A 23 year old male developed abdominal pain, diarrhoea, and vomiting several hours after poisoning with acute triphenyltin intoxication in a suicide attempt. Severe ataxia, dysmetria, nystagmus, and blurring of vision soon supervened. Disturbance of consciousness and confusion developed 12 days later and lasted for two months. A delayed sensorimotor polyneuropathy was shown by electrophysiological studies to be due to axonal degeneration and demyelination. The neuropathy rapidly recovered after consciousness was regained.Organotins are widely used in agricultural practice for their bactericidal, antiparasitic, fungicidal and molluscicidal properties. The neurotoxicity of triethyltin and trimethyltin has already been recognised in both human cases and animal studies."l Triphenyltin (TPhT) The patient became confused and occasionally semicomatous after the fifth day in hospital. A follow up EEG on 18 November revealed a moderate slowing of background activity (4-6 Hz) with periodic paroxysmal generalised spikes or sharp waves, recurring every 1-2 seconds (fig lb). A lack of definite diagnosis indicated preference for conservative treatment only.The patient gradually regained consciousness two months after admission. In late December 1986, a crucial piece of information was obtained: the patient had attempted suicide using a molluscicidal agent. Mass spectrometric analysis confirmed this agent to be triphenyltin compound. In early January 1987 the patient began to improve. There was no more nystagmus. Moderate weakness in the lower limbs with mild wasting in the small foot muscles was found; the tendon reflexes were absent in the lower limbs and hypoactive in the upper. A detailed evaluation of sensory function was impossible. Motor conduction velocities were reduced: median nerve in the left 45-7 ms, ulnar nerve 45-2 ms, peroneal nerve 29-9 ms, posterior tibial nerve 33-7 ms. Sensory conduction velocities were also slowed: left median nerve 46-8 ms, ulnar nerve 37-8 ms, sural nerve 32-6 ms. Motor and sensory action potential (MAP and SAP) amplitudes were severely decreased: peroneal nerve MAP 0 5 mV, posterior tibial nerve MAP 4-5 mV, and sural nerve SAP 5 uV. Electromyography of the small muscles of the