Rapsyn congenital myasthenic syndrome worsened by fluoxetine

Amy C. Visser, Ruple S. Laughlin, William J Litchy, Eduardo E. Benarroch, Margherita Milone

Research output: Contribution to journalArticle

5 Scopus citations

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 Hz 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.

Original languageEnglish (US)
Pages (from-to)131-135
Number of pages5
JournalMuscle and Nerve
Volume55
Issue number1
DOIs
StatePublished - Jan 1 2017

Keywords

  • congenital myasthenic syndrome
  • fluoxetine
  • myasthenia
  • RAPSN, rapsyn gene
  • repetitive nerve stimulation
  • RNS

ASJC Scopus subject areas

  • Physiology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Physiology (medical)

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