A longitudinal analysis of brain volume changes in myelin oligodendrocyte glycoprotein antibody-associated disease.

BACKGROUND AND PURPOSE: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a relapsing demyelinating condition. There are several cross-sectional studies showing evidence of brain atrophy in people with MOGAD (pwMOGAD), but longitudinal brain volumetric assessment is still an unmet need. Current recommendations do not include monitoring with MRI and assume distinct attacks. Evidence of ongoing axon loss will have diagnostic and therapeutic implications. In this study, we assessed brain volume changes in pwMOGAD over a mean follow-up period of 2 years and compared this to changes in people with multiple sclerosis (pwMS). METHODS: This is a retrospective single-center study over a 7-year period from 2014 to 2021. MRI brain scans at the time of diagnosis and follow-up in remission were collected from 14 Caucasian pwMOGAD, confirmed by serum myelin oligodendrocyte glycoprotein immunoglobulin G antibody presence, detected by live cell-based assays. Total brain volume (TBV), white matter (WM), gray matter (GM), and demyelinating lesion volumes were assessed automatically using the Statistical Parametric Mapping and FMRIB automated segmentation tools. MRI brain scans at diagnosis and follow-up on remission were collected from 32-matched pwMS for comparison. Statistical analysis was done using analysis of variance. RESULTS: There is evidence of TBV loss, affecting particularly GM, over an approximately 2-year follow-up period in pwMOGAD (p < .05), comparable to pwMS. WM and lesion volume change over the same period were not statistically significant (p > .1). CONCLUSION: We found evidence of loss of GM and TBV over time  in pwMOGAD, similar to pwMS, although the WM and lesion volumes were unchanged.

Gray matter, white matter and cerebrospinal fluid abnormalities in Parkinson's disease: A voxel-based morphometry study.

Background: Parkinson's disease (PD) is a chronic neurodegenerative disorder characterized by bradykinesia, tremor, and rigidity among other symptoms. With a 70% cumulative prevalence of dementia in PD, cognitive impairment and neuropsychiatric symptoms are frequent. Materials and methods: In this study, we looked at anatomical brain differences between groups of patients and controls. A total of 138 people with PD were compared to 64 age-matched healthy people using voxel-based morphometry (VBM). VBM is a fully automated technique that allows for the identification of regional differences in gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF) allowing for an objective comparison of brains of different groups of people. We used statistical parametric mapping for image processing and statistical analysis. Results: In comparison to controls, PD patients had lower GM volumes in the left middle cingulate, left lingual gyrus, right calcarine and left fusiform gyrus, also PD patients indicated lower WM volumes in the right middle cingulate, left lingual gyrus, right calcarine, and left inferior occipital gyrus. Moreover, PD patients group demonstrated higher CSF in the left caudate compared to the controls. Conclusion: Physical fragility and cognitive impairments in PD may be detected more easily if anatomical abnormalities to the cingulate gyrus, occipital lobe and the level of CSF in the caudate are identified. Thus, our findings shed light on the role of the brain in PD and may aid in a better understanding of the events that occur in PD patients.