XXXX correlate with cortical thinning in @entity15 .

@entity1 @entity121 @entity75 @entity62 @entity15 @entity922
OBJECTIVE: It has been suggested recently that cortical pathology in @entity15 ( @entity15 ) may, at least partly, be caused by factors in cerebrospinal fluid (CSF). We thus hypothesized that @entity15 -related tissue changes in compartments close to the CSF, such as @entity75 , might correlate with cortical pathology. METHODS: We investigated a cohort of 160 @entity1 , comprising 91 with a @entity922 ( @entity922 ) and 69 with relapsing-remitting @entity15 (RRMS; mean age: @entity922 : 31.4    9.0; RRMS: 33.0    8.7 years; mean disease duration: @entity922 : 7.2    15 months; RRMS: 8.0    6.5 years, Expanded Disability Status Scale (median, min-max): @entity922 : 1, 0-3.5; RRMS: 1.25, 0-4) with 3.0T magnetic resonance imaging. @entity15 lesions were segmented semiautomatically on fluid-attenuated inversion recovery images. To quantify periventricular lesion load (PV-LL), we generated ventricle masks and dilated them by a voxel factor of 3. Lesions within the dilated ventricle margin were classified as periventricular. Cortical thinning was assessed by @entity121 ( @entity121 ) and compared to data from 58 healthy controls (HCs; mean age: 29.1    7.4 years). RESULTS: Compared to HC, @entity922 and (even more so) RRMS @entity1 demonstrated significantly reduced @entity121 . Even after controlling for ventricular volume and total lesion load, increased periventricular lesion occupancy (percentage of PV-LL) significantly correlated with decreased @entity121 in RRMS (r = -0.295; p = 0.015), but not in @entity922 (r = 0.032; p = 0.768) @entity1 . INTERPRETATION: The correlation between increased periventricular lesion burden and decreased @entity121 indicative of subpial cortical pathology supports the concept that common CSF-mediated factors might play a role in the accumulation of @entity62 in @entity15 .
