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

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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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Neuromyelitis Optica: Looking at the Brain for Clues

Figure 2 ERG amplitude reduction in the follow-up study

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 1 Box plot of the venous diameter in lesions

Figure 4 Neuromyelitis optica spectrum disorder brain lesions

Figure MRI of anti-MOG-IgG–associated myelitis

Figure 2 Spinal cord lesions

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

Figure 1 Coronal MRI images showing the evolution of white matter abnormality and atrophy of patient 1 Coronal MRI images showing the evolution of white.

Figure 1 Percent positivity by clinical feature Overall, 6

Figure Facial photograph during headache attack and brain and upper cervical cord MRI Facial photograph during headache attack and brain and upper cervical.

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 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.

Figure Immune checkpoint inhibitor–induced encephalitis before and after treatment with natalizumab Immune checkpoint inhibitor–induced encephalitis before.

Figure Radiographic and histopathologic findings (A) Brain MRI at presentation shows multiple areas of T2 hyperintensity in the mesial temporal lobes,

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 1 MRI, pathology, and EEG findings(A) Axial fluid-attenuated inversion recovery (FLAIR) MRI sequences of the brain showing right frontal and parietal.

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 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 MRI and histology of demyelinating lesion(A) Symmetric T2 hyperintensity in the midbrain with relative sparing of cerebral peduncles. MRI and histology.

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

Figure 1 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.

Figure 2 Lesion localization visualized in the top view of the model

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 Schematic overview of flow cytometry Schematic overview on the analysis of peripheral immune cells by flow cytometry. Schematic overview of flow.

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 Family tree with the HLA haplotyping of 6 members of the family

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

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

Figure Postcontrast axial and coronal brain MRI in a patient with CLIPPERS treated with hydroxychloroquineT1-weighted spin echo post IV gadolinium contrast.

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 MRI brain 6 weeks post admission (A–C) Symmetrical high signal changes on fluid-attenuated inversion recovery sequences predominantly affecting.

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

Figure 1 Association between serum levels of IL-18 and hippocampal volume in patients with schizophrenia Scatter plots show a positive correlation between.

Figure 1 Evolution of MRI findings during interleukin (IL)–7 therapy

Figure 1 Anti-Epstein-Barr virus nuclear antigen-1 IgG quartile antibody status differences in MRI measures Anti-Epstein-Barr virus nuclear antigen-1 IgG.

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

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

Figure 1 Brain MRI Brain MRI (A) Axial fluid-attenuated inversion-recovery images show perilesional edema in both cerebellar hemisphere and hypointense.

Figure 1 Annualized percentage brain volume change

Figure 2 BVL according to on-study disability worsening

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 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.

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

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

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 Serial brain MRI of the patient with encephalitis and spontaneous recovery accompanying IgLON5 autoimmunity Serial brain MRI of the patient with.

Figure 1 MRIs (case 1)‏ MRIs (case 1) An enlarging T2 lesion in the cerebral white matter near the angular gyrus and a new lesion in the left middle cerebellar.

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 4 Patient 3 MRI evolution over time

Figure 3 Patient 2 MRI evolution over time before relapse

Figure 1 Segmentation of the normal-appearing periependymal white matter Segmentation of the normal-appearing periependymal white matter The figure demonstrates.

Figure 5 C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo.

Figure 2 Patient 1 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 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 (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 2 Representative brain MRIs from patients with neuromyelitis optica Lesions are localized at sites of high aquaporin-4 expression (white dots). Representative brain MRIs from patients with neuromyelitis optica Lesions are localized at sites of high aquaporin-4 expression (white dots). Patient 1: around the 3rd ventricle and hypothalamus; patient 2: around the 4th ventricle; patient 3: around the 4th ventricle and aqueduct; patient 4: periependymal, around lateral ventricles, cervical lesion extends into the brainstem; patient 5: thalamus, hypothalamus, optic chiasm, around the 4th ventricle, subpial in cerebellar hemispheres; patient 6: around the 4th ventricle and cerebellar peduncles. Modified with permission from Pittock et al. Arch Neurol 2006. Copyright © 2006 American Medical Association. All rights reserved. Anastasia Zekeridou, and Vanda A. Lennon Neurol Neuroimmunol Neuroinflamm 2015;2:e110 © 2015 American Academy of Neurology