Affordable Access

deepdyve-link
Publisher Website

Early movement restriction leads to enduring disorders in muscle and locomotion.

Authors
  • Delcour, Maxime1
  • Massicotte, Vicky S2
  • Russier, Michaël1
  • Bras, Hélène3
  • Peyronnet, Julie3
  • Canu, Marie-Hélène4
  • Cayetanot, Florence3
  • Barbe, Mary F2
  • Coq, Jacques-Olivier1, 3
  • 1 Neurosciences Intégratives et Adaptatives, UMR 7260, CNRS, Aix-Marseille Université, Marseille, France. , (France)
  • 2 Department of Anatomy and Cell Biology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA.
  • 3 Institut de Neurosciences de la Timone, UMR 7289, CNRS, Aix-Marseille Université, Marseille, France. , (France)
  • 4 Université de Lille, EA 7369 « Activité Physique, Muscle et Santé » - URePSSS - Unité de Recherche Pluridisciplinaire Sport Santé Société, 59000 Lille, France. , (France)
Type
Published Article
Journal
Brain Pathology
Publisher
Wiley (Blackwell Publishing)
Publication Date
Nov 01, 2018
Volume
28
Issue
6
Pages
889–901
Identifiers
DOI: 10.1111/bpa.12594
PMID: 29437246
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Motor control and body representation in the central nervous system (CNS) as well as musculoskeletal architecture and physiology are shaped during development by sensorimotor experience and feedback, but the emergence of locomotor disorders during maturation and their persistence over time remain a matter of debate in the absence of brain damage. By using transient immobilization of the hind limbs, we investigated the enduring impact of postnatal sensorimotor restriction (SMR) on gait and posture on treadmill, age-related changes in locomotion, musculoskeletal histopathology and Hoffmann reflex in adult rats without brain damage. SMR degrades most gait parameters and induces overextended knees and ankles, leading to digitigrade locomotion that resembles equinus. Based on variations in gait parameters, SMR appears to alter age-dependent plasticity of treadmill locomotion. SMR also leads to small but significantly decreased tibial bone length, chondromalacia, degenerative changes in the knee joint, gastrocnemius myofiber atrophy and muscle hyperreflexia, suggestive of spasticity. We showed that reduced and atypical patterns of motor outputs, and somatosensory inputs and feedback to the immature CNS, even in the absence of perinatal brain damage, play a pivotal role in the emergence of movement disorders and musculoskeletal pathologies, and in their persistence over time. Understanding how atypical sensorimotor development likely contributes to these degradations may guide effective rehabilitation treatments in children with either acquired (ie, with brain damage) or developmental (ie, without brain injury) motor disabilities. © 2018 International Society of Neuropathology.

Report this publication

Statistics

Seen <100 times