Mutation in the neuronal voltage-gated sodium channel SCN1A in familial hemiplegic migraine.
By Martin Dichgans, T. Freilinger, G. Eckstein, E. Babini, B. Lorenz-Depiereux, S. Biskup, Michel D. Ferrari, J. Herzog, A. M. van den Maagdenberg, M. Pusch and 1 more. The Lancet, 2005
854 citations recorded by the source corpus.
Subfields: Neurology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/2bcc7cc48746ed0cb3ed2ca46fa4f71ca5e7ce9d
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Citations in the corpus
- Pathophysiology of Migraine: A Disorder of Sensory Processing. (2017, background): “Mutations within the SCN1A gene located on chromosome 2q24 represent the underlying cause for FHM3 (215).”
- Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain (2013, background): “In agreement with the human data, mice carrying FHM mutations have shown increased susceptibility to CSD and altered synaptic transmission [36,68,125,127].”
- PATHOPHYSIOLOGY OF MIGRAINE (2006, background): “Most recently, mutations in the voltage-gated sodium channel gene SCN1A have been identified as the cause for FHM-III (Dichgans et al, 2005).”