Figure 1. Brain MRI follow-up of Sjögren syndrome–associated type II mixed cryoglobulinemic cerebral vasculitis treated with rituximab Brain MRI follow-up.

Slides:



Advertisements
Similar presentations
Date of download: 7/2/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Stroke in a Healthy 46-Year-Old Man JAMA. 2001;285(21):
Advertisements

Copyright © 2015 by the American Osteopathic Association.
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.
Nat. Rev. Neurol. doi: /nrneurol
Case One serial imaging.
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 1 Brain MRI findings in the present case
Figure 2 Evolution of MRI abnormalities in faciobrachial dystonic seizures Axial fluid- attenuated inversion recovery (FLAIR)-weighted images from patient.
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 Spinal cord lesions
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 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.
Axial magnetic resonance (MR) imaging
Figure 3 Example of venous narrowing
Figure Immune checkpoint inhibitor–induced encephalitis before and after treatment with natalizumab Immune checkpoint inhibitor–induced encephalitis before.
Figure 1 MRI head in faciobrachial dystonic seizures (A) Axial fluid-attenuated inversion recovery image from patient 3 in table 2 shows T2-weighted hyperintensity.
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
VW-MR imaging to differentiate among causes of intracranial arterial stenosis when angiography findings are inconclusive. VW-MR imaging to differentiate.
Figure Brain MRI and biopsy specimens from the pontine lesion
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 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 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.
Common VW-MR imaging pitfalls.
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.
Patient 2: CNS vasculitis in a 37-year-old woman with systemic lupus erythematosus. Patient 2: CNS vasculitis in a 37-year-old woman with systemic lupus.
Figure 3 Ultra-high-field MRI at 7.0T (patients 5 and 6)‏
Figure MRI and histology of demyelinating lesion(A) Symmetric T2 hyperintensity in the midbrain with relative sparing of cerebral peduncles. MRI and histology.
Figure 2 Example of venous narrowing
Figure 1 MRI of inflammatory myelitis before and after treatment
Figure 3. Brain imaging and neuropathologic studies in patient PT-5 diagnosed with progressive multifocal leukoencephalopathy Brain imaging and neuropathologic.
Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.
Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.
Figure Genetic deletion and MRI changes with EHMT1 deletion
Figure Postcontrast axial and coronal brain MRI in a patient with CLIPPERS treated with hydroxychloroquineT1-weighted spin echo post IV gadolinium contrast.
Figure 3 Correlation of lipid indexes to MRI measures of disease severity in multiple sclerosis Correlation of lipid indexes to MRI measures of disease.
Figure 1 Evolution of MRI findings during interleukin (IL)–7 therapy
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 2 Brain MRI at 1 year of age
Figure 1 Brain MRI Brain MRI (A) Axial fluid-attenuated inversion-recovery images show perilesional edema in both cerebellar hemisphere and hypointense.
Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.
Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.
Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.
Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521
Patient 6: 24-year-old woman with primary angiitis of the CNS
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.
Supratentorial and posterior fossa PML
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)
Pial vasodilation. Pial vasodilation. A, Axial GRE T2 image shows a left frontal sulcal SAH (black arrowhead), possibly located in the “watershed” territory.
A, FLAIR demonstrating acute infarct within a superficial distribution
Imaging at the time of presentation.
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 2 Clinical data and variation of sNfL levels of patients 4–6 with ATZ-treated MS Clinical data and variation of sNfL levels of patients 4–6 with.
Figure 3 Patient 2 MRI evolution over time before relapse
Figure 1 Segmentation of the normal-appearing periependymal white matter Segmentation of the normal-appearing periependymal white matter The figure demonstrates.
A 42-year-old woman who presented with altered mental status and lethargy. A 42-year-old woman who presented with altered mental status and lethargy. FLAIR.
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,
Figure MRI T1 coronal images show homogenous hyperintense lesion involving the right trigeminal nerve root (white arrows) in A and B and Meckel's cave.
A 21-year-old woman with a right sensory-motor deficit and aphasia for 60 minutes. A 21-year-old woman with a right sensory-motor deficit and aphasia for.
Presentation transcript:

Figure 1. Brain MRI follow-up of Sjögren syndrome–associated type II mixed cryoglobulinemic cerebral vasculitis treated with rituximab Brain MRI follow-up of Sjögren syndrome–associated type II mixed cryoglobulinemic cerebral vasculitis treated with rituximab In case 1, axial T2-weighted image (A) demonstrates multifocal subcortical/deep white matter hyperintensities and residual parenchymal hematoma in the right frontal lobe, whereas MR angiography (B) shows segmental areas of arterial narrowing (arrows) of the cortical branches of the left middle cerebral artery. Three months after rituximab infusion, MR angiography (C) shows normalization of arterial calibre of the cortical branches of the left middle cerebral artery (arrows). In case 2, MR angiography (D) shows multifocal stenosis of the pericallosal artery (arrows). Three years after rituximab infusion, MR angiography (E) shows persistent stenosis (white arrows) and a mild dilatation of the previous narrow arterial segment (black arrow). MR = magnetic resonance. Bertrand Lioger et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e253 © 2016 American Academy of Neurology