Figure Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately.

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Hereditary sensory and autonomic neuropathy type 1

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Figure 1. Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD)‏ Absence of anti–neurofascin-155 (NF155)

Figure 2 Medial occipital lobe (designated by visual cortical brain regions) hypometabolism in anti–NMDA receptor encephalitis Medial occipital lobe (designated.

Figure 2 GlyR antibody binding

Figure 1 Stiff-person syndrome spectrum patient serum bound to membranes of live GlyRα1-transfected HEK293 cells Stiff-person syndrome spectrum patient.

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

P. James B. Dyck, MD, Jennifer A. Tracy, MD Mayo Clinic Proceedings

Figure 1 Percent positivity by clinical feature Overall, 6

Figure Sural nerve electron microscopy

Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production

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 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.

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

Figure. Patient imaging

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 Muscle biopsy images demonstrating a pauci-immune necrotizing autoimmune myopathy in illustrative cases 1 and 2 (A–D) Case 1 deltoid muscle. Muscle.

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 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 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 Binding of the patient's IgG to Purkinje cells is inhibited by pretreatment of rat tissue with anti-VGCC antibodies, confirming specificity of.

Figure 2 Histochemical and immunohistochemical staining and electron microscopic examination of structures in the brain biopsy Hematoxylin & eosin staining.

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 1 Time points of blood sampling

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

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 4 Representative images of skin biopsy sample

Figure 2 CD4+ and CD8+ T cells accumulate in the CSF in GABAB receptor antibody–associated LE CD4+ and CD8+ T cells accumulate in the CSF in GABAB receptor.

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 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 Patients with acute anti–NMDA receptor encephalitis have marked hypometabolism of the visual cortical brain region correlating with the medial.

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 3 Detection of synapsin Ia, Ib, and IIa in cell-based assays, colocalization of patient IgA and commercial synapsin antibodies in hippocampus sections.

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 2 Relative concentration (in mAb equivalents) of JCV Ab in samples tested prior to IVIg (“pre-IVIg”), within 30 days of IVIg (“during IVIg”), and.

Figure 1. Antibodies to MOG in a proportion of adult patients with MS

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 Clinical findings and CNS immunoreactivity of CSF IgA of a patient with limbic encephalitis (A) Cranial MRI of a 69-year-old man with limbic encephalitis.

Figure 1 B cells and plasma cells accumulate in the CSF in GABAB receptor antibody–associated LE B cells and plasma cells accumulate in the CSF in GABAB.

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

Figure 2 Analysis of muscle and nerve histopathology and muscle mtDNA deletions (A) Representative muscle biopsy shows a cytochrome c oxidase (COX)-negative.

Figure Disease course and neuropathology of CASPR2 encephalitis(A) Summary of the most important changes during the disease course. Disease course and.

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 Clinical status and autoantibody titers in rituximab-treated patients with anti-CNTN1/NF155 chronic inflammatory demyelinating polyneuropathy.

Figure Imaging, histology/immunohistochemistry, and schematic course of treatment with corresponding clinical and radiologic disease activity Imaging,

Figure Forty-two months of follow-up of clinical symptoms in parallel with therapeutic interventions and antibody titers/B-cell count Forty-two months.

Figure 2 Histopathological features in CIDP

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

Figure ND5 and MCARNE phenotype

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 3 Effect of IVIg on endogenous relative concentration (in mAb equivalents) of JCV AbSix patients shown in this figure have had John Cunningham virus.

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

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

Figure 2 Brain biopsy of 2 patients with anti-MOG encephalitis initially misdiagnosed with small vessel CNS vasculitis Brain biopsy of 2 patients with.

Figure 3 Muscle biopsy showing myofiber atrophy and degeneration

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 Clinical course and CSF/serum NMDA receptor (NMDAR) antibody (ab) titers of mother and infant Titers were measured with immunohistochemistry of.

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 2 Cell-based assay demonstrating differential binding of AChR antibodies to the adult and fetal receptorsThe fetal (gamma subunit specific) and.

Figure 3 Bilateral optic atrophy and sural nerve biopsy of patient AII-2 Bilateral optic atrophy and sural nerve biopsy of patient AII-2 (A) Red-free photographs.

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

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.

Figure Myelin binding of high-level MBP IgA antibodies from a patient with MS Myelin binding of high-level MBP IgA antibodies from a patient with MS (A)

Figure 1 Standard treatment scheme and antibody titer changes

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Figure Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately 3–4 weeks after onset of peripheral neuropathy, NMDAR antibody (ab) titers started to appear in CSF (red) and serum (blue). Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately 3–4 weeks after onset of peripheral neuropathy, NMDAR antibody (ab) titers started to appear in CSF (red) and serum (blue). NMDAR encephalitis showed response to immunotherapy with methylprednisolone (MP), IV immunoglobulin (IVIg), plasma exchange (PE), and rituximab. Curves for neuropathy and encephalitis demonstrate global clinical impression (arbitrary units) to visualize the sequence of clinical symptoms. mRS = modified Rankin Scale. (B–D) Patient's serum (green, Alexa Fluor 488, Jackson ImmunoResearch, Suffolk, UK) showed the typical pattern in rat hippocampus (dilution 1:400, B) and NMDAR-transfected HEK293 cells (C) but not control-transfected cells (D). Red nuclear stain was performed with TO-PRO-3 iodide (Invitrogen, Karlsruhe, Germany). (E.a) Semithin section stained by methylene blue illustrates severe reduction of myelinated fibers, affecting both thin and thickly myelinated fibers. Also, profound axonal loss (asterisks), acute axonal degeneration (arrows), and single axon regeneration clusters are visible (box E.b: higher magnification). (F) Teased fibers show short internodal segments (arrows). (G) Higher magnification demonstrates hypomyelinated and shortened segments (sign of demyelination) and alignment of ovoids (sign of acute axonal degeneration). Harald Prüss et al. Neurol Neuroimmunol Neuroinflamm 2014;1:e14 © 2014 American Academy of Neurology