Patterns of Regional Gray Matter and White Matter Atrophy in “Cortical Multiple Sclerosis” (P6.130)

OBJECTIVE: To investigate the patterns of regional atrophy of the brain gray matter (GM) and white matter (WM) in patients with “cortical” multiple sclerosis (cort-MS) in comparison to classical MS (c-MS) using voxel-based morphometry (VBM). BACKGROUND: Cort-MS is a rare form of the disease characterized by a severe progressive cognitive impairment, focal cortical syndromes, cortical signs with a relative sparing of motor, sensory and cerebellar functions. Little is known about the contribution of GM and WM damage to cognitive and psychiatric symptomatology in cort-MS. DESIGN/METHODS: Following a neurological and an extensive neuropsychological evaluation for language, memory, visuo-spatial abilities, attention, executive functions and depressive symptoms, nine cort-MS patients were enrolled. As control groups, 9 classic MS patients (c-MS), matched for education, age at onset, EDSS and disease duration to cort-MS patients (p ranging from 0.2 to 0.8) and 9 sex- and age-matched healthy controls (HC) were also studied. All subjects underwent a brain MRI exam, including a fluid attenuation inversion recovery (FLAIR) and a high-resolution T1-weighted scans. VBM was used to assess between group differences of GM and WM volumes (SPM8). RESULTS: FLAIR and T1 lesion loads were higher in cort-MS vs c-MS patients (p=0.005 and p=0.002 respectively). Compared to HC, MS patients had cortical and subcortical GM atrophy and WM atrophy of the corpus callosum and bilateral corticospinal tracts. No GM/WM area was more atrophied in c-MS vs cort-MS patients. Compared to c-MS, cort-MS patients had GM atrophy of fronto-temporal-parietal areas and the cingulum and WM atrophy of the cingulum, bilateral cerebral peduncles and right inferior and left superior longitudinal fasciculus. CONCLUSIONS: GM and WM atrophy of key brain regions known to be related to cognitive functions contribute to differentiate cort-MS from c-MS. Higher susceptibility to neurodegenerative processes in these areas could underlie the clinical presentation of this disease form. Study Supported by: