Transient global amnesia

Amnesia globale transitoria

R. Galimi

UO di Neurologia, Azienda Ospedaliera della Valtellina e della Valchiavenna, Presidio Ospedaliero di Sondalo (SO)


To review the clinical aspects, new imaging findings and recent clinicoepidemiological data with regard to the phenotype, functional anatomy and putative cellular mechanisms of transient global amnesia (TGA). Despite several new hypotheses concerning the pathogenesis of TGA, there is still no consensus about its cause. Herein, the evidence in support of and against the main pathogenic hypotheses are critically evaluated.


Relevant literature published since the first reports of TGA published in 1956 is reviewed, with the aim of accurately describing the demographic and clinical features of TGA. A systematic review of the literature on the relationships between focal ischaemia, migraine, epileptic phenomena, venous flow abnormalities and TGA was performed by searching the literature for all relevant studies. References were identified through searches with the search terms “amnesia”, “transient global amnesia”, “TGA”, “hippocampus” and “CA1”. Only papers published in English were included.


Classical proposals about its possible aetiology (epilepsy, vascular disease and migraine) and other new theories (Leao’s spreading depression or influence of stress) have been assessed. While there is data in favour and against hypotheses of the aetiology of TGA, there is no current consensus which satisfactorily explains the nature of this type of amnesia. A number of recent neuroimaging studies suggests involvement of the mesial temporal area (amygdala and hippocampus) and/or thalamus leading to transient disruption of blood flow, and appearing as focal magnetic resonance (MR) hyperintensities showing restricted diffusion on diffusion-weighted MR imaging (DW-MRI).


TGA is defined as a selective deficit of memory that appears suddenly and lasts less than 24 hours. The present state of knowledge about memory deficits associated with TGA is still limited, and there are still several aspects that require clarification, particularly regarding recovery. Recent neuroimaging findings suggest that transient perturbation of hippocampal function is corrrelated with TGA, as focal lesions can be reliably detected in the CA1 field of the cornu ammonis with DW-MRI. Future research should focus on elucidating the pathophysiological correlates of the acute phase, particularly on deciphering which trigger induces the pathophysiological cascade that affects CA1 neurons.

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