sensibility in the
external auditory canal, upon the membrana tympani, and the mucoos
membrane of the tympanic cavity. Some patients complain of subjec-
tive auditory sensations, and hallucinations of hearing may occur in
hysterical seizures.

Smell and taste may suffer in a similar manner. The patients de-
tect by their odor objects wliich are unrecognizable by healthy per-
sons. Or they are excited to such a degree by certain odors, especially
of flowers, as to give rise to hysterical attacks. These patients often
manifest a penchant for disagreeable odors, such as that of asafoetida,
burnt feathers, etc. There may also be diminution or abolition of olfac-
tion on one or both sides, the former particularly in hemiansBsthesia;
this may be associated with anaesthesia of the nasal mucous membrane.
Sneezing spasms are observed occasionally.

Similar symptoms are noticed on the part of the organ of taste. The
patients are often capable of tasting the minutest trace of this or that
substance; they acquire an unconquerable antipathy to certain articles, a
predilection for others (sometimes for ill-tasting substances^. They
sometimes have a craving for indigestible articles, such as ink, chalk,
lead pencils, etc. (pica hysterica).

Among the disturbances of individual organs, those of the di^stive
apparatus are probably the most frequent. These often begin m the
buccal cavity. We have previously mentioned that disturbances of
deglutition may result from hysterical paralysis of the muscles of the
palate and cBSophagus. These disturbances become more marked if the
tongue is paretic or paralyzed. This also interferes with articulation.

in some cases, profuse salivation occurs, either during an hysterical
attack or independently. In other cases, there is an abnormal diminu-
tion of the salivary secretion. The patients then complain of dryness

FUNCTIONAL DISEASES OF THE BBAXN. 297

and pain in the mouth; fissares form not infreqaently^ particularly on
the tongue, and the mucous membrane of the mouth is unusually red.

Globus hystericus is an almost pathognomonic sign of hysteria, and
is attributed to ascending peristaltic spasms of the muscular coat of the
cesophagus. The patients experience a sensation as if a round body were
ascending from the stomach along the oesophagus. The starting-point
of the globus is sometimes referred lower, in the pelvic region. The
symptom may develop spontaneously, or is produced by mental excite-
ment, or it is a precursor of an hysterical seizure. It may be produced
at times by compression of hysterical pressure points.

Spasms of deglutition sometimes occur on attempting to oat or at
the mere sight of food (hydrophobia hysterica).

Eructations are observed not infrequently. They occur spontane-
ously and last for days, even weeks, op they are produced by irritation
of hysterical pressure points.

There is often a great accumulation of gas in the stomach and intes-
tines. The oririn of the large amounts of gas is attributed by some
writers to exhalations from tne vessels of the mucous membrane or to
rapid decomposition of the gastro-intestinal contents. In our opinion, it
is the result of the swallowing of air, which, on account of temporary
incontinence of the pylorus as the result of disturbances of innervation,
passes rapidly into the intestines. The application of faradism, and
methodical massage of the abdomen, will generally expel the gas through
the mouth and anus, almost as rapidly as it has accumulated.

Some patients suffer from obstinate vomiting. Soon after ingestion,
the food IS rejected almost unchanged, and hardlv anything may be re-
tained. It is often surprising how well this is tolerated by the patient.

HsBmatemesis sometimes occurs, and even very large amounts of blood
may be vomited. This is evidently the result of vaso-motor disturb-
ances of the gastric mucous membrane. In some cases, the blood is dis-
charged through the rectum.

Tnese symptoms often arouse the suspicion of gastric ulcer, and the
diagnosis is not always easy. The differential diagnosis is rendered espe-
cially difficult by the presence of gastric pain, which in other cases is the
sole hysterical rastric symptom. The intensity of the gastralgia is some-
times so great that the patients writhe in pain. There are also epigastric
pains which are located in the abdominal walls, and are recognized by
their superficial position.

Many patients also present vigorous epigastric pulsations, which aro
the result of local vaso-motor changes in the abdominal aorta.

The liver and spleen may bo tender in places, and occasionally
swollen.

In one of my cases, hysterical attacks could always be produced by pressure on
the spleen; in another patient, paroxysmal attacks of hepatic pain had led to the
diagnosis of gall-stones.

Intestinal pain is a more frequent symptom, and is either the result of
intestinal distention with gas, or of spasm of the intestinal walls.
Borbor^gmus is also a frequent symptom in hysteria. Digestion is dis-
turbed in many patients; constipation is generally present. Hysterical
seizures may be loUowed by watery diarrhoea — the result of vaso-motor
and secretory disturbances.

Among the hysterical changes in the respiratory apparatus, we have

298 FITNCTIOXAL DISEASES OF THE BBAIX.

already mentioned paralysis of the vocal cords and its sequels. Spasm
of the vocal cords may also occur.

In some patients, there is marked ansBsthesia^ in others hypa-
aesthesia of tne laryngeal mucous membrane. This is generally as-
sociated with a similar condition of the pharyngeal mncoas membrane.
In the former event, the patient tolerates very well the introduction of
the laryngoscope and the contact of the sound with the inside of the
larynx. Laryngeal hyperaesthesia is accompanied by f reqaent coughing.
True asthmatic attacKS are sometimes produced pj hysteria. Panlysi
of the diaphragm, generally of one-half, is observed occasionally, and
this may put the patient in danger of suffocation. Spasms of the dia-
phragm are more irequent and, if clonic in character, are manifested bj
hiccough. Hysterical singultus sometimes continues for days and weeks.
Carr6 nas called attention to the occurrence of hysterical pulmonarf
hemorrhage; it must probably be explained as the result of vaso-motor
disturbances.

According to Empereur, less oxygen is consumed by hysterical indiTidQak;
furthermore, oxygen is 8t;ored up in the system, because the patients do not ex-
hale as much oxygen in the expired carbonic acid as is inhaled with each inspizi-
tion. Counard mentions paroxysmal painful swelling of the breast, which is not
alone tense, but may also oe red and unusually warm; it contains small nodoki
The swelling sometimes occurs during hysterical seizures or with the menses.

The circulatory apparatus presents central and peripheral distnrbancM
of innervation. Attacks of palpitation or cardialgia are not infrequent;
even Basedow's disease has been attributed to Tiysteria. The pulse is
extremely variable as regards strength and fulness within a short period,
and, since the heart's action may be unchanged, it is reasonable to as-
sume that this is the result of peripheral changes in the arteries. There
is sometimes temporary inequality of the pulse in corresponding arteries
on the two sides of the body.

The urine sometimes presents striking changes. The patients maj
suddenly void larjje amounts of clear urine of low specific gravity (urina
spastica). This is especially apt to occur after an hysterical seixnre.
In rare cases, there is oliguria or even anuria hysterica. For days and
weeks, the patients pass very little or no urine. In its stead, there is
profuse watery emesis, the vomited matters containing larger or smaller
quantities of urea, although too small in amount to act as a complete sub-
stitute for the renal excretion. Hysterical polyuria and oliguria are
probably the result of secretory disturbances.

The patients often complain of vesical tenesmus, and are compelled
to micturate every few minutes. Others suffer from retention, so that
the catheter must sometimes be resorted to for weeks and months.

With regard to diseases of the sexual apparatus, we must determine
whether the changes present are the causes or the results of hysteria.
This is not always easy. For example, menstrual disturbances not in-
frequently precede the outbreak of hysteria, while in other cases they
follow it. The symptoms of hyperasstnesia are often present. Ovarialgia
has been previously mentioned. Uterine neuralgia is also observed at
times. HyperaBsthesia of the vagina is sometimes manifested by in-
tolerable pruritus vaginae or insatiable sexual desire. In some patients,
the hyperaesthesia is so great that coitus is intensely painful, and vaginis-
mus is produced. In other cases, there is anaesthesia of the vaginal
mucous membrane, and no voluptuous sensations are produced daring

FITNCrnONAL DISEASES OF THE BBAIN. 299

coitus. Some hysterical patients complain of watery secretions from
the genitalia, evidently as a result of vaso-motor and secretory disturb-
ances. The course of hysteria varies greatly when conception occurs in
hysterical individuals. In some, the symptoms disappear at once, and
may even remain absent for a long time after delivery. In others, the
symptoms increase, or at first increase and then diminish.

I have found in sevend instances that women who remained hysterical dar-
ing pregnancy give birth to children who died after repeated eclamptic attacks.
One woman, who suffered from several hystero- epileptic attacks during pregnancy)
ffave birth to a child which presented marked chorea, and died of eclampsia at
the age of two months.

Disturbances of the general condition hardly ever remain absent in
hysterical patients. They feel ill, are moody and depressed, and often
complain of obstinate insomnia. There may be complete anorexia or in-
satiable boulimia, sometimes attacks of increased thirst. Certain writ-
ers apply the term hysterical fever to paroxysmal increase of tempera-
ture without a matenal basis.

The psychical condition suffers to a greater or less extent. It is
characteristic of these patients that they exaggerate their suffering and
endeavor to attract the attention of the physician and others to their mal-
ady. In doing so they do not shrink from lying and simulation. Frogs,
snails, insects are shown and are claimed to have been vomited, or evacu-
ated from the anus or vagina. Others claim to have vomited faeces; still
others, that they have eaten nothing for weeks, until they are caught at
night secretly satisfying their hunger. Complaint is occasionally made
of fever. The thermometer in the axilla does, indeed, show an increase
in the bodily temperature, but this results from friction of the ther-
mometer between the folds of the shirt. Our suspicions should be
aroused if the temperature alone is elevated, while pulse and respiration
are unchanged. Some patients increase the frequency of the pulse by
voluntarily increasing the rapidity of the respiratory movements, u
the patients think themselves neglected, they sometimes mutilate them-
selVes, push needles under the skm, or swallow them, make preparations
for suicide, but generally in such a manner that they may be prevented
from carrying out their object.

Many patients are unable to control their emotions. Slight causes
produce laughing or crying spasms, or sad events cause laughing spasms
and vice versa.

Delirium, melancholia, mania, and other grave psychopathies some-
times develop.

The occurrence of somnambulistic, ecstatic, and similar conditions
may also be referred to. Some patients remain for months in a somno-
lent condition. Attacks of i)rofound syncope are frequent.

It is impossible for us to describe all the combinations in which the
various symptoms of hysteria may appear. Remissions and exacerba-
tions are of frequent occurrence, the latter not infrequently at the period
of menstruation, or after mental excitement.

The disease always runs a chronic course, and generally lasts for life.
While it is probably going too far to say that every woman carries within
her the germs of hysteria, it is nevertheless true that very slight causes
suffice to make a woman hysterical. The disease is rarely the cause of
death. This is most apt to occur in hvstero-epileptic attacks, and in
spasm of the vocal cords, or paralysis of the circo-arytsBuoidei postici, and

300 FdNOnOKAL DISSA8E8 OF TH£ BSADT.

in attempts at suicide^ which may terminate fatally, althoagh genenDj
not meant in earnest.

IV. Diagnosis. — The diagnosis is generally easy. It is true thik
very few symptoms are pathognomonic of hysteria, out the ensembk,
the frequent changes, and the sudden appearance of entirely opposite
conditions generally leave no room for douot.

V. Prognosis. --The prognosis as regards recovery is not favorabk,
but the patient's life is rarely endangered. The more nnmerooB tin
symptoms, the more severe the hystero-epileptic attacks, and the mon
marKed the mental affection, the more umavorable is the case.

VI. Tkeatment. — Prophylactic measures possess no slight import-
ance. They must be employed particularly in individuals who come of
hysterical and nervous families. The cmldren should be generoudy
nourished^ hardened bodily and mentally^ they should avoid over-apph-
cation in school, and be kept away from hysterical individuals.

If hysteria has developed, we must first endeavor to meet the canal
indications, and these vary, as a matter of course, with the etiology.

Friedrich recently obtained good effects from cauterization of the
clitoris. Extirpation of the ovaries has also been performed.

Against the disease itself more can be done b^ moral treatment than
by drugs. The best results will be obtained by mm who secures the con-
fidence of the patient.

AsafoBtida, valerian, musk, potassium bromide, arsenic, gold, silver,
copper, etc., have been recommended, but we have never ootained anj
special benefit from these remedies. Electrical applications (central nnd
peripheral galvanization and faradization, ana electric baths) often
fail us.

Great caution should be exercised in the administration of narcotics.

I have often derived benefit from the daily employment of protracted
lukewarm baths (30° R., thirty to forty minutes' duration), especially if
irritative symptoms predominated. Liebermeister recommends cool
baths (15° R.) followed by walking, until the patient feels warm.

Individual hysterical symptoms must sometimes be treated with local
remedies. In hysterical paralyses, the patients must J>e compelled to
exercise the limbs vigorously every day. in paralysis of the legs, for
example, the patient is placed on her feet, supported under the arms,
and, if necessary, dragged around with force. Hysterical contractures
are treated by passive stretching of tha muscles, massage, and the fara-
die current, in h^'sterical anaesthesia, the faradic brush often produces
rapid effects. Upon the outbreak of hysterical spasms, we may order
cold baths and douches, or the electrical brush.

12. Cerebral Neurasthenia^

1. The causes and significance of neurasthenia have been discussed on page
147. In some cases, cerebral symptoms predominate (cerebral neurasthenia); the
combination of cerebral and spinal symptoms is called general neurasthenia;
those cases in which vaso-motor symptoms predominate are known as vaso-motor
neurasthenia.

2. Cerebral neurasthenia is characterized by ready excitability and exhaustion
of the brain. The patients are generally moody, complain of neadache; some
suffer from insomnia, others from excessive somnolence. They feel incapable of
bodily, and particularly of mental work, are confused and forgetful. Some com-
plain of dizziness, dream a good deal at night, speak in their sleep, and suffer
from excessive pollutions. They are unusually sensitive to bright light and loud
noises. Others complain of impaired vision, flashes of light before Uie eyesy and

DISEASES OF THE SYMPATHETIC. 301

flootoma. There is not infrequently impairment of hearing and subjectiye audi-
tory senBations.

Some patients feel anxious and 0{>pre8sed in the presence of many indi-
Tiduals; others only feel well and free in company. Many are tortured by the
most various forms of terror. Walking across a large space, a visit to theatres
and concerts, a railway ride, etc., produce a feeling of fear and dread of danger
to life.

The patients not infrequently change color very quickly, complain of shooting
heat and then of coldness, perhaps of parsesthesisB. The symptoms may be con-
fined to circumscribed nerve tracts, or may be unilateral (hemi neurasthenia).

Neurasthenia is often manifested by functional disturbances of individual
organs. Persons who are compelled to speak a good deal soon suffer from a
feeling of exhaustion in the larynx, hoarseness, and a sensation of tickling. The
patients often complain of dyspncea, and attacks of palpitation of the heart are
frequent. There is diminish^ thirst and appetite, disturbances of digestion,
flatulence, and changes in the urinary excretion.

8. The diagnosis, prognosis, and treatment are the same as in spinal neuras-
thenia. Very rapid results are often, though not constantly, obtained by electri-
cal applications. The methods recommended are: Galvanism longitudinally,
transversely, or obliquely through the skull, or a large electrode to the head, the
other to tiie feet, or central galvanization; also galvanization of the cervical
sympathetic or the cervical cord, faradization of the head, or the application of
tne faiadic brush to lar^e surfaces of the skin. At first, a weak current
should be employed; the sittings should not be too long or repeated too quickly.

PART V.
DISEASES OF THE SYMPATHETIC.

Little is known positively concerning diseases of the sympathetic.
Seliance was formerly placed upon anatomical changes to prove the fre-
quency of clinically demonstrable diseases of the sympathetic; but this
mode of proof has been discredited since Lubimon showed that changes
in the sympathetic may be found in most corpses.

Diseases of the sympathetic may exist independently, or they may be
aecondary to diseases of the brain or spinal cord. The latter is readily
explained by the fact that the sympathetic receives certain nerve tracts
from the cerebro-spinal axis.

We have previously considered several affections of the sympathetic,
viz. : BasedoVs disease, stenocardia, Addison's disease. We will add the
following:

1. nemicrania. Migraine.

I. Etiology. — ^Unilateral headache is as frequent as it is annoying,
particularly in the female sex. The disease often develops in childhood;
at all events, a predisposition is manifested from the age of fifteen to
twenty-five years. In a case reported by Bohn, hemicrania seems to
have been congenital. Heredity can often be demonstrated. Either
hemicrania or neuroses of various kinds are apt to occur in the patient's
family. The higher classes seem to be affected more frequently than
the laboring classes. There is no doubt, from our own experience, that
mental strain is connected with the origin of the disease in some in-
stances. At other times, it is the result of acquired nervousness, such
as is particularly apt to develop after chlorosis, ansdmia, vital losses of
all kinds, protracted diseases, excesses. It is often associated with
hysteria. It is observed occasionally after infectious diseases, especially
gout and rheumatism. It has also been known to develop during preg-

802 DISEASES OF THE SYMPATHEnO.

nancy^ and disappear after delivery. Oppenheim recently called atten-
tion to the fact that bemicrania sometimes precedes for a long time
marked tabetic symptoms. Hack attributes certain cases to morbid
swelling of the infenor turbinated bone, and obtained good effects fiom
treating the latter with the galvano-cautery. In not a few cases the
cause remains unknown.

The individual attacks of hemicrania may be the result of menstrua-
tion^ bodily or mental strain, excitement, overloading of the stomach,
constipation, vivid impressions upon the senses, etc.

II. Symptoms. — The svmptoms begin suddenly, or they may be pre-
ceded by prodromata. The latter last one or more hours, sometimee
several days. They consist of a feeling of discomfort, dalness in the
head, rush of blood to the head, dizziness, nausea, tinnitus aurium, etc

In some cases, the patients are awakened from sleep by the violent
headache, others feel tolerably well early in the morning, out the drmded
symptoms gradually grow stronger and stronger, generally last until
night, and do not disappear untU sleep occurs in the following night.
An attack rarely lasts more than one day.

The pain is described as dull, boring, or crushing; as a rule, the

{latients do not describe the shooting, tearing pains of other neuralgiM.
t sometimes has a throbbing character, and increases with each puiflh
tion. The pain is generally confined to one side of the head, usually the
left. In some patients, its situation varies in difFerent attacks (hemi-
crania alternans), or it is originally unilateral, and then extends gradn-
ally to the other side. Even if the pain is unilateral, it often extends
beyond the median line, while in other cases it does not reach the latter.

The patients sometimes localize the pain chiefly in the forehead, the
temples, or the vertex, more rarely in the occipital region. In many
cases, the entire side of the head is uniformly sensitive. In some patient^
the pain also affects the back of the neck, and complaint is made*of stiff-
ness in this region. Painful pressure points are absent, but a larger area
at the apex of the parietal bone is often tender on pressure. The inten-
sity of the pain generally increases on coughing, straining, or bending
over. Many patients complain of pain in the orbit and of impaired
mobility of the eye.

The painful half of the head is often extremely sensitive to gentle
contact with the skin, while strong pressure is often oorne without pain.
Gentle pulling upon the hairs is often very painful. In patients who
have suffered from hemicrania for years, the hair upon the affected side
of the head is often scanty, prematurely gray, occasionally dry and
ragged. It is also said that the hairs sometimes become erect during an
attack.

Very many patients are overcome by the severity of the pain to such
an extent that they are entirely incapable of mental or bodily work.
They are extremely sensitive to bright light and loud noises; many com-
plain of flashes of light before the eyes, visual hallucinations, scotoma,
and even hemianopsia has been described. Others complain of impair-
ment of hearing, tinnitus auriiim, or other abnormal auditory sen-
sations.

Many patients are pale and feel chilly; the pulse is somewhat accel-
erated; they suffer from frequent yawning and eructations, the tongue
becomes coated, and vomiting occurs. In other cases meteorism de-
velops, the patients suffer from frequent desire to go to stool, and after

DISEASES OF THE SYMPATHETIC. 303'

the attack pass unusual quantities of a pale^ watery urine^ in which I
discovered albumin on several occasions.

The duration and number of the attacks vary greatly. Months and
years sometimes elapse before another attack appears, or women experi-
ence an attack before or during, rarely after, each menstrual period, or
they recur in series, and are then followed by comjjaratively long, free
intervals. The disease sometimes persists for life; in women it not in-
frequently ceases spontaneously at the menopause.

In the majority of cases, the symptoms described are the only ones
observed. In other cases, vaso-motor and trophic changes also occur, and
can hardly be explained except as the result of implication of the cervi-
cal sympathetic, or the vaso-motor centre. This is also indicated by the
presence of pressure points in the neck, corresponding to the superior
and middle ^nglia of the cervical sympathetnic, and over the lower-
most cervical or upper dorsal vertebrae. Not all cases, however, are the
result of disturbances of the sympathetic.

The sympathetic form of hemicrania (vaso-motor hemicrania) may be
the result 01 spasmodic or paralytic conditions. The former is known
as hemicrania sympathico-spastica, the latter as hemicrania sympathico-
par^tica. Mixed forms also occur.

Hemicrania sympathico-spasticu also presents symptoms, apart from
the unilateral headache, which indicate tetanus of the vessels of the
head supplied by the cervical sympathetic. The affected half of the face
is unusually pale and cool. Ihe temperature in the external auditory
canal may be diminished 0.6° C. The temporal artery appears narrow
and hard. The pupil on the painful side is dilated, the eye sunken.
Pressure on the carotid of the anected side increases the pain, compres-
sion of the one on the healthy side generally diminishes it. Active sali-
vation is sometimes observed ; in one case Berger collected two pounds of
saliva during a single attack. As thetetanus of the muscular fibres of
the vessels subsides towards the close of the attack, the walls of the ves-
sels relax, the face reddens and grows warm, the conjunctiva is injected,
the secretion of tears increased, and the pupil narrowed. Many patients
also complain of a general feeling of increased heat, of acceleration of
the pulse, and palpitation of the heart; vesical tenesmus is experienced,
and the patients pass large quantities of watery urine or sometimes thin
stools. Among late sequelsB of the disease are mentioned obliteration of
the folds of the skin upon the affected half of the head, thickening of the
walls of the temporal artery, thickening and nodular formations of the
skin.

The symptoms of hemicrania sympathico-paralytica remind us of
those produced by section of the cervical sympathetic in animals. The
painful side of the head is red and hot, the pupil is narrow, the eye
sometimes sunken, and the palpebral fissure narrowed; there is some-
times slight ptosis. During the attack, Moellendorf observed a scarlet
color of tne fundus of the eye, redness of the papilla, the boundaries of
which were somewhat effaced, abnormal fulness of the retinal arteries
and veins, sinuosity and nodular distentions of the retinal veins, and in-
jection of the episcleral vessels. Increased secretion of sweat (epidroeis
unilateralis) is sometimes observed upon the affected half of the head
and face. The temporal artery and, in many cases, the carotid are
dilated and pulsate vigorously. Pressure upon the latter may relieve the
pain, compression of che carotid on the healthy side increases the pain.
Berger demonstrated increased tactile sensibility of the integument of

304 DISEASES OF THE SYMPATHETIC.

the affected side during the attack. The pulse is sometimes mmsually
slow, the radial artery small and hard. Towards the end of the attack,
the redness of the face disappears, and is replaced by pallor and coolness,
and dilatation of the pupil as the results of secondary narrowing of the
vessels.

III. Anatomical Changes and Pathogenesis. — Nothing is known conoern-
ing the anatomical changes in hemicrania.

In the larf^e proportion of cases, in which sympathetic symptoms are ahsent,
the pathogenesis remains obscure. Much also remains unexplained concemiog
the sympathetic forms. Even the localization of the pain is unsettled — whether
in the dura and pia mater or in certain provinces of the central nervous sjsten.
Du Bois-Reymond believes that the pain is the result of compression and irritatiai
of the sensory nerves in the walls of the vessels, owing to the spasm of the vts-
sels. Eulenberg attributes it to the numerous changes of intracranial pressure
resulting from the changes in the amount of blood within the skuiL

IV. Diagnosis. — The diagnosis of hemicrania is easily made. It
could only be mistaken for trigeminal or occipital neuralgia^ but tbisii
distinguished by the presence of painful pressure points. If distinct
sympathetic disturbances are present, we can readily distinguish between
tne spastic and paralytic forms of the disease.

V. Prognosis. — The prognosis is good so far as regards danger to
life, but bad as regards recovery. As a rule, the disease cannot be re-
lieved permanently. It generally disappears spontaneously with advanc-
ing years, and in women at the menopause.

VI. Treatment. —Prophylactic measures should be adopted in indi-
viduals who possess an hereditary tendency to the disease. In such
individuals the mental and physical education should be such as to avoid,
as much as possible, the causes of the disease.

Such measures should also be continued in order to preyent the re-
currence of attacks. Light, nourishing diet, daily evacuation of the
bowels, ayoidance of mental and bodily overwork, constitute important
elements of treatment. In anaemic individuals iron preparations, in
nervous patients the nervines are indicated. Ve^y good effects are often
obtained from a change of air. Some patients feel better at the sea-
shore, others in the mountains. In puffy, plethoric individuals, with a
tendency to disturbances of digestion, cures at Kissingen, Hombaig,
Carlsbad, etc., are indicated.

Electricity is often resorted to, the galvanic current transversely and
longitudinally through the skul), galvanization of the neck or cervical
sympathetic, treatment of painful points with the anode. .In the spastic
form the anode, in the paralytic form the cathode should be applied to
the cervical sympathetic. The faradic current has also been employed,
particularly the primary current. Good effects have been obtained from
the electrical hand, the patient taking one electrode in his hand, the
physician grasping the other one and then stroking the head and face
with his moistened free hand. Electrical baths and general faradization
have also been recently recommended.

To relieve the individual attack, the patient should remain in a
quiet, easily darkened room, and should be kept free from noise and ex-
citement. He should assume the horizontal position, with the head as
low as possible. Many feel great relief after taking a cup of strong
coffee, others from swallowing small pieces of ice. While the pains are
increased in many cases after eating, in others great relief is felt after a
hearty meal. It is often said that the pain improves after eructation

DISEASES OF THE BYMPATHETIO. 305

and vomiting^ so that many patients put the finder into the throat in
order to produce emesis. The pain is occasionally alleviated by strong
pressure on the head^ the application of an ice-bag, compresses of cold
water or vinegar, applications of ether, chloroform, or turpentine, and
inhalation of ammonia. In the spastic form, good results have been ob-
tained from inhalation of amyl nitrite (3 to 6 drops), in the paralytic
form from the subcutaneous injection of ergotinum Bombellon (one-half
syringeful diluted with an equal amount of water). Nitroglycerin has
l>een recently recommended.

2. Progressive Facial Hemiatrophy.

{Facial Trophoneurosis. Neurotic Facial Atrophy. Prosospodysmor^

phia.)

L Etiology. — This term is'applied to atrophy of the panniculus adi-
posus and skin of one-half of the face, which gradually increases and
gives rise to serious deformity. The faciid bones and muscles, the
palate and tongue may also take part in the atrophy. The disease is not
irequent. Lewin recently succeeded in collecting the reports of only
sixty-eight cases — forty-one in males, twenty-seven in females. The
light and left halves ox the face were affected with equal frequency. As
a rule, the disease begins from the age of ten to sixteen years, rarely be-
yond the age of twenty-five years.

The influence of heredity is not proven, but several of the patients
came of nervous families, or had manifested other nervous symptoms
(trigeminal neuralgia, facial spasm, headache, epilepsy).

The disease sometimes followed traumatism, wnich either afFected
the face directlj;, acted centrally (injury to the skull) or upon the cer-
vical sympathetic. It has also been observed after infectious diseases
(measles, scarlatina, small-pox, typhoid fever, but particularly diph-
theria).

The first symptoms sometimes developed during the puerperal period.

In some cases no cause can be discovered.

II. Symptoms. — The symptoms develop unexpectedly, or they may
be preceded by prodromata for months and even years. The latter con-
sist of neuralgiform pains, paraesthesisd of various kinds, and even cere-
bral symptoms (vertigo, headache, spasms), etc. In Emminghaus' case,
twitchings of the muscles of mastication were described.

The transition from the prodromal to the manifest symptoms is
sometimes formed by changes in the hairs (beard, brows, scalp). They
become more scanty, and sometimes fall out entirely; their color becomes
lighter, often even of a silver gray. These abnormalities sometimes
occur only in patches; in other cases they follow the facial atrophy.

As a rule, the atrophy begins with the formation of light patches upon
the integument of the face. Their color is cicatricial white, yellowish,
or brownish-yellow. The originally white patches often assume a yellow
or brownish color in the further course of the disease. At first there is
generally only one patch, but this is followed by others. The patches
may coalesce with one another. In the beginning they sometimes de-
velop only along certain nerve tracts.

The patches become more and more depressed. The panniculus
adipoBus Deneath them atrophies and the skin grows thinner. At the
time the latter is adherent firmly to the underlying bones, and
20

soe

DlbSAHES or THB STXFAT^STIO.

60metimeB desquamatea very actively. Not infreqnently the &ce ia t»-
versed by a Beries of deep, cicatrix-like places. In other caees, the atrofh;
ig more Qniform; while the healthv Bidt appears blooming, the diseued
side looks shrunken and old (vide Fig. 12a). The eye is generkU;
ahfunken (atrophy pf the orbital cellulo-fatty tissue) and the {nlpcbnl
fissure is sometimes dilated, sometimes narrowed. On the affected sJ*
the mouth is sometimes slightly open, on account of atrophv of the m-
bicnlariB oris and the traction of the atrophic integument, 'fhe extern»l
nasal opening and the auditory canal are not infrequently BomewbU
enlarged. In many cases the face is drawn towards the diseased side.

Cutaneous sensibility is unchanged in the majority of cases. Some
patients state that, in testing with a needle, a sensation is felt as if Uu

Tbe r>oe lo left-dded proKnailTe tacl*! tioot^.

skin were coated with varnish or rubber. In a few oases, diminntioQ of
tactile sensation and of electro-ciitauGDus sensibility has been obsenred.
Some patients complain of parteBthesiae of the atrophic side of the face.
The cutaneous temperature is unchanged. The secretion of 8w«ut is
unaffected at first, but in very advanced cases it is sometimes diminished
or abolished. The production of sebum is very soon diminished or abol-
ished. Laude noticed, in one case, diminution of the secretion of ceru-
men. The power of blushing is unaffected, and the arteries on the dis-
eased aide are normal. In one case, Eulenburg and Landois noticed a
greater elevation of recoil in the carotid pulse cur\-e on the affected aide.
The atrophy sometimes attacks the bonce, cartilages, and moscles.
Virchow states that atrophy of the bones is eBpecially apt to occur when
the disease begins in early youth. The bones contain more or less deep

DISEASES OF THE SYMPATHETIO. 307

farrows or abnormal ridges^ and are thinned and shortened. The max-
illsB and hard palate are attacked with special intensity. Absence of a ca-
nine tooth or one or more molar teeth from the deformed jaws has been
noticed in several cases. The nasal and auricular cartilages, sometimes
those of the eyelids, may also undergo atrophy and deformity.

The tongue upon the afFected side of the face is sometimes dimin-
ished in size and, when protruded, deviates to the diseased side. The
muscular tissue of the soft palate mav also undergo atrophy. In a few
cases, the patients suffered from diphtheria, and the atrophic side was
then affected to a more marked degree.

The facial muscles may also be attacked by atrophy. The electrical
excitability of the muscles is unchanged, iibrillary muscular twitch-
ings were observed in a few cases.

The muscular atrophv generally remains confined to the muscles of
the face, tongue, and palate. In one case, disturbances of articulation
were observed, especially in the articulation of the lett*er r.

The organs of special sense remain intact. In one case, there was
. diminution in the power of hearing, and Wolff observed narrowing of the
field of vision.

Brunner and Seeligmueller described irritative sjrmptoms on the part
of the cervical sympathetic: dilated pupils, pale slun, lowered tempera-
ture, absence of perspiration, and pain on pressure over the sympatnetio
ganglia.

In two cases, similar cutaneous changes appeared on the correspond-
ing limbs. Two cases of bilateral facial atrophy have been reported.

The course of the disease generally extends over several years. Be-
missions sometimes occur; in other cases the disease comes to a stand-
still, but the deformity persists for life. There is no danger to life, but
in one case Delamare obiBcrved increasing excitement, and finally insan-
ity.

in. Natubb of the Disease. — No post-mortem examinations have been
made. Bitot and Laude regard the disease as a local atrophy of the panniculus
adiposus of unknown origin. But the fact that not alone the skin, but also the
bones, cartilages, and muscles take part in the atrophy indicates that the causes
are more general in character, probably vaso-motor or trophic. In our opinion, the
disease is probably the result of tropnio disturbances, which either onginate di«
rectly from the cervical sympathetic or from disease of the trophic fibres in the
trigeminus (particularly m the spheno-palatine and Ghuserian ganglia) and the
f adal nerve.

lY. DiAGKOSis. — The diagnosis is easy. The disease is distinguished
from congenital asymmetrv of the face by its later development, the
presence of pigmented patches and changes m the hairs. These features
will also differentiate the disease from the acquired facial atrophy of
scoliosis and caput obstipum.

V. Pbognosis. — The prognosis is unfavorable as regards recovery,
since treatment has been entirely unavailing. Peripheral and central
electrization have been employed without benefit.

3. Facial ffemihyper trophy.

1. Unilateral facial hypertrophy is extremely rare. Lewin recently collected
ten cases.

The disease is always congenital. The progress of the disease after birth kept
pftoe with the general conditions of development.

aoB

' THE STMl'ATHBTIO.

B. The hypertrophy affected parliaularly the soft parta of the fac« (Ttd« E^
130), and also the ear, tonsil, and tongue. Hypertropliy^ of the teeth, appet IM
loner jawa was observed in one case. The sebaceoua awretion was increiued. a»l
the folliclea projected as little nodule«, or the sebum hud oolleoted in pI«oes in da
shape ot cruBts and ecalea. Tiiere vas generally a considerable flo<f of nUin. is
one case active secretion from the othernise uncbanged cmr. Ttie clie«k irw
BomeCimes reddened acd felt warm subjectively. Blood veasels, Drgaus of fpitM
smse, and secretion of aneat uiichaQgi>d. In Friedreich's case, there wnsdimu.
ished sense of taste on the hypertrophic half of the tongue. Other DOtiivsbJ*
features were pigmentation of the skin, increased growtli and abnormally dui
color of tbe hair, occaaionally diniiniBhed power of mimicry. Mental function
generally intact; in one caae hydrocrphalua and zeneral convulsions.

An autopsy was obtained in Friedreich's case, nut the results were negative.

Id some cases the hypertrophy also involved the correflpondisg half otthe

yeara. After Schieirk.

and right 1«% wese hjper-

Co7iiiitio)is of ike Cervical SympatheHc.

I. Symptoms. — Among the symptoma of irritative conditions of the
cervical sympathetic, dilatation of the pupil or mydriasis spastica (Ui«
result of contracture of the dilator pupillte) is the most frequent. En-
largement of the palpebral fissure and the protrusion of the eyeball are
Bometimes noticed on the affected side (irritation of Mueller's tnoscie).
Thepower of accommodation suffers not infrequently.

Vaso-motor changes are often overlooked on account of tlieir fleeting
character. They are manifested by pallor of the corresponding halftrt
the face, diminution of temperature (0.9° C. in the external audi ton
canal), and diminutionor abolition of perspiration. The temporal ima
carotid arteries are eometimes less full on the affected side.

Trophic changes sometimes appear very early, and in one case had
advanced so rapidly within a weefe that the emaciation of the cheek was
noticed by the patient. It is uncertain whether these changes must be
attributed to special trophic fibres or to the diminished amount of blood
in the arteries.

Tbe cervical sympathetic and its ganglia are sometimes tender on
pressore.

Tbe symptoms may be temporary or persist for life. Czeimwk and

DISEASES OF THE 8TMPATHETI0. 309

Gerhardt observed a case in which ocnlo-pnpillary symptoms alone oc-
curred as the result of pressure on a tumor of the neck. Widd observed
exaoerbfttions and remissions during the course of a phlegmon of the
neck.

Irritative and paralytic symptoms sometimes alternate with one
another.

The patients feel very little discomfort^ but may be disfigured by the
extensive atrophy of the face.

II. Etiology. — ^Among the chief causes are diseases of the organs of
the neck, associated with pressure upon or extension of inflammation to
the cervical sympathetic ^glandular tumors, phlegmon of the cellular
tissue, parotid tumors, goitre, aneurisms, fall, blow, stab or gunshot
wounds in the neck).

The symptoms sometimes occur in diseases of the cervical cord, from
which the oculo-pupillary sympathetic fibres take their origin (fracture,
dislocation, exostoses, and tumors of the vertebrae, infiammation, soften-
ing, and hemorrhage of the cervical cord).

Perhaps the disease occurs occasionally as an independent neurosis.

III. Diagnosis, Prognosis, Treatment. — The diagnosis is not
difficult. If goitre and palpitation of the heart are also present, protru-
sion of the eyeball might lead us to mistake the condition for Basedow's
disease; but in the latter the symptoms are almost always bilateral.

The prognosis and the treatment depend upon the primary disease.

5. Paralytic Conditions of the Cervical Sympathetic,

I, Symptoms. — Oculo-pupillary, vaso-motor, and trophic symptoms
also occur in paralytic conditions of the cervical sympathetic; the first
are the most constant.

The pupil on the affected side is narrow (paralytic myosis), and it is
sometimes oval instead of round. It reacts to light, but often slowly.
The pupil dilates under the action of atropine, but not to such a marked
extent as the other one; if both pupils are treated with calabar, the
affected one contracts more markedly than the healthy one.

Slight ptosis is sometimes noticeable. We also find narrowing of the
palpebral nssure and sinking in of the eyeball; the latter is often espe-
cifuly marked in the later stages of the disease, and is then the result
of atrophy of the orbital cellular tissue. Diminution of intraocular

Sressure and secondary fiattening of the cornea are sometimes observed.
[yopia mav be produced by disturbances of accommodation following
paralysis of the muscles of the iris.

Vaso-motor changes are shown by increased fulness and sinuosity of
the vessels, redness, increased warmth, subjective feeling of heat, in-
creased production of sweat, tears, and saliva on the affected side. Ele-
vation of temperature cannot always be demonstrated objectively. The
symptoms mentioned sometimes extend to the cervical and upper thora-
cic region. Homer and Nicati distinguish two stages of paralysis of the
sympathetic; in the second, the vaso-motor symptoms are said to become
converted into the opposite ones: sensation of aiminished heat, slighter
fulness of the arteries, pallor, and anhidrosis.

To the latter stage belong the trophic changes which are charac-
terized by emaciation of one side of the face.

Central symptoms are sometimes observed, and are attributed to in-

810 DISEASES OF THE SYICPATHBTIO.

creased blood supply to one cerebral hemisphere. These include uni-
lateral or bilateral headache, dizziness, and even impairment of memory.

Subjective sjrmptoms are absent in the majority of cases, unless pro-
duced by the primary disease.

W. Etiology. — The causes are similar to those of irritatiye condi-
tions of the cervical sympathetic: iujuries (fall, blow, etc.), tumors of
the lymphatic glands, and the parotid, phlegmons in the neck, goibt,
etc. It is sometimes observed in phthisis as the result of adhesom
between the sympathetic and the apex of the diseased lung. It aJao
occurs in diseases of the cervical spine and spinal cord.

Attention has been called to tne frequent association of paralysis d
the cervical sympathetic, and of the brachial plexus, as the result of co-
incident injury to the cervical sympathetic, or to the communicating
branches between the sympathetic and brachial plexus. It is probable
thai; the disease may also develop as an independent rheumatic affection.

III. Diagnosis, Pbognosis, Tbeatment. — The diagnosis is easy.
Prognosis and treatment depend on the primary disease. Otto effected
a cure by galvanization of the cervical sympathetic, but recovery is gen-
erally unattainable.

1*0 reach the superior cervical ganglion with the electrode, the latter
should be passed in between the angle of the jaw and the outer end of
the greater cornu of the hyoid bone. It is advisable to place the
cathode in this region, while the anode is applied to an indifferent root,
or upon the other side of the cervical spine at the level of the nfth
and seventh vertebrae.

G. Symmetrical Gangrene.

I. Etiology.— The disease has been observed most frec^uently in women; a
certain predisposition is created bv ansBmia, delicate constitution, and nervous-
ness. Some patients mention a cold as the cause of the ditiease. Nedopil reports
a case in which this cause was associated with mental excitement. The affectioa
has also been observed after infectious diseases (typhus, intermittent fever, syj^
ilis). In some cases the disease itself creates the impression of an infectious'pro-
cess.

II. Symptoms. — The symptoms appear most frequently in the toes and fingers,
more rarely in the nose and ears. In a few cases the symptoms have also hixn
observed upon the integument of the chest.

A feeling of coldness, then a livid, cyanotic color, parsBsthesisB, and blunted
sensibility, more rarely hypersesthesia, sometimes neuralgiform pains open the
scene. At first the symptoms present remissions and exacerbatioms, later they in^
crease in intensity. Subcutaneous ecchymoses or vesicles develop in some cases.
In such places the skin then becomes blackish and undergoes gangrene, which
may lead to the loss of the phalanges, or lay bare large parts of the surface. The
symmetrical distribution of the gangrene on both sides of the bodv is especiillT
noteworthy. Tlie mucous membranes escape, but in one case I observed swell-
ine and hemorrhages of the Rums. High fever (4r C.) and enlargement of the
spleen have been observed; Bameau found sugar in the urine. The symptonu
may run an acute (one to two weeks), subacute, or chronic course.

The disease is regarded as a vascular spasm with secondary local asphyxia.
Its symmetrical occurrence indicates that the spasm is located in the vaso-motor
centre (medulla oblongata ?).

III. Diagnosis, Prognosis, Treatment.— The diagnosis is easy. It is distin-

fuished from the gangrenous form of ergotin poisoning by the previous history,
he prognosis is serious, although the disease rarely proves fatal. Treatment:
electricity (peripheral and central), massage, quinine, iron, if necessary surgical
interference.

DISEASES OF THE SYMPATHETia 311

7. Myxedema.

{Cacheosic pachydermique.)

EnoiXKHT. — ^Myzosdema occurs chiefly in women (twenty-seven females in
thirty-one cases collected by Morran). As a rule, it does not develop before the
period of puberty; it is rare in childhood and beyond the age of fift^ jears. It
has been attributed most frej^uently to colds, also pregnancy, parturition, lacta-
tion and sexual disturbances in general, to atrophy of the thymus gland, and in
one case to excitement. It is said to occur often in nervous mdividualB.

n. Symptoms. — ^The symptoms consist, in the main, of cachexia, oedema, and
nervous disturbances.

The most striking feature is the oedematous swelling which attacks the fore-
beadf cheeks, eyelids, nose, and lips. The lids can only be half closed, and form
thick sacs; the physiognomv chan^ so that the expression becomes stolid, ani-
mal, and coarse. Increased secretion of tears and saliva has been described in
several oases.

The limbs also undergo considerable swelling and increase in size, the fingers
and toes being most affected. The trunk may Sso present oedematous swellinf^
Unlike ordinary oedema, the pressure of the fingers leaves no depression In the skin,
because the fiuid accumulated in the cutis and subcutaneous cdlular tinue con-
tains a large amount of mucin, and has a semisolid consistence. The skin has an
alabaster or waxy yellow color and feels cool. The patients also complain of a
sensation of coolness, and even the bodily temperature has been found lowered
in several cases (to 86.4° C.)> The pulse is sometimes slow. The secretion of per-
spiration and sebum is often diminished, the skin dry and wrinkled; a few red
patches are sometimes found.

The mucous membranes (mouth, larynx, digestive tract) are often thickened.
The voice becomes hoarse, monotonous, sometimes indistinct and nasal.

Paraastheeisd are frequent, and the changes in theinteg[ument may be preceded
by pallor or a livid color. As a rule, the patients complain of anorexia and con-
stipation; cachexia and albuminuria graduallv develop. Then follow apathy,
somnolence, muscular weakness, delirium, hallucinations, and mental impaur-
ment.

The disease runs a progressive, but chronic course (average duration, sixteen
and one-half years).

Nothing is known positively concerning the nature of the disease. The view
Is gaining ground that it is nervous in its ori^n, some locating it in the vaso*
motor centre of the medulla oblongata, others m the sympathetic.

IIL Trbatmbnt.— Massage, pilocarpine, peripheral and central electrization,
qoinine, iron, nourishing diet.

8. Hydrops articulorum intermittens.

I. 8TMPT0MS.~This condition is manifested by paroxysmal swelling of the
joints, especially of the knees. The swelling occurs at such regular intervals as
to arouse the suspicion of m^ria. The interparoxysmal periods vary from one
to three or four weeks. The attack lasts four to six, sometimes even eight days.
The swoUen joint is free from inflammatory changes; in exceptional cases it is
painful. The duration of the disease varies from several months to twenty-five
years.

II. Etiology. — ^The causes of the disease are unknown. In two cases it was
preceded by intermittent fever. It has also been observed in association with
Basedow's disease and vaso-motor angina pectoris.

IIL Treatment. — Quinine, arsenic, ana ergotin have been employed in treat-
ment. Pierson obtained good results from galvanization of the neck. Electri-
zation of the crural and sciatic nerves and the joint itself should also be tried.

SECTION VI.

DISEASES OF THE MUSCLES.

1. Pseudo-hypertrophy of the Muscles.

(Atrophia musculorum lipom^tosa. Dystrophia musculorum progressiva.
Juvenile muscular atrophy. Hereditary muscular atrophy.)

I. Etiology.— The disease develops most frequently in children.
The deformity of the muscles and limbs is sometimes noticeable im-
mediately after birth (rare), sometimes the changes develop gradualljat
the age of two years or later. The majority of cases begin before the
fifteenth year.

The male sex is most frequently affected (amoug one hundred and
twenty-five cases, one hundred and three boys, and twenty-two girlsaod
women).

The greatest etiological influence is exercised by heredity, and this
disease probably includes all cases which have been described as heredi-
tary progressive muscular atrophy.

It often affects several children in one family, although no other relatives had
been attacked. In other cases, maternal relatives had been affected, bat the
mother, as a rule, escaped. In two cases, I observed heredity on the paternal aide.
The rarity of the latter occurrence is owing to the fact that males, when affected,
either die or become impotent before arriving at a marriageable age. In nin^ of
my cases, four occurred in Jews.

In the hereditary cases, the male sex is chiefly affected.

The disease sometimes follows infectious diseases ^variola, measles,
scarlatina, diphtheria, typhoid fever). Some ascribe the disease to
scrofula.

Injury, cold, and exposure are also mentioned as causes. Perhaps
this explains the more frequent occurrence of the disease in the poorer
classes.

In a number of cases, other nervous disturbances (idiocy, hydro-
cephalus, asymmetry of the skull, convulsions, etc.) were also present.

II. Symptoms. — The chief symptom is increase of size, with dim-
inished power, of certain groups of muscles.

If the disease is congenital, the deformity arising from increased
volume of the muscles is occasionally noticeable immediately after birth.
In other cases it develops gradually. The patients fii;pt complain of a
slight tired feeling in walking, and a tendency to fall. Dragging pains
develop on account of the over-strain of the muscles. If the disease be-

DISSUEB O? TEB KOSOISS.

318

gins before the children are able to walk, this power ia sometimes learned
Terj late (fourth or fifth year).

The increased volume of the maacles gradually becomes more
promiuent. It is most marked in the culves, next in the extensors of
the .highs and in the buttocks; then it may estend to other groups of
muBcles. The muscles of the lower limbs are often paeu do-hype rtrop hie,
while those of the back and upper limba are markedly atrophied {vide
Pig. 131). In rare cases, the pseudo-hypertrophy extends to all the
tuusctes, even to those of the face. Hypertrophy of the tongue has also
been observed, and gives rise to difficnity in speech and deglutition.

The more the «ize of the muscles increases the mors marked become
the disturbances iu their function. These are espe-
cially noticeable in walking and standing. In walk- '''o. i3i.
iug, the patients lift the foot naasnally high, an ac- _
count of the drooping of the toes. The gait becomes
waddling, the axis of the pelvis and trunk being moved
forcibly from one side to the other with every step.
Atrophy of the muscles of the back generally produces
marked lordosis in the lumbar spine, while there ia
well-marked kyphosis in the dorsal region. Weakness
of the muscles of the buttocks and back interferes with
sitting down and rising. In sitting down, the patients
drop like an inert mass; in rising, they aid themselves
by means of tlie hands and arras. If placed on the
floor, they rise by clirahing up their own body (placing
the hands progressively higher and higher upon the
thighs).

In dorsal decubitus, the foot ia g'cnerally in pee
varo-eouinUB position. The hip and Knee joints are
often flexed, the thigh abducted.

The muscular changes are generally, though not
always, equally far advanced on both sides of the
body.

The hypertrophic muscles are generally soft and
flabby, more rarely they are firm and hard (marked
proliferation of the interstitial connective tissue).

Fibrillary twitchings are absent. The mechanical
excitability of the muscles is abolished in very ad-
vanced cases.

The electro- muscular excitability diminishes, and
finally disappears with the increasing disappearance »iiii*'M?ophj or'thn
of the muscular structure. taok musciua. After

The skin over the affected muscles is often bluish- "" ™"*'
red and marbled, and is cold to the feel (even 9° C, lower than the axil-
lary temperature). The production of heat in the diseased muscles ia
diminished. The congestion of the skin has been attributed to com-
pression of the vessels in the muscles. Outanoous sensibility is un-
changed. The skin presents a great tendency to inflammation, so
that alight pressure may auffice to produce gangrene and suppuration.
The subcutaneous adipose tissue is almost always very abundantly
developed. There ia aiminution of perspiration and active desquama-
tion of the epidermis. The patellar tendon reflex was absent in some
cases,
_Afl A mlOj appetite and sleep are normal, the bladder acta promptly.

*914 DISEASES OF THE HUBOLBS.

ConBtipation U often present, especially if the abdominal matele! m
pamlyzed. The patients often suffer from bronchitis uid may die ft*
pulmonary comphcationB (weakuesa of the respiratory ronscW). C»riiie
hypertrophy has been observed in a namber of casea, aad the puts n
souictimes slow {forty to sixty heats a minute).

The mental faculties are often unaffected. In other cases apstiij,
even imbecility and idiocy have been observed.

Traces of leucin, tyrosin, and sugar have been found in the ariw;
the amount of urea is sometimes diminished. Polyuria is mendonwi ia
a few cases.

The disease runs a chronic coarse and may last more than tvnlj
years. The patients gradually lose the power of moTing about and m
confined to tbe bed. Death is the result of intercurrent diseasee, panl-
ysis of the respiratory muscles or increaeiag marafimtu.

nuclear prollfcraUDQ oF thS latendtlol

muaclea. ittet Ebatelo i
hrp«rtroptiic abras ; X. af.'iltopMc Bbrea. Enlu^ 400 times.

IV. Anatomical Changes. — The brain, spinal cord, and sym-
pathetic have been found intact. In a few cases, lesions of the cord
have been reported, but they were either accidental complications or un-
reliable. The peripheral nerves are generally unchanged, but a few
writers have reported interstitial proliferation of fat (wliieh also takei
place under otner circumstances), narrowing, flattening, and gray di*-
coloration, proliferation of interstitial connective tissue, atrophr and difr
appearance of the nerve fibres. AH these changes are probably the re-
sult of disuse of the muscles.

The muscles have a pale or butter-yellow appearance; in advanoei
cases they look like a lump of fat.

An abuudant development of fat sometimes takes place in the £
aud tendons.

DieeASRS OF THE HITSOLBa.

dfuiced iDientitL&l proUfention otfat.

Mrnai perimysium and the adventitious lymph sheaths of the blood-reasela. The
IndividuHl muacular bundles are thus wLdely separated, aud the interstitial con-
iMCtive tiaaue coat&ins on uausual number of celU (coaneotive- tissue and round

cellaj. The mure the iatHrstitial tissue increases, tlie luore the muscular Bubatanoe
disappears an the result of campreasion. In some cases, the proctma soeius to atop
-^ t£is Btage, and the mueclea remtiin very firm.

316 DISEASES OF THE XUSCLES.

Ab a rule, adipose tissae derelops in the new-formed oonnectiTe tifloe* tibe
cells taking up fat and thus becoming oonTerted into fat o^la. The mnscs&r
fibres disappear more and more, and the moscle is thus converted finally into i
clump of fat.

In the majority of cases, the fibres simply grow smaller until they diaappev;
sometimes they present the phenomena of ZSenker's degeneration. Martim ibo
described the formation of vacuolsd and canals, which were filled with albomi-
noid fluid. All these phenomena are also observed in other conditions.

In a few cases, the muscular fibres are in a condition of cloudy swelling, t»ttj
degeneration, and nuclear proliferation. Oohnheim also described hypertrophic
muscular fibres (singly and in groups), some of which had undergone diem-
mous division.

The changes in the muscles are best followed in small pieces which have been
removed from the living subject by the harpoon or knife.

Different views are entertained concerning the nature of the disease. In oor
opinion, it is myopathic in its origin. The theory of its identity with progresate
muscular atrophy is combated by the following facts: a, Pseodohypenrophj
occurs almost exclusively in youth; 6, it always beffins in the lower limbs; e, the
electrical irritability of the muscles is different; d, it ui exquisitely hereditary.

IV. DiAOXOSis. — The recognition of the disease is easy except at the
outset^ when the examination of the muscle may be necessary to clear up
the case.

It must be differentiated from: a, spinal progressive muscular
atrophy : pseudo-hypertrophy does not begin in the interossei, the the-
nar and nypothenar eminences, but in the lower limbs; it is oftm
hereditary, begins at the beginning of puberty, and does not present
fibrillary contractions, or degeneration reaction; b, acute spinal infantik
paralysis, with secondary hyperplasia of the pannicnlns adiposus; in the
latter, the symptoms begin suddenly and are not progressive; the muscles
do not react to the induced current; c, spitial paralysis and secondarj
development of fat in the paralyzed muscles; tne paralysis per se existe
for a longer period and to a more marked degree than is accounted for
by the proliferation of fat.

V. Prooxosis. — The prognosis is unfavorable, the few reports of
improvement or recovery being unreliable.

VI. Treatment. — The most promising measures appear to be mas-
sage, faradization, galvanization, and alcoholic inunctions of the affected
muscles. Little can be hoped for from potassium iodide, arsenic, and
other nervines,

2. True Hypertrophy of the Muscles.

I. Anatomical Chanobs.— A few cases of this disease have been observed. The
muscles increase in size from enlargement of the individual muscular fibres.
Auerbach found the hypertrophic fibres of the biceps and deltoid muscles 1S5 n
and 120 /i in width, while fibres of corresponding muscles in other bodies were
only 75 // and 110 /i wide (V^ = 0.001 mm.). The transverse striation is intact or
unusually distisct. The muscle nuclei are enlarged and increased in number; no
chimges in the interstitial connective tissue.

II. Symptoms.— The symptoms develop graduallv. In Berger's case they were
preceded by neuralgiform pains and paraBsthesisB; this case also presented objec-
tive sensory disturbances, which are generally absent. The limbs are usually
affected, most frequently the muscles of the arms, next those of the lower limbs
(particularly the c^ves and extensors of the thighs), next those of the trunk.
The disease may be unilateral or bilateral. The muscles are unusually large, bat
their power is generally diminished. This is supposed to be owine to the fact
that tne blood-vessels no longer suffice to nourish the hypertrophic fibres, perhaps
also the intact terminal plates of the nerves no longer prove sufficient. Auerbaoi
noticed increased power during movements of brief duration, and Friedreich
found the muscular power unchanged in a case in which some of the musdes

DrSEABES OF THE SIUSCLES.

were atrophied. Berfter deecribed fibrillary conlractionfl. The eleotrioal excita-
bility IB itenerally uncban^d, iliough occtuionaliy diiniuiahed. Benedtkt noticed
increased iDenhanical excitability of tbe muaclea. This writer ^Iso observed, as a
com plication, vaao-motor dieturDancee (livid color, sensatioa oF cold) and paralf Hia
of the aympathetic (rednesn of the face and unilateral hyperhidrosiB).

III. Etiology.— The causes mentioned are typhoid fever, overstrain of the
muscles, and injuries. In Friedreich's case, the disease waa congenital.

IV. Diagnosis. Prognosis. Trratment.— With the aid of microscopic exami-
oatioD of the excised piece of muscle, the diagnosis is easy. The proKBoais is
grave, as the disease advances uninterruptedly. Treatment has been hitherto
useless ,

3, Progressive Ossification of the Muscles. Myositis ossificans progres-
siva s. multiplex.

I. Etiot-oot, — Hardly more than twenty-five cases of thia diaeoae
hare been reported. It generally begins during childhood {before the
age of fifteen years), once it appeared at the age of eight mouths; it
aJmoat always begins within the eecond decennium. The male sei is
affected more frequently than the female. The causes are generally
unknown; the disease has been attributed to cold, injury, and straiu.

II. SYMPT0M3. — Tho first changes generally appear in the muscles
of the nape of the neck and back. Then they extend to the muscles of
the neck, shoulders, aud arms, later to the lower limbs. Even the mus-
cles of mastication, the facia! and palatal muacles may be affected. Tha
abdominal muscles, tongue, laryngeal muscles, sphincters, musolea of the
genitals, diaphragm, heart, and small muscles of the hand are never
attacked.

The process may or may not begin aimultaneo'usiy in the correspond-
ing muscles on both sides of the body. It runs a chronic course, and
may last more than twenty years. It ia characterized by paroxysms, the
intervals varying from weeks to yeura. The attacks generally occur
without any known cause, more rarely they follow an injury.

Each attack begins with severe pain in a circumscribed part of the
mnscle, but the pain not infrequently radiates over a large area. The
akin over the painful part is hot, red, tense, and cedematous, the oadema
often being very extensive. There is often more or less rise of tempera-
ture. These symptoms subside in a few days, and a tense, usually
doughy tumor can then be felt over the painful spot. In favorable oases
this disappears in a few days, leaving behind stiffness and impaired
mobility.

In other cases the swelling becomes hard, the muscle undergoes con-
tracture, and gives rise to deformity. The process corresponds anatom-
ically to the formation of a connective-tissue muscle callosity.

In still other cases, ossification ensues. A hard, at first movable body is
felt, which gradually increases in eise. In this way the muscle ia replaced by
bony tissue. The bony masses may be round, nodular, flat, or irregularly stellate.
They gradually adhere to the underlving bone, and become immovable. The
bones themselves often contain multiple exoetoses.

If the muscles of the back are affected, the patients are stiff a» a rod, are una-
ble to turn and lie down. Disease of the muscles of the neck and throat renders
the head immovable. Affection of the thoracic muscles acts like a firm cuirass,
produces dyspnwa, and permits breathing by the action of the diaphragm alone.
Ossification of the muscles of mastication interferes so seriously with the fngea-
tion of food as to render artificial feeding necessary. Finally the patient may
become immovable, even passive movementa being impossible.

Some points of ossification occaaionally soften and disappear, even within
eight or ten days. In one case, Davy found diminution of the phosphate of lime

318 DI8SA8S8 OF THS 1CIJS0LE8*

in the urine. Gtorhardt and Peter obeeired Donnal amount of xxreA, dimination
of uric acid, earthy phosphates, and kreatinin«

The patients generally die from inanition or from diseases of the respiratorf
apparatus and suffocation.

Tachycardia and unilateral hyperhidrosis of the head, tabes dorsalis and poly*
aria have been obserred as oomphcations.

in. Ajnatomioal Chamges. — ^The process is supposed to run its coarse in thefol*
lowing manner; a. inflammatory proliferation of the interstitial connective tifiBne.
5. Compression atrophy of the muscular fibres, c. Bone formation in the nev-
formed connective tissue. The osseous substance is provided with periosteom
and nutritive canals for the blood-vessels. The formation of cartilage is moi-
tioned in one case.

IV. Diagnosis, Pbognosis, Treatment. —The diagnosis is easy. The diaetn
is distinguished from other bony tumors of the muscles by its prog^reasive, multi-
ple chiuw^ter. The prognosis is unfavorable.

Treatment: at first antiphlogosis, particularly rest, ice-bags, and potraiom
iodide internally. After relief of the acute symptoms, careful massage, iodine
baths, inunctions with tincture of iodine, potassium iodide, iodoform, or mercmit
ointment. «

Mercury, sarsaparilla, guaiac, colchicum, nitric acid, lactic acid, and phoqifaato
of lime have been administered internally.

4. Ischmmic Muscular Paralysis.

It is well known that paralvsis and contracture develop not infreqaently after
the application of tight bandages, and have been attributed to ischsdmia of the
muscIeB. It has been shown that such paralyses may be produced in ^nlmah,
and that they correspond microscopically to myositis. Poensgen recently rep<nrted
a case in which a cold is said to have been the cause of purely myogenic paal-
ysis.

This look is the proper'

COOPER MEDICAL COLL;.u.:,

SAN FRANCISCO. CAU

and is not to be removed from the
I/ibrary Room by any person or
under any pretext whatever.

SEOTIOE" VII.

DISEASES OF THE SKIN.

PART I.
INFLAMMATIONS OF THE SKIN.

DERMATITIDES.

a. Eetthematous Inflammations of the Skin.

1. The chief manifest symptom of erythematous dermatitis is redness
of the affected portions of the skin. This may also be the result of sim-
ple cutaneous hypersemia, so that we distinguish erythema hyperssmicum
simplex and erythema exsudatiyum. In the latter^ the distention of
the vessels is associated with exudation of a serous, sometimes of a
bloody fluid in the immediate vicinity of the cutis. Hence, pressure
upon the skin leaves behind a yellowish or hemorrhagic patch.

Simple erythema often is converted into the exudative form; the latter
is sometimes an intermediate stage, which leads to the formation of vesi-
cles and even of necrosis of the skin.

2. Erythema exsudativum is divided into three groups, according as
it depends on local, toxic, or general causes.

Exudative erythema from local causes has the same etiology as hyper-
8Bmic erythema, viz., injuries, heat, the action of caustic substances.

Toxic exudative erythema is that form which generally follows the
administration of medicinal agents, such as quinine, salicylic acid, anti-
pyrine, chloral hydrate, strychnine, digitalis, copaiba, opium (medicinal
exanthems). The redness of the skin is either diffuse or patchy, the

Satches being sometime^) more or less elevated. Some persons possess a
istinct idiosyncrasy with regard to such eruptions.
We will now discuss in detail the erythemata produced by general
causes.

1. Nettle Rash. Urticaria.

(Cnidosis.)

I. Symptoms. — Urticaria consists of the development of wheals (pom-
phi) on the skin. These consist of elevations whose surface is more ex-
tensive than their height, and which may attain the size of the palm of
the hand. They are either red or pale in the centre and surrounded by

820 DTFLAMM ATION8 OF THE SKIN.

a red periphery. They itch, and disappear very rapidly without desqna-
matiou, in rare eases are followed hy slight pigmentation.

The skin between the wheals may be normal or reddened. The
wheals often may be prodaeed bv irritating the intact skin with the naQ
or other hard substance. If a wlieal is pricked and compressed upon the
the sides, a little drop of clear or bloody serum exudes^ and the wheal
^ows distinctly smaller. This indicates that the process is the resnlt of
inflammatory transudation in the superficial layers of the cutis.

The wheals are sometimes so closely aggregated that they coalesce (artictria
conferta), or they are arranged in chain-like, but irregular rows (urticaria gyrala).
In rare cases, the wheals develop into tirm nodes (urticaria tuberoea) or form
small itchy papules (urticaria panulosa s. lichen urticatus). Finally, the ^idenili
over the wheals may be raisea lil» a vesicle (urticaria miliaria).

The wheals aie most abundant in the face and trunk, next on the
neck and limbs. On the lids, lips, and prepuce they are often associated
with distinct oedema of the skin. They may appear at night and diasp-
pear during the day.

Wheals may also form on the mucous membrane of the cheeks, uTiih,
epiglottis, and oesophagus. Trousseau^s experience that cutaneous nrti-
cana may alternate with asthma-like attacks arouses the suspicion that
the lower air-passages may also be attacked.

The eruption is preceded not infrequently by febrile, gastric prodro-
mata. The patients feel chilly, the oodily temneratnre is increased,
there is sometimes a peculiar feeling of anxiety and shortness of breatL
In addition, they suffer from anorexia, coated tongue, diarrbcea, or obsti-
nate constipation. At tlie end of a few hours or days, the characteristic
eruption appears. In some cases, the general symptoms appear after the
outoreak of the eruption; in others, tliey are rudimentary or entirely ab-
sent.

The subjective symptoms consist mainly of intolerable pruritni,
which is increased especially by warmth. In two cases, Leube obsenred
albuminuria during the eruption.

The individual wheals generally last a very short time, often onlyi
few minutes, but others are constantly sprouting up on other parts of
the integument. The entire eruption may last only a few hours, or it
continues for several days, or relapses occur at certain intervals, or finally
the disease runs an uninterrupted chronic course for several years.

II. Anatomical Changes. — In wheals produced in rabbits, J.
Keumann found anlema of the superficial layers of the cutis, swelling of
the lowermost cell layers of the rete Malpignii, and anaemia of the cutis
vessels. In wheals removed from the human subject, Vidal found dilata-
tion of the blood-vessels and lymphatics, and white blood -globules out-
side of tlie walls of the vessels, partly in groups in the meshes of the
connective tissue, partly between the cells of the rete Malpighii.

III. Etiology. — The causes of the disease may be external (local) or
internal.

The former include cutaneous irritants, such as contact with the
stinging nettles rhus toxicodendron, certain caterpillars and moUuscs,
the stings of insects (fieas, bedbugs, flies, etc.), application of Lister's
gauze, exposure to a cold wind, etc.

Many individuals possess such sensitive cutaneous nerves that, althoqgh they
do not suffer from urticaria, any desired figure upon the skin may be produosd

INFLAMMATIONS OF THE SKIN. 821

by contact with a hard substance (urticaria factitia). The irritated spot first be*
comes pale, then red, and finally a wheal develops.

Among the internal causes is the ingestion of certain dm^s and arti-
oles of diet. The mere contact of these substances with the oiiccal mu-
cous membrane is sometimes sufficient to produce the urticaria. This is
evidently the result of reflex nervous influences. The substances in ques-
tion include strawberries^ fat meats and sausages^ certain kinds of wine,
oysters, lobsters, mussels, herring, vinegar, etc., or quinine, antipyrine,
opium, chloral hydrate, arnica, cubebs, copaiba, turpentine, etc.

In other cases, the reflex irritation starts from the gastro-intestinal
mucous membrane (gastro-intestinal catarrh, worms').

Urticaria occurs not infrequently in diseases of the uterus and ova-
ries. It may appear at the menstrual period, or even take the place of
menstniation.

It is sometimes observed in general diseases (cancer, phthisis, dia-
betes, Bright's disease) and in infectious diseases (relapsing fever,
typhoid fever, measles, scarlatina, intermittent fever).

Urticaria is not infrequent in jaundice, as the result of local cutane-
ous irritants or of the violent itching and scratching of the skin. It has
been observed in several cases of puncture of hepatic echinococci and in
hepatic colic.

It may also be a prodrome of other skin diseases, such as prurigo and
pemphigus.

Urticaria is sometimes produced by direct nervous influences, for
example in individuals who have suffered from neuralgia, after violent
emotions, and also in hysteria.

The disease sometimes appears epidemically in connection with
epidemics of erysipelas. In not a few cases, no cause can be discovered.

Most authors are agreed that urticaria is an angioneurosis of the
skin, but it must not be forgotten that much is left unexplained by this
term.

IV. Diagnosis. — The disease can hardly be mistaken for any other,
but we must not remain satisfied until the special cause of the attack
has been discovered.

V. PBOQNOSis.T-Many cases recover in a short time. 3ut it must
not be forgotten that the chronic form of the disease may be severe,
often incurable, and may drive the patient to distraction.

VI. Tbeatment. — The treatment must first be directed towards the
removal of the exciting cause.

Not much can be expected from internal remedies; potassium bro-
mide, arsenic, ergotin, and atropine have been recommended. Oarbolic
acid in pill form acted well in some of our cases. In intermittent urti-
caria, quinine should be administered. Shoemaker cured a case of
chronic urticaria with sulphuric acid.

Oarbolic acid is the best external application; in a violent case., cool
compresses of a five-per-cent solution; m milder cases inunctions of car-
bol-vaseline (3ij. • 3xx.) or chloral hydrate ointment (3i. : 3xx.),
t. i. d. We may also apply ether, chloroform, eau de cologne, lemon
juice, or acetic acid.

The diet should be light, the clothing and bed covering not too
warm*

nm.uatATioKs or i

I. Stmptoms.-

i. Erythema Xodosum.

-la. thia disease, leJ, blnish-red or greenish nodes
appear first, aud in many caeea excluaivelv, upou the anterior surface of
the legs, their size varying from that o! a hazelnut to that of a fist.
The nodes are isolated, and the ekin over them is destitute of folds,
shining, and tense. They are warm to the fi-el and tender on pressure,
and the surrounding integument is slightly oelematous. Similar ones
occur not infrequently upon other parts of the limbs, more rarely on the
face, or eveu thu buccal mucous membrane.

1 ths

The development of the eflQorescence is sometimes remarkably mpid.
It begins either as hyperiemic patches, or aa red, wheal-like elevations,
which gradually increase in extent and height. Later they assume a
more hemorrhagic appearance, become bluish-red or green, then yellowish,
and finally fade away. In rare cases, slight desquamation is left over.

In exceptional cases, the nodes uudergo ulcerative degeneration. In others,
the inflammatory process results ia the production of vesicles and pustules.
Purpura and wheals are sometimee found in addition to the characteristic nodes.

The general condition is sometimes very little affected, and the
patient merely experiences u slight burning and pricking in the affected
parts.

The outbreak of the nodes is aometimes preceded by anorexia,
malaise, and febrile movement. The fever increases upon taeir appear-
ance and the patients often fall into a depressed and tearful mood.

Pains and slight swelling of the joints are observed very often, and
many believe that erythema nodosum and articular rhenmatism bear
intimate relations to one another. The articular affection is said to
give rise, at times, to ankylosis. Endocardial murmurs arc heard not
infrequently; they are either ansemic or febrile, very rarely organic in
character. The disease lasts three to four weeks, and almost always
ends in recovery. In a few cases, fatal pleiiro-pneumonia, inflamma-
tions of the serous membranes, and ulcerations of tlie mucous mem-
branes have been observed as complications. In one case it was followed
by miliary tuberculosis of the meninges. According to Oehme and
Uffelmann, it offers a certain predisposition to pulmonary phthisie;
according to others, it may he followed oy endocarditis.

II. Etiology. — The disease occurs moat frequently in yonngwomen,
and is not rare in childhood. The patients are often chlorotic and
feeble, or suffer from uterine diseases and. menstrual disturbances; it
sometimes takes the place of missed menses. Several cases have been
observed after folUmilar angina. It occurs often in scrofula, and also in
individnalB who come of phthisical families. It may also be associated
with syphilis, and Siiessmann observed the disease run its course under
the clinical history of quotidian intermittent fever. Recently I obsen-ed
two cases after acnte gonorrhtea, A certain predisposition to the disease
is created by ejhauating influences, such as protracted diseases. Ery-
thema nodosum sometimes appears in the form of an epidemic, {larticn-
larly in the autunin and spring, and in such cases is often associated with
herpes and erysipelas.

INFLAMMATIONS OF THE SKIN* 323

We regard the disease as an infectious process, in which the cutaneous
changes merely constitute one of the most striking symptoms. Its epidemic ap-
pearance and cyclical course, the severe constitutional symptoms, the intimate
relations to affection of the joints and perhaps to endocarditis, the simultaneous
occurrence of erysipelas and herpes, favor this view. Hebra regards the disease
as an inflammation of the cutaneous lymphatics. Bohn explains it as the result
of embolism of cutaneous vessels, and as identical with peliosis rheumatica.
According to Pardon, it is the result of vaso-motor disturbances.

III. Diagnosis. — The disease may possibly be mistaken for trauma-
tism^ small-pox^ scarlatina, syphilis.

The occurrence of nodes on symmetrical parts, the swelling of the joints, and
febrile general disturbance will serve to exclude trauma.

The di£ferentiation from small-pox may be difficult. It is important to know
whether variola is prevailing at tne time. But erythema nodosum is not often
attended with the formation of vesicles and pustules.

The disease cannot be mistaken for scarlatina unless carelessly examined,
especially as the cutaneous lesions of erythema nodosum are not dififuse.

Syphilis is recognized by the previous history, the presence of syphilitic cica-
rices and the results of treatment with mercury and potassium iodide.

IV. Peoonosis. — The prognosis is almost always good, except that
the deyelopment of nodes upon the respiratory mucous membrane may
proye dangerous, the joint affection may lead to ankylosis, and, accord-
ing to some writers, valvular lesions may be left over.

V. Tbeatment, — The ti*eatment consists of rest and nourishing diet;
quinine in case of fever. Struempel obtained good results with salicylio
acid. Local treatment is unnecessary, unless there is severe burning or
pain in the nodes. We may then apply compresses of lead water, lia.
ammon. acetici (5^), carbolic acid (2^), or may brush the nodes witn
collodion or iodoform ointment ( 3 i. : 3 xx.).

3. Multiform Exudative Erythema.

(Erythema Polymorphon. Erythanthema Essentials. Herpes Iris.)

1. Symptoms. — Multiform exudative erythema is closely allied to
erythema nodosum, but is more variable in its external appearances.

At first we find red patches, as large as a pea, which grow pale on pres-
sure; they gradually increase on size and become raised. They almost
always occur first on the dorsum of the hand and foot, then on the legs
and forearms, then on other parts. The mucous membrane of the
month, pharynx, and genitals may also contain raised hyperssmic patches,
which may eive rise to excoriations. In rare cases, the disease begins in
the face and extends downwards.

The larger patches and nodes soon become cyanotic and red, and
coalesce in part. They present transitions between blue, green, and
yellow.

After a while the patches often undergp further changes. While the
centre ^rows pale, the periphery remains injected (erythema annulare),
new, injected patches sprout up at the periphery, or finally adjacent
efflorescences coalesce and form twisted, garland-like figures. If the
erjrthema retains its nodular form, it is known as erythema papulatum
8. tuberculatum.

In addition, we sometimes find wheals, purpura, vesicles, and pus-
tules. The nodes at the periphery are sometimes surrounded by a ring
of vesicles (herpes iris).

3M vm^AJDurmsB op the skis.

In mmT ctteCy tlie diteue rans m trpicml cooTse, and is often pre-
ceded bj tiie prodiomatm described in the oonsideratioii of erythema
nodosnin. A riie of tempentoie feren mbove 40^ C.) sometimes cod-
tinaes for a certain lens^th of time alter the deTelopment of the catute-
ou£ changes. Anicamr changes maj oocor, and likewise sniemic,
febrile, rarelv omnic, cardiac mnimnis. Enlargement of the liyer sod
spleen has been obserred, sometimes complications with pleurisy^ pneu-
monia« albnminnria, and renal hemorrhage. The subjectiYe symptoms
are generailj trifling: slight homing and pricking in the nodes.

As a rare, the disease lasts from one to two months; Lippe reports a
case of eight months' doration. A fatal termination is exceptional.

II. Etiology. — ^The disease occurs mainly in yoimg women who
suffer from chlorosis^ menstrual disturfaances, or uterine diseases. A
predisposition is also created by syphilis or cachexia.^ Lewin observed
the disease frequently in women suffering from urethritis.

In oar opinioD, this disease, like etjtb e ma nodosum, is infections. like the
bitter, it oocurs in epidemics in the spring and antnmn, but in some individoab
the disease returns at certain seasons of the year.

IV. Diagnosis and Tbbatxext. — ^The same mistakes are possible
that have been mentioned in describing erythema nodoeum. The trest-
ment is also similar to that of the latt^ disease.

4. Acrodfnta.
{Erythema Epidemicum.)

In 1828 to 1830 this disease was observed as an epidemic in France, and it is
also said to occur in the Orient.

It often began with gastro-enteritic symptoms: nausea, Tomiting, anorexia,
colic, and diarrhoea. An erythematous inflammation then appeared^ fint upon
the hands, later extending along the limbs to the trunk. The formation of
wheals and vesicles has also been noticed. The skin then deeqaamated and left
behind a deep dark color, particularly over the chest and abdomen. In addition,
disturbances on the part of the nervous system: a feeling of formication, tremor,
Mral^^sis of the limbs and bladder. Ophthalmia was a frsquent complioationL
Duration of the disease, several weeks or months; fatal termination nol infrS'
quent. It is probably the result of poisoning with spoiled grain.

5. PeUdgra.

I. EnOLOOT.^The disease is endemic in certain parts of Spain, France, Boa-
mania, but particularly in Northern Italy. In Lombardy, for example, nK>re than
thirtv per cent of the population have been attacked. In 1879, nearly 96,000 in-
dividualn were attacked in Italy, nearlv 41,000 in Lombardy alone. The disesse
also occurs sporadically in other locabties.

Among the Italians the disease occurs only amon^ the rural population, and
almost always among those who use maize as an article of diet. Some attribate
the disease to the non-nitrogenous character of maize, but it must be remembered
that pellafi:ra is sometimes absent in certain districts, despite the almost exdosivs
use of maize as an article of food. Others state that in tne affected districts, the
maize employed is unripe and mouldy. Attention has been called to the fact thst
the disease does not prevail in those countries in which maiae Is used only when
dried. Opinions also differ as to whether the disease is prodnoed by certain fimgi.
or by noxious chemical substances.

According to these views, the disease belongs to the same catemry as thoss
produced by the ingestion of spoiled cereals. But it is said thiUpellagia may de-
velop in those who never come in contact with maize, so that it is looked npoa
bv some as the result of poor nourishment and bad surroundings. It is *^*^ daimedJ
tnat the disease i^ hereditarv.

nO'LAMMATIONS OF THE 8KIN. 325

n. Symptoms. — The chief symptoms are cutaneous changes, disturbances of
digestion, and nervous disturbances. The disease is generally chronic and may
last ten to fifteen years.

The first symptoms begin in April to June, and subside in autumn, to reap-
pear more severely in the following year.

On those parts which are exposed to the sun, erythematous patches develop;
these desquamate at a later period, and leave behind a dark olive discolorariun.
The skin becomes fissured ana covere<l with ulcers, crusts, and nodes. The mucous
membrane of the mouth and the nails become diseased. The patients Auflfer
from fever and diarrhoea, complain of formicAtion in the hands, muscular tre-
mor, paralysis. Ptosis, hemeralopia, and diplopia make their appearance. The
patients are profoundly depressed and insanity may develop. Dt^ath occurs finally
irom increasing exhaustion.

III. Anatomical Changes. — ^These are practically unknown.

IV. Treatment.— Recovery can be looked for only at the onset of the dis-
ease. We shouM order j2:ood food, ariienite of potash and acetate of potash.
Qood results are also said to liave been obtained from sulphur waters and baths.

J. Vesicle-like Inflammations of the Skin. Debmatitides

VESICULOSiE.

1. Eczerna*

J. Etiology. — The causes of eczema may be local or general.
The local causes may be mechanical^ thermal^ or chemical.

The mechanical causes include obstinate scratching and rubbing the skin (in
itching skin eruptions, such as prurigo, puritus, or urticaria, in scabies, wearing
a rough hat, stiff collar, suspenders, etc.); constant friction of two opposed sur-
faces of the skin; finally, the eczema of the lower limbs produced by varicose
veins.

Eczema caloricum often develops in the summer upon those parts of the in-
tegument which are exposed to the sun.

The (proup of chemical causes is very large. Thus, cutaneous applications of
turpentine, croton oil, mustard, tartar emetic, mercurial and iodine preparations
may give rise to eczema. In certain individuals eczema is produced even by the
application of bland ointments. It is also observed in those who work in irritat-
ing substances (washerwomen, bakers, book-binders, mirror-polishers, etc.). It
also occurs from wearing underclothing colored in poisonous dyes, particluriy ar-
senical aniline colors.

Among the eczemas of chemical origin must be included those produced
by constant contact with perspiration, as in the axilla, inguinal folds, etc. It
may develop on the lobe of the ear, as the result of discharge from the ear, on
the evelids, as the result of profuse lachrymation in conjunctivitis, on the upper
lip after coryza, on the genitals after leucorrhcea. It is not infrequent upon the
nates of infants who suffer from diarrlioea, and in whom the buttocks are for a
longtime in contact with the diarrhoeal stools.

Symptomatic eczemas include those which are the result of internal
diseases. There is danger, however^ of mistaking an accidental compli-
cation as an etiological factor. Thus^ the closeness of the relation be-
tween rickets or scrofula and eczema has been overestimated. It is
known that patients suffering from Bright's disease and diabetes often
suffer from obstinate eczema^ and gastro-enteritic diseases and uterine
affections often present the same complication. In some women^ eczema
oconra with a certain regularity at the menstrual period, in others it de-
velops during each pregnancy. Violent mental excitement is occasion-
ally meiitioned as a cause.

Eczema is somewhat more frequent in the male sex. Age possesses
little influence^ except that the disease is rare before the age of six
months. The influence of heredity is not proven, nor does the disease
possess contagious properties.

Some individuals manifest a predisposition to eczema. It develops

826 INFLAMMATIONS OF THE SKIN.

in them after very trifling causes, and local causes produce it in a reflex
manner in parts not directly attacked.

ir. Symptoms and Diagnosis. — The outbreak of eczema is pre-
ceded not infrequently by prodromata, particularly if the eruption is not
the result of local causes. The patients feel chilly and weak, look pale
and exhausted, and have slight fever. These symptoms generally sub-
side with the outbreak of the eruption, but reappear at each relapse or
exacerbation.

Eczema results in the production of an itching eruption, which is
more often chronic than acute. It may appear in the form of closely
aggregated, irregularly distributed, pale-rea or dark-red papules (eczemi
papulosum), of small vesicles (eczema vesiculosum), or of pnstales
(eczema pustulosum). The skin may be red and moist (eczema rubrom
et madidans); or the vesicles rupture, and their contents dry into thin,
honey-yellow, rubber-like crusts (eczema crustosum); or the pustules
are converted into thick, grayish-green or brownish- red cmsts (eczemi
impetiginosum); or, finally, the integument is red, but does not weep,

and is covered with thin, numerous scales (eczema squamosum).

All these forms are different stages of the same fundamental process. Thii is
shown by the simple experiment of applying an irritant, such as croton oil, to the
skin. Mild action of the oil produces erythema, at first hypersemic, then exuda-
tive ; stronger action results m eczema papulosum. If the irritant acts still more
vigorously, serous, later purulent vesicles develop on the papules (eczema vesico-
losura and pustulosum) ; when their contents dry, eczema crustosum and im-
})etiginosum result. If the crusts fall off, a reddened, weepini^ cutis often appears
(eczema rubruni et mudidans). As the process heals, the weepinp^ ceases, and
fine scales form (eczema squamosum). If the irritant action is slight, eczema
papulosum alone is produced. If the irritation is very intense, the preceding
stages may l>e skipped, and eczema vesiculosum or pustulosum forms at once.

The various stages of development are sometimes found side by side in the
same individual.

Eczema may be partial or general (rare), acute (duration, two to
eight weeks), or chronic.

Eczema of the scalp (eczema capillitii) appears commonly in the form
of impetiginous or squamous eczema. In the former we find thick, pray-
ish-green or dirty-brown crusts, intimately adherent to the hairs. They
are mixed with sebaceous secretion, and may diffuse a sour, rancid smell.
If not kept clean, the scalp is apt to harbor lice, and, on the other hand,
lice may give rise to impetiginous eczema. In such cases, the occiput
and parietal regions often present prominences which, npon removal of
the crusts, discharge green, creamy pus. The presence of pediculi is
also shown by the nits on the hairs. In filthy individuals, the hairs
may be matted together into an inextricable mass, containing crusts,
innumerable lice and nits, and give rise to a pestilential stench (plica
polonica).

Impetiginous eczema may be circumscribed or involve the entire
scalp, and may also extend to the forehead, ear, and neck. The ad-
jacent lymphatic glands are very often swollen.

In infants, impetiginous eczema of the scalp may be secondary to
seborrhoea, the secretion decomposing and irritating the scalp.

If tlie crusts are removed, the corium appears reddened and weep-
ing. When recovery takes place, the weeping ceases, and the reddened
surface becomes covered with fine, white scales (eczema squamosum).
In some cases, eczema squamosum develops as such. It is an annoying

INFLAMMATIONS OF THS 8Km. S27

and often obstinate affection, the scalp being always coyered with more
or less numerous white scales.

Ecsema of the scalp is distinguished from seborrhoea by the fact that, in the
latter, after removal of the crust the surface is not red or weeping, the glands
are not swollen, and the disease does not extend beyond the scalp. It is dis-
tinguished from favus by the absence of spores in the crusts, and of the sulphur-
y^low color, plate-like snape and peculiar smell of the favus crusts. Psoriasis
of the scalp is associated with characteristic patches of psoriasis in other parts
of the body.

Eczema faciei may extend over the entire face or be confined to cer-
tain parts. ' Diffuse eczema is not infrequent in infants beyond the age
of fire months. It generally appears as eczema crustosum or eczema
mbrum et madidans. In the former^ the face is covered with light-yellow
crusts, which are often so closelj aggre^ted as to form a sort of mask;
in the latter^ the face is red^ moist, and sticky. The fluid is alkaline
and very poor in cellular constituents. Eczema crustosum is often
found in some parts of the face; eczema rabrum et madidans, in other
parts which are on the way to recovery.

Eczema of the ear is apt to attack the posterior surface of the concha;
it appears generally as eczema crustosum or impetiginosum. The
concna is often very much swollen, and the swelling of the external
auditory canal may interfere with audition. £czema is often compli-
cated with otorrhoea, or the former creeps along the external auditory
canal. In some cases, the otorrhoea is primary, and gives rise to eczema.
The latter often leaves behind deep and painful rhagades, which are
sometimes covered with a gray, lardaceous coating, and emit a foul odor.

Eczema nasi affects the nostrils or the nasal mucous membrane. The
nostrils are sometimes occluded by crusts, so that the patients are forced
to breathe through the mouth. Snoring, stenotic sounds are produced
on attempting to breathe tli rough the nose. This condition is not de-
void of danger in the new-born and nurslings, and may give rise to
venous stasis, cyanosis, and pulmonary congestion. In not a few cases,
moreover, the aisease is the starting-point of facial erysipelas. If the
eczema attacks the outer integument of the nose^ very painful fissures
may form in the naso-labial folds.

Eczema labiorum often gives rise to considerable swelling and de-
formity of the lips; they are thickly covered with brown or bloody
crusts,* and contain numerous painful, bleeding rhagades.

Eczema superciliorum and eczema palpebrarum produce great de-
formity. In the latter, the free border of the lid is not infrequently
affectea, and there may be secondary blepharitis.

Eczema barbce (usually pustular or impetiginous) is still more annoy-
ing. Unlike sycosis, it very often extends beyond the beard. The two
diseases are apt to be mistaken if the eczema extends to the hair folli-
cles, and allows the hair to be readily removed with the tweezers.

Eczema nuchce usually extends from the scalp. It often occurs inde-
pendently in fat babies, in whom it develops between the horizontal
folds of skin as the result of friction. If cleanliness is not enforced,
these parts may undergo gangrene and ulceration^ and, in rare cases,
death has occurred in collapse or eclampsia.

Eczema mammm is more frequent in women than in men. In stout
women, eczema intertrigo develops not infrequently under the folds of
the breast. In nursing women, eczema often occurs around the nipple.

828 OTFLAMHATIONS OF THE BKIK.

and is frequently associated with very painful rhagades. Very MTere
eczema may extend to the mammary gland, and give rise to mastitis.

Eczema umbilici is observed particularly in obese indiyidoals, and is
extremely obstinate.

Eczema of the genitals occurs in both sexes. In males, it attacks tli»
scrotum and dorsum penis, while the glans and inner surface of the pre-
puce escape. The scrotum is affected particularly in those parts whicli
are in contact with the thighs. The disease may be associated with
marked inflammatory oedema, so that the scrotum and penis are swollen
and misshapen. After it has lasted a long time, the sKin may undergo
thickening and deform the genitals. The inflammation often extends
to adjacent parts of the integument.

In women, the labia majora and mons yeneris are most freqaentlj
affected, but the eczema sometimes extends to the labia minora and
even to the vagina, giving rise to pruritus and secondary leacorrhosa. In
other cases, leucorrhoea causes secondary eczema of the external genitals.

Eczema ani is annoying from the intolerable itching, and may gire
rise to painful rhagades, muco-purulent inflammation of the rectum, or
prolapsus ani.

Eczema extremitatum is found not infrequently upon symmetrical
parts of the limbs. In eczema of the folds of the elbow or the popliteal
spaces, rhagades often form and interfere with the movements of the
upper or lower limbs. The disturbances become still greater if the
extensor and flexor surfaces are affected at the same time.

Eczemxi interdigitale is extremely annoying, and, if pustnlar in char-
acter, may be mistaken for scabies. Eczema digitorum sometimes
affects only certain parts of the fingers; if the tips are attacked, the
patients generally complain of formication in the fingers. The nails are
sometimes involved, and may be exfoliated.

Eczema voice manu?n often produces epidermoidal thickenings and
deep-red, bleeding, or weeping rhagades. It may be mistaken for
psoriasis, but in this affection patches of psoriasis are present in other
parts. Eczema vesiculosum and pustulosum are also found here, but,
as a rule, the thick epidermis interferes with the production of fully
developed vesicles.

Eczema antibrachiorum appears not infrequently as a papular or
vesicular variety, in the former, the skin is rod, hot, and covered with
numerous flat or pointed elevations; in the latter, it presents vesicles
filled with fluid. Both forms occur not infrequently in harvest time as
eczema caloricum. I have also observed them as the result of contact;
with rhus toxicodendron.

In Eczema anticrurium, the reddened skin feels sticky, and is cov-
ered with very fine, clear drops. The fluid stains the underclothing
yellow, and stiffens it. In tlie process of recovery, there is often a
transition to scjuamous eczema.

Eczema universdo is rare. In many cases, the term may not be used
literally, since some ])arts of the skin are intact.

In the majority of cases, eczemas disappear without leaving sequelaB.
If very persistent, they may reduce the patient on account of the loss of
appetite, and the disturbance of sleep caused by pruritus. Chronic ec-
zema is sometimes followed by albuminuria; but, on the other hand,
nephritis may also give rise to eczema.

III. Anatomical Changes. — The same anatomical changes are

IBFLAMMATIONS OF THE SKIN. 329

found as in the formation of papules^ vesicles^ and pustules in other
eruptions.

In papular eczema are found: dilatation of the vessels in the upper
layers of the cutis, serous exudation, emigration of white blood-globules,
a^d swelling of the cells of the rete Malpighii. In vesicular eczema, the
epidermis is separated in places from the rete Malpighii by the inter-
position of serous fluid. The vesicles are not infrequently multilocular^
the septa being composed of flattened cells of the rete Malpighii, which
have been pressed together, if numerous round cells enter the serous
contents, pustular eczema develops. The pus-corpuscles are derived in
part from the vessels of the cutis, in part from the cells of the rete Mal-
pighii. A complete restitutio ad integrum may take place, but, in
chronic cases, the cutis is unusually rich in cells, thickened, the blood-
vessels and lymphatics are dilated, the sebaceous glands and hair follicles
have partly disappeared, the sweat glands degenerated. Occasionally
there is infiltration of the subcutaneous cellular tissue with round cells^
and unusual pigmentation of the deeper layers of the rete Malpighii.

IV. Prognosis. — The prognosis, as regards complete and permanent
recovery, is only unfavorable if the disease is the result of incurable con-
stitutional causes.

V. Treatment. — The treatment depends mainly on the etiology.
If the disease is the result of local injuries alone, local remedies alone
are indicated.

In papular eczema, characterized by redness and heat of the skin, we
may apply cool compresses of liq. alumin. acet. (1^), aqua plumbi or
aqua plumbi Goulardi and water aa. To relieve violent itching, dust tho
parts at night with carbol-vaselin (1 : 15). If the pruritus is not severe,
apply some dusting powder twice a dav, for example, 3 Flor. zinci, Sem»
lycopod., aa 3i.; Amyli, 3iv. M. D. 8.

As a general thing, vesicular and pustular eczema re<}uire treatment
with bland oils or ointments, for example, the application of ol. olivsB,
ol. amygdal., or unguent, simplex, etc.

In eczema crustosum or impetiginosum, the crusts must first be
removed. This may be done by frequent application of the above-men-
tioned oils for two hours, or the application to the skin of a piece of
flannel dipped in oil.

After the crusts are removed, the eczema is thus converted artificially
into an eczema rubrum et madidans, and may be treated as such. In
our opinion, the best ointment hitherto recommended in this disease is
ung. diachylon Hebrss; if the itching is violent, it may be mixed with
can>olic acid (1 : 60), if there is profuse weeping, with tannic acid
(3 : 50). The ointment is smeared on pieces of old linen, and carefully
applied with a flannel bandage. Unna impregnates mull with the oint-
ment« and applies this directly as a bandage.

The number of ointments recommended in eczema is legion. Niemeyer extols
white precipitate ointment as an almost sovereign remedy, and also obtained
good results from corrosive sublimate (1 : 800). Lead and zmc ointments, oint-
ments of nitrate of silver, subnitrate of bismuth, etc., are also recommended.

In squamous eczema, the skin should bo anointed several times a day
and strewn with the previously 'mentioned dusting powder. In very
obstinate cases, tar preparations may be employed. 01. rusci or ol. fagi
et ol. oliv. flfi may be applied once a day, so long as the scales are freely
desquamated, "f hen tne applications may be made at longer intervals^

830 IKFLAJC1CATION8 OF THE BON.

but must be continued until the formation of scales ceases. In marked
infiltration and thickening of the skin, good results are obtained from
Aoap inunctions or applications of caustic potash (1 : 2 of water). The
latter is applied once a week, and followed immediately bj cold compressM
to relieve the pain.

Indifferent baths and cold-water cures are useful in some cases.

If rhagades have formed behind the ear, salicylated cotton smeared
with ointments may be applied. In eczema of the nose, tampons
smeared with ointments should be introduced several times a day. In
eczema of the scrotum, a suspensory bandage must be worn. In eczema
of the rectum, suppositories containing oxide of zinc or tannic acid niBj
be introduced.

The internal remedies include iron, iodine, and arsenic^ according to
the constitutional condition of the patient.

2. Miliaria.

Miliaria forms small, scattered vesicles which are transparent and
•clear (miliaria crystallina), or are surrounded by a red zone (miliaria
rubra), or present a cloudy, almost purulent appearance (miliaria alba).
They occur exclusively or chiefly on parts which are covered by clothing,
and are almost always the result of increased production of sweat
(sudamina).

The eruption appears in healthy individuals after profuse sweating
in hot weather, or is produced artificially by sweat cures and cataplasms.
It often develops during the crisis of acute febrile diseases. It is fre-
quent in acute articular rheumatism, in the stage of recovery from typhoid
fever, in phthisis, miliary tuberculosis, pyaemia, puerperal fever, measles,
scarlatina, small-pox, the cold sweats of cholera, and even in agonal
sweating.

A very trifling increase of cutaneous perspiration will produce sudamina in
some individuals. On account of the varying irritability of the skin, miliazia
<;ry3tanina persists as such, while in others, it is rapidly converted into the two
other forms. Sometimes, indeed, miliaria crystaUina remains almost entirelj
absent.

Miliaria crystallina forms clear vesicles, varying from the sixe of a
millet seed to tnat of a pin's head; in rare cases a few attain the dimen-
sions of a pea. When punctured, they discharge a clear fluid of a neu-
tral or feebly alkaline reaction. The smallest vesicles are often better
felt than seen. Sometimes there are thousands of vesicles on the skin,
in other cases only a few. They sometimes disappear very rapidly.
The fluid evaporates, the epidermis sinks in, forming small white ele-
vations, or the vesicles rupture and the superflcial layers of the epi-
dermis are cast off. The eruption gives rise to no notable symptoms, at
the most to slight pricking and itchinff. In some cases new outbreaks
continue to form, so that the eruption lasts several days or weeks. In
not a few cases it passes into

Miliaria rubra, — The contents of the vesicles become cloudy and a
red zone forms around the periphery," as the result of decomposition of
the vesicular contents and irritation of the deeper layers of the skin.

If the cloudiness increases and the red zone disappears, miliaria alba
is the result. Both forms heal by desiccation of the contents of the ves-

INFLAMMATIONS OF THE SKIN. 331

idea and dosqaamation of the superficial epidermis. Treatment is un-
necessary.

Haigkt's examinations show that the vesicles are situated above the
Biccretorj ducts of the sweat glands, and consist of elevation of the stra-
tum corneum. The^ are the result of occlusion or insufficient calibre of
the excretory ducts m question.

c. Vesiculab Inflammation of the Skin. Debmatitis Bullosa.

Pemphigus,

{PomphoUx.)

I. Symptoms. — The chief symptom of pemphigus is the occurrence
of vesicles upon the skin, varying from the size of a pea to that of the
palm of the hand or eyen more. The contents of the vesicle are, at first,
of a wine-yellow color, transparent, serous, and of neutral reaction; later
they become alkaline, cloudy, and pus like. The vesicles either rupture
spontaneously, laying bare the red weeping corium, which is gradually
covered with epidermis, and leaves behind a red, later brown patch; or
their contents dry into thin yellow, brown or blackened crusts which fall
off.

Cloeel^r aggregated vesicles are known as pemphigus confertus, isolated ones
as pempm^s disseminatus. In very rare cases only a single vesicle forms (pem-
phig^ solitarius). If the vesicles are arranged in rows, the term pemphigus
gjrratus is applied; if young vesicles form around an older one, pemphigus
circinatas. vesicles whose contents have a bloody color are called pemphigus
hemorrhagicus.

Vesicles have also been observed upon the mucous membrane of the
lips, cheek, pharynx, nose, epiglottis, bronchi, vagina, gastro-intestinal
tract, and conjunctiva. The development of vesicles upon the epiglottis
may lead to fatal oedema of the glottis, and it is also claimed that pem-
phigus of the gastro-intestinal mucous membrane may be followed by
perforation.

Three varieties of pemphigus have been distinguished, viz. : pemphi-
gus acutus, chronicus, and foliaceus.

a. As a rule, acute pemphigus does not last more than a month. It
is more frequent in children than in adults; and may be epidemic in
maternity hospitals. As a rule, the first vesicles appear, in the new-
born, from the fourth to the ninth days. A number of cases of direct
contagion have been observed. It has also been found that when a large
number of cases occurred in a town, the children had been cared for by
a certain midwife. Inoculations with the contents of the vesicles, how-
ever, almost always are followed by negative results. Cases have been
observed in which the disease ran a febrile course and terminated fatally,
generally as the result of complication with pneumonia or gastro-enter-
itis.

Acute pemphigus may also occur in adults, but rarely runs an apyrex-
ial course. The eruption is often preceded for one to tnree days by pro-
dromata, viz., general malaise, anorexia, disturbed digestion, chill and
fever. The temperature increases with the appearance of the eruption,
and mav recur at each new outbreak. AVo often notice ervthematous
and nrticaria-like places, upon which the vesicles form. The vesicle is
often surrounded by a red zone, gradually increases in size and becomes

332 INFLAMHATI0K8 OF THE SKIN.

tense, causes a disagreeable sensation of tension. It finally bursts or
dries, .while new ones form in other parts.

Vesicles in the mouth produce pain and fcetor ex ore; the buccal mu-
cous membrane appears macerated in places. In pemphimis of the bron-
chi, membranous structures are sometimes expectoratea (vide YoL L,
page 223).

Cardiac murmurs, enlargement of the spleen, ocK^asionally albumina-
ria and hsematuria have been observed as complications.

b. Chronic pemphigus lasts months and eren years. In some cases
the eruption continues uninterruptedly, in others there . are periods of
health followed by relapses. The disease may be entirely apyrexial, or
there are temporary elevations of temperature. The patients may rad-
ually grow very feeble, Bright's disease and waxy degeneration oi the
large abdominal glands may develop, and finally the patients may die
from f^eneral marasmus. Stokes reported one case of exfoliation of all
the nails following pemphigus of the fingers, and another case in which
the vesicles appeared upon the scalp. A fatal termination is almost inr
evitable if the disease is converted into:

c. Pemphigus foliaceus. This form may also develop as such from
the start, and Behrend described an epidemic of this kind in the neir-
born.

In pemphigus foliaceus, as a rule, the vesicles are small and flaccid,
so that the epidermis upon them appears wrinkled. When the vesicle
bursts, new skin does not form, so that new vetoxoles continually recur,
and the corium is laid bare more or less extensively. Hebra also ob-
served a necrotic (diphtheritic) deposit upon the exposed corium. The
disease almost always terminates fatally with the symptoms of increasing
exhaustion.

II. Anatomical Changes. — Recent vesicles are multilocular, the
septa consisting of agglomerated scales of epidermis; older vesicles are
unilocular. Upon the inner surface of the raised epidermis, there are
often small appendages which correspond to follicles. The cells of the
rete Malpighii are often broken up into granular masses, and the pa-
pillae infiltrated with round cells.

In one caso oC pemphigus foliaceus J. Neumann observed dilatation of the
sweat glands.

On perforation of the vesicles, the fluid almost always discharges
readily, but Kuester reported a case in which some of the vesicles con-
tained a gelatiuus mass which was not discharged. The fluid contains
changed white and red blood-globules, the remains of epithelium cells,
granular detritus, and schizomycetes. In our opinion, however, the
presence of the latter does not justify a conclusion as to the parasitic na-
ture of the disease.

The chemical constitution of the fluid does not differ essentially from that of
vesicles produced by a burn or a fly blister. Urinary analyses also give negative
results.

III. Etiology. — The disease is more frequent in children than in
adults, and in men than in women. Heredity has been occasionally no-
ticed. It has been observed during pregnancy or the puerperal condition.
Some cases are contagious in their origin. They may occur in infec-
tious diseases, viz., pyaemiii, puerperal fever, ulcerative endocarditis.

INFLAMMATIONS OF THE SKIN. 838

scarlatina, measles, small-pox, intermittent fever, and syphilis. Syphi-
litic pemphigus occurs almost always in children. It appears mainly,
sometimes almost exclusively, on the soles of the feet and palms of the
hand. The eruption is sometimes present at hirth or in still-born babes.
Toxic pemphigus sometimes follows the administration of potassium
iodide or bromide, and salicylic acid.

IV. Diagnosis. — The aiagnosis is generally easy. It may be mis-
taken for malingering (action of blisters), burns, eczema, herpes iris, im-
petigo, urticaria bullosa, and erythema bullosum.

Baerensprung detected intentional f raad bv finding, with the microscope, bits
of the win^ of tne Spanish fly upon the 'vesicles.

The vesicles of bums are recognized by the previous history.

Eczema produces smaller vesicles, and the ^neral condition is unaffected.

The differential diagnosis from herpes iris is extremely difficult at first, but is
decided b^ the subsequent history.

In urticaria bullosa the itching is intolerable and wheals are also j^resent.

In erythema bullosum we also find characteristic firm nodes which are not
covered with vesicles.

V. Pbognosis. — This depends upon the nature and etiology of the
disease. In pemiphigus foliaceus recovery is rare, in the acute form it is
the rule. In chronic pemphigus the prognosis becomes serious if ex-
haustion and albuminuria make their appearance.

VI. Tbeatment. — Prophylaxis is important in some cases, particu-
larly in pempliigus neonatorum (isolation of affected infants, avoidance
of too hot baths, etc.).

Little can be expected from the administration of internal remedies.
Iron, quinine, arsenic, iodine, acids, etc., have been tried.

If the patients complain of pain in the vesicles, the latter should be
punctured and powdered with :

5Flor. zinci,

Semin. lycopod &S.3i-

AmyU/..! 3v.

M. D. S. To be used as a dusting powder; or the vesicles are covered

with linen which has been smeared with carbolized oil, carbol-vaseline,

etc. In addition, wo may give a dailv lukewarm bath (30** B.) containing

5 x.-xvi. of soda, or a corrosive suolimate bath ( 3 i'-iij») every other

day* In pemphigus foliaceus permanent baths may be recommended.

In other respects symptomatic treatment.

d. PusTULAB Inflammations of the Skin. Dermatitides

PUSTULOSJE.

1. Impetigo and Ecthyma,

I. StMPTOMS AND ETIOLOGY. — The terms impetigo and ecthvma
are applied to eruptions consisting of scattered pustules; secondary
crusts are still more frequent than the pustules.

The term impetigo was formerly applied to pustules which do not exceed the
size of a pea, ecthyma to larger ones, but there are such numerous trandtions
between the two that the distmction has been abandoned.

Hebra showed that in the large majority of cases, impetigo and
ecthyma are symptoms of underlying processes.

334 INFLAMMATIONS OF THE SKIN.

Their causes may be local (idiopathic) or general (symptomatic).

The local causes^ like those of eczema, are mechanical, thermal, or
chemical (vide page 325).

Among the general causes are pyaemic processes, syphilis, glandeni,
and post-mortem wounds; also protracted, exhausting diseases, particu-
larly typhoid fever.

Impetigo sometimes occurs in healthy persons without any demon-
strable cause, lasts one to two weeks, is accompanid by fever, and then
disappears entirely. The disease here develops idiopathjcallv. This it
also true of the contagious impetigo of Tilbury Fox, and the herpeti-
form impetigo of Hebra.

In contagious impetigo, pustules first appear upon the face, then
upon the scalp, neck, trunk, and limbs, in a lew cases upon the buccal
mucous membrane and tonsils. The pustules dry up and form crusts,
and the latter fall off without leaving a cicatrix.

The eruption is sometimes preceded by febrile prodromata, and the
fever lasts several days after the outbreak of the eruption. As a rule, it
recovers spontaneously by the end of the second week, often earlier,
sometimes not until the sixth week. Unna observed several relapses.

A number of epidemics have been observed and several nnaoubted
cases of infection. Several writers performed successful inoculatiou
with the contents of the pustules, even upon the affected individnaL

The contents of the pustules contain pus-oorpuscles, epithelium cells ani
Rranular detritus. Micrococci have also been found. Kaposi observed higher
Fungi with fructification organs, and regards the disease as i>araaitic. Other
writers could not confirm these results.

Impetigo herpetiformis was first observed by Hebra in five cases
in pregnant women or soon after delivery. Recovery occurred only in
one case. The following was the clinical history:

The eruption began on the inner surface of the thighs, and then ex-
tended to the anterior surface of the abdomen; the face and limbs, even
the tongue, were sometimes attacked. Groups or circles of pustules first
appeared and dried into crusts; these were followed by new crops in the
vicinity. Upon removal of the crusts a reddened, weeping, but never
ulcerated surface was exposed; it was sometimes covered with a smeary,

frayish-white deposit, which occasionally emitted a disagreeable odor.
Proliferations were sometimes observed upon the affected integument.
The eruption and also subsequent relapses were precedea by chills
and elevation of temperature. Bloody diarrhoea was observed occasion-
ally. Death occurred from increasing exhaustion.

II. Diagnosis. — The diagnosis is easy. It is important to distin-
guish between ordinary and syphilitic impetigo. In the latter, other
signs of syphilis are generally present, and, on removing the crusts, we
find a deep, crater-like loss of substance covered with a grayish-yellow
mass; in ordinary impetigo, the loss of substance is confined to the
epidermis.

Contagious impetigo is distinguished from impetiginous eczema by
the absence of itching.

III. Pboqnosis. — This depends upon the etiology. In conti^oos
impetigo, it is very good; in the herpetiform variety, it is almost always
fatal.

IV. Tbeatment. — The treatment must first be directed against tho

INFLAMMATIONS OF THE SKIN. 335

primary disease. In addition^ the crusts should be thoroughly oiled,
and, after their removal, the affected parts treated with bland oint-
ments.

2. Acne Vulgaris.

( Varus.)

Acne vulgaris is an inflammation of the sebaceous glands, and in
places of the hair follicles, which gives rise to the formation of red papules>
nodes, and pustules. It is divided into five classes, viz., acne dissemi-
nata, frontalis, cachecticorum, syphilitica, and artificialis.

a. Acne disseminata is a very wide-spread affection. It is very rare
in childhood, but almost always begins at puberty and often lasts for
years.

The eruption is most profuse and constant on the forehead, chesty
and back, rarer on the arms and thighs; the soles of the feet and palms
of the hand always escape (absence ox sebaceous glands). Arlt observed
acne of the conjunctiva.

Seborrhoea and the formation of comedos are generally observed at
the same time. Indeed, the latter gives rise in many places to acne,
because the stasis produced by the comedo results in innammatory irri-
tation. In the mildest form we find little red papules, in the middle of
which is a black comedo (acne punctata), in otner places a pustule has
formed upon the nodules (acne pustulosa). The inflammation extends
not infrequentlv to the adjacent cutis, and forms red, very painful nodes,
from the size oi a pea to that of a bean (acne indurata); in many casea^
pus does not escape until the scalpel is introduced very deeply. The
papules, nodes, pustules, and comedos may be so numerous as to cause
great deformity. Exacerbations and remissions are noticeable.

The nature of the etiological relation between puberty and acne is
entirely unknown.

On microscopical examination, the excretory portion of the sebaceous
follicle is found occluded by thickened sebum, the gland itself is dilated
and filled with fat granules, cellular detritus, and pus-corpuscles. The
adjacent cutis is congested, and more or less infiltrated with round cells.
If lateral pressure is exercised upon the acne, the plug of sebum with its
black heaa first appears, and is followed by milky or purulent, pasty or
more fiuid contents.

b. Acne frontalis is distinguished from acne disseminata, as regards its
mode of development, by the fact that it is not preceded by the forma-
tion of comedos. It occurs exclusively on the forehead, particularly
near the hair. The papules or pustules are fiat, and often carry a small,
central crust. This is deeper than the periphery of the nodule, so that
the latter forms a sort of wall. When the crust drops off, a slightly de-
pressed cicatrix remains.

c. Acne cachecticorum develops after long protracted and exhausting
diseases; it is associated not infrequently with pityriasis tabescentium
and lichen scrophulosorum. It is probably produced by hyperplasia of
the epithelium of the sebaceous follicles, as the result of cachexia with
subsequent inflammatorv irritation.

d. Acne syphilitica (vide article on Syphilis, Vol. IV.).

e. Acne artificialis. The best known form is tar acne, produced by
local applications or by inhalations of tar vapor. If the skin is coated
with tar, black specks (particles of tar) are observed in the sebaceous

336 INFLAMMATIONS OF THE SKIN.

follicles^ and later the acne changes appear. If tar is inhaled, it is
probably deposited in part in the sebaceous follicles, and there produces
inflammation. Tar acne is also produced in those who work in tar pro-
ducts (creasote, benzin, petroleum, etc.). Acne also develops from the
use of iodine and bromine preparations and chrysarobin ointment.

The diagnosis of all the varieties of acne is easy, the prognosis is un-
favorable 80 far as regards thorough and permanent cure.

In acne cachecticorum, reliance must be placed on cod-liver oil,
tonics, and nutritious food; local treatment is hardly necessary.

In acne disseminata, we should first attempt to prevent the formation
of comedos. If there is an abundant formation of papules or nodes, mer-
curial ointment should besmeared on leather and applied at night to the
affected parts. The next morning the skin is carefully washed with the
following: IJ Saponis virid., 3 iij., Spiritus vini, | iv. ; filtra et adde OL
lavandul., 01. bergamot®, && gtt. v. M. D. S. To be used eztemallj.
Large, painful nodes should be poulticed, and then incised. If there is a
proiuse formation of pustules, these should be punctured, and their
contents discharged; the skin may then be covered with Hebra's
diachylon plaster.

We may briefly mention the following other plans of treatment: a. Applica-
tions of oorroeive sublimate (fi^, | to is^. : S iiiss.); b. application of tinct. iodin.,
tinct. benzoes, or tinct. canthnrid. ; o. treatment with sulphur or glycerin soapK
d. (2iei89r8 sulphur paste) Lac. sulph., Elali. carbon., Glycerin., Spirit, vin. diiat.,
&&. M. D. S. Smeared on leather, and applied every night, removed with soap
in the momiuB;, etc. All these remedies seek to produce active desquamation oif
the superficial layers of epidermis, and thus to keep the excretory ducts of the
glands free.

3. Acne Mentagra.

{Sycosis.)

I. Etioloot. — The term sycosis is applied to a chronic inflammatory
process in the hair follicles, which gives rise to the formation of papules,
nodes, diffuse infiltrations of the skin, pustules, and crusts. Two forms
are distinguished, the parasitic (produced by tricophyton tonsurans),
and the non-parasitic.

The disease is obserred almost exclusively in bearded men. A dense
growth and very thick hairs in the beard predispose to sycosis.

The causes of non-parasitic sycosis are unknown. Among those
which have been assumed are shaving with a dull razor, uncleanliness.
irritation by snuff, highly spiced food. In some cases, it follows eczema.
Chronic coryza may also give rise to sycosis if the secretion constantly
flows upon the upper lip, and irritates" the follicles.

Hebra believes that in sycosis a new hair g^ws in an old liair follicle before
the previous one has fallen out, and thus produces mechanical irritation and
inflammation of the hair follicle. Werthheim assumes that the beiod hairs are
too tliick. 80 that the follicle does not afford sufficient room for the transrene
section of the hair.

Parasitic sycosis is produced by direct infection with herpes tonsu-
rans, either from animals ^cow, horse, dog) or from man to man.

The disease affects the nead most frequently, and has therefore been
called folliculitis barbae. More rarely it attacks the eyebrows or lid«,
still less frequently the hair of the axilla, mons veneris, the vibriss© of

IBTLAMMATI0S3 OP THE BKIK. 837

I noae, or the scalp. In the latter locality, the disease is almost

always secondary to eczema,

II. Symptoms. — The deyelopment of the eruption is generallypre-
ceded by a feeling of tension and pricking in the affected parts. Tlion
there appear red papules and nodes, whose centre is perforated by a hair.
Adjacent nodes come in contact, and form diflrise nodular elevations;
not infrequently there are extensive infiltrations of the skin. Pustules
appear in places upon the nodes, and either rupture epontaneonsly or
dry into yellow or grayish-^'ellow crusts, which are likewise perforated
by a hair. In those localities in which a hair is situated in the pustule)

HiJr contklDlDB CuQRi (i

Hmd

the former is readily removed on making traction. The root portion
appears thickened, and the root sheatha infiltrated with pus; the hair is
often bent at an angle immediately above the bulb. In parasitic eycosis,
the hair is peculiarly drv, fibrillaled, and discolored. After removal of
the hair, alittle drop of creamy pus often escapes.

If the crusts are softened and i-emoved, we often find reddened but
dry surfaces, which are sometimes elevated like condylomata, present
the appearance of proud fiesh, or are perforated like a sieve, the indl-
Tidnal openings containing pus. After the process has lasted for some
time, certain parts of the skin mav be entirely destitute of hair. This

idition persiata, inasmuch as the liair follicles have been obliterated by

888 INFLAMMATIONS OF THE 6EIN.

the inflammation. The snbmaxillary lymphatic glands become swollen
if the cutaneous changes are extensive.

In non-parasitic sycosis, the changes described are confined stnctlj
to the beard; in the parasitic form, they are apt to extend to adjacent
parts of the face or neck. The changes characteristic of herpes tonsa-
rans make their appearance in sharply defined circles, which are corered
with little yesicles or scales.

. Non-parasitio sycosis may last a yery lon^ time, sometimes even more
than thirty years. Parasitic sycosis generally runs a rajiid course.

III. Diagnosis. — The diagnosis is easy. Sycosis is disting[iiished
from eczema by the fact that in the latter the affected skin is moist and
itching, and that it is not confined to the hairy parts. The microscope
readiljr distinguishes parasitic from non-parasitic sycosis; in the former,
the hairs contain threads and spores of tricophyton tonsurans (vide Fig.
135).

The fungus is formed earliest between the hair and inner root sheath, then it
spreads into the root sheaths, finally into the substance of the hair. The bain
become transparent if treated for fifteen to twenty minutes with potash (f : 8).
Among four hundred examinations, Michelson and Schueppel found the fungus
only in one hair out of twenty.

IV. Progkosis. — The prognosis is good. The disease may recoyer
spontaneously, and is amenable to treatment, but it exhibits a tendenc7
to relapse.

V. Trbatmekt. — In non-parasitic sycosis, the beard should be
closely clipped if the disease is extensive. The beard should be shaved
daily, even long after the disease has recovered, in order to prevent a
relapse. Crusts are removed by fatty inunctions (two hours), pustules
are opened, and the hairs contained therein are removed daily with a
pair of tweezers. Only one hair should be grasped at a time and trac-
tion made in the direction of the hair. The entire diseased district
should not be treated in the first few sittings, since this may give rise to
peculiar conditions of excitement, and even to syncope. Epilation must
be continued until the formation of nodes and pustules has ceased.
Behrend has recently employed the sacrificator with success. The re-
maining infiltration may be treated with Hebra's diachylon plaster or
mercurial ointment; if the infiltration is very thick, with Zeissl's sul-
phur paste.

Parasitic sycosis may be treated with applications of turpentine,
corrosive sublimate, nitrate of silver, acetic acid, or powdered sulphur.

Appendix.

Hebra applied the term sycosis framboesiformis to an affection located at the
border of the neck and hair, and which gives rise at first to the development of
nodes, each of which is perforated by a hair. Later, the coalescence of the nodes
causes a raspberry-like infiltration of the hairs, and which, in many cases, cannot
be removed except by cauterization or excision. The disease is chronic; it is per-
haps the result of mechanical causes (friction of the collar.'

4. Acne Rosacea,

I. Symptoms and Anatomical Changes. — The disease occurs
exclusively upon nou-hairy portions of the face, generally the nose, next
the cheeks, chin, or glabella. It may also e^^end continuously oyer

TSFLAlDtATIQSB OF THE SKIN. OOV

large portions of the face, sometimes to the border of the hair, and even
to the back of the neck.

In the mildest grades, there is anusual redness of the skin, parti;
diffuse, partly in the form of unusuall; dilated and sinnoiis cutaDeouq
vessels. It usually increases after estiug or excitement. It is often as*
Bociated with seborrlioea.

As the disease grows more severe, soft, painless, red nodnles, varying
from the size of a lentil to that of a pea, appear npon the reddened skin.
In addition, there is often an abundant development of comedos and
acne vnlgaris. Puatnles are rarely observed.

The process is the resnlt of marked dilatation and in part of new-
formation of vessels of the cutis, dilatation of the sebaceous glands, with
stagnation of their secretion, and the formation of a gelatinous connec-
tive tissue in the cutis. Spontaueous recovery is possible,
even in this stage, by absorption of the newly formed ^"^ '"■
connective tissue. In the majority of cases, hovever, the
process continues to advance.

L^rge nodes then develop, generally situated on a broad
base, more rarely pedunculated. If the disease attacks
the nose, great deformity is produced; the organ some-
times attains the size of two fists, and looks liKe a large
roogh potato, etc. (rhinophyma).

II. £tioloot. — la many cases, the disease is the result
of alcoholic excesaee.

Tbe greateat danger is run by wine drinkers, next hy brandjr
drinkera, flnalljr by beer drinkers. Those wines which are rich in
ethereal oils and acid are the meet injurious in their effects. In
whiskey drinkers, the nose ia usually smooth and bluish-red; in
wine bibbers it is generally covered with red protuberances; in
beer drinkers, with cyanotic cul^ercles.

Acne rosacea is sometimes found in individuals who
suffer from diseases of the digestive tract (stomach, intes<
tines, liver).

In women, it is almost always the reaalt of diseases
of the sexual apparatus: amenorrhcea, uterine diseases. It
is most frequent in females at the beginning of puberty or
the menopause; in males, it develops beyond the age of
35 years. In some women, the first signs appear during
pregnancy or childbed. It has been often ooserved after
protracted cold-water cures. **'^iii''"?*^

Finally, tbe disease may follow local injuries (frequent wari&iuian-
exposure to rough winds or to fire).

III. DiAOKOBiB.— The diagnosis of the disease is easy. It may pos-
sibly be mistaken for frost-hites, lupus, carcinoma, syphilis, and rhino-
scleroma.

Id frost-bites, the skin is bluish-ted, and the cutaneous veins are not dilated.

Lupus erythematosus is characterized by profuse formation of scales and the
development of cicatrices.

In lupus vulgaris, there are brownish-red nodules, which are apt to break
down and cicatrize.

Carcinoma, as a rule, soon ulcerates. This is also true of syphilis; in addition,
other evidences of syphilis are noticeable.

IV. Pbogitosis. — The disease is often very obstinate. The de-

840 DTFLAMMATIONS OF THE SKDT.

f ormity is often so great that the patients are a laughing-stock in the
community.

V. Tbeatment. — We must first endeavor to remove the cause of tlu
disease, and this in itself is sometimes sufficient to effect a care. In ad-
dition, local treatment must be adopted.

In the mildest form (simple redness), we recommend that the skin
be brushed every ni^ht with collodion or sublimate coUodipn (gr. } : f i.)-
We have also obtamed good results from an ointment of tannin and
ergotin (ung. diach. HebrsB, 3 v., acid, tannic, erffotin.^ ^ 3 ss. M. D. S.
To be smeared on linen, and applied every night).

The second srade of the disease may be treated with mercnrial oint*
ment and, if there is marked vascularization, by scarification with a
lancet-shaped needle (Fi^. 136). ZeisseFs sulphur paste, iodine and
sulphur preparations may oe employed to relieve marked infiltrations.

Cases of the third grade must be treated by surgical interference,
i. e.y removal of the new-formations.

e. SCALE-FOBMING INFLAMMATIONS OF THB SKOT. DEBMATinDES

Squamosje.

1. Psoriasis.

I. Symptoms. — Psoriasis is a chronic skin disease which leads to the
production of abundant scales possessing a gloss like that of. mother-of-
pearl. If these are removed with the nail, a reddened, easily bleeding
base makes its appearance.

The individual efflorescences begin as a reddened, slightly elevated
patch, which is covered, at the end of a few days, with an increasing
number of scales, and, at the same time, increases in size. The smallest
efflorescences form little dots which shine like asbestos (psoriasis punc-
tata); when they attain the size of a lentil, the skin looks as if sprinkled
with mortar (psoriasis guttata). In some places, the scales disappear in
the centre of the patch, but extend further at the periphery (psoriasis
orbicularis). Adjacent patches not infrequently coalesce and produce
complicated figures (psoriasis gyrata). If tne scales extend contmnonflj
over a large area, it is known as psoriasis diffusa. The term psoriasis
nigra is employed when the scales have a brownish or blackish appear-
ance (particularly in old cases).

The eruption first appears on the extensor side of the elbows and
knees, and tnese parts are rarely unaffected in extensive psoriasis. As a
rule, the scalp is next affected, thick hillocks of scales being formed and
matting the hairs together. At the border of the hair, the patches often
extend to the adjacent integument of the face and neck. The concha
and external auditory canal are very often affected, but there are many
oases in which the eruption extends over the entire body. The mucous
membranes are always intact. The volar surfaces of the hands and feet
are rarely affected, in contradistinction to psoriasis syphilitica. Psoriasis
sometimes develops on the nails; white patches nrst appear^ then the
nail thickens, becomes lamellated, and crumbles to pieces.^

In some patients, a few patches persist, perhaps for life; in others,
there may be very little unchanged integument. Remissions and exacer-
bations occur very often. The eruption sometimes disappears sponta-
neously, and remains absent for months and years. As a rale^ the cauae
of the relapse cannot be ascertained.

Very violent exacerbations may be associated with slight fever, pain
in the joints, and neunilgic aymptoma. The patients often suffer no
sabjectivo disturbancea, but at first some complain of itching. If the
paoriaais is very marked at the lar^e joints, very painful rhagadea develop
not infrequently, and render motion distreaaing. In inveterate paoritisia
of the face, we alao find painful fissurea, occoaionally also ectropium, Aa
a rule, individuals suffering from extensive psoriaaia do not perspire much.
Cutaneous senaibility is sometimes diminiched, and albuminuria has alas
been observed. If tho disease is very obstinate and extensive, tbe patient
may suffer from anoresia, with increaeing feebleness and exhauating
diarrhcEQ, and theae symptoms occasionally terminate fatallv-

If spontaneous recovery enauea, the scales fall off, the atin is at 6rst
red and infiltrated, but gradually growa pale and returns to the normal.
In some caaea, pigmented spots persist apou tbe legs.

Etioloot. — Little is known concerning the causes of tbe disease.
Heredity exercisea an important influence; tbe inheritance ia sometimes
direct from the parents, sometimes from tbe grandparents or collateral
branches of the family. The predisposition to psoriasis alone is inher-
ited, and the development of tbe disease requires the interposition of
certain external irritants.

The latter include traumatism. Hence the early appearance of psorU
asis on tbe elbows or knees, because these parts are particularly subject
to friction. J. Neumann showed that tbe disease not infrequently fol-
lows eczema intertrigo, the latter being secondary to traumatism.

All other statements with regard to the etiology of paoriofiia are either
improbable or unproven.

Next to eczema, psoriasis ia tho most frequent of akin diseases. Aa a
rule, it does not begin before the sixth year, nor after the fortieth year^
It seems to be somewhat more frequent in men than in women,

IHFLAIQCATIONS OF THE flXIir.

According to a few atatementa which hare been made, psoriaHiB iicofr
tagiom.

FuDBUi threads trom ths paorlul* membruie. Af Mr Lang.

of forceps, and placed in a flve-per-cent solution of potaah. After the scalee bm
swollen and become transparent (at the end of a few minutes), we will Uni be-
tween them, round, oval, and elongated spores. 0.006 to 0.008 mm. brcnd and
twice as long (Tide Fig. 137). If the membrane is placed in a solution of polash
nrhich haa b^n mixed with equal parts of glycerin and water, the spores will de-
velop, at the end of two or three hours, into lonft, rarely branched threads, whoM
free end is either rounded or swollen (ride Fig. 188).

III. Anatokical Changes. — Siace some of the lesions disappear
after death, sections musb be taken from the living subject.

In the cutis are observed elongation and increased breadth of the pa>

INFLAMMATIONS OF THE SKIN. 843

T)ill89, dilatation and sinuosity of the vessels, profuse emigration of white
blood-globules, and accumulation of the latter, particularly upon the
outer wall of the vessels. J. Neumann also found the sweat glands filled
with round cells. In the rete Malpighii the lowermost palisade-like epi-
thelium cells, which are arranged normally in one row, now occupy
several rows ; the higher epithelium cells have lost their processes, and
also present nuclear proliferation and fission.

rv. Diagnosis. — The disease possibly may be mistaken for eczema
squamosum, seborrhoea capillitii, pityriasis rubra, pemphigus foliaceus,
lichen ruber, luous erythematosus, lupus eicfoliativus, rupia, psoriasis
syphilitica, favus, and herpes tonsurans.

Eczema squamosum presents marked pruritus, often weeps, and is preceded
by the formation of vesicles.

Seborrhoea capillitii occurs particularly in the new-bom, never extends beyond
the border of the hair, and, upon removal of the crusts, a red, bleeding surface is
not exposed.

Pityriasis rubra is distinguished from psoriasis by its course ; it leads to ma*-
rasmus and serious general disturbances. This is also true of pemphigus folia-
ceus, in which, moreover, vesicles are formed.

In lichen ruber, the efflorescences are smaller, covered with fewer scales, and,
as a rule, are arranged in contiguous groups.

Lupus erythematosus develops chiefly on the nose and cheeks; on removal of
the scales, their lower surface is found to present prolongations which project into
the sebaceous follicles; after recovery from lupus, cicatrices and pigmentations
are left over.

Lupus exfoliativuB produces fewer scales, and^on their removal the surface is
found reddened, but not bleeding.

After removal of a rupia crust, a deep, crater-shaped ulcer appears, with a
lardaceous base.

Psoriasis syphilitica is attended with a slighter formation of scales, which ad-
here more firmly, the base is brownish-red; it is localized on the palms of the
hands and soles of the feet, and other evidences of syphilis are present.

Favus and herpes tonsurans are recognized with tne aid of the microscope by
the presence of the characteristic fungi.

V. Prognosis. — The prognosis is almost always good as regards life,
but is unfavorable as regards complete recover}', since it is impossible to
prevent relapses.

VI. Treatment. — Internal treatment should be combined with ex-
ternal treatment.

We have succeeded in almost every case with the following simple
plan. The patient receives:

IJ Aq. amygdal. amar.,

Liq. potass, arsenit &a. ^ ss.

M. D. St Five drops t. i. d. after meals; the dose is increased by
one drop every third day.

In addition, the patient should take a daily bath at 30° B. (lasting
two hours), in which 3 iij.-vi. of potassium sulphate are dissolved. Im-
mediately after the bath, the following ointment is rubbed into the
patches with a brush, until the scales are removed as thoroughly as pos-
sible.

Ij, Sapo. virid.,
Picis liquidaa,
Lact. sulphur.,

Siiirit. vini dilut •• ..ua si.

M. D. S. To be used externally.

344 ISFUkJOCATIOXd OF TH£ SKIN.

Wa will mention a few other remediet which have been employed in this d»
MUM. a, Internal remedies. Iodine and mercurial preparations, carbolic add,
Mil icy lie acid, tar preparations, copaiba, carbonate of ammonia, phoephonu,
tUi, ; ttlNO exclusive meat diet. 6, External remedies. Subcutaneous injections
I if arseul(!al preparations, douches, hydropathic packs, permanent baths, cures -n
Aix, KnmsnAch, Pfaffers, etc., preparations of tar, iodine, and sulphur, cauteri-
Kallon witli acetic acid or corrosive sublimate, chrjsarobin ( 3 ij, : yaselin 3x.),
pyrugalllu lu^iU ( 3 i* : z.)i thymol, iodoform.

2. Pityriasis Rubra.

I. RYMt*T(^)lA.— This is a very rare disease. The skin reddens and desqns-
iu«t«M wuhout any previous efflpresence. Later the skin grows thinner, is teiuK,
Aiul «p)HM«rs to liave become too small for the body. The face assumes a stiff,
iiuMik-hk%) «)xpreii»ion, the limbs are m a forced position, midway between flexioii
tiiuk i».\tt»iui\>u. Khagades form here and there. Alopecia often develops at a
UkWv |H>ri\Hi. The disease sometimes starts from a certain part, sometimes it is
UtUuno hxHii the be|nnninK:at all events, it tends to spread over the entire body.

lHk0 duik^<ie is alm^wt always chronic, and may last several years. Qangrene
lUf vvftaiu part* hMi been observed. At the same time marasmus sets in, and
^i iiiiii*4t«iii fatally,

U. lU\viNv>Qiis.— Il is distinguished from squamous eczema bv the absence of
uKM.^iuv\» \^ tho skin and of nuirkeii itching. In lichen ruber, the formation of
•K-^iU".^ i<« tiU^ud^l with the development of nodules; lupus erythematosus ocean
I hioit\ lu lite fnc^.

Ul. VMrv^MK\KL OHJLXOESL—Hebra found, at the onset, profuse infiltratioQ
oL iho u^uH*r la vers of the cutis with round celU. later atrophy of the epidermis
:iuvl ^Ki^ull^rv IkvIv. jitT\>phy of the sweat glands and sebaceous glands, snd
M.-K«u»«kd of the cutis tissue. ' Phthisical changes have been observed in the lungi
tiud lUUNitine^.

IV. b^nv^UH) V. —The causes and nasore of the disease are unknown.

V . \^Kv\iNv\>;^--The prvV"V>?-* ^a* f.^rmerly re^^arded as absolutely fatal, bat
3\»iuo \\4.^^ of revvverv hAve S?er. recv:::»r recx>rted.

\ I. IVsLirMSNT.— lr.terr.Al .i,;:ai=j,scr:i5:o£i of arseaic or carbolic acid, exter-
ikilA tv*;:vs and fa::y ir.uuv;;ou:k

»»

\ . \ v.> In V. vv\ vt: n> y r.-.: >x:y. DzsitATixiDEs Pjlpulos^

I >\v^**,vv< — :V-:r,r.^ :> .ii-rwcc.-iiic ':t tjie appearance of scat-

.v'.'vvl "Ai .'.;.,>, ..'/•'.•. :..,' <::^ ;: a •; "*> r.fA.i :: :':i-i: of a hempiseed, which
v.. .,: v\Nx>«.\v> : -,' ".^i-.i. ,vl:r ;: :^: >i:r. r JLrf pale r»r^i. On punc-
... V. . ,\ .- v,-\>v:> .^ ,*V\4r i<— .:> 1.::.:. Tie i.:s«?ase is cbjoaic, and is

,' ,^ -*. xw . ,■ • X .! ».i- ; .1. iixc. r?--? rally towards the

. . .^ . ,^ ■ >: .,.. .» ; ••• •. *. ».-: ::': 7:r-i:~ if r of life. Thev

. » • vvi i<^ » .' > •..-':> ^ '"..-iT i. riie oaamcteristic

s . . .v^ \. . .> , «-.» . • •. r L-Ti:*. s..-* that they are

•s . XV ,.»_ :, \: vi .< r: i*:: n:r: i-i more above

■. 's « » v.. ' N % .V. $ m::^;*" ■ i:«i "i^-f l-f-r?* ilien upon the

. ^ -. . ... -. » .>, . .V ^^ . V :.-.• ijTtrAT ~r«:z the face.

'.V... V -.-■.: ^ * -^-i : .-■-s: i>4ZiAt:::i of ihe skin,

.x* . > ,, . • :.;. ^ *.' .. tl'.tL t^ sriicrr. e'bovs,

\ », - \ '.....>. s;..> .. .'. . i^ii. rizlii-La alwavs

V. -. ^ •.- ■:..^'::. fSTc-Jiiillr when the
V . ..;. . 1* ^5"^-. :■,•-'■< - "■:-■.'■: AS the re-
s. .--.:. ^..:^ r>,' irei of the

INFLAMMATIONS OF THE SKIN. 345

scratched papule acquires a bloody crast, or is converted into a pustule.
Pustules^ eczema^ and urticaria also develop in places which are free
from prurigo papules. The lymphatic glanas become swollen, particu-
larly in the groins, where they may form masses as large as a pigeon's
egg. These are somewhat characteristic of the disease, and are known
as prurigo buboes. The glands rarely suppurate. After the disease has
lasted a long time, the skin assumes a brown color (melasma), and feels
infiltrated and thickened. The furrows of the skin are not infrequently
unusually ^deep. The skin is generally di^, produces but little perspira-
tion, ana is often covered with scales. Warty elevations are sometimes
found upon the le^s, and the muscular system may undergo considera-
ble emaciation. The general condition may Coffer from disturbed sleep.
Remissions and exacerbations are frequent. The symptoms increase
during the winter, and may disappear almost entirely during the sum-
mer.

II. EnoLOOT. — The causes of the disease are unknown. Heredity
seems to exert an influence in some cases, but since prurigo does not de-
velop before the end of the first year, we must assume that merely the
premsposition of the skin to prurigo is developed. It has been attributed
to highly spiced diet, scrofula, rickets and phthisis (?). It is more fre-
quent in males than in females, and also among the children of the

• poorer classes.

III. Anatomical Changes. — Hebra attached chief importance to
the collection of a fluid substance between the cells of the rete Malpig-
hii, which served to nourish the cells, but was secreted in excessive
amounts. J. Neumann noticed cell proliferation in the papillad, and
swelling of these bodies by inflammatory, purely serous exudation.

Derov states that each papule is perforated by a hair. He also de-
scribed hypertrophy of the arrector pili, increased development of the
external root sheath and bulbous involutions of the hair follicles. These
changes are of minor importance. Gay noticed dilatation of the lymph
spaces in the cutis. The following changes have also been described:
Inroliferation of the cells of the rete Malpighii, proliferating processea
in the sweat glands, in old cases atrophy of the sebaceous and sweat
glands, and abnormtd deposit of pigment in the layers of the cutis.

Schwioimer claims that prurigo is a trophoneurosis. In our opinion, however,
the pruritus is secondary to the development of the prurigo papules.

IV. Diagnosis. — The diagnosis is easy, if we bear in mind the char-
acteristic shape and distribution of the efflorescences. We must be
careful to avoid regarding secondary cutaneous changes as the primary
lesion.

V. PB0QN0Si8.-r-The disease is capable of recovery if treated early,
^ Permanent recovery is not infrequent in children. But if the disease
' has lasted more than four years, complete recovery will hardly ever be

obtained.

VI. Treatment. — Much cannot be expected from the use of inter-
nal remedies. Arsenic and carbolic acid have been particularly recom-
mended. The general condition should also be treated.

The following is the simplest and most certain plan of local treat-
ment: Every night the patient is rubbed with green soap; in the morn-
ing he takes a bath (for two hours) at 30^ K., I iij.-vi. of potassium
sulphate being added to each bath. Then the entire skin is anointed

346 CEFUJOIATIOSB OP THE 8KIX.

with carboI-Tueline (3 : 50). This plan must be continned for a long
time, even after the papule^ bare disappeared.

Good effects hare been obiained from sabooteneoos in jeetioiis of pilocarpine
or carbolic add. The tzeatment reoominended for psoriasis is also much in ▼Qgu
for prorigo.

2. Lichen Scrophulowrum.

I. SncPTOics. — In this disease are foand papnles abont the size of t
pin's head, of a pale red, lirid red or brown-red color, with a little ^aik
upon the apio^. If the letter is remored with the nail, the moath of a
hair follicle appears, the ricinitv of which is slightly raised like a indl.
These papules are generallj arranged in round groups, rarely in circuit
lines. Tnev itch slightly or not at aU, and disappear spontaneoiulT
after branny desquamation. The disease is chronic, and often lasts for
years.

The first efBorescences appear upon the back, chest, and abdomen,
later upon the limbs, particularly the flexor surfieices; finally, the face
and scalp may be affected. In adranced cases, large areas may be in-
Tolved. Acne and eczema may also be present, the latter particnlsrlj
on the genitalia.

II. Etiology. — The disease is most common in children, especisUj
in boys. It is rare beyond the age of 20 years. The patients generdlj
present the eridences of scrofula. The skin is often very pale, and is
peculiarly fatty to the feel. In exceptional cases, phthisical changes are
noticed.

III. Anatomical Changes. — Kaposi found infiltration of the cutis
with round cells in the immediate vicinity of the hair follicle and its se-
baceous glands, and in the papillae immediately adjacent to the follicle,
njuiid cells in the follicles themselres, and accumnlation of epidermis
cells in the mouth of the hair follicle.

IV. DiAGXOSis. — The diagnosis is easy. In sqnamons eczema^ there
is severe itching, and many papules are converted into resides and pus-
tules. Lichen syphiliticus affects chiefly the flexor surfaces of theUmbs,
and the papules are often as large as a pea.

V. Prognosis. — The prognosis is good, since there is no danger to
life and the disease is not incurable.

VI. Treatment. — This consists of the internal and external adminis-
tration of cod-liver oil. one tablespoonful internally morning and even-
ing:, inunctions externally t. i. d., and the parts then coTered with flan-
nel.

3. Lichen Ruber,

I. Symptoms. — This extremely rare disease appears as scattered pap-
ules, as large as a pin's head, of a pale red or brownish-red color: thev
are sometimes pointed and covered with thin scales, sometimes flat, ani
appear urabilicated. Both forms are very often combined.

The first pa])ules appear on the chest, abdomen, genitalia, or flexor
surfaces of the limbs. Xew ones gradually appear and finally they are
so closely aggregated as to come in contact. In the coarse of" vear^, al-
most the entire integument may be attacked. The scalp, aidllse, and
mons veneris are generally unaffected, the hairs of other parts fall out.

Peripheral circles of papules sometimes sprout up aronnd central

INFLAMMATIp2<S QF THE SKIN. 347

OTieSy or the latter disappear^ leaving behind pigmentation and cicatri-
cial changes, while the process extends at the periphery.

in old cases, the palms of the hands and soles of the feet are covered
with thickened, fissured epidermis, the nails are also thickened, brittle,
brownish, or thinned. The papules have also been observed on the mu-
cous membrane of the mouth. The red, scaly skin is often diffusely in-
filtrated, and painful, bleeding rhagades are formed; the limbs are Kept
semi-flexed, and movement is painful.

If the process is left to itself, increasing marasmus sets in, and finally
death. In .some cases sleep is disturbed by pruritus, and this accelerates
the collapse.

II. Etiology. — The disease is more frequent in men. It develops
mainljr between the ages of ten and forty years, rarely earlier, though
Kaposi reports a case in a child of eight months. It causes are un-
known.

III. Anatomical Changes. — Examination of the skin shows noth-
ing which has not also been observed in other chronic skin diseases. We
may mention infiltration of the papillsB with round cells ; obliteration,
sometimes dilatation of blood-vessels in the papillsa ; occasionally colloid
degeneration of the walls of the vessels. In umbilicated papules, the
papillae corresponding to the umbilication are atrophied; the external
root sheath of the hair follicles is unusually well developed; hypertrophy
of the arrectores pili; fibrillation of the lower end of tne hairs; increase
of the cells in the rete Malpighii and epidermis.

IV. Diagnosis. — The diagnosis is generally easy. The disease is
distinguished from papular and squamous eczema by the fact that vesi-
cles and pustules have generally oeen present in the latter affections.
Psoriasis forms thicker scales, and the patches increase peripherally,
while lichen papules always retain the same size. Lichen ruber is dis-
tinguished from lichen scrophulosorum by the absence of a tubercular
etiology, and by the different distribution of the eruption.

V. Prognosis, Treatment. — The prognosis is good, since Hebra
found that successful results are obtained by the internal or subcuta-
neous administration of arsenic In marantic individuals, ^ood diet and
iron preparations are important, li there is violent itching, the skin
shoula be anointed night and morning with carbol-vaseline (3 : 30). In-
stead of arsenic, Unna recently recommended the following ointment:
Unguent, zinc, benzoat., 3X., Acid, carbolic, 3iij., Hydrarg. bichlo-
rid., gr. iv. M. D. S. To be rubbed into the skin morning and evening.
The patient then remains between woollen blankets.

M3 SBCBEnnr asomalies of xh£ 8kzn.

PAKT IL

SECEtEIORY ANOMALIES OF THE SKIN.

A. Secbeiory Anomalies op the Sweat Glands.
L Imcrtasfd Secretion of Sweai. Hyperkidrosis.

(EpkidrosU.)

UnnsiudlT profuse prodncdon of sweat may affect the entire vaiegor
ment (hvperliidrosis aniversalis) or be confined to certain r^ons (hy-
perhidrosis localis).

Hrperhidrosis nniyersalis is often observed in weIl*nonriflhed, obese
indiTidaals who perspire profusely on slight exertion. This perspiration
is most abundant in inclosed i)ortion8 of the body (axillse, anal
groove, etc.)- The excessire perspiration often produces further cuta-
neous changes. At first sudamina develop (vide page 330). In other
cases, the skin appears macerated and slightly reddened, especially where
two surfaces rub against one another (cbukfing, intertrigo).

In epileptics, profuse diaphoresis has sometimes been observed, either
in the place ol the epileptic attacks, or shortly preceding them.

We will not consider the diaphoresis obserred during the oourae of internal
diseases, since this is a sympcom of the diseases in question.

Hyperhidrosis loealis may be unilateral or circumscribed still more
narrowly.

Unilateral hyperhidrosis has been obserred in the course of various
nervous diseases udiocv, Basedow^s disease, asthma). Pikroffskv re-
j)ort.s a case in which the ingestion of food always produced svreating on
the right side of the body. In Kaposi*s ease, it occurred upon the face
on one side, and the trunk and limbs on the opposite side.

In some cases, unilateral sweating is confineKi to the face. This has
been observed in general paralysis of the insane, in phthisis with laige
cavities (the sweating side corresponded to the side of the cavity). In
Bonder's case, it always occurred during mastication.

In one case, Riehl found that the superior ganglion of the cervical
sympathetic on the affected side was swollen and reddened, infiltrated
with round cells, the vessels distended, the ganglion cells and nerve fibres
atrophied, and containing a punctate hemorrhage.

lIy{)orhidrosis localis is sometimes verv circumscribed. • In one case,
diaphoresis occurred, at certain hours of tlieday, upon the dorsal surface
of tlio right hand and forearm. This was relieved by quinine.

Excessive sweating in the axillie not infrequently stains the clothing
of a yellowish-red color; in addition it produces a disagreeable odor of
sweat. It may be followeil by intertrigo and eczematous changes. The
parts should be washed morning and evening with:

l> Acid, tannic gr. vi.

Spirit, vin. dilut 3 iij.

and then dusted with:

SECBETOBY ANOMALIES OF THE SKIN. 349

Q Acid, salicylic. y

Flor. zinci aa 3 v.

Talci praeparat 3 x.

M, D. S. Dusting powder.

In hyperhidrosis of the palms of the hands, the parts are moist, often
clammy and cyanotic. The patients leave moist traces upon everything
they touch. If the hyperhidrosis is persistent, the epidermis, in places,
is raised in vesicles, or it has a dull white color, and scales in pore or
less extensive shreds. This is observed relativelv often in chlorotio
females who suffer from menstrual disturbances. It often ceases spon-
taneously, but relapses may occur. Hyperhidrosis of the feet is still
more annoying to the patient. Marked maceration and shedding of the
epidermis produce violent pain and may render walking impossible.
The disagreeable odor (bromhidrosis) is so pronounced that we can gen-
erally recognize the disease by the sense of smell. Hebra showed that
the bad odor results from the decomposition of the sweat which has been
absorbed by the stockings.

In slight grades, dauy foot baths, frequent change of stockings, and
the daily application of tne above-mentioned dusting powder, especially
between the toes and stocking, will suffice. In advanced cases, we may
order unguent, diachylon HebrsB, which is smeared thickly on a piece of
linen in which the foot is placed. Small pieces are inserted between the
toes. The ointment is renewed every twelve hours. In six to twelve
days the macerated epidermis is cast off, and replaced by healthy epider-
mis. The dusting powder should then be continued for a little while.

2. Diminished Secretion of Sweat, Anhidrosis {Hyphidrosis),

Anhidrosis almost always occurs as a symptom of other diseases,
such as diabetes mellitus, diabetes insipidus, chronic interstitial nephritis,
cancer, cachexia in general.

Partial anhidrosis may also be secondary to other skin diseases, over
the site of disease (eczema, prurigo, psoriasis, lichen, ichthyosis).

Finally, it may be the result of nervous influences. According to
Strauss, it occurs on the paralyzed side in peripheral facial paralysis, but
not in central paralysis. In paralyzed parts of the body, hyperhidrosis is
sometimes noticed, sometimes anhidrosis, according to the occurrence of
paralysis or irritation of the several nerve fibres which run along the
peripheral nerves.

3. Changes in the Quality of the Sweat, Parhidrosis {Osmhidrosis,
s, Bromhidrosis y Chromhidrosis, Hcemathidrosis, Urhidrosis).

Changes in the quality of the sweat may affect its odor, color, or
chemical constitution.

a. An unusual odor of the sweat is known as osmhidrosis or brom-
hidrosis. In some cases, a bad odor is observed immediately after the
secretion of the sweat; in others, it is the result of decomposition of the
secretion. Frigerio recently reported two cases in which the sweat of
idiots smelled like musk. Szokalski healed a nervous lady with hydro-
pathic packs, and for two weeks the perspiration had the odor of violets.
An urinous odor of the sweat may be detected in uremic cases.

350 SECBETORT ANOMALIES OF THE SSJN.

b. Abnormal color of the perspiration is known as chromhidrosia.
Yellow, blue, green, black, ana bloody sweat has been observed.

In jaundice the underclothing is not infrequently stained yellow by
the perspiration.

A number of cases of blue perspiration (cyanhidrosis) have been re-
ported. In 18G9 Foote collected thirty-eight deuses. It generally occurred
m women, who were often anaemic and suffered from uterine diseases.
The abnormal production of sweat was localized, most frequently on the
lower lids, most rarely on the back of the hand, never upon the posterior
surface of the bodv. Ipavic found shapeless masses oi pigment in the
secretion. The blue pigment has been found in a number of cases to be
allied to indican. In ^rgmann's case the blue color was produced by
fungi.

Bloody sweat (hsemathidrosis^ does not belong properly in this cate-
gory. It is the result of unusual fragility of the finer cutaneous veraels,
the blood being extravasated into the immediate vicinity of the sudori-
parous glands or into their lumen. This condition is often simulated.

€, Among the anomalies in the chemical constitution of the sweat
urhidrosis may be briefly mentioned. In this condition urea is excreted
upon the integument in the form of white scales. This has been ob-
served in suppression of urine in cholera or nephritis^ and is often asso*
ciated with ursemia (vide Vol, II., page 261).

B. Anomalies ix the Secretiox op the Sebaceous Olands.

I. Increased Sebaceous Secretion. SeborrhcML.

Two forms of this condition are distinguished, viz., seborrhoea
oleosa and soln^rrhiva sicca. In the former, masses of fat are deposited
on the surfiKV of the skin, and either imparl to it an unusually fatty
gU^ss, or remain as thick, fatty scales and crusts. In seborrhcea sicca,
thert* is ex^^vssive desquamation of thin scales and epidermis, mixed with
dr\>ps of fat, Iknh forms may occur in the same individual. The dis-
ease may be ireneral or Ivval.

(K Si^lH>rrha>a of the soalp is most frequent during the first year of
life. The sv*alp is ooverevi more or less extensively with fatty sosdes or
with Yellow ish-irra v. greenish-gray, or blackish crusts, which may attain
a ihvokni\?ii of s^^veraf millimetres^ The dark color is the result of ad-
mixture with dirt. These deposits never e3rtend bevond the scalp.
Thev often liavo a ranoivl o*.lor. are peculiarly fatty to ih.% feel, and are
vviu^KV4^\i A dr\^j>s of fat mixed with epidermis cells. If carefully
r^nuoNivl, the uuvlerlviug :skiu is found to be pale and unchanged, fit
tl\e mas^i\^ of s^^bum decx.^mtKve aai become irritating, the underlying
skin iwlvlcus or i: Ivcomes eczematous and moist. The hairs are apt to
vviue v*ut while !\»iuovitii: the miS5?et? of »bum.

If the vvuv!::iou is \ef: untrvnted. the profuse secretion of sebum
vwiMNs lu :hc st^wv.d or thirvl \>?ar. the accumulated masses of fat become
dv\cv ;4v.sl iuo!\^ br::tle. arid are cas5 of by the growing hairs. But the
v\^Usiuiou 55^ouId be reliev^l as *{:i:ckly as DOdsibie. If tbe deposits are
thui, the atf^vtx\l i>ar<:s should be nibbei viioroasly everv morning
aust cvc'iiiu ^-^^^^ vu. oliv^jev oL a:ity^::^iaL« or oiher fatSE* and the scalp
ibcu \^>4^h^^ ihorv^;i^i:hN w'.:h 4C'>wc sob^i^ If :her« is a thick accumula-
tion vxl tuu> uiA^seci. ^hev >hou.Ii >? rjLbcvu wi:h oil every two hours,
aud a iUuuci ^va^* V**^*^*^ -•'^ ^^'^ iettoi: whrfu ;iie crusts liave been re-

8ECRET0BT ANOMALIES OF THE SKIN. 351.

moved, at the end of twelve to twenty-four hoars, the parts should again
be washed with soap. To prevent a relapse, the washing and inunc
tions should be continued morning and evening for some time.

in adults, the disease is rarely so severe as iu infants. It occurs
much more frequently as seborrhoea sicca. There is profuse desquama-
tion of white, fat-containing epidermis scales, whicri make the hair
appear unclean, and often covers the coat collar. This condition is
known as pityriasis capillitii. It often gives rise to defluvium capillo-
rum, and finally to alopecia. After recovery from the disease, the hairs
are generally restored.

In some cases, no cause can be ascertained; in others, the condition
is preceded by inflammatory diseases of the skin (eczema, erysipelas,,
small-pox); in still others by constitutional diseases (chlorosis, syphilis).

The treatment includes general and local measures. Iron, iodine,,
and mercury must be employed according to the causal indication. At
night, the scalp should be rubbed with alcohol, in the morning with oil.

b. Seborrhcea of the face is most marked on the forehead, temples,
nose, and chin. The parts have an unusually fatty gloss, the skin feels
fatty; in rare cases, the fat collects in scales and crusts. The mouths of
the sebaceous glands are unusually wide, and contain a more or less pro-
jecting mass of fat. Dust is apt to settle upon them, giving the patients^
a speckled, dirty appearance.

In seborrhoea of the nose, the cutaneous vessels situated between the-
openings of the sebaceous ducts are injected and sinuous. The condi-
tion is not infrequently present only at the period of puberty, and is
especially severe in brunettes. Treatment is similar to that of seborrhoea
of the scalp.

c. Seborrhoea of the genitals is especially apt to develop in males who
suffer from phimosis. The smegma collects at first in the coronary sul-
cus, but may finally encrust the entire glans. In hot weather or after
exercise, the secretion is apt to decompose, produces balanitis and
balano-posthitis, and may finally give rise to excoriations and con-
dylomata. The patients often suffer from herpes progenitalis, and,
in children, the violent itching may result in onanism. If the smegma
stagnates for a long time, preputial calculi may form.

The treatment consists of relief of the phimosis by gradual disten-
tion or operation, removal of the smegma by oily inunctions, and pre-
vention of its reaccumulation bv careful washing with soap, and intro-
duction of charpie smeared with zinc ointment or with tannin and
glycerin into the preputial sac.

Seborrhoea genitaiium is also observed in females, especially in little
girls. The sebum accumulates in the vicinity of the clitoris and be-
tween the labia majora and minora.

d. General seborrhoea occurs in adults as the result of chronia
wasting diseases. The entire integument is covered with fine, fat-con-
taining scales. This condition is termed pityriasis. The patients
shoulcf be nourished as generously as possible, and should take lukewarm
baths followed by fatty inunctions.

In the new-born, the production of sebum, which forms the vemix
caseosa, sometimes continues for a few days. The little ones look as if
covered by a thin, shiny membrane, which contains numerous fissures
(ichthyosis sebacea). This may be associated with refusal to take
nourishment, and unusually low bodily temperature, so that the children
^e in collapse. If they refuse to nurse, they should be fed with the

852 8B0BETOBT ANOMALIES OF TH£ BKIN.

spoon, warming flasks applied to the body, a protracted warm \mk
(34° B.) given three or four times a day, and the entire integament
rubbed with oil.

2. Diminution of the Sebaceous Secretion. AsieatoHs.

{Oligosteatosis.)

Diminution of the sebaceous secretion may be congenital or acaniiei
The skin is unusually dry^ has a tendency to form painfal ana often
bleeding rhagades, desquamates more or less actiyely, and has a roa^
appearance.

This condition may be congenital, either alono or in combination
with cong[enital diseases of the skin, for example, prurigo and ichthyoai
The acquired form may also be associated with certain skin diseases, sad
as psoriasis, lichen ruber> etc. It may be confined to the back of the
hands and forearms in indiyiduals who wash themselyes frequentij,
especially if the water contains a good deal of lime or irritating sotp.
This is noticed particularly in the winter. The treatment consists of
inunctions of vaseline or cold cream. Olycerin, which is such a favorite
remedy among the laitv, not infrequently aggravates the disease by ex-
tracting water from the tissues. The patients should wash less fre-
quently and only in lukewarm water, and should wear gloves in winter.

3. A^wmalicit in the Excretion of Sebum, Parasteatosis.

<7. Comedo.

L Symptots. — Comoilos are little black specks which correspond to
the oxoroiory duets of tho sebaceous glands, and in places are slightly
olo\*»iovi alnne the level of the skin. On pressure, the black speck is
extrudeii. and is often followed by a yellow, spiral, thread-like structure.
The latter consists of sebum, and, under the microscope, is found to be
comjHvsevl v>f fat and fatty epidermis cells, occasionally of cholestearin
crystals* la many oases we also find downy hairs and acarus follica-
lorum.

l\uuevlvxs deveio:> mv\st abundantly in those parts which are rich ia
i^^Kavwus elands \^K^rvhead, nose, lip&. chest, and back). They may
wvur aloue. or arv ass^viaied w::h seborrhoea. They are sometimes ^
uumerv^us that :he skin pr^":5en:s a claek-^peckled appearance, or in
p;a^\v? they arv so o\\seiy a^.-wited as to form wsut-like promineuces.
I hev luay hIsk^ jr.ve rise to ir:5ar::r!ia::o:i of the sebaceous follicles (acne).

R;u^s:r.or oaV.s A::or.:ior, :o :iie constant presence of comedos on the
^u* of :r.e r.vNse ;:: :ho r.ew-bort:.

U, Kr:o:vv;\.— The oiuse^ c^f :he retention of the sebum cannot
ii^xi^kxs ;v AAvr:iu:u\L li: s*.*c:Tf caise* i: is the result of mechanical
\sv*,i3s:x*u of :>.o e\orv:or>i .*,:;:. jls cs o6i5erred in workers in tar or petro-
V;,',v.. v^r '.V, .:*,;.\:sl:;ils >»>,,\ .:i^sy::e :ie fcici that their integument is
(^i;x, ^:a^*1\ >fc^i.<h :he f:K^r w::i kx&r^ In others, it is the result of the
\\*\s\;;o;;/*A of uv.;xs;:a,>» s::f seccrt,' Cooedois often develop in anaemic
«^v,x\ ov>;.^,;s',a; v:,v\',v,:a >, vvry vri^^fn 4: ^bie penod of paberty.

11. r K vv V \ V \ t V ^s* :rvyi:rj:f r. 4 s.vcis£S^ of mecmmical removal of
O'o xv^v A' ,^ >x :v.<\ciN .-: * ^-i:.-i i^jx. <c^^ To incmee the tonus of the
s\;',>^,nV, .. ^»^A^x^s. >fcv vAJi^* -i.'^V ^^^5fc*;:ir w;»bes. for example. Hebra'a

HYPEBTEOPHY OF THE SKIN. 353

green soap (vide page 336). This should be done at night. General
treatment must be adopted in chlorotic^ scrofulous, or anaemic indi-
Tiduals.

b. Milium.

1. Milium forms light-yellow or grayish-white papules, varying from
the size of a millet seed to that of a pin's head, and which often are
slightly elevated above the surface of the skin. Upon slitting the epi-
dermis and exercising pressure, a grayish-white papule appears. Under
the microscope this is found to be composed of lamellsB oi epidermis cells
and a fat- containing nucleus. This is the result of obliteration of the
excretory duct of a sebaceous gland, so that an accumulation of epider-
mis cells takes place in a lobule, or in the entire gland, and dilates it.
The epidermis passes over the papule, so that the former must be de-
stroyed before the contents of the latter are laid bare. Milium is distin-

Juished from comedos by the fact that the latter occupy the excretory
net of the sebaceous glands.
Calcification of milium has been observed in some cases. Wagner
reported a case of colloid milium, i. e., the papules were the result of
colloid degeneration of the epidermis cells.

The disease is most frequent upon the integument of the eyelids and
t^jacent parts of the cheeks and forehead, next upon the lips, the penis,
and inner surface of the labia minora. They are sometimes so numerous
upon the corona of the glans penis as to form a wreath.

2. The disease is often noticed at the periphery of cutaneous cica-
trices, for example, those produced by burns, syphilis, or lupus. It is
also frequent in parts which have been the site of previous skin diseases,
for example, pemphigus. In some cases it seems to be the result of a
primary anomaly of secretion, inasmuch as epidermis cells are deposited
in abundance within the lobules of the gland, but do not undergo fatty
degeneration and remain within the lobule.

Euestner observed an abundant development of milium in children
born prematurely.

If they are very numerous in the face, the epidermis should be
nicked with a fine bistoury, and the contents removed by pressure.

PART III.

HYPERTROPHY OF THE SKIN.

A. HYPEBTEOPHY OF THE CUTA.NE0US PlOMEKT.

1. NCBVUS.

Nffivi are congenital accumulations of pigment in the skin. They
form brownish or brownish-black, fiat, and smooth patches (naavi spili),
or they are uneven and warty (naevi verrucosi), or pedunculated (njevi
moUusciformes), or covered with bristling, thick dark hairs (nsevi pilosi).
The size and number of the n»vi are extremely variable. They are
sometimes so numerous that the skin assumes a speckled appearance.
They are situated not infrequently along the course of certain nerves,
and, like herpes zoster, only upon one side of the body (nerve nasvi).
23

854 UYPEKTBOrHY OF THE SKIN.

The formation of the pigment has been regarded, accordingly, as the
result of trophic disturbances, and this view seems to be favor^ by the
fact that other unmistakable nervous symptoms are sometimes notice-
able. NaBvi generally present a tendency to further growth. In later
years they are occasionally the site of development of sarcoma or cancer,
and may be the source of secondary infection of other organs. Anatom-
ical examinations have shown that there is not alone an accumnlatioQof
pigment in the lowermost cell layer of the rete Malpi^hii, but that there
IS sometimes an abnormal development of pigment m the cutis and its
obliterated vessels. The question of remove by operatiou comes ap
only with regeurd to smaller n»vi.

2. Chloasma.

Chloasma is the term applied to an acquired development of pigment
in the skin, and is either a primary (idiopathic) or symptomatic skin
disease.

Idiopathic chloasma includes freckles (ephelides, lentifi^nes). These
form light-brown patches which may attain the size of a lentil, and are
especially numerous in the face (no»a and adjacent parts of the cheeks).
But since they are also found on parts which are constantly coTered with
clothing, for example, the flexor surfaces of the arms and the genitalia,
it is evident that the action of the rays of the sun is not their sole canse.
Individuals with a delicate complexion are especially apt to be affected
with freckles. They are most marked in the spring and summer, and
grow palo or even disappear in winter. They are rare before the
a^> of six years or beyond the fortieth year. They may be removed
temporarily by remedies which produce an abundant desquamation of
opidormis : so^ip inunctions, tincture of iodine, corrosive sublimate
i^r« viij. : 3 ij.V In many individuals, they disappear spontaneously
at tho vvmpleiion of puberty.

The term traumatio chloasma is applied to those pigmentations which
follow uuvhauioal irritation of the skin. It is often observed in places
U|Hn\ whioh precj^nrx? has been exercised for a long time by bandages,
otOs* al:isv^ after viv^leni and repeated scratching (prurigo, eczema, scabies,
|HsiiouUV As the effect of clothes lice, tramps sometimes acquire such
a dark w!or of the skiu as to look like mulattoes (melasmas, melano-

i'hivNAsiuA eci\^r:ouai is the term applied to the dark color of the
Atu p.:\si;u\\: iu ;i*.auy individuals vofien within a few hours) by expo-
*u;v t\^ 5 he ;^uu gfcUvi air.

tVvio x*hU\*s:uA niav be vjrvxiuv>?d by the application of irritating sub-
*;,^v,ANs ^^ ',hx^ ?sk:u. "the aVv-*-****^'- ^"^^ • mustard plaster or fly blister
\e\\ x\tXov, U\^\V':i ^ brv^^:: i:<».vl: :::*:: or of the integument.

Vtuo*-Vii t^x' s^:uv:,*iva::,* f .^rt^is of :he affection, chloasma nterinnm
^i,\xvv>\\< ?iv\v:i, y.^, :.::c" 1: forms brv>wn:sh-yellow patches which, un-
\^X\^ iV >\^Jiu'>fc "^.ii 5Cvit^Ar vdkZvh-t^s of rcirriasis versioolor, are not shin-
\'.V<* ^'->^ -*'' o^'<sv;u^::*:va:>s *iv. sio r:v>5 vV^iain the fungus (mikrosporon
t\^^ r,;*^ \N;v,s' ir ;,* ViirxT^ifcs:^ h is cc«rnfd in wtunen who menstruate
\v\wo,\i \x. >v :i:x*vr f>ocf:t c:;<^;tifc»if^ 0* lie :ii«^is and ovaries. In many
m^nv^^s ;\ x; ,v\%;:^ >v^r*v^ yc^f^vATxr^ o^j^.'i&saLa fT^avhiarum). It generally
^t^M\n^\4^^ ^\ ; V :j;?:n;*v,«o^vju.:!^^ T^ for^iuMC. cheeks, lips, and chin

\ \j^,;v>«4 vviNiis\^>\vo^:ft i$ o^iT^r. u^ i::ir^3eatlj, in marantic

HYPEBTBOPHY OF THE BKIN. 355

individuals (malarial cachexia, marasmus of syphilis, cancer, pulmonary
phthisis).

Pigmentations are not infrequently left over in places which have
been the site of chronic skin diseases.

B. Hypertbophy of the Epidermis. Kebatosis.

Cutaneous changes which depend chiefly on hypertrophic conditions
of the stratum comeum are known as keratoses. They may either exist
alone or be associated with hj^pertrophy of the papillary body.

Among the keratoses which are confined to the stratum comeum,
are a series of cutaneous changes which are so frequent that they merely
require bare mention. These include callosities (tyloma), which are gen-
erally the result of f reouently recurring pressure; corns, which are one
variety of cutaneous callosity, and horns Tcornua cutanea).

The keratoses, in which the papillary oody is affected, include warts,
condyloma acuminatum^ and ichthyosis. The latter alone possesses medi-
cal interest.

Ichthyosis,

I. Symptoms and Diagnosis. — Ichthyosis is a chronic, usually con-
genital disease, in which more or less thick deposits of epidermis form
upon the skin.

In the mildest grades, the skin is covered by irregularly formed plates
of epidermis, which are bounded by deep furrows. At the same time,
the skin feels peculiarly rough and dry, and presents a great tendency to
desquamation of the most superficial epidermis layers (ichthyosis sim-

Slex). If the central portions of the individual fields of epiaermis are
epressed, while the edges are slightly elevated, it is known as ichthyosis
scutelata. In some cases the scales, particularly at the periphery, have
a mother-of-pearl gloss. In many cases, they assume a greenish or
greenish-gray color. The highest ^rade of development of the disease is
reached in ichthyosis cornea and ichthyosis hystria. In the former,
the scales of epidermis are as hard as horn, thick, curved; in the latter,
they form prickle-like prolongations and prominences. As a matter of
course, such changes produce great deformity, particularly since the
nodules are not infrequently almost black.

Various forms of ichthyosis are sometimes observed in the same in-
dividual.

The condition may be general or circumscribed; the latter form is
less frequent.

The first changes generally appear at the end of the first year of life,
often not until much later. Oases of congenital ichthyosis have been
reported, but good authorities maintain that these cases were really in-
stances of seborrhoea. Hereditary influences are not exerted at once, but
some time after birth.

The extensor surfaces of the elbows and knees are first affected, later
the changes spread more and more, but the fiexor surfaces of the
joints, axulaB, genitals, palms of the hands, and soles of the feet almost
always remain intact. In the face and scalp, as a rule, we find merely
active desquamation; the hair of the scalp is unusually dry and* has a
tendency to fall out. The affected parts rarely perspire. Many pa-
tients complain of annoyinff pruritus. Deep, painful rhagades some-
times develop, but they rarely penetrate into the cutis. The thick, tense

356 HYPEBTBOPHT OF THE eSJS.

epidermis may interfere with the free movement of the joints, so that
they are kept almost constantly in a semi-flexed position. In marked
ichthyosis of the face, impaired mobility of the lids and ectropinm hare
been observed.

Ichthyosis is sometimes associated with other skin diseases (eczema,
lupus, measles, small-pox^.

Mapother has observea cardiac hypertrophy, which he attributes to
disturbance of the cutaneous circulation. Increase and diminution of
diuresis have been observed in this disease. In one case, W. Boeck de-
scribed the development of a cataract and retinitis pigmentosa, with
atrophy of the optic nerve.

n. Etiology. — Little is known concerning the causes of the disease.
In some families it is hereditary, and Nayler was able to trace it back for
six generations.

Sometimes only one child is attacked; in other cases, the male or the female
children. Tbe diseaae ma^ also skip a generation.

According to Qaskoni, ichthyo:>is often appears in families i^rhich suffer from
eczema, asthma, phthisis, and fcout.

It is sometimes aojqaired, particularly in parts of the bodj which have been
the site of chronic skin diseases.

Ichthyosis runs a chronic course, and generally lasts for life. Spon-
taneous recovery is exceptional. Exacerbations and remissions are ob-
served not infrequently.

III. Anatomical Ghakqes. — The anatomical changes affect not
alone the epidermis, but also the cutis and subcutaneous cellular tissue.
The panniculus adiposus is considerably atrophied, and sometimes dis-
appears almost entirely. In the cutis, we find hypertrophy of the pa-
pilla9, often to a very marked extent. Their vessels are unusually wide,
sometimes thickened. The epidermis shows considerable increase of
the cornified cell-layers, while the juicy cells of the rete Malpighii are
sometimes reduced to a single layer. There is sometimes increase of
the nuclei in the epithelium cells of the mucous layer. Some writers
mention very distinct development of the prickle layer and an excessive
amount of the intercellular substance. Brown and black pigment
granules are found within and without the epidermis cells. J. Neu-
mann observed atrophv of the sebaceous and sweat-glands.

IV. Pboonosis. — The prognosis is unfavorable, since the disease can
only be relieved temporarily. However, there is no danger to life.

V. Treatment. — Active desquamation of the epidermis should be
stimulated by inunctions of green soap at night, and a warm bath
(30° R.), containinff §viij.-xvi. of soda, every day. This object
may also be secured by protracted baths, wearing rubber garments, in-
unctions of cod-liver oil or resorcin ointment (3-20 per cent), etc. In-
ternal treatment is useless.

C. Htpebtropht of the Haies.
ffirsuties.

{Hypertrichosis. Polytrichia. Trichauxis. )

In this condition, the hairs develop in abnormal numbers or in ab-
normal parts of the body. The condition may be congenitsd or acquired.
The following are the principal forms:

HYPERTEOPHT OF THE SKIN. 357

a. Ohildren are sometimes born with very long and abundant hair on
the scalp, but this almost always drops off after a certain length of time.

b. In some cases, the entire body, including the face, is thickly cov-
ered with hair. This form is generally hereditary. The development
of the teeth in such individuals is usually defective.

c. Thick hairs develop not infrequently upon nsevi.

d. A beard sometimes appears in women, especially in those who are
sterile or suffer from menstrual anomalies.

e. An abnormal formation of hair sometimes takes place on wounds
and inflammations of the skin; also upon paralyzed limos.

/. Some individuals present an unusual development of the hair of
the beard and scalp, so tnat the hairs may flow to the ground.

If the abnormal growth is scanty, the hairs may oe renioved with
tweezers, but permanent recovery is only effected by destruction of the
hair-follicle. This may be done with caustic pastes and the galvano-
cautery.

D. Hypebtbopht of the Nails.

Onycliauxis.

The changes produced by hypertrophy of the nail substance beloujg
to the domain of surgery. The nail may increase in thickness, or it
becomes unusually long and broad, or both conditions are combined.
It is sometimes bent like a horn or claw (onychogryphosis), or is raised
from the nail-bed, or gives rise to inflammation of the nail-furrow
(paronychia). Hypertrophic nails are usually rough, brittle, uneven,
and discolored.

This condition may result from local injuries (pressure), or other
chronic skin diseases (f)soriasis. prurigo, lichen, ichthyosis, etc.) or con-
stitutional diseases (chlorosis, syphilis, pulmonary phthisia).

E. Connective Tissue Hypertrophy.
Sclerema of Adults.

{Scleroma. Sclerodermia. )

I. Symptoms. — Sclerema appears generally as a chronic change in
the skin, which gives rise to a peculiar condensation, hardening, and re-
traction of the affected parts.

The changes sometimes occur in patches (partial) or they may bo dif-
fuse. They are found most frequently in the upper half of the body.
They may develop imperceptibly so that, at the most, the patient's at-
tention is attracted by a feeling of unusual tension and slight itching,
rarely by rheumatoid pains, or they are noticed accidentally; at first the
skin 'is sometimes oedematous, or there may hare been preceding erysipe-
latous changes.

In the beginning, the skin is slightly elevated and contains a doughy
infiltration. A stnking condensation soon sets in and no longer permits
the skin to be raised into folds. This increases more and more, and the
skin becomes immovably adherent to the underlying tissues, the perios-
teum, sheaths of the tendons, or fascisB of the muscles. The skin may
look normal, or it is unusually pale and alabaster colored, or rosy-red to
brownish-red. It sometimes contains more or less numerous and large

HTPEBTBOPHT OF THB BSJfS,

patches of pigment, ia other cases certain regions contain an unQSually
small amount of pigment. The periphery of the sclerotic patches is
sometimes very much congested, particularly when the process is ad-
vancing peripherally.

The longer the disease lasts and the moro it advances the mori.'
marked hecome the symptoms in the parts first attacked. The origi-
nally eleTSted portions of the skin become more and more depressed, aud
form, in a measure, firm, band-like stripes which compress the underly-
ing structures. Thus, the chest is sometimes found divided into two
parts, or compression of veins produces oadema, etc. The skin may also
grow as thin as paper, very red, desquamating, and exquisitely atrophic.

The cutaneous functions may remain entirely intact. The produc-
tion of sebum and perspiration is usually unchanged. Cutaueoua sensi-
bility is generally retained, exceptionally it is blunted. The tempera-
ture of the skin may be increased, diminished, or normal. Other
exanthemata (aone, herpes zoster, variola) develop not infrequently upon
the sclerotic parts. Ulceration and gangrene of the skin have also been
observed.

As a matter of course, the firm sclerotic skin, acting like a narrow,
unyielding cuirass, will produce various functional disturbances and
pressure effects. In diifuse facial sclerema, the face becomes ri^d. desti-
tute of folds, incapable of expression, and the patient lives, in a mea-
sure, behind u mask. Impaired mobility and ectropium of the lids set
in, painful rhagadcs form at the month, which grows smaller and smaller.
Paulicki described a case in which he was compelled to remove several
teeth from the upper jaw in order to render possible the introduction of
food. The condition grows still more distressing if the mobility of the
arms has been almost abolished as the result of sclerotic changes around
the elbows, bands, and fingers.

Diffuse sclerema in the neck interferes with the movements of the
head. Sclerema around the joints of the limbs gives rise to stiffness of
the joints, painful rhagades, and changes iu position. In extensive
Bclerema of the integument of the thorax the patients complain of a
feeling of constriction and anxiety. Sclerema of the penis may render
erection impossible.

Similar changes are sometimes observed upon the mucous membranes
(tongue, fauces, larj'nx. vagina).

As a rule, the disease is chronic, more rarely it runs an acute course.
In the acute cases, the cutaneous changes are generally preceded by
cedema of the skin. The sclerotic parts often become soft, while others
are being diseased. Death occurs generally with the signs of increasing
marasmus. Rossbach described a combination of sclerema and Addi-
Bon's disease,

II. Anatomical Changes. — The anatomical changes appear princi-
pally in the cutis and subcutaneous cellular tissue. The epidermis is
almost entirely unchanged, with the exception of circumscribed prolife-
rations of the rete Malpighii and accumulations of pigment. The cutis
shows proliferation and condensation of the connective- tissue elements
and elastic fibres. The vessels are narrowed in places. Upon theirouter
wall, and also in other parts, are observed nest-like aocumolations of
round cells. There is also an increaso of connective tissue in the subcu-
taneous cellular tissue, wliile the adipose tissue proper disappears
more and more. Accumulations of round cells are also found in this
locality.

IITPEBTBOPHY OF THE SKIN. 359

All other cutaneous changes ai)pear to be secondary; they include ac-
cumulation of pigment in the cutis, dilatation of the excretory ducts of
the sweat glands, hypertrophy of the smooth muscular fibres, etc.

The following lesions nave been found in other organs : tubercular
changes in the lungs and other viscera, cirrhosis of the liver and kid-
neys, cardiac hypertrophy, obliteration of the thoracic duct.

III. Etiology. — Little is known concerning the causes of the dis-
ease. Among those mentioned are erysipelas, injury', mental excite-
ment, and cold. The disease is much more frequent m women than in
men. It is exceptional in childhood, and generally develops beyond the
age of twenty-five years. Cruse observed one case in which the disease
developed a few days after birth.

We know as little concerning the nature of the disease as we do
concerning its causes. Some authors regard it as an infiammation,
others as a disease of the lymphatics ; the maiority of writers regard it
as a trophoneurosis. Eulenburg recently called attention to the inti-
mate relations between scleroderma and facial hemiatrophv.

IV. Prognosis. — The prognosis is not very favorable, although a
few cases of recovery have been reported. The disease generally
advances uninterruptedly, and proves fatal by exhaustion at the end of
months or years.

V. Treatment. — The best results are obtained by massage, oily
inunctions, and the application of emplast. mercuriale. Buelau recently
cured a case with sodium salicylate ( 3 i. daily), which he administered for
months. Good effects have been obtained from galvanization of the
sympathetic and of the affected parts of the skin.

Appendix.

Sclerema Neonatorum.

I. Etiology. — The disease is similar to scleroderma in certain exter-
nal appearances, but, anatomically and etiologically, it is entirely
different. It generally attacks children during the first few months of
life ; in rare cases, it begins in the second, or even in the third year ;
in a few instances it was congenital. It occurs most frequently in the
winter, in the children of the poorer classes. The children were not
infrequently born prematurely, or were asphyxiated at birth, and suffered
from atelectasis, bronchitis, broncho-pneumonia, gastro-enteritis, or
congenital valvular disease.

II. Symptoms. — The first changes appear upon the integument of
the calves ; then it extends to the feet, thighs, abdomen, chest, face,
and upper extremities. The skin is at first oedematous and slightly
reddened ; then it becomes peculiarly rigid, cannot be raised in folds,
and is very cold. It is peculiarly smooth, and either slightly reddened
or assumes a waxy pallor. Cutaneous sensibility is diminished or
abolished. The more the cutaneous changes extend the more the
movements of the child are interfered with. If the face is attacked, it
acquires a rigid, unchangeable expression, like that of an old man. The
mouth can hardly be opened, and infants are unable to nurse. The
integument is as cold as that of a frozen corpse. The bodily tempe-
rature is constantly lowered (22° C). The pulse becomes slow and
feeble. The second heart sound is hardly audible. The children are
generally apathetic, occasionally they moan feebly.

360 ATROPHY OF THE SKIN.

Cyanosis and jaundice are observed not infrequently as the result of
changes in other organs.

Death generally occurs after increasing collapse and progressiTe
diminution of temperature. More rarely the hardened portions of akin
soften and recovery ensues, after gradual elevation of the bodily tempe-
rature. Improvement is sometimes only temporary. Death may oocor
in a few hours ; the disease rarely lasts longer than two weeks.

III. Anatomical Changes. — The anatomical changes consist nudnlj
of rigidity of the subcutaneous cellular tissue. Demme foand &ttj
degeneration of the heart muscle ; Parrot noticed ecchymoses in the
mucous membrane of the bladder. Lan^r has shown that, in the new-
bom, the fat contains larger amounts oi the solid fatty acids (pidmitin
and stearin acids) than m adults, and is therefore more solid, and
melts at a higher temperature. Hence a slight diminution of the bodfly
temperature will make it firm and rigid, ouch a depression of tempe-
rature may occur very readily from disturbances in the cutaneons circa-
lation, which are apt to develop in the diseases mentioned under the
head of Etiology.

IV. Prognosis and Treatment. — The prognosis is almost alwajs
fatal. Repeated warm baths (half-hour) at 37^ C. should be ordered.
After the bath, the child is placed in a warm bed, and warming flasb
applied to the body. Artificial feeding must be resorted to. Camphor
may be injected subcutaneously. Careful massage and faradization d
the muscles have also been employed.

PART IV.

ATROPHY OF THE SKIN.

A. Atrophy of the Cutaneous Pigment.

Leukoderma,

( Leu kopath ia. A chromat ia. )

A deficiency of cutaneous pigment is shown by the unusually white
color of the skin, either in patches or diffusely. Congenital conditions
are known as albinism, acquired conditions as vitiligo.

All forms of pigment atrophy are more frequent in negroes.

a. General albinism is shown by the brilliant white color of the
skin. The hairs are yellowish-white, and have a silky gloss. The iris
and choroid are poor in pigment, and present a red reflex in direct sun-
light. Heredity is observed in some cases.

b. Partial albinism consists of the formation of patches of light
skin. They are most frequent upon the genitalia, scalp, chest, back of
the hands and fingers, and are not infrequently situated on symmetrical
parts. The hair on the affected parts is also poor in pigment, and has
a gray or white color. The patches generally remain stationary, but
sometimes they increase gradually in size.

c. Vitiligo occurs, in the majority of cases, as an idiopathic change
in the integument. Violent excitement, exhausting diseases (typhoid
fever), and injury are sometimes mentioned as causes. The symptoms
often appear quite suddenly. Naecke states, with regard to his own

ATBOPHY OF THE SKIN. 861

case, that he noticed the first changes during a railway trip. As a rule,
the disease develops in adults, but cases have been reported at the age
of twenty-one days, five and eighteen years respectively.

This condition is easily recognized. The skin contains light white
patches with very darkly pigmented borders. In one of my cases,
a small, dark pigmented spot was found near the middle of each white
patch. The patches gradually increase in size, coalesce, and finally
occupy the greater part of the bodv. At certain times the patches may
increase rapidly in size and numoer ; then, again, they may remain
stationary lor a long time. They often follow the distribution of the
cutaneous nerves. Tne functions of the skin are unchanged.

Vitiligo occurs symptomatically in those parts of the skin which have
been subjected to injury and ulceration (white color of cutaneous cica-
trices). It develops not infrequently in localities which have been sub-
ject to protracted pressure by bandages, etc. It may follow various
cutaneous eruptions.

These conditions are characterized anatomically by deficiency of pig-
ment in the lowermost layers of the rete cells. Treatment is powerless.

B. Atrophic Changes in the Hairs.

1. Canities,

{Poliosis.)

Gray hair may be congenital or acquired. It is congenital in albin-
ism; in diffuse albinism it affects all the hairs on the body, in partial
albinism only those places which are destitute of pigment. In some
individuals, small patches of gray hair appear congenitally, indepen-
dently of albinism.

Senile canities is one of the physiological forms of this condition. It
begins, as a rule, in the temples, and then extends to the hair of the
scalp and beard. In some families it appears very early. « The process
is tne result of an insufficient supply of pigment by the hair papilla, so
that the cortical layers of the hair become poor in pigment. The gray color
begins at the hair bulb. At first, the disturbances in the formation of
pigment are occasionally temporary, so that the hairs present alternate
gray and dark portions. If tne hair grows gray independently of age,
the condition is known as premature canities. This is observed after
typhoid fever, syphilis, erysipelas, etc., if the hairs have fallen out and
tnen grown again. They not infrequently become gray and scanty.
The hairs may also grow gray after skin eruptions and cicatrices, and m
vitiligo. It is well known that premature grayness may be the result
of loose habits and violent emotions. It may also be the result of nerv-
ous infiuences. Thus the hairs sometimes grow gray in hemicrania and
neuralg[ia in the affected nerve tracts. Berger observed it in facial
paralysis.

The hairs may grow suddenly gray in consequence of violent emo-
tions. In one of these cases, Landois and Lohmer observed air-bubbles
in the gray hairs, but Kaposi claims that they may also be present in
hairs which are not gray.

362 ATBOPHY OF THE BKIN.

2. Alopecia and Atrichia.

1. Complete absence of hair may be congenital or acquired. Con-
genital atrichia is often associated with absence of the teeth; sometime
the hairs developed at the age of two or three years. Acquired atrichia
occurs occasionally after yiolent emotions. Todd described a case in
which a man who was struck by lightning lost all his hair and nails; in
another patient the loss of hair followed concussion of the brain. Crisp
observed atrichia after malaria, which was associated with ansesthesia of
the left side. It is evident, therefore, that this condition is influenced
by nervous disturbances. In some cases, however, no cause can be dis-
covered. This happened in two of my own cases. The falling out of
the hair (defluvium capillorum) generally begins on the scalp, then ex-
tends to the beard, eyebrows, eyeuds, axillae, and mons veneris, so that
the patients are entirely destitute of hair. This sometimes takes place
within a few weeks.

2. Falling out of the hair is a physiological process in old a^ (alope-
cia senilis). It is generally precedea by canities. The senile defluvium
either be^ns on the forehead and temples, and gradually extends to the
vertex, or the first bald spots appear at the vertex. The bald spots are
glossy and often covered with yellow or dirty gray scales of accumulated
sebum. Senile defluvium is observed occasionally in the beard, but this
is exceptional. The process must be attributed to senile changes in the
fikin. Koelliker lays stress on obliteration of the vessels in the hair
papillae.

3. Falling out of the hairs in earlier years is known as premature
alopecia. In some families it is the result of an inherited predisposition;
in other cases, of nervous influences (mental strain, worry, grief, hemi-
crania, dissipation).

Alopecia sometimes follows infectious and constitutional diseases
(typhoid tever, febrile infectious diseases in general, pulmonary phthisis,
cancer, and marantic conditions). Many women suffer from very marked
alopecia afte? childbed, if the condition is only temporary, a new
growth of hair makes its appearance after a while, and is occasionally
even more abundant than the preceding growth.

Alopecia is sometimes the result of local changes in the scalp. It is
associated not infrequently with seborrhoea of the scalp, also with erysip-
elas, eczema, prurigo, lupus, psoriasis, lichen, favus, herpes tonsurans,
and with variola, sycosis, and syphilides of the scalp. It is incurable if
these diseases have given rise to destruction of the hair papillae and
follicles.

4. The various forms of alopecia must be treated in almost the same
way. At first, the causal conditions must be taken into consideration.
Locally we should apply irritating alcoholic lotions, followed by inunc-
tions with oils, for example :

ij Spirit, viu. dilut • • • • § iij.

Acid, carbolic • 3 ss.

M. D. S. To be rubbed in morning and evening.

IJ 01. macidis 3 iij.

01. oliv , ♦ 3 X.

M. D. S. To be used as hair oil; or,

ATBOPHT OF THE SKIN. 363

3 Acid, carbolic • 3 ss.

Sodii salicylat 3 iss.

Vaselin 3 z**

M. D. S. To be used as pomade.

3. Alopecia areata 8, Cehu

1. The changes in alopecia areata consist of the complete loss of
liair in sharply defined, round spots, which look as if shaved with a
razor. The spots gradually increase in extent. If a number of spots are
present, adjacent ones often coalesce and produce irregularly-shaped
patches. In very advanced cases, there may be almost complete loss of
the hair on the head, and the beard may be similarly affected. The
cutaneous sensibilit3r of the bare spots is sometimes diminished. The
hairs which are situated at the boundaries of the bald spotsare
often unusually loose. In some cases the disease is hereditary or it ap-
pears in several members of the same family. It lasts for months and
years. There is often a sudden remission in the symptoms, followed by
the growth of downy hairs, later of normal hairs.

2. The majority of writers attribute the disease to trophoneurotic
disturbances. In our opinion some of the cases, at least, are parasitic in
their oririn. The distribution of the spots, their shape and ^owth,
favor the latter view more than the former. The treatment is the same
as that of alopecia.

4. Trichorhexis.

1. The ends of the hairs not inf reauently split up. This occurs par-
ticularly in long hairs, most frequently in the long nairs of the head in
women, more rarely in the long hairs of the male beard. It is probably
a nutritive disturbance, perhaps the result of the excessive growth of the
hair. The treatment consists in cutting the hair.

2. Trichorhexis nodosa occurs almost exclusively in the hairs of the
beard, rarely in those of the eyebrows. In places the hairs form nodular
distentions, which are sometimes so numerous as to present a rosary-like
appearance. The hairs are situated firmly in their follicles, but readily
break spontaneously or upon traction on the individual nodes. In
places, they run into spherical prominences and present a gnawed ap-
pearance. Under the microscope it is found that the changes begin with
a dlight spindle-shaped dilatation of the hair. Next the cortical layers
in this locality split up, while the medullary parts are often filled with
large drops of fat, and press outwards more and more. But in many
places the medullary cells are entirely absent. Finally, the cortical fibres
of the upper and lower portions of the hair look like two brushes which
are pushed into one another. The causes of the disease are unknown.
Wolfberg believes that many cases are mechanical in their origin, and
result from very strong friction of the hairs in drying them after washing.
I recently cured two cases bv advising the parties to discontinue rubbing
the head after washing. Whether all cases of trichorhexis are due to
this cause, is not settled.

864 NEUBOSE8 OF THE SKIN.

C. Atrophy of the Cutis Tissue.

Xeroderma.

Kaposi distinguished two forms of this disease, one running its oonm
with, tne other without the formation of pigment in the skin. The
skin appears peculiarly tense, thin, and shiny, or is covered with sm^
Boalos ; its sensibility is retained, but it cannot be lifted readily into
folds. The movements of the limbs are impeded, and the latter are kept
semi-flexed; ectropium and narrowing of tne nostrils and month become
noticeable. In those forms which are associated with the formation of
pigment, cancer and sarcoma of the skin developed in a number of
oases. The prognosis is unfavorable.

PABT V.

NEUROSES OF THE SKIN.

licking of the Skin. Cutaneous Pruritus.

L Etiology. — Cutaneous itching is an annoying symptom in many
•kin di^Hidivsu but we refer now only to that form which is independent
wt anatomical change in the skin, and constitutes an independent func-
tiotutl disturbance of the cutaneous sensorv nerves. It is observed not
iufriiH)UcntlY in old as:e« perhaps as the result of senile processes of inyo-
)uti\\u iu the ;!^kiu. In other oases it is the result of general diseases and
Kk>^ AtTivtious of interaAl organs, such as diabetes mellitus, Bright'sdifi-
i>i%!t\\ JAXiUxluw v*a:uvr. diseases of ihe liver, stomach, uterus, and oTaries.
JNuntu* I* svnt\o::nt^^s Uv^tioed at a very early stage of cancer. Some
>^\^iuou vv:v.vU::x v^f ir/.olerible ::chi:i^ during pregnancy, and, according
l\^ UnVa.Ix :^u< sxtuononi arse's r ?e no; Infrequently to premature labor 2
\^ Ax^vsv^^^ r,x :S^' ^evwv.l hdu! :f pre-^riazoy. Duhring applied the term
jM\i>ou:t hvti>,V,;:^ :>.* :K\?e cas^:>? ▼'irvh occur in certain individuals on
s\s-^l .^;;;u^v,v, A^vl %:v*:^r i^Y^ Prsr::;is has also been observed after

\ I S\\ ,-^^.v>ts r*x* : v'i:-^ js socMiLses fei: constantly, sometimes
\* Av^ x > x\i:v^VNms. I . :zvf j»n^ir ^t«-:, :i appears particularly at
vi^Nu >': >i.^s.'' ;n^ ".\i. c>"t: :< t-::rv ^irir^Jy :rAL Mental emotion and

«>v ow^^i X *^ i. ,^'v ^^i i.v* ^".^.f 'if 4 siiLrtre. The patients often
^^4 .4x\\./ c ^ ^^ .' ^^^' -*-'^' ^'vi^oi li-'-'Tj: r!i«e xirtiT by the itching. In
'^v*, > "*s -•> <^ cs >i.* > ' ii..> : \i' :!»,'/ i.-^ .'*:2t.>*Ilrd lo avoid society,
V .v,v >v> * V I .* >»w / ^,>.si K' Iv'^jx-^ Tr iCfarci. The patients are
,\V v%.v,» ,..lv»v^.*o^v w.^- ^"-v '^v; . :.u*^ mi T iTi-2. Sf driven to insanity

\>> xv ^ * \v v.. */5v ■^^\>- X !. ^:. "! ~\»i tCk^ rf wheals, nodnles.
.V..N...... ..N i ?. X ^ . . \.\^',i^ v:!?x "~ ^ .*?r££i iiScTilt to decide

**sv\ \,cvx V**v u->;,t>>t>^ >^ "ti" ri^itf riil*r -w^sen the causes
v*. \ N..V v.v.. ' ,v I i s**,v>i^iv: :: ^;; 7rt:rniS »* cvi age. Blight's

.\ .N^^ \N\ *v •. '. v.x*',"»»* r:.:v'^c:vTns tlts5 frst be met

^ ... V vv . x^« V. . \ >.- ■ fs ur .^.liT «»i ^'^^ting ▼ithca^-
,K, \K^N. .X ^ \ * *.*^. N ■• . * '< v^>K -:rirLv;i: frSsr^c: B Potass.

PABASITES OF THE SKIN. 365

bromid., 311].; Ext. belladonnsB, gr. ivss.; Acid, carbolic, gr. xv.; Palv.
et succ. llq., q. s. at ft. pU. No. 50. D. S. Two pills to be taken four
times a day.

A large number of other remedies have been employed in this disease. We
may mention the following; Veratrine, chloral hydrate, morphine, etc., douches
or baths with soda, corrosive sublimate, etc., applications of ether, alcohol,
chloroform.

PART VI.
PARASITES OF THE SKIN. DERMATOSES PARASITARI-S.

A. Animal Parasites. Debmatozoonoses.

1. Itch, Scabies,

I. Etiology akd Anatomical Changes. — The term itch is ap-
plied to an artificial eczema which is partly produced by the direct irrita-
tion of the acarus scabiei (sarcoptes hominis), partly by the scratching
superinduced by the intolerable pruritus occasioned by the parasite.

The acarus scabiei belongs to the family of acarinsa and to the class
arachnidsB. Each patient harbors many more female than male mites.

The female is larger than the male (the former is 0.27 to 0.45 mm.
long, 0.2 to 0.35 mm. broad; the latter is 0.23 to 0.25 mm. long, 0.16
to 0.20 mm. broad), and, to the naked eye, appears as an irregularly
round, gray, slightly transparent little nodule, which is barely visible.
Under the microscope, it is found to be shaped somewhat like a crab,
and pendulum-like movements of its eight feet and head are often ob-
served. It becomes more transparent without undergoing any other
changes, if a solution of potash (1 : 3) is added to the preparation.

The head is situated at the anterior extremity upon the dorsal sur-
face (Fig. 139). It possesses two pairs of mandibles with three segments,
and, to tne outside of these, two three-jointed palpi provided with bristles.
The lateral surfaces of the body present numerous constrictions, and
from them project two anterior and two posterior pairs of feet. The
anterior pairs have five segments , and at their free end carry a pedun-
culated sucking disk (ambulacra); the posterior pair possesses only
three segments, and terminate in long bristles. Upon the broad dorsal
surface are found numerous furrows and a number of rows of spines,
the middle ones being convex anteriorly, the posterior ones convex
posteriorly. In addition, there is a row of more or less pointed and long
thorns. At the posterior end of the body, they are arranged in four
rows, fourteen in number.

Upon the ventral surface of the female, the head can readily be
traced from the oesophagus. Near the posterior extremity is a fissure
which leads to the vagina; more or less developed ova are often
visibile in the belly (Fig. 140). At the posterior extremity is found the
anal opening, with long bristles on each side. No respiratory organs
can be discovered, and the animals can live for a long time when de-
prived of air. The female acarus is said to live twenty to sixty days.

The male acarus is smaller than the female, and the posterior pair of
feet possesses a pedunculated disk, while the third carries a long bristle,
as in the female. There are a smaller number of thorns and spines on

PABASmS OF THE I

tbn '\oTm\ mirface. Upon tfae Tentral rorfkce is seen the fork-aluped
jwiiiM, Nitnatod in a horseshoe like sheath of cbitin (Fi^. 141).

VrohMy a singlo act of sezaal intercoarse safficea for the production
of n liirf(0 numlxtr of viable ova. The latter are said to nnmber abont
ntty, onu or two ova being deposited on a single day. According to
(hiddtin, tbe male dies six to ei^bt days after intercoaree,

Whmi A fotnale aoarns is impregnated, it bores a pass^^ (acarng
• ■' ■ ' ' ■ tfae rete Malpighii. This

burrow) tlirongh the stratum comenm into I ^ „

|)riwt)si oau bo traced by placing a living acams on the skin. It boi^

<;« .-i :w iPtiwratis Vv a^i ci ibe mandibles.
.-i-vw; .T S-!*iiW«CL ;7 .'ftfc focxain* dirt or
, ■: .iVE.'wtrip « i Toacsaiw. bu^-k fai«ak. The
i-u>i .■; . K- 'Txi'-'yi. aaii T-ia ai**5aeffltlr can be
, •* : 1 :ii' t^-nl ;ini, aac ."aa ifaa he removed
■jtuvi.t,. ',"'iii '..'(i-^ li Z3si >a:rr-,-T is penerally
? ii> uau ' i^ j :!ii. Via 3LJie naj biu« a di^

iv. ^ -i ':-iM.:L-i :jiK 'ja 'ia:r-i'w teciaf at the

PARASITES OF THE 8K1N.

enrface of the epidermis with a alight, funnel-shaped dilatation, and
alao ends in a slight enlargement. The female is always found at the
blind extremity of the burrow. As it makeg its way into the skin, it
loavda ova in jto track, the older ones being at the entrance, the young-
est ones immediately behind the mother. The number of ova may
amount to fifty, but on the average only ten to twenty are present.
Mingled with the ova are black granules of fsecea. The mite dies after
having deposited a sufficient number of ova.

The acarua bores deeper and deeper into the skin, because it finds
DouriBhment only in the juicy cells of the rete Malpighii, while the irri.-

le WX1UU7 mature ociirua.

Ealitr^il 300 Umoa.

tation which it exercises produces coraification of the surrounding epi-
dermis colls, so that it is compelled constantly to geek new layers of
epithelium. The irritation is also shown by inflammatory changes in
the cutis below the burrow, so that pajiules, vesicles, and pustules form,
and elevate individual portious of the canal.

The female acari alone are found in the burrow, tho males are gener-
ally found in its vicinity in superficial furrows of the epidermis.

The ovaare oval in shape, 0.16 mm, long and U.ll mm. broad. The
youngest present numerous fission processes, while the older oues contain
the rudiments of tho head und foet. In six to twelve days the ovum de-
velops iuto a larva.

868 PAHABIIBb OF THE BEIH.

The larra (vide Figs. 143 and 144) fareftke throngh the shell of tbe
ornm, and makes its way through the burrow to the snrface of the epi-
dermis. According to Bomo writers, it makes ita way to the surface
throngh air boles in the burrow. On the average, they attain a length
of 0.15 mm. and a breadth of 0.10 mm. Sevenil free larrn are often
found in the burrow. After they have reached the surface of the epi-
dermis, they burrow a superficial neat in which they develop further.

The larvse have only six legs, and present no sexual differences. They
moult three times, according to some writers, four times. After the
first moult the animal possesses eieht legs, after the third moult it if
sexually mature. Accoroing to Gudden, the first moult takes place from
the fourteenth to seventeenth davs, and each moult lasts five days.

The disease is always the result of the direct conveyance of the larvs.

veatnl iiirfua. BoUtkhI a» tL

but this requires prolonged and intimate contact with patients suffering
from itch. It occurs most frequently from sleeping in the same bed,
and is rarely the result of contact with the hands. If nurses and moth-
ers suffer from itch, the nursling is ofteu infected, because the breast it
a favorite site of the mites. It has been erroneously held that tbe dis-
ease cannot be conveyed in the underclothing.

Scabies can be conveyed not alone from man to man, but also from
animals to man. The parasite has been found in the dog, cat, horse,
cow, sheep, rabbit, fox, elephant, etc.

Certain trades (shoemakers, smiths, bakers, tanners) present a pte-
disposition to the disease, while others, especially cigarmakers, are geo-
erally not attacked.

The disease is generally more frequent in the winter, and is more
common among men than among women.

II. STMPTOua. — The favorite habitats of the itch-mite are those
places in which the horny layer of the epidermis is thin, and the cells of
the rete Malpighii are juicy. Sach places are: the skin betfreen the fin-
gers, the flexor sarfaces of the wrist aad phalangeal joiate, the palm of

Acanu burrow,

loMtrument or tha loin*. 8%hUjr eolMfed. AlMrEftpod.

the hand in children and individaals with a delicate iiit«gament, the
extensor surface of the elbow, the anterior axillaiy fold, the nipple and
umbilicus (particularly in women), the genitalia, the region of the tro-
chanters, buttoeks, knee, and inner border of the foot. The paraaite is

870

PARASITES OF THB SKIS.

foriiealtttlj abaadant upon the battocks in iadividoalB who work in i
sitting position, for example, Bhoemakers. The acaruB is also apt to be
founom parts which are subjected to prolonged pressnre by bandage^
etc. Hebra observed itch burrovs upon the mncons membrane of the
urethra. The face is gonerallT anaffected, except in nnrtdings who u-
qoire the disease from the motner or nnrse.

The cataneouB changes prodaced b^ the parasites and by Bcraiehiiu
are not always identical locally. The itching prodaced by the aoams h
always radiated to parts which remain free from the parasite, and sach
parts are also scratcned by the patients. The scratch efflorescences ire
found chieSy in parts which are easily reached by the patient's hind
(anterior part of chest and abdomen, inner surface of tbigna and knees).

id nioutt. Alia Em™>-

The effloreacenccB of scabies are composed of papules, veaiclea, pus-
tules, crusts, aud excoriattons.

The term scabies norwegica is applied to very severe and inveteratt
cases, in which thick crusts form, particularly upon the face and scalp.
The finger nails are also afEected, being discolored, fissured, and thick-
ened. After being treated with potash, the nails are found to contais
innumerable ova, larvsa, and nests of acari (rido Fig. 1^).

The sole complication is the enlargement of the lymphatio elands in
the Ticinitv of extensive eczema. Suppuration of thebaboes nas been
observed after extensive changes on the penis.

The patients generally complain of nothing beyond intolerable itch-
ing, particularly at night. This ceases during the course of febrile dis-
eases, because tne mature acari are killed by the increased bodily tern-

PABAsriBB OF THE BKIN. 371

Seratnre. When the temperature returns to the normal, the ora
eposited in the burrows mature, and the symptoma then return.

III. DiAONOsis. — As a rule, the diagnosis is e^, but is only posi-
tive afterthe finding of the mites, ora, or lame. The burro vs, Vbi oh
should be looked for between the fingers and upon the penis, are also
characteristic, bnt they may be subjected to Buch severe scratching that
it is hardly possible to find either tliem or the parasite. Even in such
cases the diagnosis is usnaliy easy, if we bear in mind the distribution
of the efflorescences.

IV. PRoaNosiB, — The prognosis is good, since we are able to kill
the parasites, and thus remove the cause of the cutaneous lesions.

V. Tbeatmbnt. — lu order to kill the parasites, the following should
be mbbed into the skin morning and evening for two sacceseive days:

B Balaam. Peruvian.,

Styracis liquid &&ii.

M. D. S. To be rubbed in morning and evening, and after the sec

ond day a warm bath should be taken daily for three days and the parta
washed with soap. In addition, the underclothing and' bedding should
be changed and tailed, the remainder of the clothing exposed to hot va-
por in order to kill any parasites which may be present in these articles.
To relieve the eczema produced by the mitea, we recommend oily
inunctions, bland ointments, or the ordinary remedies in eczema.

We may mention some of the other remedies which have been employed la
this disease: Carbolic acid, naphthol, naphtholin, ol. bergamottee, sulphur, mer-
curj, far, etc. The followjug ointmento may be mentioned:

5 Calcia !»i;.

Sulphur, citrin Z xiij.

Coquecum.Aq I'^**

Ad remanent |x.

D. S. To be rubbed in.

B Flor. sulphur.,

01. cadinl Ml v.

Sapon. virid.,

Azimg. porci A&Jz.

H. D. S. To be rubbed in.

872

PABASITE8 OF THB SKIN.

9 Styrao. liquid,,

Flor. Bulpnur.,

Cretsd albad fi& 3 iij.

Sapon. virid.,

Axunff. porci &SLZyL

M. D. 8. To be used externally.

If the ointments irritate the skin too strongly, they may give rise to albumi-
nuria, but this is a rare event.

Fig. 146.

2. Acarusi FoUiculorum,

{Demodez folliculorum. Macrogaster platypus. )

In many individuals this parasite is found in the sebaceous and hair
follicles^ but does not give rise to any other cutaneous changes. It is
found with special frequency on the bald head of old people,
next upon the forehead^ cheeks^ nose^ upper lip^ and external
auditory canal. It may be obtained by expressing the con-
tents of the follicles^ and then placing the latter, with a
drop of oil, upon the object glass. As many as twenty
have been found in a single follicle.

The anatomical (vide Fig. 146) characteristics are: An
elongated, cylindrical, worm-shaped animal, 0.08-0.12 mm.
long, 0.02 mm. broad; at the anterior end are two man-
dibles and two lateral palpi; on the thoracic portion, four
pairs of feet; the abdomen is four times as long as the
anterior portion. Smaller, six-legged mites hayo also been
described.

When conveyed to animals, it is said that severe cutane-
ous lesions are produced.

'<i^

Acarus foUi-
culorum.
Enlarged.

3. Lice, Fediculi.

There arc three varieties of lice, viz. : Pedicnlus capitis,
pediculus vestimentorum, and pediculus pubis.

a. Pediculus capitis (head louse) is found only on the
scalp. It is about two mm. long, and has six feet provided
with hooks. The females are always more numerous than
the males. In fertilization, the female sits upon the male.
The former lays about fifty ova, or nits. These adhere to
the hairs by means of a sheath of chitin which surrounds the
hairs (Fig. 148, a). The oldest ova are those situated next to the scalp.
At the end of three to eight days the young escape from the ova, and are
fully developed in eighteen to twenty days. Within six weeks, the fe-
male may bear six thousand young.

An artificial eczema is produced upon the scalp, inasmuch as the
lice give rise to pruritus, and the consequent itching mechanically irri-
tates the scalp. In combing, the painful spots are spared, so that the lice
find favorable conditions for development within the sticky hairs and
upon the bleeding skin, which is covered with pustules or crusts. Finally,
the hairs form a densely matted mass, containing pus, crusts, and blood,
and which often has a nauseous and quite characteristic smell. The ec-
zema often extends to the adjacent skin, the neighboring lymphatic
glands become swollen, tlie "pskU^iiU are sleepless on account of tne in-

PABA8ITB8 OF THE BKIK. dT3

tolerable itching, lose their appetite, and run down in health. The back

jf the head is particularly apt to be affected.

In making a diagnosis, our attention should be directed to the pree-

enec ot nits; the nearer they are to the tips of the haira the older ia
11 the disease,

j^H Treatment consists of the application to the hair of ung. hydrarg.
^^kinereum, or of the following:

^^H Q 01. petri italici 3 iiss.

^^H 01. olivce I i.

^^M Balsam. Peruvian. Zij.

^H U. D. S. Externally.

I^H^ Sia. UT. Fio. UB. Fm. ISO,

lou

In this manner the lice and nita are killed; they must then be re-

Iioved by diseiitangliag and combing the hair. The chitin sheaths ad-
ere very firmly to the hair, and are removed more readily by washing
'ith vinegar.
b. I'ediculus vestimentorum (clotliea louao) ia the largest variety of
Duse in man, and attains a length of three to five millimetres (Fig. 14d).
Its habitat are the folds of clothes, particularly of the shirt. It is found
chiefly on the neck and between tlio shoulder blades, on the sacrum,
sateSj external sorfaoe of the thigh, and immediately above the what-

874 PABA8ITE8 OF THB SKJS.

joint. It deposits its ova in a rosary-like arrangement within the folds
of the skin, and rarely leaves its habitat except to seek uoarishment on
the skin. It is, therefore, rarely found on the skin, but most be sought
for in the folds of the underclothing. Its sting produces pruritus and
wheals. Individuals who have suffered from body lice for a long time
present open wounds, crusts, pustules, excoriations, even furuncles and
extensive ulcers. When the efflorescences recover, they are followed at
first by white cicatrices, but later they give rise to a aeep*bro¥m, even
blackish diffuse pigmentation of the skin.

The treatment consists in placing the clothes in a vessel heated to
60-65^ B., and thus killing the parasites. The eruption is treated in
the ordinary way.

c. Pediculus pubis (crab louse) is only one millimetre in length (Fig.
150), and is found most frequentlv in the hair on the genitaliu. It may
also occur in the hairs of the axillae, limbs, chest, beard, and eyebrow^
but not upon the scalp. It is acquired most frequently daring coitus,
and gives rise to itching and eczema. Treatment similar to that of
pediculus capitis.

4. Fleas. Pulices.

a. The common flea, pulex irritans, has its habitat in the folds of
the underclothing. Its sting produces a minute extravasation of blood,
which is surrounded by a hyperaemic zone, which grows pale on pressure.
The latter also disappears spontaneously with great rapidity, while the

Eetechia lasts for days. Dirty individuals are often covered with flea
iteSj and if they are dull and suffer from high fever, difficulty in diag-
nosis may arise if typhoid fever is prevalent. Chief importance must Se
attached to the distribution of the petechiae, and to the presence of
roseola around some of them. In individuals with a delicate skin, fleas
give rise to wheals.

b. Sand flea (pulex penetrans) is found in America, most freouentlT
on sandy beaches. The female bores into the skia, gorges itself with
blood, and in two to five days produces inflammatory clianges in the
skin, which may terminate in ulceration, gangrene, and even erysipelas,
lymphangioitis, and tetanus.

5. Bed Bug. Oimex lectularius.

The sting of the bed-bug produces wheals, not infrequently a reflex
eruption of urticaria, which is attended with annoying pruritus. As a
result of the scratching, the wheals are often excoriated and covered
with crusts. The diagnosis is not always easy.

6. Guinea Worm, Filaria Medinensis. •

This worm is found chiefly on the west coast of Africa. It may at-
tain a length of one metre. Its habitat is the subcutaneous cellular
tissue which it probably reaches from within, inasmuch as it is swallowed
in the drinking-water and carried by the blood-vessels to the periphery
of the body. It gives rise to abscesses of the skin, ulcerations, furuncles,
and gangrene, producer fev^x, aiid even convulsions. If it projects

PARASITES OF THE SKIN.

375

from an open wound, it should be wound around
a little stick, and gradually withdrawn in the
course of a few hours.

Fio. 151.

7. Cysticerci of the Skin. Cysticercus celluloses

subcutaneus.

Cysticerci of the skin generally form round
or slightly flattened tumors, which are usually as
large as a hazelnut. They are painless on pres-
sure, have a peculiar, firm, cartilaginous resist-
ance, and are movable to a certain extent. They
are most apt to be mistaken for swollen lym-
phatic glands, and a positive diagnosis can onlv
oe made by extirpation. We then find a dull
white vesicle which, when cut open, discharges
a clear fiuid, and, upon its inner surface, con-
tains the head which is recognizable externally
by a thickening and slight depression of the
vesicle. The head often moves vigorously under
the microscope fvide Vol. II., Fig. 29).

Hundreds oi cysticerci are often found in
one individual, in other cases only a few. They
may gradually grow smaller and disappear, whife
new parasites sprout up in other localities.
Cysticerci are often found in other organs, viz.,
the brain, eye, and other viscera.

In rare cases, the patients also harbor tape-
worms. Self-infection is conceivable only in the
event that proglottides passed from the intes-
tines into the stomach, and were there dissolved
by the gastric juice.

The treatment consists of extirpation of the
tumors, if they are not too numerous.

B. Vegetable Parasites of the skin.
Debmatomycoses.

1. Pityriasis versicolor.

I. Symptoms and Etiology. — Microsporon
furfur, the fungus of pityriasis versicolor, proli-
ferates in horny layers of the epidermis, and,
according to Gudden, also penetrates the epider-
moidal portions of the hair follicles.

The skin is covered with orange-yellow,
brownish-yellow, or dark-brown patches which
are slightly elevated above the adjacent skin,
and glisten slightly or not at all; in old cases, they
are scaly ana fissured. They can be readily
removed by scratching with the finger-nail.
This lays bare the reddened cutis which bleeds from numerous small
openings.

If the epidermis scales are placed on an object glass, and a drop of

Female Guinea Worm.
Natural size.

176 PASASTrxs OF TSB acnt.

potash (1 : 3) added, the fnngi become cleorl; risible at the end d
ten to fifteen minatefl, after the epidermis cells have HWoUen and become
transparent. Tbej form round Leaps of spherical conidia, witb a dia-
meter of 0.005-0.007 mm. They contain not infreqnently a nncleos-Iike
structnre or granular protoplasm (vide Fig. 152). Myceliam threada
are also present. The older ones contain transverse partitions and one
or more nuclei in the individoal snbdiTiaions. Id some places, the round
oonidia sprout into mycelium threads; in others, couiclia sproDt from the
latter.

The patches of pityriasis versicolor are almost alirays fonnd on cot-
ered portions of the body. They generally appear tlrst on the cheat, then
extend gradually to the neck, alidomeu, and Iwck. They are sometimes
found in the azillie, on the mens veneris, in the inguinal folds, and on the
inner sarfaoe of the thigha. In exceptional cases, they are present in
the face, never on the hands and feet.

Large portions of the integument are often changed in the manner
described, as a result of the cMilescence of smaller patches. The centre

fta.iEa

, Urcellum tbrends ; 0. CooldlA ; e. EpIthellDm call*.

of the patches sometimes clears up, which the change continues to ex-
tend at the periphery.

Subjective aymptoms arc entirely absent, or there is slight itching,
especially while perBpirlng.

The diseaae does not occur during childhood or old age. Exacerba-
tions and remissions nre noticeable, und sometimes the disease disappears
temporarily. Koehner succeeded in inoculating the fungus upon his
own integument and upon that of rabbits; but infection from man to
man is rarely observed in practice.

II. D1AGNO8I8. — The ready desquamation of the pigment patches
distinguishes tliis from most otner pigment changes of the skin, and, in
addition, the fungus is readily found with the microscope.

III. Treatment. — This consists chiefly of cleanlmess. The skin
should be rubbed, for several successive evenings, with sapo viridis or
with:

5 Sapon. virid.,

Lact. Bul]>hur.,

Picis liquid.,

Spta. Tin. dilut au 3 i.

M. U. 9. To be rubbed in at night.

PAS&8ITE8 OF THB SKIN. oTT

and in the morning it shoald be carefully washed with a woollen cloth.
No spot shonld be oTerlooked, since it will serve as a fresh startiag'
point for the disease.

Z, Favut,

( Tinea favosa. Porrigo favosa. Dermatomycosis achorina. )

I. Stuptohs and Akatohioal Changes. — The fungua of fams
(Acharion s. Oidinm Schoenleinii) is foand almost always on the scalp.
When present on other parts, it Btarte, as on the scalp, from the hair-fol-
licles. It rarely affects the nails (onychomycosis favosa).

The disease appears at first as yellow points (as laree as a pin's head)
beneath the epidermis; they are perforated by a hair. The spots
gradually increase to the size of a pea, bean, or ten-cent jiece. At the
same time, a central umbilication appears, while the penphery becomes
elevated, and the so-called favus cnp is thus shaped like a plate.

AeboTloa SchoenleliiUfTOD) the lower l«r«n of Hie fknia cup. After Ekpod.

When the favas cnps are separate, the disease is known as favus
dispersas; when they coalesce, as favus confertus. In old cases, the
entire scalp may be attacked. The deposits on the skin not infrequently
lose their original salphnr color, and become whitish-yellow, light gray,
or dirty gray.

If tne favus crusts are removed, they may be ground between the
fingers, and emit a peculiar mouldy, musty odor. If particles are treated
with water or potash, and examined under the microscope, they are
found to consist, apart from a few epidermis cells, fat drops, grannlar
dotrituB, and schizomycetes, of numerous gonidia and mycelium threads
of Achorion Schoenleinii (Fig. 153). The gonidia preuomiaate in the
lower layers of the crusts; the mycelium threads, in the upper layers.
The gonidia are round, baud-shaped, or cask-shaped, and are found
singly or in groups or rows, while tne myceliam threads are segmented,
and m places branched.

Achorion Schoenleinii belongs to the mould fun^ (bviihomfoetea). It can be
conveyed to other individuals. The old view that it is Identical with the fungui
of pityriasis versicolor and herpes has been abandoned.

8T8

FABABITB» OF THB BEIN.

The inoreaaing derelopment of the favus trusts is attended irith im-
portant changes in the hairs and epidermis. At first the ftingua devel-
ops only in the funnel-shaped space situated at the opening of the hair-
follicle, bo that it is surrounded like a ring by epidermis. But it soon
Bpreads deeper into the follicle, and gives rise to nutritive disturbanceB

in the hair, partly as the result of pressure, partly by destruction of the
hair-papilla. The fungus passes between the external and internal root-
sheaths of the hair, later it perforates the upper cuticle of the hair, and
enters the cortical layers. The mycelia predominate in this repon
(vide Fig. 154). The hairs appear dry, destitute of gloss, break readily.
a be readily removed on slight traction, or fall out spontaneously. If

PABA8ITES OF THE SKIS. ' 379

the papilla has been destroyed^ regeneration of the hair is impossible, and
the part remains permanently bald.

If a crust is removed in tne earlier stages, the cutis is often found to
be red and slightly moist. Later it is covered with young epidermis,
80 that the removal of the crust shows a delicate, glistening epidermis,
which looks almost like a cicatrix. Atrophy of the sebaceous glands,
cvstoid formations in them, in rare cases cutaneous ulcerations have
also been observed.

The development of favus is associated with itching. Eczema of the
scalp and swelling of the adjacent lymphatic glands are sometimes ob-
served as complications. In a few cases herpes tonsurans and favus have
been noticed in the same individual.

In filthy persons, favus may last thirty years or more, the masses of
the fungus accumulating above each other in thick crusts.

If favus develops on other parts of the body, the crusts generally fall
off at an earlier period and spontaneous recovery occurs, except in rare
cases.

In favus of the nails (onychomycosis favosa), the nails are thickened,
fissured, brittle, and destitute of gloss, are exfoliated in parts, and on
the addition of potash are found to contain Achorion Schoenleinii. The
infection probably is the result of scratching the scalp which is covered
with favus.

II. Etiology. — The disease is either conveyed from animals, or from
man to man. It is often found in mice, but the fungus is generally con-
veyed to man by the cat, the latter being infect^ by mice or rats.
Favus has also been observed in dogs, rabbits, chickens, cows. The
greater the degree of uncleanliness the greater is the danger of infection
of one individual by another. The disease is most frequent in children
or youn^people, and also in the male sex.

III. Diagnosis. — The diagnosis is rendered extremely easy by the
aid of the microscope, so that a mistake is hardly possible.

IV. Prognosis, — The prognosis is good, except that the hair will
not be restored in parts whicn have become bald, if the hair follicles
have been destroyed.

V. Tbeathent. — In favus of the scalp, the crusts should be oiled for
two hours, and then covered with a piece of fiannel dipped in oil, until
the crusts can be entirely removed. The scalp is then carefully washed
morning and evening with green soap. After each wash, all unhealthy
looking hairs should be removed with the finders or a pair of tweezers,
together with all the hairs in the immediate vicinity of tne former crusts
(in order to prevent reinfection from the fundus which has been left in
the follicles). The parts are then rubbed with corrosive sublimate and
alcohol (gr. iij. : I iiiss.). This procedure should be continued four to
twelve weeks, and the patients should be kept under observation for
weeks afterwards, in order that the treatment may again be instituted if
a relapse occurs.

Other parasiticides have also been recommended, such as carbolic and salicylic
acids, sulphur, tar, oreasote, benzin, Peruvian balsam, styrax, turpentine, etc.

In favus of the nails, the affected parts should be excised and painted
with corrosive sublimate collodion (1 : 20).

SSU FASABITEB OP THE flKDT.

3. Herpes tonsurans.

(Tinea tondena. Trichotnt/ces a. Dermatomt/eoats tonaurans.)

I. AiTATOSiCAL CHAifOE3, — The fangns of herpes tonsamna (tri-
■cophyton tonBtiranB) is found not alOne oe the scalp, bat al90 upon parts
wfiicn are covered with downy haire. In the beam, it gifea rise to ayco-
■813 parasitaria (page 336), ana in parts of the skin which are coDstantly

Srotected and kept moist, it gives rise to eczema marginatam. It also
erelons occasionally in the substance of the noils (onychomycoaia ton-
earana).

Upon the scalp and on most other parts of the skin, the changes pn>-
daced by the fnngus appear in three forms, herpes tonauraas Teaicalo-
Bus, maculosas, and sqaamosaa. The latter ia a later atage of the other
two.

Epldfnnla scale In herpes toDHunns squBmoma. txmtslDlng more myoellK tbui

Herpes tonsurans veaiculosua is attended at first by the deTelopraent
of small, clear, cloudy, or even purulent vesicles, which are generally not
larger than a pin's heiiil. These soon dry into thin scales, at the peri-
phery of which new vesicles appear in a circle, and this may continue
until a surface larger than the palm of the hand ia affected. While re^-
iolos are still distinct in the psripheral zones, the central portions show
the changes of herpes tonsurans squamosus; indeed, the centre itself
may have entirely recovered. Adjacent circles may come in contactanil
form chain-like figures. In old and neglected cases, the larger pirt of
the surface of tlie body may bo affected.

In herpes tonsurans macnlosus wo notice, at first, small pale-r^d or
brownish-red patches, which arc slightly elevated above the healthy skin.
While the patch pales and becomes covered with thin scales, a new red
zone appears at .the periphery, and this proces3 is repeated as in the ve-
eicular form.

The fungus must be looked for in the peripheral zones. In herpes

PAEASITES OF THE BKTS. 351

fiqnamosne, they are contained in the scales; in herpes veajonlosus, in tho
epidermal covering of the veeicles, but repeated examination is often
necessary in order to discover them. In order to malf.e the microBcopi-
cal preparation transparent, a solution of potash (1 : 3) should be added.
Like the fungus of favus, tlnit of herpes tonsurans appears in the
form of round, oval, cask-shaped, honiogeneons, grannlar, or nucleated
gouidin and t bread -shaped mycelia {Fie. 165), but the latter are more
abundant than in the favus fungus. They are often branched, and filled
with granular protoplasm, vacuoles, or nucloi. The fungus is situated
between the cells of the stratum com«nm and the upper cells of tlierete
ilalpighii.

ria. lie.

Herpes tonsurans of tho scalp occurs most frequently in the equa-
10U8 form. The circles often extend to the integument of the forehead
• napo of the neck. Within the circles the hairs breal; very readilv, ao
lat spots which are alino!!t bald arc found upon the scalp. The naira
__« readily removed by traction, and. under tno microscope, it is found
that tho fungus has penetrated between the root sheatna of the hair
follicle, and also into tho cortical substance of the hair (vide Fig. 156).
As a rule, the pupilhi is not destroyed, eo that the hair is restored, after re-
moval of the fundus.

Onychomycosis tonsuraoB causes opacity, thickening, fisanring of the
Diiil which may finally be exfoliated. It affects only the finger nails,
irobably aa the i-oauH of aelf-infectlon in scratching herpetic patches,
"he herpes on the akin is sometimes recovered, ultnough onychomy-

S>i PAKUITEB OF TBK SSIN.

coii? continnes. The /nn^s elements are distinctly risible, ander the
microsco{)e. in nail scrapings which have been cleared up br the addi-
tion of potash (vide Fig. 15T).

Syoo^is paraeitaria has been diwnssed on page 33G. Huebner hti
shown that the eczema marginatum of Hebra is nothing more tban
herpes tonsurans. It is observed most freqnently on the inner surface
of the thigh ami scrotum, and may eitend to the pubes and perinenm.
It occuM more rarely in the axiMse. the folds under the breast, umbilicus,
or other parts. It forms hypenemic patches, which are covered with
resides, pustule-, Ecales, and crusts, and have a zigzag, sharp liorder.
The microscope reveals fungi in the ecales. bat, according to Ilebrn,
they never penetrate into the hair follicles. The peculiar appearance of
eczema marginatum is probably owing to the fact that the diseased

V. --

irlcLii)byt[n&. Potash pr^iiaratlan.

parta, on account of their protected position, are constantly bathed in a
tvarni. n;oist utnioi-phcre, or that herpes tonsurans complicates a pre-
existing iM-zemji.

Till' iiisi'ti-e niiiy liiiJfc for years, but Bpontaupous recovery sometime!
takes pl:ii-(-.

Thf sulpji'i'tivi' syniptums consist merely of itching, and even this is
not cunsuiiit.

II. Kri'ii-Dtn". — Inoctiliition proves that the disease is produced by
the fungus, hifcitiun fri)nim:in to man is more frequent than in farus.
and the disciisc nccurs cnik'niically in families, schools, and barrack;.
It is somotimos rnnv('vi.'d from barber shops through the medium of
nnclean shaving ntensiis. In other cases, it is contracted from animal
JdofT. cut, horse, ctnv, nibbii). The disease has also been observed iu
individuals who live in damp apartments, constantly use damp under-
clothing or bedding, or warm poultices. It is observed most freciuently

PABASITES OF THB SKIN. 383

in the spring and autumn, and in damp weather, and chiefly attack
children and young people.

III. Diagnosis, Prognosis, Tbeatmbnt. — The diagnosis is ren-
dered positive by the discovery of the fungus. The prognosis is good,
the treatment similar to that of favus, but recovery is effected more
rapidly.

INDEX.

Abdominal muBcles, panUysis of, 80

spasm <jf , 45

reflex of, 222
Abscess of the brain, 288

spinal cord, 84
Absentia epileptica, 206
Acanis follicalorum, 872

scabiei, 866
Achorion Schoenleinii, 877
Achromatia, 860
Acne artiflcialis, 885

cachecticorpni, 885

disseminata, 885

frontalis, 885

mentagra, 886

punctata, 885

pustulosa, 885

rosacea, 838

vulgaris, 885
Acrodynia, 824
.^Isthesiometer, 64
Ageusis, 71
Agraphia, 209
Albinism, 860
Alcohol paralysis, 155
Alexia, 209
Alopecia, 862

areata, 868

Celsi, 868
Amimia, 210

Amyotrophic lateral sclerosis, 186
Amyotrophy, spinal prosressive, 122
An»mia of the brain, 210

spinal cord, 77
AnaBsthesia, 62

dolorosa, 67, 85

gustatory, 71

olfactory, 70

trigeminal, 68
Anarthria, 177
Aneurism of cerebral arteries, 246

miliary, of cerebral arteries, 220
Anhidrosis, 849
Anosmia, 70
Anuria, hysterical, 298
Ape-hand, 28
Aphasia, 205

amnesic, 207

ataxic, 205

motor, 205
25

Aphasia, sensory, 206

total, 206
Apoplexy, cerebral, 218

of the cerebral meninges. 260

of the medulla oblongata, 185

of the spinal meninges, 172

spinal, 79
Apraxia. 209
Arm centre, cortical, 192
Arsenic paralysis, 154
Articular changes in tabes dorsalis, 108
Articular neuralgia, 62
Ascending spinal paralysis, 149

degeneration of spinal cord, 184
Asemia, 205

Associated movements, 225
Asteatosis, 852
Asymbolia, 205
Ataxia, 100

hereditary, 180
Athetosis. 288

Atrophic infantile paralysis, 114
Atrichia, 862

Atrophia musculorum lipomatosa, 813
Atrophy of the brain, 252

of face, unilateral, 805

of skin, 860
Auditory disturbances in facial paraly-
sis. 6
Aura, epileptic, 264
Axillary paralysis, 26

Base of brain, focal symptoms in dis-
eases of, 204
Baraasthesiometer, 68
Beirs palsy, 1
Beriberi, 75
Blepharospasm, 89
Boroorygmus, hjrsterical, 297
Brachial neuralgia, 58
Brach-Romberg symptom, 107
Brain, diseases of, 190

abscess, 288

ansBmia* 210

atrophy, 252

cancer, 240

cysts, 289

apoplectic, 219^

embolism, 229

encephalitis, 288

386

I2a>£X.

Brain, encephalitis, congenital, 238

glioma, 2d9

hemorrhage, 218
punctate, 229

hyperaetmia, 218

hypertrophy, 251

neuroses, 2o2

oedema, 217

parasites, 245

thrombosis, 229

tumors, 289
Bromine acne, 886
Bromliidrosis, 849
Brown-Sequard's paralysis, 188
Bulbar myelitis, 188

nuclei, paralysis of, 176
Bulbar paralyi^iSt apoplectit'orm, 186

chronic, 176
Bulimia, hysterical, 299

Cachexie pachydermique, 811
Callositas, 855
Canities, 361
Capsule, external, 208

internal, 197
Capillary hemorrhages in brain, 229

in spinal cord, 81
Caput oDstipum, paralytic, 15

spastic, 42
Catalepsy, 291

Carbon bisulphide paralysis, 154
Carbonic oxide gas paralysis, 154
Causalgia, 54
Central convolutions, focal symptoms

in diseases of, 192
Centrum ovale, focal symptoms in dis-
eases of, 196
Cerebellar peduncles, focal symptoms

in diseases of, 203
Cerebellum, focal symptoms in diseases

of, 203
Cerebral arteries, aneurism of, 246
Cerebral cortex, focal symptoms in dis-
eases of, 191
Cerebral hemorrhage, 218
Cerebral meninges, diseases, 253
hemorrhage, 260
inflammation, 253
Cerebral nerves, exit of, 205
vessels, diseases of, 229
aneurism, 246.
distribution, 209
embolism, 229
syphilis, 230
thrombosis. 229
sinus, inflammation of, 256
symptoms, diffuse, 190
focal, 190
Cerebro-spinal sclerosis, 91
Cervico-brachial neuralgia, 53

occipital neuralgia, 61
Chapman's rubber bag, 81
Cheirospasm, 155
Chloasma, 353
Choked disk, 243
Cholesteatoma of brain, 239

Chorea, 277

congenital, 277

gravidarum, 278

poflt-hemiple^c, 282

prsehemiplegic, 282
Chromhidrosis, 849
Cimex lectularius, S74
Cincture feeling, 85
Clavus hystericus, 2115
Claw hand, 24, 128
daustrum, 208
Clothes lice, 878
Cnidosis, 819
Coccygodynia, 62
Comedo, 852

Compression-myelitis, 144
Concussion, spinal, 143
Conditions, epileptoid, 267
Conduction, delayed, 106

paths of, in spinal oord, 181
Contractions. diple^c» 127
Contracture, hysterical, 288

seoondaiy, 181
Copiopia, hysterical, 296
Corpora quadrigemina, focal symptonif

in diseases of, 208
Corpus striatum, focal symptoms in

diseases of, 199 ^

Cortical centres, motor ^silepsy, 191
Cramp, 45

Crura cerebelli, focal symptoms in dis-
eases of, 208
Crura cerebri, focal symptoms in dis-
eases of, 199
Crural nerve, neuralgia of, 58

paralysis, 31
Crutch paralysis, 18
Crises, gastric, 95

intestinal, 106
Cyanhidrosis, 850
Cysticercus of brain, 245

skin, 375
Cysts, apoplectic, 219

Decubitus, acute, 86
Defluvium capUlorum, 862
Degeneration of lateral columns, 131

of posterior columns, 110

reaction, 7

secondarv of cord, 130
Demodex folliculorum, 872
Dermatitis, 819
Dermatomycoses, 875
Dermatoses parasitarisd, 865
Dermatozoonoses, 865
Dermoid cyst of brain, 289
Descending degeneration of spinal owd,

Diaphragm, neuralgia, 58

paralysis, 29

spasm, 44
Diplegia facialis, 9
Double sensation, 66, 106
Duchenne's disease, 812
Dura mater, cerebral, diseases of, 253

spinal, diseases of, 163

INDEX.

387

Dysaesthesia, 86

Dystrophia musculorum progressiva,
812

Echinococcus of brain, 245

spinal meninges, 175
Eclampsia, 270
Ecthyma, 888
Ectropium, paralytic, 5
Eczema, 825

caloricum, 825

capiUitii, 826

faciei, 827

marginatum, 880
Embolism of cerebral arteries, 229

of medulla oblongata, 186
Emprosthotonus, 247
Encephalitis, 288
Encephalomalacia, 220
Encephalorrhagia, 218
Enohondroma of brain, 239

spinal meninges, 175
Enteralgia, hysterical, 297
Ephelides, 858
Ephidrosis, 848
Epidermidophytes, 842
Epilepsy, 262

hystero-, 294

Jacksonian, 194
Epileptoid conditions, 267
Epiphora, 5

Erb s supraclavicular point, 27
Ergotism, 154
Erythema, epidemic, 824

exudative, 828

hypersBmic, 819

noaosum, 822
Etat cribl6, 215

Facial hemiatrophy, 805

hypertrophy, 807

neuralgia, 46

paralysis, 1

spasm, 86
Fatty emboli of brain, 280
Favus, 877

Fibrillary twitchings, 126
Fibroma of brain, 289

medulla oblongata, 188

spinal meningtfs, 175
Filana medinensis, 874
Flexibility of muscles, waxy, 291
Folie musculaire, 281
Friedreich's disease, 180
Fright paralysis, 151

Oastric crises in ataxiii, 109

Gteingrene, symmetrical, 810

Olobus hystericus, 297

Qlossalgia, 50

Qlossoplegia, 16

Gluteal paralysis, 84

Glosso-labio-laryngeal paralysis, 176

Graphospasm, 155

Guinea worm, 874

Gustatory nerves, diseases of, 70

Gustatory nerves, diseases of, ageusia,
71
hypergeusia, 71
parageusia, 71

Hair, diseases of, 861
HsBmathidrosis, 850, 172
Haamatoma of dura mater, 254
HsBmatomyelia, 79
HsBmatomvelitis, 79
Haematorrhachis, 172
BsBmoptysis, hysterical, 298
Head tetanus, 276
Hemorrhage of brain, 218
medulla oblongata, 185
spinal meninges, 172
spinal cord, 79
Hemianaesthesia, 199
Hemianopsia, 195

Hemiatrophy, facial progressive, 805
Hemichorea, 281
Hemicrania, 801
Hemihypertrophy, facial, 807
Hemiopia, 195
Hemiplegia, alternate, 201
cerebral, 222
hysterical, 298
spinal, 189
Hereditary ataxia, 180
Herpes iris, 828

tonsurans, 880
Heterotopia, 289
Hiccough, 48
Hirsuties, 856
Hydrocephaloid, 211
Hydrocephalus, 247
acquired, 248
acute, 248
congenital, 250
external, 249
intermeningeal, 247
Hydromyelia, 98
Hydrophobia, hysterical, 297
Hydrops articulorum intermittens, 811
Hyperacusis, 6
Hyperasmia of brain, 218

spinal cord, 78
Hyperaesthesia, gustatory, 69

olfactory, 70
Hypergeusia, 70
Hyperhidrosis. 848
Hyperosmia, 69
Hypertrichosis, 856
Hypertrophy of brain. 251
face, unilateral, 807
hair, 856
nails, 857
skin, 858
Hyphidrosis, 849
Hypoglossal paralysis, 16

spasm, 41
Hysteria, 291
Hystero-epilepsy, 294

Ichthyosis, 855
Impetigo, 888

888

IBTDEX.

Infantile paralysis, 114

acute atrophic, 114

cerebral, 288

spinal, 114
Infectious paralysis, 151
Intercostal neuralgia, 55
Intestinal crises in ataxia, 110
Ischialgia, 58
Itch, 3S5
Itching, cutaneous, 364

Jacksonian epilepsy, ld4
Joint changes in ataxia, 108

neuralgia of, 62 •

Keratosis. 355
Kussmaul-Landry paralysis, 149

Lagophthalmus, paralytic, 5
Laryngeal crises, in ataxia, 110
Lateral sclerosis, 112
Latissimus dorsi, paralysis of, 29
Lingual spasm, 41

paralysis, 16
Lead paralysis, 151
Lenticular nucleus, focal symptoms in

diseahes of, 199
Lenti^ines. 853
Levator anguli scapuldB. paralysis of,

29
Leptomeningitis, 167
Leukoderma, 360

Leukomyelitis, chronic posterior, 100
Leukopathia, 360
Lice, 872
Lichen ruber, 346

scrophulosorum, 346
Lipomatosis musculorum progressiva,

812
Locomotor ataxia, 100
Lum bo-abdominal neuralgia, 57

Macrogaster platypus, 872
Malum Cotunnii,' 58
Mastodynia, 59
Median paralysis, 22
Medulla oblongata, diseases, 176

compression, 189

emboliflm, 186

hemorrhage, 185

inflammation, 188

injurieH, 189

thromboslH, 186

tumors, 188
Melasma, 354
Meniere's disease, 290
Meningeal a|>oplexy, 172, 260
Meninges, anatomy of, 260
Meningitis, spinal, 167
Mentagra, 336>
Microsporon furfur, 376
Migraine, 301
Miliaria, 330
Miliary aneurisms of cerebral arteries,

220
Milium, 353

Mogij^phia, 155
Mnitipie sclerosis, 91
Muscles, diseases of, 313

ischsBmic paralysis, 818

pseudo-hypertrophy, 812

of mastication, spasm of, 40

progressive ossification, 317
Muscular atrophy, hereditary, 812

juvenile, 812

spinal, 122
Muscular hypertrophy, false, 312

true, 816
Muscular spasms, primary spinal, 169
Muscular twitchings, fibrillary, 126
Musculo-cutaneous nerve, paralysis (^

26
Myelitis, acute, 82

apoplectiform, 83

chronic, 90

disseminated, 91

hemorrhagic, 83
Myelo-malacia, BS
Myelo-meningitiB, chronic, 90
Myxoedema, 811
Myositis ossificans progressiva, 817

Nsevus, 353
Nerves, diseases. 1

inflnmmation, 71
Nerves of arms, combined paralrsis ot

27
Neuralgia, 46

alveolar, 50

ano- vesical, 62

cervico- brachial, 53

cervico-occipital, 51

ciliary, 49

crural, 58

facial, 46

inferior alveolar. 50

inframaxillary, 50

infraorbital, 49

intercostal, 55

lingual, 50

lumbo-abdominal, 57

mental, 50

mammary, 57

obturator, 58

of joints, 62

ophthalmic, 49

phrenic, 53

sciatic, 58

spermatic. 61

supraorbital, 49

supra maxillary, 49

trigeminal, 46
Nettle rash, 819
Neurasthenia, cerebral, 300

spinal, 148
Neuritis, 71

multiple, 74

nodose, 72
Neuroses of the brain, 262

joints, 62

skin, 364

spinal cord, 147

INDEX.

889

Nictitating spasm, 40

Nucleus lenticularis, focal symptoms

in diseases of, 199
Nystagmus, 95

Obturator neuralg^, 58

paralysis, 83
Occipital lobe, focal symptoms in dis-
eases of, 195
Occipital neuralgia, 51
(Edema of brain, 217
Olfactory nerve, diseases, 69

anosmia, 70

hyperosmia, 69

parosmia, 70
Oligosteatosis, 852
Oliguria, hysterical, 298
Onychauxis, 857
Onychogryphosis, 857
Onychomycosis favosa, 877

tonsurans, 880
Ophthalmia, neuro-paralvtic, 69
Ophthalmic neuralgia, 49
Opisthotonus, 274
Osmhidrosis, 849
Ovarialgia, 295
Ovum hystericum, 295
Ozyokoia, B

Pachymeningitis, cerebral, 258

external spinal, 162

internal spinal, 164
PapilUtis, 248
Parageusia, 71
Paralysis, acute ascending, 149

agitans, 288

arsenic, 154

after acute diseases, 151

alcohol, 155

bisulphide of carbon, 154

carbonic oxide, 154

facial, 1

fright, 151

fflosso-labio-laryngeal, 176

infectious, 151

lead, 152

motor trigeminus, 18

phosphorus, 154

psychical spinal, 151

railway, 148

reflex, 150

spastic, 112

toxic spinal, 161
Paraplegia, urinary, 150
Parasteatods, 852
Parhidrosis, 849

Parietal lobes, focal symptoms in dis-
eases of, 194
Parkinson's disease, 288
Parosmia, 70

Patellar tendon reflex, 107
Pectoral muscles, panUyis of, 28
Pediculus capitis, 872

pubis, 874

▼estimentonim, 878

Pedunculi cerebri, focal symptoms in

diseases of, 199
Pellagra, 824
Pemphigus, 881
Perimeningitis spinalis, 162
Perineuritis, 72
Peripachymeningitis spinalis externa,

152
Peroneal paralysis, 84
Pharyngeal crises in ataxia, 110
Phlebitis of cerebral sinuses, 257
Phosphorus paralysis, 154
Phrenic nerve, neuralgia, 58

paralysis, 80
Piano-player's spasm, 158
Pica hysterica, 295
Pigment atrophy of skin, 860

emboli of brain, 280
Pityriasis rubra, 844

versicolor, 875
Pleurosthotonus, 274
Plica polonico, 826
Polioencephalitis, acute, 288
Poliomyelitis, acute infantile, 114

chronic, 122

of adults, 120
Poliosis, 861
Polysesthesia, 66
Polyneuritis, 74
Polytrichia, 856
Pompholix, 831

Pons, focal symptoms in diseases of, 201
Post-hemiple^ic chorea, 282
Prsehemiplegnc chorea, 282
PrsBpucial calculi, 851
Pressure points, hysterical, 295

Valleix', 48
Progressive muscular atrophy, 122
Prosopalgia, 46
Prosoplegia, 1
Prosopodysmorphia, 805
Prosospasmus, 86
Prurigo, 844
Pruritus, 864
Psoriasis, 840
Pulex irritans, 874

penetrans, 874
Pupils, reflex rigidity of, 109

Radial paralysis, 18
Railway paralysis, 148
Raphania, 154
Reflex epilepsy, 268

hysteria, 292

paralysis, 150

vertigo, 290
Rhinoph^ma, 889
Rhomboids, paralysis of, 29
Risus sardomcus, 278

Saltatory spasms, 161
Band flea, 874
Sarcoptes hominis, 865
Scabies, 865
Sciatica, 58

Sclerema adultorum, 3S7

Scleroderma. 357
Scleroma, 357
Sclerosis, multiple. 01

of lateral columns. U2
of posterior coluniOB, 100
periependymal . 9(1
Sebaceous eecretion, anomalies of, 3!
Beborrliusa. 350

Serratus magnus, paraljsia of, 37
Singultus, 43
Sinuses, cerebral. inSammation of, i

IhniiubosiB of, 257
Skiu, diaeasex of, 310
atrophy, BCD
■ hypertropliy, 353
iDSammationB, 310
erythematous, 319
papular, 344
pUBtular, 333
BCaly, 310
vesicle-like. 32S
vesicular, 331

paraaiteB. animal, 3S5
vegetable, 375

secretory anomalies, 348
Sleep parBilysis, 19
Spasmus nictitans, 40
Spastic gait, 114

spinal paralysis, 113
Speecn centres, 'cortical, 208
Spermatio neuralgia, 61
Spinal accessory, paralysis of, 14
Spinal cord, diseases of. 77

abscess, 84

acute inflammation of anterior
boms, 114

acute injuries, 141
• 77

formation of cavities in, 9S
functional weakness, 143
hemorrhage, 79

L = _ ,jg

chronic, 00

irritation, 147

lateral sclerosis, 113

multiple scleroais, Ql

punctata hemorrhages, 81

scleroais of poBterior columos, 100

Bscondary degeaeratioD, 130

tumors, 93

unilateral lesions, 138
Spinal meningee, diseases of, 1(12

hemorrhage, 173
Status eclamplicus, 370

epilepticns. 366

hystero-epilepticus, 294
i, Vitus' dance, 377

paralytic conditions of, 309
Syncope, 313
Syringomyelia. 98

Tabes dorsalis, 100

spasmodica. 113
Tactile sensation, eiaminatiou of, W
Tar acne, 335
Tegmentum, 201
Teleerapher's spasm, 158
Tendon reflexes, 107
Tenosinitis hypertrophica, 31
Tetany, 158
Tetanus, 371
Thalamus opticus, focal symptoms ii

diseases of, 199
Tbermfesthesio meter, 65
Thrombosis of cerebral sinuses, 25S

vessels, 22B
Thomsen's disease, 163
Tibial paralysis, 34
Tic convulsif, 37

doulonreui, 48

rotatoire, 43
Tinea favosa. 377

tondens. 880
Tosic spinal paralyses, 151
Tremor. 388
Trichauxis, 3B0
Trichomycosii
Tricophyt" ■
Trichorhe ... ...

Trigeminal ansistbeBia, 68

neuralgia, 46

paralysis, 13

spasm, 40
Trismus, 373

Trophoneurosis facialia, 305
Trousseau's phenomenon, 159
Tumors of brain, 338

medulla oblongala, 188

spinal cord, B8

spinal meninges, 174

Ulnar paralyais. 33
Urine, spastic, 308
Urticaria, 319

Vaginismus, 298
Valleis' pressure points, 48
Varus. 335
Vertigo, 289

a stomacho Ueso, 390

cardiac, 390

epileptic. 267

senile, 289
Vitiligo, 360

WaiT flexibility of muaclu, 381
Word blindneBs, 309

deafness, 308
Writer's spasm, 156
Xeroderma, 864
Zone, epileptogenic, 368

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