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Medline ® Abstract for Reference 24

of 'Myopathies of systemic disease'

24
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Hypokalemic weakness in hyperaldosteronism: activity-dependent conduction block.
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Krishnan AV, Colebatch JG, Kiernan MC
SO
Neurology. 2005;65(8):1309.
 
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.
AD
The Institute of Neurological Sciences, Prince of Wales Hospital, University of New South Wales, Randwick, Sydney, NSW, Australia.
PMID