Figure 1. Spinal cord MRI and immunofluorescence staining of the patient's serum and controls on different tissues and recombinant cell substrates Spinal.

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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.

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Figure 2 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)

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 Muscle biopsy from a patient with a slowly progressive (24 years) HMGCR antibody–associated myopathy syndrome (A) Hematoxylin & eosin stain, (B)

Figure 2 GlyR antibody binding

Figure 1 Immunofluorescence pattern of patient septin-5-immunoglobulin G binding to mouse tissues Immunofluorescence pattern of patient septin-5-immunoglobulin.

Figure MRI of anti-MOG-IgG–associated myelitis

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

Figure 2 Association of serum IgG reactivity with MRI measures of disease severity Association of serum IgG reactivity with MRI measures of disease severity.

Figure 2 Serums of patients with stiff-person syndrome spectrum disorders containing GlyRα1-Binding IgG specifically induces internalization of GlyRα1.

Figure Neuroimaging and pathology

Figure 3 Immunohistochemical analyses of positive and negative Epstein-Barr virus (EBV) control tissues using immunostaining Immunohistochemical analyses.

Figure 2 Disease progression slowed during each round of Treg infusions and correlated with increased Treg suppressive function Disease progression slowed.

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 3 Example of venous narrowing

Figure DPPX antibodies as detected by fluorescence-based immunohistochemistry and a cell-based assayImmunohistochemistry displayed binding of the patient's.

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

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

Figure 4 Detection of EBER+ cells in MS and control brains by in situ hybridization Detection of EBER+ cells in MS and control brains by in situ hybridization.

Figure 1 Reactivity of the patients' antibodies with rat brain and HEK cell-based assays Rat hippocampal dentate gyrus neuropils were stained with patient.

Figure 1 ERG peak time delay at baseline

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 2 Brain-infiltrating immune cells mainly consist of CD8+ memory T cells Immunofluorescence staining of brain-infiltrating immune cells. Brain-infiltrating.

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 5 Cytokine release and stimulation of cells during alemtuzumab treatment Cytokine release and stimulation of cells during alemtuzumab treatment.

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 2 Mean serum concentrations of BIIB033 vs time(A) Single ascending dose study and (B) multiple ascending dose study. Mean serum concentrations of.

Figure Widespread leptomeningeal enhancementAxial T1 fat-saturated postcontrast image (A) demonstrates abnormal leptomeningeal enhancement of bilateral.

Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.

Figure 3 Ultra-high-field MRI at 7.0T (patients 5 and 6)‏

Figure 1 GABAB expression in the thymus(A–C) Staining of thymus tissue with anti-cytokeratin (A) and anti-GABAB antibody (B, C double immunofluorescence).

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 1 VGCC antibody uptake in cerebellar slice culture

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 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 3 Correlation of lipid indexes to MRI measures of disease severity in multiple sclerosis Correlation of lipid indexes to MRI measures of disease.

Figure 6 Cellular composition after tissue dissociation

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. Radiologic and pathologic findings

Figure 1 Imaging of disease onset and treatment response Repeat MRI scans including fluid-attenuated inversion recovery (FLAIR) (A) and T2 fast field echo.

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 Leptomeningeal inflammationPostcontrast T1-weighted MRI: abnormal leptomeningeal enhancement over the frontoparietal lobes and interhemispheric.

Figure 2 Pre- and posttreatment contrast-enhanced MRI of second toxoplasmosis lesion in case 1(A) Contrast-enhanced MRI demonstrated a second ring-enhancing.

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

Figure 1 Determination of anti-Tr/DNER by indirect immunofluorescence(A) Slide with 10 reaction fields as used for the study. Determination of anti-Tr/DNER.

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

Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF and.

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

Figure 2 MRIs (cases 2 and 3)‏

Figure 1 Tissue processing methods and cellular viability

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

Figure 2 Brain MRI features of 3 representatives patients with MS who experienced WNS after FTY withdrawal Brain MRI features of 3 representatives patients.

Figure 4 Patient 3 MRI evolution over time

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 1 MRI of both patients with IgG4-HP and spinal cord arteriography of the first patient MRI of both patients with IgG4-HP and spinal cord arteriography.

Figure 2. Histoimmunoprecipitation and antigen identification

Figure 1 Axial FLAIR brain MRI obtained on admission to the ICU demonstrated (A1) old hyperintense subcortical lesions (arrowhead), new superimposed on.

Figure 3. Verification of GluRd2 as the target antigen of the patient's antineural autoantibodies Verification of GluRd2 as the target antigen of the patient's.

Presentation transcript:

Figure 1. Spinal cord MRI and immunofluorescence staining of the patient's serum and controls on different tissues and recombinant cell substrates Spinal cord MRI and immunofluorescence staining of the patient's serum and controls on different tissues and recombinant cell substrates (A) MRI of the cervical spinal cord. (A.a) MRI before prednisolone treatment. (A.b) MRI after 2 weeks of prednisolone. Arrows depict longitudinal hyperintense areas that ameliorate during immunomodulation. T1+CE = T1-weighed image with contrast enhancement. (B) Cryosections of rat (B.a) or monkey cerebellum (B.b), murine whole brain (B.c), monkey exocrine pancreas (B.d), and recombinant HEK293 expressing the pancreatic autoantigen CUZD1 (B.e) were incubated with the patient's serum (1:100). Nuclei were counterstained by incubation with TO-PRO-3 iodide. Scale bar: 50 μm. Ramona Miske et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e255 © 2016 American Academy of Neurology