Organophosphate-induced delayed polyneuropathy (OPIDP) is a rare toxicity 
resulting from exposure to certain organophosphorus (OP) esters. It is 
characterised by distal degeneration of some axons of both the peripheral and 
central nervous systems occurring 1-4 weeks after single or short-term 
exposures. Cramping muscle pain in the lower limbs, distal numbness and 
paraesthesiae occur, followed by progressive weakness, depression of deep tendon 
reflexes in the lower limbs and, in severe cases, in the upper limbs. Signs 
include high-stepping gait associated with bilateral foot drop and, in severe 
cases, quadriplegia with foot and wrist drop as well as pyramidal signs. In 
time, there might be significant recovery of the peripheral nerve function but, 
depending on the degree of pyramidal involvement, spastic ataxia may be a 
permanent outcome of severe OPIDP. Human and experimental data indicate that 
recovery is usually complete in the young. At onset, the electrophysiological 
changes include reduced amplitude of the compound muscle potential, increased 
distal latencies and normal or slightly reduced nerve conduction velocities. The 
progression of the disease, usually over a few days, may lead to 
non-excitability of the nerve with electromyographical signs of denervation. 
Nerve biopsies have been performed in a few cases and showed axonal degeneration 
with secondary demyelination. Neuropathy target esterase (NTE) is thought to be 
the target of OPIDP initiation. The ratio of inhibitory powers for 
acetylcholinesterase and NTE represents the crucial guideline for the 
aetiological attribution of OP-induced peripheral neuropathy. In fact, 
pre-marketing toxicity testing in animals selects OP insecticides with 
cholinergic toxicity potential much higher than that to result in OPIDP. 
Therefore, OPIDP may develop only after very large exposures to insecticides, 
causing severe cholinergic toxicity. However, this was not the case with certain 
triaryl phosphates that were not used as insecticides but as hydraulic fluids, 
lubricants and plasticisers and do not result in cholinergic toxicity. Several 
thousand cases of OPIDP as a result of exposure to tri-ortho-cresyl phosphate 
have been reported, whereas the number of cases of OPIDP as a result of OP 
insecticide poisoning is much lower. In this article, we mainly discuss OP 
pesticide poisoning, particularly when caused by chlorpyrifos, dichlorvos, 
isofenphos, methamidophos, mipafox, trichlorfon, trichlornat, 
phosphamidon/mevinphos and by certain carbamates. We also discuss case reports 
where neuropathies were not convincingly attributed to fenthion, malathion, 
omethoate/dimethoate, parathion and merphos. Finally, several observational 
studies on long-term, low-level exposures to OPs that sometimes reported mild, 
inconsistent and unexplained changes of unclear significance in peripheral 
nerves are briefly discussed.