Hippocampal modifications in transient global amnesia.

Abstract Transient global amnesia (TGA) is an acute and transient syndrome with a remarkably stereotypical set of signs and symptoms. It is characterized by the abrupt onset (no forewarning) of massive episodic memory impairment, both anterograde and retrograde. Ever since it was first described, TGA has fascinated neurologists and other memory experts, and in recent years, there has been a surge of neuroimaging studies seeking to pin down the brain dysfunction responsible for it. Several pathophysiological hypotheses have been put forward, including the short-lived suggestion of an epileptic mechanism. All the available data indicate that the brain modifications are reversible, and that the mechanism behind TGA is of a functional nature. However, while diffusion-weighted imaging studies have clearly identified the hippocampus and, more specifically, the CA1 area, as the locus of brain modifications associated with TGA, researchers have yet to determine whether the origin of the mechanism is vascular or neurochemical. Spectroscopy may provide a means of settling this issue once and for all.