The stolen memory: a case of transient global amnesia

Transient global amnesia (TGA) is a clinical syndrome characterized by the abrupt onset of anterograde amnesia without other neurological deficits. The ability to lay down new memories recovers gradually, in minutes to hours, with an average of 4 to 6 hours (1), leaving only a dense amnesic gap for the duration of the episode. Transient global amnesia is likely to be due to an acute impairment of the hippocampus (2) but the etiopathogenesis is debated. Ischemia, epileptiform activity, and psychological factors may contribute to TGA. The strongest argument in favor of the ischemic etiology is the presence of a small area of restricted diffusion-weighted imaging (DWI) signal in the hippocampus, which appears in the magnetic resonance imaging (MRI) scan data of most patients with TGA (1 and 3). Diffusion-weighted imaging hypersignal indicates cytotoxic edema; therefore, it is considered the hallmark of brain ischemia (4). Nevertheless, an analysis of risk factors leads to the conclusion that the cerebrovascular etiology is unlikely, even in individuals with DWI lesions (5). An epileptic origin has been considered (6) but it appears unlikely, because of the long duration and the low recurrence rate of the episodes and the absence of convulsions, impairment of consciousness, or other signs of cortical dysfunction (7). Finally, psychogenic origin has been proposed: TGA commonly occurs in periods of stress, overwork, and emotional arousal (7) or after stressful events, pain, or sexual intercourse. As follows, we describe a patient with TGA in whom the clinical, neuroimaging, and electroencephalogram (EEG) findings demonstrate a transient, reversible, dysfunction of the hippocampus.