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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.

Published byΑνάργυρος Γιαννακόπουλος Modified over 5 years ago

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Presentation on theme: "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."— Presentation transcript:

1 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 and radiologic course(A) The T2 contrast-enhanced sequence on day 3 shows an extensive central cord lesion extending from C2 to T7. The cord is swollen. Multiple areas of contrast enhancement were present throughout the cord (not shown). (B) Day 438: The cord edema has resolved and there is no longer contrast enhancement (not shown). Posterior fossa (C) and supratentorial (D) white matter changes were evident on a T2-weighted scan performed 3 days after symptom onset. These changes resolved on follow-up imaging (not shown). (E) The myelin oligodendrocyte glycoprotein antibody (MOG-Ab) titer fell rapidly following the commencement of immunotherapy (reference range < 1:160; red line). There was a steady improvement in modified Rankin Scale (mRS) score over 200 days (mRS = 1). Katrina A. Morris et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e88 © 2015 American Academy of Neurology

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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. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein MRI features of patients with MS who had antibodies.
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 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 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 Medial occipital lobe (designated by visual cortical brain regions) hypometabolism in anti–NMDA receptor encephalitis Medial occipital lobe (designated.

Figure 2 Medial occipital lobe (designated by visual cortical brain regions) hypometabolism in anti–NMDA receptor encephalitis Medial occipital lobe (designated.
Figure MRI of anti-MOG-IgG–associated myelitis

Figure MRI of anti-MOG-IgG–associated myelitis
Figure 2 Spinal cord lesions

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 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 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 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 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 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 3 Example of venous narrowing

Figure 3 Example of venous narrowing
Figure Brain MRI and biopsy specimens from the pontine lesion

Figure Brain MRI and biopsy specimens from the pontine lesion
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-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 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 Quantitative spinal cord MRI maps and segmentations

Figure 1 Quantitative spinal cord MRI maps and segmentations
Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.

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