Figure 2 2010 Prevalence for MS cumulated over 10 years in the United States per 100,000 population by age and sex 2010 Prevalence for MS cumulated over.

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Figure Pedigrees of the SCA42 families identified in this study

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Figure EDSS, FS scores, and Modified MSFC scores

Figure 2 ERG amplitude reduction in the follow-up study

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

Figure 3 Pedigree of familial idiopathic transverse myelitis

Figure 1 Box plot of the venous diameter in lesions

Figure 2 Needle biopsy of the left vastus lateralis

Figure 2 Spinal cord lesions

Figure 4 Correlation of age with [11C](R)-PK11195 binding in the normal-appearing white matter (NAWM) and thalami Correlation of age with [11C](R)-PK11195.

Figure 1 Hierarchical clustering (HCL) outcome of all tested samples with the expression profile of the case report set as unknown Hierarchical clustering.

Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production

Figure 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.

Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.

Figure 1 Comparison of miR-150-5p (log scale), prednisone dose (mg), and QMG score between the thymectomy (ETTX) and prednisone groups Comparison of miR-150-5p.

Figure 2 Neurochemical profiles for each neurocognitive trajectory

Figure 3 Age, pretreatment, sex, and leukopenia do not influence CD19+ cell repopulation Age, pretreatment, sex, and leukopenia do not influence CD19+

Figure Pedigree of the family

Figure 4 Detection of EBER+ cells in MS and control brains by in situ hybridization Detection of EBER+ cells in MS and control brains by in situ hybridization.

Figure 1 Linear relationship between CSF inflammation and glucose in meningitis; analysis stratified by diagnostic category (aseptic, n = 115 and microbial,

Figure 2 Luciferase assays of transiently transfected HEK 293 cells with reporter constructs containing the 766-bp wild-type KCNJ18 or c.-542 T/A mutant.

Figure 3 Gene expression in CSF cell pellets

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure Association of hippocampal subfield volumes to cognition by neopterin level, volumes, and cognition adjusted for age, education, race, sex, and.

Figure 1 Dominant and recessive missense and nonsense variants in neurofilament light (NEFL)‏ Dominant and recessive missense and nonsense variants in.

Figure 2 Forest plots for subgroup analyses

Figure 3 Temporal trends in FALS incidence

Table 4 Associations in SNP array data between the Braak stage and previously known AD risk loci (341 variants) comparing participants with Braak stage.

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

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 3 Receiver operating characteristics for CSF glucose (n = 225) and serum/CSF glucose ratio (n = 156) as predictors for microbial meningitis Receiver.

Figure 1 Characteristics of the German National MS Cohort

Figure 2 Linkage analysis of chromosome 19

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 Family tree with the HLA haplotyping of 6 members of the family

Figure 4 Relative abundances of the order Clostridiales and its family members are differentially changed by therapy Relative abundances of the order Clostridiales.

Figure 2 Functionally significant genes

Table 2 Rs number, gene, OR, 95% CI, and permutation p value for the statistical significant variants resulted from allelic association analysis association.

Figure 1 Family pedigree and DNA sequencing results

Figure 4 Voltage-clamp recordings of KCNJ18 carrying the patient's SNVs expressed in Xenopus laevis oocytes under control conditions and after application.

Figure 1 [18F]florbetapir standardized uptake value ratio analytical method [18F]florbetapir standardized uptake value ratio analytical method Flowchart.

Figure Alluvial plot of modified Rankin Scale (mRS) scores during and at the end of hospital stay Alluvial plot of modified Rankin Scale (mRS) scores during.

Figure 3 Comparisons of quantitative spinal cord MRI measures and brain atrophy in RIS vs. healthy controls (adjusted for age and sex)‏ Comparisons of.

Figure 1 Flowchart of patient inclusion

Figure 6 Cellular composition after tissue dissociation

Figure 1 Histamine flare in patients and controls

Figure 2 Changes in fatigue under treatment

Figure 1 Considerations for concussed athletes leading to medical care or return to sport (RTS)‏ Considerations for concussed athletes leading to medical.

Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.

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

Figure 2 Kaplan-Meier survival graphs for 10-year risks of overall and post-90-day recurrent ischemic stroke (IS) and death Kaplan-Meier survival graphs.

Figure 1 Stacked bar chart depicts the proportion of patients with diffusion-weighted imaging (DWI)+ and DWI− scans categorized by index event type TIA.

Figure 1 Annualized percentage brain volume change

Figure 2 BVL according to on-study disability worsening

Figure 2 Repopulation of CD19+ cells in low and high BSA patients and calculation of the BSA Repopulation of CD19+ cells in low and high BSA patients and.

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 1 bvFTD PINBPA network

Figure 2 Seizure outcomes

Figure 2 Overview of apheresis therapies

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Figure 2 Pedigrees of families and segregation analysis of variants c

Figure 1 ASO functions ASO functions Target mRNA fates depending on ASO mechanism of action that is determined by where the ASO is targeted and by ASO.

Figure 3 Within-group comparisons (before–after)‏

Figure 2 Between-group comparisons

Figure 1 Segmentation of the normal-appearing periependymal white matter Segmentation of the normal-appearing periependymal white matter The figure demonstrates.

Figure 2 Time from incident ADS event to MS diagnosis

Figure 4 Venn diagram for B-cell Sup proteins compared with proteins from exosome-enriched fractions from a human B-cell line Venn diagram for B-cell Sup.

Figure 3 A receiver operating characteristic curve of days to IVMP as a predictor of failure to regain 0.2 logMAR (20/30) vision (AUC 0.84, p < 0.001)‏

Figure (A and B) Effect of canakinumab in muscle strength measured in each patient as mean bilateral GF (A) and TMS (B) during the mean study period of.

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Figure 2 2010 Prevalence for MS cumulated over 10 years in the United States per 100,000 population by age and sex 2010 Prevalence for MS cumulated over 10 years in the United States per 100,000 population by age and sex Higher and lower estimates adjusted to 2010 US Census based on combined datasets from the multiple sclerosis (MS) algorithm inclusive of the following: Truven, Optum, Department of Veterans Affairs, Medicare, and Medicaid (full data available for all age and sex estimates in data table e-7 available from Dryad, https://doi.org/10.5061/dryad.pm793v8). (A) Lower-estimate and (B) higher-estimate 2010 MS prevalence in the United States per 100,000 population. Mitchell T. Wallin et al. Neurology 2019;92:e1029-e1040 Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.