Electrophysiological studies in acute organophosphate poisoning.

Abstract

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-

Phrenic nerve conduction studies in acute organophosphate poisoning

“…3,17 Our data suggest that respiratory muscle (diaphragmatic) weakness is a major contributing factor in the development of respiratory failure in acute OP poisoning. Reduced amplitudes of the diaphragmatic CMAPs were noted in 60% of initial neurophysiological studies.…”

The Study of Clinical Features of Organophosphorus Poisoning in Indian Society

“…In severe poisoning, patients may have convulsive seizures. 8 Muscarinic, Nicotinic, and CNS symptoms according to amount of poisoning are observed in observation. We found that 41.5% patients were unable to tell the amount of poisoning, 24.4% patients had taken less than 5 grams, and 34.1% patients had taken more than 5 grams of poison.…”

Commentary: An electrophysiological study of the intermediate syndrome of organophosphate poisoning

“…In patients with severe OP intoxication, abnormalities suggestive of membrane instability (positive sharp and fibrillation potentials) can occur. 4,6 In conclusion, patients with IMS can be monitored with electrophysiological studies, and the results correlate well with clinical findings in acute OP poisoning. 1,7-9…”