Figure 3 Archetypal MS clinical course depicted over 20 years

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Nat. Rev. Neurol. doi: /nrneurol

Figure 1 The topographical model of multiple sclerosis, clinical (A) and subclinical (B) views The topographical model of multiple sclerosis, clinical.

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 3 Associations of [11C](R)-PK11195 binding to disability and diffusion tensor imaging (DTI) changes in patients with MS Associations of [11C](R)-PK11195.

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

Figure 2 Spinal cord lesions

Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.

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 Coronal MRI images showing the evolution of white matter abnormality and atrophy of patient 1 Coronal MRI images showing the evolution of white.

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 1 Evolution of multiple sclerosis

Figure 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.

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 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)

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 Punctate PML lesions visualized by highly resolving T2

Figure 2 Forest plots for subgroup analyses

Figure 2. ROC curves for different group comparisons

Figure 1 Characteristics of the German National MS Cohort

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 2 Example of venous narrowing

Figure 2 Lesion localization visualized in the top view of the model

Figure 1 Illustration of white matter– and lesion-associated regions of interest (ROIs)‏ Illustration of white matter– and lesion-associated regions of.

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

Figure 3 Analysis of the prognostic value of IL-10–producing B cells or IL-6/IL-10–B-cell ratio measurements in patients with RIS/CIS MS Analysis of the.

Figure 2 Cerebral and spinal MRI (A) Restricted diffusion of both optic nerves (arrows) on diffusion-weighted and apparent diffusion coefficient imaging.

New Insights into Multiple Sclerosis Clinical Course from the Topographical Model and Functional Reserve Stephen C. Krieger, MD, James Sumowski, PhD

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

Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.

Figure 2 Individual EDSS scores

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 Phenotype and functional properties of B cells in MS and HCs at baseline Phenotype and functional properties of B cells in MS and HCs at baseline.

Figure Correlation between the Kurtzke Expanded Disability Status Scale and the relative expression of hsa-miR-337-3p Correlation between the Kurtzke Expanded.

Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases Distribution of MOG IgG antibody in pediatric demyelinating diseases (A)

Figure 2 Reduced frequency of central memory CD4 T cells in patients with PML Reduced frequency of central memory CD4 T cells (CD4Tcm) (p < ), naive.

Figure 5 Autopsy Mycoplasma DNA analysis

Figure 1 Evolution of MRI findings during interleukin (IL)–7 therapy

Figure 1 Anti-Epstein-Barr virus nuclear antigen-1 IgG quartile antibody status differences in MRI measures Anti-Epstein-Barr virus nuclear antigen-1 IgG.

Figure 1 BG-12 treatment reduced total circulating B cells and had variable effects on memory B cells BG-12 treatment reduced total circulating B cells.

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 3 Pedigrees of 3 multiplex families with NLRP3 mutations and MS The patient numbers refer to the patients listed in table 1. Pedigrees of 3 multiplex.

Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.

Figure 1 Radiologic features of patients with white matter syndromes in association with NMDA receptor antibodies Radiologic features of patients with.

Figure 2 Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing.

Figure 1 Levels of miR-150 are elevated in patients with multiple sclerosis (MS) and patients with clinically isolated syndrome (CIS) who convert to MS.

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

Figure 4. The N:M ratio is significantly increased in patients with ALS and correlates with disease progression The N:M ratio is significantly increased.

Figure 1 Volcano plot Peptides (n = 2,260) showing distribution of fold change and statistical significance. Volcano plot Peptides (n = 2,260) showing.

Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.

Figure 4 Four representative disease-course archetypes

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

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

Figure 2 MRIs (cases 2 and 3)‏

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

Figure 3 Freedom from clinical disease activity during 36 months of fingolimod treatment Freedom from clinical disease activity during 36 months of fingolimod.

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 2 Clinical data and variation of sNfL levels of patients 4–6 with ATZ-treated MS Clinical data and variation of sNfL levels of patients 4–6 with.

Figure 2 Time from incident ADS event to MS diagnosis

Figure 2. Percentage of CD16− monocytes in the blood is reduced during disease progression Percentage of CD16− monocytes in the blood is reduced during.

Figure 2 Region of interest (ROI)-specific [11C](R)-PK11195 binding in patients with relapsing-remitting MS (RRMS), patients with secondary progressive.

Figure 4 Illustration of a practice effect by examining longitudinal performance measures in patients with MS and cohabitants (A) Response time for each.

Figure 4 Longitudinal analysis of peripheral immune cell composition Frequency of naive, central memory (Tcm), and effector memory (Tem) CD4 T cells over.

Presentation transcript:

Figure 3 Archetypal MS clinical course depicted over 20 years Archetypal MS clinical course depicted over 20 years Still images from 5 key time points in this 20-year clinical course depiction are shown. (A) RIS: lesions emerge as topographical peaks that are apparent as T2 lesions on MRI but have not crossed the clinical threshold. (B) CIS: the first lesion (circled) to cross the clinical threshold denotes CIS. Lesions arising in the shallow end are more likely to cross the clinical threshold, as there is less functional reserve in these regions. (C) RRMS: the emergence of subsequent subthreshold lesions defines RRMS by the McDonald criteria. The second clinical relapse (circled) defines clinically definite MS—in this example, a brainstem attack. Additional lesions denote ongoing disease activity, i.e., “base effects.” (D) SPMS is characterized by a gradual decline in functional capacity, revealing the underlying lesion topography above the clinical threshold. Disability is driven here principally by the dropping threshold, i.e., “surface effects” (downward arrow). Progression takes the form of a patient's particular disease topography, unmasking existing deficits and recapitulating symptoms of prior relapse—in this example, multifocal myelopathy and brainstem/cerebellar signs. (E) SPMS with activity is demonstrated by a new relapse (circled) occurring in the context of progressive disease. CIS = clinically isolated syndrome; MS = multiple sclerosis; RIS = radiologically isolated syndrome; RRMS = relapsing-remitting MS; SPMS = secondary progressive MS. Stephen C. Krieger et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e279 © 2016 American Academy of Neurology