Peripheral neuritis and increased spinal cord neurochemicals are induced in a model of repetitive motion injury with low force and repetition exposure

Brain Res. 2008 Jul 7:1218:103-13. doi: 10.1016/j.brainres.2008.04.029. Epub 2008 Apr 23.

Abstract

Performance of high repetition tasks with or without force is associated with peripheral tissue inflammation, decreased nerve function and motor dysfunction. Here, we examined whether a low repetition task with negligible force (LRNF) produces fewer tissue and behavioral pathologies than previously observed with high repetition tasks using our rat model of repetitive motion injury (RMI). Thirty-seven rats were randomized into control or LRNF groups, the latter reaching and grasping a 45 mg food pellet at a rate of 3 reaches/min. This task was performed in 4, 0.5 5 h sessions with 1.5 5 h rest periods for 3 days/week for up to 12 weeks. Examination of distal median nerve, forelimb flexor tendons and bones for ED1-positive cells (macrophages and osteoclasts) revealed increases in nerve and bone in week 12. The nerve also contained increased TNF-alpha expressing cells in week 12. Examination of spinal cord dorsal horns revealed increased immunoexpression of Substance P in week 8 and neurokinin-1 in weeks 8 and 12 in the superficial lamina. Motor behavioral analyses showed no changes in reach rate across weeks, slightly reduced task duration (a measurement of voluntary task participation) in week 12, but significantly increased extra arm movement reversals during reaching in week 8. These extra movement reversals were corrections for missed food pellets during a reach. Thus, performance of even a low repetition, negligible force upper extremity task for 3 months can induce mild peripheral tissue inflammation, neurochemical increases in spinal cord dorsal horns, and declines in fine motor control.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Behavior, Animal
  • Bone and Bones / metabolism
  • Cumulative Trauma Disorders / complications*
  • Cumulative Trauma Disorders / pathology*
  • Disease Models, Animal
  • Ectodysplasins / metabolism
  • Enzyme-Linked Immunosorbent Assay / methods
  • Feeding Behavior / physiology
  • Female
  • Median Nerve / physiopathology
  • Neuritis / etiology*
  • Psychomotor Performance / physiology
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Neurokinin-1 / metabolism*
  • Spinal Cord / metabolism*
  • Substance P / metabolism*
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism
  • Upper Extremity / innervation

Substances

  • Ectodysplasins
  • Receptors, Neurokinin-1
  • Tumor Necrosis Factor-alpha
  • Substance P