000			nab a22 7a 4500
999			_c16288 _d16288
003			PC16288
005			20210625062820.0
008			210224b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_9305 _aLlamas Velasco, Sara _eNeurología
100			_91498 _aSierra Hidalgo, Fernando _eInstituto de Investigación i+12
100			_92621 _aCeballos Rodríguez, Rosa María _eNeurología
100			_92592 _aMéndez Guerrero, Antonio _eNeurología
100			_91470 _aRuiz Morales, Juan Manuel _eNeurología
245	0	0	_aFlecainide-induced myoclonus. _h[caso clínico]
260			_bClinical neuropharmacology, _c2014
300			_a37(2):65-6.
500			_aFormato Vancouver: Velasco SL, Sierra-Hidalgo F, Rodríguez RM, Guerreo AJ, Morales JR. Flecainide-induced myoclonus. Clin Neuropharmacol. 2014 Mar-Apr;37(2):65-6.
501			_aPMID: 24614665
504			_aContienen 13 referencias
520			_aFlecainide 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.
710			_9267 _aServicio de Neurología-Neurofisiología
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc16288.pdf _ySolicitar documento
942			_2ddc _cCAS _n0