Articles: hyperalgesia.
-
Sleep disturbance is a commonly reported co-morbidity in chronic pain patients, and conversely, disruption of sleep can cause acute and long-lasting hypersensitivity to painful stimuli. The underlying mechanisms of sleep disruption-induced pain hypersensitivity are poorly understood. Confounding factors of previous studies have been the sleep disruption protocols, such as the 'pedestal over water' or 'inverted flower pot' methods, that can cause large stress responses and therefore may significantly affect pain outcome measures. ⋯ These results show that acute and low-stress sleep disruption causes mechanical and heat hypersensitivity in rats. Mechanical and heat hypersensitivity exhibited differential sensitivity to pharmacological agents, thus suggesting dissociable mechanisms for those two modalities. Ultimately, this model could help identify underlying mechanisms linking sleep disruption and hypersensitivity.
-
Comparative Study
Hyperalgesia and increased sevoflurane minimum alveolar concentration induced by opioids in the rat: A randomised experimental study.
Perioperative opioids reduce inhalational anaesthetic requirements. The initial hypoalgesia may, however, be followed by a rebound hyperalgesia. ⋯ Opioid-induced hyperalgesia was associated with an increase in the MAC in normal rats who had not undergone surgery. Both effects lasted 21 days and were prevented by ketamine.
-
This study determined whether individuals with mild knee pain due to osteoarthritis (OA) experience hyperalgesia and central sensitivity by comparing them with age-matched and sex-matched control participants and determined whether these levels are associated with pain intensity. This study also determined whether these individuals experience significantly poorer quality of life than age-matched and sex-matched controls and whether pain and function predict quality of life. ⋯ Individuals with mild knee pain due to OA experience mechanical (but not thermal) hyperalgesia that relates to pain intensity. They have a reduced quality of life that is predicted by pain intensity. More aggressive pain management for mild knee OA pain is indicated to improve the quality of life for individuals who are not yet candidates for joint replacement.
-
J Magn Reson Imaging · Apr 2015
Spinal and supraspinal processing of thermal stimuli: an fMRI study.
To assess and characterize responses to innocuous/noxious thermal stimuli and heat allodynia using functional spinal magnetic resonance imaging (spinal fMRI). ⋯ Spinal fMRI successfully demonstrates increased spinal activity and secondary changes in activation of supraspinal centers involved in pain modulation caused by peripheral nociceptor sensitization. J. Magn. Reson. Imaging 2015;41:1046-1055. © 2014 Wiley Periodicals, Inc.
-
There is increasing evidence that inflammatory (M1-polarized) macrophages drive the nonresolving neuroinflammation that causes neuropathic pain after nerve injury. As interleukin-4 (IL-4) promotes the suppressive (M2-polarized) state in macrophages, we examined whether exploiting an IL-4-mediated pathway could ameliorate M1 macrophage-dependent neuropathic pain. The mRNA and protein expression of IL-4 receptor α chain (IL-4Rα) were upregulated in accumulating F4/80 macrophages in injured sciatic nerve (SCN). ⋯ These effects of IL-4 were based on that IL-4 treatment increased the proportions of pSTAT6 and CD206 macrophages in injured SCN on day 14 after PSL. We found that neuropathic pain can be ameliorated by IL-4 treatment, which exerts its therapeutic effect on accumulating macrophages through a STAT6-dependent pathway. A shift in macrophage phenotype from the inflammatory to the suppressive phenotype, driven by IL-4R signaling, may have benefits in the treatment of neuropathic pain.