Abstract

See related article, pages 67–71. Transient global amnesia (TGA) was generally believed to have a psychogenic, epileptic, or thromboembolic etiology until the frequent comorbidity with migraine and the common accompanying symptoms (headache and dizziness) pointed toward cortical spreading depression as a pathogenic suspect.1,2 More recently, based on evidence that Valsalva-like activities may represent the precipitating factors in most TGA patients, cerebral venous congestion leading to venous ischemia was hypothesized as a possible pathophysiologic mechanism.3 Corroborating this hypothesis, the prevalence of internal jugular vein (IJV) valve incompetence, as assessed by ultrasound, was found to be more prevalent in patients with TGA than in controls.4–8 In all of these studies, IJV valve incompetence was detected in 97 of 131 patients (74%) and in 65 of 191 controls (34%). In this issue of Stroke, Cejas and coauthors9 confirmed these findings in a larger population, reporting IJV valve insufficiency in 113 patients with TGA (79.5%) and in 10 controls (25%). Apparently, this could solve …

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