Figure 3 Electron microscopy images of brain autopsy case II-2

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47-year-old with progressive upper limb weakness Teaching NeuroImages Neurology Resident and Fellow Section © 2014 American Academy of Neurology.

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Paul M. George, Gary K. Steinberg Neuron

Figure 1 Summary of prior diagnostic workup in neuromuscular disorder cases Summary of prior diagnostic workup in neuromuscular disorder cases Percentage.

Figure 1 Imaging, histopathology, and molecular evaluation of case 1 with definite leptomeningeal angiomatosis Imaging, histopathology, and molecular evaluation.

Figure 2 Needle biopsy of the left vastus lateralis

Figure 1 Immunofluorescence pattern of patient septin-5-immunoglobulin G binding to mouse tissues Immunofluorescence pattern of patient septin-5-immunoglobulin.

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 Sural nerve electron microscopy

Figure 2 Muscle pathology of patients 2, 26, 11, 9, 32, and 48

Electron Microscopy at Scale

Figure 2 Immunopathologic analysis of all 3 Rasmussen encephalitis cases Immunopathologic analysis of all 3 Rasmussen encephalitis cases (A) Perivascular.

Figure Immune checkpoint inhibitor–induced encephalitis before and after treatment with natalizumab Immune checkpoint inhibitor–induced encephalitis before.

Figure 2 FXTAS Rating Scale scores for case 1

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 1 MRI, pathology, and EEG findings(A) Axial fluid-attenuated inversion recovery (FLAIR) MRI sequences of the brain showing right frontal and parietal.

Figure 2 Neuropathologic examination for lymphoma etiology (patients 1–4)‏ Neuropathologic examination for lymphoma etiology (patients 1–4) Immunohistochemical.

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.

Volume 50, Issue 1, Pages (January 2014)

Figure MRIs and histopathology of the biopsy specimens

Figure 1 Genetic profile of 90 patients with dysferlin deficiency

Figure 2 Histochemical and immunohistochemical staining and electron microscopic examination of structures in the brain biopsy Hematoxylin & eosin staining.

Figure 3 Temporal trends in FALS incidence

Figure 1 All patients with pediatric genetic movement disorders, their genetic diagnoses, and type of genetic investigations All patients with pediatric.

Figure 2 Specific brain MRI findings of 8 patients

Figure 5 Neurite structure is not disrupted by the lack of neurofilament light (NEFL)‏ Neurite structure is not disrupted by the lack of neurofilament.

Figure Chronic inflammatory demyelinating polyneuropathy–like picture in patient with proven Creutzfeldt-Jakob disease (A) Example of partial conduction.

Figure 1 Mutations in SPG7 in a family with primary lateral sclerosis

Figure 2 Gross autopsy findings

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. Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem Neuropathologic diagnosis of Creutzfeldt-Jakob disease (CJD) at postmortem.

Figure 1 Within-groups sum of squares vs number of clusters Within-groups sum of squares vs number of clusters to determine the number needed for k-means.

Figure 2 Light microscopy images of brain autopsy case II-2

Figure 4. Electron microscopic findings in AP-5 patient cells

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 5 Autopsy Mycoplasma DNA analysis

Figure 1 Kernel density plots

Figure 1 Mutated CTSF in adult-onset neuronal ceroid lipofuscinosis and patients with frontotemporal dementia Mutated CTSF in adult-onset neuronal ceroid.

Figure 1 Patterns of study retention The proportion of individuals actively participating in the study is displayed over the course of the study. Patterns.

Figure 5 Electron microscopy of transfected HeLa cells and Dnm1Ftfl neurons (A) Electron microscopy (EM) of HeLa cells transfected with wild type (WT)

Figure 4 Unspecific MRI findings and facial dysmorphy in patients with germline variants Unspecific MRI findings and facial dysmorphy in patients with.

Figure 4 Gray and white matter structural connectivity analyses in patients with PPA according to KIAA0319 genotype Pattern of gray matter (A) and white.

Figure 2. Patient stratification by the reported duration of symptoms and disease severity at the time of assessment Patient stratification by the reported.

Figure Brain MRI findings before and during appearance of lymphoproliferative disorder and pathology findings of cerebellar lesion Brain MRI findings before.

Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial.

Figure ND5 and MCARNE phenotype

Figure Neurologic, gastrointestinal, and dermatologic findings

Figure MRI brain comparison prior and after treatment and brain biopsy findings MRI brain comparison prior and after treatment and brain biopsy findings.

Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.

Figure 4 CHCHD2 but not TOP1MT expression rescues molecular defects

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 Brain biopsy of 2 patients with anti-MOG encephalitis initially misdiagnosed with small vessel CNS vasculitis Brain biopsy of 2 patients with.

Figure 2 Neuroimaging characteristics of TARDBP carriers

Figure 2 Assessment of fluctuation in fatigue scores using environmental data The relationship between fatigue (as measured by the Modified Fatigue Impact.

Early MR imaging study at the age of 4 months in a patient with autopsy-proved infantile Alexander disease. Early MR imaging study at the age of 4 months.

A 53-year-old male patient with temporal lobe epilepsy (case 31).

Figure 1. MBP-specific IFN-γ+ but not IL-17+ frequencies are significantly different between patients with MS and HCs MBP-specific IFN-γ+ but not IL-17+

Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.

Figure 3. Temporal trends in individual serum lipid fractions in ICH patients by APOE allele carrier status Temporal trends in individual serum lipid fractions.

Brain biopsies from different patients showing typical sarcoid granuloma (short arrows) with a Langerhans-type giant cell (long arrow) (H&E, original magnification.

Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF and.

Figure 6 Multiple target epitopes exist in the N-terminal domains of Caspr2 (A) Multidomain deletion constructs of Caspr2 were generated to determine which.

Figure 3 Bilateral optic atrophy and sural nerve biopsy of patient AII-2 Bilateral optic atrophy and sural nerve biopsy of patient AII-2 (A) Red-free photographs.

Figure 3 Changing appearance of the frontal cortex with age associated with increasing myelination Changing appearance of the frontal cortex with age associated.

Figure 2 Striatal dopamine transporter binding with the SNCA A53E mutation Transaxial planes of [123I]FP-CIT SPECT on the striatal level are presented.

Figure 4 Patient 3 MRI evolution over time

Representative electron microscopic image from a patient with SMGN

Electron microscopy. Electron microscopy. A, 8 h after irradiation. An endothelial cell is seen protruding into the lumen of the vessel. Arrow head, a.

Figure 1 Representative radiologic and pathologic images of patients with brain somatic mutations in SLC35A2 Representative radiologic and pathologic images.

Newborn pattern of cerebral glucose metabolism.

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Figure 3 Electron microscopy images of brain autopsy case II-2 Electron microscopy images of brain autopsy case II-2 (A) Frontal cortex. Intraneuronal storage of lipofuscin-like inclusions. Magnification: ×5,750. (B) Occipital cortex. Neuronal inclusion showing a granular pattern and densely packed short lamellar profiles, coarser granular compounds, and lipid droplets. Magnification: ×41,000. (C) Nucleus dorsomedialis of the thalamus. Intraneuronal intermingled granular and lamellar complexes. Magnification: ×27,000. (D) Temporal cortex. Predominance of fingerprints in a neuronal inclusion. Magnification: ×52,500. (E) Brain biopsy of a 34-year-old female patient without neuronal ceroid lipofuscinosis (control). Intraneuronal classical lipofuscin. Magnification: ×41,000. (F) Electron microscopic examination of skin biopsy case II-5. Lipofuscin-like inclusion with an uncommon heterogeneous pattern in an endothelial cell of a blood vessel. Magnification: ×27,000. Scale = 1 μm. Julie van der Zee et al. Neurol Genet 2016;2:e102 © 2016 American Academy of Neurology