P1074 Regional Brain Volume Differences in patients with CIS A voxel- based Morphometry study Rumaiza Alyafeai a, Deborah Pareto b, Jaume Sastre-Garriga a, Angela Vidal-Jordana a, Manel Alberich b, Cristina Auger b, Mar Tintoré a, Alex Rovira b, Xavier Montalban a The developed GM damage in ON patients a Department of Neurology-Neuroimmunology and Multiple Sclerosis Centre of Catalonia (Cemcat), Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona. Barcelona, Spain. b Magnetic Resonance Unit. Radiology Department. Hospital Universitari Vall d’Hebron. Universitat Autònoma de Barcelona. Barcelona, Spain. P1074 Introduction & Purpose Relevant brain atrophy is present in patients with clinically isolated syndromes (CIS), particularly in the thalami, and other deep grey matter structures. In this study we aim to further characterize the clinical correlates of regional grey matter damage at CIS presentation and its short-term evolution by using voxel-based Morphometry (VBM). Methods From a longitudinal on-going CIS inception cohort 133 consecutive patients were selected. Out of these, 19 patients were excluded mostly due to incomplete or non-standardized MRI protocol, or segmentation errors. Finally, 114 patients (66 females) were analyzed. Baseline mean age was 33.4 years (SD 7.9) and median EDSS 1.5 (range 0 - 4). A Brain 3T-MRI at baseline (3 months) and follow-up (12 months) was acquired (including a 3D T1-weighted sequence [MPRAGE]). Patients with CIS were classified according to: 1) fulfillment of Barkhof criteria at baseline MRI, dichotomised as follows: 0-1-2 criteria were considered as Barkhof Low (BL, n=80) and 3-4 criteria as Barkhof High (BH, n=34); 2) the presence/absence of oligoclonal bands: OCB+ (n=53) or OCB- (n=47); 3) the initial clinical presentation: Optic Neuritis (ON, n=51) or other CIS topography (OTHER, n=63). For voxel-based data analysis we used VBM pipelines implemented in SPM8. The cross-sectional analysis was performed using a 2-sample t-test comparing the cohort subgroups at baseline (BL vs BH, OCB+ vs OCB-, ON vs OTHER). To check for longitudinal changes at one year between subgroups we used a flexible factorial design. Changes were considered significant at p<0.05 FWE-corrected level, on extended threshold of 30 voxels. Results Baseline cross-sectional analyses showed significant grey matter (GM) atrophy in BH compared to BL patients mainly affecting the thalami (figure 1), while no differences were observed between the other subgroups at baseline (OCB+ vs OCB- / ON vs OTHER). Longitudinal analyses by subgroups showed significant GM atrophy in: 1. postcentral, cingulum, lingual, paracentral , parietal and frontal giri of the BH group compared to BL (figure 2A); 2. cingulate, postcentral and supplementary motor area of OCB+ patients compared to OCB- (figure 2B); 3. lingual occipital, postencentral and cingulum in ON patients compared with OTHER (figure 2C). Figure 1 reveals areas of significant thalami atrophy in BH patients compared to BL; no areas of significant grey matter atrophy in BL compared to BH patients were observed. Baseline differences between the other complementary subgroups were not observed. A C B Figure 2 shows the differential changes when comparing subgroups in the longitudinal analyses. Patients in the BH (A), OCB+ (B) and ON (C) groups develop significantly more GM atrophy in specific regions than their complementary groups of BL, OCB- and OTHER. Conclusions Significant grey matter losses in specific brain regions are already visible from the CIS stage. Grey matter damage is more significant in patients with other signs of severity (presence of OCB or fulfillment of Barkhof criteria) Grey matter damage is associated with clinical presentation in patients presenting with optic neuritis. The developed GM damage in ON patients compared to Non-ON patients, is nicely associated with their clinical presentation and maybe a demonstration of trans-synaptic degeneration. SWI Disclosures R Alyafeai Current MSIF fellow D Pareto has recieved speaking honoraria from Novartis and Genzyme. J Sastre-Garriga has received compensation for consulting services and speaking honoraria from Merck-Serono, Biogen-Idec, Teva, Sanofi-Aventis and Novartis. M Tintoré has received compensation for consulting services and speaking honoraria from Bayer-Schering, Merck-Serono, Biogen-Idec, Teva, Sanofi-Aventis and Novartis. X Montalban has received speaking honoraria and travel expenses for scientific meetings, has been a steering committee member of clinical trials or participated in advisory boards of clinical trials in the past with Bayer Schering Pharma, Biogen Idec, EMD Merck Serono, Genentech, Genzyme, Novartis, Sanofi-Aventis, Teva Pharmaceuticals and Almirall. A Rovira serves on scientific advisory boards for NeuroTEC and on the editorial board of the American Journal of Neuroradiology and Neuroradiology, has received speaker honoraria from Bayer Schering Pharma, Sanofi-Aventis, Bracco, Merck Serono, Bracco, Teva Pharmaceutical Industries Ltd. and Biogen Idec, receives research support from Bayer Schering Pharma, and serves as a consultant for Novartis email: Ralyafeai@cem-cat.org Multiple Sclerosis Center of Catalonia | Clinical Neuroimmunology Unit | MR Unit (IDI) Department of Radiology. Vall d’Hebron University Hospital | Barcelona (Spain)