A number of studies have shown that physical exercise improves neuropathic pain, but the exact mechanism underlying exercise–induced analgesia is not fully understood. It has been known that macrophages play important roles in the peripheral nervous system with regard to management of pain. Activated macrophages were categorized as M1 (classically activated) and M2 (alternatively activated), and several studies demonstrated that M1 macrophages are associated with the development of pain by releasing pro­inflammatory cytokines, while M2 macrophages are involved in the relief of pain via production of anti–inflammatory cytokines. Although these results suggest that M2 macrophages may contribute to exercise–induced analgesia, it has never been examined whether physical exercise changes phenotypes of activated macrophages in injured nerves, and thereby contributes to the attenua­tion of neuropathic pain. Therefore, we examined the effects of running exercise on the changes of macrophage polarity in injured sciatic nerve of neuropathic pain model mice. Male C57BL ⁄ 6J mice received partial sciatic nerve ligation (PSL) on the right sciatic nerves, and were divided into five groups: Naïve, PSL–Sedentary, PSL–Runner, Sham–Sedentary and Sham–Runner mice. The Runner mice ran at a speed of 7 m/min for 60 min/day, 5 days/week from 2 days after PSL operation. PSL–Sedentary mice developed remarkable mechanical allodynia and thermal hyperalgesia, but the pain behaviors were significantly attenuated in PSL–Runner mice. After PSL, the number of CD68⁺ M1 macrophages was increased in injured sciatic nerves, but running exercise induced significant decrease of these macrophages. On the other hand, the number of CD206⁺ M2 macrophages in PSL–Runner mice was significantly increased within the proximal parts of injured sciatic nerve compared with that of PSL–Sedentary mice. Changes in the ratio of macrophage subtypes (Intermediate, M1 and M2) indicated that running exercise increased both Intermediate and M2 subtypes within proximal parts of injured sciatic nerves. The present study indicated that running exercise attenuated neuropathic pain at least partly by changing balance between M1 and M2 macrophages in injured sciatic nerve, and suggested that activation of M2 macrophages may contribute to produce exercise–induced analgesia in neuropathic pain condition.

抄録全体を表示

   The speed of change in pain intensity as measured by the visual analog scale (VAS) was investigated in patients with acute low back pain (LBP). Each patient was initially treated with oral nonsteroidal anti–inflammatory drugs (NSAIDs). Clinical outcome was determined by patient self–assessment on the day of the last visit and classified into four groups: healed, improved, marginal, and unidentified. Data were analyzed for 131 cases in the healed (n=55), improved (n=62), and marginal (n=14) groups. VAS values at the first and last visits were denoted as VAS–f and VAS–l, respective­ly. ∆VAS, the speed of change in the VAS value per day was calculat­ed by dividing the change in the VAS value by the number of days elapsed. The initial ∆VAS (∆VAS–i) and the ∆VAS throughout the study (∆VAS–t) were calculated between the first and second visits and between the first and last visits, respective­ly. VAS–f was not relevant to outcome, while VAS–l was strongly cor­related with outcome, as expected. Both ∆VAS–i and ∆VAS–t were significantly correlated with outcome. Patients in the healed and improved groups showed higher ∆VAS–i values as compared with those in the marginal group. A ∆VAS–i over 5 mm/day predicted favorable outcomes. The ∆VAS–i can be regarded as a predictor of outcome in acute LBP. Speedy pain relief should be planned for patients with acute LBP with a low ∆VAS–i to prevent a change to chronic LBP.

抄録全体を表示

   We previously reported on how patients catastrophize pain after total knee arthroplasty (TKA), indicating the importance of patient education in preventing pain catastrophizing. This study aimed to examine whether patient education reduces postoperative pain catastrophizing and to assess the effectiveness of video–based postoperative patient education.
   TKA was performed at the Fukuoka Rehabilitation Hospital between October 2012 and December 2013. We established a control group comprising patients who had undergone TKA between October 2012 and December 2013 and underwent normal postoperative rehabilitation, and a video group comprising TKA patients who had undergone TKA between June 2013 and December 2013 and underwent preoperative and postoperative (3 and 5 weeks postoperatively) patient education in addition to their normal rehabilitation. Their education comprised a 7–minute video, followed by an explanation by their physical therapist (PT), who also provided appropriate responses to the patients’ questions. The video covered topics such as early–stage post­operative rehabilitation (expanding range of motion and muscle strengthening), and indoor and outdoor walking practice, as well as showed actual patients undergoing rehabilitation. The pain catastrophizing scale (PCS) was used to assess preoperative and postoperative (3 and 5 weeks after surgery) pain catastrophizing, and the numerical rating scale (NRS) was used for postoperative assessments. The total PCS score was defined as the sum of PCS scores in the following subscales: rumination, helplessness, and magnification. The validity of the differences in PCS and visual analog scale scores was compared using 2–way analysis of variance and post hoc Bonferroni correction. The statistical significance level was set at < 5%.
   No significant differences in preoperative and postoperative total PCS scores or in the PCS scores in the magnification and helplessness subscales in both postoperative periods were noted between the two groups. However, the video group had significantly lower PCS scores for rumination in both postoperative periods. In addition, the video group generally had significantly lower pain scores at postoperative 5 weeks.
   Based on our findings, patients may concretely predict their pain by viewing the video provided by their PT during patient education. The video may reflect whether patients should allow their psychological condition to dictate their physical functions, given their present pain or condition. The influence of the patient’s psychological condition may be related to pain allevia­tion at postoperative 5 weeks. Thus, video–based patient education is an effective modality for stabilizing patients’ postoperative psychological conditions and alleviating postoperative pain.

抄録全体を表示

   Whereas the central nervous system usually cannot regenerate, axons within the peripheral nervous system regenerate spontaneously and rapidly after injury. To study molecular mechanisms of peripheral nerve regeneration, we established the sciatic nerve transection–regeneration model by using a combination of tabulation and osmotic mini–pump to deliver drugs at a constant rate for at least 4 weeks and have recently demonstrated that endo­thelin (ET)–1 was involved in the nerve regeneration. In the present study, to clarify which receptors of ET–1 mediated its action, we examined the effect of ET_AR and ET_BR antagonists on the functional recovery. Mice started to resume mechanical responses of their hind paws 5 weeks after the sciatic nerve transection and returned to the level before operation by 7 weeks. Time course of the functional recovery is well cor­related with that of nerve regeneration assessed by elongation of axons express­ing yellow fluores­cent protein and application of fluoro–ruby, a fluores­cent retrograde tracer, to the distal stump of the transected nerve. The ET_BR antagonist, but not ET_AR antagonist, delayed the functional recovery in the model mice. Taken together with ET_BR expression in Schwann cells, these results demonstrate that ET–1 is involved in peripheral nerve regeneration via ET_BR.

抄録全体を表示

   We have previously reported the efficacy of 5 Hz repetitive transcranial magnetic stimulation (rTMS) of the primary motor cortex (M1) in relief of central post–stroke pain (CPSP). The objective of this study was to explore changes of functional connectivity related to CPSP condition, and to assess changes of functional connectivity induced by rTMS in patients with CPSP. In 14 patients with CPSP and 14 control subjects, resting–state functional MRI were taken. Twelve of these patients received 5 Hz–rTMS of M1, and underwent resting–state functional MRI before and after rTMS. Functional connectivity associated with motor and default mode networks increased in patients with CPSP compared with control subjects. Moreover, functional connectivity associated with default mode network and anterior cingulate cortex decreased after rTMS. These findings suggest that several functional networks are involved in pathophysiology of CPSP and mechanisms of action of rTMS.

抄録全体を表示