JOURNAL O f THE INDIAN MEDICAL ASSOCIATION CALCUTTA, AUGUST 16, 1963

The disease usually affects people belonging to the lower income group who happen to live principally on khesari dal. Human lathyrism, also called neurolathyrism is characterised by weakness, spasticity and rigidity of

LATHYRISM
yathyrism,

the leg muscles with increased deep reflexes. The higher functions, cranial nerves, trunk and upper extremities escape so that the morbid anatomy is confined to the lower dorsilumbar region of the spinal cord. city,13' 14> 15 other While most workers blamed investigators16 incriminated Lathyrus sativus seed itself for its neurotoxiVicia sativus seeds as the real offender, the toxic principle being divicine. In any case the precise causative agent has, however, not been identified. Surprisingly enough and contrary to the popular belief, patients with features of lathyrism have been reported from South India in nonlathyrus eating population.17"18 On theother hand, several workers19'21 considered that deficiency of certain factors in the diet, e.g., vitamin A or carotene, tryptophane and methionine are in some way related to the disorder. Metallic poisoning (selenium, manganese, etc.) has also been incriminated for the neurological features of the disease on the basis of high selenium or manganese content of the
13

a crippling disease, has been known

centuries among the peasants in India, and the 'Hindu literature in medicine has a mention of s disorder. In the 17th century, it was attrito eating of the vetch, lathyrus and this is yet generally held. It is mostly prevalent | India, though outbreaks have been reported >m several European continental countries. ice the beginning of this century onefindsfrelt reports of the disease, Having occurred in lie or .epidemic form in several provinces, tcularly Bihar, Madhya Pradesh and Uttar idesh. '
1 10 :

Except for a few sporadic cases, the

se has not been encountered in West Bengal.11 :ent outbreak in this State investigated in [ail by Chaudhuri et al. the report of which irs elsewhere in this issue will, therefore, be eiterest.
if, A. G.Brit. Med. J., 2 : 707, 1903. ^BUCHANAN, A.Report of Lathyrism in the Central ices in 1896-1902, 1904, Nagpur. toy, D. M.Indian Med. Gaz., 8 6 : 263, 1951. LCTON, H. W.Ibid., 57 : 241, 1922.
|HCCOMBIE YOUNG, T. C Indian J. Med. Res., 15 :

12

ACTON,

H.

W.

AND CHOPRA,

R.

N.Indian

Med.

Gaz.,
14

57 : 432, 1922.
MEGAW, J. W. D. AND GUPTA, J. C.Ibid., 62 : 299,

1927. ANAPATHY, K. T. AND DwiVEDi, M. P.Studies on Epidemiology of Lathyrism, Lathyrism Enquiry i. Unit, Gandhi Memorial Hospital, 1961, Rewa r, H.Indian J. Med. Res., 18 : 51, 1930. JD, S. K.Antiseptic, 41 : 514, 1944.

1927.
15
16

JACOBY, H.Ibid.,

81 : 246, 1946.

ANDERSON, I/. A. P., HOWARD, A. AND SIMONSEN, J.

L.Indian J. Med. Res., 12 : 613, 1925.

17

MINCHIN, R. L. K.Brit.

Med. J., 1 : 253, 1940.

RANJAN, N. P.Ibid., 4 1 : 652, 1944.

glrfAI,, s . B.Indian Med. Gaz., 84 : 468, 1949. FCHAUDHURI, R. N.Annual Rep. Calcutta School "Med., 1959-60, 1961, Supdt. Govt. Printing, West Govt. Press, Alipore, p . 34.
AUDHURI, R. N., CHHETRI, M. K., SAHA, T. K.

GOPALAN, C.Trans. Roy. Soc. Trop. Med. Hyg., 4 4 : 333, 1950. 19 MEIVLANBY, E.Nutrition and Disease, 1934, Oliver & Boyd, London, p. 136.
20

18

BASU,

K.

P.,

NATH,

M.

C,

GHANI,

M.

O. AND

MUKHERJEE, R.Indian J. Med. Res., 2 4 : 1027, 1937.

31

RUDRA, M. N., CHOWDHURY, L. M. AND SINHA, S.

P. P./. Indian M. A., 41 : 169, 1963.

P.Indian

Med. Gaz., 87 : 89, 1952.

207

28

]. INDIAN M. A., VOL. 41, NO. 4, AUGUST 16, 1963 increasingly recognised. Collagen diseases occur',

Lathy rus sativus seeds.22"23 This is comparable to hepatolenticular poisoning. It is thus obvious that there is still many gaps in our knowledge regarding the aetiological background of the disease. The recent reported outbreaks have been studied by Chaudhuri et al. clinically,
11

degeneration

due

to

copper

ring in relation to the connective tissue, disseminated sclerosis occurring in relation to the myelin sheaths of the central nervous system, Hashimoto's disease occurring in relation to the thyroid gland have been attributed to the same mechanism. It may be that the antigen-antibody reaction in lathyrism occurs in relation to the nervous tissue of the spinal cord, the injurious effect depending upon prolonged consumption of khesari and the activity of the autoimmune mechanism, the site of predilection being the most vulnerable part of the spinal cord, viz,, dorsilumbar region. The authors found that the subjects were taking khesari for 3-5 months every year during the said period, and they think such periodical stimulation of the antigen-antibody reaction important for finally bringing about the overt clinical syndrome. Persons in whom the reactions are mild may only show biochemical abnormality and herein lies the slender possibility for the prophylaxis of the disease. At this stage, besides elimination of the sensitising agent from the diet, use of steroids may halt the progress of the reactions which may ultimately culminate in the disease. This no doubt entails costly and comprehensive biochemical survey of the inhabitants in the lathyrus growing regions but is worth consideration, in view of the fact that the end stage of the disease is crippling to the sufferer and burdensome to the family and the State. In any case, all measures to discourage the use of lathyrus as the staple diet should be taken,> and replacement of the poor cultivators' lathyrus crops by paddy, especially during periods of scarcity, will go a long way to prevent the disease, as is borne out by the experiences gained in the reported outbreak of West Bengal.

epidemiologically and biochemically.

Floods and poverty had driven many inmates of the particular rural area to cultivate khesari and live exclusively on the cheap product seasonally for 4-5 years during which period the disease appeared in the community. Some members of the affected family and many others in the area consuming similar food, however, escaped. The authors suggest that the disease in some of these individuals might have been subclinical or at biochemical level only. In fact, slighter forms are rarely ever recognised clinically or reported. Basing their conclusions on biochemical and haematological investigations the authors for the first time point out that the disease may be the result of antigen-antibody reactions, the auto-antigen being related to the khesari protein and nervous tissue complex. The hyperglobulinaemia, particularly increased gammaglobulin, elevated ESR and positive thymol turbidity test all may be no doubt to some such mechanism and, therefore, the present work opens up a new field for investigation which should ultimately establish or deny the suggested view. Autoimmune diseases, i.e., diseases resulting from antigen-antibody reactions, the antibody being produced against one's own cells are being
M
23

RUDRA, M.
SADASIVAN,

N. Nature,
T. S.,

170 : 124,
B.,

1952.
JOHN, V. T.,

SULOCHANA, C.

SUBBARAM, M. R. AND GOPAUN, C Curr. Sei., I960.

2 9 : 86,