Articles: hyperalgesia.
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Journal of pain research · Jan 2015
ReviewBuprenorphine - an attractive opioid with underutilized potential in treatment of chronic pain.
Despite proven clinical utility, buprenorphine has not been used widely for the treatment of chronic pain. Questions about "ceiling effect" or bell-shaped curve observed for analgesia in preclinical studies and potential withdrawal issues on combining with marketed μ-agonists continue to hinder progress in expanding full potential of buprenorphine in the treatment of cancer and noncancer pain. Mounting evidence from clinical studies and conclusions drawn by a panel of experts strongly support superior safety and efficacy profile of buprenorphine vs marketed opioids. ⋯ The receptor pharmacology and pharmacokinetics profile of buprenorphine is complex but unique and contributes to its distinct safety and efficacy. The buprenorphine pharmacology also allows it to be combined with other μ-receptor opioids for additivity in efficacy. Transdermal delivery products of buprenorphine have been preferred choices for the management of pain but new delivery options are under investigation for the treatment of both opioid dependence and chronic pain.
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Nummular headache (NH) is most commonly a localized unifocal headache; however, some patients infrequently exhibit multifocal symptomatic painful head areas retaining all features of NH. We present the pressure pain sensitivity map of an adolescent with multifocal NH. ⋯ This is the first pain sensitivity map of a patient with multifocal NH. Our results support peripheral mechanisms are maintained in multifocal NH.
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Neuropathic pain is a well-known type of chronic pain caused by damage to the nervous system. Until recently, researchers have found that increased generation of reactive oxygen species (ROS) contributes to the development of exaggerated pain hypersensitivity during neuropathic pain. ⋯ Taken together, our results suggest that administration of EGb761 can ameliorate neuropathic pain, and further indicate that JNK, which is activated by both exogenous and endogenous ROS, might be the mechanism underlying the effects of EGb761 on CCI neuropathic pain.
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Chronic stress alters the hypothalamic-pituitary-adrenal axis, increases gut motility, and increases the perception of visceral pain. We investigated whether epigenetic mechanisms regulate chronic stress-induced visceral pain in the peripheral nervous systems of rats. ⋯ Chronic stress increases DNA methylation and histone acetylation of genes that regulate visceral pain sensation in the peripheral nervous system of rats. Blocking epigenetic regulatory pathways in specific regions of the spinal cord might be developed to treat patients with chronic abdominal pain.
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A subset of the population receiving opioids for the treatment of acute and chronic clinical pain develops a paradoxical increase in pain sensitivity known as opioid-induced hyperalgesia. Given that opioid analgesics are one of few treatments available against clinical pain, it is critical to determine the key molecular mechanisms that drive opioid-induced hyperalgesia in order to reduce its prevalence. Recent evidence implicates a splice variant of the mu opioid receptor known as MOR-1K in the emergence of opioid-induced hyperalgesia. Results from human genetic association and cell signaling studies demonstrate that MOR-1K contributes to decreased opioid analgesic responses and produces increased cellular activity via Gs signaling. Here, we conducted the first study to directly test the role of MOR-1K in opioid-induced hyperalgesia. ⋯ These findings suggest that MOR-1K is likely a necessary contributor to the development of opioid-induced hyperalgesia. With further research, MOR-1K could be exploited as a target for antagonists that reduce or prevent opioid-induced hyperalgesia.