Arjen Lindenholz

142 CHAPTER 6 Table 2. Associations between the presence of parenchymal changes and the intracranial vessel wall lesion burden. Outcome as present/absent Unadjusted relative risk (±95%CI) P-value Adjusted relative risk (±95%CI) P-value Infarcts Any anterior circulation infarct 1.05 (0.99-1.12) 0.086 1.05 (0.98-1.12) 0.151 Cortical infarcts 1.06 (0.98-1.15) 0.151 1.07 (0.98-1.17) 0.129 Infarcts often caused by SVD 1.23 (1.09-1.39) 0.001 1.18 (1.03-1.35) 0.017 Small subcortical infarcts NA NA NA Lacunes of presumed vascular origin 1.20 (1.04-1.40) 0.016 1.13 (0.95-1.34) 0.174 Deep grey matter infarcts 1.29 (1.04-1.60) 0.019 1.25 (0.98-1.60) 0.069 Cortical microinfarcts 1.14 (0.93-1.38) 0.212 1.07 (0.85-1.36) 0.565 White matter hyperintensities (Fazekas grade) Periventricular (0/1 vs. 2/3) 1.34 (1.16-1.55) < 0.001 1.21 (1.02-1.42) 0.026 Deep (0/1 vs. 2/3) 1.22 (1.05-1.41) 0.008 1.09 (0.89-1.33) 0.417 Table 2 . Included for analysis, n = 82. The unadjusted and adjusted (for age and sex) relative risks including their 95% confidence interval (CI) for the presence of cerebral parenchymal changes with the total number of anterior vessel wall lesions as included variable. A p-value < 0.05 was considered to indicate a statistically significant difference. A log-binomial regression model was used with a robust variance estimator. White matter hyperintensity Fazekas grade is described as: 0 = absence or single punctate white matter hyperintensity, 1 = ‘caps’ or pencil-thin lining or multiple punctate lesions, 2 = smooth ‘halo’ or beginning confluency of lesions, 3 = large confluent lesions or irregular hyperintensities extending into the deep white matter. 28 CMI; cortical microinfarct, NA; not applicable (only 1 count), SVD; small vessel disease.