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

Slides:



Advertisements
Similar presentations
Gliomatosis cerebri with spinal metastasis presenting with chronic meningitis in two boys  Yi-Heng Lin, Yen-Wen Chang, Shih-Hung Yang, Hsiu-Hao Chang,
Advertisements

Figure 2. A patient with multifocal nodular lesions diagnosed with CNS tuberculosis A patient with multifocal nodular lesions diagnosed with CNS tuberculosis.
Figure 2 ERG amplitude reduction in the follow-up study
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 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.
Figure MRI of anti-MOG-IgG–associated myelitis
Figure 2 Spinal cord lesions
Figure Neuroimaging and pathology
Figure 3 Immunohistochemical analyses of positive and negative Epstein-Barr virus (EBV) control tissues using immunostaining Immunohistochemical analyses.
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.
Figure Facial photograph during headache attack and brain and upper cervical cord MRI Facial photograph during headache attack and brain and upper cervical.
Figure 3 Example of venous narrowing
Figure 2 Immunopathologic analysis of all 3 Rasmussen encephalitis cases Immunopathologic analysis of all 3 Rasmussen encephalitis cases (A) Perivascular.
Figure Muscle biopsy of the left biceps showing the characteristic pathologic findings in BCIM Muscle biopsy of the left biceps showing the characteristic.
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 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 4 Detection of EBER+ cells in MS and control brains by in situ hybridization Detection of EBER+ cells in MS and control brains by in situ hybridization.
Figure Brain MRI and biopsy specimens from the pontine lesion
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 1 Histopathologic features of case 1 (A–G) and case 2 (H–L)‏
Figure 5 Increased frequency of parenchymal CD138- and LMP-1–positive cells in MS Increased frequency of parenchymal CD138- and LMP-1–positive cells in.
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 2 Neuropathology of PML lesions in a patient with MS treated with fingolimod Neuropathology of PML lesions in a patient with MS treated with fingolimod.
Figure 2 T2-weighted and subtraction images
Figure MRI and immunologic findings
Figure 2 Histopathologic findings of patients with both inflammatory myopathy and myasthenia gravis Histopathologic findings of patients with both inflammatory.
Figure 4 Neuropathology of MOG and AQP4 antibody–associated demyelinating lesions in the brain The biopsy specimen revealed a small actively demyelinating.
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 Sections of muscle biopsy specimens stained with hematoxylin & eosin (HE)‏ Sections of muscle biopsy specimens stained with hematoxylin & eosin.
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 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.
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 MRI of inflammatory myelitis before and after treatment
Figure 1 Illustration of white matter– and lesion-associated regions of interest (ROIs)‏ Illustration of white matter– and lesion-associated regions of.
Figure 3. Brain imaging and neuropathologic studies in patient PT-5 diagnosed with progressive multifocal leukoencephalopathy Brain imaging and neuropathologic.
Figure 4 Autopsy immunochemistry results
Figure 1 MRI findings over time
Figure Imaging, histology/immunohistochemistry, and schematic course of treatment with corresponding clinical and radiologic disease activity Imaging,
Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.
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 MRI brain comparison prior and after treatment and brain biopsy findings MRI brain comparison prior and after treatment and brain biopsy findings.
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
Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521
Ingo Kleiter et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e504
Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453
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 2 MRIs (cases 2 and 3)‏
Figure 1 Imaging and histopathologic characteristics of patients with CNS-FHL Imaging and histopathologic characteristics of patients with CNS-FHL FLAIR.
Figure 2 Brain MRI features of 3 representatives patients with MS who experienced WNS after FTY withdrawal Brain MRI features of 3 representatives patients.
Figure A 57-year-old man with relapsing-remitting MS (RRMS) and new-onset ataxia A 57-year-old man with relapsing-remitting MS (RRMS) and new-onset ataxia.
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
Figure 1 Representative radiologic and pathologic images of patients with brain somatic mutations in SLC35A2 Representative radiologic and pathologic images.
Figure 5 C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo.
Figure 2 Patient 1 MRI evolution over time
Figure 1 MRI of both patients with IgG4-HP and spinal cord arteriography of the first patient MRI of both patients with IgG4-HP and spinal cord arteriography.
Figure 4 C5B3 decreased NMOSD mouse model lesions in vivo
Figure 1 Axial FLAIR brain MRI obtained on admission to the ICU demonstrated (A1) old hyperintense subcortical lesions (arrowhead), new superimposed on.
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 MRI and neuropathologic characteristics of the tumefactive demyelinating lesion in our patient MRI and neuropathologic characteristics of the tumefactive demyelinating lesion in our patient T1-weighted imaging revealed a nodular and linear enhancement with gadolinium in the center of the lesion (A and B). FLAIR imaging revealed an extensive hemispheric white matter lesion with a mass effect in the left fronto-parieto-temporal lobe (C and D). The high-intensity lesion observed on FLAIR images appeared as a lesion of slightly lower signal intensity on diffusion-weighted images (E) and exhibited an increased apparent diffusion coefficient value (F), suggestive of vasogenic edema. An existing periventricular lesion was detected in the right posterior ventricular horn without gadolinium enhancement (A, C, arrow). FLAIR imaging of the brain (G) and T2-weighted imaging of the cervical cord (H) before TDL development showed typical MS lesions (arrow indicates a cervical lesion). We performed a biopsy of the enhanced lesion. Parenchymal inflammatory infiltrates were invariably present and were accompanied by foamy macrophages and reactive astrocytes (I). Perivascular lymphocytic cuffing and Creutzfeldt-Peters cells (inset) were also observed (hematoxylin and eosin stain, scale bar = 300 μm, inset scale bar = 25 μm) (J). Demyelination was observed as a loss of Luxol fast blue staining (Klüver-Barrera stain, scale bar = 200 μm) (K). Relative axonal preservation (IHC stain for neurofilaments, scale bar = 200 μm) (L). Extensive macrophage infiltration presenting with lipid-laden foamy macrophages (IHC for CD68, scale bar = 200 μm) (M). Relative glial fibrillary acidic protein preservation within the TDL (IHC for GFAP scale bar = 200 μm) (N). Continuous sections of the perivascular lymphocytic cuffing lesion (O: IHC for CD3; P: IHC for CD8; Q: IHC for CD4; R: IHC for CD20, scale bar = 200 μm). Inflammatory infiltrates were composed of lymphocytes (O), most of which were CD8-positive cytotoxic T lymphocytes (P). Scattered CD4-positive helper T cells (Q) and relatively fewer B cells were observed (R). CD4-positive T lymphocytes tended to accumulate predominantly in the parenchymal tissue (Q). FLAIR = fluid-attenuated inversion recovery; IHC = immunohistochemical; TDL = tumefactive demyelinating lesion. Kazumasa Okada et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e484 Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.