MRI differences between MOG antibody disease and AQP4 NMOSD

Salama, Sara; Khan, Majid; Shanechi, Amirali Modir; Lévy, Michaël; Izbudak, Izlem

doi:10.1177/1352458519893093

Cited by 98 publications

(120 citation statements)

References 27 publications

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“…with 12 years' experience). 9 Then, 3DT1 images were lesion-filled and segmented for gray matter. Tract-Based Spatial Statistics (TBSS) were conducted on fractional anisotropy (FA) and mean diffusivity (MD) using DTI images.…”

Section: Image Processingmentioning

confidence: 99%

Brain structural and functional alterations in MOG antibody disease

et al. 2020

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Background: The impact of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) on brain structure and function is unknown. Objectives: The aim of this study was to study the multimodal brain MRI alterations in MOGAD and to investigate their clinical significance. Methods: A total of 17 MOGAD, 20 aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4 + NMOSD), and 28 healthy controls (HC) were prospectively recruited. Voxel-wise gray matter (GM) volume, fractional anisotropy (FA), mean diffusivity (MD), and degree centrality (DC) were compared between groups. Clinical associations and differential diagnosis were determined using partial correlation and stepwise logistic regression. Results: In comparison with HC, MOGAD had GM atrophy in frontal and temporal lobe, insula, thalamus, and hippocampus, and WM fiber disruption in optic radiation and anterior/posterior corona radiata; DC decreased in cerebellum and increased in temporal lobe. Compared to AQP4 + NMOSD, MOGAD presented lower GM volume in postcentral gyrus and decreased DC in cerebellum. Hippocampus/parahippocampus atrophy associated with Expanded Disability Status Scale ( R = −0.55, p = 0.04) and California Verbal Learning Test ( R = 0.62, p = 0.031). The differentiation of MOGAD from AQP4 + NMOSD achieved an accuracy of 95% using FA in splenium of corpus callosum and DC in occipital gyrus. Conclusion: Distinct structural and functional alterations were identified in MOGAD. Hippocampus/parahippocampus atrophy associated with clinical disability and cognitive impairment.

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Section: Image Processingmentioning

confidence: 99%

Brain structural and functional alterations in MOG antibody disease

et al. 2020

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“…Optic nerve involvement is most commonly longitudinally extensive and bilateral, with a propensity for intracranial segments including the optic chiasm (17).…”

Section: Aquaporin-4 Antibody Neuromyelitis Optica Spectrum Disorder mentioning

confidence: 99%

“…There is variable deep gray matter involvement, with a predilection for the thalamus ( 18 ). Cortical involvement with or without meningeal enhancement has been described as a rare but distinct pattern in MOG-AD, and is characterized on imaging as FLAIR hyperintensity and swelling with reduced diffusivity ( 17 , 20 – 22 ).…”

Section: What Are the Typical Radiological Features Of Relapsing Inflmentioning

confidence: 99%

Relapsing Demyelinating Syndromes in Children: A Practical Review of Neuroradiological Mimics

et al. 2020

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Relapsing demyelinating syndromes (RDS) in children encompass a diverse spectrum of entities including multiple sclerosis (MS) acute disseminated encephalomyelitis (ADEM), aquaporin-4 antibody associated neuromyelitis optica spectrum disorder (AQP4-NMOSD) and myelin oligodendrocyte glycoprotein antibody disease (MOG-AD). In addition to these, there are "antibody-negative" demyelinating syndromes which are yet to be fully characterized and defined. The paucity of specific biomarkers and overlap in clinical presentations makes the distinction between these disease entities difficult at initial presentation and, as such, there is a heavy reliance on magnetic resonance imaging (MRI) findings to satisfy the criteria for treatment initiation and optimization. Misdiagnosis is not uncommon and is usually related to the inaccurate application of criteria or failure to identify potential clinical and radiological mimics. It is also notable that there are instances where AQP4 and MOG antibody testing may be falsely negative during initial clinical episodes, further complicating the issue. This article illustrates the typical clinico-radiological phenotypes associated with the known pediatric RDS at presentation and describes the neuroimaging mimics of these using a pattern-based approach in the brain, optic nerves, and spinal cord. Practical guidance on key distinguishing features in the form of clinical and radiological red flags are incorporated. A subsection on clinical mimics with characteristic imaging patterns that assist in establishing alternative diagnoses is also included.

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“…Auch bei dieser Entität finden sich nicht selten große Läsionen in den Hirnhemisphären sowie Läsionen in den Hirnschenkeln und im Hirnstamm. Die Area postrema ist seltener betroffen als bei NMOSD [58].…”

Section: Zerebrale Symptomeunclassified

Aquaporin-4- und Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierte Optikusneuritis: Diagnose und Therapie

Wildemann

Horstmann

Korporal-Kuhnke

et al. 2020

Klin Monbl Augenheilkd

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ZusammenfassungDie Optikusneuritis (ON) ist vielfach die erste Manifestation einer AQP4-Antikörper-vermittelten NMOSD (AQP4: Aquaporin-4, NMOSD: Neuromyelitis-optica-Spektrum-Erkrankung, Engl.: neuromyelitis optica spectrum disorders) oder einer Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierten Enzephalomyelitis (MOG-EM; auch MOG antibody associated disorders, MOGAD). Für beide Erkrankungen wurden in den vergangenen Jahren internationale Diagnosekriterien und Empfehlungen zu Indikation und Methodik der serologischen Testung vorgelegt. Seit Kurzem liegen zudem Ergebnisse aus 4 großen, internationalen Phase-III-Studien zur Behandlung der NMOSD vor. Mit dem den Komplementfaktor C5 blockierenden monoklonalen Antikörper Eculizumab wurde 2019 erstmalig ein Medikament zur Langzeitbehandlung der NMOSD, die bislang vornehmlich Off-Label mit Rituximab, Azathioprin und anderen Immunsuppressiva erfolgt, auf dem europäischen Markt zugelassen. Für die erst vor wenigen Jahren erstbeschriebene MOG-EM stehen inzwischen Daten aus mehreren retrospektiven Studien zur Verfügung, die eine Wirksamkeit von Rituximab und anderen Immunsuppressiva in der Schubprophylaxe auch in dieser Indikation nahelegen. Viele der zur Therapie der MS zugelassenen Medikamente sind entweder unwirksam oder können, wie z. B. Interferon-β, eine Verschlechterung des Krankheitsverlaufes bewirken. Beide Erkrankungen werden im Akutstadium mit hochdosierten Glukokortikoiden und Plasmapherese oder Immunadsorption behandelt. Diese Behandlung sollte möglichst rasch nach Symptombeginn eingeleitet werden. Insbesondere die MOG-EM ist durch eine oft ausgeprägte Steroidabhängigkeit gekennzeichnet, die ein langsames Ausschleichen der Steroidtherapie erfordert, und schließt viele Fälle der bislang meist als „idiopathisch“ klassifizierten „chronic relapsing inflammatory optic neuropathy“ (CRION) ein. Unbehandelt kann sowohl die NMOSD- als auch die MOG-EM-assoziierte ON zu schweren, persistierenden und oft bilateralen Visuseinschränkungen bis hin zur Erblindung führen. Beide Erkrankungen verlaufen meist relapsierend. Neben den Sehnerven sind häufig das Myelon sowie der Hirnstamm und, vor allem bei NMO-Patienten, das Dienzephalon betroffen; supratentorielle Hirnläsionen im kranialen MRT sind, anders als früher gedacht, kein Ausschlusskriterium, sondern häufig. In der vorliegenden Arbeit geben wir einen Überblick über Klinik, Diagnostik und Therapie dieser beiden wichtigen Differenzialdiagnosen der MS-assoziierten und idiopathischen ON.

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MRI differences between MOG antibody disease and AQP4 NMOSD

Cited by 98 publications

References 27 publications

Brain structural and functional alterations in MOG antibody disease

Brain structural and functional alterations in MOG antibody disease

Relapsing Demyelinating Syndromes in Children: A Practical Review of Neuroradiological Mimics

Aquaporin-4- und Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierte Optikusneuritis: Diagnose und Therapie

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