Abstract 204: Regional Hypoperfusion is Associated with Cortical Thinning in Asymptomatic Carotid Artery Disease

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Objective: Cortical thinning has been reported in patients with cerebrovascular disease and degenerative dementia, but the direct impact of regional hypoperfusion on cortical pathology has been difficult to establish. We examined the association between regional cerebral blood flow (rCBF) and regional cortical thickness (rCT) in a cohort of patients with unilateral high-grade internal carotid artery (ICA) disease without history of stroke.

Methods: Twenty-seven patients age 73±10yrs, 11F with unilateral ICA stenosis ≥80% or occlusion but no stroke underwent MRI, including high resolution T1 (MPRAGE) and tissue specific pseudocontinuous arterial spin labeling (ts-pCASL) to assess cortical thickness and gray matter resting CBF. Cortical thickness was measured in each hemisphere in the primary motor cortex (M1--Brodmann Area 4) by a blinded investigator using Freesurfer software (http://surfer.nmr.mgh.harvard.edu/), and in visual cortex (V1, Brodmann area 17) as a control for nonspecific effects in the posterior circulation. Paired t-tests were used to assess hemispheral asymmetry for rCBF and for rCT in M1 on the occluded vs unoccluded side. Linear regression was used to predict the effect of rCBF on rCT in M1 on the occluded side.

Results: Cortex was 0.08mm thinner on the side of ICA occlusion in M1 (95%CI=0.04-0.11, p=0.0003). There was no rCT asymmetry in V1 (p=.276). rCBF was 9.3 ml/100gm*min-1 lower in M1 of the occluded hemisphere (95%CI=5.1-13.5, p<.0001). Cortical blood flow in M1 was a significant predictor of cortical thickness in M1 on the side of the occluded ICA (adj R2=.128, p=.038).

Conclusion: Cortical thinning occurred in M1 on the side of carotid occlusion in the absence of stroke, and correlated with lower rCBF. Brodmann area 4 was chosen to represent the distal field of the carotid artery. Our finding demonstrates an important effect of chronically reduced blood flow on brain pathology, and suggests that a broader definition of “symptomatic” carotid artery disease may be needed.

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