{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,31]],"date-time":"2023-10-31T07:42:50Z","timestamp":1698738170326},"reference-count":17,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,3,29]],"date-time":"2013-03-29T00:00:00Z","timestamp":1364515200000},"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":[[2013,5]]},"abstract":"Introduction<\/jats:title>In mitochondrial disease, it is likely that energy substrate depletion leads to paralysis of ATPase<\/jats:styled-content>\u2010dependent pumps, resulting in membrane depolarization. Axonal depolarization has been demonstrated in a crisis, but not in the resting state. We, therefore, stressed axons using ischemia to see if this would reveal abnormal responses, as occurs in diabetes mellitus.<\/jats:p><\/jats:sec>Methods<\/jats:title>Excitability of median nerve axons at the wrist was studied in 13 patients with MELAS<\/jats:styled-content> (6 with glucose intolerance) and 17 control subjects in response to ischemia due to inflation of a cuff around the arm for 10 min.<\/jats:p><\/jats:sec>Results<\/jats:title>There were no significant differences in preischemic measures of axonal excitability or in the intra\u2010 and postischemic responses.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>Although depolarization has been noted to occur spontaneously during a crisis, we could not demonstrate a defect of axonal ATP<\/jats:styled-content>\u2010dependent mechanisms. The mechanisms underlying axonal excitability and neuropathy in diabetes may not apply to MELAS<\/jats:styled-content>. 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