Visuospatial dysfunction is associated with posterior distribution of white matter damage in non-demented cerebral amyloid angiopathy.

Abstract

Cerebral amyloid angiopathy (CAA) is a well-recognized contributor to cognitive decline in the elderly. The posterior cortical predilection of CAA pathology would cause visuospatial dysfunction, which is still underexplored. We aimed to investigate whether the visuospatial dysfunction in CAA is associated with the posterior distribution of small vessel disease (SVD) imaging markers. We recruited 60 non-demented CAA cases from a Chinese prospective cohort and 30 cases with non-CAA SVD as controls. We used the Visual Object and Space Perception (VOSP) battery to evaluate visuospatial abilities, and multivariable regression models to assess their associations with SVD imaging markers. There was visuospatial dysfunction, especially visual object perception impairment, in CAA compared to controls (Z-score of VOSP: -0.11±0.66 vs. 0.22±0.54, p=0.023). The VOSP score in CAA was independently related to the fronto-occipital gradient of white matter hyperintensity volumes (coefficient = 0.03, 95% confidence interval [CI] = 0.003-0.05, p=0.030) and mean fractional anisotropy values on diffusion tensor imaging (coefficient = 4.72, 95% CI = 0.97-8.48, p=0.015), but not the severity of global SVD imaging markers or the gradient of lobar cerebral microbleeds with adjustments for age and global cognition score. This finding suggests that the damage of posterior white matter rather than global disease severity may be a major contributor to visuospatial dysfunction in CAA.