AI Article Synopsis

  • This study investigated walking difficulties in people with multiple sclerosis (PwMS) by comparing their ankle proprioception and plantarflexor muscle performance to healthy controls.
  • Results showed that while PwMS had intact movement detection and joint position sense, they had slower reaction times and reduced muscle performance compared to controls, indicating potential areas of impairment.
  • Despite lower voluntary activation and torque during maximal contractions, PwMS did not exhibit muscle damage, suggesting that their issues may stem from neural drive rather than muscle strength itself.

Article Abstract

Background: A common and disruptive symptom of multiple sclerosis is difficulty in walking. Deficits in ankle proprioception and in plantarflexor muscle function may contribute to these mobility issues. In this study, ankle proprioceptive ability and plantarflexor performance of people with multiple sclerosis (PwMS) were compared to healthy controls to determine whether multiple sclerosis causes impairments in these systems.

Methods: PwMS (n = 30, median EDSS 4.0, IQR 2) were compared to age- and sex-matched healthy controls (n = 30) across tests of ankle proprioception and plantarflexor muscle performance. Proprioceptive tests: detection of passive movement, reaction time and ankle joint position sense. Plantarflexor performance: strength, fatigue, recovery and voluntary activation (level of neural drive) of the plantarflexor muscles, assessed through brief and sustained fatiguing (2 min) isometric maximal voluntary contractions with nerve stimulation to evoke superimposed and resting muscle twitches.

Results: PwMS had unimpaired movement detection and joint position sense but had a slower reaction time to respond with plantarflexion to an imposed ankle movement (between group difference = 0.11 [95% CI; 0.05 to 0.17] s). During brief, maximal contractions PwMS produced lower torque (difference = -25.1 [-42.0 to -8.2] Nm) with reduced voluntary activation (difference = -14.6 [-25.1 to -4.1]%) but no impairment of the muscle itself (resting twitch torque difference = 0.3 [-2.8 to 2.2] Nm). At the end of the fatiguing contraction, neural drive decreased for PwMS (-19.5 [-27.1 to -11.9]%, p <0.0001) but not for controls (-2.5 [-6.9 to 1.8]%, p = 0.242). Fatigue did not affect the resting twitch size for controls (-1.3 [-2.7 to -0.03] Nm, p = 0.134) or PwMS (-0.1 [-1.1 to 1.0] Nm, p = 0.90).

Conclusions: PwMS showed no deficit in their ability to sense ankle position or imposed movements but were slow when a motor response was required. Their plantarflexor muscles produced similar torque with electrical stimulation but voluntary strength was impaired.  Both groups experienced overall fatigue following the 2-minute maximal voluntary contraction but PwMS also had significantly reduced neural drive indicating central fatigue. PwMS showed mainly central deficits in motor output at the ankle with little impairment of proprioceptive acuity.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.msard.2020.102584DOI Listing

Publication Analysis

Top Keywords

multiple sclerosis
16
ankle proprioceptive
8
people multiple
8
ankle proprioception
8
proprioception plantarflexor
8
plantarflexor muscle
8
plantarflexor performance
8
healthy controls
8
reaction time
8
joint position
8

Similar Publications

An MRI assessment of mechanisms underlying lesion growth and shrinkage in multiple sclerosis.

Ann Clin Transl Neurol

January 2025

NMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.

Objective: To assess the pathological mechanisms contributing to white matter (WM) lesion expansion or contraction and remyelination in multiple sclerosis (MS).

Methods: We assessed 1,613 lesions in 49 people with relapsing-remitting MS in the CCMR-One bexarotene trial (EudraCT 2014-003145-99). We measured lesion orientation relative to WM tracts, surface-in gradients and veins.

View Article and Find Full Text PDF

This proceedings article summarizes the inaugural "T Cells in the Brain" symposium held at Columbia University. Experts gathered to explore the role of T cells in neurodegenerative diseases. Key topics included characterization of antigen-specific immune responses, T cell receptor (TCR) repertoire, microbial etiology in Alzheimer's disease (AD), and microglia-T cell crosstalk, with a focus on how T cells affect neuroinflammation and AD biomarkers like amyloid beta and tau.

View Article and Find Full Text PDF

Previously, our metabolomic, transcriptomic, and genomic studies characterized the ceramide/sphingomyelin pathway as a therapeutic target in Alzheimer's disease, and we demonstrated that FTY720, a sphingosine-1-phospahate receptor modulator approved for treatment of multiple sclerosis, recovers synaptic plasticity and memory in APP/PS1 mice. To further investigate how FTY720 rescues the pathology, we performed metabolomic analysis in brain, plasma, and liver of trained APP/PS1 and wild-type mice. APP/PS1 mice showed area-specific brain disturbances in polyamines, phospholipids, and sphingolipids.

View Article and Find Full Text PDF

We examine disease-specific and cross-disease functions of the human gut microbiome by colonizing germ-free mice, at risk for inflammatory arthritis, colitis, or neuroinflammation, with over 100 human fecal microbiomes from subjects with rheumatoid arthritis, ankylosing spondylitis, multiple sclerosis, ulcerative colitis, Crohn's disease, or colorectal cancer. We find common inflammatory phenotypes driven by microbiomes from individuals with intestinal inflammation or inflammatory arthritis, as well as distinct functions specific to microbiomes from multiple sclerosis patients. Inflammatory disease in mice colonized with human microbiomes correlated with systemic inflammation, measured by C-reactive protein, in the human donors.

View Article and Find Full Text PDF

Objectives: This case series describes adults with aquaporin 4 immunoglobulin G-seropositive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD) who switched treatment from eculizumab to satralizumab.

Methods: Case information for patients with AQP4-IgG+ NMOSD who received satralizumab for ≥6 months was obtained from US healthcare providers from April 2022 to January 2024. Patient characteristics, examination findings, diagnostic test results, treatment response, and adverse events were recorded.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!