Author Of 2 Presentations
P0708 - Differential MRI biomarkers between MOGAD, AQP4-NMOSD and RRMS: a MAGNIMS multicenter study (ID 1335)
Abstract
Background
Clinical and imaging features of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) may overlap with those of aquaporin 4-neuromyelitis optica spectrum disorder (AQP4-NMOSD) and relapsing remitting multiple sclerosis (RRMS). There is an unmet need for MRI biomarkers which reflect biological mechanisms involved in MOGAD and can help in the differential diagnosis.
Objectives
We aim to identify imaging features able to differentiate between non-acute MOG-antibody disease, AQP4-NMOSD and RRMS.
Methods
In this ongoing retrospective, cross-sectional MAGNIMS study, we analyzed data collected from 8 centers. All subjects (n=352) had brain and cervical cord 3T MRI. Quantification of MRI biomarkers included brain white matter lesions (WMLs), cortical lesions (CL), brain parenchymal fraction (BPF), white matter fraction (WMF), cortical and deep grey matter fractions (GMF) and cross-sectional cervical cord area (CSA) at C1-C2. Linear regression models were used to compare MRI measures between groups, corrected for age, sex, and centre. Statistical significance was considered when p was <0.05.
Results
91 patients with MOGAD (50F, mean age: 41yrs [±15]), 85 with AQP4-NMOSD (68F, 49yrs [±14]), 90 with RRMS (56F, 41yrs [±11]) and 87 healthy controls (HCs) (54F, 36yrs [±11.6]) were collected. The most common phenotypes at onset were optic neuritis and transverse myelitis in MOGAD (93%) and AQP4-NMOSD (87%). WMLs were detected in 57% MOGAD, 79% AQP4-NMOSD, all RRMS (100%) patients, and in 15% HCs. The mean lesion load and number of lesions were higher in RRMS than both MOGAD (p=0.007, p<0.001) and AQP4-NMOSD (p=0.001, p<0.001). At least one CL was seen in 8% patients with MOGAD (total n=8), 10% patients with AQP4-NMOSD (n=7), and in 69% patients with RRMS (n=150). All patient groups showed lower BPF than HCs, with lower WMF in MOGAD and RRMS than HCs (all p<0.01). Between groups, deep GMF was lower in RRMS than MOGAD (p<0.001) and AQP4-NMOSD (p=0.001). CSA was reduced in all disease groups when compared to HCs (all p<0.01) and lower in AQP4-NMOSD than RRMS (p=0.01).
Conclusions
This ongoing study indicates that MOGAD and AQP4-NMOSD share similar MRI features, and no specific MRI biomarker can distinguish between them. Patients with AQP4-NMOSD showed greater spinal cord atrophy than RRMS, and RRMS patients had a higher number of cortical lesions, and greater deep GM atrophy than AQP4-NMOSD and MOGAD. The next step is to investigate whether lesion distribution differs between the two antibody-mediated disease.
P0945 - Brain choroid plexus volume in Multiple Sclerosis versus Neuromyelitis Optica Spectrum Disease (ID 1476)
Abstract
Background
Neuromyelitis optica spectrum disease (NMOSD) and multiple sclerosis (MS) have a different pathophysiology. Accumulating evidence suggests that the choroid plexus plays a pivotal role in the pathogenesis of MS. However, MRI data comparing the choroid plexus volume between MS and NMOSD are scarce.
Objectives
To compare the choroid plexus volume in MS vs. NMOSD in vivo using high-resolution 3D MRI data. Migraine patients and healthy individuals served as control groups.
Methods
We included 95 MS patients [45% secondary progressive (SP); mean age 51.0±11.5 years; disease duration 20.8±10.4 years, 62% female; median Expanded Disability Status Scale (EDSS) 4.0], 43 NMOSD patients [28/43 anti-aquaporin 4 antibody positive; 11/43 anti-myelin oligodendrocyte glycoprotein antibody positive; 87% female; mean age 50.0±13.8 years; disease duration 6.8±7.3 years, median EDSS 3.0], 38 migraine patients [mean age 39±13 years, 79% female; 15/38 migraine with aura] and 65 healthy individuals [HCs, mean age 41±17 years, 48% female]. The choroid plexus of the lateral ventricles and T2-weighted (T2w) white matter lesions (WMLs) were segmented fully automated on T1-weighted (T1w) magnetization-prepared rapid gradient echo (MPRAGE) images and fluid attenuated inversion recovery sequences (FLAIR, voxel size of both sequences 1x1x1 mm3), respectively, using a supervised deep learning algorithm (multi-dimensional gated recurrent units). Total intracranial volume (TIV) and lateral ventricle volumes were assessed fully automated using Freesurfer. All outputs were reviewed and manually corrected (if necessary) using 3D-Slicer by trained raters who were blinded to the clinical information. Group differences were analyzed using multivariable generalized linear models (GLMs) adjusted for age, gender, TIV and lateral ventricle volume. Cohens’ d was used to calculate the standardized difference between the respective groups. Given p-values are adjusted for multiple comparisons (Bonferroni).
Results
Mean choroid plexus was larger in MS compared to NMOSD (1907±455 vs. 1467±408 µl; p<0.001, d=0.86), HCs (1663±424 µl; p=0.007, d=1.17) and migraine (1527±366 µl; p=0.02, d=0.72). There was no statistical difference in the choroid plexus volume between NMOSD, migraine and HCs. The choroid plexus was marginally larger in RRMS than SPMS (1959±482 vs. 1875±476 µl; p=0.28; d=0.17) and in untreated MS patients compared to MS patients on disease modifying therapy (2111±382 vs. 1876±459 µl; p=0.36). However, these differences did not reach statistical significance after correction for multiple comparisons. There was no association between the choroid plexus volume and total T2w WML volume in MS.
Conclusions
Patients with MS have larger choroid plexus than HCs, migraine and NMOSD patients. Further studies are warranted to investigate the respective roles of the choroid plexus in the pathogenesis of MS and NMOSD.
Presenter Of 1 Presentation
P0945 - Brain choroid plexus volume in Multiple Sclerosis versus Neuromyelitis Optica Spectrum Disease (ID 1476)
Abstract
Background
Neuromyelitis optica spectrum disease (NMOSD) and multiple sclerosis (MS) have a different pathophysiology. Accumulating evidence suggests that the choroid plexus plays a pivotal role in the pathogenesis of MS. However, MRI data comparing the choroid plexus volume between MS and NMOSD are scarce.
Objectives
To compare the choroid plexus volume in MS vs. NMOSD in vivo using high-resolution 3D MRI data. Migraine patients and healthy individuals served as control groups.
Methods
We included 95 MS patients [45% secondary progressive (SP); mean age 51.0±11.5 years; disease duration 20.8±10.4 years, 62% female; median Expanded Disability Status Scale (EDSS) 4.0], 43 NMOSD patients [28/43 anti-aquaporin 4 antibody positive; 11/43 anti-myelin oligodendrocyte glycoprotein antibody positive; 87% female; mean age 50.0±13.8 years; disease duration 6.8±7.3 years, median EDSS 3.0], 38 migraine patients [mean age 39±13 years, 79% female; 15/38 migraine with aura] and 65 healthy individuals [HCs, mean age 41±17 years, 48% female]. The choroid plexus of the lateral ventricles and T2-weighted (T2w) white matter lesions (WMLs) were segmented fully automated on T1-weighted (T1w) magnetization-prepared rapid gradient echo (MPRAGE) images and fluid attenuated inversion recovery sequences (FLAIR, voxel size of both sequences 1x1x1 mm3), respectively, using a supervised deep learning algorithm (multi-dimensional gated recurrent units). Total intracranial volume (TIV) and lateral ventricle volumes were assessed fully automated using Freesurfer. All outputs were reviewed and manually corrected (if necessary) using 3D-Slicer by trained raters who were blinded to the clinical information. Group differences were analyzed using multivariable generalized linear models (GLMs) adjusted for age, gender, TIV and lateral ventricle volume. Cohens’ d was used to calculate the standardized difference between the respective groups. Given p-values are adjusted for multiple comparisons (Bonferroni).
Results
Mean choroid plexus was larger in MS compared to NMOSD (1907±455 vs. 1467±408 µl; p<0.001, d=0.86), HCs (1663±424 µl; p=0.007, d=1.17) and migraine (1527±366 µl; p=0.02, d=0.72). There was no statistical difference in the choroid plexus volume between NMOSD, migraine and HCs. The choroid plexus was marginally larger in RRMS than SPMS (1959±482 vs. 1875±476 µl; p=0.28; d=0.17) and in untreated MS patients compared to MS patients on disease modifying therapy (2111±382 vs. 1876±459 µl; p=0.36). However, these differences did not reach statistical significance after correction for multiple comparisons. There was no association between the choroid plexus volume and total T2w WML volume in MS.
Conclusions
Patients with MS have larger choroid plexus than HCs, migraine and NMOSD patients. Further studies are warranted to investigate the respective roles of the choroid plexus in the pathogenesis of MS and NMOSD.