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Faciobrachial dystonic seizures result from fronto–temporo–basalganglial network involvement
• Faciobrachial dystonic seizures (FBDS) are caused by autoantibodies to leucine-rich glioma-inactivated1 proteins, a component of the voltage-gated potassium channel complex (VGKC-complex) and precede the clinical presentation of limbic encephalitis. • The exact pathophysiology of FBDS is not known...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5573798/ https://www.ncbi.nlm.nih.gov/pubmed/28879090 http://dx.doi.org/10.1016/j.ebcr.2017.06.001 |
Sumario: | • Faciobrachial dystonic seizures (FBDS) are caused by autoantibodies to leucine-rich glioma-inactivated1 proteins, a component of the voltage-gated potassium channel complex (VGKC-complex) and precede the clinical presentation of limbic encephalitis. • The exact pathophysiology of FBDS is not known and whether they are seizures or movement disorder is still debated. • We suggest the fronto-temporo-basal ganglia network involving the medial frontal and temporal regions along with the corpus striatum and substantia nigra being responsible for the clinical phenomenon of FBDS. • The varied clinical, electrical and imaging features of FBDS in our cases and in the literature are best explained by involvement of this network. • Entrainment from any part of this network will result in similar clinical expression of FBDS, whereas other electro-clinical associations and duration depends on the extent of involvement of the network. |
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