Incident subcortical infarcts induce focal thinning in connected cortical regions.

Objective: Brain atrophy is common in subcortical ischemic vascular disease, but the underlying mechanisms are poorly understood. We set out to examine the effects of incident subcortical infarcts on cortical morphology. Methods: A total of 276 subjects with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, an inherited small vessel disease, were enrolled in a prospective study. Incident subcortical infarcts were identified on follow-up magnetic resonance scans after 18, 36, and 54 months using difference images. Probabilistic fiber tracking and cortical thickness measurements were applied to study the longitudinal relationship between incident infarcts and connected cortical areas. Cortical thickness was assessed before and after infarction using FreeSurfer software. Focal cortical thinning was defined as change of cortical thickness in the connected region of interest exceeding the global change of cortical thickness. Results: Nine subjects had a single incident infarct during the follow-up and were suitable for analysis. There was a strong correlation between the probability of connectivity and mean focal cortical thinning (p = 0.0039). In all subjects, there was focal cortical thinning in cortical regions with high probability of connectivity with the incident infarct. This pattern was not observed when using control tractography seeds. Conclusions: Our findings provide in vivo evidence for secondary cortical neurodegeneration after subcortical ischemia as a mechanism for brain atrophy in cerebrovascular disease. Neurology (R) 2012;79:2025-2028