Serial 7 T MRI demonstrates reversible hippocampal T2 abnormalities in transient global amnesia
Background Transient global amnesia (TGA) often shows tiny punctate hippocampal CA1 lesions on diffusion-weighted imaging (DWI). Whether these lesions represent truly transient structural alterations remains unsettled. Ultra–high-field 7-tesla (7 T) MRI increases spatial resolution and lesion conspicuity. However, the evolution of hippocampal T2 signal at 7 T from the acute phase through short-term follow-up has not been systematically examined. Objective To determine, using serial 7 T MRI, whether hippocampal T2-weighted imaging (T2WI) abnormalities visible in acute TGA are consistently detectable acutely and completely disappear by approximately 2 weeks. Methods Single-center consecutive case series of six patients with clinically defined TGA and DWI-confirmed CA1 lesions who underwent serial 7 T MRI, including acute imaging and follow-up at 14–18 days. The primary outcome was complete resolution of hippocampal T2 hyperintensity. Secondary outcomes were acute T2 detection rate, lesion distribution, and concordance with DWI. Results Six patients (4 men), median age 69 years (range 50–76), all fulfilled the diagnostic criteria of TGA and no neurological deficits. Acute 7 T MRI was performed at a median of 37 h after symptom onset. Acute phase: All 6/6 showed focal hippocampal CA1 hyperintensity on 7 T T2WI, colocalizing with DWI/ADC abnormalities. Follow-up (day 15–18): T2 hyperintensity resolved in 6/6 with no visible residual signal abnormality or structural atrophy. Follow-up 7 T DWI demonstrated complete disappearance of the previously identified diffusion abnormalities in all patients. Interpretation: Even at ultra-high field, hippocampal T2 abnormalities are fully reversible within approximately 2 weeks. Conclusion Serial 7 T MRI demonstrates that hippocampal T2WI lesions in TGA are consistently visible acutely and uniformly disappear by 2 weeks, providing high-field structural evidence that typical TGA is a transient phenomenon. These findings refine the temporal profile of hippocampal signal evolution and contribute to mechanistic understanding of CA1 vulnerability in TGA.