Conduction block during and after ischaemia in chronic inflammatory demyelinating polyneuropathy.
A previous study suggested that axonal hyperpolariza tion produced by maximal voluntary contraction could accentuate conduction block in symptomatic patients with chronic inflammatory demyelinating polyneuropathy (CIDP). If this is so, conduction block should occur with hyperpolarization due to other causes such as the release of ischaemia. The effects of ischaemia on axonal excitability and on impulse conduction were therefore studied in 12 healthy control subjects and seven patients with symptomatic CIDP. The compound muscle action potential (CMAP) of abductor pollicis brevis was recorded in response to supramaximal stimuli to the median nerve at the wrist alternating with measurements of axonal excitability before, during and after ischaemia for 10 min produced by inflation of a sphygmomanometer cuff around the arm. During ischaemia, the amplitude/area of the maximal CMAP was reduced in the patients by 10% and, after release of ischaemia, it was attenuated by 19%. There were only slight changes in the CMAPs in the healthy controls. The attenuation of the CMAP during ischaemia presumably results from depolarization-induced inactivation of Na(+) channels in axons critically dependent on the number of functioning Na(+) channels for action potential generation. The attenuation of the CMAP after release of ischaemia paralleled the post-ischaemic hyperpolarization and was probably precipitated by it. This study provides suggestive evidence that axonal depolarization can produce conduction block in CIDP, in addition to providing confirmation that axonal hyperpolarization can also do so. In patients with chronic demyelinating disorders, conduction block can probably result from a wider range of physiological stresses than previously appreciated, such as natural activity, ischaemia or recovery from transient ischaemia--all of which could produce fluctuations in symptoms.
Cappelen-Smith
Cecilia
C
Prince of Wales Medical Research Institute, University of New South Wales and Department of Clinical Neurophysiology, The Prince of Wales Hospital, Sydney, NSW, Australia.
Lin
Cindy S-Y
CS
Kuwabara
Satoshi
S
Burke
David
D
D000200:Action Potentials; D000328:Adult; D000368:Aged; D001132:Arm / Q000098:blood supply; D001369:Axons / Q000502:physiology; D005260:Female; D006801:Humans; D007249:Inflammation; D007511:Ischemia / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply / Q000503:physiopathology*; D009407:Nerve Block; D020277:Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / Q000503:physiopathology* / Q000628:therapy*