No abstract

No abstract

Since the large case series of Fisher and Adams, 1 the clinical characteristics of transient global amnesia (TGA) have been well described, including an acute amnesic episode with anterograde amnesia and no other cognitive impairment, no disturbances of consciousness, reiteration of questions, and a high rate of trigger factors (ie, pain, medical procedures, emotional stress, sexual activity). Although an exhaustive definition of the etiology and pathophysiology behind the disorder is missing, the transient dysfunction of the bilateral hippocampi (and in particular of CA1 neurons, particular susceptible to metabolic stress) represents the neuroanatomical basis for this clinical picture, and different hypothesis have been postulated on the pathological mechanisms that lead to this clinical symptomatology, like hypoxic-ischemic events, migraine-related mechanisms, venous flow abnormalities, psychological mechanisms, and epilepsy-related activity. 2

No abstract