Effects of Athermal Shortwave Diathermy Treatment on Somatosensory Evoked Potentials and Motor Evoked Potentials in Rats With Spinal Cord Injury.

STUDY DESIGN: A study on shortwave diathermy (SWD) versus no treatment following induced spinal cord injury (SCI) in rats. OBJECTIVE: To investigate the effects of athermal SWD treatment on somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) and hindlimb movements in rats with SCI. SUMMARY OF BACKGROUND DATA: SWD has been proven to improve vascular circulation and reduce inflammation. However, there have been few studies on neuroprotective effect of SWD on SCI. METHODS: Twenty-four female Sprague-Dawley (SD) rats were randomly divided into four groups: sham, SCI, SWD, and intact groups. The SCI model was established using the modified Allen weight-drop method. The SWD group received 15 sessions of athermal SWD treatment over a 3-week period of time at 24 hours after SCI. While the sham group and SCI group received no treatment after surgery. Hindlimb movements were evaluated by the Basso, Beattie, and Bresnahan (BBB) scale before surgery, and on days 1, 7, 14, and 21 after the surgery, respectively. The SEP and MEP measurements were simultaneously performed to detect the responses of neural conduction. RESULTS: The week-by-week BBB scores showed a gradual improvement in the rats of both SCI and SWD groups from the first week to the end of the study; however, the BBB scores of the SWD group were higher than those of the SCI group over the course of 3 weeks. Data from the SEP and MEP measurements showed a significant improvement in the SWD group compared with the SCI group at each time point of observation, with a more prominent increase of amplitude and a more evident reduction of latency. There was a linear correlation between the BBB scores and the latency and amplitude of SEPs or MEPs. CONCLUSION: Athermal SWD treatment might facilitate the recovery of locomotor function and exert neuroprotective effect on the SCI. LEVEL OF EVIDENCE: N/A.

Blocking of BDNF-TrkB signaling inhibits the promotion effect of neurological function recovery after treadmill training in rats with spinal cord injury.

STUDY DESIGN: Experimental study. OBJECTIVES: To investigate the role of BDNF-TrkB signaling that promotes the recovery of neurological function in rats with incomplete spinal cord injury (SCI) after treadmill training (TT). SETTING: Rehabilitation Medicine Center of the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. METHODS: Forty rats were divided into five groups: (i) Sham; (ii) SCI and phosphate-buffered saline (PBS) (SCI/PBS); (iii) SCI-TT/PBS; (iv) SCI/TrkB-IgG; and (v) SCI-TT/TrkB-IgG. The intrathecal catheter and T10 contusion SCI model was established. At 7-day post SCI, the BDNF-TrkB signaling was blocked by TrkB-IgG. Exercise began at 8th day after SCI and continued for 4 weeks. The BBB scale and motor-evoked potential (MEP) were used for the evaluation of the locomotor functions. The BDNF/TrkB, PSD-95, SYP synthesis, and neuroprotective effect was determined by western blot, Nissl, or immunohistochemistry staining. RESULTS: The expression of BDNF and TrkB in the SCI-TT/PBS group was 1.46 ± 0.09 and 1.70 ± 0.22, respectively, higher than that in SCI/PBS group (0.51 ± 0.04 and 0.76 ± 0.07, respectively), relative to the Sham group. The BBB scores in the Sham, SCI/PBS, SCI-TT/PBS, SCI/TrkB-IgG, and SCI-TT/TrkB-IgG groups were 21.00 ± 0.00, 7.63 ± 0.74, 12.13 ± 1.36, 7.88 ± 0.64, and 8.75 ± 0.88, respectively. The percentages of MEP responders/non-responders were 100, 0, 75, 0, and 50%. The MEP latencies in Sham, SCI-TT/PBS, and SCI-TT/TrkB-IgG groups were 6.65 ± 0.19, 13.32 ± 2.95, and 19.55 ± 4.55 ms, respectively. The number of NeuN+ neurons, the cell body area of motor neurons, PSD-95, and SYP expression in the SCI-TT/PBS group was significantly higher than that in the SCI/PBS, SCI/TrkB-IgG, and SCI-TT/TrkB-IgG groups. CONCLUSION: The BDNF-TrkB signaling is a critical pathway in exercise training that promotes the recovery of neurological function in rats with incomplete SCI.