Introduction

OPIDN, sometimes also called organophosphate induced delayed polyneuropathy (OPIDP) is a rare, delayed neurotoxic effect, which occurs 1-5 weeks after severe toxicity from some cholinesterase inhibitors. However, it is not thought to be due to the effects on acetylcholinesterase itself.  (Jamal 1997; Clegg and van Gemert 1999; Jokanovic, Stukalov et al. 2002; Erdman 2004)

Although it is usually associated with organophosphorus compounds including nerve agents, several cases have been reported that are possibly related to carbamates.  (Clark 2002; Abou-Donia 2003)

Etiology

The cause of this condition is unknown. (Jamal 1997) While some have associated this condition with inhibition of an enzyme called neurotarget esterase (NTE), this association more recently has been called into question.  (Jamal 1997; Abu-Qare and Abou-Donia 2002; Walker and Nidiry 2002; Abou-Donia 2003)

Pathology

The condition is associated with symmetrical sensory-motor axonal degeneration of the peripheral nerves and spinal cord. (Marrs and Dewhurst 2000; Abu-Qare and Abou-Donia 2002) The lesion, a form of chemical transection known as Wallerian-type degeneration, is followed by myelin degeneration of distal portions of the long and large-diameter tracts of the central and peripheral nervous system. (Abou-Donia 2003)

Signs and Symptoms

Early symptoms

These include sharp, cramp-like pains in the calves. (Jokanovic, Stukalov et al. 2002)

Severity

Less severe cases exhibit a characteristic high-stepping gait. (Marrs and Dewhurst 2000) The initial muscle weakness gives rise to a clumsy, shuffling gait. (Ecobichon 1996) The most disabling featureis the paralysis of the legs. In severe cases, quadriplegia with foot and wrist drop are seen, as well as mild pyramidal signs. (Jokanovic, Stukalov et al. 2002)

Progression

The neuropathic findings begin peripherally and proceed proximately. Lower extremity paresthesias may appear with a “stocking-glove” distribution and progress to weakness, ataxia, depression of deep tendon reflexes, and paralysis with occasional progression to the arms and hands.  (Aaron and Howland 1994; Tareg et al. 2001; Clark 2002; Jokanovic, Stukalov et al. 2002)

Pain and weakness spreads rapidly, and patients become unsteady and unable to keep their balance. (Jokanovic, Stukalov et al. 2002)

This is subsequently replaced by spasticity, hypertonicity, hyperreflexia, clonus, and abnormal reflexes, indicative of damage to the pyramidal tracts and a permanent upper motor neuron syndrome. (Ecobichon 1996)

Treatment

No specific treatment has been identified. (Marrs and Dewhurst 2000) The early administration of pralidoxime and atropine does not seem to prevent the condition. (Tareg et al. 2001)

Prognosis

Patients with mild cases recover over several months; those with more serious polyneuropathies have persistent effects.  (Clegg and van Gemert 1999; Kwong 2002) Recovery affects only sensory nerves, while motor neurons may permanently lose function. The prognosis for functional recovery depends on the degree of pyramidal involvement, with ataxia and paralysis representing a permanent outcome in severe cases. (Jokanovic, Stukalov et al. 2002)

Progress Check