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Rapsyn congenital myasthenic syndrome worsened by fluoxetine
Author(s) -
Visser Amy C.,
Laughlin Ruple S.,
Litchy William J.,
Benarroch Eduardo E.,
Milone Margherita
Publication year - 2017
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.25244
Subject(s) - fluoxetine , congenital myasthenic syndrome , repetitive nerve stimulation , discontinuation , medicine , depression (economics) , weakness , anesthesia , acetylcholine receptor , myasthenia gravis , surgery , serotonin , receptor , economics , macroeconomics
ABSTRACT Introduction : Fluoxetine is a selective serotonin reuptake inhibitor and long‐lived open channel blocker of the acetylcholine receptor, often used in the treatment of slow‐channel congenital myasthenic syndromes (CMS). Methods : We report a 42‐year‐old woman who had a history of episodic limb weakness that worsened after initiation of fluoxetine for treatment of depression. Genetic testing for CMS revealed a homozygous pathogenic mutation in the rapsyn ( RAPSN ) gene (p.Asn88Lys). Electrodiagnostic testing was performed before and 1 month after discontinuation of fluoxetine. Results : The 2 H z repetitive nerve stimulation of the fibular and spinal accessory nerves showed a baseline decrement of 36% and 14%, respectively. One month after discontinuing fluoxetine, the spinal accessory nerve decrement was no longer present, and the decrement in the fibular nerve was improved at 17%. Conclusions : This case demonstrates worsening of both clinical and electrophysiologic findings in a patient with CMS secondary to a RAPSN mutation treated with fluoxetine. Muscle Nerve 55 : 131–135, 2017