• Claudio Baracchini, Simone Tonello, Filippo Farina, Federica Viaro, Matteo Atzori, Enzo Ballotta, and Renzo Manara.
• Department of Neurological Sciences, University of Padua School of Medicine, Via Giustiniani, 5, 35128, Padova, Italy. claudiobaracchini@tin.it
• Stroke. 2012 Sep 1; 43 (9): 2289-92.

Background And PurposeTransient global amnesia (TGA) has been associated with an increased prevalence of internal jugular valve insufficiency and many patients report Valsalva-associated maneuvers before TGA onset. These findings have led to the assumption of hemodynamic alterations in intracranial veins inducing focal hippocampal ischemia. We investigated this hypothesis in patients with TGA and control subjects.MethodsSeventy-five patients with TGA and 75 age- and sex-matched healthy subjects were enrolled into a cross-sectional study. Extracranial and transcranial high-resolution venous echo-color-Doppler sonography was performed blindly in all patients and control subjects. Blood flow direction and velocities were recorded at the internal jugular veins, basal veins of Rosenthal, and vein of Galen, both at rest and during Valsalva-associated maneuvers.ResultsMean age of patients with TGA was 60.3±8.0 years (median, 60 years; range, 44-78 years); 44 (59%) were female (female/male ratio: 1.42). Internal jugular valve insufficiency (left, right, or bilateral) was found to be more frequent in patients with TGA than in control subjects: 53 (70.7%) versus 22 (29.3%; P<0.05). Blood flow velocities in the deep cerebral veins of patients with TGA did not differ from control subjects both at rest and during Valsalva-associated maneuvers. Intracranial venous reflux was neither observed in patients with TGA nor in control subjects despite unilateral or bilateral internal jugular valve insufficiency during prolonged and maximal Valsalva-associated maneuvers.ConclusionsThis study, although confirming the association between TGA and internal jugular valve insufficiency, challenges the hypothesis that cerebral venous congestion plays a significant role in the pathogenesis of TGA.

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