Abstract
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.
Publication types
-
Case Reports
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Action Potentials / drug effects
-
Action Potentials / physiology
-
Humans
-
Hyperaldosteronism / complications*
-
Hyperaldosteronism / physiopathology
-
Hypokalemia / blood
-
Hypokalemia / complications*
-
Hypokalemia / physiopathology
-
Ion Channels / physiology
-
Male
-
Middle Aged
-
Motor Neurons / metabolism
-
Muscle Weakness / drug therapy
-
Muscle Weakness / etiology*
-
Muscle Weakness / physiopathology
-
Neural Conduction / drug effects
-
Neural Conduction / physiology
-
Peripheral Nerves / metabolism
-
Peripheral Nerves / physiopathology
-
Peripheral Nervous System Diseases / etiology*
-
Peripheral Nervous System Diseases / physiopathology
-
Potassium / blood
-
Potassium / therapeutic use
-
Sodium-Potassium-Exchanging ATPase / drug effects
-
Sodium-Potassium-Exchanging ATPase / physiology
-
Treatment Outcome
Substances
-
Ion Channels
-
Sodium-Potassium-Exchanging ATPase
-
Potassium