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Cervical artery dissection (CeAD), a common cause of ischemic stroke in young and middle-aged adults, accounts for ∼15% of all stroke in patients <50 years old.1 Etiologies, including motor vehicle whiplash and other mechanical traumas, are readily identified and widely publicized. Although the pathogenesis of spontaneous CeAD remains uncertain, patient-specific characteristics may increase the risk of such events. Hypertension, migraine, and recent infection may increase risk, whereas hypercholesterolemia and obesity may protect against spontaneous CeAD.2–5 The identification of underlying genetic etiologies lends credence to the notion that CeAD is in fact a multifaceted disease.6 Evaluating protein expression profiles and related biological pathways of connective tissue disorders for less penetrant genetic variations and epigenetic drivers represents an area of active research.
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Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial
See page 724
- © 2018 American Academy of Neurology
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