Differential brainstem atrophy patterns in multiple sclerosis and neuromyelitis optica spectrum disorders among Hong Kong Chinese (P2.080)

Objective: To study the brainstem atrophy patterns in multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD) patients. Background: MS and NMOSD present similarly as relapsing attacks of neuroinflammation and can mimic one another. However, it is increasingly recognized that the two disorders differ significantly in natural history, neuroimaging findings, underlying pathologies, treatment response and prognosis. MS is more prevalent in Caucasians while NMOSD is more prevalent in Asians. In previous studies, it was shown that brainstem involvement is common both clinically and radiologically, in both of our local MS and NMOSD patients. We hypothesized that the brainstem volume is significantly reduced in both diseases, and the pattern of volume loss is different between MS and NMOSD as the medulla seems more commonly and severely affected in NMOSD. Design/Methods: Semi-automated segmentation and volumetric measurement of brainstem structures were performed and compared among MS, NMOSD and healthy controls (HC). Clinical symptoms and severity were graded using Expanded Disability Status Scale and Kurtzke Functional System Scores. Associations between the imaging and clinical parameters were assessed by partial correlation and multiple regression analyzes. Results: MR images of 17 MS patients, 13 NMOSD patients and 18 HC were investigated. Normalized whole brainstem, midbrain and pons volumes are significantly smaller in MS subjects compared to HC (−5.2%, p =0.027; −8.3%, p =0.000 and −5.9%, p =0.048 respectively) while only the normalized medulla volume is significantly smaller in NMOSD subjects compared to HC (−8.5% vs HC, p =0.024). Comparing MS and NMOSD subjects, normalized midbrain volume is smaller in MS (−5.0%, p =0.014) while normalized medulla volume is smaller in NMOSD (−8.1%, p =0.032). Smaller whole brainstem, pons and medulla oblongata volumes were associated with greater disability in NMOSD patients. Conclusions: Our findings revealed different patterns of brainstem atrophy between MS and NMOSD patients. This could be related to different underlying pathologies and pathogenetic mechanisms. Disclosure: Dr. Lee has nothing to disclose. Dr. Mak has nothing to disclose. Dr. Chiu has nothing to disclose. Dr. Barkhof has received personal compensation for activities with Bayer Schering Pharma, Biogen Idec, Sanofi Genzyme, Janssen Research, Merck Serono, Novartis, Roche, Synthon BV, and Teva Neuroscience as a consultant or a speaker. Dr. Chan has nothing to disclose.