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

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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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Copyright © 2010 American Medical Association. All rights reserved.

Figure EDSS, FS scores, and Modified MSFC scores

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 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)

Figure 2. Infliximab treatment effect

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 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 2. Change in total PSPRS score from baseline to each study visit for all participants Change in total PSPRS score from baseline to each study visit.

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 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum.

Figure 1 Patient flow diagram

Figure 3 Example of venous narrowing

Figure 3 JCV index changes in JCV+ patients

Figure 1 ERG peak time delay at baseline

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

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

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

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 1 Characteristics of the German National MS Cohort

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 Example of venous narrowing

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

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 4 Aquaporin-4 immunoglobulin G (AQP4-IgG) index in time-matched paired serum-CSF specimens: 3 attack/preattack pairs and 7 bridge/remission pairs.

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

Figure 2 Individual EDSS scores

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. Antibodies to MOG in a proportion of adult patients with MS

Figure Correlation between the Kurtzke Expanded Disability Status Scale and the relative expression of hsa-miR-337-3p Correlation between the Kurtzke Expanded.

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 2 Spectrum of abnormal CT scanning of patients with bacterial meningitis presenting with a minimal Glasgow Coma Scale score Spectrum of abnormal.

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 2 Clinical and autoantibody status of 2 CNTN1 or NF155+ patients not receiving rituximab Despite corticosteroids and methotrexate treatment, patient.

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 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. Heat map of antibody binding patterns to glycolipid targets in Guillain-Barré syndrome (GBS) cases and controls Heat map of antibody binding.

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 Clinical course and overview of the treatment protocols♦ = neuroradiologic evidence of new disease activity; ★ = CD19+ reconstitution. Clinical.

Figure 3 Fluorescence-activated cell sorting (FACS) employing cells singly transfected with M1-AQP4 or M23-AQP4 or cotransfected with both AQP4 isoforms.

Figure 2 Kaplan-Meier survival curves for the fingolimod cohort In each graph, bottom tertile: solid line; middle tertile: long dashed line; top tertile:

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

Figure 2 Overview of apheresis therapies

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

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

Kaplan-Meier estimation of diabetes-related survival curves in patients grouped according to increased 24-h proteinuria (A), the presence of preexisting.

Figure 6 Multiple target epitopes exist in the N-terminal domains of Caspr2 (A) Multidomain deletion constructs of Caspr2 were generated to determine which.

Figure 1 Cell gating and binding curve from FACS experiments and M23 and M1 antibody titers during relapses and remission Cell gating for fluorescence-activated.

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

Figure 3 C5B3 blocked MAC formation

Figure 4 Patient 3 MRI evolution over time

Figure 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 4 C5B3 decreased NMOSD mouse model lesions in vivo

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 1 EDSS score (A), T2LV (B) and T1LV (C) courses in patients who experienced WNS after FTY withdrawal EDSS score (A), T2LV (B) and T1LV (C) courses.

Figure 2 Correlations of subcortical gray matter SUVRs with the EDSS score, T25FW, and BPV in MS Correlations of subcortical gray matter SUVRs with the.

Figure (A and B) Effect of canakinumab in muscle strength measured in each patient as mean bilateral GF (A) and TMS (B) during the mean study period of.

Presentation transcript:

Figure 1 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability (A) Months from onset to develop NMO according to the onset attack type: patients with optic neuritis, and those with longitudinally extensive transverse myelitis (LETM) aged <30 years, converted earlier than patients with LETM aged >30 years or with brainstem syndrome (p < 0.001). (B) Months from onset to use a cane (Expanded Disability Status Scale [EDSS] score 6.0) by age at disease onset: older patients were significantly more likely than younger patients to develop motor disability over time (p < 0.001). (C) Years from onset to use a cane by antibody status in NMO patients: at 5 years after onset, 26% of aquaporin-4 immunoglobulin G (AQP4-IgG)–positive patients, 19% of double-seronegative patients, and none of the myelin oligodendrocyte glycoprotein (MOG)–IgG-positive patients were expected to need a cane to walk (EDSS score 6.0) (p = 0.089). EDSS score 6.0 = intermittent or unilateral assistance required to walk 100 meters with or without resting. ON = optic neuritis. Maria Sepúlveda et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e225 © 2016 American Academy of Neurology