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Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype.

Pröbstel AK, Rudolf G, Dornmair K, Collongues N, Chanson JB, Sanderson NS, Lindberg RL, Kappos L, de Seze J, Derfuss T - J Neuroinflammation (2015)

Bottom Line: Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48).MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions).Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. anne-katrin.proebstel@usb.ch.

ABSTRACT

Background: Antibodies against myelin oligodendrocyte glycoprotein (MOG) have been identified in a subgroup of pediatric patients with inflammatory demyelinating disease of the central nervous system (CNS) and in some patients with neuromyelitis optica spectrum disorder (NMOSD). The aim of this study was to examine the frequency, clinical features, and long-term disease course of patients with anti-MOG antibodies in a European cohort of NMO/NMOSD.

Findings: Sera from 48 patients with NMO/NMOSD and 48 patients with relapsing-remitting multiple sclerosis (RR-MS) were tested for anti-aquaporin-4 (AQP4) and anti-MOG antibodies with a cell-based assay. Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48). MOG-seropositive patients tended towards younger disease onset with a higher percentage of patients with pediatric (<18 years) disease onset (MOG+, AQP4+, MOG-/AQP4-: 2/4, 3/31, 0/13). MOG-seropositive patients presented more often with positive oligoclonal bands (OCBs) (3/3, 5/29, 1/13) and brain magnetic resonance imaging (MRI) lesions during disease course (2/4, 5/31, 1/13). Notably, the mean time to the second attack affecting a different CNS region was longer in the anti-MOG antibody-positive group (11.3, 3.2, 3.4 years).

Conclusions: MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions). Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

No MeSH data available.


Related in: MedlinePlus

Brain MRI abnormalities in an anti-MOG antibody-positive patient. Axial T2-FLAIR (fluid-attenuated inversion recovery) brain MRI of a MOG-seropositive NMO patient 31 years after disease manifestation with combined optic neuritis and transverse myelitis showed multiple abnormalities fulfilling Barkhof criteria and resembling multiple sclerosis lesions.
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Fig2: Brain MRI abnormalities in an anti-MOG antibody-positive patient. Axial T2-FLAIR (fluid-attenuated inversion recovery) brain MRI of a MOG-seropositive NMO patient 31 years after disease manifestation with combined optic neuritis and transverse myelitis showed multiple abnormalities fulfilling Barkhof criteria and resembling multiple sclerosis lesions.

Mentions: MOG-seropositive patients showed brain lesions during the disease course more frequently (2/4) as compared to AQP4-seropositive (5/31) and seronegative (1/13) patients. Follow-up brain MRI in two MOG-seropositive patients revealed juxtaventricular lesions in one patient, and lesions in the thalamus and corpus callosum in another patient fulfilling the Barkhof criteria (Figure 2). All of the patients had longitudinally extensive transverse myelitis (LETM) in the cervical and/or thoracic spinal cord.Figure 2


Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype.

Pröbstel AK, Rudolf G, Dornmair K, Collongues N, Chanson JB, Sanderson NS, Lindberg RL, Kappos L, de Seze J, Derfuss T - J Neuroinflammation (2015)

Brain MRI abnormalities in an anti-MOG antibody-positive patient. Axial T2-FLAIR (fluid-attenuated inversion recovery) brain MRI of a MOG-seropositive NMO patient 31 years after disease manifestation with combined optic neuritis and transverse myelitis showed multiple abnormalities fulfilling Barkhof criteria and resembling multiple sclerosis lesions.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4359547&req=5

Fig2: Brain MRI abnormalities in an anti-MOG antibody-positive patient. Axial T2-FLAIR (fluid-attenuated inversion recovery) brain MRI of a MOG-seropositive NMO patient 31 years after disease manifestation with combined optic neuritis and transverse myelitis showed multiple abnormalities fulfilling Barkhof criteria and resembling multiple sclerosis lesions.
Mentions: MOG-seropositive patients showed brain lesions during the disease course more frequently (2/4) as compared to AQP4-seropositive (5/31) and seronegative (1/13) patients. Follow-up brain MRI in two MOG-seropositive patients revealed juxtaventricular lesions in one patient, and lesions in the thalamus and corpus callosum in another patient fulfilling the Barkhof criteria (Figure 2). All of the patients had longitudinally extensive transverse myelitis (LETM) in the cervical and/or thoracic spinal cord.Figure 2

Bottom Line: Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48).MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions).Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. anne-katrin.proebstel@usb.ch.

ABSTRACT

Background: Antibodies against myelin oligodendrocyte glycoprotein (MOG) have been identified in a subgroup of pediatric patients with inflammatory demyelinating disease of the central nervous system (CNS) and in some patients with neuromyelitis optica spectrum disorder (NMOSD). The aim of this study was to examine the frequency, clinical features, and long-term disease course of patients with anti-MOG antibodies in a European cohort of NMO/NMOSD.

Findings: Sera from 48 patients with NMO/NMOSD and 48 patients with relapsing-remitting multiple sclerosis (RR-MS) were tested for anti-aquaporin-4 (AQP4) and anti-MOG antibodies with a cell-based assay. Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48). MOG-seropositive patients tended towards younger disease onset with a higher percentage of patients with pediatric (<18 years) disease onset (MOG+, AQP4+, MOG-/AQP4-: 2/4, 3/31, 0/13). MOG-seropositive patients presented more often with positive oligoclonal bands (OCBs) (3/3, 5/29, 1/13) and brain magnetic resonance imaging (MRI) lesions during disease course (2/4, 5/31, 1/13). Notably, the mean time to the second attack affecting a different CNS region was longer in the anti-MOG antibody-positive group (11.3, 3.2, 3.4 years).

Conclusions: MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions). Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

No MeSH data available.


Related in: MedlinePlus