Polyneuropathy induced by n-hexane intoxication in Taiwan.

Abstract

n-Hexane and methyl n-butyl ketone share a common metabolite, 2,5-hexanedione, a potent neurotoxin. Neurotoxic effects to both peripheral and central nervous systems may occur after occupational exposure or recreational abuse of n-hexane. Initial clinical manifestations include numbness and tingling sensation in the toes and fingers, followed by progressive weakness and areflexia, particularly in the distal limbs. Chronic low-dose n-hexane exposure, often observed in industrial workers, apparently causes axonal loss with sensory impairment. Subacute high-dose n-hexane exposure, often observed in glue-sniffers, can cause axonal swelling and secondary demyelination with muscle wasting and weakness. Electrophysiological studies demonstrate prominent prolongation of distal latencies, slowing of nerve conduction velocities, and conduction block with temporal dispersion particularly in severely intoxicated patients. Pathological hallmarks include giant axonal swelling with secondary demyelination and relative loss of large myelinated fibers. Giant axons are accumulated by 10 nm neurofilaments. The clinical course tends to be biphasic with "coasting" for 2-3 months, followed by a slow recovery for about 1-2 years after cessation of exposure to n-hexane. Prognosis is usually favorable. Severely affected patients may develop sequelae of muscle wasting, foot drop, and spasticity. Increased awareness of the n-hexane neurotoxicity in industrial workers and glue sniffers as well as use of safe solvents and adequate ventilation systems are important for preventing n-hexane toxicity.