Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.

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Teaching NeuroImages Neurology Resident and Fellow Section © 2013 American Academy of Neurology A 51-year-old woman with triplegia and blindness.

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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 1 Initial brain imaging (A–C) patient 1; (D–F) patient 2; (G–I) patient 3; (J–L) patient 4; and (M) patient 2. Initial brain imaging (A–C) patient.

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 4 Neuromyelitis optica spectrum disorder brain lesions

Figure 1 Brain MRI findings in the present case

Figure 4. Brain imaging and neuropathologic demonstration of Epstein-Barr virus (EBV) encephalitis in patient PT-10 Brain imaging and neuropathologic demonstration.

Figure 2 Evolution of MRI abnormalities in faciobrachial dystonic seizures Axial fluid- attenuated inversion recovery (FLAIR)-weighted images from patient.

Figure 1 Percent positivity by clinical feature Overall, 6

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 3 JCV index changes in JCV+ patients

Figure 1 MRI head in faciobrachial dystonic seizures (A) Axial fluid-attenuated inversion recovery image from patient 3 in table 2 shows T2-weighted hyperintensity.

Figure 1 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody.

Figure 3. MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis.

Figure Longitudinal MRI study data demonstrating evolution of central pontine myelinolysis(A, B) Axial T2-weighted MRI of the brain from January 9, 2014,

Figure MRI and leptomeningeal biopsy findings in Vogt-Koyanagi-Harada syndrome involving the cerebellopontine angle(A) Coronal and (B) axial gadolinium-enhanced.

Figure 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.

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

Figure 1 Neuropathologic examination of brain areas with normal MRI appearance and with gadolinium enhancement (patient 1)‏ Neuropathologic examination.

Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.

Figure MRIs and histopathology of the biopsy specimens

Figure 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)

Figure 2 Exemplary MRI of a patient with contrast enhancement on postcontrast FLAIR MRI of a 54-year-old patient with viral meningitis caused by varicella-zoster.

Figure 2 7T MRI can differentiate between early PML and MS lesions Two different patterns of brain lesions were observed using 7T MRI: ring-enhancing lesions.

Figure 2 DTI values between the hepatitis C group and controls(A) DTI FA values, (B) DTI diffusion values. *Statistically significant at FDR-adjusted p.

Figure 1 Time points of blood sampling

Figure 2 Concordance of results for commercial cell-based assay (CBA) and fluorescence-activated cell sorting (FACS) assays, FACS titers, and disease activity.

Figure 2 JCV index JCV index (A) Fifty samples of natalizumab-treated patients with multiple sclerosis were assessed twice for their anti-JCV antibody.

Figure 2 Representative brain MRIs from patients with neuromyelitis optica Lesions are localized at sites of high aquaporin-4 expression (white dots).

Figure 1 MRI of inflammatory myelitis before and after treatment

Figure 1 Radiologic features of human myelin oligodendrocyte glycoprotein immunoglobulin G–positive patients with cranial nerve involvement Radiologic.

Figure 1 Illustration of white matter– and lesion-associated regions of interest (ROIs)‏ Illustration of white matter– and lesion-associated regions of.

Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.

Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,

Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.

Figure 2 Pathologic diagnosis of CAA-related vascular inflammation Hematoxylin & eosin staining (A) revealed focal intramural inflammation including lymphocytes,

Figure 1 JCV serostatus JCV serostatus (A) Serostatus of 1,921 natalizumab-treated patients with multiple sclerosis, with JCV− patients shown in black.

Figure 5 Pairwise correlations between selected patient-reported outcomes and performance tests in patients with MS (A) The number of pairwise correlations.

Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.

Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.

Figure Clinical and radiologic course(A) The T2 contrast-enhanced sequence on day 3 shows an extensive central cord lesion extending from C2 to T7. Clinical.

Figure 1 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to.

Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases Distribution of MOG IgG antibody in pediatric demyelinating diseases (A)

Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.

Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.

Figure 1 Relapse and rituximab historyThe figure shows rituximab (RTX) treatment history as well as relapse history for 100 days prior to the first RTX.

Figure 3 Clinical and MRI outcomes by quartiles of increasing CD56bright natural killer (NK) cell countsAll data are mean and upper 95% confidence interval.

Figure 1 Patterns of study retention The proportion of individuals actively participating in the study is displayed over the course of the study. Patterns.

Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.

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.

Figure 1 MRI findings over time

Figure 1 Representative spinal cord MRIs from patients with neuromyelitis optica Longitudinally extensive transverse myelitis of the cervical (A) and cervicothoracic.

Figure 2 Correlation between wGRS and age at onset The figure shows the correlation between weighted genetic risk score (wGRS) and age at onset in all.

Figure 2. Detection of KIR4.1 autoantibodies using LIPS

Figure 1 Full-length MOG cell-based assay using a serum dilution of 1:160 as a cutoff for positivity (red line in both plots)(A) Myelin olidgodendrocyte.

Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.

Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.

Figure 2 Assessment of fluctuation in fatigue scores using environmental data The relationship between fatigue (as measured by the Modified Fatigue Impact.

Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.

Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521

Ingo Kleiter et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e504

Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453

Figure 2 MRIs (cases 2 and 3)‏

Figure MRI demonstrating cerebellar encephalitis, longitudinally extensive transverse myelitis, and pathology of seminoma(A) Parasagittal T1 postcontrast.

Figure 2 Time from incident ADS event to MS diagnosis

Figure 2 Patient 1 MRI evolution over time

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 2. Percentage of CD16− monocytes in the blood is reduced during disease progression Percentage of CD16− monocytes in the blood is reduced during.

Figure 4 Illustration of a practice effect by examining longitudinal performance measures in patients with MS and cohabitants (A) Response time for each.

Figure 1 MRIs MRIs (A and B) Axial FLAIR images of the brain demonstrate multifocal parenchymal lesions including the right hippocampus, right midbrain,

Presentation transcript:

Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that were not confined to the optic nerve but extended to the soft tissues around the optic nerves (perineural enhancement) (A–D), which were not observed in the neuromyelitis optica group (E and F) or the multiple sclerosis group (G and H). Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that were not confined to the optic nerve but extended to the soft tissues around the optic nerves (perineural enhancement) (A–D), which were not observed in the neuromyelitis optica group (E and F) or the multiple sclerosis group (G and H). All MRIs were T1-weighted with gadolinium enhancement. Red lines in A, C, E, and G highlight the level where the transverse images in B, D, F, and H are taken. Sung-Min Kim et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e163 © 2015 American Academy of Neurology