Pain
-
Prolotherapy is widely used in pain control and tissue repair in pain medicine. The classical mode is injection with hypertonic dextrose in muscle or perimysium. However, the analgesic mechanism is still not known. ⋯ Moreover, intramuscular dextrose injection induced phosphorylated extracellular signal-regulated kinase expression in dorsal root ganglion neurons expressing substance P; the phosphorylated extracellular signal-regulated kinase expression was inhibited by the ASIC1a antagonist PcTx1. The optimal settings for prolotherapy in fibromyalgia-like pain are dextrose dependent and volume dependent, and the peripheral antinociception involves ASIC1a and substance P signaling in muscle afferents. This study suggests a possible mechanism of action of dextrose prolotherapy in noninflammatory muscle pain such as fibromyalgia and provides insights into treating other types of chronic pain.
-
Nociceptive and pruriceptive neurons in the dorsal root ganglia (DRG) convey sensations of pain and itch to the spinal cord, respectively. One subtype of mature DRG neurons, comprising 6% to 8% of neurons in the ganglia, is responsible for sensing mediators of acute itch and atopic dermatitis, including the cytokine IL-31. How itch-sensitive (pruriceptive) neurons are specified is unclear. ⋯ Accordingly, lentiviral re-expression of TMEM184B in mutant embryonic neurons restores Wnt signatures. Together, these data demonstrate that TMEM184B promotes adult somatosensation through developmental Wnt signaling and promotion of proper pruriceptive gene expression. Our data illuminate a new key regulatory step in the processes controlling the establishment of diversity in the somatosensory system.
-
Long-term opioid use in patients with chronic noncancer pain (CNCP) can lead to opioid use disorder (OUD) and has been associated with hyperalgesia and reduced quality of life (QoL). Studies suggest antihyperalgesic properties of buprenorphine, and buprenorphine or naloxone (BuNa) has shown beneficial effects on QoL in patients with OUD without CNCP. This study investigated the added value of BuNa in patients with CNCP with OUD on self-reported pain, pain thresholds, pain tolerance, and QoL. ⋯ We found that conversion of full μ-receptor agonists to BuNa, in patients with CNCP with OUD, was accompanied with lower self-reported pain, higher pain thresholds, higher pain tolerance, and improved QoL. Despite several study limitations, these data suggest that BuNa might be of value in patients with CNCP with OUD. Future studies should investigate long-term effects of BuNa in randomized trials.