Contributions
Abstract: P787
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Introduction: Neuromyelitis optica spectrum disorders (NMOSD) consist of clinically similar, but pathogenically distinct autoimmune disorders of the CNS. Pathogenic antibodies against aquaporin-4 (AQP4-IgG) can be detected in ~70% of NMOSD patients. Antibodies against myelin-oligodendrocyte-glycoprotein (MOG-IgG) are detected in a proportion of NMOSD patients seronegative for AQP4-IgG. Spinal cord involvement and subsequent cord atrophy is common in NMOSD. Spinal cord lesion characteristics and spinal cord atrophy (SCA) patterns have not been compared between both NMOSD subgroups.
Objectives: To investigate spinal cord lesion prevalence and SCA in AQP4-IgG+ and MOG-IgG+ NMOSD.
Aims:
1) Comparison of spinal cord lesion prevalence, distribution, and length.
2) Comparison of SCA measured with mean upper cervical cord area (MUCCA) and total cord volume (TCV).
Methods: MRI of 40 AQP4-IgG+ and 15 MOG-IgG+ NMOSD patients, in non-acute myelitis stage (median = 18 weeks, range = 3 - 89 weeks), were analysed. Lesion characteristics (prevalence, location, length measured as vertebral segments) were recorded and MUCCA and TCV were measured by semi-automatic segmentation (JIM7.0 Cord Finder).
Results: In chronic stage NMOSD, prevalence of spinal cord lesions was 65% in AQP4-IgG+ and 33% in MOG-IgG+ patients (Chi-square = 3.2 5, p= 0.071). Similarly, the proportion of patients with cervical and thoracic lesions was higher in the AQP4-IgG+ group than in the MOG-IgG+ group (cervical: AQP4-IgG+ 50%, MOG-IgG+ 25%, Chi-square = 2.90, p= 0.089; thoracic and lumbar: AQP4-IgG+ 35%, MOG-IgG+ 15%, Chi-square = 1.54). Mean lesion length was not different between groups (total mean ± SD: AQP4-IgG+ = 3.08 ± 1.6; MOG-IgG+ = 4.10 ± 3.6, p= 0.571). SCA measures were not different between both subgroups as measured with MUCCA (AQP4-IgG+ 69.2 ± 7.6 mm2, MOG-IgG+ 71.3 ± 12.3 mm2, p= 0.549) or TCV (AQP4-IgG+ 17697.3 ± 2226.5 mm3, MOG-IgG+ 18534.8 ± 4538.5 mm3, p = 0.548).
Conclusions: Overall, AQP4-IgG+ and MOG-IgG+ NMOSD subtypes did not differ significantly in spinal cord MRI lesion characteristics (prevalence, distribution, or length). However, a trend towards a higher prevalence of spinal cord lesions was found overall and in the cervical cord of AQP4-IgG+ compared to MOG-IgG+ patients. SCA seems to occur in both subtypes to a similar extent. Whether spinal cord MRI can reflect the different neuroinflammatory mechanisms in NMOSD would have to be investigated in a larger cohort.
Disclosure: CC, MS, and NB have nothing to disclose.
KR 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, all unrelated to this work.
JBS received speaking fees and travel grants from Bayer Healthcare, Sanofi-aventis/Genzyme, Biogen and Teva Pharmaceuticals, unrelated to the present scientific work. AUB 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. FP reports research grants and speaker honoraria from Bayer, Teva, Genzyme, Merck, Novartis, MedImmune and is member of the steering committee of the OCTIMS study (Novartis), all unrelated to this work.
Abstract: P787
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Introduction: Neuromyelitis optica spectrum disorders (NMOSD) consist of clinically similar, but pathogenically distinct autoimmune disorders of the CNS. Pathogenic antibodies against aquaporin-4 (AQP4-IgG) can be detected in ~70% of NMOSD patients. Antibodies against myelin-oligodendrocyte-glycoprotein (MOG-IgG) are detected in a proportion of NMOSD patients seronegative for AQP4-IgG. Spinal cord involvement and subsequent cord atrophy is common in NMOSD. Spinal cord lesion characteristics and spinal cord atrophy (SCA) patterns have not been compared between both NMOSD subgroups.
Objectives: To investigate spinal cord lesion prevalence and SCA in AQP4-IgG+ and MOG-IgG+ NMOSD.
Aims:
1) Comparison of spinal cord lesion prevalence, distribution, and length.
2) Comparison of SCA measured with mean upper cervical cord area (MUCCA) and total cord volume (TCV).
Methods: MRI of 40 AQP4-IgG+ and 15 MOG-IgG+ NMOSD patients, in non-acute myelitis stage (median = 18 weeks, range = 3 - 89 weeks), were analysed. Lesion characteristics (prevalence, location, length measured as vertebral segments) were recorded and MUCCA and TCV were measured by semi-automatic segmentation (JIM7.0 Cord Finder).
Results: In chronic stage NMOSD, prevalence of spinal cord lesions was 65% in AQP4-IgG+ and 33% in MOG-IgG+ patients (Chi-square = 3.2 5, p= 0.071). Similarly, the proportion of patients with cervical and thoracic lesions was higher in the AQP4-IgG+ group than in the MOG-IgG+ group (cervical: AQP4-IgG+ 50%, MOG-IgG+ 25%, Chi-square = 2.90, p= 0.089; thoracic and lumbar: AQP4-IgG+ 35%, MOG-IgG+ 15%, Chi-square = 1.54). Mean lesion length was not different between groups (total mean ± SD: AQP4-IgG+ = 3.08 ± 1.6; MOG-IgG+ = 4.10 ± 3.6, p= 0.571). SCA measures were not different between both subgroups as measured with MUCCA (AQP4-IgG+ 69.2 ± 7.6 mm2, MOG-IgG+ 71.3 ± 12.3 mm2, p= 0.549) or TCV (AQP4-IgG+ 17697.3 ± 2226.5 mm3, MOG-IgG+ 18534.8 ± 4538.5 mm3, p = 0.548).
Conclusions: Overall, AQP4-IgG+ and MOG-IgG+ NMOSD subtypes did not differ significantly in spinal cord MRI lesion characteristics (prevalence, distribution, or length). However, a trend towards a higher prevalence of spinal cord lesions was found overall and in the cervical cord of AQP4-IgG+ compared to MOG-IgG+ patients. SCA seems to occur in both subtypes to a similar extent. Whether spinal cord MRI can reflect the different neuroinflammatory mechanisms in NMOSD would have to be investigated in a larger cohort.
Disclosure: CC, MS, and NB have nothing to disclose.
KR 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, all unrelated to this work.
JBS received speaking fees and travel grants from Bayer Healthcare, Sanofi-aventis/Genzyme, Biogen and Teva Pharmaceuticals, unrelated to the present scientific work. AUB 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. FP reports research grants and speaker honoraria from Bayer, Teva, Genzyme, Merck, Novartis, MedImmune and is member of the steering committee of the OCTIMS study (Novartis), all unrelated to this work.