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Figure 2 Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing.

Published byIngvar Månsson Modified over 5 years ago

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Presentation on theme: "Figure 2 Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing."— Presentation transcript:

1 Figure 2 Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing testing with either myelin olidgodendrocyte glycoprotein antibody (MOG-Ab) or oligoclonal blands (OCBs), the additional testing of the respective other is represented by arrows to the respective outcomes. Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing testing with either myelin olidgodendrocyte glycoprotein antibody (MOG-Ab) or oligoclonal blands (OCBs), the additional testing of the respective other is represented by arrows to the respective outcomes. A MOG-Ab–positive test predicted a non–multiple sclerosis (MS) diagnosis, whereas OCB positivity was highly predictive of MS. Eleven of 15 OCB- positive patients developed MS (73%), whereas 11 of 14 OCB-positive and MOG-Abs–negative patients developed MS (79%). The one MOG-Ab–positive and OCB-positive patient did not have MS, and all MOG-Ab–positive and OCB-negative cases had a non-MS course, compared to 91% if only OCB was negative. Of the 14 patients not tested for intrathecal OCBs, 7 patients tested positive for MOG-Ab; 2 patients from the antibody-positive and 2 from the antibody-negative groups had a diagnosis of MS at 1-year follow-up. ADEM = acute disseminated encephalomyelitis; CIS = clinically isolated syndrome; N/D = not done; ON = optic neuritis; TM = transverse myelitis. Yael Hacohen et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e81 © 2015 American Academy of Neurology

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Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein MRI features of patients with MS who had antibodies.

Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein MRI features of patients with MS who had antibodies.
Figure 3 Brain MRI findings in patients with MOG-Ab Extensive brain lesions with large diameter (A and B), posterior reversible encephalopathy–like lesions.

Figure 3 Brain MRI findings in patients with MOG-Ab Extensive brain lesions with large diameter (A and B), posterior reversible encephalopathy–like lesions.
Figure 5 Mononuclear cell subset isolation from spinal cord of mice with experimental autoimmune encephalomeylitis Mononuclear cell subset isolation from.

Figure 5 Mononuclear cell subset isolation from spinal cord of mice with experimental autoimmune encephalomeylitis Mononuclear cell subset isolation from.
Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.

Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.
Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.

Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.
Figure 3 Archetypal MS clinical course depicted over 20 years

Figure 3 Archetypal MS clinical course depicted over 20 years
Figure 2 Disease progression slowed during each round of Treg infusions and correlated with increased Treg suppressive function Disease progression slowed.

Figure 2 Disease progression slowed during each round of Treg infusions and correlated with increased Treg suppressive function Disease progression slowed.
Figure 1 Percent positivity by clinical feature Overall, 6

Figure 1 Percent positivity by clinical feature Overall, 6
Figure 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.

Figure 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.
Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.

Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.
Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum.

Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum.
Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.
Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.

Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.
Figure 3 Multifocal visual-evoked potentials in optic neuritis Figure shows the visual-evoked potentials (VEPs) in 52 sectors of the retina. Multifocal.

Figure 3 Multifocal visual-evoked potentials in optic neuritis Figure shows the visual-evoked potentials (VEPs) in 52 sectors of the retina. Multifocal.
Figure 2 NMDAR-Ab levels, clinical syndromes, and therapy in 8 informative patients with white matter syndromes in association with NMDAR-Ab NMDAR-Ab levels,

Figure 2 NMDAR-Ab levels, clinical syndromes, and therapy in 8 informative patients with white matter syndromes in association with NMDAR-Ab NMDAR-Ab levels,
Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.

Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.
Figure 2 Primary and secondary outcomes reported in multiple sclerosis (MS) disease-modifying therapy (DMT) clinical trials Primary and secondary outcomes.

Figure 2 Primary and secondary outcomes reported in multiple sclerosis (MS) disease-modifying therapy (DMT) clinical trials Primary and secondary outcomes.
Figure 1 Biomarkers associated with different clinical phases in MS

Figure 1 Biomarkers associated with different clinical phases in MS
Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.

Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.
Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

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