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NEUROLOGY 2005;65:1309-1312
© 2005 American Academy of Neurology
Brief Communications

Hypokalemic weakness in hyperaldosteronism: Activity-dependent conduction block

Arun V. Krishnan, MBBS, James G. Colebatch, DSc and Matthew C. Kiernan, PhD

From the Institute of Neurological Sciences, Prince of Wales Hospital; Prince of Wales Medical Research Institute and Prince of Wales Clinical School, University of New South Wales, Randwick, Sydney, NSW, Australia.

Address correspondence and reprint requests to Dr. Matthew Kiernan, Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney, NSW 2031, Australia; e-mail: m.kiernan{at}unsw.edu.au

The authors describe a 48-year-old man who presented with acute weakness. Serum K+ was 1.7 mmol/L, and investigations established hyperaldosteronism. Nerve excitability studies during hypokalemia demonstrated that axons were of high threshold with a fanning out of threshold electrotonus, consistent with hyperpolarization. Activity-dependent conduction block was induced by voluntary contraction. Excitability abnormalities resolved with K+ replacement. Activity-dependent conduction block induced by normal activity may contribute to weakness and paralysis developing with hypokalemia.

Supported by grants from the National Health and Medical Research Council of Australia and the Australian Association of Neurologists (A.V.K.).

Disclosure: The authors report no conflicts of interest.

Received February 25, 2005. Accepted in final form July 11, 2005.






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