Aetiology of transient global amnesia.
Publication/Presentation Date
8-1-1998
Abstract
The pathophysiology of transient global amnesia (TGA) has been obscure since the definition of this syndrome more than 30 years ago. Current hypotheses include migraine, seizure, or transient cerebral arterial ischaemia. However, none of these potential mechanisms explain both the absence of other neurological signs or symptoms during TGA, and its frequent precipitating activities: many of which would be expected to result in marked increases in venous return from the arms to the superior vena cava. Patients with TGA also commonly have a Valsalva manoeuvre at the onset of attacks. I suggest that a Valsalva manoeuvre, blocking venous return through the superior vena cava, may allow brief retrograde transmission of high venous pressure from the arms to the cerebral venous system, resulting in venous ischaemia to the diencephalon or mesial temporal lobes and to TGA.
Volume
352
Issue
9125
First Page
397
Last Page
399
ISSN
0140-6736
Published In/Presented At
Lewis S. L. (1998). Aetiology of transient global amnesia. Lancet (London, England), 352(9125), 397–399. https://doi.org/10.1016/S0140-6736(98)01442-1
Disciplines
Medicine and Health Sciences
PubMedID
9717945
Department(s)
Department of Medicine
Document Type
Article