SUMMARY Electrophysiological studies in suicidal patients with organophosphate poisoning are reported. Patients often developed muscular weakness of variable severity owing to diplorisation block at nicotinic receptors. During such paralysis nerve conduction velocity and distal latencies were normal even in severely paralysed patients. The amplitude of the compound action potential was smaller than in controls and often showed a repetitive response. The amplitude tended to be lower in those more severely affected. On repetitive stimulation there was usually no decrement with three stimuli per second and only occasional decrement at 10 per second. At 30Hz several cases showed a decrement even in the absence of paralysis. This response to repetitive stimuli is thus quite distinct from that seen in either myasthenia or Eaton Lambert syndrome. On three occasions after poisoning with dichlorovos there was first anticholinesterase insecticide poisoning and later delayed neurotoxicity as seen with triorthocresylphosphate. These cases showed all the features of a severe pure motor axonal degeneration neuropathy.Organosphosphate insecticide poisoning is the commonest mode of suicidal poisoning in India today.'The drug is usually ingested and the patients are commonly admitted with miosis, fasciculations, pulmonary oedema and froth at the mouth due to the muscarinic, nicotinic and central manifestations of cholinergic poisoning. We have described before the neurological manifestations seen in 200 consecutive cases.2 We divided the signs into Type I, that is, those present on admission and responding promptly to atropine therapy and Type II as those appearing sometime after commencement of treatment and basically not influenced by atropine. Type I signs are believed to be cholinergic effects at muscarinic receptors and include bilateral pyramidal signs and impairment of consciousness and miosis. Type II are believed to be due to acetylcholine excess at nicotinic receptors. Type II paralysis appears from 12-72 hours after poisoning and lasts up to 5-6 days. This Type II paralysis is clearly different from delayed neurotoxicity, which appears only after 8-12 days and lasts much longer.3 Delayed neurotoxicity after a prior episode of clinical organophosphate anticholinesterase poisoning is furthermore very uncom-

SUMMARY In a study of enteric fever, cerebellar ataxia was found to be the commonest neurological manifestation, second only to toxic delirium. Excluding toxic delirium (found in 25-30% of cases) neurologic deficit was noted in 5-0% of a series of 718 consecutive cases; 2-3% showed cerebellar ataxia, either as an isolated feature or in association with other lesions. The ataxia usually appeared in the second week, and lasted a mean of 9-4 days. In 90% of cases it had cleared completely within a month.

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