Figure Rapid progression of lesions after natalizumab treatment(A) MRI from February 2012. Rapid progression of lesions after natalizumab treatment(A)

Slides:

Advertisements

Similar presentations

Neurology Resident and Fellow Section

Advertisements

Nat. Rev. Neurol. doi: /nrneurol

Copyright © 2015 by the American Osteopathic Association.

Figure 1 Perivenous distribution of multiple sclerosis lesions

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 Lumbar spine MRI obtained on hospital day 2 demonstrating nerve root enhancement and evolution of CSF and electrodiagnostic findings Lumbar spine.

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 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 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.

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 1. Prebiopsy and postbiopsy MRI

Dabrafenib and Trametinib Treatment for Erdheim-Chester Disease With Brain Stem Involvement Ahmed Al Bayati, MD, Thomas Plate, MD, Mahmood Al Bayati,

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

Figure 3. MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis.

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

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.

Chapter 16 Neurologic Dysfunction and Kidney Disease

Figure MRI and immunologic findings

Figure Widespread leptomeningeal enhancementAxial T1 fat-saturated postcontrast image (A) demonstrates abnormal leptomeningeal enhancement of bilateral.

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

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 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 1 Reibergram (CSF/serum quotient diagram) of all included patients Increasing albumin quotients reflect increasing blood-brain barrier dysfunction.

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 Imaging of disease onset and treatment response Repeat MRI scans including fluid-attenuated inversion recovery (FLAIR) (A) and T2 fast field echo.

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 Imaging, histology/immunohistochemistry, and schematic course of treatment with corresponding clinical and radiologic disease activity Imaging,

Figure 1 Representative spinal cord MRIs from patients with neuromyelitis optica Longitudinally extensive transverse myelitis of the cervical (A) and cervicothoracic.

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 2 Frequency of the proportion of total WMLs with central veins in PPMS, RRMS, and SVD Frequency of the proportion of total WMLs with central veins.

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 Kaplan-Meier survival curves for the fingolimod cohort In each graph, bottom tertile: solid line; middle tertile: long dashed line; top tertile:

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

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

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 4 Patient 3 MRI evolution over time

Figure 3 Patient 2 MRI evolution over time before relapse

Figure 2 Patient 1 MRI evolution over time

Figure 1 Axial FLAIR brain MRI obtained on admission to the ICU demonstrated (A1) old hyperintense subcortical lesions (arrowhead), new superimposed on.

Axial magnetic resonance imaging (MRI) of a 30 year old man with relapsing remitting multiple sclerosis (MS) showing multiple periventricular lesions:

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 Rapid progression of lesions after natalizumab treatment(A) MRI from February 2012. Rapid progression of lesions after natalizumab treatment(A) MRI from February 2012. Axial fluid-attenuated inversion recovery (FLAIR) and sagittal T2 scans reveal scattered white matter lesions and a short-segment lesion at T3 (arrow). (B) MRI from September 2013. Axial FLAIR images reveal progression of disease from prior imaging. (C, D) MRI after second natalizumab treatment in November 2013. Axial FLAIR images (C) reveal marked progression, and sagittal T2 scan (D) reveals a longitudinally extensive lesion from T6 to T12. (E, F) MRI demonstrating relapse after initiation of rituximab. Axial T1 postcontrast (E) shows an enhancing lesion in the brachium pontis, and sagittal T2 (F) reveals a new cervical lesion. Michael D. Kornberg, and Scott D. Newsome Neurol Neuroimmunol Neuroinflamm 2015;2:e66 © 2015 American Academy of Neurology