BACKGROUND: While the efficacy of pulsed radiofrequency (PRF) for shoulder pain has been demonstrated, its efficacy on the saphenous nerves for knee osteoarthritis (OA)-associated pain has only been reported in observational studies. OBJECTIVES: The aim of this study was to compare saphenous nerve PRF to placebo for knee OA-associated pain. STUDY DESIGN: Patients, practitioners, and outcome assessor-blinded randomized placebo-controlled trial. SETTING: Pain management clinics at 2 hospitals in Japan. METHODS: Patients were randomly allocated to the PRF (n = 37) or placebo group (n = 33). Patients aged 40-85 years with refractory anteromedial knee pain. PRF in the saphenous nerve under ultrasound guidance. The placebo group underwent the same procedure, but with motor stimulation. The primary endpoint was the average pain intensity measured using the visual analog scale (VAS) at the 12-week post-treatment visit; secondary outcomes included the average VAS at 1 and 4 weeks, and pain intensities at rest, in flexion, at standing, and at walking. Other secondary outcomes were knee pain, symptoms, activities of daily living, knee-related quality of life, mobility, range of motion, and adverse events. RESULTS: In the PRF group, the mean VAS score was 52.41 ± 26.17 at 12 weeks, while in the sham group, the mean VAS score was 63.06 ± 27.12 (P < 0.05). There were no significant differences between the groups in any of the secondary outcomes. LIMITATIONS: Patients with comorbidities were excluded from this study. The follow-up time was limited to 12 weeks. CONCLUSIONS: Ultrasound-guided saphenous nerve PRF proved to be effective for at least 12 weeks in patients with knee OA and showed no adverse events. KEY WORDS: Pulsed radiofrequency treatment, knee osteoarthritis, saphenous nerve, ultrasound-guided, randomized controlled trial, pain, pain management, placebo

The review was performed to investigate the functional brain alterations in patients with various kinds of chronic pain including fibromyalgia, chronic low back pain, migraine and the other chronic pain conditions. In these patients functional connectivity was different not only in the sensorymotor system but also in the affective and reward system. New technology have allowed us to identify and understand the neural mechanisms contributing to chronic pain, which provides us novel targets for future research and treatment.

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Objective. We aimed to investigate the relationship between alterations in spontaneous brain activity and demographic characteristics in patients with functional somatic syndrome (FSS) and associated pain.Materials and Methods. Thirty-four FSS patients participated, each undergoing a 5-min resting-state fMRI scan. We performed seed-based correlation analysis on individual data as the first-level of analysis. The seed regions were the periaqueductal gray, dorsal ⁄ rostral anterior cingulate cortex (ACC), insula, amygdala, and posterior cingulate cortex. Multiple regression of group data was performed as the second-level of analysis. The independent variables were age, average pain intensity on a numerical rating scale, pain duration, and hospital anxiety and depression scale (HADS) and pain catastrophizing scale (PCS) scores.Results. Left amygdala-left insula functional connectivity had a significant positive correlation with average pain intensity. Left rostral ACC-left anterior insula functional connectivity was significantly negatively correlated with pain duration. Right amygdala functional connectivity significantly negatively correlated with HADS anxiety scores. Furthermore, functional connectivity of the right amygdala-right parahippocampal gyrus and right rostral ACC-right thalamus were significantly positively correlated with PCS.Conclusions. We found that the functional connectivity of several brain regions related to pain processing relate to the demographic characteristics of FSS patients. This suggests that alterations in spontaneous brain activity relating to pathological pain are modulated by several demographic characteristics. Dysfunction of the brain is one of the pathophysiological mechanisms leading to FSS.