Musculoskeletal pain is associated with altered motor control that, despite short-term benefit, is hypothesised to have long-term consequences, contributing to the development of chronic pain. However, data on how motor control is altered when pain is sustained beyond a transient event are scarce. Here, we investigated motor adaptation, and its relationship with corticomotor excitability, in the transition to sustained muscle pain. Twenty-eight healthy individuals were injected with nerve growth factor into the right extensor carpi radialis brevis muscle on days 0 and 2. Motor adaptation and corticomotor excitability were assessed on day −2, before injection on days 0 and 2, and again on days 4 and 14. Motor adaptation was quantified during a radial–ulnar movement as kinematic variability of wrist flexion–extension and pronation–supination, and as electromyographic (EMG) variability of extensor carpi radialis brevis activity. Pain, muscle soreness, and functional limitation were assessed from days 0 to 14. Pain, muscle soreness, and functional limitation were evident at days 2 and 4 (P < 0.001). Electromyographic variability reduced at days 4 and 14 (P < 0.04), with no change in kinematic variability (P = 0.9). However, data revealed variation in EMG and kinematic variability between individuals: some displayed increased motor variability, whereas others a decrease. Individuals who displayed an increase in EMG variability after 4 days of pain also displayed an increase in corticomotor excitability (r = 0.43, P = 0.034). These findings suggest individual adaptation of the motor system in the transition to sustained pain that could have implications for clinical musculoskeletal pain disorders.
The movement strategy adopted by an individual in the transition to sustained pain is related to his/her motor cortical strategy, but the strategy differs between individuals.
aSchool of Science and Health, Western Sydney University, New South Wales, Sydney, Australia
bFaculty of Health, University of Canberra, Australian Capital Territory, Canberra, Australia
cDepartment of Health Science and Technology, Aalborg University, Aalborg, Denmark
dCenter for Neuroplasticity and Pain (CNAP), SMI, Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark
eNeuroscience Research Australia, New South Wales, Sydney, Australia
Corresponding author. Address: Neuroscience Research Australia, Margarete Ainsworth Building, 139 Barker St (PO Box 1165), Randwick, NSW 2031, Australia. Tel.: +61 421568494. E-mail address: email@example.com (S.M. Schabrun).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received January 10, 2019
Received in revised form April 25, 2019
Accepted April 29, 2019
Online date: May 8, 2019