Coexisting cortical atrophy plays a crucial role in cognitive impairment in moderate to severe cerebral small vessel disease patients.

Whether white matter lesion (WML) is associated with vascular cognitive impairment in cerebral small vessel disease (CSVD) remains controversial; some severe CSVD patients retain normal cognitive function, and cortical thinning associated with WMLs has also been recently reported. The contribution of cortical atrophy to vascular cognitive impairment in severe CSVD and whether WML affects cortical atrophy remain unknown. From November 2012 to January 2015, 50- to 80-year-old patients with moderate to severe WMLs or more than four lacunar infarctions and cognitive complaints, excluding those with large vascular diseases diagnosed by transcranial cerebral Doppler, were recruited. The patients were divided into CSVD groups with or without vascular cognitive impairment-no dementia (VCIND) according to scores on neuropsychological tests that evaluated five cognitive domains. Based on these results, 16 patients were included in the CSVD with VCIND group, and 12 were included in the CSVD without VCIND group. T1, T2, 3D-MPRAGE, and diffusion tensor imaging were performed, and gray matter volume and fractional anisotropy (FA) values were compared between the two groups. Gray matter volume, especially in the frontal cortex, bilateral calcarine sulcus, and fusiform gyrus, was considerably lower in the CSVD with VCIND patients, with 24,619 fewer voxels. In addition, the FA values of 1,583 voxels were lower in the CSVD patients with VCIND than in those without. In conclusion, cortical atrophy is associated with cognitive impairment in moderate to severe WML or lacunar infarction patients, suggesting that cortical atrophy might be secondary to white matter damage in vascular cognitive impairment caused by CSVD.