Poster Session 3. Diagnosis and differential diagnosis. Abstracts Multiple Sclerosis Journal 2018; 24: (S2) SAGE Publications

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1 Abstracts Multiple Sclerosis Journal 208; 24: (S2) Poster Session 3 Diagnosis and differential diagnosis P970 Prediction of conversion to multiple sclerosis using the 207 McDonald and 206 MAGNIMS criteria in patients with clinically isolated syndrome A. Miclea, A. Salmen, R. Wiest 2, F. Wagner 2, A. Hoepner 3, L. Schrewe, G.-C. Zoehner, N. Kamber, A. Chan, R. Hoepner Department of Neurology, Inselspital, Bern University Hospital and University of Bern, 2 Department of Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland, 3 Banking & Finance group, Michael Smurfit, Graduate Business School & UCD Lochlann Quinn School of Business, University College Dublin, Dublin, Ireland Introduction: In 206 and 207, new diagnostic criteria were proposed for the diagnosis of multiple sclerosis (MS) prompting the need to investigate their sensitivity and specificity. Objectives: To retrospectively compare the 206 MAGNIMS with the 207 McDonald criteria by evaluating their accuracy of predicting the conversion to MS in a single-centric cohort of patients diagnosed with clinically isolated syndrome (CIS) according to the 200 McDonald criteria. Methods: The retrospective analysis was performed at the Bern University Hospital in Switzerland (ethical approval: KEK-BE ). It was investigated if at the time point of CIS diagnosis, patients already fulfilled the 207 McDonald, the 206 MAGNIMS or three modified sets of diagnostic criteria. Parameters of disease activity were retrospectively assessed until clinical and/ or radiological conversion to MS or in non-converters for a maximum of 5 years. Results: From the 27 included patients, 67 (52.8%) converted clinically and/or radiologically to MS (median duration:. years, 25th-75th percentile: ). Retrospectively applying the 207 McDonald and 206 MAGNIMS criteria to patients with CIS and investigating the conversion to MS, resulted in a sensitivity of 0.89 (mean, 95% confidence interval: ) and 0.6 ( ) and a specificity of 0.3 ( ) and 0.5 ( ), respectively. Adding individual modifications, i.e. optic nerve involvement or requirement of 3 periventricular lesions for periventricular involvement to the 207 McDonald criteria and presence of oligoclonal bands to the 206 MAGNIMS criteria, did not increase the predictive accuracy. Conclusions: The 207 McDonald criteria had the highest predictive accuracy in estimating the conversion from CIS to MS. Therefore, we conclude that the 207 McDonald criteria are a valuable tool for the early diagnosis of MS in the real world setting. Conflict of Interest and Sources of Funding Statement: On behalf of all authors, the corresponding author states that there is no conflict of interest. This research was supported by the Swiss Multiple Sclerosis Society, which is a non-profit organization (quality of life research grant, applicant RH). Authors disclosures: A Miclea, A Hoepner, GC Zoehner and N Kamber report no disclosures. A Salmen received speaker honoraria and/or travel compensation for activities with Almirall Hermal GmbH, Biogen, Merck, Novartis, Roche and Sanofi Genzyme, none related to this work. R Wiest received research support from the Swiss National Fonds (320030L_70060, 32003B_6007 and 33IC30_66827) and the Swiss Heart Foundation. F Wagner received a research grant from the Swiss Multiple Sclerosis Society. L Schrewe received travel grants from Genzyme Sanofi. A Chan has received personal compensation for activities with Bayer, Biogen, Genzyme, Merck, Novartis, Roche, Teva. He received research support from the Swiss National Fonds (SNF, No _72952), Genzyme and UCB. He serves in the editorial board for Clinical and Translational Neuroscience and the Journal of International Medical Research. R Hoepner received research and travel grants from Novartis and Biogen Idec. He also received speaker s honoraria from Biogen, Novartis, Merk and Almirall. He is supported by the Swiss Multiple Sclerosis Society. P97 Differential diagnosis of multiple sclerosis with machine learning-based central vein sign recognition J. Richiardi,2, P. Maggi 3, M.J. Fartaria,2,4, F. La Rosa,4, J. Jorge 5, P. Sati 6, D.S. Reich 6, R. Du Pasquier 3, R. Meuli, M. Bach Cuadra,7, T. Kober,2,4 Department of Medical Radiology, Lausanne University Hospital, 2 Advanced Clinical Imaging Technology, Siemens Healthcare AG, 3 Department of Neurology, Lausanne University Hospital, 4 Signal Processing Laboratory (LTS5), 5 Laboratory of functional and metabolic imaging, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland, 6 National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States, 7 Center for Biomedical Imaging, University of Lausanne, Lausanne, Switzerland Introduction: The central vein sign (CVS), the presence of a vein at the center of white matter (WM) lesions, is a promising imaging marker to differentiate MS from its mimics. Lesions and veins are well contrasted on FLAIR* MRI images, but manually classifying perivenular and non-perivenular lesions is time-consuming. 208 SAGE Publications 0.77/

2 Poster Session 3, 24 (S2) 53 Objectives: We propose two approaches to automatically detect the CVS: deep learning or a state-of-the-art vessel-filtering approach. We compare their performance and potential for clinical applicability. Methods: Patients with an established MS diagnosis (n=6) or other MS-mimics (n=7) underwent 3T MRI at the Erasme University Hospital (Brussels, Belgium). Brain WM lesions were manually segmented, and perivenular assessment was done on FLAIR* images by an expert neurologist, following NAIMS guidelines [Sati et al., Nat. Rev. Neurol., 206; Maggi et al., Ann. Neurol., 208], yielding 202 perivenular and 22 non-perivenular lesions. A convolutional neural network (CNN) was designed and trained on 35 3D lesion patches (+36 for validation in each of 0 crossvalidation folds) to classify lesions with and without CVS, keeping 63 lesions (5 patients) unseen for final testing. A vesselness filter was also optimized for CVS classification, with average filter response within the lesion mask as the imaging marker. After both algorithms, patients were classified as MS if 50% or more of their lesions were classified as CVS ( 50% rule ), as MS-mimic otherwise. Lesion-level performance was evaluated by specificity, sensitivity, and area under the curve (AUC) on the test set. Patient-level performance was evaluated on the validation set (28 patients) due to the small size of the test set. Results: Compared to expert visual assessment, at lesion level the CNN reached 8% sensitivity, 7% specificity, and 79% AUC, with near-instant classification (vesselness filter 8%, 57%, 74% resp., around.5 seconds per lesion). At the patient level, the CNN had sensitivity 9%, specificity 88% (vesselness filter 50%, 82% resp.). Conclusions: The relatively high performance and speed of the proposed automated approaches are promising and show potential for clinical applicability. The CNN performed better than the vesselness filter, without need for lesion masking. Relatively simple improvements to the CNN training and architecture should further increase its performance, which might ease translation of the CVS imaging biomarker into clinical practice. Jonas Richiardi: Salary paid in part by Siemens Healthcare AG Switzerland Pietro Maggi: Supported by the ECTRIMS Clinical Training Fellowship Program Ma rio Joa o Fartaria: Salary paid by Siemens Healthcare AG Switzerland Francesco La Rosa: Nothing to disclose Joa o Jorge: Nothing to disclose Pascal Sati: Nothing to disclose Daniel S. Reich: No s relevant to the content of this abstract Renaud Du Pasquier: Nothing to disclose Reto Meuli: Nothing to disclose Meritxell Bach Cuadra: Nothing to disclose Tobias Kober: Salary paid by Siemens Healthcare AG Switzerland P972 Sensitivity and specificity of 207 McDonald criteria for multiple sclerosis in patients with clinically isolated syndrome F. Gobbin, A. Marangi, R. Orlandi, S. Monaco, M.D. Benedetti, A. Gajofatto AOUI Verona Neurologia, Azienda Ospedaliera Universitaria Integrata Verona, Verona, Italy Introduction: In 207 the McDonald criteria for multiple sclerosis (MS) diagnosis were revised in order to update them based on the most recent medical evidence. According to the revised criteria, symptomatic and cortical lesions on MRI can be used to demonstrate dissemination in space and time (DIS and DIT). In addition, the presence of cerebrospinal fluid (CSF)-specific oligoclonal bands allows a diagnosis of MS in patients fulfilling DIS requirements at any time. The purpose of our study is to evaluate and compare the sensitivity and specificity of 207 McDonald criteria and 200 McDonald criteria in patients presenting with a clinically isolated syndrome (CIS). Methods: To do this we included patients with a first demyelinating event suggestive of MS (i.e. CIS) who were followed at Verona University Hospital MS Centre up to April 208. Inclusion criteria were: CIS onset after 2007; no more than 2 months between onset of symptoms and first clinical evaluation at study Centre; brain and spinal cord MRI with gadolinium and CSF analysis for oligoclonal bands performed within 9 months from onset; follow up brain MRI less than 24 months from onset. Study patients data were retrospectively collected from available database and medical records. Fulfilment of 200 and 207 McDonald criteria was assessed for each patient using baseline MRI to demonstrate DIS and both baseline and follow-up MRI plus CSF analysis to demonstrate DIT. Sensitivity and specificity of diagnostic criteria were calculated using conversion to clinically definite MS (CDMS) as the gold standard. Results: As of April 208, 55 eligible patients were included. Of these 33 were female (60%). Median age at onset was 30 years (range 34-38). Onset location was optic nerve in 2 patients, brainstem/cerebellum in, cerebral hemisphere in 4, and spinal cord in 28. Median follow up time was 5 months (38-8).Twenty-six patients (47.3%) converted to CDMS. 200 McDonald criteria showed a sensitivity of 80.8% (95% confidence interval: %) and a specificity of 44.8% ( %). 207 McDonald criteria had 00% ( %) sensitivity and 3.8% ( %) specificity. Discussion: the preliminary data of our study show that 207 McDonald criteria substantially increase sensitivity for MS diagnosis in CIS patients, compared to McDonald 200 criteria. However, the revised criteria seem to significantly reduce specificity. Gobbin Francesca: nothing to disclose Marangi Antonio: nothing to disclose Orlandi Riccardo: nothing to disclose Multiple Sclerosis Journal 208; 24: (S2)

3 532 Poster Session 3, 24 (S2) Monaco Salvatore: nothing to disclose Benedetti Maria Donata: nothing to disclose Gajofatto Alberto: nothing to disclose P973 Performance of the 200 and 207 revised McDonald criteria in an Italian retrospective cohort of patients with clinically isolated syndrome V. Camera, D. Ferraro, F. Vitetta 2, R. Bedin, N. Fini 2, P.F. Nichelli, P. Sola 2 Biomedical, Metabolic and Neurosciences, University of Modena and Reggio Emilia, 2 Neurology Unit, Azienda Ospedaliero-Universitaria di Modena, Modena, Italy Introduction: The 200 revised McDonald diagnostic criteria for multiple sclerosis (MS) have been updated in December 207, in order to anticipate diagnosis and, subsequently, treatment, in clinically isolated syndrome (CIS) patients with a high risk of developing MS. Objective: The aim of this study is to investigate the performance of the 200 and 207 revised McDonald criteria in diagnosing MS in patients with CIS, in a retrospective single-center Italian cohort. Material and methods: We retrospectively selected patients with a typical CIS suggestive of MS between 202 and 207, with at least six months of follow-up, and no history of previous neurological symptoms. Patients were included in the analysis in the presence of baseline cerebrospinal fluid (CSF) analysis, baseline brain and spinal MRI (within 3 months from onset) and a further follow-up brain and spinal scan performed after 3-2 months. Patients who developed primary progressive MS were excluded. Results: Of 207 selected CIS patients, 29 fulfilled the inclusion criteria and were further analyzed. Mean age at onset was 36 ±.6 years and female/male ratio was 2.5:. At onset, a MS diagnosis was possible in 6.3% (n=79) of patients using the 207 criteria and in 20.8% (n=26) using the 200 criteria (p < ). One-hundred and fourteen subjects (88.4%) had dissemination in space (DIS) according to the 200 criteria, and a further three patients (2.3%) fulfilled the 207 DIS criteria. Twenty-six (22.8%) patients fulfilled the 200 DIT criteria, while 207 DIT criteria were met by a further thirty-four (29.8%) patients using MRI and by further forty-one patients (36%) on the account of CSF oligoclonal bands (OCBs). The median time to MS diagnosis was four months (interquartile range-iqr:-8 months) following application of the 200 and one month (IQR:0-2 months) following application of the 207 criteria (p < 0.00). The proportion of patients with a MS diagnosis using the 200 and 207 criteria was 49% and 84%, respectively during the first three months (p < 0,0000) and 8.5% and 96.5% throughout the first year (p =0.0004). Conclusions: The 207 McDonald criteria enable a MS diagnosis in more than 80% of CIS patients during the first three months from disease onset. This is mainly due to the reintroduction of CSF OCBs and to the loss of distinction between symptomatic and asymptomatic lesions in the new DIT criteria. Valentina Camera: nothing to disclose Diana Ferraro: has served on scientific advisory boards for Biogen Idec, Novartis and Roche and has received travel grants and/or speaking honoraria from Teva, Merck Serono, Genzyme, Biogen and Novartis. Francesca Vitetta: has served on scientific advisory boards for Merck Serono and Teva and has received travel grants and/or speaking honoraria from Teva, Merck Serono, Genzyme and Biogen. Roberta Bedin: nothing to disclose Nicola Fini: nothing to discolse Paolo Frigio Nichelli: nothing to discolse Patrizia Sola: has served on scientific advisory boards for Biogen Idec and Teva; she has received funding for travel and speaker honoraria from Biogen Idec, Merck, Teva, Sanofi Genzyme, Novartis and Bayer and research grants for her institution from Bayer, Biogen, Merck, Novartis, Sanofi and Teva. P974 Treatment in attacks of NMOSD: steroids versus plasma exchange in a Colombian cohort L.M. Giraldo, A.M. Pino-Pérez,2, C. Restrepo- Aristiza bal,2, F. Álvarez-Gómez,2, C.A. Franco,2, J.V. Tobón,2, P.A. Mazo, J.L. Ascencio 3, M.I. Zuluaga,2 Neurologia, Instituto Neurológico de Colombia, 2 Neurologia Clínica, Universidad CES, 3 Neuroradiología, Instituto Neurológico de Colombia, Medellín, Colombia Background: Neuromyelitis optica spectrum disorders (NMOSD) are a group of inflammatory disorders of the central nervous system characterized by acute attacks to the optic nerve and longitudinally extensive myelitis. In general, attacks are treated with high-dose intravenous glucocorticoids followed by plasma exchange (PLEX) in case of refractoriness. Recently, the possibility of starting with steroids associated to plasma exchange has been raised in order to impact on severe outbreaks. Objective: To compare the outcome of relapses in patients with NMOSD treated with steroids versus PLEX. Methods: A retrospective review of patients with NMOSD records was made. Data of all admissions to the Instituto Neurológico de Colombia were evaluated. The primary outcome was defined as complete improvement at 6 months. The Expanded Disability Status Scale (EDSS) score was calculated at baseline, nadir, discharge and follow up (6 months). Results: A total of 88 attacks in 55 patients were included, 38 (69.%) anti-aquaporine-4 positive. The median number of attacks was 2 (-2). Thirty-eight (43.2%) patients had spinal cord attacks, followed by attacks in the optic nerve 28 (3.8%). Sixtyseven attacks [44 patients, 93.2% female, mean age at debut 43.9 (3.4) and median disease duration 5 years (3-8.5)] were treated with steroids alone. Nineteen attacks [9 patients, 88.9% female, mean age at debut 5 (.7), and median disease duration 6 years (3-2)], were treated with PLEX (two attacks steroids and PLEX, one PLEX alone, and 6 PLEX after steroids). PLEX patients had a significantly higher EDSS at baseline (4.5 vs.0; p = 0.03), Multiple Sclerosis Journal 208; 24: (S2)

4 Poster Session 3, 24 (S2) 533 nadir (8.0 vs 5.0; p < 0.05) and at discharge (8.0 vs 5.0; p < 0.05). During the follow up 35% of the steroid treatment group while 47.% of the PLEX group achieved a complete improvement (p= 0.6) with a delta EDSS of.0 at 6 months. Conclusions: In this study there were no differences found when comparing the primary outcome in NMOSD patients according to the treatment with steroids versus PLEX. Both treatments can provide clinical improvement in acute relapses of NMOSD. Lilliana M Giraldo: nothing to disclose Angélica M Pino-Perez: nothing to disclose Carolina Restrepo-Aristizabal: nothing to disclose Felipe Alvarez-Gomez: nothing to disclose Cesar A Franco: nothing to disclose Jose Vladimir Tobon: nothing to disclose Paula A Mazo: nothing to disclose Jose Luis Ascencio: nothing to disclose Maria I Zuluaga: nothing to disclose P975 A brief language-independent and self-administered computerized test for cognitive assessment in multiple sclerosis (MS) S.-M. Khaligh-Razavi,2, M. Sadeghi 3, M. Khanbagi, C. Kalafatis 2,4, S.M. Nabavi Brain and Cognitive Sciences, Royan Institute for Stem Cell Biology and Technology, Tehran, Islamic Republic of Iran, 2 Cognetivity Ltd, London, United Kingdom, 3 Tehran University, Tehran, Islamic Republic of Iran, 4 South London & Maudsley NHS Foundation Trust, London, United Kingdom Cognitive impairment is common in patients with multiple sclerosis (MS), and occurs in up to 65% of these patients. However, it is not routinely assessed in the clinic setting. The currently available reference tests for assessing cognitive impairment in MS are typically long and need a clinician to administer the test. We developed a 5-minute computerized cognitive assessment tool based on a rapid visual categorization task, in which a series of carefully selected natural images of varied difficulty are presented to participants. The test is self-administered and independent of language and culture. We refer to this test as the Integrated Cognitive Assessment test (ICA). To determine the validity of ICA in cognitive assessment for MS, we compared it with the pen-and-paper Brief International Cognitive Assessment for MS (BICAMS) test. BICAMS consists of the following three tests and takes about 5 to 20 mins to administer: the Symbol Digit Modalities Test (SDMT), the learning trials from the California Verbal Learning Test (CVLT-II), and the Brief Visual Memory Test-Revised (CVLT-R). Ninety-five MS patients and eighty-three healthy controls participated in the experiment. ICA had excellent test-retest reliability (r=0.96), and was highly correlated with the BICAMS battery of tests (correlation with SDMT: 0.80; CVLT-II: 0.76; BVMT-R: 0.67). ICA has advantages over BICAMS because of its efficient administration, shorter duration, automatic scoring, language independency, and potential for medical record or research database integration. Thus, we suggest ICA as a practical tool for routine screening of cognitive performance in the MS clinic. Dr. Khaligh-Razavi serves as the chief science officer at Cognetivity ltd. Other authors declared no potential conflicts of interest with respect to the research. -Maryam Sadeghi: nothing to disclose -Mahdiyeh Khanbagi : nothing to disclose -Seyed Massood Nabavi: nothing to disclose Funding: This study was designed and conducted by investigators from Royan Institute, Brain and Cognitive Science Dept.; and was funded in part by grants from Cognetivity ltd. The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data. P976 The review of systems questionnaire discriminates medically unexplained neurologic symptoms from neurologic disease in a multiple sclerosis referral clinic B. Jones, W. Kilgo, J. Rinker Neurology, University of Alabama at Birmingham, Birmingham, AL, United States Distinguishing multiple sclerosis (MS) from medically unexplained symptoms (MUS) is a major challenge for specialty MS clinics. Misdiagnosis of MS may expose patients to medical, psychological, social, and financial harm. Overreliance on testing such as MRI may lead to over diagnosis of MS. Focusing on aspects of the face-to-face encounter may improve discrimination between neurologic disease and MUS. The review of systems (ROS) is used to collect information about symptoms affecting a range of organ systems. Patients responding yes to a high percentage of ROS items have been shown to correlate with MUS in specialty clinics in otolaryngology, gastroenterology, and epilepsy. Presented here are the results of a retrospective review from a specialty MS clinic examining the utility of the ROS in predicting the presence of MUS. Consecutive new patients seen in the University of Alabama MS Clinic from October 207 through 3 March 208 were included. Demographics, reason for referral, and final diagnosis were collected in addition to ROS questionnaires. Those without a completed ROS were excluded. Subjects were dichotomized by the presence or absence of MUS by physician impression. ROS yes responses were converted to a percent positive response (PPR) score for each subject. Odds ratios predicting MUS by PPR were determined by logistic regression. A receiver operating characteristic (ROC) curve was constructed to assess strength of ROS in diagnosing MUS, and sensitivity and specificity of ROS were reviewed for varying PPR cutoffs. All statistical analyses were performed using JMP 3.0. Of 384 encounters, 66 completed ROS questionnaires, and 27 (6.2%) had MUS. Subjects were 76.5% female, 74.% white, and mean age was 47.4 ± 3.8 years. Mean ROS PPR was 38.7 ± 8.75% for subjects with MUS and 23.8 ± 5.9% for all others. Multiple Sclerosis Journal 208; 24: (S2)

5 534 Poster Session 3, 24 (S2) Odds ratio (OR) per unit change in PPR as a univariate predictor of MUS was 0.93 (p< 0.00). In a multivariate model, age, sex, and ethnicity did not predict MUS. Area under the ROC curve for PPR on ROS was When subjects responded yes to >45% of items, ROS predicted MUS with 52% sensitivity and 94% specificity. Patients with high PPR on ROS questionnaire are likely to have MUS. The ROS is a valuable, specific, and inexpensive tool to employ in the evaluation for MS or related disorders. While clinical judgement remains paramount, high PPR on ROS should act as a red flag for MUS. Benjamin Jones receives salary support for fellowship training through an institutional grant from Biogen. William Kilgo reports no s. John Rinker receives research funding from Biogen for an unrelated study. P977 Longitudinally extensive transvers myelitis: a single instution experience E. Yilmaz, M.A. Tuncer, F. Khasiyev, E. Gümeler 2, A.T. Ilıca 3, R. Göçmen 2, R. Karabudak Hacettepe University Neurology, 2 Hacettepe University Radiology, Hacettepe University Faculty of Medicine, 3 Division of Radiology, Turkish General Stuff,Clinic, Ankara, Turkey Introduction and aims: Longitudinally extensive transverse myelitis (LETM) is defined as a spinal cord lesion that extends over three or more vertebral segments. The clinical presentation of LETM consist of paraparesis or tetraparesis, sensory disturbances, and gait, bladder, and bowel dysfunction. LETM encompasses a broad list of differential diagnoses where many of which have widely variable treatments and outcomes. In this study, we aimed to describe the epidemiological, clinical, radiologic, laboratory findings and treatment outcomes of LETM patients. Methods: In this retrospective single-center study, all LETM patients who have been followed up in our center between April January 207 were evaluated in terms of epidemiological, clinical, radiological, cerebrospinal fluid findings, etiologies and treatment outcomes. Results: Total 05 patients ( 3 males,74 females ) were reviewed. Median age of onset was 40 (range 2-76 years).we classified our patients according to their etiologies as autoimmune diseases (n=70), infections (n=8, 7,6%), vascular pathologies (n=6,5,7%), others ( n=4, 3,3% hydrocephalus, radiation myelitis, Leber hereditary optic neuropathy, hypertensive myelopathy, B2 deficiency trauma etc.), and undetermined etiologies(n=8 7,6%). Autoimmune disease presenting with LETM were neuromyelitis optica (NMO) (n=43, 40,9%); multiple sclerosis (MS) (n=8,7,6%); connective tissue disorder (n=5 4,2%); acute disseminated encephalomyelitis (n=); parainfectious (n=2) and paraneoplastic syndrome (n=2). Clinically 35 patients (33,3%) had optic neuritis either simultaneus or later onset with LETM. Among them 26 were clinically diagnosed as NMO, one had MS, one had Behçet s syndrome, one had Leber s hereditary optic neuropathy, and the last had connective tissue disorder. LETM presenting with paraneoplastic syndrome were finally diagnosed as B cell lymphoma and gastric adenocarcinoma. Conclusions: To predict the prognosis of the first LETM relapse, the radiological and cerebrospinal fluid findings is essential. Although the final differential diagnosis is mainly among the central nervous system demyelinating autoimmune diseases group there can be some other diseases that are totaly different in terms pathogenesis and therefore treatment. Our series represents different final diagnosis that should be included during the clinical work-up of the patient. Ezgi YILMAZ: nothing to disclose. Aslı TUNCER: nothing to disclose. Farid Khasiyev: nothing to disclose. Ekim Gümeler: nothing to disclose. Ahmet Turan ILICA: nothing to disclose. Rahşan GOCMEN: nothing to disclose. Rana KARABUDAK: nothing to disclose. P978 Neuromyelitis optica misdiagnosed as multiple sclerosis: a hospital-based study A. Villa, V. Fernandez, L. Melamud Buenos Aires University, Buenos Aires, Argentina Background: Neuromyelitis optica spectrum disorders (NMOSD) is a severe inflammatory disease affecting the Central Nervous System. Despite the discovery of the specific biomarker, aquaporin-4 antibody (AQP4-Ab) more than 0 years ago, misdiagnosis remains a problem. Objective: The aim of the study is to determine which proportion of patients with NMOSD were initially misdiagnosed as Multiple Sclerosis (MS). Materials and methods: We performed a retrospective hospitalbased study and obtained information from medical records of patients with diagnosis of NMOSD according to 205 criteria who were referred for a medical consultation at a General Hospital in Buenos Aires, Argentina between 2006 and 206. Results: Of 7 NMOSD patients, we collected data from 52 patients. 2/52 (23%) were diagnosed as having MS at the beginning of the disease. Median duration of misdiagnosis was 4.5 years. 7/2 patients (58%) were diagnosed as MS before the 2006 NMO diagnostic criteria (3 with transverse myelitis and 4 with optic neuritis as first symptom). 5/2 patients (42%) were diagnosed as MS after that time (3 had optic neuritis, transverse myelitis and the other one an area postrema syndrome as first symptoms). 7/2 (58%) patients were treated with disease-modifying therapy (DMT). 6/2 received beta-interferon and the other one glatiramer acetate. All of these patients persisted with relapses despite the treatment. In /2 misdiagnosed patients, testing for AQP4-Ab was available, being positive in 6/ (58%), similar to the seropositivity rate in this whole sample. Multiple Sclerosis Journal 208; 24: (S2)

6 Poster Session 3, 24 (S2) 535 Conclusions: NMOSD is frequently misdiagnosed as MS, leading to unnecessary and potentially serious risks for patients and significant implications for health care systems. Nothing to disclose P979 Are recurrent myelitis a prodromic phase of inflammatory diseases or a distinct inflammatory condition? L. Cacciaguerra,2, E. Pagani, M. Radaelli 2, V. Martinelli 2, G. Comi 2, M. Filippi,2, M.A. Rocca,2 Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, 2 Department of Neurology, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy Background: Acute transverse myelitis is a frequent presentation of a clinically isolated syndrome. A subgroup of these patients experiences recurrent myelitis (RM) without other neurological manifestations, thus not allowing the diagnosis of a specific inflammatory condition, such as multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD). In this study, we evaluated whether patients with RM show differences in lesion distribution and white matter (WM) tract involvement compared to those with NMOSD and MS. Methods: Brain WM lesion distribution was obtained from the T2-lesion masks of 7 RM subjects, 20 NMOSD and 20 relapsing-remitting MS patients matched for age and disease duration. Lesional volumes (LV) were split among WM tracts of the Johns Hopkins University (JHU) atlas, co-registered in the standard Montreal Neurological Institute (MNI) space. The impact on each region (minimum of 5 voxels) was assessed. Intragroup and intergroup analyses of LV distribution and WM involvement were performed. Results: RM patients had a selective damage of the motor pathways: superior corona radiata (CR) 8% of LV, middle cerebellar peduncle (MCP) 3%, cortico-spinal tract (CST) 2% (p vs other tracts=0.03). MS and NMOSD patients showed a higher involvement of the optic radiations (OR) and of the CR (p=0.04, p=0.03 respectively than other regions). The intergroup comparison of patients LV distribution confirmed the preferential involvement of MCP (p=0.007) and CST (p=0.04) in RM vs MS, while no difference emerged from the comparison between RM vs NMOSD. The analysis of WM tracts involvement confirmed the preferential damage of the OR and CR in NMOSD and MS (NMODS p=0.03, MS p=0.02 than other tracts), while RM patients had a preferential involvement of posterior CR (78.6%, p 0.0 vs other tracts). Conclusions: Despite a monomorphic clinical presentation, RM patients experience the involvement of the motor pathway also in the brain, suggesting a different pathogenetic mechanism from other WM diseases. L. Cacciaguerra, E. Pagani, and M. Radaelli have nothing to disclose V. Martinelli reports consultancy, speaking fees and/or travel expenses from Biogen Dompé SG, Merck Serono, Bayer Schering, Novartis, Sanofi Aventis, Genzyme Europe and Teva Pharmaceuticals. G. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, ExceMED. M. Filippi is Editor-in-Chief of the Journal of Neurology; received compensation for consulting services and/or speaking activities from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). M.A. Rocca received speakers honoraria from Biogen Idec, Novartis, Genzyme, Sanofi-Aventis, Teva, Merck Serono, and Roche and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla. MS Variants P980 Clinical and therapeutic predictors of relapse and disability outcomes in neuromyelitis optica spectrum disorder A. Kunchok, C. Malpas 2, D. Horakova 3, E. Havrdova 3, R. Alroughani 4, M. Terzi 5, B. Yamout 6, R. Karabudak 7, C. Boz 8, S. Ozakbas 9, J. Olascoaga 0, M. Simo, F. Granella 2, P. McCombe 3, T. Csepany 4, R. Bergamaschi 5, Y. Fragoso 6, T. Al-Harbi 7, R. Turkoglu 8, J. Lechner-Scott 9, G. Laureys 20, E. Pucci 2, P. Sola 22, D. Ferraro 22, A. Altintas 23, F. Grand Maison 24, G. Izquierdo 25, S. Eichau 26, A. Lugaresi 27, M. Marriott 2, I. Kister 28, H. Butzkueven 29, T. Kalincik 2, MSBase study group Neurology, 2 Royal Melbourne Hospital, The University of Melbourne, Melbourne, VIC, Australia, 3 Charles University in Prague and General University Hospital, Prague, Czech Republic, 4 Amiri Hospital, Sharq, Kuwait, 5 Mayis University, Medical Faculty, Samsun, Turkey, 6 American University of Beirut Medical Center, Beirut, Lebanon, 7 Hacettepe University Faculty of Medicine, Ankara, 8 KTU Medical Faculty Farabi Hospital, Trabzon, 9 Dokuz Eylul University, Izmir, Turkey, 0 Biodonostia Health Research Institute, San Sebastian, Spain, Semmelweis University, Budapest, Hungary, 2 University of Parma, Parma, Italy, 3 Royal Brisbane Hospital, Brisbane, QLD, Australia, 4 University of Debrecen, Debrecen, Hungary, 5 IRCCS Mondino Foundation, Pavia, Italy, 6 Universidade Metropolitana de Santos, Santos, Brazil, 7 King Fahad Specialist Multiple Sclerosis Journal 208; 24: (S2)

7 536 Poster Session 3, 24 (S2) Hospital Dammam, Khobar, Saudi Arabia, 8 Haydarpasa Numune Training and Research Hospital, Instanbul, Turkey, 9 John Hunter Hospital, Newcastle, NSW, Australia, 20 Universitary Hospital Ghent, Ghent, Belgium, 2 UOC Neurologia, Macerata, 22 Azienda Ospedaliera Universitaria, Modena, Italy, 23 Istanbul University Cerrahpasa School of Medicine, Instanbul, Turkey, 24 Neuro Rive-Sud, Quebec, QC, Canada, 25 Hospital Universitario Virgen Macarena, 26 Universitario Virgen Macarena, Sevilla, Spain, 27 Department of Biomedical and Neuromotor Science, University of Bologna, Bologna, Italy, 28 New York University Langone Medical Center, Multiple Sclerosis Comprehensive Care Center, New York, NY, United States, 29 Monash University, Melbourne, VIC, Australia Introduction: Neuromyelitis optica spectrum disorder (NMOSD) is a central nervous system autoimmune inflammatory condition associated with aquaporin-4-immunglobulin antibodies which results in demyelination. Understanding clinical and therapeutic predictors of relapses can aid management and prognostication of this disease Aim: To evaluate the effect of clinical and therapeutic predictors on risk of relapse and change in disability in NMOSD Methods: This MSBase cohort study of NMOSD patients (n=399) examined predictors of relapse in a Anderson-Gill survival model and change in expanded disability status score (EDSS) in a mixed effects model. A secondary analysis was conducted in the NMOantibody positive subgroup ( core region affected: spinal cord, optic nerve or brainstem, n=202). Results: Age (HR=0.82 per decade, p=0.003), disease duration (HR=0.95 per year, p=0.02), spinal cord onset (HR=0.6, p=0.007), brainstem onset (p=0.53, p=0.009) and treatment with azathioprine (HR=0.5, p< 0.00), mycophenolate mofetil (HR=0.24, p=0.06) were associated with a reduced risk of relapse in NMOSD. Treatment with glatiramer acetate (HR=.82, p=0.028), interferon-β (HR=.57, p=0.03) and acute therapies - corticosteroids (HR=.87, p < 0.00), intravenous immunoglobulin (HR=3.49, p=0.00) were associated with an increased risk of relapse. In the NMO-antibody positive subgroup, similar treatment effects on the risk of relapse were seen for azathioprine, mycophenolate mofetil, glatiramer acetate, corticosteroids and intravenous immunoglobulin. Age (p< 0.00), disease duration (p< 0.00), glatiramer acetate (p=0.00), and therapies used in acute relapses - cyclophosphamide (p=0.0), intravenous immunoglobulin (p=0.00) and plasma exchange (p< 0.00) were associated with a more pronounced increase in EDSS in the NMOSD cohort. Optic nerve onset (p=0.048), proportion of time pregnant (p=0.02) and treatment with azathioprine (p< 0.00), mycophenolate mofetil (p=0.043) and rituximab (p=0.029) - were associated with a slower increase in EDSS in the NMOSD cohort. The immunotherapies and age and disease duration showed similar associations in the NMO-antibody positive subgroup. Conclusion: Treatment with azathioprine, rituximab and mycophenolate mofteil are associated with a slower increase in EDSS in NMOSD and a lower risk of relapses. The risk of relapses declines and accumulation of disability increases with age and disease duration in NMOSD. Amy Kunchok received research support from Biogen. Charles Malpas - nothing to disclose Dana Horakova received speaker honoraria and consulting fees from Biogen, Merck, Teva and Novartis, as well as support for research activities from Biogen and research grants from Charles University in Prague [PRVOUK-P26/LF/4], Czech Minsitry of Education [PROGRES Q27/LF] and Czech Ministry of Health [NT3237-4/202]. Eva Kubala Havrdova received speaker honoraria and consultant fees from Actelion, Biogen, Celgene, Merck, Novartis, Roche, Sanofi and Teva, and support for research activities from Czech Ministry of Education [project Progres Q27/LF]. Raed Alroughani received honoraria as a speaker and for serving on scientific advisory boards from Bayer, Biogen, GSK, Merck, Novartis, Roche and Sanofi-Genzyme. Murat Terzi received travel grants from Novartis, Bayer-Schering, Merck and Teva; has participated in clinical trials by Sanofi Aventis, Roche and Novartis. Bassem Yamout did not declare any competing interests. Rana Karabudak did not declare any competing interests. Cavit Boz received conference travel support from Biogen, Novartis, Bayer-Schering, Merck and Teva; has participated in clinical trials by Sanofi Aventis, Roche and Novartis. Serkan Ozakbas did not declare any competing interests. Javier Olascoaga serves on scientific advisory boards for Biogen, Novartis, Sanofi and Roche; has received speaker honoraria from Almirall, Biogen, Bayer, Sanofi, Merck, Novartis and Roche and research grants from Biogen, Merck, Novartis and Teva. Magdolna Simo received speaker honoraria from Novartis, Biogen, Bayer Schering; congress/travel compensation from Teva, Biogen, Merck, Bayer Schering. Franco Granella received research grant from Biogen, served on scientific advisory boards for Biogen, Novartis, Merck, and Sanofi-Aventis and received funding for travel and speaker honoraria from Biogen, Merck, Sanofi-Aventis, and Almirall. Pamela McCombe received honoraria and consulting fees from Novartis, Bayer Schering and Sanofi and travel grants from Novartis, Biogen and Bayer Schering. Tunde Csepany received speaker honoraria/ conference travel support from Bayer Schering, Biogen, Merck, Novartis and Teva. Roberto Bergamaschi received speaker honoraria from Bayer Schering, Biogen, Genzyme, Merck, Novartis, Sanofi-Aventis, Teva; research grants from Bayer Schering, Biogen, Merck, Novartis, Sanofi-Aventis, Teva; congress and travel/ accommodation expense compensations by Almirall, Bayer Schering, Biogen, Genzyme, Merck, Novartis, Sanofi-Aventis, Teva. Yara Fragoso received honoraria as a consultant on scientific advisory boards by Novartis, Teva, Roche and Sanofi-Aventis and compensation for travel from Novartis, Biogen, Sanofi Aventis, Teva, Roche and Merck. Talal Al-Harbi did not declare any competing interests. Recai Turkoglu did not declare any competing interests. Jeannette Lechner-Scott accepted travel compensation from Novartis, Biogen and Merck. Her institution receives the honoraria for talks and advisory board commitment from Bayer Health Multiple Sclerosis Journal 208; 24: (S2)

8 Poster Session 3, 24 (S2) 537 Care, Biogen, Genzyme Sanofi, Merck, Novartis and Teva, has been involved in clinical trials with Biogen, Novartis and Teva. Guy Laureys did not declare any competing interests. Eugenio Pucci served on scientific advisory boards for Merck, Genzyme and Biogen; he has received honoraria and travel grants from Sanofi Aventis, Novartis, Biogen, Merck, Genzyme and Teva; he has received travel grants and equipment from Associazione Marchigiana Sclerosi Multipla e altre malattie neurologiche. Patrizia Sola served on scientific advisory boards for Biogen Idec and TEVA, she has received funding for travel and speaker honoraria from Biogen Idec, Merck, Teva, Sanofi Genzyme, Novartis and Bayer and research grants for her Institution from Bayer, Biogen, Merck, Novartis, Sanofi, Teva. Diana Ferraro received travel grants and/or speaker honoraria from Merck, TEVA, Novartis, Biogen and Sanofi-Genzyme. Ayse Altintas received personal fees and speaker honoraria from Teva, Merck, Biogen - Gen Pharma, Roche, Novartis, Bayer, Sanofi-Genzyme; received travel and registration grants from Merck, Biogen - Gen Pharma, Roche, Sanofi-Genzyme and Bayer. Aysun Soysal did not declare any competing interests. Francois Grand Maison received honoraria or research funding from Biogen, Genzyme, Novartis, Teva Neurosciences, Mitsubishi and ONO Pharmaceuticals. Guillermo Izquierdo received speaking honoraria from Biogen, Novartis, Sanofi, Merck, Roche, Almirall and Teva. Sara Eichau did not declare any competing interests. Alessandra Lugaresi is a Bayer, Biogen, Genzyme, Merck Advisory Board Member. She received travel grants and honoraria from Roche, Bayer, Biogen, Merck, Novartis, Sanofi, Teva and Fondazione Italiana Sclerosi Multipla (FISM). Her institution received research grants from Bayer, Biogen, Merck, Novartis, Sanofi, Teva and Fondazione Italiana Sclerosi Multipla (FISM). Mark Marriott - nothing to disclose Ilya Kister served on scientific advisory board for Biogen and received research support from Guthy-Jackson Charitable Foundation, National Multiple Sclerosis Society, Biogen,, and Novartis. Helmut Butzkueven served on scientific advisory boards for Biogen, Novartis and Sanofi-Aventis and has received conference travel support from Novartis, Biogen and Sanofi Aventis. He serves on steering committees for trials conducted by Biogen and Novartis, and has received research support from Merck, Novartis and Biogen. Tomas Kalincik served on scientific advisory boards for Roche, Genzyme-Sanofi, Novartis, Merck and Biogen, steering committee for Brain Atrophy Initiative by Genzyme, received conference travel support and/or speaker honoraria from WebMD Global, Novartis, Biogen, Genzyme-Sanofi, Teva, BioCSL and Merck and received research support from Biogen. P98 AQP4-autoimmunity in Japan and Germany - a comparative retrospective study in neuromyelitis optica spectrum disorders A.U. Brandt,2, M. Mori 3, H.G. Zimmermann, N. Borisow, F. Schmidt, A. Uzawa 3, H. Masuda 3, R. Ohtani 3, K. Sugimoto 3, J. Liu 3, K. Ruprecht 4, J. Bellmann-Strobl,5, S. Kuwabara 3, F. Paul,5 NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany, 2 Department of Neurology, University of California Irvine, Irvine, CA, United States, 3 Department of Neurology, Chiba University, Chiba, Japan, 4 Department of Neurology, Charité - Universitätsmedizin Berlin, 5 Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Berlin, Germany Introduction: Neuromyelitis optica spectrums disorders (NMOSD) are autoimmune inflammatory conditions of the central nervous system, which share an overlapping clinical phenotype with optic neuritis and myelitis and may also show brain and brainstem involvement. Disease presentation and prognosis differ substantially between different regions in the world. Contrasting patients in different regions potentially allows investigating disease-relevant factors derived from environment but also genetic background in NMOSD. Objectives: To investigate differences in disease presentation, course and treatment of NMOSD between Germany and Japan. Aims: To recognize modulators of NMOSD in order to better understand disease mechanisms and aid in future treatment development Methods: Retrospective, two center study involving one German center and one Japanese center, both large referral centers for NMOSD. Data was collected from ongoing prospective observational studies in both centers. Patients were included, if they fulfilled the 205 IPND criteria for NMOSD and tested seropositive for aquaporin-4 IgG. Results: A total of 38 patients were included from Berlin (35 female), 54 from Chiba (48 female). Mean disease duration was 8±7 years in Berlin and 3± years in Chiba. Patients in Chiba had a very similar age at disease onset (42±5 years) as patients in Berlin (42.5±5.3years, W=06.5, p= ). Histogram analysis revealed three peaks of onset, which were present in both the Japanese and German cohorts: ) around 20 years of age, 2) around 40 years of age, and 3) around 60 years of age. Patients in Chiba presented more frequently (2 from 54 patients) with brain attacks (area postrema, brainstem or cerebral syndrome) than patients from Berlin (4 from 36 patients, p=0.008). Treatment in Chiba relied mostly on corticosteroids alone or in combination with azathioprine, whereas Berlin patients were treated most often with rituximab or azathioprine. Conclusions: Aquaporin-4-IgG seropositive NMOSD patients show different clinical disease phenotypes in Germany and Japan and are treated differently. Underlying factors investigating the cause of different disease characteristics should be investigated further in a prospective study and might allow insight into genetic or environmental disease modulators. Alexander U. Brandt is cofounder and shareholder of Motognosis and Nocturne. He is named as inventor on several patent applications regarding MS serum biomarkers, OCT image analysis and perceptive visual computing. Masahiro Mori: nothing to disclose. Multiple Sclerosis Journal 208; 24: (S2)

9 538 Poster Session 3, 24 (S2) Hanna G. Zimmermann received a research grant from Novartis and speaking fees from Teva. Nadja Borisow: nothing to disclose. Felix Schmidt: nothing to disclose. Akiyuki Uzawa: nothing to disclose. Hiroki Masuda: nothing to disclose. Ryohei Ohtani: nothing to disclose. Kazuo Sugimoto: nothing to disclose. Jia Liu reports: nothing to disclose. Klemens Ruprecht was supported by the German Ministry of Education and Research (BMBF/KKNMS, Competence Network Multiple Sclerosis) and has received research support from Novartis and Merck Serono as well as speaking fees and travel grants from Guthy Jackson Charitable Foundation, Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/genzyme, Teva Pharmaceuticals, Roche and Novartis. Judith Bellmann-Strobl has received travel grants and speaking fees from Bayer Healthcare, Biogen Idec, Merck Serono, sanofiaventis/genzyme, Teva Pharmaceuticals, and Novartis. Satoshi Kuwabara serves as academic editor for JNNP. Friedemann Paul serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate editor for Neurology Neuroimmunology & Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; and received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA. P982 Early clinical predictors of severe MS C. Malpas, S. Sharmin 2, D. Horakova 3, E.K. Havrdova 3, M. Trojano 4, G. Izquierdo 5, R. Bergamaschi 6, P. Sola 7, D. Ferraro 7, A. Lugaresi 8, A. Prat 9, M. Girard 9, P. Duquette 9, P. Grammond 0, F. Grand Maison, S. Ozakbas 2, V. Van Pesch 3,4, F. Granella 5, R. Hupperts 6, E. Pucci 7, C. Boz 8, G. Iuliano 9, Y. Sidhom 20, R. Gouider 20, D. Spitaleri 2, H. Butzkueven 22,23,24, A. Soysal 25, T. Petersen 26, F. Verheul 27, R. Karabudak 28, R. Turkoglu 29, C. Ramo-Tello 30, M. Terzi 3, E. Cristiano 32, M. Slee 33, P. McCombe 34, R. Macdonell 35, Y. Fragoso 36, J. Olascoaga 37, A. Altintas 38, T. Kalincik 39,40, MSBase Study Group The University of Melbourne CORe, Department of Medicine Royal Melbourne Hospital, 2 Department of Neurology, CORe Unit, Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Melbourne, VIC, Australia, 3 Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University in Prague and General University Hospital, Prague, Czech Republic, 4 Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari, Bari, Italy, 5 Hospital Universitario Virgen Macarena, Sevilla, Spain, 6 IRCCS Mondino Foundation, Pavia, 7 Department of Neuroscience, Azienda Ospedaliera Universitaria, Modena, 8 Department of Biomedical and Neuromotor Science, University of Bologna, Bologna, Italy, 9 Hopital Notre Dame, Montreal, Canada; CHUM and Universite de Montreal, Montreal, 0 CISSS ChaudiËre-Appalache, Levis, Neuro Rive-Sud, Quebec, QC, Canada, 2 Dokuz Eylul University, Konak/Izmir, Turkey, 3 Cliniques Universitaires Saint-Luc, 4 UniversitÈ Catholique de Louvain, Brussels, Belgium, 5 Department of Medicine and Surgery, University of Parma, Parma, Italy, 6 Zuyderland Ziekenhuis, Sittard, The Netherlands, 7 UOC Neurologia, Azienda Sanitaria Unica Regionale Marche - AV3, Macerata, Italy, 8 KTU Medical Faculty Farabi Hospital, Trabzon, Turkey, 9 Ospedali Riuniti di Salerno, Salerno, Italy, 20 Department of Neurology, Razi Hospital, Manouba, Tunisia, 2 Azienda Ospedaliera di Rilievo Nazionale San Giuseppe Moscati, Avellino, Italy, 22 Central Clinical School, Monash University, 23 Department of Neurology, The Alfred Hospital, 24 Department of Neurology, Box Hill Hospital, Monash University, Melbourne, VIC, Australia, 25 Bakirkoy Education and Research Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey, 26 Kommunehospitalet, Arhus C, Denmark, 27 Groene Hart Ziekenhuis, Gouda, The Netherlands, 28 Hacettepe University, Ankara, 29 Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey, 30 Hospital Germans Trias i Pujol, Badalona, Spain, 3 Medical Faculty, 9 Mayis University, Samsun, Turkey, 32 Hospital Italiano, Buenos Aires, Argentina, 33 Flinders University, Adelaide, SA, 34 University of Queensland, Brisbane, QLD, 35 Austin Health, Melbourne, VIC, Australia, 36 Universidade Metropolitana de Santos, Santos, Brazil, 37 Instituto de InvestigaciÛn Sanitaria Biodonostia, Hospital Universitario Donostia, San Sebastian, Spain, 38 Istanbul University Cerrahpasa School of Medicine, Istanbul, Turkey, 39 CORe Unit, Department of Medicine, University of Melbourne, 40 Department of Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia Introduction: The course of disability progression in MS varies across individuals. A subset of patients will rapidly accrue disability relatively early in the course of the disease. This phenotypic profile has been described as severe MS. The early detection of such patients is critical to accurate prognosis, and may inform optimal treatment strategies. A number of possible clinical predictors have been identified, however a consensus is yet to emerge regarding early diagnostic criteria for severe MS. Aims: To evaluate whether clinical factors observed in the first year since symptom onset can identify patients who will develop severe MS. Methods: Patient data were obtained from MSBase. Inclusion criteria were (a) first recorded disability score (EDSS) within 2 months of symptom onset, (b) at least 2 recorded EDSS scores, and (c) at least 0 years of observation time. Patients were classified as having severe MS if they: (a) reached EDSS >= 6 within 0 years of symptom onset, (b) EDSS >=6 was confirmed and sustained over >=6 months, and (c) EDSS >=6 was sustained until the end of follow-up. Clinical predictors included patient variables (sex, age at onset, baseline EDSS, disease duration at first Multiple Sclerosis Journal 208; 24: (S2)