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Dravet syndrome classically features “febrile and afebrile, generalized and unilateral, clonic or tonic-clonic seizures, that occur in the first year of life in an otherwise normal infant and are later associated with myoclonus, atypical absences, and partial seizures. All seizure types are resistant to antiepileptic drugs. Developmental delay becomes apparent within the second year of life and is followed by definite cognitive impairment and personality disorders.”1 This description, which is much centered on epilepsy and cognitive impairment, predates the identification of SCN1A as the disease-causing gene2 and experimental work suggesting that haploinsufficiency causes reduced sodium currents in GABAergic inhibitory interneurons,3 and that the protein expression clusters predominantly in the axon initial segments of the nodes of Ranvier.4
Footnotes
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