Background and Purpose— Aneurysmal subarachnoid hemorrhage (aSAH) may have detrimental effects on white matter microstructure, which may in turn explain the cognitive impairments that occur often after aSAH. We investigated (1) whether the white matter microstructure is altered in patients with aSAH compared with patients with an unruptured intracranial aneurysm and (2) whether these abnormalities are associated with cognitive impairment 3 months after ictus. Methods— Forty-nine patients with aSAH and 22 patients with an unruptured intracranial aneurysm underwent 3T brain magnetic resonance imaging, including a high-resolution diffusion tensor imaging sequence. Patients with aSAH were scanned 2 weeks and 6 months after ictus. Microstructural white matter alterations were quantified by the fractional anisotropy and mean diffusivity (MD). Cognition was evaluated 3 months after ictus. Results— Patients with aSAH had higher white matter MD 2 weeks after ictus than patients with an unruptured intracranial aneurysm (mean difference±SEM, 0.3±0.01×10 −3 mm2/s; P ≤0.01), reflecting an abnormal microstructure. After 6 months, the MD had returned to the level of the unruptured intracranial aneurysm group. No between-group differences in fractional anisotropy were found (−0.01±0.01; P =0.16). Higher MD at 2 weeks was associated with cognitive impairment after 3 months (odds ratio per SD increase in MD, 2.6; 95% CI, 1.1–6.7). The association between MD and cognitive impairment was independent of conventional imaging markers of aSAH-related brain injury (ie, cerebral infarction, hydrocephalus, total amount of subarachnoid blood, total brain volume, or white matter hyperintensity severity). Conclusions— Patients with aSAH have temporary white matter abnormalities in the subacute phase that are associated with cognitive impairment at 3 months after ictus.

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Objective:To investigate the association of silent vascular lesions, imaging negative ischemia, and symptomatic cerebrovascular disease with long-term progression of brain atrophy and cerebrovascular lesions in patients with arterial disease.Methods:Within the SMART-MR study, stroke status of participants at baseline was classified as no cerebrovascular disease (reference group, n=829), symptomatic cerebrovascular disease (n=206), silent vascular lesion (n=157), and imaging negative ischemia (n=90) based upon clinical and MRI findings. Using linear mixed models, changes in brain and white matter hyperintensity (WMH) volumes at baseline and during 12 years of follow-up were studied in stroke classifications. Relative risks were estimated for new infarcts during follow-up associated with stroke classifications. Analyses were adjusted for age, sex, cardiovascular risk factors, and medications.Results:Symptomatic cerebrovascular disease associated with 0.35 SDs (95%CI 0.24-0.47) smaller brain volume and 0.61 SDs (95%CI 0.48-0.74) larger WMH volume at baseline, and increased risk for new infarcts during follow-up (risk ratio (RR) 2.89; 95%CI 2.00-4.16). Silent vascular lesions associated with 0.15 SDs (95%CI 0.01-0.88) smaller brain volume, 0.02 SDs (95%CI 0.01-0.03) steeper brain atrophy slope, and 0.48 SDs (95%CI 0.32-0.64) larger WMH volume at baseline, in addition to increased risk for lacunes (RR 2.08; 95%CI 1.48-2.94). Individuals with imaging negative ischemia had increased risk for cortical infarcts (RR=2.88; 95%CI 2.17-3.82).Conclusions:Patients with symptomatic cerebrovascular disease, silent vascular lesions, or imaging negative ischemia have different course of brain volume loss and cerebrovascular lesions development. These findings may have implications for future stroke risk and dementia and need further investigation.

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