Evidence of early cortical atrophy in XXXX : relevance to white matter changes and disability.

@entity1 @entity32 @entity66 @entity75 @entity16 @entity393 @entity62 @entity15
OBJECTIVE: To assess cortical @entity62 ( @entity62 ) changes in @entity15 and establish their relevance to clinical disability and to inflammatory changes of white matter (WM) in @entity1 with the relapsing-remitting (RR) and primary progressive (PP) forms of the disease. METHODS: Conventional MRI examinations were obtained in @entity1 with definite @entity15 who had either the RR or the PP form of the disease. An automated analysis tool was used with conventional T1-weighted MR images to obtain total and cortical brain volumes normalized for head size. Total @entity75 load was estimated on conventional proton density and T2-weighted MR images. The relationship between volumetric MR measures and scores of clinical disability was assessed. RESULTS: Normalized cortical volumes (NCV) were lower for both RR and PP @entity15 @entity1 than for normal control subjects (p < 0.001) but were similar between the two @entity1 groups (p > 0.5). NCV decreases in both @entity1 groups were detected even in those @entity1 with @entity66 duration (<5 years; p < 0.001 in RR @entity15 and p < 0.05 in PP @entity15 ) and minimal @entity75 volume (<5 mL; p < 0.0001 in RR @entity15 and p < 0.005 in PP @entity15 ). Measures of NCV in individual @entity1 were negatively correlated with T2-weighted lesion volume (r = -0.47, p < 0.001) and disease duration (r = -0.25, p < 0.05) only in the @entity1 with RR @entity15 . NCV correlated with Expanded Disability Status Scale scores across all of the @entity1 , but the strength of the correlation was stronger (p < 0.05) for PP (r = -0.64, p < 0.0001) than for RR (r = -0.27, p = 0.04) @entity15 @entity1 . CONCLUSIONS: These data confirm substantial neocortical @entity393 in @entity15 @entity1 and suggest that neocortical @entity62 pathology may occur early in the course of the disease in both RR and PP @entity15 @entity1 and contribute significantly to @entity16 . Although a proportion of this neocortical pathology may be secondary to WM @entity32 , the extent of the changes suggests that, especially in @entity1 with PP @entity15 , an independent neurodegenerative process also is active.
