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Human Serum Anti-aquaporin-4 Immunoglobulin G Detection by Cell-based Assay
Published on: April 5, 2019
Brain structural alterations in MOG antibody diseases: a comparative study with AQP4 seropositive NMOSD and MS
Yunyun Duan1,2, Zhizheng Zhuo1,2, Haiqing Li3,4
1Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Background:
Brain structural alterations and their clinical significance of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) have not been determined.
Methods:
We recruited 35 MOGAD, 38 aquaporin 4 antibody positive neuromyelitis optica spectrum diseases (AQP4+ NMOSD), 37 multiple sclerosis (MS) and 60 healthy controls (HC) who underwent multimodal brain MRI from two centres. Brain lesions, volumes of the whole brain parenchyma, cortical and subcortical grey matter (GM), brainstem, cerebellum and cerebral white matter (WM) and diffusion measures (fractional anisotropy, FA and mean diffusivity, MD) were compared among the groups. Associations between the MRI measurements and the clinical variables were assessed by partial correlations. Logistic regression was performed to differentiate MOGAD from AQP4+ NMOSD and MS.
Results:
In MOGAD, 19 (54%) patients had lesions on MRI, with cortical/juxtacortical (68%) as the most common location. MOGAD and MS showed lower cortical and subcortical GM volumes than HC, while AQP4+ NMOSD only demonstrated a decreased cortical GM volume. MS demonstrated a lower cerebellar volume, a lower FA and an increased MD than MOGAD and HC. The subcortical GM volume was negatively correlated with Expanded Disability Status Scale in MOGAD (R=-0.51; p=0.004). A combination of MRI and clinical measures could achieve an accuracy of 85% and 93% for the classification of MOGAD versus AQP4+ NMOSD and MOGAD versus MS, respectively.
Conclusion:
MOGAD demonstrated cortical and subcortical atrophy without severe WM rarefaction. The subcortical GM volume correlated with clinical disability and a combination of MRI and clinical measures could separate MOGAD from AQP4+ NMOSD and MS.
Insights
Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) shows brain atrophy, particularly in grey matter, correlating with disability. MRI and clinical data effectively distinguish MOGAD from similar conditions.
Area of Science:
- Neuroimmunology
- Neuroimaging
- Neurology
Background:
- Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is an inflammatory demyelinating condition.
- Brain structural changes and their clinical relevance in MOGAD are not well-established.
Purpose of the Study:
- To investigate brain structural alterations in MOGAD using multimodal MRI.
- To determine the clinical significance of these alterations and their utility in differentiating MOGAD from AQP4+ NMOSD and MS.
Main Methods:
- Multimodal brain MRI was performed on 35 MOGAD patients, 38 AQP4+ NMOSD, 37 MS patients, and 60 healthy controls.
- Analysis included brain lesions, parenchymal volumes (grey and white matter), and diffusion tensor imaging (FA, MD).
- Associations between MRI metrics and clinical disability (EDSS) were assessed; logistic regression was used for classification.
Main Results:
- MOGAD patients exhibited cortical and subcortical grey matter atrophy, unlike AQP4+ NMOSD and MS.
- Subcortical grey matter volume reduction in MOGAD correlated negatively with Expanded Disability Status Scale (EDSS).
- Combined MRI and clinical data achieved high accuracy (85-93%) in classifying MOGAD versus AQP4+ NMOSD and MS.
Conclusions:
- MOGAD is characterized by cortical and subcortical grey matter atrophy without significant white matter rarefaction.
- MRI-derived subcortical grey matter volume is a potential biomarker for clinical disability in MOGAD.
- Integrated MRI and clinical assessment aids in differentiating MOGAD from AQP4+ NMOSD and MS.
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