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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,

Published byŠtěpánka Řeháková Modified over 5 years ago

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Presentation on theme: "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,"— Presentation transcript:

1 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, clinical syndromes, and therapy in 8 informative patients with white matter syndromes in association with NMDAR-Ab (A–C) Cases 1–3 presented initially with brainstem encephalitis; Cases 1 and 2 relapsed with encephalopathy, psychiatric features, movement disorder, and dysautonomia. Case 2 had additional seizures. In both, the diagnosis of NMDAR-Ab encephalitis was made at the time of relapse. Case 3 had a monophasic illness and did not have any of the clinical characteristics of NMDAR-Ab encephalitis. (D, E) Cases 4 and 5 presented with herpes simplex virus encephalitis (HSVE) and then had a neurologic relapse, which correlated with raised NMDAR-Abs in both serum and CSF and demonstrated a clinical response to immunotherapy with reduction of antibody levels. (F) Case 8 presented with optic neuritis and poor visual recovery, which prompted a neuroinflammatory screen and the identification of the antibody positivity. She only received a course of steroids 1 year into her illness and 3 years later had a neurologic relapse. (G) Case 9 presented initially with 2 episodes of acute disseminated encephalomyelitis (ADEM) and relapsed at 1 year with optic neuritis. He was also MOG-Ab positive, which remain detectable even when NMDAR-Abs are no longer detectable and when the patient had clinically recovered. (H) Case 10 had recurrent episodes of hyperventilation, dizziness, and double vision; did not receive any treatment; and both her clinical and radiologic features remained unchanged. Ab = antibody; CSF Ab × 10 = NMDAR antibody titers in CSF (all between 1:20 and 1:50) multiplied by 10 to provide visibility in comparison to serum levels; IVIg = IV immunoglobulin; IVMP = IV methylprednisolone; LeukoE = radiologic leukoencephalopathy; Lt = left; MMF = mycophenolate mofetil; NMDAR = NMDA receptor; ON = optic neuritis; PLEX = plasma exchange; Rt = right; Serum Ab titer = titer measured by endpoint dilution. Yael Hacohen et al. Neurol Neuroimmunol Neuroinflamm 2014;1:e2 © 2014 American Academy of Neurology

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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 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 GlyR antibody binding

Figure 2 GlyR antibody binding
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 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 2 Serums of patients with stiff-person syndrome spectrum disorders containing GlyRα1-Binding IgG specifically induces internalization of GlyRα1.
Figure 4 Correlation of age with [11C](R)-PK11195 binding in the normal-appearing white matter (NAWM) and thalami Correlation of age with [11C](R)-PK11195.

Figure 4 Correlation of age with [11C](R)-PK11195 binding in the normal-appearing white matter (NAWM) and thalami Correlation of age with [11C](R)-PK11195.
Figure 4 Proposed therapy scheme for anti-LGI1 encephalitis

Figure 4 Proposed therapy scheme for anti-LGI1 encephalitis
Figure 1 Percent positivity by clinical feature Overall, 6

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

Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum.
Figure Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately.

Figure Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately.
Figure 4 Relation of neuropsychological deficits and intrathecal immune cell subsets in GABAB receptor antibody–associated limbic encephalitis Relation.

Figure 4 Relation of neuropsychological deficits and intrathecal immune cell subsets in GABAB receptor antibody–associated limbic encephalitis Relation.
Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.
Figure 2 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.

Figure 2 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.
Figure 3 Multifocal visual-evoked potentials in optic neuritis Figure shows the visual-evoked potentials (VEPs) in 52 sectors of the retina. Multifocal.

Figure 3 Multifocal visual-evoked potentials in optic neuritis Figure shows the visual-evoked potentials (VEPs) in 52 sectors of the retina. Multifocal.
Figure. Patient imaging

Figure. Patient imaging
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 Reactivity of the patients' antibodies with rat brain and HEK cell-based assays Rat hippocampal dentate gyrus neuropils were stained with patient.
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 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 Clinical course and response to therapy in 6 Australian patients with HMGCR antibodies The clinical course, creatine kinase (CK) levels, Medical.

Figure 2 Clinical course and response to therapy in 6 Australian patients with HMGCR antibodies The clinical course, creatine kinase (CK) levels, Medical.
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 MRI, pathology, and EEG findings(A) Axial fluid-attenuated inversion recovery (FLAIR) MRI sequences of the brain showing right frontal and parietal.
Figure 1 Evolution of visual function after acute optic neuritis Figure shows the measurement of high-contrast visual acuity (VA) using the Early Treatment.

Figure 1 Evolution of visual function after acute optic neuritis Figure shows the measurement of high-contrast visual acuity (VA) using the Early Treatment.

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