title: Electrophysiological investigation of toxic neuropathies.
abstract: Electrophysiological changes are correlated with pathological processes. Marked slowing of conduction is found in segmental demyelination due to delayed nodal excitation or short lengths of continuous conduction. Secondary demyelination causes slow conduction in hexacarbon neuropathy. Slight reduction in maximal conduction velocity is attributable to selective damage to large fibres in acrylamide neuropathy. Sensory nerve action potential amplitude is a sensitive measure of peripheral nerve function and comparison of abnormalities in different nerve segments may indicate the nature of the underlying pathological change. Other abnormalities may be elucidated by double stimuli; eg repetitive activity due to cholinesterase inhibition only occurs after the first of two closely spaced stimuli. Activity-related excitability changes may be detected by measuring the amplitude of the response to a submaximal stimulus at varying times after a maximal shock and is increased and prolonged by the pyrethroid deltamethrin.
mesh_terms: D000200:Action Potentials; D004553:Electric Conductivity; D004594:Electrophysiology; D006801:Humans; D009046:Motor Neurons / Q000502:physiology; D009132:Muscles / Q000503:physiopathology; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000175:diagnosis / Q000503:physiopathology; D009475:Neurons, Afferent / Q000502:physiology; D011930:Reaction Time