Autoantigen-specific CD4+ T cells acquire an exhausted phenotype and persist in human antigen-specific autoimmune diseases.

Pro-inflammatory autoantigen-specific CD4+ T helper (auto-Th) cells are central orchestrators of autoimmune diseases (AIDs). We aimed to characterize these cells in human AIDs with defined autoantigens by combining human leukocyte antigen (HLA)-tetramer-based and activation-based multidimensional ex vivo analyses. In aquaporin4-antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD) patients, auto-Th cells expressed CD154, but proliferative capacity and pro-inflammatory cytokines were strongly reduced. Instead, exhaustion-associated co-inhibitory receptors were expressed together with FOXP3, the canonical regulatory T cell (Treg) transcription factor. Auto-Th cells responded in vitro to checkpoint inhibition and provided potent B cell help. Cells with the same exhaustion-like (ThEx) phenotype were identified in soluble liver antigen (SLA)-antibody-autoimmune hepatitis and BP180-antibody-positive bullous pemphigoid, AIDs of the liver and skin, respectively. While originally described in cancer and chronic infection, our data point to T cell exhaustion as a common mechanism of adaptation to chronic (self-)stimulation across AID types and link exhausted CD4+ T cells to humoral autoimmune responses, with implications for therapeutic targeting.

Investigation of health care use and a possible prodrome before the first attack in NMOSD and MOGAD.

BACKGROUND: Prodromal phases are well recognized in many inflammatory and neurodegenerative diseases, including multiple sclerosis. We evaluated the possibility of a prodrome in aquaporin-4 antibody positive (AQP4+) neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD) using health administrative data. METHODS: We investigated individuals with AQP4 + NMOSD and MOGAD, confirmed by medical chart review, in Ontario, Canada. Each NMOSD and MOGAD participant was matched 1:5 to general population controls by sex, birth year, immigrant status, and region. Total outpatient visits and hospitalizations were compared in the 5 years preceding the incident attack in multivariable negative binomial models. RESULTS: We identified 96 people with AQP4 + NMOSD, matched to 479 controls, and 61 people with MOGAD, matched to 303 controls. In the 5 years preceding the incident attack, health care use was elevated for outpatient visits and hospitalizations for the NMOSD cohort (adjusted rate ratio (aRR): 1.47; 95% confidence interval (CI): 1.25-1.73; aRR: 1.67; 95% CI: 1.19-2.36, respectively) but not for MOGAD. Rate ratios steadily increased in NMOSD for outpatient visits in the 2 years preceding the incident attack. CONCLUSION: Our findings support a prodromal phase preceding clinical onset of AQP4 + NMOSD. Earlier recognition and management of NMOSD patients may be possible.

Impact of autoantibodies against myelin oligodendrocyte glycoprotein in paediatric acquired demyelinating disease: Intellectual functioning and academic performance.

Paediatric acquired demyelinating syndromes (pADS) attack white matter pathways in the brain during an important period of development. Affected children can experience poor functional outcomes, including deficits in specific cognitive domains. Understanding risk factors for poor outcome will guide clinical management of these children. One clinical phenotype which may differentially impact cognitive outcomes is the presence of autoantibodies to myelin oligodendrocyte glycoprotein (MOG). Preliminary research has suggested that cognitive difficulties exist in paediatric patients who test positive for MOG antibodies or MOGAD (Myelin Oligodendrocyte Glycoprotein Associated Disease) however, they experience a less severe profile compared to seronegative counterparts. The current study assesses children diagnosed with pADS who tested positive or negative for MOG-ab using standardised assessments of both intellectual functioning and academic ability. The results show that a subset of MOGAD patients experience clinically significant sequalae in intellectual functioning and academic ability. The neuropsychological profile also differed between children with and without MOG-ab positivity, with seronegative patients more likely to show a clinically relevant difficulties at the individual patient level. Whilst no differences existed at the group-level; the current study demonstrates the relative additional risk of intellectual/academic difficulty associated with MOG-ab seronegativity. This research further supports the growing perspective that MOG-positivity confers a more favourable neuropsychological outlook than is the case for their seronegative counterparts. This broadening consensus offers reassurance for clinicians, families, and patients.

Isolated Intracranial Hypertensions as Onset of Myelin Oligodendrocyte Glycoprotein Antibody Disease.

Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is characterized by multiple phenotypic conditions such as acute disseminated encephalomyelitis, optic neuritis, and myelitis. MOGAD's spectrum is expanding, with potential symptoms of increased intracranial pressure that are similar to idiopathic intracranial hypertension (IIH). We report a boy with new-onset continuous headache and a brain MRI at onset suggesting idiopathic intracranial hypertension (IIH). The patient showed resistance to treatment with acetazolamide and, after one month, developed optic neuritis in the left eye. Laboratory tests documented positive MOG antibodies (anti-MOG) in the serum. The final diagnosis was MOGAD, with the initial symptoms resembling IIH.

Successful Maintenance Therapy with Intravenous Immunoglobulin to Reduce Relapse Attacks and Steroid Dose in a Patient with Refractory Myelin Oligodendrocyte Glycoprotein Antibody-positive Optic Neuritis.

A 25-year-old Japanese man developed visual disturbance with eye pain and was diagnosed with optic neuritis associated with anti-myelin oligodendrocyte glycoprotein antibodies. His symptoms improved temporarily after steroid therapy but chronically relapsed many times after tapering the steroid dose. He became highly steroid-dependent and was referred to our department for reconsideration of the treatment strategy. Maintenance intravenous immunoglobulin (IVIg) therapy successfully decreased the annual recurrence rate from 1.15 to 0.27 times/year and the maintenance dose of oral prednisolone from 35 to 5 mg/day. Maintenance IVIg therapy is a promising option for preventing disease relapse in such cases.

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Complicated by Pachymeningitis: A Case Report.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare autoimmune disorder that primarily affects the central nervous system (CNS). We present a unique case of MOGAD complicated by pachymeningitis, which is characterized by inflammation of the dura mater. The clinical presentation included vertigo, nausea, and vomiting. A diagnostic workup confirmed MOGAD complicated by pachymeningitis. This case underscores the diverse clinical manifestations of MOGAD and highlights the challenges in diagnosis and management, particularly when complicated by rare manifestations like pachymeningitis.

Study of seasonality of attacks in MOG antibody-associated disease.

BACKGROUND: Seasonal variation in attacks of acute disseminated encephalomyelitis (ADEM1) is reported in some studies. Myelin oligodendrocyte glycoprotein (MOG) antibodies are found in up to 50 % of ADEM cases. Despite this, there has been no adequately powered study of seasonality in MOG antibody-associated disease (MOGAD). We sought to determine whether there was an effect of season on incidence of total attacks and onset attacks of MOGAD. METHODS: We searched the large national Oxford-based NMO Service database to identify attacks of MOGAD occurring between 2010 and 2021. Month of each attack was extracted and Edwards' test of seasonal variation was applied to determine whether there was a seasonal effect on total attacks and onset attacks. RESULTS: Neither incidence of total attacks nor incidence of onset attacks varied significantly by month. CONCLUSION: There is no evidence of seasonal fluctuations in the incidence of MOGAD attacks in the UK.

The positive predictive value of MOG-IgG testing based on the 2023 diagnostic criteria for MOGAD.

Background: Myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD) is a relatively new disease entity in the field of demyelinating disorders. Its first diagnostic criteria have recently been published. Objectives: We evaluated the positive predictive value (PPV) for MOG-IgG testing and report the clinical and radiologic features with respect to the recently published criteria. Methods: A retrospective study was conducted at three centers in Dallas, Texas. Patients with positive MOG-IgG testing on cell-based assays at any time were included. Positive cases were reviewed by at least two neuroimmunologists for fulfillment of the criteria. Results: We included 235 patients. The PPV of seropositivity at any time was 78.3% overall, 52.6% for low titer, and 90.1% for high titer. Children had a higher PPV than adults (93.9% versus 67.2%). Positive predictive value was 6.3% in those without a core clinical demyelinating attack. Children more often have the typical imaging features of MOGAD in optic neuritis than adults. Conclusions: We report a PPV of 78.3% for MOG-IgG testing using the 2023 MOGAD diagnostic criteria. Children had higher PPV and frequency of supporting imaging features. Careful consideration is necessary when assigning patients with no core demyelinating event and low titers a MOGAD diagnosis.

The pharmacological management of myelin oligodendrocyte glycoprotein-immunoglobulin G associated disease (MOGAD): an update of the literature.

INTRODUCTION: Myelin oligodendrocyte glycoprotein-immunoglobulin G associated disease (MOGAD) is a clinical entity distinct from multiple sclerosis and aquaporin-4 (AQP4+)-IgG-positive neuromyelitis optica spectrum disorder. There is a lack of evidence regarding the efficacy and safety of current treatments used for MOGAD. AREAS COVERED: In this article, the authors review the currently available literature on the pharmacological management of MOGAD. This article is based on an extensive search for articles including meta-analyses, clinical trials, systematic reviews, observational studies, case series and case reports. EXPERT OPINION: Intravenous high-dose methylprednisolone is the most common therapy for acute attack with patients having a good treatment response. In cases with poor recovery, intravenous immunoglobulins (IVIG) or plasma-exchange proved to be effective. Maintenance therapies include mycophenolate mofetil, azathioprine, IVIG, oral corticosteroids, rituximab, and interleukin-6 receptor (IL6-R) antagonists. Rituximab is the most used drug while IL6-R antagonists emerged as an effective option for people not responding to current treatments. Larger prospective studies with longer follow-ups are needed to confirm whether the blockage of the IL6-R is an effective and safe option. Since there is no evidence of major safety issues related to the new available therapies, the authors believe that waiting for disease activity to consider a possible treatment change, is an unwise approach.

Rituximab Therapy for Immune-Mediated Neurological Diseases: Our Experience at a Tertiary Care Centre.

INTRODUCTION: Rituximab (RTX) is a monoclonal anti-CD20 chimeric antibody that inhibits B cell activity. However, it is an appealing substitute for traditional immunomodulatory drugs as a swiftly acting, targeted therapy with mounting evidence of efficacy and tolerance in numerous neuroinflammatory conditions. We discuss the scientific evidence for the use of RTX in neurological illnesses, as well as the dose, safety, and other practical elements of prescription. AIM: This study aims to assess and correlate the effects of RTX on immune-mediated neurological disorders. OBJECTIVES: The primary objective of this study is to determine the outcomes in patients treated with RTX for the following conditions: myasthenia gravis (MG), autoimmune encephalitis, multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody disease (MOGAD), immune-mediated peripheral neuropathy, and inflammatory muscle disease. The secondary objective is to assess adverse drug reactions in patients treated with RTX. METHODS: This is a prospective observational study conducted at a tertiary care centre. The data were analyzed for the period from May 2022 to May 2024. Approval was obtained from the institutional ethics committee before commencing the study, and written informed consent was obtained from all patients. RESULTS AND CONCLUSIONS: A total of 56 patients were included in the study. The distribution of patients according to diseases is as follows: MG (17), MS (11), NMOSD (10), MOGAD (7), immune-mediated peripheral neuropathy (6), autoimmune encephalitis (3), and inflammatory muscle disease (2). However, one patient was lost to follow-up in the autoimmune encephalitis group. All patients experienced improvements in symptoms, and no relapse episodes have been reported except for one patient who had a relapse in the inflammatory muscle disease group. During the infusion process, some adverse drug reactions, such as chills and rigors, were observed, and two patients experienced major side effects, such as Pott's disease and cryptogenic organizing pneumonia. Nevertheless, overall, rituximab shows promise as an off-label immunosuppressive treatment for the aforementioned neurological immune-mediated diseases.

Long term outcome in non-multiple sclerosis paediatric acquired demyelinating syndromes.

OBJECTIVES: We aimed to study the risks of relapse and long term disability in children with non-MS acquired demyelinating syndromes (ADS). METHODS: In this prospective, multi-centre study, from the 14 UK pediatric neurology centres, children (<16 years) experiencing a first episode of ADS were recruited from 2010 to 2014. Case report forms were collected prospectively. RESULTS: A total of 269 children were recruited and followed up for a median of 7.2 years. Median age at onset was 9y (IQR 9.5-14.5, 126 females). At last follow-up, 46 (18 %) had MS, 4 AQP4-Ab NMOSD and 206 (80 %) had other ADS, of which 27 (13 %) relapsed. Relapsing MOGAD was the diagnosis in 12/27, 6 were seronegative and 9 did not have antibodies tested. Frequency of relapse differed according to first presentation in non-MS ADS, being least likely in transverse myelitis (p = 0.025). In the non-MS group, MOG-Ab was predictive of relapse (HR = 8.42; p < 0.001) occurring 8 times as often decreasing over time. Long-term difficulties did not differ between children with monophasic vs relapsing diseases. CONCLUSION: The risk of relapse in non-MS ADS depends on initial diagnosis, and MOG-Ab positivity. Long-term difficulties are observed regardless of relapses and are determined by presenting phenotype.

Diagnostic criteria for optic neuritis in the acute and subacute phase: clinical uses and limitations.

BACKGROUND: A recent international consensus panel proposed diagnostic criteria for optic neuritis and a new classification. We aimed to investigate the clinical relevance of these diagnostic criteria and classification, in a cohort of patients hospitalized for a suspected diagnosis of optic neuritis. METHODS: We included all patients hospitalized between 2017 and 2022 in our tertiary center for (sub)acute loss of visual acuity suggestive of optic neuritis. Clinical and paraclinical criteria obtained within the first 3 months of symptoms were collected, as well as the final diagnosis which could be optic neuritis or non-optic neuritis. We constructed a contingency table comparing diagnoses based on physician experience to those based on the recently proposed criteria. The subtypes of optic neuritis based on the new classification were compared to subtypes based on the clinician experience. RESULTS: Two hundred fifty-seven patients were included in this study. Prevalence of optic neuritis in our cohort was 88.3%. Sensitivity and specificity of a correct diagnosis using the new criteria were, respectively, 99.5% and 86.7%. The proposed diagnostic criteria overdiagnosed four patients with optic neuritis and missed the diagnosis in one patient. According to the recent classification, idiopathic optic neuritis and clinical isolated syndrome were reclassified mainly as single isolated optic neuritis. CONCLUSION: In our specific cohort of patients hospitalized for acute and subacute optic neuropathy highly suspect of optic neuritis, we found that recently proposed diagnostic criteria and classification of optic neuritis are relevant for our clinical practice. Our interpretation of clinical requirement for definite and possible optic neuritis diagnosis might explain our excellent sensitivity and our high percentage of definite optic neuritis, relative to previous publications. The moderate specificity (86.7%) underlines the importance to include all contextual data in consideration for the diagnosis. The simplification of subgroups is useful, but our study highlights the complexity to find the adequate subgroup for seronegative NMOSD.

Assessment of international MOGAD diagnostic criteria in patients with overlapping MOG-associated disease and multiple sclerosis phenotypes.

BACKGROUND: The clinical spectrum and diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) has evolved in the setting of an optimized anti-MOG-IgG cell-based assay and expert consensus. The McDonald criteria for MS have been revised multiple times to improve the accuracy and specificity of diagnosis on a framework based on clinical presentation, MRI findings, and CSF results. While the uses of MS and MOGAD diagnostic criteria are helpful for typical cases, such utility for patients with overlapping clinical, laboratorial, and imaging features is unknown, posing diagnostic and management uncertainties. OBJECTIVES: To report a multicenter cohort of patients with overlapping phenotypic features of MOGAD and MS and evaluate the application of new MOGAD diagnostic criteria. METHODS: A collaborative retrospective cohort study was performed to identify patients with both positive serum anti-MOG-IgG and fulfillment of the MS revised 2017 McDonald criteria. Clinical and radiographic features of patients fulfilling inclusion criteria were reviewed longitudinally, including relapses, repeated MRI, and MOG-IgG testing in detail to allow the panel of expert opinion to assign to each case. The International MOGAD Panel proposed criteria were applied at onset and last follow-up to each case and compared to the expert author diagnosis assignment based on presentation, clinical and imaging features, and response to treatment. RESULTS: Ten of 225 (4%) MOG-IgG seropositive cases met study inclusion criteria [seven of 10 were female; age at initial event: eight adults (mean age 26.8 years), two adolescents (mean age 14.5 years)]. AQP4-IgG was negative for all. Apart from serum titers of MOG-IgG, distinguishing clinical and radiographic features [i.e., clinical severity of the initial demyelinating event, radiographic features (optic nerve/spine/brain), and presence/absence of lesion normalization on serial scans] led to consensus of three separate classifications differing by degrees of shared features of MOGAD and MS. Patients were classified by expert panel into (1) Classic MOGAD even with MS-like, well-defined brain lesions, when severe events and most T2 lesions normalized (n = 5; MOG-IgG titers 1:100, 1:20, 1:160, 1:40, 1:200); (2) Classic RRMS included cases thought to have likely false positive or clinically irrelevant MOG-IgG, due to mild clinical events and no radiographic normalization of well-defined MS-like lesions (n = 3; MOG titers 1:20, 1:100, 1:40); (3) MOGAD and MS overlapping phenotype was defined by those with a combination of mild and severe clinical events, partial T2 lesion normalization, both well- and ill-defined lesions (n = 2; MOG titers 1:20, 1:100). The application of the International MOGAD Panel criteria categorized five patients (50%) in agreement with expert assignment. One additional patient was classified in agreement to assignment when MOGAD criteria were applied after serial MOG-IgG titers testing. DISCUSSION: While the International MOGAD Panel diagnostic criteria have helped with accuracy for the diagnosis of this condition, in a group of patients seropositive for MOG-IgG with overlapping clinical and imaging features of RRMS criteria review may lead to increased accuracy. Serial serologies, repeated imaging, close attention to clinical course, and response to therapy are possible variables to consider for further refinement of MOGAD diagnostic criteria.

Spinal movement disorders in NMOSD, MOGAD, and idiopathic transverse myelitis: a prospective observational study.

BACKGROUND: Retrospective studies suggest that spinal movement disorders, especially tonic spasms, are prevalent in NMOSD. However, there have been no prospective studies evaluating spinal movement disorders in NMOSD, MOGAD, and idiopathic transverse myelitis (ITM). METHODS: Patients referred to a tertiary neuroimmunology clinic for spinal cord demyelination (excluding MS) were evaluated. All patients answered a movement disorders survey and underwent a movement disorder-focused exam. Movement disorders were compared among patients with NMOSD with and without AQP4-IgG, MOGAD, and ITM. Patients with and without involuntary movements were also compared to identify predictors of spinal movement disorders. RESULTS: Sixty-three patients were evaluated from 2017 to 2021 (71% females, median age 49 years, range 18-72 years, median disease duration 12 months, range 1-408). Of the total, 49% had ITM, 21% had NMOSD without AQP4-IgG, 19% had NMOSD with AQP4-IgG, and 11% had MOGAD. Movement disorders were present in 73% of the total patients and were most frequent in NMOSD with AQP4-IgG (92%) and least frequent in MOGAD (57%). The most frequent spinal movement disorders were tonic spasms (57%), focal dystonia (25%), spinal tremor (16%), spontaneous clonus (9.5%), secondary restless limb syndrome (9.5%), and spinal myoclonus (8%). Multivariate analysis showed that longitudinally extensive myelitis and AQP4-IgG are independent risk factors for the development of spinal movement disorders, while MOG-IgG and African American race were associated with a lower risk of developing these movement disorders. CONCLUSIONS: Spinal movement disorders are highly prevalent in non-MS demyelinating disorders of the spinal cord. Prevalence rates exceed those reported in MS and retrospective NMOSD studies.

Extremely Longitudinally Extensive Transverse Myelitis in a Patient With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.

Longitudinally extensive myelitis with 15 or more vertebrae in length is extremely rare, with limited evidence regarding clinical features and therapeutic response. We report a case of a 29-year-old male patient with extremely longitudinally extensive myelitis ultimately diagnosed as myelin oligodendrocyte glycoprotein-associated disease (MOGAD). The patient presented with an acute onset of meningismus, limb weakness, sensory disturbance below the C5 level, ataxia, and urinary retention. T2-weighted imaging on MRI showed an extremely longitudinally extensive spinal cord lesion ranging from C2 to the medullary conus, together with a left pontine lesion. Positive anti-myelin oligodendrocyte glycoprotein antibodies were serologically detected, which led to the diagnosis of MOGAD. Intravenous methylprednisolone followed by 1 mg/kg oral prednisolone with taper resulted in complete symptomatic and radiological resolution. The striking complete resolution despite the symptomatic and radiological severity observed in this case has been described in a few previously reported MOGAD cases. Extremely longitudinally extensive myelitis with excellent therapeutic response may be a characteristic presentation of MOGAD.

Unravelling the Complexity of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare autoimmune disorder characterized by recurrent episodes of demyelination affecting the central nervous system. The following case report showcases a thorough analysis of a 21-year-old female patient presenting with MOGAD, outlining her clinical presentation, diagnostic workup, treatment protocol, and long-term management outcomes. Through a multidisciplinary approach, we aim to augment the understanding of this complex neurological entity and steer optimal therapeutic interventions.

A burning encephalitis: Fluid-attenuated inversion recovery-hyperintense lesions in Anti-myelin oligodendrocyte glycoprotein-associated encephalitis with seizures in anti-myelin oligodendrocyte glycoprotein-associated encephalitis with seizures-A case report and review of the literature.

FLAMES, or fluid-attenuated inversion recovery-hyperintense lesions in anti-myelin oligodendrocyte glycoprotein (anti-myelin oligodendrocyte glycoprotein)-associated encephalitis with seizures, represents a rarely documented syndrome characterized by ambiguous features. Positioned within the spectrum of inflammatory demyelinating diseases of the central nervous system, it is regarded as a distinct subset of myelin oligodendrocyte glycoprotein antibody-associated disease, the latest classification in this domain. Myelin oligodendrocyte glycoprotein antibody-associated disease exhibits a diverse clinical spectrum, spanning from solitary optic neuritis or myelitis to multifocal central nervous system demyelination, manifesting as acute disseminated encephalomyelitis, or cortical encephalitis accompanied by seizures, delineating the fluid-attenuated inversion recovery-hyperintense lesions in anti-myelin oligodendrocyte glycoprotein-associated encephalitis with seizures syndrome. We present a compelling case study of a 30-year-old individual with a history of recurrent seizures initially diagnosed with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes. However, the disease's progression more closely resembled self-resolving cerebral cortical encephalitis linked with myelin oligodendrocyte glycoprotein antibodies. In addition, we undertake a systematic review of literature cases to explore the diagnostic significance of magnetic resonance angiography, fluid-attenuated inversion recovery, and specialized markers such as diffusion-weighted imaging and perfusion in discerning fluid-attenuated inversion recovery-hyperintense lesions in anti-myelin oligodendrocyte glycoprotein-associated encephalitis with seizures syndrome and elucidating its distinctive characteristics.

Deciphering the conformational dynamics of Myelin Oligodendrocyte glycoprotein in the myelin sheath.

Myelin Oligodendrocyte Glycoprotein (MOG) is a transmembrane protein in the myelin sheath. It acts as an auto-antigen under certain unknown conditions causing demyelination, thus resulting in Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease (MOGAD). The significance of glycosylation in the conformational dynamics of the extracellular region (EC1) of the MOG were evident from the previous computational studies. Here, in this study, we performed the molecular dynamics simulation of the entire human MOG in the myelin sheath for 100 ns using the NAMD program. The results indicated that the EC1 and cytoplasmic region (CP) dominate the conformational rigidity of the protein, and enhance its interaction with lipids. This in turn helps in maintaining the myelin integrity in the presence of glycan. The transmembrane regions have reduced interaction with lipids in the glycosylated system. Moreover, the C-terminal extracellular region 2 (EC2) behaves exactly opposite to that of EC1 in the glycan presence. This may be attributed to the glycosylation site in the EC1 region. Hence, not only the region EC1 (having 3 crucial epitopes) but even the CP region were important for understanding the proper function of MOG in the glycan presence.Communicated by Ramaswamy H. Sarma.

Diagnostic Criteria for Multiple Sclerosis, Neuromyelitis Optica Spectrum Disorders, and Myelin Oligodendrocyte Glycoprotein-immunoglobulin G-associated Disease.

The diagnostic workup of multiple sclerosis (MS) has evolved considerably. The 2017 revision of the McDonald criteria shows high sensitivity and accuracy in predicting clinically definite MS in patients with a typical clinically isolated syndrome and allows an earlier MS diagnosis. Neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein-immunoglobulin G-associated disease (MOGAD) are recognized as separate conditions from MS, with specific diagnostic criteria. New MR imaging markers may improve diagnostic specificity for these conditions, thus reducing the risk of misdiagnosis. This study summarizes the most recent updates regarding the application of MR imaging for the diagnosis of MS, NMOSD, and MOGAD.