Electrophysiological Studies in Acute Organophosphate Poisoning
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J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.50.11.1442 on 1 November 1987. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry 1987;50:1442-1448 Electrophysiological studies in acute organophosphate poisoning R S WADIA, S CHITRA, R B AMIN, R S KIWALKAR, H V SARDESAI From the Neurology Clinic Sassoon General Hospitals and Ruby Hall Clinic, Pune, India 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 ofparalysis. This response to repetitive stimuli is thus quite distinct from that seen in either myasthenia or Eaton Lambert syndrome. On three occasions after was insecticide poisoning and later delayed poisoning with dichlorovos there first anticholinesterase guest. Protected by copyright. neurotoxicity as seen with triorthocresylphosphate. These cases showed all the features of a severe pure motor axonal degeneration neuropathy. Organosphosphate insecticide poisoning is the com- mon and in our experience with over 2000 cases of monest mode of suicidal poisoning in India today.' organophosphate poisoning we have seen this on only The drug is usually ingested and the patients are com- three occasions, each time after ingestion of Dichlo- monly admitted with miosis, fasciculations, pul- rovos.4 We report here our electrophysiological stud- monary oedema and froth at the mouth due to the ies during the hospital admission for acute muscarinic, nicotinic and central manifestations of organophosphate poisoning. cholinergic poisoning. We have described before the neurological manifestations seen in 200 consecutive Materials and methods cases.2 We divided the signs into Type I, that is, those present on admission and responding promptly to The patients reported here were admitted for acute therapy and Type II as those appearing organophosphate poisoning, usually ingested for suicidal atropine purposes, to the Sassoon Hospital or Ruby Hall Clinic, sometime after commencement of treatment and Pune. They were treated as usual with atropine and pyridine- basically not influenced by atropine. Type I signs are 2 aldoxime methiodide (2 PAM). In the early stages 2-PAM believed to be cholinergic effects at muscarinic recep- was not easily available in India and some cases received tors and include bilateral pyramidal signs and only atropine. In the original series of 200 cases2 42 devel- impairment of consciousness and miosis. Type II are oped Type II paralysis and 17 died. The nerve conduction believed to be due to acetylcholine excess at nicotinic studies reported here include cases from that series and 21 receptors. Type II paralysis appears from 12-72 several studied subsequently. A total of 66 cases including http://jnnp.bmj.com/ hours after poisoning and lasts up to 5-6 days. This cases who had no clear weakness were studied in detail. Type II paralysis is clearly different from delayed Nerve conduction was studied using standard techniques and recording from surface electrodes on the abductor digiti neurotoxicity, which appears only after 8-12 days minimi for the ulnar nerve and extensor digitorium brevis and lasts much longer.3 Delayed neurotoxicity after a for the lateral popliteal nerve. The organophosphates chiefly prior episode of clinical organophosphate anti- used in these cases were diazinon, malathion, fenthion and cholinesterase poisoning is furthermore very uncom- sumithion. The frequency of the neurological signs here mentioned and the time course of the paralysis (onset and seen on October 2, 2021 by Address for reprint requests: Dr R S Wadia, Poona Medical Founda- duration) vary with the drug used but the clinical signs tion, Ruby Hall Clinic, Department of Medicine and Neurology, 40 were similar5 and all the organophosphate insecticides are Sassoon Road, Pune 411 001, India. studied together in this series. The initial studies of these cases were reported at the Second International Congress on Received 7 February 1986 and in revised form 18 March 1987. Muscle Diseases in Newcastle and has been published as an Accepted 26 March 1987 abstract. 1442 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.50.11.1442 on 1 November 1987. Downloaded from Electrophysiological studies in acute organophosphate poisoning 1443 Table I Pairalrti signs in organopho.)phate poisoning: total +2SD (ca.se.s:- 101 in 350 (cases pOarah'Otic 60- Inability to lift ncck 87 Inability to sit up 99 Ophthalimloparcsis 27 56- Slow eye movement 39 S 0 Facial weakness 52 Swallowing difficulty 14 0 Limh weakness proximal more than distal 86 52 0 . Arellexia 52 tn 0 0 Respiratory paralysis 37 E * 00 S DeatIh 333 >, 48- 0 0 0 S 0 0 0 * 0. 0 0 ' 44- 0 Observations 0 0 @0 0 0 In two separate series of 200 cases and 150 cases 40' 0 0 respectively Type II paralysis signs were noted in a 0 0 0 total of 101 cases (49%). Table 1 lists the signs. Cases with only three or less of the signs listed were consid- 36' ered mild. Those with 4-6 signs were considered mod- 34 0 erately affected and those with more than six sign§ 32 were considered severe. The nerve conduction velocities in the ulnar and Control NO Mild Moderate Severe lateral popliteal nerves are shown in figs 1 and 2. deficit guest. Protected by copyright. Though the figs show that the mean velocities were Fig 2 Motor nerve conduction velocities in the lateral least in the severely affected and serially better in the popliteal nerve. moderate, mild and no deficit groups, the differences are not significant. Moreover, it is important to note that the slowest velocities noted were 39m/s in the only six readings in the entire series were actually a lateral popliteal and 47m/s in the ulnar nerve and little outside the range of normal for our laboratory. Suffice to say that even in extremis with the patients on a respirator, with minimal limb movement nerve conduction velocities were invariably over 45 m/s in +2 SD the ulnar and 38m/s in the lateral popliteal nerve. 70* 0 Figure 3 shows distal latencies in these cases. Again 0 though these were a little more in the severely 0 0 there was no case with distal 66' affected, latency outside 0 the range of normal in our laboratory. .0 0 0.00 Decrement was looked for in cases with weakness 62- * 0 0 and in those without. Tests were done stimulating the ulnar nerve at the wrist and recording from the 0 .0 0 0 E 0 abductor digiti minimi. Only two cases (who went LA *0 0 58- 0 into respiratory paralysis 24 hours later) showed dec- rement at 3 Hz. At 10 Hz only four cases showed dec- 0 http://jnnp.bmj.com/ .0 0 rement. The two cases with decrement at 3 Hz and > 54- 0 0 four cases with decrement at 10Hz were repeated at 0 30 Hz and also showed decrement at this rate. Of 18 00 0 0 50- 0 cases with no deficit seven showed decrement at -2SD 0 30 Hz. Decrement at 30 Hz was noted in 12 of 19 with 0 mild deficit, three of seven with moderate deficit, and 46- seven of seven with severe deficit. Figure 4 shows one case showing decrement at 30 Hz. In cases the eight on October 2, 2021 by decrement tests was repeated more than once after the 42- onset of paralysis. We found that significant decre- Controls No M ild Moderate Severe ment may last for 4-11 days after onset of paralysis. (n =50) deficit The amplitudes of the compound action potential Fig 1 Motor nerve conduction velocity in ulnar nerve. were also studied. In the early part of the study the J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.50.11.1442 on 1 November 1987. Downloaded from 1444 Wadia, Chitra, Amin, Kiwalkar, Sardesai 56 Ulnar nerve Lateral popliteal 50 4.5- * 0 4*0 - 0 0 @0 00 tn 2 SD 0 0 0 0 E 35 - 0 * 0 T 0 0 .@0a *1.0 0 >80 0 0 0 0 * 0 o 25-I I I I ** ..0 20- 0 0 -2SD 0 0 1 5 0 0 -20 * 0 Controls Mild Moderate Controls Mild Moderate (mean ±2SD) to severe to severe guest. Protected by copyright. Fig 3 Distal latencies in ulnar and lateral popliteal. action potentials were measured with both electrodes tional peaks flattened out on repetitive stimuli. The on the muscle belly. The amplitude we measured was response on repeated stimuli is the characteristic of clearly reduced to a mean of 60% of our control repetitive activity6 ' and is the method by which it is series. In 17 cases we have measured the amplitude recognised. When looking for it specifically repetitive with the standard belly tendon electrode placement. activity was noted in precisely 60% of the cases but Figure 5 shows these results and shows that the was seen in all the cases with clinical signs. We amplitude tended to be lower in the more severely believed at one time that decrement may be seen in affected cases and was below the lower limit of con- cases which did not show repetitive activity. Figure 7 trol (mean-2SD) in several.