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

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Date of download: 6/6/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Lessons Learned From Fatal Progressive Multifocal.

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Neurology Resident and Fellow Section

Neurology Resident and Fellow Section

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

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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

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Figure 2 Evolution of MRI abnormalities in faciobrachial dystonic seizures Axial fluid- attenuated inversion recovery (FLAIR)-weighted images from patient.

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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

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Figure 3 MRI findings in opportunistic infections of the CNS

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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.

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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.

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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.

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Presentation transcript:

Figure Radiologic and pathologic findings Fluid-attenuated inversion recovery (FLAIR) sequence with a single large T2-hyperintense signal involving the left frontoparietal lobe (A) with gadolinium-enhanced (Gd+) T1-weighted imaging (T1WI) demonstrating a small central area of contrast enhancement (B). Radiologic and pathologic findings Fluid-attenuated inversion recovery (FLAIR) sequence with a single large T2-hyperintense signal involving the left frontoparietal lobe (A) with gadolinium-enhanced (Gd+) T1-weighted imaging (T1WI) demonstrating a small central area of contrast enhancement (B). FLAIR sequence demonstrating ongoing new T2 lesions involving bilateral hemispheres (C) with evidence of blood-brain barrier opening, with Gd+ T1WI again corresponding to the left parietal lobe lesion (D). Preferential involvement of the central portion of the corpus callosum (known as “snowball” lesions) (E) as well as a central callosal hole (F). FLAIR sequence demonstrating extensive T2-hyperintense lesions (G) with corresponding postcontrast T1WI confirming leptomeningeal enhancement along the left parietal hemisphere (H) days after the patient's first natalizumab infusion. (I) Low-power Luxol fast blue (LFB) hematoxylin & eosin (H&E) stain demonstrates white matter with patchy myelin loss. Myelin loss was most prominent in the perivascular white matter, with greater perivenular than periarterial involvement. (J) High-power view of perivascular macrophages also contained small particles of LFB– and periodic acid-Schiff–positive material consistent with the myelin accumulation, which can be seen in demyelinating disorders. (K) Vascular deposits of C3d. (L) A venule infiltrated by macrophages and lymphocytes. There is evidence of vascular compromise characterized by marked red cell extravasation. (M) Neurofilament stain, an axonal marker, showed relative preservation of axons; however, axons were focally distended and showed evidence of axonal injury (yellow arrowheads). Lana Zhovtis Ryerson et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e151 © 2015 American Academy of Neurology