Effects of Intensity of Electroacupuncture on Chronic Pain in Patients With Knee Osteoarthritis

A Randomized Controlled Trial

Zheng-tao Lv; Lin-lin Shen; Bing Zhu; Zhao-qing Zhang; Chao-yang Ma; Guo-fu Huang; Jing Yin, Ling-ling Yu; Si-yi Yu; Ming-qiao Ding; Jing Li; Xiao-cui Yuan; Wei He; Xiang-hong Jing; Man Li

Disclosures

Arthritis Res Ther. 2019;21(120) 

In This Article

Discussion

In this study, participants with KOA who received strong or weak EA had significantly improved VAS, WOMAC, NPRS, ES, and PPI but not CPM after 1 week of treatment than those who received sham EA. Additionally, strong EA and weak EA further increased CPM value than sham EA, and the effect of strong EA was better than weak EA after 2 weeks of treatment. Therefore, at least 2 weeks duration is necessary for EA to exert a clinical effect on KOA, with strong EA being the most effective in alleviating pain intensity and increased CPM value of KOA, thus preventing the development of chronic pain.

There is a growing body of evidence suggesting that CPM may be an important predictor of chronic pain and assessor of therapeutic effect.[31] CPM is a psychophysical experimental measure of the endogenous pain inhibitory pathway in humans,[32] a phenomenon in which one noxious stimulus prevents the pain generated by another noxious stimulus.[33] Less-efficient CPM have been reported in people with chronic pain, and impaired CPM might have a role in the development and maintenance of chronic pain.[34–36]

In humans, to our knowledge, ours is the first study to assess the efficacy of EA in improving the CPM in patients with KOA. Since CPM modulates the transmission of nociceptive signals involving the periaqueductal gray, rostral ventromedial medulla, and subnucleus reticularis dorsalis,[37,38] the strength of CPM may reflect the function of the endogenous pain inhibitory system. Endogenous opioid peptides, GABA, serotonin, and the noradrenergic system are involved in the regulation of descending pain control.[39–41] Our results suggested that 1 week of strong or weak EA treatment is not sufficient for repairing CPM and that at least 2 weeks of EA is needed to enhance the synthesis of endogenous analgesic neurotransmitters and strengthen the function of the endogenous pain inhibitory system. Thus, although EA has an immediate effect on pain intensity, a cumulative effect is required for EA to repair CPM value. In addition, EA intervention was well tolerated, with only a 7.2% attrition rate. Our low dropout rate and low incidence of adverse events highlight the feasibility of EA in treating KOA.

CPM is specifically activated by peripheral A and/or C fibers. Weak EA with low-intensity current (less than 1 mA) has been demonstrated to mainly stimulate large fibers (Aβ fibers), which may not activate CPM function.[8] Instead, this harmless stimulation may only inspire an analgesic effect through the spinal mechanism of gate control theory.[9] In contrast, strong EA with high-intensity current (more than 2 mA) stimulates thin fibers (Aδ and/or C fibers) and may activate CPM function.[10] In this study, we mainly discussed the influence of EA intervention on KOA patients based on previous findings of CPM involvement in the analgesic mechanism of acupuncture.[42,43] In our study, CPM (the DNIC-like function in human) was assessed by measuring the rate of change in VAS before and after nociceptive cold water stimulus. All participants in the three groups had significant improvement in CPM function after 2 weeks treatment. Participants who received strong or weak EA had significantly better CPM function than those who received sham EA, excluding the placebo effect of sham EA. As the previous study[44] showed that true EA was better than the placebo effect of sham EA but the study was not an RCT, ours is the first study in RCT to prove that the effect of true EA (strong EA and weak EA) is better than the placebo effect of sham EA.

Strong EA had a better effect on repairing CPM function than weak EA, suggesting that high-intensity current (the maximum tolerable intensity of current) was the ideal electric current intensity of EA that could prevent the development and maintenance of chronic pain of KOA. Our results are in line with the previous study that high intensity (to tolerance but subnoxious) of EA is better than low intensity (strong but comfortable) of EA in reducing experimental pain in healthy human volunteers.[11] Our results are also the first to show that strong EA was better than weak or sham EA in alleviating pain intensity and inhibiting chronic pain of KOA.

ITT analysis indicated that there was no significant difference in CPM improvement between sham EA and weak EA/strong EA at the end of week 1; the positive effect of strong EA on CPM function seems to become apparent beginning in week 2. These findings were further confirmed by the PP analysis. All recruited participants were of Han ethnicity, many of whom knew about or had been exposed to acupuncture. The pain in participants with KOA who hold a positive attitude toward acupuncture is more likely to improve.[45] There are some limitations in our study. First, although the participants were not aware of which type of EA they received, it was not possible to blind the acupuncturists who administered EA. Participant expectations and their existing positive attitude toward acupuncture, acupuncturists' confidence in treatment, and interaction between participant and acupuncturist may have influenced the outcomes to some extent. Second, the inability to directly assess the correlation between treatment expectancy and the specific effects of EA on CPM function prevented the determination of the magnitude of these different effects. In addition, imaging studies, such as X-ray, were not performed. Therefore, we could not conclude whether and how the severity of disease affected the treatment response. Finally, the duration of EA intervention was only 2 weeks because our goal was to evaluate the short-term effect of EA. Thus, future studies are required to explore the long-lasting effect of EA in improving CPM function in patients with KOA.

Comments

3090D553-9492-4563-8681-AD288FA52ACE

processing....