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Hemifacial spasm, vertebrobasilar dolichoectasia and neurofibromatosis type 1. [artículo]

Por: Pablo Fernández, Eduardo de [Neurología] | Posada Rodríguez, Ignacio Javier [ Neurología, ] | Sierra Hidalgo, Fernando [Instituto de Investigación i+12].
Colaborador(es): Servicio de Neurología-Neurofisiología | Instituto de Investigación imas12.
Editor: Journal of Clinical Neuroscience, 2012Descripción: 19(7):1046-7.Recursos en línea: Solicitar documento Resumen: Hemifacial spasm (HFS) is usually produced by compression of the facial nerve by tortuous blood vessels at the root exit zone, including vertebrobasilar dolichoectasia (VBD). Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder with a variety of symptoms, affecting mainly the skin and nervous system. Cerebrovascular abnormalities are becoming a recognized complication of the disease and the most constantly described lesions are stenosis and occlusions affecting the internal carotid artery. VBD has rarely been associated with NF1. We report a 38-year-old female patient with HFS produced by VBD with NF1 presenting with other cerebrovascular abnormalities associated with this disease. We discuss the possible association between these three entities, assuming that a causal relationship may be established and that VBD is part of the spectrum of vascular abnormalities caused by NF1 in this patient.
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Artículo Artículo PC2109 (Navegar estantería) Disponible

Formato Vancouver:
de Pablo-Fernández E, Correas-Callero E, Sierra-Hidalgo F, Posada IJ. Hemifacial spasm, vertebrobasilar dolichoectasia and neurofibromatosis type 1. J Clin Neurosci. 2012 Jul;19(7):1046-7.

PMID: 22480682

Contiene 5 referencias

Hemifacial spasm (HFS) is usually produced by compression of the facial nerve by tortuous blood vessels at the root exit zone, including vertebrobasilar dolichoectasia (VBD). Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder with a variety of symptoms, affecting mainly the skin and nervous system. Cerebrovascular abnormalities are becoming a recognized complication of the disease and the most constantly described lesions are stenosis and occlusions affecting the internal carotid artery. VBD has rarely been associated with NF1. We report a 38-year-old female patient with HFS produced by VBD with NF1 presenting with other cerebrovascular abnormalities associated with this disease. We discuss the possible association between these three entities, assuming that a causal relationship may be established and that VBD is part of the spectrum of vascular abnormalities caused by NF1 in this patient.

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