title: Performance of a high-repetition, high-force task induces carpal tunnel syndrome in rats.
abstract: METHODS
  A randomized controlled prospective experimental study with some repeated measures.
  
  
  OBJECTIVE
  To characterize behavioral, sensory, motor, and nerve conduction decrements, and histological changes in the median nerve in rats trained to perform a high-force repetitive task.
  
  
  BACKGROUND
  Understanding of work-related carpal tunnel syndrome is hampered by the lack of experimental studies of the causes and mechanisms of nerve compression induced by repetitive motion. Most animal models of nerve compression have not employed voluntary repetitive motion as the stimulus for pathophysiological changes.
  
  
  METHODS
  Thirty Sprague-Dawley rats served as controls for 1 or more studies. Ten rats were trained to pull on a bar with 60% maximum force 4 times per minute, 2 h/d, 3 d/wk for 12 weeks. Motor behavior and limb withdrawal threshold force were characterized weekly. Grip strength and median nerve conduction velocity were measured after 12 weeks. Median nerves were examined immunohistochemically for ED1-positive macrophages, collagen, and connective tissue growth factor.
  
  
  RESULTS
  Reach rate and duration of task performance declined over 12 weeks. Grip strength and nerve conduction velocity were significantly lower after 12 weeks than in controls. Limb withdrawal threshold increased between weeks 6 and 12. Median nerves at the level of the wrist showed increases in macrophages, collagen, and connective-tissue growth-factor-positive cells. These effects were seen in both the reach and nonreach limbs.
  
  
  CONCLUSIONS
  This animal model exhibits all the features of human carpal tunnel syndrome, including impaired sensation, motor weakness, and decreased median nerve conduction velocity. It establishes a causal relationship between performance of a repetitive task and development of carpal tunnel syndrome.
authors.affiliation: Department of Physical Therapy, Temple University, Philadelphia, PA 19140, USA. brian.clark@temple.edu
authors.forename: Brian D
authors.initials: BD
authors.lastname: Clark
authors.forename: Talal A
authors.initials: TA
authors.lastname: Al-Shatti
authors.forename: Ann E
authors.initials: AE
authors.lastname: Barr
authors.forename: Mamta
authors.initials: M
authors.lastname: Amin
authors.forename: Mary F
authors.initials: MF
authors.lastname: Barbe
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D002349:Carpal Tunnel Syndrome / Q000503:physiopathology*; D003094:Collagen / Q000032:analysis; D055513:Connective Tissue Growth Factor; D005260:Female; D017874:Immediate-Early Proteins / Q000032:analysis; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis; D008264:Macrophages / Q000166:cytology / Q000378:metabolism; D008475:Median Nerve / Q000737:chemistry / Q000503:physiopathology; D009431:Neural Conduction / Q000502:physiology; D011446:Prospective Studies; D011597:Psychomotor Performance / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013647:Task Performance and Analysis
chemical_list: C526317:CCN2 protein, human; C526316:CCN2 protein, rat; D017874:Immediate-Early Proteins; D036341:Intercellular Signaling Peptides and Proteins; D055513:Connective Tissue Growth Factor; D003094:Collagen