Transient global amnesia

Alfredo Ardila PhD (Dr. Ardila of Florida International University has no relevant financial relationships to disclose.)
Martin R Farlow MD, editor. (Dr. Farlow of Indiana University received research grant support from Accera, Biogen, Eisai,  Eli Lilly, Genentech, Roche, Lundbeck, Chase Pharmaceuticals and Boehringer Ingelheim; honorariums from Eisai, Forest Laboratories, Pfizer, Eli Lilly and Company and Novartis for speaking engagements; and fees from Accera,  Alltech, Avanir,   Biogen, Eisai Med Res, Inc., Eli Lilly and Company, FORUM Pharmaceuticals, Genentech, Inc., Grifols, Helicon, INC Research, Lundbeck, Medavante, Medivation, Merck,  Neurotrope Biosciences, Novartis, Pfizer, Prana, QR Pharm., Riovant Sciences Inc., Roche, Sanofi-Aventis, Schering-Plough, Toyama Pharm and UCB Pharma for consultancy. His spouse was employed by Eli Lilly.)
Originally released September 18, 1995; last updated May 22, 2015; expires May 27, 2018

Overview

Transient global amnesia represents an episode of acute onset of transient global anterograde amnesia, with a variable degree of impairment of retrograde memory, which is not associated with any other major neurologic signs or symptoms. Resolution is gradual, with subjective recovery occurring in two thirds of patients within 2 to 12 hours and, in almost all, within 24 hours. In this article, the author explains that the etiology is still controversial and could be explained by an ischemic event due to arterial thromboembolic ischemia in a subgroup of patients with increased vascular risk factors. PET studies usually show hypometabolism in the hippocampi and mesial temporal lobes. An acute effect on hippocampal cornu ammonis neurons has been proposed as the functional correlate of amnesia, reflecting a transient disruption in the hippocampus memory circuits. It has been suggested that not only is memory affected, but executive functions are diminished as well.

Key points

 

• Transient global amnesia is characterized by acute onset of transient global anterograde amnesia that is not associated with any other major neurologic signs or symptoms.

 

• Amnesia resolves gradually, usually within about 2 to 12 hours.

 

• Recurrence is low, about 2.5% to 5% per year.

 

• In a significant percentage of cases, a precipitant factor (physical or psychological) can be identified.

Historical note and terminology

Fisher and Adams coined the term "transient global amnesia," but this syndrome was first described in 1956 by Bender as the "syndrome of [an] isolated episode of confusion with amnesia" and by Guyotat and Courjon as "les ictus amnesiques" (Bender 1956; Guyotat and Courjon 1956; Fisher and Adams 1958). Probably before 1950 it was interpreted either as a psychogenic amnesia or as an amnesia occurring after an emotional shock (Gil et al 2010). The essential features are an episode of acute onset of transient global anterograde amnesia, with a variable degree of impairment of retrograde memory, which is not associated with any other major neurologic signs or symptoms (Bender 1956). Since this syndrome's recognition, controversy has surrounded its pathogenesis, treatment, and prognosis.

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