Periependymal Abnormalities in Neuromyelitis Optica Spectrum Disorders and Multiple Sclerosis: A Case-Control Study (P07.066)

Abstract

Objective: Our aim is to evaluate differences in lesional pattern between Neuromyelitis optica spectrum disorders (NMOsd) and Multiple Sclerosis (MS). Background NMOsd and MS differ with respect to clinical course, prognosis and treatment, but cannot always be reliably differentiated based on brain MRI. Periependymal abnormalities are reported in both conditions, but there are no studies that examine differences in the lesional pattern of periependymal abnormalities in MS and NMOsd. Design/Methods: We evaluated MR images of 17 NMO IgG seropositive patients with NMOsd and equal number of age, sex and disease duration-matched MS patients. The sequences evaluated were axial T1 postcontrast, axial FLAIR and sagittal FLAIR. A neuroradiologist blinded to the diagnosis evaluated MRIs with respect to periventricular lesional pattern (A=no lesions,B=smooth periventricular, C=smooth+periventricular lesions, D=only periventricular lesions, E=diffuse irregular confluent); ependymal enhancement; genu and splenium ependymal hyperintensity (graded as thin, medium or thick); 9Dawson fingers9-type lesions on FLAIR images. Group comparison was carried out with Fisher9s exact test (two-tailed). Results: Distribution of patterns follows: Pattern A) 8 NMOsd vs none MS (p=0.003); Pattern B) 5 NMOsd vs. 1 MS (p=0.17); Pattern C) 3 NMOsd vs. 5 MS (p=0.69); Pattern D) 1 NMOsd vs. 3 MS (p=0.60); pattern E) 0 with NMOsd vs. 8 MS (p=0.003). Genu hyperintensity on FLAIR was noted in 8/17 NMO (6 thin, 1 medium and 1 thick) and 9/17 MS (4 thin, 2 medium and 3 thick) (p=1). Splenium FLAIR hyperintensity in 5/17 NMO (2 thin, 1 medium and 2 thick) and 8/17 MS (2 thin, 3 medium and 3 thick) (p=0.48). Dawson fingers in 6/17 NMO and in 15/17 MS (p=0.04). Conclusions: Our study suggests that certain periependymal lesional patterns may be useful to discriminate NMOsd from MS. 9Dawson finger9 appear to be more common in MS than in NMOsd. Large prospective studies are necessary to validate our findings. Disclosure: Dr. Raz has nothing to disclose. Dr. Kister has nothing to disclose. Dr. Omari has nothing to disclose. Dr. Herbert has received personal compensation for activities with Biogen Idec, Teva Neuroscience, Serono, Inc., and Bayer Pharmaceuticals Corporation as a consultant.Dr. Herbert has received research support from Teva Neuroscience, Novartis, Biogen Idec, BioMS, and INC Research. Dr. Lui has nothing to disclose. Dr. Loh has nothing to disclose.