Brain, Vol. 126, No. 4, 1001-1008,
April 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg087
Activity-dependent hyperpolarization and impulse conduction in motor axons in patients with carpal tunnel syndrome
1 Prince of Wales Medical Research Institute, University of New South Wales, 2 Department of Clinical Neurophysiology, Prince of Wales Hospital and 3 College of Health Sciences, University of Sydney, Australia
Correspondence to: Professor David Burke, Office of Research and Development, College of Health Sciences, Medical Foundation Building-K25, University of Sydney, NSW 2006, Australia E-mail: d.burke{at}chs.usyd.edu.au
The differing contributions of axonal attenuation, ischaemia, demyelination and remyelination to the pathophysiology of carpal tunnel syndrome remain unresolved. Previous studies indicate that the hyperpolarization of motor axons produced by voluntary contractions may precipitate conduction block in chronic acquired demyelinating polyneuropathies. The present study investigated whether this axonal hyperpolarization can produce or accentuate conduction block in carpal tunnel syndrome, thereby implicating demyelination as a significant factor in its pathogenesis. Studies were performed in 12 patients with mild to moderate carpal tunnel syndrome and compared with 12 healthy control subjects. Using the technique of threshold tracking, the compound muscle action potential (CMAP) of abductor pollicis brevis (APB) was recorded in response to supramaximal stimuli to the median nerve at the wrist, alternating with measurements of axonal excitability. After a voluntary contraction of APB for 60 s, there was a lesser hyperpolarizing threshold increase in the patients (
18%), than in controls (37%). The changes in strength–duration time constant and supernormality were appropriately smaller in the patients. The amplitude and area of the maximal CMAP was not significantly altered in either group. Activity-dependent conduction block was not precipitated in the carpal tunnel syndrome patients even though this degree of axonal hyperpolarization was sufficient to produce conduction block in chronic inflammatory demyelinating polyneuropathy. These studies support the view that demyelination may not be a critical factor in the slowing of impulse conduction in mild to moderate carpal tunnel syndrome.