Therapeutic ultrasound in combination with treadmill training reduces neuropathic pain more than either modality alone. - GreenMedInfo Summary
Therapeutic Ultrasound and Treadmill Training Suppress Peripheral Nerve Injury Induced-Pain in Rats.
Phys Ther. 2016 Apr 28. Epub 2016 Apr 28. PMID: 27126126
Ching-Hsia Hung
BACKGROUND: Although evidence suggests that therapeutic ultrasound (TU) in combination with treadmill training (TT) suppresses nerve injury-associated pain, the molecular mechanisms for this action are not clear.
OBJECTIVE: The purpose of this research was to study the possible beneficial effects of TU and TT, alone and in combination, on two clinical indicators of neuropathic pain and to correlate these findings with changes in inflammatory mediators within the spinal cord. Our experimental model used the well-known chronic constriction injury (CCI) of the rat sciatic nerve.
DESIGN: An experimental study.
METHODS: Each group contained 10 rats. Group 1 underwent only the CCI procedure. Group 2 underwent a sham-operation where the sciatic nerve was exposed but not ligated. Group 3 had the sham-operation followed by both TT and TU. Groups 4, 5, and 6 underwent the CCI procedure followed by TT alone, TU alone, and both the TT and TU interventions, respectively. Heat and mechanical sensitivity, interleukin-6 (IL-6), IL-10, and ionized calcium binding adaptor molecule 1 (iba-1) were evaluated.
RESULTS: Compared to Group 1 animals, TT and/or TU produced smaller decreases in mechanical withdrawal threshold and heat withdrawal latencies. The combination of TT and TU was more effective than either treatment alone. In addition, rats who received these treatments did not express the upregulation of IL-6 and iba-1 in their spinal cords on postoperative days 14 and 28, as was found in the Group 1 animals.
LIMITATIONS: These experimental findings may not be generalizable to humans.
CONCLUSIONS: The combination of TU + TT reduces neuropathic pain more than either modality alone. This beneficial effect appears related to down-regulation of pro-inflammatory IL-6 and iba-1, while up-regulating the anti-inflammatory IL-10.