Is there really evidence for neurodegeneration in Dravet syndrome? Commentary on the publication by Selvarajah et al

Our understanding of the pathophysiological complexity of Dravet syndrome (DS) is becoming increasingly intricate and nuanced. Non-canonical roles of the most commonly implicated gene, SCN1A, encoding the alpha-1 subunit of the sodium channel, are emerging. SCN1A diseases are complex conditions, with morbidities beyond seizures rightly receiving more attention. Sophisticated, targeted therapies are being developed based on improved understanding of the underlying neurobiology. It is therefore important that the pathophysiology and natural history of DS are rigorously explored. This can be challenging when longitudinal data are sparse, and when previous treatments and events complicate cross-sectional data.