Feb., 1941]

PRESENTED TO

T a vnnvw THE ARMY MEWCAL LIBRARY

i DRY S PARALYSIS: BANERJEA & THE ASS'N. OF MILITARY SURGEOHS 65

Original Articles

CLINICAL OBSERVATIONS ON LANDRY'S PARALYSIS 1/

(Based on a study of 10 cases)

By J. C. BANERJEA, m.b., m.r.c.s. (Eng.),

m.r.c.p. (Lond.) Uony, Jr. Visiting Physician, Medical College Hospi

a

and

M. N. DE, m.b., m.r.c.p. (Lond.)

Professor oj Medicine, Medical College, Calcutta

Landry, in 1859, described a Lining

terized by an acute flaccid Par?X treading in the lower limbs and ^apid'y ?eck, upwards to involve the trunk, upl

'

Since the bulbar and the respiratory c

aralysis then, this syndrome of acute

ascending para^y & has been observed by various

gross number of diseases associated wit

pathological lesions of the nervousy > .

as (a) an ascending form of acute

poliomyelitis, (b) acute asce diphtheritic

(c) acute polyneuritis, specially 1

origin, (d) intrathecal haemorrhag > ^ and vaccinal and post-erythematous { '

^ an(j measles) encephalomyelitis, U) ? ? 1933). rarely (g) disseminated sclerosis ( 'm,ed \n This syndrome has also occasions

y antirabic

the course of typhoid fever a

inoculation. It is therefore desirabl<e, term

interest of clarity, that the use o> ^

'

Landry's paralysis' should be .

w^ere those cases of acute ascending par J little sensory and sphincteric disturbanc^^ marked, or absent, muscular wasting

is iyors and

recovery is complete among Jrhe s system gross pathological changes m the

ne

are absent in the autopsy cases.

Etiology The aetiology of the disease is not de

known. It is probably an acute form of po y

neuritis of toxic or infective origin. 0f resemblance of the disease to some V acute anterior poliomyelitis, post-vaccm^ e

Phalomyelitis and rabies is strongly gg

of an infection by a neurotropic vir..

infective agent has probably a ec

t-vp 0f

[or the lower motor neurones, mesp hlood- the mode of entry, whether via 'the bloott

stream or the axis cylinders of the ;nfec_

nerves. The possibility of a bactei1 d

tion is extremely doubtful, thoug ,

(1903) attributed some of his case, to

bacterial agent, a micrococcus.

Pathology On a naked-eye examination

the spma Qme

fjnd specially its grey matter s* .

_es

^yperaemia with a few punctiform haemo

Microscopical examination reveals vascular engorgement and varying grades of degenera- tive changes in the anterior horn cells and the cells of Clarke's column, such as chromatolysis and diffuse fatty changes. These changes are

most marked in the lumbo-sacral enlargement which is the seat of the first paralysis. Peri- vascular infiltration, neuronophagia and neuro- glial proliferation are absent. Slight fatty changes may be seen in the skeletal muscles. The cerebro-spinal fluid is clear and may show normal or increased pressure. The protein content is normal or slightly increased. The cell content is either normal or may show a

slight lymphocytosis. In one of our cases the

lymphocyte count was 20 per c.mm. Spon- taneous coagulation of the fluid due to a high protein content has been reported by some

observers. Enlargement of the liver, spleen and mesenteric lymph nodes is not infrequent.

Clinical features

Incidence.?Landry's paralysis is undoubtedly a rare disease. There were only seven cases in 49,284 admissions into the Medical College Hospital during the last 14 years, viz, 1926 to 1939. We came across three cases in the Howrah General Hospital during the last 5

years 1935 to 1939. According to Aring (1936) there were only seven cases in about 30,000 admissions into the Boston City Hospital from 1st September, 1933 to 1st August, 1934. The disease occurs usually between 16 and 54 years (Collier and Adie, 1929). In our series the

age incidence was between 15 and 37 years. Males are more frequently affected than females. The ratio of males to females is 9 : 1 in our series. Mode of onset.?The onset, though sometimes

sudden, is usually gradual, ushered in by certain prodromal symptoms such as malaise, headache, insomnia, slight fever, anorexia, vomiting, diarrhoea, dull aching pains in the

back and limbs and numbness of the extremities. In our series, the premonitory symptoms were as follows :?slight or moderate fever in six cases, vomiting and diarrhoea in one, pain and tingling sensation in the limbs in two and transient stiff- ness of the neck in one. It is interesting to note that in two cases premonitory symptoms were conspicuously absent.

Psychical functions.?Consciousness is re-

tained throughout the illness. Intelligence, memory and judgment are unimpaired. Speech is usually normal.

Cranial nerve functions.?The cranial nerves are usually not involved except in severe cases. AVe have noted the infra-nuclear type of facial paralysis in three cases (unilateral in two, bilateral in one), dysphagia in four, hoarseness of voice in two, palatal paralysis in three, and diminished sensibility over the area of supply of the trigeminal nerve in one. Nystagmus indicating an involvement of the vestibular nerve or the cells of Clarke's column was

66 THE INDIAN MEDICAL GAZETTE [Feb., 1941

observed in one case. The occurrence of diplopia or ptosis has been reported in the literature, but we have not come across any- such symptoms. Motor junctions.?-Weakness first appears

in the muscles of the lower limbs, one limb being affected a few hours earlier than the other. The proximal muscles are more affected than the distal, so that the movements of the fingers and toes may be present, though the limbs cannot be moved. In severe cases, the paralysis rapidly spreads upwards, in the course of a few hours to a few days, involving succes- sively in the order of their innervation from the spinal cord, the muscles of the trunks, upper limbs, neck and those supplied by the bulbar nuclei. In some cases the muscular weakness

may start in the face, neck or the upper limbs and then spread downwards to the trunk and the lower limbs. Such a descending type of

Landry's paralysis was observed in two of our cases (vide cases 1 and 10). The paralysed muscles are flaccid and slightly tender on pres- sure. Wasting is usually absent but it may occur in a moderate degree, in cases where

recovery is delayed beyond 2 or 3 weeks. It was present in two of our cases. Fibrillary tremors are absent. The electrical reactions are usually normal, but in cases associated with muscular wasting a partial reaction of degene- ration may be present, as in two of our cases.

Sensory junctions.?In most cases there is no

objective loss of sensation. In three out of ten

cases, a blunting of the sensibility to light touch and pin-prick over the distal parts of the limbs was present. In one of these three cases there was, in addition, a diminished

sensibility of the conjunctivae and cornese with

astereognosis and loss of sense of position in the fingers and toes.

Reflexes.?The superficial and deep reflexes are either absent or diminished in the affected area. The plantar reflex, if present, is flexor. In our series the deep reflexes (knee and ankle jerks) were absent in all, the superficial reflexes were absent in seven, sluggish in one and

present in two. The functions of the sphincters are, as a rule, unimpaired though occasionally, as in two of our cases, retention of urine may occur in the early days but it clears up spon- taneously in a few days. Some difficulty in

emptying-the rectum may also be present, as in one of our cases.

Trophic junctions.?Vasomotor changes or

changes in the nutrition of the skin and nails are absent. Bed-sores are not known to occur. ??VConstitutional symptoms?The constitu- tional symptoms are usually mild. The disease

is, in most instances, afebrile except in the

presence of bronchial or pulmonary, complic- ations. In six out of our ten cases the course was febrile.

Blood picture.-?There is no distinctive blood picture of the disease. The average total

leucocyte count was 7,063 per c.mm., the maxi- mum being 11,856 and the minimum 6,500.

Course and prognosis.?In unfavourable cases which constituted about 60 per cent of the total number in our series, the paralysis extended in the course of 6 to 13 days, either to the cervical region of the spinal cord, causing death by res- piratory failure, or to the muscles of deglutition leading to death from aspiration broncho- pneumonia. Out of six deaths in our series, five were due to respiratory failure and one was due to bulbar paralysis. In two of the fatal cases respiratory failure was associated with diaphragmatic paralysis. In favourable cases, the paralysis ceases to spread and con-

valescence begins. The power of movement gradually returns, first in those muscles which were affected last. The distal muscles of the limb recover earlier than the proximal. ^

period varying from 3 to 6 months is often required for complete recovery. In two of our cases the recovery period was 2 and 4 months, respectively. In two other cases recovery was not complete even after 7 months and 2 years of convalescence. The occurrences of relapses and recurrences are unknown.

Diagnosis The diagnosis of a typical case of Landry's

paralysis presents little or no difficulty. The onset of a rapidly spreading flaccid paralysis of the limbs and trunk, the absence of muscular wasting, sensory loss and sphincter disturbances and the occurrence of complete recovery if the patient survives are diagnostic features of the disease. Of course, in atypical cases the pres- ence of slight sensory loss, muscular wasting with reaction of degeneration and sphincteric disturbances may throw doubt as to the real nature of the disease, but it must be remem- bered that these clinical features per se do not contra-indicate the diagnosis of Landry's para- lysis. In such cases, however, before arriving at a diagnosis we have to differentiate it froin (?) acute ascending type of poliomyelitis) (?) acute ascending myelitis and (c) intra- thecal haemorrhage. From the acute ascending type of poliomyel'

itis, it is distinguished by (i) its rarity in child- hood, (ii) wide-spread nature of the paralysis> and (Hi) absence of high fever, signs of menin- geal irritation, marked muscular wasting and reaction of degeneration. A high polymorph0' nuclear leucocytosis in the peripheral blood with a -lymphocytosis in the cerebro-spinal fluid is

strongly suggestive of poliomyelitis. The preS- ence-of. a residual wasting on recovery excludes the diagnosis of Landry's paralysis. From acute ascending myelitis it is easily

differentiated by the absence of severe sensory loss below the level of the lesion, sphincteri0 disturbances, bed-sores, and Babinski's sig*! (unless the lumbo-sacral enlargement of the cord is- affected or the transverse lesion is severe and

complete). Moreover, in the former disease*

Feb., 1941] LANDRY'S PARALYSIS : BANERJEA & DE 67

the motor paralysis, semJory imultaneoUSly.

sphincter paralysis _ ?ccurf, of syphilitic Besides, acute myelitis w

oft? ,

a lympho- origin and hence associated positive cytosis of the cerebro-spinal fluid

<

cerebro- Wassermann reaction of the serum ^ ^g_ spinal fluid. Intrathecal hsemorr g

t|lc tinguished from Landry s para y iysis> simultaneous appearance of m? jf an(j by sensory loss and sphincter incon

1

b'ro_spinal the presence of hemorrhagic

""The distinction of Landry's P"?1? no pra?

acute polyneuritis is artificial ??''?' {0?;cs tical value. Both the conditions

h , goth

on pathological and elinical gi ?

toxic are due to a toxic blood state lower agent in both has a selective action ^ neurones, both motor and sensory. some instances of acute

_ polyneur

^

s

eXperi- rabies, lead poisoning, diphtheria,. action 0f mental curare poisoning, the sele nr neurones the toxin is confined to the lower

motor neuro

only.

Treatment

In the absence of any specific remedy ^ treatment consists in (a) the m

nutrition general body resistance by adequ ^ere be and correction of associated ,an^u\vDOthetical any, (b) the elimination of tl

purgatives toxins by diuretics, enemata, m y , fluid, and daily drainage of cerebro- p relief (c) prevention of complications,

a

of symptoms. , resistance :

(a) Maintenance of the bod essen-

For^this purpose adequate nouris 11

easily tial. The diet should be bght and easi y

assimilable and yet should consis bohyUrates sary quantities of proteins, *ats'

^ere is' and vitamins, specially vitamin Jt5i. ,

an associated anaemia, it must be 1

doses the appropriate drugs, viz, iron 1

or liver-extract injections, accor g

hypochromic or hyper chromic. _ usually , (b) Elimination of toxins : Toxins, ai > usua^y

eliminated by the skm, kidneys retic bowels. Hence the administration of

a _

and diaphoretic mixture and of mere _ Some tlves is useful in ensuring ellmma^phvo_Sninal of the toxin is circulating in the

c m> 0{

fluid and daily withdrawal of 15 nfltll're will cerebro-spinal fluid by a lumbar P^ct certainly reduce the toxic load and neip

recovery of the nerve celK _ os^ (c) Prevention of complications .

ar(jed serious complication that is to

_

S?

against is the paralysis of the rc?P"'o Z.nDed b^lbar muscles. The patient should be llP to help respiration and prevent yp V -ne c?ngestion. Hypodermic injections

of y

sulphate in doses of grain VI?'. c?"\\\-pr and .? adults have been very helpful.. o >

Adie (1929) advocate injection of atropine _g

check the progress of the respiratory P y

and to prevent the accumulation of exudates in the bronchioles which may lead to collapse broncho-pneumonia. We have had beneficial results in some of our cases from the daily administration of vitamin Bx (thiamine chlo-

ride), in the form of betaxin, in doses of 4,000 international units for 2 weeks. When res-

piratory paralysis supervenes artificial respira- tion should be continued with the aid of a

Drinker's apparatus till the crisis is over. In cases of bulbar paralysis, there is great diffi-

culty in feeding and maintaining nutrition.

Besides, aspiration broncho-pneumonia is a

common complication. In such cases feeding by the nasal or oesophageal tube should be resorted to. The mouth should be kept scru- pulously clean by the use of antiseptic washes.

(cl) Relief of symptoms : The symptoms such as pain, pyrexia and retention of urine are fortunately not persistent. Still the use of

analgesics and antipyretics, such as aspirin and salicylates, is indicated in the presence of pain and pyrexia. If there is retention of urine the bladder should be catheterized every 8 hours under strict aseptic precautions.

Case reports Case 1.?S., Muslim, male, aged 24 years, was

admitted on 27tli September, 1937, with the complaint of inability to move both the upper and lower limbs. This developed in the course of 3 days about 2

weeks before admission. The order of affection was

tight fingers, right forearm, right arm, left fingers, left

forearm, left arm and then the legs. He had no

premonitory symptoms, nor did any constitutional dis- turbance accompany the paralysis. Past history?kala- azar 14 years back. Family history?nothing contri-

butory. Personal history?an employee in Bata Shoe

Co., Ltd. He prepared rubber sheets for soles of shoes. Moderate smoker. No other addiction. None else in the workshop similarly affected. General examination-

average build and nutrition. No amemia, cyanosis, or

jaundice. Temperature?98.4?F. Pulse/respiration? 72/20. Nervous system?higher cerebral functions

unimpaired; sleep?good; speech?normal. Cranial nerve functions?normal." Motor functions?loss of

power in the muscles of both upper and lower limbs, more marked on the right side. Muscles?flabby, no wasting noticed on admission, but he developed some degree of wasting during the course of the illness. Fibrillary twitching absent. Sensory functions? unimpaired. Calf muscles slightly tender on pressure. Reflexes: abdominal reflex?sluggish; plantar reflex? flexor and sluggish; deep reflexes?absent; sphincters? normal. Trophic functions?normal. Alimentary sys- tem: spleen?just palpable; liver?not palpable. Respiratory system?no abnormality detected even

though a careful watch was kept for any sign of involvement of the diaphragm and inter-costal muscles. Cardio-vascular and urinary systems showed no

abnormality. Laboratory findings?Blood: haemoglobin ?80 per cent; leucoeytes?9,900 per c.mm.; poly- morphonuclears?56 per cent. Wassermann reaction? negative. Electrical reaction?partial reaction of

degeneration in the affected muscles. Patient was

discharged on 1st February, 1938. Cured without any residual paralysis. Case 2?P. K. M., developed Landry's paralysis in

the course of an attack of epidemic dropsy. He was admitted on 25th July, 1938, with the following complaints:?(i) Swelling of the feet and legs with a red flush for 10 days, (n) fever varying between 101 ?F. and 100?F. for- the first. 5 days, none for the last

.4.. days, (iii).. inability ..to move, tha lower. limbs for

3 days, (iv) difficulty in swallowing for 3. days,

68 THE INDIAN MEDICAL GAZETTE [Feb., 1941

(v) nasal intonation of voice for 2 days, (vi) palpita- tion for 10 days and (vii) hoarseness of voice for 5 days. Past history?nothing of importance. History of epidemic dropsy in the family. Personal history nothing contributory. General examination?patient toxic, no anaemia, cyanosis or jaundice. Temperature? 100?F. Pulse/respiration?152/38. Nervous system? higher cerebral functions?normal; sleep?good; speech ?normal. Cranial nerve functions?paresis of the soft palate and right side of the face; hoarseness of voice and dysphagia; no other abnormality. Motor functions ?paralysis of the muscles of the lower limbs and paresis of the muscles of the upper limbs. Sensory functions unimpaired. Both superficial and deep reflexes absent. Sphincters normal. Trophic changes absent. Skull and vertebral column normal. Respiratory system?air entry into lungs moderate. Alimentary system?tongue thickly coated and dry; liver enlarged two fingers and tender; spleen?not palpable. Cardio-vascular system? heart sounds weak and rapid. Urinary system?nothing abnormal. Laboratory findings?Blood: haemoglobin? 70 per cent; leucocytes?7,126 per c.mm.; polymorpho- nuclears?SO per cent. Sedimentation rate 37.5 mm.

per hour. Patient succumbed on 28th July, 1938, on the 12th day of the illness, from paralysis of the diaphragm. Case 3.?A. B. D., Hindu, male, aged 37 years, was

admitted on 26th July, 1938, with the following com- plaints:?(i) Pain in the legs, (ii) inability to move the lower limbs and (Hi) fever. He had at first pain in the medial aspect of the thighs but this extended down to the legs later on. Fever developed 2 days later and paralysis of the lower limbs 3 days later. Past, family and personal history?nothing of importance. General examination?build and nutrition ?poor; ansemia present; no jaundice or cyanosis. Temperature?100?F. Pulse/respiration?118/26. Ner- vous system?higher cerebral functions unimpaired; sleep?good; speech?normal. Cranial nerve functions normal. Motor functions?paralysis of the muscles of the lower limbs. Paresis of the muscles of the upper limbs. Sensory functions normal. Some wasting of the paralysed muscles present. Fibrillary twitchings? absent. Reflexes?superficial reflexes absent; knee and ankle jerks absent; biceps, triceps and supinator jerks normal. Sphincters?control of the vesical sphincter was lost but is now normal; defsecation normal. Trophic functions normal. Skull and vertebral column normal. The respiratory, alimentary and circulatory systems showed no abnormality. Laboratory findings? Blood: haemoglobin?65 per cent; leucocytes?9,672 per c.mm.; polymorphonuclears?79 per cent. Urine? B. coli on culture. No abnormality detected in the stool. Patient was discharged on 3rd September, 1938, in a much improved condition.

Case 4.?L. P., Chinese, male, aged 25 years, was admitted with the following complaints:?(i) weakness of both upper and lower limbs, (ii) fever, (iii) difficulty in breathing, and (iv) difficulty in swallowing solid food. He developed the above complaints in the course of 10 days in the following order: fever, weakness of the lower limbs and weakness of the upper limbs. Past, family and personal history?nothing contributory. General examination?build and nutrition moderate. Cyanosis present; no jaundice or anaemia. Nervous system?higher cerebral functions unimpaired; speech normal; sleep good. Cranial nerve functions?difficulty in swallowing solid food; no other abnormality. Motor functions?loss of power in the muscles of both upper and lower limbs; slight wasting; fibrillary twitchings absent. Sensory functions unimpaired, only tender calf muscles during the early stage. Deep reflexes absent. Trophic functions unimpaired. Skull and vertebral column normal. Respiratory system?sucking in of the epigastrium during inspiration (paralysis of

diaphragm); rate 30 per minute. Cardio-vascular and alimentary systems?nothing abnormal. Laboratory findings?B1 )d: leucocytes 6,500 per c.mm., poly- morphonucL 'S 69 per cent; Wassermann reaction negative. Uriue and stool?nothing abnormal. Patient died of respiratory failure on the 13th day of the "illness.

Case 5.?N. K. B., Hindu, male, aged 20 years,y . I admitted with the following complaints:?(i) Pareslflr=t the upper and lower limbs for 5 days, weakness m developed in the lower limbs, (ii) intermittent feV '

(Hi) nasal intonation of voice for 5 days and (iy) culty in swallowing liquids. Past and family history ,

nothing contributory. General examination?build nutrition average. Cyanosis present. Temperature^ 100?F. Pulse/respiration?104/36. Nervous system, higher cerebral functions normal; sleep normal; sP^e0{ normal. Cranial nerve functions?nasal voice (paralysis the soft palate); difficulty in swallowing liquids; no otn abnormality. Motor functions?paresis of the muse of the upper limbs; complete paralysis of the muscl. of the lower limbs; no wasting. Fibrillary twitch"^ absent. Sensory function unimpaired. Reflexes?o? j superficial and deep reflexes absent. Sphincters normj Trophic changes?nil. Skull and vertebral column, normal. Respiratory system?sucking in of the eP* gastrium during inspiration (paralysis of diaphragm' Alimentary and cardio-vascular systems?n?tnm? abnormal. Died of respiratory failure on the 8th o

of the disease. 1st Case 6.?S. B., male, aged 30 years, admitted on 3j December, 1937, with all the signs and symptoms sim1'

to those of N. K. B. (case 5) except that there was p paralysis of the diaphragm. The bulbar involvemeP was more marked. Patient died on 1st January, w*

' I on the 6th day of his illness, 24 hours after admission- <

Case 7.?K. S., Buddhist, aged 25 years, was admit*^ on 4th April, 1939, with the following complaints: (i) fever?5 days, (ii) severe pain in left lower lina|p. 3 days; the pain spread to the right lower limb W next day, (in) loss of power of the left lower 3 days, (iv) loss of power of the right lower li^SL 2 days and (v) retention of urine?24 hours. patient took some purgative 4 days back as a result which he had six loose stools and two vomits and tbe he developed the above complaints. General examm9 tion?patient exhausted; build and nutrition?modera^y Nervous system?higher cerebral functions norm9' Cranial nerve functions?nystagmus present; no

abnormality. Motor functions?paralysis of both lo^i, limbs; no wasting. Fibrillary twitchings absent. Ne slightly rigid. Sensory functions?unimpaired. Refle* '

?superficial: abdominal present; plantar?no respons" Knee and ankle jerks absent; biceps and triceps sluggish. Sphincters?retention of urine, no evacuati0 of the bowels; patient had to be catheterized and gi^ei enemata. Trophic changes?nil. Skull and vertebra column normal. Respiratory, alimentary, urinary cardio-vascular systems revealed nothing abnorm9' Laboratory findings?Blood: hajmoglobin 70 per leucocytes 11,856 per c.mm.; polymorphonuclears^ 74 per cent. Urine and stool?nothing abnorm9^ Blood urea?50 mg. per cent. Wassermann reaction negative. Electrical reaction?reaction of degenerate in the muscles of both lower limbs. Patient y .

discharged on 21st May in a much improved conditio*^ sphincters became normal; power in the lower lim^ was gradually returning and the patient could m?' his right great toe.

g I Case 8.?Mrs. R., Anglo-Indian, female, aged 37 ye^"J

was admitted on 2nd June, 1935, with the folIoWiP* complaints:?(i) pain and tingling sensation all oV ,

the body, _ (ii) pricking sensation in the hands and }e

and (Hi) inability to walk or stand. General examm tion?build and nutrition moderate. Jaundice, an?111' and cyanosis?nil. Temperature?98.4?F. Pulse/respi1'9 tion?-84/24. Nervous system?higher cerebral fuD

j tions_ unimpaired; sleep normal; speech norm9j Cranial nerve functions?diminished conjunctival corneal sensibility on both sides. Paralysis of ^ facial nerve on both sides (infra-nuclear type). v? i of ̂

pharyngeal and palatal reflexes. Hoarseness

voice. Motor functions?complete paralysis of muscles of the lower limbs; paresis of the muscles the upper limbs; muscles flaccid; no wasting; c% ordination lost (as shown by the finger-nose teS

Sensory functions?loss of sensation to light touch both legs up to the middle of the thighs; hyperaesthe-i of the soles of the feet; joint sense in the fingers 9?

Feb., 1941] LANDRY'S PARALYSIS : BANERJEA & DE 69

toes lost; astereognosis present. absent; biceps, no response; knee and ankle j Sphincters?: triceps and supinator jerks si ?c - ?

vertebral normal. Trophic changes?nil. b

,? tarv cardio- column?normal. Respiratory, 'abnormal. vascular and urinary systems-notmoderately Laboratory finding?Wassermann May, 1935, positive. Patient was discharged on . , weakness almost completely cured but for a slight

laciai ^

of the right side. , nA 07 vears, was

Case 9.?B. L., Hindu, male, aged 37:^complaint admitted on 8th November, 1938, wi h {or of loss of power of both lower and upper 8 days. General examination bui

Temperature moderate. Anajmia and ,3au^ice ,,+p Nervous 98?F., pulse- 80, and respiration 20 per ^ed; sleep system?higher cerebral functions P

functions? normal; speech normal; cranial n muscles unimpaired. Motor functions?paralysi upper of tl,o lower limbs; paresis of the moscks off ^ limbs. Sensory functions?slight blu J= Sphincters over the lower limbs. Vertebral normal. Trophic changes?absent, dku 1

tient was

column normal. Respiratory jpV: uef0re death, reported to have respiratory dimcu Cardio- Alimentary system?spleen slightly e o '^normal/ vascular and urinary systems no b

^ per Laboratory findings?Blood: leucocj

^ ^ ^

c.mm.; polymorphonuclears 68 per ce ,

c^jon of rings and crescents found. (.iear 20 cells serum doubtful. Cerebro-spinal fluid; \ mann' reaction Per c.mm. (majority lymphocytes); v\ ass failure strongly positive. Patient died oif r ]P

^ digease. 3 days after admission on the 11th d^y years, was Case 10.?M. M., Hindu male, aged

to y laints

admitted on 12th January, 1939, with lower iimbs. of tingling and weakness in the uppei t:ced in the The weakness and tingling were first ?build upper limbs 8 days ago. General exammtion^. and nutrition moderate; jaundice anc|__Nervous no cyanosis. Pulse/respiration

iu / ?

normal; system?higher cerebral functions norm ,

g-s Qf the speech normal. Cranial nerve functions 1

Motor right side of the face; no otherahn bmbs paretic; functions?muscles of the upper and lo\ cpnSory func- no pasting; fibrillary twitching absen

.

^ over the tions?impairment of sensation to lig Reflexes? distal parts of the upper and lower

limbs *?fnciers both superficial and deep reflexes a - >

vertebral normal. Trophic changes?nil. Skull . r?jeg 9olumn normal. Respiratory system , spleen in both lungs. Alimentary system-~~~hv __nothing lust palpable. Cardio-vascular system

abnormal. Urinary system?nothing a cent;

ratory findings?Blood: haemoglobin pev leucocytes 6,500 per c.mm.; polymorph Jeve\0ped cent; Wassermann reaction negative. Pa ^ Paralysis of the diaphragm 4 days after

admission

died on the 13th day of the illness.

Comments A typical case of Landry's paralysis is

characterized by (1) ascending flaccid par

lysis unassociated with any wasting o m >

(2) loss of tendon reflexes, (3) absence of sen

s,0I>y loss and sphincter disturbances an

(4) absence of reaction of degeneia io .

study of our cases however reveals that s

(cases 1, 3, 4, 7, 8, 9 and 10) P^sentedone or more atypical features; thus

case 1

wasting of the affected muscles with partial re

action of degeneration; case 3 showe<cl^ome +' n_ of the paralysed muscles, as

well as

of urine though lasting for the firs ?

Case 4 also showed some wasting of the c

.

m^scles. In case 7 there was retention o

ar^d fseces for a few days. Moreover, a 1

of degeneration was present in the muscles of lower limbs. In cases 8, 9 and 10 there was

blunting of sensation to cotton-wool and pin- prick over the lower limbs. In case 8, there were in addition some loss of sensibility over

the cornea and conjunctiva, astereognosis and loss of sense of position of the fingers and toes. Further analysis reveals that there was sdme

residual paralysis in one of the lower limbs in cases 7 and 3 even after 7 months and 2

years of convalescence respectively. The pres- ence of a positive Wassermann reaction of the serum in case 8 and of a positive Wassermann reaction of the cerebro-spinal fluid in case 9 was a mere coincidence. A much more interesting finding is the presence of a few malignant ter- tian rings and crescents in case 9. It may be

argued that in this case Landry's syndrome was caused by a malignant tertian infection and its concomitant embolic lesions of the spinal cord. But such a hypothesis was untenable because the patient was afebrile, quite conscious and his blood examination revealed both rings and crescents indicative of an old infection.

Summary

(1) An attempt has been made to define

Landry's paralysis. (2) Its aetiology and pathology have been

briefly discussed.

(3) The clinical picture of the condition has been described in detail on the basis of an

analytical study of ten cases.

(4) The prognosis and differential diagnosis have been dealt with.

(5) Ten case notes have been appended. (6) The atypical features of Landry's para-

lysis have also been commented upon.

Acknowledgment

We take this opportunity to extend our grate- ful thanks to Lieut.-Colonel J. C. De, i.m.s., the Superintendent, Medical College Hospitals, Calcutta, and to Lieut.-Colonel B. H. Singh, i.M.S., the Superintendent, General Hospital, Howrah, for their kind permission to utilize the case records. Our thanks are also due to Dr.

Amulya Ratan Roy and Dr. I. Ilias for much valuable assistance in collecting the case reports.

REFERENCES

Abing, C. D. (1936). The Practitioners' Library of Medicine and Surgery, 9, 298. D. Appleton-Century Co., London.

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