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Abstract Details

Grey Matter Pathology and Corpus Callosum Atrophy Contributes to Cognitive Dysfunction in Multiple Sclerosis Patients
MS and Related Diseases
P06 - (-)
128
BACKGROUND: Studies with conventional magnetic resonance imaging (MRI) indicate that cognitive impairment in multiple sclerosis (MS) patients is not fully explained by the burden of T2 lesions in the brain, and probably better related to grey-matter pathology. Other non-conventional MRI techniques such as double inversion recovery (DIR) and corpus callosum volume (CCV) have been applied to MS cognitive studies with seemingly better correlation but few data address these relationships.
DESIGN/METHODS: We prospectively studied 43 RRMS patients with cognitive testing using Rao's Brief Repeatable Battery of Neuropsychological Tests (BRB-N) and MRI in a 3T scanner including FLAIR, volumetric T1, and DIR sequences. Pure cortical lesions (CoL) and mixed white/grey matter lesions (MixL) were segmented on DIR, and white-matter lesion load (WML) in FLAIR sequences using a semiautomatic thresholding technique (MIPAV software). CCV was measured in volumetric T1 with FreeSurfer.
RESULTS: We included 10 male and 33 female RRMS patients with mean age 30.8 years, 6.5 years of disease duration, and median EDSS of 2.0. Mean number of deficits in BRB-N was 2.0. All MRI measures were related to the score of selective reminding test (mostly CCV, R=0.53, p<0.001), symbol-digit modalities test (mostly number of CoL; R=-0.51, p<0.001), and PASAT (mostly WML; R=-0.67, p<0.0001). The CCV was related to all BRB-N subtests, except verbal fluency. Overall number of deficits in BRB-N was also related to all MRI measures and mostly to number of CoL and MixL (R=0.52, <0.01; R=0.51, p<0.001, respectively), and CCV (R=-0.51, p<0.001).
CONCLUSIONS: Cognitive impairment in RRMS patients is strongly related to the burden of lesions in both white and grey matter. Corpus callosum atrophy and grey matter lesions provide valuable insight into the pathological process leading to cognitive dysfunction in MS.
Authors/Disclosures
Alfredo Damasceno, MD
PRESENTER
No disclosure on file
Benito P. Damasceno, MD, PhD (Neurology Department, Medical School, State University of Campinas (UNICAMP)) No disclosure on file
Fernando Cendes, MD, PhD, FAAN (Departamento de Neurologia; FCM; UNICAMP) Dr. Cendes has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for UCB Pharma. Dr. Cendes has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for UCB Biopharma. Dr. Cendes has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for United Medical – Brazil. Dr. Cendes has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Zodiac Pharma . Dr. Cendes has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Eurofarma – Brazil . Dr. Cendes has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Epilepsia. Dr. Cendes has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Frontiers in Neurology - Epilepsy. The institution of Dr. Cendes has received research support from São Paulo Research Foundation - FAPESP. The institution of Dr. Cendes has received research support from Conselho Nacional de Desenvolvimento Científico e Tecnológico - Brazil . The institution of Dr. Cendes has received research support from NIH.
Alan J. Thompson, MD, FRCP, FAAN (UCL Institute of Neurology) No disclosure on file