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PATHOGENESIS OF TRANSIENT GLOBAL AMNESIA BASED ON MRI FINDINGS-CASE SERIES
PATHOGENESIS OF TRANSIENT GLOBAL AMNESIA BASED ON MRI FINDINGS-CASE SERIES
Abstract
Background and Aims
The etiology, pathophysiological mechanisms, and anatomical correlates of transient global amnesia (TGA) remain obscure. Focal MRI-signal diffusion-weighted imaging (DWI) changes in the hippocampus are present in patients with TGA, but these lesions exact localization, long-term outcome, and pathophysiological nature remain unknown.
Methods
Our study is a single-center, retrospective study, including 34 patients (13 men and 21 women; mean age 66.6 ± 9 years; range, 54-82 years) diagnosed with TGA. Most of our patients underwent diffusion-weighted 1.5-T MRI within four days following the onset of TGA symptoms.
Results
Risk factors found in our TGA patients: dyslipidemia in 70.59% of cases, arterial hypertension in 58.82%, diabetes mellitus in 23.53%, coronary artery disease & atrial fibrillation in 8.82% each. Prior to the clinical event, 41.8% of the patients received antiaggregants and 2.9% anticoagulants. 11 patients reported a possible trigger event (e.g., Valsalva, head extension, sports activity, and emotional distress) before the amnestic episode. In most patients, symptoms resolved within 2 hours. DWI MRI showed hippocampal lesions in 16 patients (47.06%): left-sided in 11 patients (68.75%), right-sided in three patients (18.75%), and bilateral lesions in two patients (12.5%). MRI was positive in 70% of the cases in the first 48 hours from the event, but only in 16.7% of cases if performed after 96 hours.
Conclusions
Our study supports the TGA's ischemic background, mostly involving the dominant hemisphere hippocampus. Vascular risk factors are prevalent in this pathology, particularly hyperlipidemia and hypertension. MRI was much more frequently positive if performed early following the clinical event.