Flecainide-induced myoclonus. [caso clínico]
Por: Llamas Velasco, Sara [Neurología]
| Sierra Hidalgo, Fernando [Instituto de Investigación i+12] | Ceballos Rodríguez, Rosa María [Neurología] | Méndez Guerrero, Antonio [Neurología ] | Ruiz Morales, Juan Manuel [Neurología].
Colaborador(es): Servicio de Neurología-Neurofisiología | Instituto de Investigación imas12.
Tipo de material: 
ArtículoEditor: Clinical neuropharmacology, 2014Descripción: 37(2):65-6.Recursos en línea: Solicitar documento Resumen: Flecainide is a class 1c antiarrhythmic that acts by blocking sodium channels to reduce intracardiac conduction and is used mainly in the treatment of supraventricular arrhythmias. Dizziness, visual disturbances, headache, and nausea are commonly associated with flecainide, but severe central nervous system toxicity is rare. Here, we report the case of a 71-year-old woman with a history of renal transplantation who developed severe myoclonus 24 hours after being started on flecainide, 100 mg 2 times a day, because of atrial fibrillation. This symptom completely disappeared once the drug was removed. Only 2 patients presenting with flecainide-induced myoclonus have been previously reported. Although the exact pathophysiologic explanation of this phenomenon remains unclear, it is well known that the susceptibility to severe flecainide toxicity is increased in patients with chronic kidney disease.
| Tipo de ítem | Ubicación actual | Signatura | Estado | Fecha de vencimiento |
|---|---|---|---|---|
Caso clínico
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PC16288 (Navegar estantería) | Disponible |
Formato Vancouver:
Velasco SL, Sierra-Hidalgo F, Rodríguez RM, Guerreo AJ, Morales JR. Flecainide-induced myoclonus. Clin Neuropharmacol. 2014 Mar-Apr;37(2):65-6.
PMID: 24614665
Contienen 13 referencias
Flecainide is a class 1c antiarrhythmic that acts by blocking sodium channels to reduce intracardiac conduction and is used mainly in the treatment of supraventricular arrhythmias. Dizziness, visual disturbances, headache, and nausea are commonly associated with flecainide, but severe central nervous system toxicity is rare. Here, we report the case of a 71-year-old woman with a history of renal transplantation who developed severe myoclonus 24 hours after being started on flecainide, 100 mg 2 times a day, because of atrial fibrillation. This symptom completely disappeared once the drug was removed. Only 2 patients presenting with flecainide-induced myoclonus have been previously reported. Although the exact pathophysiologic explanation of this phenomenon remains unclear, it is well known that the susceptibility to severe flecainide toxicity is increased in patients with chronic kidney disease.
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