Clinical and electrophysiological studies of carbon disulphide polyneuropathy.
A clinical and electrophological study was performed on 30 patients with chronic carbon disulphide poisoning. Although the measurements of motor conduction velocity and of terminal latency were within the normal range in the subclinical stage, estimation of nerve excitability threshold showed distal motor hypoexcitability, thus proving a very effective means for the early detection of carbon disulphide polyneuropathy. The distal muscle fatigue found in 35% of patients was confirmed by the decrement (more than 10%) in the amplitude of muscle evoked potentials in the abductor digiti minimi muscle in response to repetitive stimulation of the ulnar nerve. Association of the above findings with the significant electrophysiological changes, viz., decrease in the amplitude of sensory evoked potentials on stimulation of the digital fibres, mild slowing of sensory conduction velocity in the peripheral nerves, and decrease in the amplitude of evoked potentials in the distal muscles, suggest that the carbon disulphide polyneuropathy would be underlain by a primary distal axonopathy.
D000328:Adult; D002246:Carbon Disulfide / Q000506:poisoning*; D004576:Electromyography; D005071:Evoked Potentials / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000187:drug effects; D009431:Neural Conduction / Q000187:drug effects; D009468:Neuromuscular Diseases / Q000139:chemically induced; D010525:Peripheral Nerves / Q000187:drug effects; D011115:Polyneuropathies / Q000139:chemically induced*; D012677:Sensation / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*
D002246:Carbon Disulfide