{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T18:51:32Z","timestamp":1790016692515,"version":"4.0.1"},"reference-count":19,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2002,6,3]],"date-time":"2002-06-03T00:00:00Z","timestamp":1023062400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2002,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Multiple nerve excitability measurements have been proposed for clinical testing of nerve function, and an important determinant of excitability is membrane potential. We report a patient with acquired hypokalemic paralysis in whom multiple excitability indices (stimulus\u2010response curve, strength\u2010duration properties, threshold electrotonus, recovery cycle) were measured during and after an acute hypokalemic attack (serum K<jats:sup>+<\/jats:sup> level, 2.1 mEq\/L and 4.5 mEq\/L, respectively). During hypokalemia, there was a shift of the stimulus\u2010response curve to the right, a decrease in strength\u2010duration time constant, a \u201cfanning\u2010out\u201d of responses during threshold electrotonus, a reduction in relative refractory period, and an increase in superexcitability; all of these indicate axonal hyperpolarization, presumably due to the K<jats:sup>+<\/jats:sup> equilibrium potential being more negative. These indices returned to normal 20 h later, associated with normalization of the serum K<jats:sup>+<\/jats:sup> level. These results demonstrate that the changes associated with hypokalemic paralysis are not confined to muscle and that axons undergo hyperpolarization in vivo. Multiple excitability measurements can be used as a tool to identify changes in membrane potential of human axons. \u00a9 2002 Wiley Periodicals, Inc. 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