Abstract
In multiple sclerosis, magnetic resonance imaging (MRI) new silent lesions contribute to the diagnostic criteria, have prognostic value, and are used in treatment monitoring; but in aquaporin-4 antibody neuromyelitis optica spectrum disorder (AQP4-NMOSD), they are rare between attacks. Their frequency and their association with relapses in adults with myelin oligodendrocyte glycoprotein antibody disease (MOGAD) are still unclear. To examine the frequency and characteristics of MRI new silent lesions in MOGAD and AQP4-NMOSD. This retrospective cohort study analyzed clinical and MRI data of 404 patients with MOGAD or AQP4-NMOSD between February 1, 1994, and April 1, 2021; data were prospectively recorded on the Oxford NMOSD clinical database under follow-up. The study was conducted at the Oxford National Referral Center for NMOSD. Participants included patients with MOGAD and AQP4-NMOSD who were treated within the Oxford National NMO Specialist Service. Seropositive MOGAD and AQP4-NMOSD patients who had MRIs during attacks and the remission phase of their disease. Frequency of new silent lesions detected by either attack MRIs (during the acute clinical event) or remission MRIs (performed outside of a relapse and at least 3 months from last attack). Median time to next relapse in the presence of definite (reference MRI performed at least 4 weeks from last attack onset), probable (reference MRI performed during last attack), and no new silent lesions on remission MRIs was also evaluated. One hundred eighty-two MOGAD patients and 222 AQP4-NMOSD patients were included. Of the MOGAD patients, 113 (62%) were female, median age at onset was 28 years (range, 2-72), and median follow-up was 52 months (range, 11-253). Of the AQP4-NMOSD patients, 189 (85%) were female, median age at onset was 43 years (range, 2-82), and median follow-up was 87.5 months (range, 11-260). MOGAD patients had 296 attack MRI sessions and 167 remission MRI sessions. New attack silent lesions were found in 97 of 296 (33%) attack MRI sessions, whereas new remission silent lesions were found in 5 of 167 (3.0%) remission MRI sessions. Median time from remission scan to the next relapse in the presence of definite or probable new remission lesions was 2 months (IQR, 1-6), whereas in the absence of any new remission lesions it was 73 months (IQR, 20-104; hazard ratio, 23.86; 95% CI, 7.51-75.79; P < .001). AQP4-NMOSD patients had 470 attack MRI sessions and 269 remission MRI sessions. New attack silent lesions were detected in 88 of 470 (18.7%) attack MRI sessions, whereas new remission silent lesions were found in 7 of 269 (2.6%) remission MRI sessions. Median time from remission scan to the next relapse in the presence of definite or probable new remission lesions was 5 months (IQR, 2-6), whereas in the absence of any new remission lesions it was 85 months (IQR, 29-167; hazard ratio, 21.23; 95% CI, 8.05-53.65; P < .001). In contrast to that reported in multiple sclerosis, results of this cohort study suggest that new remission silent lesions are rare on follow-up scans in MOGAD and AQP4-NMOSD and appear to indicate a high risk of imminent relapse.
Highlights
Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a relatively newly described demyelinating disease of the central nervous system, without predominance by sex or racial category.[1]
Median time from magnetic resonance imaging to relapse was shorter in the presence of new magnetic resonance imaging remission lesions (2 and 5 months) than in their absence (73 and 85 months) in both myelin oligodendrocyte glycoprotein antibody disease (MOGAD) and AQP4-NMOSD cohorts, respectively. Meaning These findings suggest that new silent lesions are rare in MOGAD and AQP4-NMOSD during remission and appear to precede imminent relapses
In contrast to that reported in multiple sclerosis, results of this cohort study suggest that new remission silent lesions are rare on follow-up scans in MOGAD and AQP4-NMOSD and appear to indicate a high risk of imminent relapse
Summary
Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a relatively newly described demyelinating disease of the central nervous system, without predominance by sex or racial category.[1]. It is characterized by serum MOG IgG1 autoantibodies whose pathogenetic role has not been proven yet. Its clinical phenotype is broad, most frequently presenting with unilateral or bilateral optic neuritis, and transverse myelitis, brain and brainstem attacks, and a rarer cortical syndrome with seizure.[1,2]. 50% of patients have a relapsing course,[2] this appears less in children.[3]. AQP4-NMOSD may present with severe optic neuritis, longitudinally extensive transverse myelitis, and area postrema, brainstem, diencephalic, and cerebral syndromes.[1,4]. AQP4-NMOSD may present with severe optic neuritis, longitudinally extensive transverse myelitis, and area postrema, brainstem, diencephalic, and cerebral syndromes.[1,4] The prompt distinction between MOGAD, AQP4-NMOSD, and multiple sclerosis (MS) may be challenging for clinicians because the diseases share some clinical and magnetic resonance imaging (MRI) characteristics, which may hamper the treatment of patients
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