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.
|Original language||English (US)|
|Number of pages||4|
|State||Published - May 27 2003|
ASJC Scopus subject areas
- Clinical Neurology