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In vitro electrophysiological studies were conducted using whole cell patch\u2010clamp to explore biophysical properties of wild\u2010type and mutant K<jats:sub>V<\/jats:sub>3.1 channels.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Symptoms began at between 3 and 15 years of age (median\u2009=\u20099.5), with progressively severe myoclonus and rare tonic\u2013clonic seizures. Ataxia was present early, but quickly became overshadowed by myoclonus; 10 patients were wheelchair\u2010bound by their late teenage years. Mild cognitive decline occurred in half. Early death was not observed. Electroencephalogram (EEG) showed generalized spike and polyspike wave discharges, with documented photosensitivity in most. Polygraphic EEG\u2013electromyographic studies demonstrated a cortical origin for myoclonus and striking coactivation of agonist and antagonist muscles. Magnetic resonance imaging revealed symmetrical cerebellar atrophy, which appeared progressive, and a prominent corpus callosum. Unexpectedly, transient clinical improvement with fever was noted in 6 patients. To explore this, we performed high\u2010temperature in vitro recordings. At elevated temperatures, there was a robust leftward shift in activation of wild\u2010type K<jats:sub>V<\/jats:sub>3.1, increasing channel availability.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>MEAK has a relatively homogeneous presentation, resembling Unverricht\u2013Lundborg disease, despite the genetic and biological basis being quite different. A remarkable improvement with fever may be explained by the temperature\u2010dependent leftward shift in activation of wild\u2010type K<jats:sub>V<\/jats:sub>3.1 subunit\u2013containing channels, which would counter the loss of function observed for mutant channels, highlighting <jats:italic>KCNC1<\/jats:italic> as a potential target for precision therapeutics. Ann Neurol 2017;81:677\u2013689<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.24929","type":"journal-article","created":{"date-parts":[[2017,4,5]],"date-time":"2017-04-05T23:34:45Z","timestamp":1491435285000},"page":"677-689","source":"Crossref","is-referenced-by-count":84,"title":["Myoclonus epilepsy and ataxia due to <scp><i>KCNC<\/i><\/scp><i>1<\/i> mutation: Analysis of 20 cases and <scp>K<\/scp><sup>+<\/sup> channel properties"],"prefix":"10.1002","volume":"81","author":[{"given":"Karen L.","family":"Oliver","sequence":"first","affiliation":[{"name":"Epilepsy Research Centre, Department of Medicine University of Melbourne, Austin Health Heidelberg Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvana","family":"Franceschetti","sequence":"additional","affiliation":[{"name":"Department of Neurophysiology C. 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