Painful and disabling musculoskeletal disorders remain prevalent. In rats trained to perform repetitive tasks leading to signs and dysfunction similar to those in humans, we tested whether manual therapy would prevent the development of the pathologies and symptoms. We collected behavioral, electrophysiological, and histological data from control rats, rats that trained for 5 weeks before performing a high-repetition high-force (HRHF) task for 3 weeks untreated, and trained rats that performed the task for 3 weeks while being treated 3x/week using modeled manual therapy (MMT) to the forearm (HRHF + MMT). The MMT included bilateral mobilization, skin rolling, and long axis stretching of the entire upper limb. High-repetition high-force rats showed decreased performance of the operant HRHF task and increased discomfort-related behaviors, starting after training. HRHF + MMT rats showed improved task performance and decreased discomfort-related behaviors compared with untreated HRHF rats. Subsets of rats were assayed for presence or absence of ongoing activity in C neurons and slow Aδ neurons in their median nerves. Neurons from HRHF rats had a heightened proportion of ongoing activity and altered conduction velocities compared with control and MMT-treated rats. Median nerve branches in HRHF rats contained increased numbers of CD68+ macrophages and degraded myelin basic protein, and showed increased extraneural collagen deposition, compared with the other groups. We conclude that the performance of the task for 3 weeks leads to increased ongoing activity in nociceptors, in parallel with behavioral and histological signs of neuritis and nerve injury, and that these pathophysiologies are largely prevented by MMT.
Manual therapy prevented functional and pathophysiological changes in rats that volitionally perform a task that leads to the development of a repetitive motion disorder.
aDepartment of Biomedical Sciences, University of New England College of Osteopathic Medicine, Biddeford, ME, United States
bDepartment of Anatomy and Cell Biology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States
cSquamish Integrated Health, Squamish, BC, Canada
Corresponding author. Address: Department of Biomedical Sciences, University of New England College of Osteopathic Medicine, Biddeford, ME 04005, United States. Tel.: 207 590 8949. E-mail address: firstname.lastname@example.org (G.M. Bove).
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Received August 15, 2018
Accepted November 05, 2018