Figure Brain MRI and biopsy specimens from the pontine lesion

Slides:

Advertisements

Similar presentations

Figure 2. A patient with multifocal nodular lesions diagnosed with CNS tuberculosis A patient with multifocal nodular lesions diagnosed with CNS tuberculosis.

Advertisements

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 4 Neuromyelitis optica spectrum disorder brain lesions

Figure 1 Brain MRI findings in the present case

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

Histopathologic features (all images at ×10 magnification).

Figure MRI of anti-MOG-IgG–associated myelitis

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 Vertebral artery angiogram and tissue pathology

Figure Neuroimaging and pathology

Figure 1 Coronal MRI images showing the evolution of white matter abnormality and atrophy of patient 1 Coronal MRI images showing the evolution of white.

Case 2. Case 2. A and B, T2-weighted images (fast spin-echo sequence with parameters of 4500/96 [TR/TE]) show diffuse hyperintense lesions in the white.

Figure 3 Example of venous narrowing

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

Figure 1. Prebiopsy and postbiopsy MRI

Figure Clinical presentation of daclizumab side effects with skin rash and meningoencephalomyelitis Clinical presentation of daclizumab side effects with.

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 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 Nuclear Nrf2 expression after fumarate therapy A new left occipital fluid-attenuated inversion recovery hyperintense (A), T1 hypointense (B), and.

Figure MRI and leptomeningeal biopsy findings in Vogt-Koyanagi-Harada syndrome involving the cerebellopontine angle(A) Coronal and (B) axial gadolinium-enhanced.

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 4 Comparison of 7.0T and 3.0T MRI (patients 5 and 6)‏

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

Figure MRIs and histopathology of the biopsy specimens

Figure 2 T2-weighted and subtraction images

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 7T MRI can differentiate between early PML and MS lesions Two different patterns of brain lesions were observed using 7T MRI: ring-enhancing lesions.

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

Figure 4 Neuropathology of MOG and AQP4 antibody–associated demyelinating lesions in the brain The biopsy specimen revealed a small actively demyelinating.

Figure Chronic inflammatory demyelinating polyneuropathy–like picture in patient with proven Creutzfeldt-Jakob disease (A) Example of partial conduction.

Figure MRI and neuropathologic characteristics of the tumefactive demyelinating lesion in our patient MRI and neuropathologic characteristics of the tumefactive.

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

Figure Radiologic and pathologic findings Fluid-attenuated inversion recovery (FLAIR) sequence with a single large T2-hyperintense signal involving the.

Figure 2 Example of venous narrowing

Figure 1 Radiologic features of human myelin oligodendrocyte glycoprotein immunoglobulin G–positive patients with cranial nerve involvement Radiologic.

Figure 3. Brain imaging and neuropathologic studies in patient PT-5 diagnosed with progressive multifocal leukoencephalopathy Brain imaging and neuropathologic.

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

Figure 2 Pathologic diagnosis of CAA-related vascular inflammation Hematoxylin & eosin staining (A) revealed focal intramural inflammation including lymphocytes,

Figure Postcontrast axial and coronal brain MRI in a patient with CLIPPERS treated with hydroxychloroquineT1-weighted spin echo post IV gadolinium contrast.

Figure MRI brain 6 weeks post admission (A–C) Symmetrical high signal changes on fluid-attenuated inversion recovery sequences predominantly affecting.

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 4 Autopsy immunochemistry results

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

Figure 1 Radiologic features of patients with white matter syndromes in association with NMDA receptor antibodies Radiologic features of patients with.

Figure 1 MRI findings over time

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 Brain MRI Brain MRI (A) Axial fluid-attenuated inversion-recovery images show perilesional edema in both cerebellar hemisphere and hypointense.

Figure Brain MRI findings before and during appearance of lymphoproliferative disorder and pathology findings of cerebellar lesion Brain MRI findings before.

Figure 1 Brain MRI features in patients with deletions upstream of LMNB1 Brain MRI features in patients with deletions upstream of LMNB1 All images are.

Figure Neurologic, gastrointestinal, and dermatologic findings

Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.

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 1 Detailed overview of treatment course and paraclinical findings Maximum intensity projection maps of supratentorial inversion recovery images.

Hematoxylin-eosin (A) and luxol fast blue (B) staining of the lesion seen in the cerebellum of case 2. Hematoxylin-eosin (A) and luxol fast blue (B) staining.

Figure 6 P2Y12 is highly expressed in CD68+ and CD163+ cells during parasitic brain infectionIn a case of Schistosoma mekongi infection, hematoxylin and.

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

Figure 1 MRIs (case 1)‏ MRIs (case 1) An enlarging T2 lesion in the cerebral white matter near the angular gyrus and a new lesion in the left middle cerebellar.

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

Figure Rapid progression of lesions after natalizumab treatment(A) MRI from February Rapid progression of lesions after natalizumab treatment(A)

Figure FDG-PET, lymph node biopsy, and brain MRI

Figure 4 Patient 3 MRI evolution over time

Figure 3 Patient 2 MRI evolution over time before relapse

A 69-year-old man with small-cell carcinoma from the lung

Figure 1 MRIs MRIs (A and B) Axial FLAIR images of the brain demonstrate multifocal parenchymal lesions including the right hippocampus, right midbrain,

Presentation transcript:

Figure Brain MRI and biopsy specimens from the pontine lesion Brain MRI and biopsy specimens from the pontine lesion (A) Brain MRI with and without contrast. Fluid-attenuated inversion recovery sequences demonstrate T2 hyperintense lesions in the pons, right middle cerebellar, bilateral basal ganglia, left frontal and parietal lobes (not shown). The lesions in the pons and cerebellar peduncle were contrast-enhancing. (B, C) Brain pathology specimens. Gross brain pathology (not shown) was remarkable for 2 regions of softening with red discoloration, the first measuring 1 cm in the left parietal white matter and the second measuring 2 cm in the pons with extension into the middle cerebellar peduncle. (B) Luxol fast blue and periodic acid-Schiff–stained section from the pons showed the interface of a hypercellular lesional area with myelin loss (left half of field) with relatively less involved white matter (right half of field). (C) CD68 immunohistochemistry revealed numerous macrophages in the involved area. CD68 specifically labels phagocytic cells of the brain, including macrophages and microglia. The larger reactive cells are intact macrophages, with foamy cytoplasm by hematoxylin & eosin staining (not shown), and the smaller more intensely stained cells include smaller phagocytes and fragmented phagocytes. No nonspecific staining of neurons was present. Original magnification: 100×. Michael J. Bradshaw et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e205 © 2016 American Academy of Neurology