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Figure 2. Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem.

Published byΓοργοφόνη Κεδίκογλου Modified over 5 years ago

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Presentation on theme: "Figure 2. Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem."— Presentation transcript:

1 Figure 2. Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem
Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem (A) Cerebellar vermis shows typical changes of CJD including spongiform encephalopathy, gliosis, and neuronal loss (hematoxylin and eosin × 100 actual magnification) and (B) synaptic pattern (PrP) immunoreactivity (12 F10 PrP antibody × 100 actual magnification). Note there is no evidence of any inflammatory cells. Boaz Kim et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e248 © 2016 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 4. Brain imaging and neuropathologic demonstration of Epstein-Barr virus (EBV) encephalitis in patient PT-10 Brain imaging and neuropathologic demonstration.

Figure 4. Brain imaging and neuropathologic demonstration of Epstein-Barr virus (EBV) encephalitis in patient PT-10 Brain imaging and neuropathologic demonstration.
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 Vertebral artery angiogram and tissue pathology

Figure Vertebral artery angiogram and tissue pathology
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 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.

Figure 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.
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 Anti-LINGO-1 (Li81) does not affect cytokine production

Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production
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 2 Immunopathologic analysis of all 3 Rasmussen encephalitis cases Immunopathologic analysis of all 3 Rasmussen encephalitis cases (A) Perivascular.

Figure 2 Immunopathologic analysis of all 3 Rasmussen encephalitis cases Immunopathologic analysis of all 3 Rasmussen encephalitis cases (A) Perivascular.
Figure 1 Histopathologic features of a chronic active and a chronic plaque in the MS brain Histopathologic features of a chronic active and a chronic plaque.

Figure 1 Histopathologic features of a chronic active and a chronic plaque in the MS brain Histopathologic features of a chronic active and a chronic plaque.
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 Muscle biopsy images demonstrating a pauci-immune necrotizing autoimmune myopathy in illustrative cases 1 and 2 (A–D) Case 1 deltoid muscle. Muscle.
Figure Brain MRI and biopsy specimens from the pontine lesion

Figure Brain MRI and biopsy specimens from the pontine lesion
Figure Radiologic and histopathologic findings in a patient with IgG4-related intracranial hypertrophic pachymeningitis(A–D) Radiologic findings over 10.

Figure Radiologic and histopathologic findings in a patient with IgG4-related intracranial hypertrophic pachymeningitis(A–D) Radiologic findings over 10.
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 2 Neuropathologic examination for lymphoma etiology (patients 1–4)‏ Neuropathologic examination for lymphoma etiology (patients 1–4) Immunohistochemical.

Figure 2 Neuropathologic examination for lymphoma etiology (patients 1–4)‏ Neuropathologic examination for lymphoma etiology (patients 1–4) Immunohistochemical.
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.
Figure 1 Neuropathologic examination of brain areas with normal MRI appearance and with gadolinium enhancement (patient 1)‏ Neuropathologic examination.

Figure 1 Neuropathologic examination of brain areas with normal MRI appearance and with gadolinium enhancement (patient 1)‏ Neuropathologic examination.

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