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POISONOUS FOOD GRAINS                                            699

presence of an active neurotoxin in Kesari Dal, while during the investigation of an
outbreak of lathyrism in Bhopal State in Central India in the year 1944-45 Dr. Shourie
did not find that the seeds of Lathyrus sativus were contaminated with the seeds of
Vicia sativa, and he thought that the disease was due to the existence in Lathyrus
sativus of a toxin affecting the pyramidal tracts.02 From the evidence collected in the
districts of Patna, Monghyr and Darbhanga in Bihar State, Dr. Lai suggests that lathyrism
is caused by the toxin or toxins present in the pulse, which act on and damage the
nerve cells, already devitalized by the individual living for a prolonged period on a
poor diet consisting largely of Kesari Dal and lacking in vitamin A.G3 It is also sug-
gested that the poisonous symptoms may be due to the absence of tryptophan, an essen-
tial amino-acid, which is very deficient in the grains of Lathyrus sativus, especially when
this pulse forms the bulk of the protein part of the diet.04

Symptoms.—The onset of the disease often comes on suddenly. On waking up in the
morning or whilst working in the field, the patient may notice weakness in his legs
and difficulty in sitting down and getting up from a squatting position. He is then
unable to walk without the aid of a stick, and later assumes a spastic gait owing to the
rigidity of the muscles of the calves and thighs. Lastly complete paraplegia of the lower
limbs occurs. There is no atrophy or loss of the tone of the muscles and no reaction of
degeneration. Sensation is normal although there is muscular pain. The knee-jerks are
increased, ankle clonus is well-marked and Babinski's sign is present. There is no
loss of consciousness, nor is there any involment of the bladder and rectum.

Treatment.—Stop the dal and administer a generous diet rich in vitamin A and
carotena*. Apply massage and electricity.

Post-mortem Appearances.—Death in the acute stage is very rare. There may be
sclerosis of the lateral columns of the spinal cord.

Lolium Temulentum (Darnel, Mostuki, Mochni).—This weed belongs to N.O. Grami-
nacese, and grows in wheat fields in the Upper Gangetic Plain, the Punjab, Sind, Western
Himalayas, and Kashmir State. The grains of this weed are similar to wheat grains
in shape, but are much smaller in size. They owe their poisonous properties to a pyri-
dine base, called temuline, contained in an endophytic fungus which attacks the

Accidental cases of poisoning have occurred from these grains being ground in mis-
take with wheat grains and then made into bread. Recently, an epidemic occurred in
Aden, where some 450 people suffered from poisonous symptoms by eating wheat flour
contaminated with the flour of the grains of this weed.66

Symptoms.—Giddiness, headache, muscular weakness, tremors, symptoms of gastro-
intestinal irritation, dilatation of the pupils, stupor and even coma. No case of death has
yet been recorded.

Stigmata Maides (Maize, Indian Corn, Maccai or Butta),—This corn belongs to N.O.
Graminse and is cultivated everywhere. It is affected by a special kind of fungus, which
causes pellagra, when eaten. However, pellagra is now regarded as a deficiency disease
due to lack of fat-soluble vitamin A in maize.

Paspalam Scrobiculatum (JCodro or Kodon).—The poison is supposed to reside in
the husk of the grain, which is often used by poor people as an article of food. The
poison is removed by boiling.

Symptoms.—These are giddiness, intoxication, dilated pupils, tremors, delirium,
convulsions, stupor and coma.

A family consisting of a woman, aged 50, a man, aged 22, and two boys, aged 9 and
12, was attacked by vomiting and giddiness about an hour-and-a-half after taking an
evening meal consisting of chapatis made from some flour of fcodon. They then became un-
conscious. The pulse was small and quick, and the extremities cold. They regained
consciousness in about an hour, but the young man was unconscious for some time.
They all had tremors, and recovered the following morning.67

62.    Ind. J. Med. Res., Vol. XXXIII, No. 2, Oct. 1945, pp. 239-47 ; see also D, M, Roy,
Ind. Med. Gaz., June 1951, p. 263.

63.    Ind. Med. Gaz., Oct. 1949, p. 468.

64.   Haviland Minchin, Brit. Med. J., Feb.'17, 1940, p. 253.

65.    S. D, S. Greval and P. N. Bhaduri, Ind. Med. Gaz., Aug. 1946, p. 294.

66.    D. Brinton, Proc. Roy. Soc. oj Med., Vol. XXXIX, Feb. 1946, p. 173.

67.    A. Swarup, Ind. Med. Gaz., July 1922, p. 257.