[Transient global amnesia - benign memory blackout].

Dtsch Med Wochenschr

Campus Klinikum Nürnberg, Paracelsus Medizinische Universität, Nürnberg.

Published: June 2024

AI Article Synopsis

  • - Transient global amnesia (TGA) is a temporary condition primarily affecting older adults, causing short-term memory loss for new information, lasting 30 seconds to 3 minutes, while other cognitive functions remain intact.
  • - Recent data suggests TGA occurs more frequently than previously thought, with about 15 cases per 100,000 people annually, and episodes typically resolve within 24 hours, but 10% may experience future episodes.
  • - MRI scans often reveal small lesions in the hippocampus in TGA patients, but the precise causes and mechanisms are still unclear; potential triggers include physical exertion and anxiety, and reassurance for concerned relatives is part of managing TGA.

Article Abstract

Transient global amnesia (TGA) is a typical clinical syndrome characterized by acute, predominantly anterograde amnesia. New epidemiological data assume a significantly higher annual incidence than previously assumed, namely around 15 cases per 100,000 people. Those affected, usually over the age of 50, cannot remember new memory content for longer than 30-180 seconds and therefore ask repetitive questions about current events. All other cognitive functions are unimpaired, and everything previously learnt, e.g. driving or cooking, can be carried out. The episodes are self-limiting and by definition subside within 24 hours. At least 10% of those affected will experience 1-5 recurrences in the future. The punctate lesions in the hippocampus, which are found on MRI in at least 50% of patients after 24-72 hours, are distributed 2/3 unilaterally and 1/3 bilaterally. Using 7 Tesla MRI the frequency of detected lesions increases to 90% compared to 50% with 1.5 or 3 Tesla. Beyond the punctiform hippocampal lesions, other memory-related network disorders, including the default network, are also suggested to be involved in the pathomechanism of TGA. TGA etiology and pathophysiology are not known in detail. Vascular, migraine-like, epilepsy-like, and psychogenic mechanisms are discussed. Triggers of the episodes are often physical exertion with a Valsalva character. Management is aimed at identifying the syndrome based on the typical clinical presentation and ruling out possible differential diagnoses with similar symptoms. During the TGA, the usually anxious relatives should be reassured of the benign and inconsequential nature of the episode.

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Source
http://dx.doi.org/10.1055/a-2190-5900DOI Listing

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