Treatment of slow-channel congenital myasthenic syndrome with fluoxetine.
The authors found that fluoxetine significantly shortens at 5 microM/L and nearly normalizes at 10 microM/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 microM/L). Both patients showed marked subjective and objective improvement by quantitative muscle strength testing and electromyography.
Harper
C Michel
CM
Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA. harper.michel@mayo.edu
Fukodome
Takayasu
T
Engel
Andrew G
AG
D000328:Adult; D018680:Cholinergic Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D004341:Drug Evaluation; D004342:Drug Hypersensitivity / Q000209:etiology; D005260:Female; D005473:Fluoxetine / Q000494:pharmacology / Q000627:therapeutic use*; D005799:Genes, Dominant; D006801:Humans; D020125:Mutation, Missense; D020294:Myasthenic Syndromes, Congenital / Q000188:drug therapy*; D017354:Point Mutation; D011802:Quinidine / Q000009:adverse effects; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000235:genetics* / Q000502:physiology; D016896:Treatment Outcome
D018680:Cholinergic Antagonists; D011950:Receptors, Cholinergic; D005473:Fluoxetine; D011802:Quinidine