Transient ischemic attack results in delayed brain atrophy and cognitive decline

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Abstract

Background and Purpose-Transient ischemic attack (TIA) initiates an ischemic cascade without resulting in frank infarction and, as such, represents a novel model to study the effects of this ischemic cascade and secondary neurodegeneration in humans. Methods-Patients with suspected TIA underwent acute brain perfusion imaging, and those with acute ischemia were enrolled into a prospective observational study. We collected baseline and 90-day magnetic resonance imaging, including MP-RAGE (high-resolution T1 sequence) and cognitive assessment with the Montreal Cognitive Assessment. Brain morphometry and within patient statistical analysis were performed to identify changes between baseline and 90-day imaging and clinical assessments. Results-Fifty patients with TIA with acute perfusion lesions were studied. All patients experienced a decrease in global cortical gray matter (P=0.005). Patients with anterior circulation TIA (n=31) also had a significant reduction in the volume of the pons (P<0.001), ipsilesional parietal lobe (P<0.001), occipital lobe (P=0.002), frontal lobe (P<0.001), temporal lobe (P=0.003), and thalamus (P=0.016). Patients with an anterior perfusion lesion on acute imaging also had a significant decrease in Montreal Cognitive Assessment between baseline and day 90 (P=0.027), which may be related to the volume of thalamic atrophy (R2=0.28; P=0.009). Conclusions-In a prospective observational study, patients with TIA confirmed by acute perfusion imaging experienced a significant reduction in global gray matter and focal structural atrophy related to the area of acute ischemia. The atrophy also resulted in a proportional decreased cognitive performance on the Montreal Cognitive Assessment. Further studies are required to identify the mechanisms of this atrophy.

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Bivard, A., Lillicrap, T., Maréchal, B., Garcia-Esperon, C., Holliday, E., Krishnamurthy, V., … Parsons, M. (2018). Transient ischemic attack results in delayed brain atrophy and cognitive decline. Stroke, 49(2), 384–390. https://doi.org/10.1161/STROKEAHA.117.019276

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