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LETTER TO EDITOR
Year : 2004  |  Volume : 52  |  Issue : 1  |  Page : 128--129

Clinical characteristics of organophosphate-induced delayed polyneuropathy

S Kumar 
 Neurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632004, India

Correspondence Address:
S Kumar
Neurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632004
India




How to cite this article:
Kumar S. Clinical characteristics of organophosphate-induced delayed polyneuropathy.Neurol India 2004;52:128-129


How to cite this URL:
Kumar S. Clinical characteristics of organophosphate-induced delayed polyneuropathy. Neurol India [serial online] 2004 [cited 2020 Jul 2 ];52:128-129
Available from: http://www.neurologyindia.com/text.asp?2004/52/1/128/6728


Full Text

Sir,

I read with interest the recent article by Chatterjee et al.[1] They report a patient with organophosphorus (OP) poisoning who developed intermediate syndrome (IS) and organophosphate-induced delayed polyneuropathy (OPIDP) in succession. However, I would like to make certain comments regarding the diagnosis of OPIDP in this case.

OPIDP as a clinical syndrome is well known and was described even before the association of IS with OP poisoning became known. The prevalence of OPIDP is variable; however, it occurred in 22% of patients with OP poisoning in a recent study.[2] OPIDP occurs within a period of one week to five-six months of the ingestion of an OP compound, almost exclusively in patients with preceding acute cholinergic toxicity related to severe acute exposure (to an OP compound). However, there are occasional reports of OPIDP developing in a patient without prior cholinergic toxicity following a low-dose chronic exposure to OP.[3]

The neuropathy in OPIDP is typically a symmetrical sensorimotor neuropathy, with a distal predominance.[4] Initial symptoms are paraesthesia in the lower limbs and pain in the calves, followed by motor involvement of the lower limbs, manifested by leg weakness, foot drop and muscle hypotonia. The neuropathy in OPIDP is motor-predominant, and pure sensory neuropathy does not occur. If sensory symptoms are present, they are always milder than the motor component. Upper limb symptoms are always preceded by lower limb involvement. OPIDP is typically a “dying-back” neuropathy as revealed by clinical, electrophysiological and nerve biopsy data.[4] The neuropathy has a typical “subacute” course of progression over a two-week period.[5] In addition, features of pyramidal tract and posterior column involvement may be noted later in the course of illness. The patient reported by Chatterjee et al presented with a wrist drop and had features of right radial nerve palsy alone (even after electrophysiological studies) without any involvement of the lower limbs. This does not fit with the description of OPIDP as mentioned above and an alternative etiology for the same should be considered.

References

1Chatterjee M, Sarma PSA. Unusual neurological complications in a case of organophosphate poisoning. Neurol India 2003;51:290-1.
2Aygun D, Doganay Z, Altintop L, Guven H, Onar M, Deniz T, et al. Serum acetylcholinesterase and prognosis of acute organophosphate poisoning. J Toxicol Clin Toxicol 2002;40:903-10.
3Kaplan JG, Kessler J, Rosenberg N, Pack D, Schaumburg HH. Sensory neuropathy associated with Dursban (chlorpyrifos) exposure. Neurology 1993;43:2193-6.
4Vasilescu C, Alexianu M, Dan A. Delayed neuropathy after organophosphorus insecticide (Dipterex) poisoning: a clinical, electrophysiological and nerve biopsy study. J Neurol Neurosurg Psychiatry 1984;47:543-8.
5Singh S, Sharma N. Neurological syndromes following organophosphate poisoning. Neurol India 2000;48:308-13.