Transient epileptic amnesia is significantly associated with discrete CA1-located hippocampal calcifications but not with atrophic changes on brain imaging.

Background: The exact etiology of transient epileptic amnesia (TEA) is currently unknown. In older individuals, common neurodegenerative dementias and small-vessel diseases (SVDs) could be major contributors. We examined these hypotheses on the basis of imaging analysis.

Methods: In total, 36 TEA patients were compared with 25 healthy controls for (1) cortical atrophic changes (in the mesial temporal, frontal, anterior temporal, and parietal regions) using four established MRI-based visual rating scales, and for (2) SVD evidence using two MRI-based visual rating scales (Fazekas and MARS scores). In 24 TEAs cases, there were also brain CT scans available that were compared with 57 controls for the presence of hippocampal calcifications (HCs).

Results: We did not find significant differences in cortical atrophy between TEAs and controls, nor did we observe a different SVD brain load on MRI. However, TEAs were significantly associated (p < 0.01) with uni- or bilateral CA1-located HCs in half of the patients compared with the controls (less than 20 %).

Conclusions: This study argues in favor of a hippocampal-restricted SVD (as indicated by HCs) as one of the major etiologies of TEA, while neurodegenerative dementias are probably minor causes. It furthermore highlights the pivotal role of the CA1 hippocampal subfield in the pathophysiology of this syndrome.