Neue Aspekte zur Pathophysiologie der transienten globalen Amnesie

Zusammenfassung

Typischer Befund der transienten globalen Amnesie (TGA) sind umschriebene hippocampale Läsionen, die am besten mit 24 Stunden Latenz zur Episode nachgewiesen werden. In der Erforschung der Ursachen und möglicher Auslöser der TGA wurden in den vergangenen Jahren unterschiedliche pathophysiologische Ansätze verfolgt. So konnte durch größere Studien, die weder eine erhöhte Schlaganfallinzidenz nach TGA, noch eine entsprechende Konstellation der Risikofaktoren bei TGA-Patienten fanden, die TGA gegenüber der arteriellen Ischämie abgegrenzt werden. Ein wichtiges Thema blieb der Einfluss zerebralvenöser Auffälligkeiten: Obwohl mehrere Studien eine hohe Prävalenz einer Jugularvenenklappeninsuffizienz bei TGA-Patienten berichteten, wurde eine hämodynamische Relevanz dieses Befundes, die eine Rolle bei der Entstehung der TGA spielen könnte, nicht gefunden. Neuere Hypothesen postulieren eine Glutamat-vermittelte Hyperexzitabilität mit zytotoxischer Schädigung des Hippocampus, insbesondere der CA1-Neurone. Diese fokussieren auf die mögliche Rolle von Stress und seine gedächtnisrelevanten Auswirkungen. Weiterhin konnten aus funktionellen bildgebenden Studien neue Erkenntnisse über die im Rahmen der TGA beeinträchtigten zerebralen – mit dem Hippocampus verbundenen – Netzwerke gewonnen werden. Die vorliegende Übersichtsarbeit greift wesentliche Aspekte der wissenschaftlichen Veröffentlichungen der letzten Jahre zur TGA auf, die zum Verständnis der Pathophysiologie der TGA beitragen sollen, und geht insbesondere auf die Aspekte einer möglichen stressvermittelten Ätiologie ein.

Abstract

Small hippocampal lesions are a characteristic finding in transient global amnesia (TGA) that become detectable approximately 24 hours after the clinical episode. In research into the causes and possible triggers of TGA different pathophysiological approaches have been followed in recent years. Several large trials have found no evidence for a higher incidence of stroke or vascular risk factors in TGA patients, thereby further distinguishing TGA from arterial ischemic disease. The relevance of cerebral venous abnormalities remained an important topic: Even though several studies have reported a higher prevalence of jugular venous reflux in TGA patients, hemodynamic alterations as a possible pathophysiological mechanism of TGA could not be demonstrated. Newer hypotheses have postulated a glutamate-mediated hyperexcitability with consecutive cytotoxic damage of the hippocampus and especially of the hippocampal CA1 neurons. These concepts focus on the possible role of stress and its effects on memory. New results have been obtained from functional imaging studies with respect to the memory networks affected in TGA. In this review, we describe new insights into the pathophysiology of TGA from recent scientific publications highlighting the possible role of stress-mediated processes for the development of TGA.

Schlüsselwörter

Amnesie - Hippocampus - Stress - MRT

Keywords

amnesia - hippocampus - stress - MRI

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