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Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
Brain atrophy in NMOSD and MOGAD: a meta-analysis of volumetric and DTI biomarkers
Ariel Rechtman1,2, Omri Zveik1,2, Adi Vaknin-Dembinsky1,2
1Department of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Background:
Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are demyelinating diseases of the central nervous system. Brain atrophy is well recognized in multiple sclerosis; however, approximately 50% of studies report no significant difference in overall brain volumes when comparing NMOSD patients with healthy controls (HCs). To quantitatively assess differences in brain volume and white matter integrity in NMOSD and MOGAD patients compared to HCs through a meta-analysis.
Methods:
A systematic literature search of English articles in PubMed was performed through December 2024. We analyzed sixty-one studies that met the inclusion criteria, providing volumetric MRI or diffusion tensor imaging data with HC comparisons. Outcomes of interest included brain volume, and DTI parameters. Standardized mean differences were computed, and random-effects meta-analyses were performed to account for study heterogeneity.
Results:
The studies included data from 1,786 NMOSD patients, 376 MOGAD patients, and 1,936 HCs. NMOSD patients exhibited significantly lower total brain, gray, and white matter volumes compared to HCs. Notable atrophy was observed in several regions including the accumbens, brainstem, caudate, cerebellum, hippocampus, putamen, and thalamus. MOGAD patients have reduced brain volume compared to HCs. Furthermore, comparisons demonstrated that NMOSD patients had significantly lower brain and gray matter volumes than MOGAD patients.
Conclusion:
Our meta-analysis confirms substantial brain atrophy in NMOSD patients compared to both HCs and individuals with MOGAD, indicating a more pronounced neurodegenerative impact than previously recognized. These findings carry important clinical implications by enhancing our understanding of disease-specific imaging biomarkers.
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