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Abstract #3161

Transient Global Amnesia: Multi-timepoint 3T and 7T MRI Analysis of Acute Hippocampal Lesions - A One-year Longitudinal Prospective Study

Barbara Daria Wichtmann1,2, Zeynep Bendella1, Mónica Ferreira2, Martin Reuter2,3, Christine Kindler2,4, Theodor Rüber2,5, Alexander Radbruch1,2, Gabor C. Petzold2,6, Daniel Paech1,3, Tony Stöcker2, Felix Jürgen Bode2,6, and Niklas Michael von Danwitz2,6
1Department of Neuroradiology, University Hospital Bonn, Bonn, Germany, 2German Center for Neurodegenerative Diseases, Bonn, Germany, 3Department of Radiology, Mass General Brigham, Boston, MA, United States, 4Department of Neurology, University Hospital Bonn, Bonn, Germany, 5Department of Epileptology, University Hospital Bonn, Bonn, Germany, 6Department of Vascular Neurology, Center of Neurology, University Hospital Bonn, Bonn, Germany

Synopsis

Keywords: Other Neurodegeneration, Neuro, High-Field MRI, Transient Global Amnesia

Motivation: Transient global amnesia (TGA) presents with temporary DWI-visible hippocampal lesions. The long-term implications of these lesions remain unclear, particularly whether they cause permanent structural changes.

Goal(s): To evaluate whether acute TGA-associated hippocampal lesions lead to permanent structural changes detectable with state-of-the-art neuroimaging.

Approach: 18TGA patients underwent same-day comparative 3T and 7T MRI scanning at three timepoints over one year (24-72h, 1 month, 12 months post-event), utilizing high-resolution morphological and diffusion-weighted imaging.

Results: Initial DWI-hyperintense lesions were detected in 16/18 patients, but no residual signal changes or structural abnormalities were observed at either field strength during follow-up examinations, suggesting complete resolution without permanent damage.

Impact: Leveraging ultra-high field MRI, this study provides evidence for clinicians and patients that acute hippocampal lesions in TGA do not result in chronic structural changes. The comprehensive multi-timepoint imaging protocol establishes a methodological framework for future investigations into TGA pathophysiology.

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