Articles: hyperalgesia.
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Opioids are the frontline analgesics in pain management. However, chronic use of opioid analgesics causes paradoxical pain that contributes to the decrease of their efficacy in pain control and the escalation of dose in long-term management of pain. The underling pathogenic mechanism is not well understood. ⋯ Surprisingly, ablating microglia using these specific and effective approaches did not cause detectable impairment in the expression of hyperalgesia induced by morphine. We confirmed this conclusion with a behavioral test of mechanical and thermal hyperalgesia, in male and female mice, and with different species (mouse and rat). These findings raise caution about the widely assumed contribution of microglia to the development of opioid-induced hyperalgesia.
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Randomized Controlled Trial
Anodal transcranial direct current stimulation reduces secondary hyperalgesia induced by low frequency electrical stimulation in healthy volunteers.
The aim of the study was to determine whether transcranial direct current stimulation (tDCS) reduced pain and signs of central sensitization induced by low frequency electrical stimulation in healthy volunteers. Thirty-nine participants received tDCS stimulation under 4 different conditions: anodal tDCS of the primary motor cortex (M1), anodal tDCS of the dorsolateral prefrontal cortex (DLPFC), anodal tDCS over M1 and DLPFC concurrently, and sham tDCS. Participants were blind to the tDCS condition. ⋯ Overall, these findings suggest that anodal tDCS over M1 suppresses pain, and that anodal tDCS over DLPFC modulates secondary hyperalgesia (a sign of central sensitization) in healthy participants. PERSPECTIVE: Anodal transcranial current stimulation (atDCS) at the left motor cortex and the dorsolateral prefrontal cortex increased the electrically-evoked pain threshold and reduced secondary hyperalgesia in healthy participants. Replication of this study in chronic pain populations may open more avenues for chronic pain treatment.
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Curr Pain Headache Rep · Feb 2022
ReviewModulatory Effects of Stem Cells on Opioid Receptors and Neuroinflammation.
This narrative review examines stem cell therapy and its effect on opioid therapy in neuropathic pain. ⋯ Stem cell therapy has shown promise in neuropathic pain and opioid tolerance, with a notable common pathway (the P2X4 receptor). Opioid therapy frequently has poor efficacy in patients who suffer from neuropathic pain. There is evidence that the presence of neuropathic pain itself causes changes to the opioid receptor, decreasing the therapeutic potential of this modality. The efficacy of opioid therapy is further decreased in this patient population after chronic opioid exposure, which leads to opioid tolerance and in some cases opioid-induced hyperalgesia. There is growing evidence that stem cell therapy has potential to treat neuropathic pain and may simultaneously decrease opioid tolerance and hyperalgesia. Opioid-induced hyperalgesia occurs via mu-opioid receptor-dependent expression of P2X4 receptors on microglia. Intrathecal stem cell therapy provides analgesic properties due to the significant reduction of P2X4R expression in spinal cord microglia, thereby directly decreasing chronic neuropathic pain.