Transient Global Amnesia

Author:

Enzinger Christian1,Thimary Felix1,Kapeller Peter1,Ropele Stefan1,Schmidt Reinhold1,Ebner Franz1,Fazekas Franz1

Affiliation:

1. From the Department of Neurology (C.E., S.R., R.S., F.F.) and the Section of Neuroradiology (C.E., F.T., F.E.), Department of Radiology, Medical University of Graz, Graz; and the Department of Neurology (P.K.), Villach, Austria.

Abstract

Background and Purpose— A hypoxic-ischemic origin of transient global amnesia (TGA) has been suggested on the basis of the observation of infarctlike diffusion-weighted imaging (DWI) abnormalities in some affected individuals. We tested this hypothesis by comparing vascular risk factors, magnetic resonance imaging (MRI) markers of cerebral small-vessel disease, and other evidence of a cerebrovascular disorder between TGA patients with (DWI+) and without (DWI−) DWI lesions and normal community-based controls. Methods— We retrospectively identified 86 patients hospitalized for TGA (mean±SD age, 65.9±10.9 years; 62% female). Brain MRI at 1.5 T was assessed for DWI lesions exhibiting restricted diffusion (ie, DWI+), white-matter hyperintensities, lacunes, and chronic infarcts (median time lag to clinical onset, 66.6±54.6 hours). Vascular risk factors and findings from duplex sonography, ECG, and echocardiography were recorded. A 1:2 age- and sex-matched sample of 172 elderly subjects (mean±SD age, 65.6±9.3 years; 62% female) free of neuropsychiatric disease served for comparison. Results— DWI lesions were observed in 10 patients with TGA (11.5%; mean±SD age, 68.3±5.4 years; 8 women). They were all small and located in the mesiotemporal region (9 left hemisphere, 5 right hemisphere). The vascular risk profile of TGA patients and concomitant changes on brain MRI were comparable with those of healthy controls and did not show significant differences between DWI+ and DWI− subjects. A comprehensive diagnostic workup also provided no evidence for a higher rate of cerebrovascular disorder-related abnormalities in either the total group of TGA patients or TGA DWI+ patients. Conclusions— These findings do not support a cerebrovascular etiology of TGA, even in those individuals showing acute DWI lesions. Other pathophysiologic mechanisms need to be explored.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Advanced and Specialised Nursing,Cardiology and Cardiovascular Medicine,Clinical Neurology

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