Figure 1 Imaging of disease onset and treatment response Repeat MRI scans including fluid-attenuated inversion recovery (FLAIR) (A) and T2 fast field echo.

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Neurology Resident and Fellow Section

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Nat. Rev. Neurol. doi: /nrneurol

Figure 1 Perivenous distribution of multiple sclerosis lesions

A 54-year old woman with subacute encephalopathy

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 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

Fluid-attenuated inversion recovery magnetic resonance imaging at the onset of the clinical investigation (A, B) and 2 months later (C, D). Fluid-attenuated.

Figure Patient 1's ictal EEG and brain MRI and patient 2's ictal EEG and polygraphic recording(A) Patient 1's EEG showing an ictal discharge over right.

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

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 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.

Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.

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 3 Ultra-high-field MRI at 7.0T (patients 5 and 6)‏

Figure 2 DTI values between the hepatitis C group and controls(A) DTI FA values, (B) DTI diffusion values. *Statistically significant at FDR-adjusted p.

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 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,

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 1 Patients with acute anti–NMDA receptor encephalitis have marked hypometabolism of the visual cortical brain region correlating with the medial.

Figure 5 Pairwise correlations between selected patient-reported outcomes and performance tests in patients with MS (A) The number of pairwise correlations.

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

Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.

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 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 2 Assessment of systemic disease activityTc99 scintigraphy (A) and fluorodeoxyglucose PET imaging (B, C) at disease onset 2 years before acute deterioration.

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.

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 Imaging and histopathologic characteristics of patients with CNS-FHL Imaging and histopathologic characteristics of patients with CNS-FHL FLAIR.

Figure 1 Selection of the study population

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

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 MRI at presentation The axial diffusion-weighted image (A) showed restricted diffusion throughout the cortical ribbon of the right hemisphere.

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 1 Imaging of disease onset and treatment response Repeat MRI scans including fluid-attenuated inversion recovery (FLAIR) (A) and T2 fast field echo (B) sequences. Imaging of disease onset and treatment response Repeat MRI scans including fluid-attenuated inversion recovery (FLAIR) (A) and T2 fast field echo (B) sequences. All images were acquired on a 3T MRI scanner. Upon initiation of immunosuppressive treatment in April 2009, there was a rapid resolution of FLAIR hyperintensities within 8 weeks. In response to the following maintenance therapy, the number of microbleeds markedly dropped. Andreas Traschütz et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e165 © 2015 American Academy of Neurology