OCT retinal nerve fiber layer thickness differentiates acute optic neuritis from MOG antibody-associated disease and Multiple Sclerosis

Chen, John J.; Sotirchos, Elias S.; Henderson, Amanda D.; Vasileiou, Eleni S; Flanagan, Eoin P.; Bhatti, M. Tariq; Jamali, Sepideh; Eggenberger, Eric; Dinome, Marie; Frohman, Larry; Arnold, Anthony C.; Bonelli, Laura; Seleme, Nicolás; Mejia-Vergara, Alvaro J.; Moss, Heather E.; Padungkiatsagul, Tanyatuth; Stiebel‐Kalish, Hadas; Lotan, Itay; Hellmann, Mark A.; Hodge, Dave; Oertel, Frederike Cosima; Paul, Friedemann; Saidha, Shiv; Calabresi, Peter A.; Pittock, Sean J.

doi:10.1016/j.msard.2022.103525

Cited by 40 publications

(28 citation statements)

References 43 publications

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“…Optical coherence tomography (OCT) is an essential part of the diagnostic evaluation of optic neuritis and this imaging diagnostic test can be useful for confirming an optic neuropathy as well as potentially discriminating between MOGAD, AQP4-IgG+NMOSD and MS (124)(125)(126)(127)(128). In the acute setting of MOGAD optic neuritis, the peripapillary retinal nerve fiber layer (pRNFL) is often significantly thickened, and indeed the median thickness was greater in MOGAD at 164 µm vs. MS at 103 µm in one study (129). Over 3-6 months after optic neuritis, there is progressive thinning of the pRNFL and the macular ganglion cell and inner plexiform layer (mGCIPL); the thinning of the mGCIPL tends to occur earlier and within a few weeks of the attack while the pRNFL thinning takes longer to develop possibly due to the slowly resolving optic nerve head edema (130).…”

Section: Optical Coherence Tomographymentioning

confidence: 99%

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

et al. 2022

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Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is the most recently defined inflammatory demyelinating disease of the central nervous system (CNS). Over the last decade, several studies have helped delineate the characteristic clinical-MRI phenotypes of the disease, allowing distinction from aquaporin-4 (AQP4)-IgG-positive neuromyelitis optica spectrum disorder (AQP4-IgG+NMOSD) and multiple sclerosis (MS). The clinical manifestations of MOGAD are heterogeneous, ranging from isolated optic neuritis or myelitis to multifocal CNS demyelination often in the form of acute disseminated encephalomyelitis (ADEM), or cortical encephalitis. A relapsing course is observed in approximately 50% of patients. Characteristic MRI features have been described that increase the diagnostic suspicion (e.g., perineural optic nerve enhancement, spinal cord H-sign, T2-lesion resolution over time) and help discriminate from MS and AQP4+NMOSD, despite some overlap. The detection of MOG-IgG in the serum (and sometimes CSF) confirms the diagnosis in patients with compatible clinical-MRI phenotypes, but false positive results are occasionally encountered, especially with indiscriminate testing of large unselected populations. The type of cell-based assay used to evaluate for MOG-IgG (fixed vs. live) and antibody end-titer (low vs. high) can influence the likelihood of MOGAD diagnosis. International consensus diagnostic criteria for MOGAD are currently being compiled and will assist in clinical diagnosis and be useful for enrolment in clinical trials. Although randomized controlled trials are lacking, MOGAD acute attacks appear to be very responsive to high dose steroids and plasma exchange may be considered in refractory cases. Attack-prevention treatments also lack class-I data and empiric maintenance treatment is generally reserved for relapsing cases or patients with severe residual disability after the presenting attack. A variety of empiric steroid-sparing immunosuppressants can be considered and may be efficacious based on retrospective or prospective observational studies but prospective randomized placebo-controlled trials are needed to better guide treatment. In summary, this article will review our rapidly evolving understanding of MOGAD diagnosis and management.

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Section: Optical Coherence Tomographymentioning

confidence: 99%

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

et al. 2022

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“…OCT also facilitates the differential diagnosis between ON and myelin oligodendrocyte glycoprotein antibody associated disorder (MOGAD). Thus, while pRFNL thickening is above 5 µm in all patients with MOGAD, in MS, only 54% of cases have this associated change [ 174 ].…”

Section: The “Big” Picture Behind the Ms Triadmentioning

confidence: 99%

Optic Neuritis in Multiple Sclerosis—A Review of Molecular Mechanisms Involved in the Degenerative Process

Ciapă¹,

Șalaru

Stătescu

et al. 2022

CIMB

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Multiple sclerosis is a central nervous system inflammatory demyelinating disease with a wide range of clinical symptoms, ocular involvement being frequently marked by the presence of optic neuritis (ON). The emergence and progression of ON in multiple sclerosis is based on various pathophysiological mechanisms, disease progression being secondary to inflammation, demyelination, or axonal degeneration. Early identification of changes associated with axonal degeneration or further investigation of the molecular processes underlying remyelination are current concerns of researchers in the field in view of the associated therapeutic potential. This article aims to review and summarize the scientific literature related to the main molecular mechanisms involved in defining ON as well as to analyze existing data in the literature on remyelination strategies in ON and their impact on long-term prognosis.

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“…On OCT, optic disc swelling during the acute phase of ON in MOGAD can be evidenced by thickening of the pRNFL. A recent study has investigated the potential of pRNFL, not only for diagnosing acute ON in MOGAD, but also for differentiating MOGAD from MS [36]. The study showed that during acute ON, pRNFL measurements in MOGAD are significantly higher than that in MS (164 µm vs. 103 µm).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…The study showed that during acute ON, pRNFL measurements in MOGAD are significantly higher than that in MS (164 µm vs. 103 µm). Furthermore, with a cutoff of 118 µm, a sensitivity of 74% and a specificity of 82% can be reached to distinguish acute MOGAD-ON from acute MS-ON [36].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Neuro-ophthalmological Presentation of Optic Neuritis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease

Lin

Asseyer

Buenrostro

et al. 2022

Klin Monbl Augenheilkd

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(English) Myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD) is a rare demyelinating autoimmune disorder of the central nervous system. MOGAD frequently manifests with severe, bilateral, and recurrent optic neuritis (ON) episodes and is an important differential diagnosis to multiple sclerosis and aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorders. The clinical manifestations of MOGAD commonly include, besides ON, transverse myelitis, acute disseminated encephalomyelitis, or brainstem encephalitis. In this article, we summarize the current knowledge of the neuro-ophthalmological presentation of MOGAD-ON. We describe epidemiological aspects, including the association with COVID-19 and other infections or vaccinations, clinical presentation, and imaging findings of MOGAD-ON in the acute stage and during remission. Furthermore, we report findings regarding prognosis, treatment response, and changes in ON-unaffected eyes. Specifically, we touch upon findings on visual acuity, visual fields, visual evoked potentials, as well as structural changes assessed with optical coherence tomography. Moreover, we elaborate on how to differentiate MOGAD from its differential diagnoses, including other neuroinflammatory disorders (multiple sclerosis and neuromyelitis optica spectrum disorders), but also idiopathic intracranial hypertension. (Deutsch) Die Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierte Erkrankung (MOGAD) ist eine seltene demyelinisierende Autoimmunerkrankung des zentralen Nervensystems. MOGAD äußert sich häufig durch schwere, bilaterale und wiederkehrende Episoden von Retrobulbärneuritis (optic neuritis, ON) und ist eine wichtige Differenzialdiagnose der Multiplen Sklerose und den Aquaporin-4-IgG-assoziierten Neuromyelitis optica-Spektrum-Erkrankungen. Zu den klinischen Manifestationen von MOGAD gehören neben ON häufig transversale Myelitis, akute disseminierte Enzephalomyelitis oder Hirnstammenzephalitis. In diesem Artikel fassen wir den aktuellen Kenntnisstand der neuro-ophthalmologischen Präsentation von MOGAD-ON zusammen. Wir beschreiben epidemiologische Aspekte, einschließlich des Zusammenhangs mit COVID-19 und anderen Infektionen oder Impfungen, die klinische Präsentation und die bildgebenden Befunde von MOGAD-ON im akuten Stadium und in Remission. Darüber hinaus berichten wir über Befunde zur Prognose, zum Ansprechen auf Therapie, und zu Veränderungen bei nicht betroffenen Augen. Insbesondere diskutieren wir Befunde zu Sehschärfe, Gesichtsfeld, visuell evozierten Potentialen sowie zu strukturellen Veränderungen, die mittels optischer Kohärenztomographie untersucht werden. Darüber hinaus führen wir aus, wie sich MOGAD von anderen neuroinflammatorischen Erkrankungen (Multiple Sklerose und Neuromyelitis-optica-Spektrum-Erkrankungen), aber auch von idiopathischer intrakranieller Hypertonie abgrenzt.

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OCT retinal nerve fiber layer thickness differentiates acute optic neuritis from MOG antibody-associated disease and Multiple Sclerosis

Cited by 40 publications

References 43 publications

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

Optic Neuritis in Multiple Sclerosis—A Review of Molecular Mechanisms Involved in the Degenerative Process

Neuro-ophthalmological Presentation of Optic Neuritis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease

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