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

Slides:



Advertisements
Similar presentations
Study Design 121 Relapsing-remitting MS patients randomized to –Stress Management Therapy MS active treatment* 16 individual sessions conducted over 24.
Advertisements

Defining the Clinical Course of Multiple Sclerosis.
Thrice-Weekly Glatiramer Acetate for Relapsing Forms of Multiple Sclerosis: Findings from the GALA Study Fred D. Lublin, MD Saunders Family Professor of.
Date of download: 6/3/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Effect of Anti-CD25 Antibody Daclizumab in the Inhibition.
Capturing the Costs of End-of-Life Care: Comparisons of Multiple Sclerosis, Parkinson's Disease, and Dementia  Paul McCrone, PhD  Journal of Pain and.
Four Known Types of MS Clinically isolated syndrome (CIS)
Brain health: time matters in multiple sclerosis
Figure EDSS, FS scores, and Modified MSFC scores
Figure 2 ERG amplitude reduction in the follow-up study
Nat. Rev. Neurol. doi: /nrneurol
Volume 383, Issue 9936, Pages (June 2014)
Figure 2. Infliximab treatment effect
Figure 1 The topographical model of multiple sclerosis, clinical (A) and subclinical (B) views The topographical model of multiple sclerosis, clinical.
The Business Case for Adult Disability Care Coordination
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 3 Archetypal MS clinical course depicted over 20 years
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 2 Disease progression slowed during each round of Treg infusions and correlated with increased Treg suppressive function Disease progression slowed.
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 1 Patient flow diagram
A pilot trial of treprostinil for the treatment and prevention of digital ulcers in patients with systemic sclerosis  Lorinda Chung, MD, David Fiorentino,
Figure 3 Example of venous narrowing
Figure 1 Evolution of multiple sclerosis
Functional Neurologic Symptoms: Assessment and Management
Nat. Rev. Neurol. doi: /nrneurol
Capturing the Costs of End-of-Life Care: Comparisons of Multiple Sclerosis, Parkinson's Disease, and Dementia  Paul McCrone, PhD  Journal of Pain and.
Figure 1 ERG peak time delay at baseline
Figure 2 Primary and secondary outcomes reported in multiple sclerosis (MS) disease-modifying therapy (DMT) clinical trials Primary and secondary outcomes.
Figure 1 Cerebral MRI during the disease course Cerebral MRI with multiple cerebral supratentorial lesions during the disease course: periventricular lesions.
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.
Long-term influence of combined oral contraceptive use on the clinical course of relapsing–remitting multiple sclerosis  Giulia Gava, M.D., Ilaria Bartolomei,
Figure 2. ROC curves for different group comparisons
Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.
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.
The Development of the Rotigotine Transdermal Patch
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 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 3 Correlation of lipid indexes to MRI measures of disease severity in multiple sclerosis Correlation of lipid indexes to MRI measures of disease.
Fig. 1 Kaplan-Meier plot presenting no difference in progression to RA in patients with clinically suspect ... Fig. 1 Kaplan-Meier plot presenting no difference.
Figure 3 Clinical and MRI outcomes by quartiles of increasing CD56bright natural killer (NK) cell countsAll data are mean and upper 95% confidence interval.
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 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 1 Clinical status and autoantibody titers in rituximab-treated patients with anti-CNTN1/NF155 chronic inflammatory demyelinating polyneuropathy.
Volume 33, Issue 4, Pages xiii-xiv (November 2015)
Figure 1 Annualized percentage brain volume change
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 Clinical course and overview of the treatment protocols♦ = neuroradiologic evidence of new disease activity; ★ = CD19+ reconstitution. Clinical.
Figure 2 Kaplan-Meier survival curves for the fingolimod cohort In each graph, bottom tertile: solid line; middle tertile: long dashed line; top tertile:
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 3 Freedom from clinical disease activity during 36 months of fingolimod treatment Freedom from clinical disease activity during 36 months of fingolimod.
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 1 EDSS score (A), T2LV (B) and T1LV (C) courses in patients who experienced WNS after FTY withdrawal EDSS score (A), T2LV (B) and T1LV (C) courses.
Figure 2 Region of interest (ROI)-specific [11C](R)-PK11195 binding in patients with relapsing-remitting MS (RRMS), patients with secondary progressive.
Figure 2 Correlations of subcortical gray matter SUVRs with the EDSS score, T25FW, and BPV in MS Correlations of subcortical gray matter SUVRs with the.
Figure 4 Illustration of a practice effect by examining longitudinal performance measures in patients with MS and cohabitants (A) Response time for each.
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.
Atrophied Brain T2 Lesion Volume at MRI Is Associated with Disability Progression and Conversion to Secondary Progressive Multiple Sclerosis The rate.
Presentation transcript:

New Insights into Multiple Sclerosis Clinical Course from the Topographical Model and Functional Reserve  Stephen C. Krieger, MD, James Sumowski, PhD  Neurologic Clinics  Volume 36, Issue 1, Pages 13-25 (February 2018) DOI: 10.1016/j.ncl.2017.08.003 Copyright © 2017 The Author(s) Terms and Conditions

Fig. 1 The 4 classic disease course phenotypes in multiple sclerosis. (Adapted from Lublin FD, Reingold SC. Defining the clinical course of multiple sclerosis: results of an international survey. Neurology 1996;46:907–11.) Neurologic Clinics 2018 36, 13-25DOI: (10.1016/j.ncl.2017.08.003) Copyright © 2017 The Author(s) Terms and Conditions

Fig. 2 Archetypal clinical course for multiple sclerosis (MS) incorporating clinical relapses, lesions, and the loss of neurologic reserve in tandem with accelerated brain atrophy. PPMS, primary progressive multiple sclerosis; SPMS, secondary progressive multiple sclerosis. (Courtesy of Dr Tim Vollmer, Aurora, CO; with permission.) Neurologic Clinics 2018 36, 13-25DOI: (10.1016/j.ncl.2017.08.003) Copyright © 2017 The Author(s) Terms and Conditions

Fig. 3 The topographical model of multiple sclerosis (MS), clinical (A) and subclinical (B) views. (A) Water is opaque, only above-threshold peaks are visible. (a) Above-threshold topographical peaks depict relapses and quantified Expanded Disability Status Scale (EDSS)/functional system disability measures. Each peak yields localizable clinical findings; the topographical distribution defines the clinical picture for an individual patient. (b) Water level at outset reflects baseline functional capacity and may be estimated by baseline brain volume. (c) Water level decrease reflects loss of functional reserve and may be estimated by metrics of annualized brain atrophy. (B) Subclinical view. The water is translucent, both clinical signs and subthreshold lesions are visible. (d) Subthreshold topographical peaks depict T2 lesion number and volume. (e) The tallest peaks (ie, the most destructive) in the cerebral hemispheres are shown capped in black as T1 black holes. (Data from Krieger SC, Cook K, De Nino S, et al. The topographical model of multiple sclerosis: a dynamic visualization of disease course. Neurol Neuroimmunol Neuroinflamm 2016;3:e279.) Neurologic Clinics 2018 36, 13-25DOI: (10.1016/j.ncl.2017.08.003) Copyright © 2017 The Author(s) Terms and Conditions

Fig. 4 Representative disease course archetype at 5 and 20 of years disease duration. The model conceptualizes relapsing and progressive contributions to disease course along a continuum: an individual’s disease course can be driven predominantly by relapses, or predominantly by progression, and those with very mild or stable disease may demonstrate neither. This archetypal disease course is shown at years 5 and 20. In progressive multiple sclerosis, several subthreshold lesions denote underlying early disease activity, which cross the clinical threshold as functional reserve declines yielding gradual accumulation of disability. (Data from Krieger SC, Cook K, De Nino S, et al. The topographical model of multiple sclerosis: a dynamic visualization of disease course. Neurol Neuroimmunol Neuroinflamm 2016;3:e279.) Neurologic Clinics 2018 36, 13-25DOI: (10.1016/j.ncl.2017.08.003) Copyright © 2017 The Author(s) Terms and Conditions