Abstract

Transient global amnesia (TGA) is a rare clinical diagnosis characterized by the sudden onset of anterograde with repetitive questioning, and lesser degree of retrograde amnesia, lasting up to 24 hours, without compromise of other neurologic functions. Several pathophysiologic mechanisms have been proposed, but none of them has been proved to explain all cases of TGA consistently. We reviewed data of TGA patients who visited Chungnam National University Hospital from 2010, January to 2017, January. A total of 324 patients under the impression of TGA, 212 patients were met TGA criteria and performed brain magnetic resonance imaging and neuropsychological tests. We compared the clinical and neuropsychological characteristics of TGA patients according to presence or absence of the hippocampal lesion on diffuse weighted images (DWI+ vs. DWI-). Ninety two patients (43.3%) with TGA had the visible hippocampal lesions on the DWIs and the most number of lesions (63.8%) were found in 12 to 48 hours after the onset of TGA. One hundred thirty five patients with TGA (64.8%) had various precipitating factors before the onset of TGA symptoms. The most distinguishing precipitating factor between the DWI+ and DWI- groups was emotional events such as crying and angry. The incidence of physical activities as a precipitating factor for TGA occurrence was increased in the spring and fall. None of neuroimaging features such as numbers of lacunae, degree of temporal lobe atrophy, or white matter hyperintensity were different, depending on the hippocampal lesions. The patients with right hippocampal lesion showed lower function of non-verbal short-term memory on RCFT but no difference found on the verbal memory function by hippocampal lesion location. Although hippocampal lesion is not always found in patients with TGA, it could give some explanations for understanding pathophysiologic mechanisms of TGA. Uncontrollable emotion or unusual strong physical activities may be associated with central venous congestion due to sudden increase of central pressure, triggering TGA onset.

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