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Peripheral and central changes combine to induce motor behavioral deficits in a moderate repetition task.

Coq-JO; Barr-AE; Strata-F; Russier-M; Kietrys-DM; Merzenich-MM; Byl-NN; Barbe-MF
Exp Neurol 2009 Dec; 220(2):234-245
Repetitive motion disorders, such as carpal tunnel syndrome and focal hand dystonia, can be associated with tasks that require prolonged, repetitive behaviors. Previous studies using animal models of repetitive motion have correlated cortical neuroplastic changes or peripheral tissue inflammation with fine motor performance. However, the possibility that both peripheral and central mechanisms coexist with altered motor performance has not been studied. In this study, we investigated the relationship between motor behavior changes associated with repetitive behaviors and both peripheral tissue inflammation and cortical neuroplasticity. A rat model of reaching and grasping involving moderate repetitive reaching with negligible force (MRNF) was used. Rats performed the MRNF task for 2 h/day, 3 days/week for 8 weeks. Reach performance was monitored by measuring reach rate/success, daily exposure, reach movement reversals/patterns, reach/grasp phase times, grip strength and grooming function. With cumulative task exposure, reach performance, grip strength and agility declined while an inefficient food retrieval pattern increased. In S1 of MRNF rats, a dramatic disorganization of the topographic forepaw representation was observed, including the emergence of large receptive fields located on both the wrist/forearm and forepaw with alterations of neuronal properties. In M1, there was a drastic enlargement of the overall forepaw map area, and of the cortex devoted to digit, arm-digits and elbow-wrist responses. In addition, unusually low current amplitude evoked digit movements. IL-1 beta and TNF-alpha increased in forearm flexor muscles and tendons of MRNF animals. The increases in IL-1 beta and TNF-alpha negatively correlated with grip strength and amount of current needed to evoke forelimb movements. This study provides strong evidence that both peripheral inflammation and cortical neuroplasticity jointly contribute to the development of chronic repetitive motion disorders.
Ergonomics; Fatigue; Injuries; Injury-prevention; Laboratory-animals; Laboratory-testing; Motion-studies; Muscle-physiology; Muscle-stress; Musculoskeletal-system-disorders; Neurological-reactions; Neurological-system; Neuromotor-disorders; Neuromotor-system-disorders; Neuromuscular-system; Neuromuscular-system-disorders; Repetitive-work; Sensory-disorders; Sensory-motor-system; Work-analysis; Author Keywords: Repetitive motion injury; Movement disorders; Primary somatosensory cortex; Primary motor cortex; Electrophysiological mapping; Inflammation; Muscle; Tendon; TNF-a; IL-1ß
Mary F. Barbe, Department of Physical Therapy, College of Health Professions, Department of Anatomy and Cell Biology, Temple Medical School, Temple University, 3307 North Broad Street, Philadelphia, PA, 19140
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Experimental Neurology
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Temple University
Page last reviewed: September 2, 2020
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