Lathyrism India Chaudhuri Et Al 1963

7/29/2019 Lathyrism India Chaudhuri Et Al 1963

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. Journal of theIndian Medical AssociationV O L U M E 41N U M B E R 4 PUBLISHED TWICE A MONTHEDITOR H. K. ROY, M.D. (CAL.) A U G U S T 16, 1963CALCUTTA

b ORIGINAL ARTICLESLATHYRISM* : A CLINICAL AND EPIDEMIOLOGICAL STUDY

R. N. C H A U D H U R I , F.R.C.P.E., F.N.I., Director and Professor of Tropical MedicineM. K. CHHETRI, M.D., M.R.C.P.**, Reader

T . K. S A H A , M.D., D.PHIL., Assistant Professor AND P. P. M I T R A , M.B.B.S., LecturerSchool of Tropical Medicine, CalcuttaLathyrism is a disease of which the most.prominent clinical feature is muscular weakness oflegs and later spastic paraplegia ; it occurs amongst"people whose staple diet is a vetch, Lathyrus. In'India, Lathyrus sativus, locally known as Khesari[da l is incriminated. We here describe an outbreakthat occurred in a remote rural area, about 250^kilometres from Calcutta, which we investigated;both locally aswell as by admitting several patientsto hospital.

EPIDEMIOLOGYIt first came to the notice of the authoritiespearly in 1960 when some apparently healthy"persons were seen limping about with or withouti:the aid of sticks. The affected locality consisted ofI several small hamlets scattered about on eitherof a river over an area of about 12 squarefmiles. Rice was the staple diet of the inhabitantspvith very little khesari (Lathyrus) but 6 years|ago there was a heavy flood which left a thickleposit of. silt and sand in the fields, making themit for paddy cultivation. So they startedrowing khesari instead, and as these plants grewluxuriantly and cost very little, they made it anmal event and had been using these grainsiberally in recent years. After harvesting in

February the seeds were stored in earthen potsWand consumed daily after removal of the husks asflour (simply-mixed with water), hand-made breador as dal (cooked in water like soup). T his wassupplemented sometimes by a little rice or wheat.After 3 or 4 months when the stock of khesari wasexhausted, they would take to rice again. Somevegetables were taken, but rarely fish, meat ormilk.The people were mostly cultivators andpossessed no land of their own and served aslabourers for which they were paid either inkhesari or money which they in turn spent on thisarticle of food, it being much cheaper than rice..It was after this heavy consumption of khesarithat cases of lathyrism began to appear, reachingthe peak period in June-July and then decliningwith the change to rice. T his sequence of eventshad been occurring every year over a period of 4or 5 years. No reliable information could beobtained as regards the extent of its incidence, butwe were able to trace 82 victims in various stagesof the disease amongst 54 families. 18 suchfamilies had each more than one person affectedup to a maximum of 4, the members falling ill inabout the same season within a period of 2 to 6weeks. The remaining families had no more than

* The earlier part of the work was carried out by the Clinical Research Unit (I.C.M.R.) at the School of Tropicalledicine, Calcutta.** Now at the Ins t i tute of Postgraduate Medical Education & Research, Calcutta.169


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170 J. INDIAN M. A., VOL. 41, NO. 4, AUGUST 16, 1963one victim in each. There were, of course, manypeople in and outside these families who escaped,though consuming similar food. Persons of allages were affected, but only 8 females wereencountered.

CLINICAL FEATURESThese are based on the history and examinationof 22 patients who were brought to Calcutta and

admitted to the Carmichael Hospital for TropicalDiseases for investigation. Except 2 girls and 1boy aged between 7 and 8 they were all adultmales. The duration of their illness varied from5 months to 5 years. All possessed fairly goodhealth except 3 who had moderate anaemia. Therewere no obvious vitamin or other nutritionaldeficiencies.Prodromal symptoms had been present in 16patients. They were: (1) Painful spasms andcramps of calf muscles and tingling sensation inthe legs in 13 cases. These occurred especially atnight and continued for varying period of 3-15days before the onset of paralysis. (2) Precipit-ancy of micturition in one case for as long as 9months, and then he found his legs stiff. (3)Heaviness of the lower limbs in one case. (4)Fever in one case.The onset of actual paralysis of lower limbswas sudden in 12 cases following some exertion,e.g., ploughing, walking a long distance orcarrying a heavy load. In others, the onset wasslow and indefinite with gradual development ofjveakness and spasticity of legs. Other symptomsresent with it were : ( 1 ) Cramps and tinglingwhich persisted to a variable degree in those whohad them in the prodromal stage, but developed

in 5 others after the onset of paralysis. (2) Painat the back in the lumbodorsal region, persistentin nature, in 16 cases. (3) Precipitancy ofmicturition in 13 cases . (4) Faecal incontinencein .4 cases. (5) Sexual impotence in 2 cases. Themotor functions gradually worsened, walking beingparticularly affected. In the majority the maxi-mum disability was reached in 2-7 months, afterwhich the condition usually remained stationary,but in a few there was further deterioration over alonger period, one of them being severely disabled.7 patients, while at hospital, were using one ortwo sticks for walking. The upper limbs wereentirely unaffected.Examination of the nervous systemHigherfunctions, speech and cranial nerves were normal.In both the lower extremities, the muscle tonewas increased, more of the flexors than extensors.Power was diminished in all. Diffuse atrophy ofmuscles was noticed in one patient and atrophy ofquadriceps on one side in 2 others. Sensory-

changes were generally absent except areas ofhyperaesthesia in one patient and loss of vibrationsense in another. Abdominal and cremastericreflexes were absent in 8 and 13 cases respectivelyand plantar reflex was bilateral extensor in all.Knee and ankle jerks were exaggerated in all,associated with ankle and patellar clonus in abouthalf. The gait was spastic with varying flexorspasms of the muscles of lower limbs.Report from School of Physical Medicine onthe neurological findings in 14 cases of the presentseries was as follows : There was upper motorneurone type of lesion in all cases and the nerveconduction was positive in all. There was noevidence of denervation except in one case (theseverely disabled one) with diffuse atrophy of themuscles of the lower limbs. Examination of theindividual muscles revealed some selective distri-bution of weakness or spasm : (a) Gluteus mdiusand maximusmarked weakness in all cases, (b)Invertors and evertors coordination testsinvertorspasm in all cases, (c) Tibialis anteriornot con-

tracting properly due to weakness and also due togastrosoleus spasm, (d) Spasm and in some casescontracture of hamstrings. These factors are res-ponsible for the characteristic gait. The spasm ofthe muscles cannot be due to peripheral mecha-nism because injection of 2 per cent lignocainehvdrochloride in the muscles did not relieve thesame.

INVESTIGATIONS(a) HaematologicalThe average haemoglobinwas about 11 g. per cent. Three patients weremoderately anaemic. Eosinophilia of 10 to 21 percent was noticed in 14 cases. Erythrocyte sedi-

mentation rate (Westergren) was elevated in allexcept 2, the average value being 33 mm./hr., butin some it was over 80. Total serum B12 level waswithin normal range.(b) BiochemicalThe most significant findingwas hyperglobulinaemia in all (Table 1). Electro-phoresis showed a significant rise in gamma-globu-lin. The average findings were as follows : serumalbumin 3"7 g. per cent, serum globulin 3"7 g. percent, gamma-globulin fraction 38 per cent. Thy-mol turbidity was above the normal range in mostof the cases.(c) Other examinationsStool had hookwormova in 20 cases and ascaris ova in 11 cases. X-raysshowed no abnormalities in chest or bones (verte-brae and long bones). The cerebrospinal fluidshowed no significant abnormality.Thus the most significant abnormalities werethe increase of serum globulin and gamma-globu-lin, elevated ESR, increased thymol turbidityand moderate rise of eosinophils.


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< ~ ^ < / _ ^ LAlHYRISMCHAUDHURI T L. 171

TABLE IS HO WIN G PLASMA PROTEINS AND SR IN THE22 PATIENTS UNDER OBSERVATIONSerum protein

SerialNo. Total(g. %) Albumin(g. %) Globulin(g. %)-Gammaglobulin

E S R(mm./hr.)? 1I 2 4! , 56- 7* 8, - 9

1011

1 2; - ' l 3r-14;.. is* 16I 17I 18 20L- 21tr 22

8-47-17-0"8-2

6-77-87-57-56-76-98-07-07-88-06-47-17-36-97-66-57-68-2

4 53-63-44-03-03-43-53-63-5

-2-33-93-34-13-43-43-73-73-94-43-44-44-2

3-93-54-64-23-74-44 03-9 '3-24-64-T3-73-74-6

' -30. 3-4

3-63-03-23-13-24-0

31-434-03 6 - 9 '27-622-0s r27-531-2 35-3 30-932-5 .27-529-7

. 36-634-233-630-537-529-436-138-3

344585154828

- 247814 583528

' 1725' 4

1922

.. 28' 1911

3418

For comparison, a series of\27 'normal' indivi-duals from the affected families having similardietetic history was investigated. Su rprising ly, 13;of them had hyperglobulinaemia (about 3"5 g. percent) along with a rise of gamma-globulin (above34 per cent). These figures were normal in theremaining 14 subjects.Further, 10 normal subjects of the localityreported to have never consumed khesari prepara-tions were also similarly investigated and the; findings were all normal.

TREATMENTWith hospital diet all the patients gained inweight with improvement in blood picture, but* there w as no ap parent effect on the neurolog ical.manifestations. Muscle relax ant like me phenesin(tolseram) also had no effect whatsoe ver. B utprostigmin injections 0'5 mg. daily for 10 daysi were distinctly beneficial. Stiffness gradua lly dimi-rnished, power of legs was regained to a certainextent and most of those using sticks could do.without them . Pre cipitanc y.. of mictu rition, and

incontinence of faeces also'd isapp eared ^in" nearly N"half the cases. T he improvemen t appeared morestrikin g in those with .shorter -duration. Sym ptoms.like backache, cramps and the tingling sensa- '.


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172 j . INDIAN M. A., VOL, 41, NO. 4, AUGUST 16, 1963important factors worth noting in this outbreakare ingestion of large quantities of the seeds andalmost entire absence of food of animal origin.Incidentally the seeds were examined and identi-fied as those of Lathyrus sativus.L,athyrism is essentially a disease of the nervoussystem. Ex perimental studies and autopsy reportsare scanty. Bu zzard and Greenfield (1921) foundon postmortem in a patient, the margins of thespinal cord presenting a honey-combed appearanceas is seen in subacute combined degeneration.Filimonoff (1926) observed sclerosis of the lateralregion of the cord, not strictly confined to thepyramidal tract, with the small blood vesselssclerosed and obliterated in places. Acton andChopra (1922) demonstrated constriction of thespinal vessels supplying the anterolateral columnin rats after feeding them with extract of Lathyrussativus. It was postulated by Acton (1922) that thelesion in the spinal cord in clinical cases of lathy-rism was due to thrombosis of blood vessels supply-ing the anterior an d an terolateral tracts ; this causeddegenerative changes which only partially affectthe crossed pyramidal tract and partially or whollythe extrapyramidal tract. The fully developed clini-cal picture in our casesparalysis, increased kneejerks, loss of abdominal reflexes and of sphinctericcontrol, pain in the lumbodorsal region andincrease in muscle tone also indicates that thelesin whatever its nature, is highly selective andlocalised in the posterolateral region of the cord,predominantly affecting the pyramidal and extra-pyramidal tracts at the upper lumbar and dorsalsegments.The epidemiological data clearly point to theaction of some toxin but the manner of its actionis unkn own . Detailed investigation in the presentseries of 22 patients revealed hyperglobulinaemia,and a rise of gamma-globulin with raised ESR,eosinophilia and the increased thymol turbidityin the majority. We suggest that lathyrism is theresult of antigen-antibody eaction and that theabove changes are but manifestations of the sameprocess/ It may be that the antigen-antibodyreaction has injurious effect on the central nervoussystem in its most vulnerable part (upper lumbarand lower dorsal segment) which results in theclinical syndrome. The history that there was aninterval of a few months between the commence-ment of lathwus intake and the onset of the illnesssuggests thahe body wasbeing sensitised duringthis period with the formation of antibodies againstthe -toxin The severity of the. reaction mustdepend on, among other possible factors, theamount of lathyrus ingested, individual susceptibi-lity and repeated sensitisation by the toxin.Identical biochemical and haematological abnor-

malities were also present in half the number of'normal' individuals in the affected families livingon similar diets. Presumably these were thepersons in whom the reactions were mild and whowere still in what may be called the biochemicalphase, whilst others in whom this mechanism wasvery active and periodically stimulated, progressedto manifest clinical disease.In lathyrism, apart from finding the nature ofthe supposed toxin, there still remain obscurepoints which require elucidation. For instance,Mackenzie (1927) opined that people suffered onlywhen Lathyrus sativiis is grown in virgin soil ornewly cultivated land and that it loses its lathyro-genic property after a few years' cultivation. Inthe outbreak under report the seeds were originallybrought from a neighbouring State (Bihar) wherelathyrism is common. Th ese seeds were distinctlyof larger size than the local variety though theybelonged to the same species. No contaminantwas detected such as seeds of Vicia sativa whichhas been incriminated by some workers as thecause of the disease (Anderson et al., 1925).SUMMARYAn outbreak of lathyrism in a hitherto un-affected rural area due to heavy consumption ofLathyrus sativus peas, tiie plants having beenwidely cultivated with seeds imported from aneighbouring endemic state, is reported.The clinical features are described.The haematological and, biochemical findingssuggest that the neurological manifestations arethe result of antigen-antibody reactions injuringthe spinal cord.Prostigmin injections definitely ameliorated the

condition specially in ca3R with shorter duration.By means of propaganda the lathyrus cultiva-tion in the area was reduced considerably and withit the disease came under control.ACKNOWLEDGMENT

The au thors thank Dr. R. h. Nath, Professor ofBiochemistry, Dr. J. B. Chatterjea, Professor of Haema-tology, Dr. S. P. Basu, Radiologist, and Professor S. R-Bose, Botanist, for help in the investigations. Thanksare also due to Dr. S. Sarkar, Physiotherapeutis t, Schoolof Physical Medicine, Calcutta, for the special neurologi-cal reports of 14 patients of the present series.REFERENCES

ACTON, H. W.Indian Med. Gaz., 57 : 241, 1922.A CT O N , H. W. AND CH O PRA , R. N.Ibid., 57 : 412, 1922.A N D E RSO N , L*. A. P. , H O W A RD , A. AND SI M O N SE N , J. L.Indian J. Med. Res., 12: 613, 1925.BUZZARD, E. F. AND GREENFIELD, J. G.The Pathologyof the Nervous System, 1921, Constable & Co.,London , p. 232.


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BASAL CELL CARCINOMAAHMAD ET AL. 173R. N.Annua l Rep . Ca lcu t t a Schoo l Trop .JYIeJ. 1959-60, 1961, Su pdt . G ovt. P rin tin g, W estBengal , Aiipore , p . 34., L. N. Z. Ges. Neurol. Psychiat., 105 : 76,1926. CTrans. Roy, Soc. Trop. M cd. Hyg., 4 4 :333, 1950.

'GUTIERREZ, F . H..Ann. Bromatol (Madrid), 2 : 261, 1950.dem10 Congress Internat . Ind. Agri . Y. Aliment(Mandit), 1954, p. 560.MACKENZIE, L> . H . h.Indian Med. Gaz., 62 : 201, 1927. R . L . H.Brit. M e d . } . , 1 : 25 3, 1940., M. N. Nature , 170 : 124, 1952.fSADASIVAN, T . S ., SULOCHANA, C . B. , JOHN, V. T.,

SUBBARAM, M. R . AND GO PA UN , C.Curr. Sei., 2 9 :86, 1960.

BASAL CELL CARCINOMA :A CLINICOPATHOLOGIC STUDY OF120 CASESK. N. AHMAD, M.D.Dem onstrator in PathologyK. M. WAHAL, M.D., D.sc, F.C.A.P.Reader in Pathology

AN DR. M. L. MEHROTRA, M.D., PH.D.Professor of PathologyDepartment of Pathology & BacteriologyK.G.'s. Medical College, Lucknow

Basal cell carcinoma is seemingly a biologicpinigma as it arises from the more primitivefpidermal basal cells and yet is biologically less[active or malignant than squamous cell carcinoma|Which arises from prickle cells, a maturer cell than|basal cell. T he other interestin g feature about thisf o u r is its histogenesis. Ew ing (1940) andg W i s (1960) believe that basal cells, of theppidermis or of the skin appendages, are thesource of this tumo ur. O ther workers, have criti-cised this view and they derive these tumoursfrom specialised basal cells destined to form skinglands (Krainz, 1921), hair matrix (Haythorn,931 ; Wallace and Halp ert, 1950 ; Swerdlow ,|958). Lever (1954) and other dermatologistsisider that these tumours arise from the primarypithelial germ cells.:-During the period 1949 to 1961, we cameross 120 cases of basal cell carcinoma whichfere thoroughly studied keeping in mind their'stogenesis, histological appearances and clinicalitures. The present communication describesfindings on this material.

METHODS AND MATERIAL " "The material for the study comprised of suitablesized pieces obtained from the lesions which wereserially cut wherever necessary. T he sectionswere stained with Harris' haematoxylin andeosin, Van Gieson's stain for collagen andVerhoeff's stain for elastic fibres.RESULTS

Age and sex incidenceOf the 120 cases, 86were males and 34 females. T he maximum ageincidence was in the fourth and fifth decades(Table 1). 23 out of 118 tum ours were in patientsunder the age of 30 years. T he youngest patientwas aged 8 years and the oldest 84 years.TABLE 1SHOWING AGE DISTRIBUTION OF 118 CASES

( A G E N O T S T A T ED I M C A S E S )

Age in years0-10 11-20 21-30 31-40 41-50 51-60 61 &above

Total cases 20 35 34 20

LocationThough the tumours were located inall the regions of the body, over 75 per cent of thetumours were on the head and face, the eyelids(30), face (31), scalp (19) and nose (6) being thesites of predilection (Table 2). T he incidence oflesions on the face was over six times more inmales than in females except in the case oftumours arising from the eyelids where the inci-dence was equal (15 males and 15 females). T hedistribution in other sites of the body did not revealany sex bias or any particular area of predilectionexcept for the tumours of the hand (5 cases) andback (3 cases) all of which were observed in males.Clinical featuresIn every instance the lesionwas a solitary one and no case of multiple tumourswas recorded in this series. T he tumours mani-fested in the majority (86 cases) as a solitary, slowgrowing nodule or as an irregular growth whichwas pigmented in 10 cases. T he remaining 34cases presented with an indolent ulcer which bledon touch. The duration of the lesions was variable,the average being 1"8 year s. In one instance thelesion had been there for 45 years, in 3 cases thetumour had existed for over 20 years and in 48cases over 2 years. T he shortest period recordedwas 2 mon ths in a 25-year old male. Regionallymph nodes were enlarged in 6 cases but unfortu-nately none was submitted for histological exami-nation.


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Journal of theIndian Medical AssociationV O L U M E 41N U M B E R 4 PUBLISHED TWICE A MONTHE D I T O R H. K. ROY, M.D. ( CAL. ) A U G U S T 16, 1963CALCUTTA

ORIGINAL ARTICLESLA T H Y R I SM * : A CLINICAL AND EPI D EM I O LO GI C A L ST U D Y

R. N. C H A U D H U R I , F.R.CP.E., F.N.I., Director and Professor of Tropical MedicineM. K. CHHETRI, M.D., M.R.C.P.**, Reader

T . K. S A H A , M.D., D.PHIL., Assistant Professor AND P. P. M I T R A , M.B.B.S., LecturerSchool of Tropical Medicine, Calcutta

Lathyrism is a disease of which the mostprominent clinical feature is muscular weakness oflegs and later spastic paraplegia ; it occurs amongstpeople whose staple diet is a vetch, Lathyrus. In'India, Lathyrus sativus, locally known as Khesaridal is incriminated. We here describe an outbreakthat occurred in a remote rural area, about 250'kilometres from Calcutta, which we investigatedboth locally as well as by admitting several patientsto hospital.

EPIDEMIOLOGYIt first came to the notice of the authorities- early in 1960 when some apparently healthypersons were seen limping about with or without-the aid of sticks. The affected locality consisted of;. several small hamlets scattered about on either;side of a river over an area of about 12 square[miles. Rice was the staple diet of the inhabitants[with very little khesari (Lathyrus) but 6 yearsago there was a heavy flood w:hich left a thickdeposit of. silt and sand in the fields, making themfj for paddy cultivation. So they startedgrowing khesari instead, and as these plants grewluxuriantly and cost very little, they made it anmual event and had been using these grainsliberally in recent years. After harvesting in

February the seeds were stored in earthen potsWand consumed daily after removal of the husks asflour (simply-mixed with water), hand-made breador as dal (cooked in water like soup). This wassupplemented sometimes by a little rice or wheat.After 3 or 4 months when the stock of khesari wasexhausted, they would take to rice again. Somevegetables were taken, but rarely fish, meat ormilk.The people were mostly cultivators andpossessed no land of their own and served aslabourers for which they were paid either inkhesari or money which they in turn spent on thisarticle of food, it being much cheaper than rice..It was after this heavy consumption of khesarithat cases of lathyrism began to appear, reachingthe peak period in June-July and then decliningwith the change to rice. This sequence of eventshad been occurring every j^ear over a period of 4or 5 years. No reliable information could beobtained as regards the extent of its incidence, butwe were able to trace 82 victims in various stagesof the disease amongst 54 families. 18 suchfamilies had each more than one person affectedup to a maximum of 4, the members falling ill inabout the same season within a period of 2 to 6weeks. The remaining families had no more than



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170 J. INDIAN M. A., VOL. 41, NO. 4, AUGUST 16, 1963one victim in each. There were, of course, manypeople in and outside these famuies who escaped,though consuming similar food. Persons of allages were affected, but only 8 females wereencountered.


admitted to the Carmichael Hospital for TropicalDiseases for investigation. Except 2 girls and 1boy aged between 7 and 8 they were all adultmales. The duration of their illness varied from5 months to 5 years. All possessed fairly goodhealth except 3 who had moderate anaemia. Therewere no obvious vitamin or other nutritionaldeficiencies.Prodromal symptoms had been present in 16patients. They were: (1) Painful spasms andcramps of calf muscles and tingling sensation inthe legs in 13 cases. These occurred especially atnight and continued for varying period of 3-15days before the onset of paralysis. (2) Precipit-ancy of micturition in one case for as long as 9months, and then he found his legs stiff. (3)Heaviness of the lower limbs in one case. (4)Fever in one case.The onset of actual paralysis of lower limbs\Vas sudden in 12 cases following some exertion,e.g., ploughing, walking a long distance orcarrying a heavy load. In others, the onset wasslow and indefinite with gradual development of^veakness and spasticity of legs. Other symptomsfcresent with it were : ( 1 ) Cramps and tinglingwhich persisted to a variable degree in those whohad them in the prodromal stage, but developed

in 5 others after the onset of paralysis. (2) Painat the back in the lumbodorsal region, persistentin nature, in 16 cases. (3) Precipitancy ofmicturition in 13 cases . (4) Faecal incontinencein .4 cases. (5) Sexual impotence in 2 cases. Themotor functions gradually worsened, walking beingparticularly affected. In the majority the maxi-mum disability was reached in 2-7 months, afterwhich the condition usually remained stationary,but in a few there was further deterioration over alonger period, one of them being severely disabled.7 patients, while at hospital, were using one ortwo sticks for walking. The upper limbs wereentirely unaffected.Examination of the nervous systemHigherfunctions, speech and cranial nerves were normal.In both the lower extremities, the muscle tonewas increased, more of the flexors than extensors.Power was diminished in all. Diffuse atrophy ofmuscles was noticed in one patient and atrophy ofquadriceps on one side in 2 others. Sensory

changes were generally absent except areas othyperaesthesia in one patient and loss of vibrationsense in another. Abdominal and cremastericreflexes were absent in 8 and 13 cases respectivelyand plantar reflex was bilateral extensor in all.Knee and ankle jerks were exaggerated in all,associated with ankle and patellar clonus in abouthalf. The gait was spastic with varying flexorspasms of the muscles of lower limbs.Report from School of Physical Medicine onthe neurological findings in 14 cases of the presentseries was as follows : There was upper motorneurone type of lesion in all cases and the nerveconduction was positive in all. There was noevidence of denervation except in one case (theseverely disabled one) with diffuse atrophy of themuscles of the lowrer limbs. Examination of theindividual muscles revealed some selective distri-bution of weakness or spasm : (a) Gluteus mdiusand maximusmarked weakness in all cases, (b)Invertors and evertors coordination testsinvertorspasm in all cases, (c) Tibialis anteriornot con-tracting properly due to weakness and also due togastrosoleus spasm, (d) Spasm and in some casescontracture of hamstrings. These factors are res-ponsible for the characteristic gait. The spasm ofthe muscles cannot be due to peripheral mecha-nism because injection of 2 per cent lignocainehvdrochloride in the muscles did not relieve the

same.INVESTIGATIONS

(a) HaematologicalThe average haemoglobinwas about 11 g. per cent. Three patients weremoderately anaemic. Eosinophilia of 10 to 21 percent was noticed in 14 cases. Erythrocyte sedi-mentation rate (Westergren) was elevated in allexcept 2, the average value being 33 mm./lir., butin some it was over 80. Total serum B12 level waswithin normal range.(b) BiochemicalThe most significant findingwas hyperglobulinaemia in all (Table 1). Electro-phoresis showed a significant rise in gamma-globu-lin. The average findings were as follows : serumalbumin 3"7 g. per cent, serum globulin 3'7 g. percent, gamma-globulin fraction 38 per cent. Thy-mol turbidity was above the normal range in mostof the cases.(c) Other examinationsStool had hookwormova in 20 cases and ascaris ova in 11 cases. X-raysshowed no abnormalities in chest or bones (verte-brae and long bones). The cerebrospinal fluidshowed no significant abnormality.Thus the most significant abnormalities werethe increase of serum globulin and gamma-globu-lin, elevated ESR, increased thymol turbidityand moderate rise of eosinophils.


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LATHYRISMCHAUDHRI ETAL ' 171H- T ABL E I S H O W I N G P L A S M A P R O T E I N S A-\> 'SR IN XHE

22 P A T I E N T S U N D E R O B S E R V A T I O N

ffSeriali No.

;- i: 22. 3* 4f 56% 7 8."- 9

1011;- 12' '13:"" H'. 1 516:- 1718 1 91 20r. 21"' 22

T o t a l(g- %)8-47-17-0

'8-26-77-87-57-56-76-98-07-07-88-06-47-17-36-97-66-57-68-2

S e r u mAl b u m i n(g . %)

4-53-63-44-03-03-43-53-63-5

.2-33-93-34-13-43-43-73-73-94-43-44-44-2

pro te inG l o b u l i n(g- % ) -

3-93-54-64-23-74-44 03-9'3-24-64-1*3-73-74-6' 303--43-63-03-23-13-24-0

G a m m aglobu l in(0 / )Wo /31-434-036-927-622-0t J t27-531-2 3 5 -3 30-932-5 .27-529-736-634-233-630-537-529-436-138-3

ESR(mm. /h r . )

344585154828. 247814 '583528

172541922.. 28' 1911. 3418

For comparison, a series of\27 'normal' indivi-duals from the affected families having similardietetic history was investigated. Surprisingly, 13;of them had hyperglobulinaemia (about 3"5 g. percent) along with a rise of gamma-globulin (above34 per cent). These figures were normal in theremaining 14 subjects.Further, 10 normal subjects of the localityreported to have never consumed khesari prepara-tions were also similarly investigated and the; findings were all normal.

TREATMENTWith hospital diet all the patients gained inweight with improvement in blood picture, but' there was no apparent effect on the neurologicalmanifestations. Muscle relax ant like mep henesin(tolseram) also had no effect whatsoever. Butprostigmin injections 0'5 mg. daily for 10 daysi Were distinc tly beneficial. S tiffness gradually dimi-nished, power of legs was regained to a certainlextent and most of those using sticks could .do _^Without them . Pre cipitancy of micturition, and

incontinence of faeces also* disappeared "in" nearlyhalf the cases. The improvement appeared morestriking in those with shorte r duration. Sym ptoms. .like backache, cramps and the tingling sensa-tion in legs however remained uninfluenced. Itshould be mentioned that placebo injections tosome patients made no difference until substituted^by prostigmin. . ~ . " . Nine months after discharge from the hospital,the patients were followed up in their villages. - It was found that those who had given up eatingkhesari maintained the improvement attained inthe hospital, but the condition of others deterio :.rated to the old state. -

CONTROL AND PREVENTION :The Director of Health Services, West Bengalwas apprised of the findings. The villagers werediscouraged by means of propaganda to cultivate . khesari and the stock was replaced by paddy as 'much as possible, and in this way the incidence ." of fresh cases went down from 29 in 1959 to 6. in -1960, 5 in 1961 and none in 1962;- ' " K " '

DISCUSSION; . _Many _ theories have been put forward to ex-.plain the aetiology of lathyrism, but the "actualcause is still in dou bt. Briefly they assume the. presence of a toxin in lathyrus or- in sometaminant of the lath yru s. crop, w hich acts on, nervous system, most probably in the absence p> .some unknown food factor. Poisoning 'by certain ; -" metals such as selenium (Rudra,*1952) and manga-nese (Gutierrez, 1950, 1954; Sadasivan .et al'., J1960) said to be present in the seeds has also beenpostulated. On the other hand," Minchin (1940)and Gopalan (1950) have described sporadic occur- rence of the syndrome in non-lathyrus-eatingpopulation in South India. Lathyrism cases rarely originate in WestBengal. Incidentally, in the year- 1949-50 a fewfamilies were affected in a rural area of HowrahDistrict and 3 patients were . admitted to thishospital. T hey were early cases and improved. considerably after a course of prostigmin injections(Chaudhuri, . 1961). ' I n .the affected area under""report, there was no known lathyrism prior to'the . present outbreak. Flood and reasons of economy" drove the villagers to grow lathyrus and consume it as their main diet for about 3 months in a year,when the disease began to occur. By this time the 'stock of lathyrus at their homes was exhausted and '-they had changed their diet to rice. Then it *"gradually began fo declined This had been going ,on for some years until steps were taken to dis-.courage the cultivation of lathynis, and thisreduced the incidence of fresh-cases to nil. Two-


9/15

j . INDIAN M. A., VOL. 4L NO. 4, AUGUST 16, 1963important factors worth noting in this outbreakare ingestion of large quantities of the seeds andalmost entire absence of food of animal origin.Incidentally the seeds were examined and identi-fied as those of Lathy rus sativus.L-athyrism is essentially a disease of the nervoussystem. E xperim ental studies and autopsy reportsare scanty. Buzzard and Greenfield (1921) foundon postmortem in a patient, the margins of thespinal cord presenting a honey-combed appearanceas is seen in subacute combined degeneration.Filimonoff (1926) observ ed sclerosis of the lateralregion of the cord, not strictly confined to thepyramidal tract, with the small blood vesselssclerosed and obliterated in places. Acton andChopra (1922) demonstrated constriction of thespinal vessels supplying the anterolateral columnin rats after feeding them with extract of Lathymssativus. It was postulated by Acton (1922) that thelesion in the spinal cord in clinical cases of lathy-rism was due to thrombosis of blood vessels supply-ing the anterior and anterolateral tracts ; this causeddegenerative changes which only partially affectthe crossed pyramidal tract and partially or whollythe extrapyramidal tract. The fully developed clini-cal picture in our casesparalysis, increased kneejerks, loss of abdominal reflexes and of sphinctericcontrol, pain in the lumbodorsal region andincrease in muscle tone also indicates that thelesion whatever its nature, is highly selective andlocalised in the posterolateral region of the cord,predominantly affecting the pyramidal and extra-pyramidal tracts at the upper lumbar and dorsalsegments.The epidemiological data clearly point to theaction of some toxin but the manner of its actionis unkno wn. Detailed investigation in the presentseries of 22 patients revealed hyperglobulinaemia,and a rise of gamma-globulin with raised ESR,eosinophilia and the increased thymol turbidityin the majority. We suggest that lathyrism is theresult of antigen-antibody eaction and that theabove changes are but manifestations of the sameprocess.' It may be that the antigen-antibodyreaction has injurious effect on the central nervoussystem in its most vulnerable part (upper lumbarand lower dorsal segment) which results in theclinical syndrome. The history that there was aninterval of a few months between the commence-ment of lathjrus intake and the onset of the illnesssuggests thahe body wasbeing sensitised duringthis period with the formation of antibodies againstthe toxin. The severity of the reaction mustdepend on, among other possible factors, theamount of lathyrus ingested, individual susceptibi-lity and repeated sensitisation by the toxin.Identical biochemical and haematological abnor-

malities were also present in half the number of'normal' individuals in the affected families livingon similar diets. Presumably these were thepersons in whom the reactions were mild and whowere still in what may be called the biochemicalphase, whilst others in whom this mechanism wasvery active and periodically stimulated, progressedto manifest clinical disease.In lathyrism, apart from finding the nature ofthe supposed toxin, there still remain obscurepoints which require elucidation. For instance,Mackenzie (1927) opined that people suffered onlywhen Lathyrus sativus is grown in virgin soil ornewly cultivated land and that it loses its lathyro-genic property after a few years' cultivation. Inthe outbreak under report the seeds were originallybrought from a neighbouring State (Bihar) wherelathyrism is common. Th ese seeds were distinctlyof larger size than the local variety though theybelonged to the same species. No contaminantwas detected such as seeds of Vicia saliva whichhas been incriminated by some workers as thecause of the disease (Anderson et al., 1925).

SUMMARYAn outbreak of lathyrism in a hitherto un-affected rural area due to heavy consumption ofLathyrus sativus peas, the plants having beenwidely cultivated with seeds imported from aneighbouring endemic state, is reported.The clinical features are described.The haematological and, biochemical findingssuggest that the neurological manifestations arethe result of antigen-antibody reactions injuringthe spinal cord.Prostigmin injections definitely ameliorated thecondition specially in caaH with shorter duration.By means of propaganda the lathyrus cultiva-tion in the area was reduced considerably and withit the disease came under control.

ACKNOWLEDGMENTThe authors thank Dr. R. L-. Nath, Professor ofBiochemistry, Dr. J. B. Chatterjea, Professor of Haema-tology, Dr. S. P. Basu, Radiologist, and Professor S. R>Bose, Botanist, for help in the investigations. Thanksare also due to Dr. S. Sarkar, Physiotherapeutist, Schoolof Physical Medicine, Calcutta, for the special neurologi-cal reports of 14 patients of the present series.

REFERENCESACTON, H. W.Indian Med. Gaz., 57: 241, 1922.A C T O N , H. W. AND C H O P R A , R. N.Ibid., 57 : 412, 1922.A N D E R S O N , L-. A. P., H O W A R D , A. AND SIMONSEN, J. L.Indian J. Med. Res., 12 : 613, 1925.BUZZARD, E. F. AND GREENFIELD, J. G.The Pathologyof the Nervous System, 1921, Constable & Co.,London, p. 232.


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BASAL CELL CARCINOMAAHMAD ET AL. 173R . N . An n u a l R e p . C a l c u t t a Sc h o o l T r o p .1959-60, 1961, Su pd t . Go v t . P r in t i ng , W es tB e n g a l , Aiipore , p . 34.L . N.Z. 6"t 'S. Ncurol. Psychiat., 1 0 5 : 76,1926.GOPALAN, C Trans . Roy, Soc . Trop. Mcd. Hyg., 4 4 :333, 1950.

G U T I E R R E Z , F . H.Ann. Bromatol (Madr id) , 2 : 261, 1950.Idem 10 Congress In te rna t . Ind . Agri . Y. A l i m e n t(Mandi t ) , 1954, p. 560.MACKENZIE, h. H . h.Indian Mcd. Gaz., 6 2 : 201, 1927. R . L . H.Brit. Mcd. ]., 1 : 253, 1940.RUDRA, M . N.Nature, 1 7 0 : 124, 1952.

' S A D A S I V A N , T. S . , S ULO CHAN A, C . B . , J O H N , V . T . ,SUBBARAM, M. R. AND GOPALAN, C.CuiT. Sei., 2 9 :86, 1960.

B AS AL C E L L C AR C I NOMA :A C L I NI C OP ATHOL OG I C S TUDY OF120 CASESK. N. AHMAD, M.D.Demonstrator in PathologyK. M. WAHAL, M.D., D.sc, F.C.A.P.Reader in Pathology

AN DR. M. L. MEHROTRA, M.D., P H . D .Professor of PathologyDepartment of Pathology & BacteriologyK.G.'s. Medical College, Lucknow

Basal cell carcinoma is seemingly a biologic^enigma as it arises from the more primitivefepidermal basal cells and yet is biologically lessactive or malignant than squamous cell carcinomat/which arises from prickle cells, a maturer cell than[basal cell. T he other interesting feature about this^tumour is its histogenesis. Ewin g (1940) andWillis (1960) believe that basal cells, of theepidermis or of the skin appendages, are thesource of this tumour. O ther workers, have criti-fbised this view and they derive these tumours3m specialised basal cells destined to form skin[glands (Krainz, 1921), hair matrix (Haythorn,p931 ; W allace and Ha lpert , 1950 ; S werdlow,J958). Lever (1954) and other dermatologists|consider that these tumours arise from the primaryoithelial germ cells.During the period 1949 to 1961, we cameIfcross 120 cases of basal cell carcinoma which^ thoroughly studied keeping in mind theiristogenesis, histological appearances and clinicalatures. T he present communication describesfindings on this material.

METHODS AND MATERIAL " ~The material for the study comprised of suitablesized pieces obtained from the lesions which wereserially cut wherever necessary. T he sectionswere stained with Harris' haematoxylin andeosin, Van Gieson's stain for collagen andVerhoeff's stain for elastic fibres.RESULTS

Age and sex incidenceOf the 120 cases, 86were males and 34 females. T he maximum ageincidence was in the fourth and fifth decades(Table 1). 23 out of 118 tumours were in patientsunder the age of 30 years. T he youngest patientwas aged 8 years and the oldest 84 years.T A B L E 1 S H O W I N G A G E D I S T R I B U T I O N OF 118 C A S E S

( AGE N O T S T A T E D I I CASES)

Ag e i n yea r s0-10 11-20 21-30 31-40 41-50 51-60 61 &above

T o t a l case s 1 2 20 35 34 20 6

LocationThough the tumours were located inall the regions of the body, over 75 per cent of thetumours were on the head and face, the eyelids(30), face (31), scalp (19) and nose (6) being thesites of predilection (Table 2). T he incidence oflesions on the face was over six times more inmales than in females except in the case oftumours arising from the eyelids where the inci-dence was equal (15 males and 15 females). T hedistribution in other sites of the body did not revealany sex bias or any particular area of predilectionexcept for the tumours of the hand (5 cases) andback (3 cases) all of which were observed in males.Clinical featuresIn every instance the lesionwas a solitary one and no case of multiple tumourswas recorded in this series. T he tumours mani-fested in the m ajority (86 cases) as a solitary, slowgrowing nodule or as an irregular growth whichwas pigmented in 10 cases. The remaining 34cases presented with an indolent ulcer which bledon touch. The duration of the lesions was variable,the average being 1"8 years. In one instance thelesion had been there for 45 years, in 3 cases thetumour had existed for over 20 years and in 48cases over 2 years. T he shortest period recordedwas 2 months in 25-year old male. Regionallymph nodes were enlarged in 6 cases but unfortu-nately none was submitted for histological exami-nation.


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. Journal of theIndian Medical AssociationV O L U M E 41N U M B E R 4 PUBLISHED TWICE A MONTHEDI TO R H. K. ROY, M.D. (CAL.) A U G U S T 16, 1963CALCUTTA

ORIGINAL ARTICLESL ATHYR I S M* : A CLINICAL AND E P I DE MI OL OG I C AL S TUDY

R. N. C H A U D H U R I , F.R.C.P.E., F.N.I., Director and Professor of Tropical MedicineM. K. CHHETRI, M.D., M.R.C.P.**, Reader

T . K. S A H A , M.D., D.PHIL., Assistant Professor AND P. P. M I T R A , M.B.B.S., LecturerSchool of Tropical Medicine, Calcutta

Lathyr ism is a disease of which the mos tprominent clinical feature is muscular weakness oflegs and later spastic paraplegia ; it occurs amongstpeople whose staple diet is a vetch, Lathy rus. InTndia , Lathyrus sativas, locally known as Khesarida l is incr imina ted. We here describe an outbreakthat occurred in a remote rural area, about 250'ki lometres f rom Calcutta , which we investigatedboth locally as well as by admitt ing several patientsto hospital .EPIDEMIOLOGYIt first came to the notice of the authori t ies-.early in 1960 when some apparently healthypersons were seen limping about with or w i thou t-the aid of st icks. The affected locality consisted of: several small hamlets scattered about on eitherjside of a river over an area of about 12 square;;miles. Rice was the staple diet of the inhabi tantsiwith very l i t t le khesar i (Lathyrus) but 6 ye a r sthere was a heavy flood which left a th ickfdeposit of. silt and sand in the fields, making themflinfit for paddy cul t iva t ion. So they star tedgrowing khesar i instead, and as these plants grew

luxuriantly and cost very l i t t le , they made it anannual event and had been using these grains^liberally in recent years. After harvesting in

Fe br ua r y the seeds were stored in e a r t h e n p o t s jand consumed daily after removal of the husks asf lour (simply-mixed with water) , hand-made breador as dal (cooked in water l ike soup) . T his wassupplemented sometimes by a little rice or wheat.After 3 or 4 months when the stock of khesari wasexhausted, they would take to rice again . Som evegetables were taken, but rarely fish, meat ormilk.The people were mostly cult ivators andpossessed no land of their own and served aslaboufers for which they were paid ei ther inkhesari or money which they in turn spent on thisarticle of food, it being much cheaper than r ice. .I t was after this heavy consumption of khesarithat cases of la thyr ism began to appear , reachingthe peak period in June - Ju ly and then decliningwith the change to r ice. T his sequence of eventshad been occurring every year over a period of 4or 5 years. No rel iable information could beobtained as regards the e x t e n t of its incidence, butwe were able to trace 82 victims in various stagesof the disease amongst 54 families. 18 suchfamilies had each more than one person affectedup to a ma ximum of 4, the members fal l ing ill inabout the same season within a period of 2 to 6weeks. The remaining families had no more than



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70 J. INDIAN M. A., VOL. 4i, NO. 4, AUGUST 16, 1963one victim in each. There wert, of course, manypeople in and outside these fannues who escaped,though consuming similar food. Persons of allages were affected, but only 8 females wereencountered.


admitted to the Carmichael Hospital for TropicalDiseases for investigation. Except 2 girls and 1boy aged between 7 and 8 they were all adultmales. The duration of their illness varied from5 months to 5 years. All possessed fairly goodhealth except 3 who had moderate anaemia. Therewere no obvious vitamin or other nutritionaldeficiencies.Prodromal symptoms had been present in 16patients. They were: (1) Painful spasms andcramps of calf muscles and tingling sensation inthe legs in 13 cases. These occurred especially atnight and continued for varying period of 3-15

days before the onset of paralysis. (2) Precipit-ancy of micturition in one case for as long as 9months, and then he found his legs stiff. (3)Heaviness of the lower limbs in one case. (4)Fever in one case.The onset of actual paralysis of lower limbsWas sudden in 12 cases following some exertion,e.g., ploughing, walking a long distance orcarrying a heavy load. In others, the onset wasslow and indefinite with gradual development ofjveakness and spasticity of legs. Other symptomsresent with it were : ( 1 ) Cramps and tinglingwhich persisted to a variable degree in those whohad them in the prodromal stage, but developedin 5 others after the onset of paralysis. (2) Painat the back in the lumbodorsal region, persistentin nature, in 16 cases. (3) Precipitancy ofmicturition in 13 cases . (4) Faecal incontinencein .4 cases. (5) Sexual impotence in 2 cases. Themotor functions gradually worsened, walking beingparticularly affected. In the majority the maxi-mum disability was reached in 2-7 months, afterwhich the condition usually remained stationary,but in a few there was further deterioration over alonger period, one of them being severely disabled.7 patients, while at hospital, were using one ortwo sticks for walking. The upper limbs wereentirely unaffected.Examination of the nervous systemHigherfunctions, speech and cranial nerves were normal.In both the lower extremities, the muscle tonewas increased, more of the flexors than extensors.Power was diminished in all. Diffuse atrophy ofmuscles was noticed in one patient and atrophy ofquadriceps on one side in 2 others. Sensory

changes were generally absent except areas ofhyperaesthesia in one patient and loss of vibrationsense in another. Abdominal and cremastericreflexes were absent in 8 and 13 cases respectivelyand plantar reflex was bilateral extensor in all.Knee and ankle jerks were exaggerated in all,associated with ankle and patellar clonus in abouthalf. The gait was spastic with varying flexorspasms of the muscles of lower limbs.Report from School of Physical Medicine onthe neurological findings in 14 cases of the presentseries was as follows : There was upper motorneurone type of lesion in all cases and the nerveconduction was positive in all. There was noevidence of denervation except in one case (theseverely disabled one) with diffuse atrophy of themuscles of the lower limbs. Examination of theindividual muscles revealed some selective distri-bution of weakness or spasm : (a) Gluteus mdiusand maximusmarked weakness in all cases, (b)Inverters and evertors coordination testsinvertorspasm in all cases, (c) Tibialis anteriornot con-

tracting properly due to weakness and also due togastrosoleus spasm, (d) Spasm and in some casescontracture of hamstrings. These factors are res-ponsible for the characteristic gait. The spasm ofthe muscles cannot be due to peripheral mecha-nism because injection of 2 per cent lignocainehvdrochloride in the muscles did not relieve thesame.

INVESTIGATIONS(a) HaematologicalThe average haemoglobinwas about 11 g. per cent. Three patients weremoderately anaemic. Eosinophilia of 10 to 21 percent was noticed in 14 cases. Erythrocyte sedi-

mentation rate (Westergren) was elevated in allexcept 2, the average value being 33 mm./hr., butin some it was over 80. Total serum B12 level waswithin normal range.(b) BiochemicalThe most significant findingwas hyperglobulinaemia in all (Table 1). Electro-phoresis showed a significant rise in gamma-globu-lin. The average findings were as follows : serumalbumin 3'7 g. per cent, serum globulin 3'7 g. percent, gamma-globulin fraction 38 per cent. Thy-mol turbidity was above the normal range in mostof the cases.(c) Other examinationsStool had hookwormova in 20 cases and ascaris ova in 11 cases. X-raysshowed no abnormalities in chest or bones (verte-brae and long bones). The cerebrospinal fluidshowed no significant abnormality.Thus the most significant abnormalities werethe increase of serum globulin and gamma-globu-lin, elevated ESR, increased thymol turbidityand moderate rise of eosinophils.


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LATHYRISMCHAUDHURI ET'L. 171fr TABLE S H O W I N G PLASM A P R O T E I N S A - \ D iSR I N I H E

22 P A T I I N T S U N D E R O B S E R V A T I O N

ffSerial' Ko.

"' 1? 21 3? 4" 56% 7" 8 * 91011'- 12' " 1 3;" 14. 1516- 1 7181 20: 21~ 22

Tota l(g- %)8-47-17-0"8-2G-77-87-57-56-76-98-07-07-88-06-47-17-36-97-66-57-68-2

S e ru mAlbumin(g . %)

4-53-63-44-03-03-43-53-63-5 2-33-93-34-13-43-43-73-73-94-43-44.44-2

pro te inGlobul in

( g . % ) 3-93-54-64-23-74-44 03-9'3-24-64- f3-73-74-6' 303-43-63-03-23-13-24-0

Gammaglobulin( / \31-434-036-9"27-622-0s r27-531-2 35-3-30-932-5 .27-529-736-634-233-630-537-529-436-138-3

E S R(m m . /hr . )344585154828_ 247814 583528

1 72541922.. 28' 1911. 3418For comparison, a series of\27 'normal' indivi-

duals from the affected families having similardietetic history was investigated. Su rprising ly, 13of them had hyperglobulinaemia (about 3'5 g. percent) along with a rise of gamma-globulin (above34 per cent). These figures were normal in theremaining 14 subjects.Further, 10 normal subjects of the localityreported to have never consumed khesari prepara-tions were also similarly investigated and the; findings were all normal.TREATMENTWith hospital diet all the patients gained inweight with improvement in blood picture, but; there was no apparent effect on the neurologicalmanifestations. Muscle relaxa nt like me phenesin(tolseram) also had no effect whatso ever. B utprostigmin injections 0"5 mg. daily for 10 daysre distinctly beneficial. Stiffness gradually dimi-nished, power of legs was regained to a certainextent and most of those using sticks could .do _^Without them . Pre cipitancy of micturition , and

incon tinence of faeces also" disappeared "irf-nearlyhalf the cases. T he improvement appeared morestriking in those with .shorter duration. Sym ptoms. .like backache, cramps and the tingling sensa-tion in legs however remained uninfluenced. Itshould be mentioned that placebo injections tosome patients made no difference until substituted^by prostigmin. . ~ . " TNine months after discharge from the hospital,the patients were followed up in their villages. - I t was found that those who had given up eatingkhesari maintained the improvement attained inthe hospital, but the condition of others deterio : rated to the old state. -

CONTROL AND PREVEN TION :The Director of Health Services, West Bengalwas apprised of the findings. The villagers werediscouraged by means of propaganda to cultivate . khesari and the stock was replaced by paddy asmuch as possible, and in this way the incidence . of fresh cases went down from 29 in 1959 to 6. in -1960, 5 in 1961 and none in 1962! .

DISCUSSION; . _ - .* ' ;Many . theories have been put forward to .ex-,plain the aetiology of lathyrism, but the actualcause is still in doub t. Briefly they assume the ;presence of a toxin in lathyrus or- in some cpn-^jtaminant of the la thyru s. crop, which acts'on-theg* ':nervous system, most probably in the absence Q . .._*,some unknow n food factor-. Poison ing 'by certain ;' * ." metals such as selenium (Rudra,-1952) and manga- . .nese (Gutierrez, 1950, 1954; Sadasivan .et'al'.-, , ^1960) said to be present in the seeds has also beenpostulated. On th e other hand," Minchin (1940)and G opalan (1950) have described sporadic occur- "rence of the syndrome in non-lathyrus-eatingpopulation in South India. Lathyrism cases rarely originate in WestBengal. Inciden tally , in the year- 1949-50 a fewfamilies were affected in a rural area of HowrahDistrict and 3 patients were . admitted to thishospital. They were early cases and improved, -considerably after a course of prostigmin injections(C haudhu ri, 1961). ' In .the affected area under" "report, there was no known lathyrism prior to'the . present outbrea k. Flood and reasons of economy" "drove the villagers to grow lathyrus and consume >it as their main diet for about 3 months in a year, . -when the disease began to occur. By this time the / ._stock of lathynis at their homes was exhausted and "-they had changed their diet to rice. Th en it ~gradually began fo decline: T his had been going ,on for some years until steps were taken to dis-,courage the cultivation of lathynis, and thisreduced the incidence of fresh-cases to nil. Two* ,


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172 j . INDIAN M. A., VOL. 41. NO. 4, A UG UST 16, 1963important factors worth noting in this outbreakare ingestion of large quantities of the seeds andalmost entire absence of food of animal origin.Incidentally the seeds were examined and identi-fied as those of Lathy rus sativus.Lathyrism is essentially a disease of the nervoussystem. Ex perim ental studies and autopsy reportsare scanty. Buzzard and Greenfield (1921) foundon postmortem in a patient, the margins of thespinal cord presenting a honey-combed appearanceas is seen in subacute combined degeneration.Filimonoff (1926) observed sclerosis of the lateralregion of the cord, not strictly confined to thepyramidal tract, with the small blood vesselssclerosed and obliterated in places. Acton andChopra (1922) demonstrated constriction of thespinal vessels supplying the anterolateral columnin rats after feeding them with extract of Lathy russativus. It was postulated by Acton (1922) that thelesion in the spinal cord in clinical cases of lathy-rism was due to thrombosis of blood vessels supply-ing the anterior andanterolateral tracts ; this causeddegenerative changes which only partially affectthe crossed pyramidal tract and partially or whollythe extrapyramidal tract. The fully developed clini-cal picture in our casesparalysis, increased kneejerks, loss of abdominal reflexes and of sphinctericcontrol, pain in the lumbodorsal region andincrease in muscle tone also indicates that thelesion whatever its nature, is highly selective andlocalised in the posterolateral region of the cord,predominantly affecting the pyramidal and extra-pyramidal tracts at the upper lumbar and dorsalsegments.The epidemiological data clearly point to theaction of some toxin but the manner of its actionis unknown. Detailed investigation in the presentseries of 22 patients revealed hyperglobulinaemia,and a rise of gamma-globulin with raised ESR,eosinophilia and the increased thymol turbidityin the majority. We suggest that lathyrism is theresult of antigen-antibody eaction and that theabove changes are but manifestations of the sameprocess: It may be that the antigen-antibodyreaction has injurious effect on the central nervoussystem in its most vulnerable part (upper lumbarand lower dorsal segment) which results in theclinical syndrome. The history that there was aninterval of a few months between the commence-ment of latrrsrus intake and the onset of the illnesssuggests thahe body wasbeing sensitised duringthis period with the formation of antibodies againstthe toxin. The severity of the reaction mustdepend on, among other possible factors, theamount of lathyrus ingested, individual susceptibi-lity and repeated sensitisation by the toxin.Identical biochemical and haematological abnor-

malities were also present in half the number of'normal' individuals in the affected families livingon similar diets. Presum ably these were thepersons in whom the reactions were mild and whowere still in what may be called the biochemicalphase, whilst others in whom this mechanism wasvery active and periodically stimulated, progressedto manifest clinical disease.In lathyrism, apart from finding the nature ofthe supposed toxin, there still remain obscurepoints which require elucidation. For instance,Mackenzie (1927) opined that people suffered onlywhen Lathyrus sativus is grown in virgin soil ornewly cultivated land and that it loses its lathyro-genic property after a few years' cultivation. Inthe outbreak under report the seeds were originallybrought from a neighbouring State (Bihar) wherelathyrism is common. These seeds were distinctlyof larger size than the local variety though theybelonged to the same species. No contaminantwas detected such as seeds of Vicia sativa whichhas been incriminated by some workers as thecause of the disease (Anderson et al., 1925).SUMMARYAn outbreak of lathyrism in a hitherto un-affected rural area due to heavy consumption ofLathyrus sativus peas, the plants having beenwidely cultivated with seeds imported from aneighbouring endemic state, is reported.The clinical features are described.The haematological and biochemical findingssuggest that the neurological manifestations arethe result of antigen-antibody reactions injuringthe spinal cord.Prostigmin injections definitely ameliorated the

condition specially in caa^ with shorter duration.By means of propaganda the lathyrus cultiva-tion in the area was reduced considerably and withit the disease came under control.ACKNOWLEDGMENTThe authors thank Dr. R. h. Nath, Professor ofBiochemistry, Dr. J. B. Chatterjea, Professor of Haema-tology, Dr. S. P. Basu, Radiologist, and Professor S. R.Bose, Botanist, for help in the invest igat ions. Thanksare also due to Dr. S. Sarkar, Physiotherapeutist, Schoolof Physical Medicine, Calcutta, for the special neurologi-cal reports of 14 patients of the present series.

REFERENCESACTON, H. W.Indian Med. Gaz., 57: 241, 1922.ACTON, H. W. AND CHOPRA, R. N.ibid., 57 : 412, 1922.A N D E RSO N , L-. A. P., H O W A RD , A. AND SIMONSEN, J. L.Indian } . Med. Res., 12 : 613, 1925.BUZZARD, E. F. AND GREENFIELD, J. G.The Pathologyof the Nervous System, 1921, Constable & Co.,London, p. 232.


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BASAL CELL CARCINOMAAHMAD ET AL. 173*CHAUDHURI, R. N.AnnuaJ Rep. Calcut ta School Trop.Met. 1959-60, 1961, Supdt. Govt. Pr in t ing , Wes tBengal , Aiipore , p. 34.' F I L I M O N O F F , L. N.Z. Gcs. Scurol. Psychiat., 105 :76,

1926.GOPAUN, CTrans. Roy, Soc. Trop. Mcd. Hyg., 44 :333, 1950.^GUTIERREZ, F. H.Ann. Bromatol (Madrid) , 2 : 261, 1950.1 dem10 Congress In te rna t . Ind. Agri . Y. Al imen t(Mandit), 1954, p. 560.' M A C K E N Z I E , h. H. L.Indian Mcd. Gaz., 62 : 201, 1927. ' I N C H I X , R. L. H.Brit. Mcd. J., 1 : 253, 1940.RUDRA, M. N . Nature , 17 0 : 124, 1952.SADASIVAN, T. S., SULOCHANA, C. B., J O H N , V. T.,SUBBARAM, M. R. AND GOPALAN, C.ClUT. Sei., 29 :

86 , 1960.

B AS AL C E L L C AR C I NOMA :A C L I NI C OP ATHOL OG I C S TUDY OF120 CASESK. N. AHMAD, M.D.Demonstrator in PathologyK. M. WAHAL, M.D., D.sc, F.C.A.P.Reader in Pathology

i

AN DR. M. L. MEHROTRA, M.D., PH.D.Professor of PathologyDepartment ofPathology & BacteriologyK.G.'s. Medical College, Lucknow

Basal cell carcinoma is seemingly a biologic enigma as it arises from the more primitive^epidermal basal cells and yet is biologically lessTactive ormalignant than squamous cell carcinoma Which arises from prickle cells, amaturer cell than.basal cell. T he other interestin g feature about this^tumour is its histogenesis. E wing (1940) and(1960) believe that basal cells, of the^epidermis or of the skin appendages, are thesource of this tumour. Other workers, have criti-cised this view and they derive these tumoursspecialised basal cells destined to form skin|glands (Krainz, 1921), hair matrix (Haythorn,1931 ; Wallace and Halpert, 1950 ; Swerdlow,1958). Lever (1954) and other dermatologistsConsider that these tumours arise from the primarytithelial germ cells.During the period 1949 to 1961, we cameross 120cases of basal cell carcinoma whichthoroughly studied keeping in mind theirjjistogenesis, histological appearances and clinicalitures. The present communication describesfindings on this material.

METHODS AND MATERIAL " "The material for the study comprised of suitablesized pieces obtained from the lesions which wereserially cut wherever necessary. The sectionswere stained with Harris' haematoxylin andeosin, Van Gieson's stain for collagen andVerhoeff's stain for elastic fibres.RESULTS

Age and sex incidence O f the 120 cases, 86were males and 34 females. T he maximum ageincidence was in the fourth and fifth decades(Table 1). 23 out of 118 tumours were in patientsunder the age of 30 years. T he youngest patientwas aged 8years and the oldest 84 years.TABLE 1SHOWING AGED I S T R I B U T I O N OF 118 CASES

(AGE NOT STATED I I CASES)

Age in years0-10 11-20 21-30 31-40 41-50 51-60 61 &above

Total cases 1 2 20 35 34 20 6

LocationThough the tumours were located inall the regions of the body, over 75 per cent of thetumours were on thehead and face, the eyelids(30), face (31), scalp (19) and nose (6) being thesites of predilection (Table 2). T he incidence oflesions on the face was over six times more inmales than in females except in the case oftumours arising from theeyelids where the inci-dence was equal (15 males and 15 females). Thedistribution in other sites of the body did not revealany sex bias orany particular area of predilectionexcept for the tumours of the hand (5 cases) andback (3 cases) all ofwhich were observed in males.Clinical featuresIn every instance the lesionwas a solitary one and no case of multiple tumourswas recorded in this series. T he tumours mani-fested in the majority (86 cases) as a solitary, slowgrowing nodule or as an irregular growth whichwas pigmented in 10 cases. The remaining 34cases presented with an indolent ulcer which bledon touch. The duration of the lesions was variable,the average being 1'8years. In one instance thelesion had been there for 45 years, in 3 cases thetumour had existed for over 20 years and in 48cases over 2 years. T he shortest period recordedwas 2 months in a 25-year oldmale. Regionallymph nodes were enlarged in 6 cases but unfortu-nately none was submitted forhistological exami-nation.

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