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Treatment of slow-channel congenital myasthenic syndrome with fluoxetine

From the Department of Neurology (Drs. Harper and Engel), Mayo Clinic, Rochester, MN; and Kawatana National Hospital (Dr. Fukodome), Japan.

Address correspondence and reprint requests to Dr. C. Michel Harper, Department of Neurology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905; e-mail: harper.michel{at}mayo.edu

The authors found that fluoxetine significantly shortens at 5 µM/L and nearly normalizes at 10 µM/L the prolonged opening bursts of slow-channel congenital myasthenic syndrome (SCCMS) acetylcholine receptors (AChR) expressed in fibroblasts. Prompted by this observation, they treated two SCCMS patients allergic to quinidine with up to 80 to 120 mg of fluoxetine per day over 3 years (serum fluoxetine + norfluoxetine levels 8 to 11 µM/L). Both patients showed marked subjective and objective improvement by quantitative muscle strength testing and electromyography.