Maximum isotope accumulation in the retrosplenial cortex during amnesia attack and its temporal change suggest cortical spreading depression as a pathophysiology of patients with transient global amnesia

Abstract

AbstractTransient global amnesia (TGA) is a clinical syndrome that is characterized by the sudden onset of anterograde amnesia and a less prominent impairment in retrograde memory lasting up to 24 h. Although several etiologies have been proposed, including migraine, epilepsy, ischemia, venous congestion, and glutamate toxicity, none sufficiently explain the disorder in its entirety. We retrospectively investigated images obtained using single‐photon emission computed tomography (SPECT), performed with 99mtechnetium hexamethylpropyleneamine oxime, from 11 patients with TGA divided into the following groups based on the timing of SPECT: during TGA (n = 2, Group 1), at the start of the attenuation of memory impairments (n = 2, Group 2), and after TGA (n = 7, Group 3). Regional isotope accumulation was examined using a three‐dimensional stereotactic surface projection (3D‐SSP) analysis. After calculating the mathematical product of the mean severity and extent ratio, unique comparable bar graphs were prepared with respect to Brodmann's areas (B). Increases in isotope accumulation were the largest in the retrosplenial cortex (B29, B30), posterior cingulate cortex (B23, B31), and precuneus (B7) in Groups 1 and 2, whereas decreases were noted in the same regions in Group 3. This is the first study to identify cerebral sites and describe changes consistent with the completion of amnesia as a symptom using an image analysis, such as a 3D‐SSP analysis. We consider cortical spreading depression (CSD) to be the etiology of TGA based on maximum isotope accumulation in the above sites and a literature review on CSD.