Hypokalemic weakness in hyperaldosteronism: activity-dependent conduction block.
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.
Krishnan
Arun V
AV
The Institute of Neurological Sciences, Prince of Wales Hospital, University of New South Wales, Randwick, Sydney, NSW, Australia.
Colebatch
James G
JG
Kiernan
Matthew C
MC
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications* / Q000503:physiopathology; D007008:Hypokalemia / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D007473:Ion Channels / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000378:metabolism; D018908:Muscle Weakness / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D010525:Peripheral Nerves / Q000378:metabolism / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000209:etiology* / Q000503:physiopathology; D011188:Potassium / Q000097:blood / Q000627:therapeutic use; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects / Q000502:physiology; D016896:Treatment Outcome
D007473:Ion Channels; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium