Articles: hyperalgesia.
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Journal of anesthesia · Feb 2016
The possible involvement of JNK activation in the spinal dorsal horn in bortezomib-induced allodynia: the role of TNF-α and IL-1β.
Bortezomib (BTZ), a widely used chemotherapeutic drug, is closely associated with the development of painful peripheral neuropathy, but the mechanism underlying the induction of this disorder by BTZ remains largely unclear. To examine this association, we have evaluated the activation of mitogen-activated protein kinase (MAPK) family members in the spinal dorsal horn and the role of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in BTZ-induced allodynia in rats. ⋯ Our results suggest that the TNF-α or IL-1β/JNK pathway in the spinal dorsal horn may play a critical role in the development of painful peripheral neuropathy induced by BTZ.
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Randomized Controlled Trial
Does Fentanyl Lead to Opioid-induced Hyperalgesia in Healthy Volunteers?: A Double-blind, Randomized, Crossover Trial.
Although opioids in general and remifentanil in particular have been shown to induce hyperalgesia, data regarding fentanyl are scarce. Thus, the authors investigated the effect of fentanyl dosing on pain perception and central sensitization in healthy volunteers using established pain models. ⋯ A higher dose of fentanyl increased hyperalgesia from 4.5 to 6.5 h in healthy volunteers while simultaneously decreasing pain scores.
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Curr. Opin. Neurobiol. · Feb 2016
ReviewAfferent hyperexcitability in neuropathic pain and the inconvenient truth about its degeneracy.
Neuropathic pain, which arises from damage to the nervous system, is a major unmet clinical challenge. Reversing the neuronal hyperexcitability induced by nerve damage is a logical treatment strategy but has proven frustratingly difficult. Here, we propose a novel explanation for that difficulty. ⋯ Despite offering multiple drug targets, this scenario is problematic: if multiple sufficient changes are triggered by nerve injury, then no single change is necessary for hyperexcitability. This so-called degeneracy compromises therapeutic interventions because drug effects on any one ion channel can be circumvented by changes occurring in other ion channels. Overcoming degeneracy demands a more integrative approach to drug discovery.
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Brain responses to nociception are well identified. The same is not true for allodynic pain, a strong painful sensation in response to touch or innocuous cold stimuli that may be experienced by patients with neuropathic pain. Brain (or spinal cord) reorganization that may explain this paradoxical perception still remains largely unknown. ⋯ Both thalamic function and structure have been reported to be abnormal or impaired in neuropathic pain conditions including in the basal state, possibly explaining the spontaneous component of neuropathic pain. A further indication as to how the brain can create neuropathic pain response in SII and insular cortices stems from examples of diseases, including single-case reports in whom a focal brain lesion leads to central pain disappearance. Additional studies are required to certify the contribution of these areas to the disease processes, to disentangle abnormalities respectively related to pain and to deafferentation, and, in the future, to guide targeting of stimulation studies.
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Neck pain has an elevated prevalence worldwide. Most people with neck pain are diagnosed as nonspecific neck pain patients. Poor recovery in neck disorders, as well as high levels of pain and disability, are associated with widespread sensory hypersensitivity. Nevertheless, there is controversy regarding the presence of widespread hyperalgesia in chronic nonspecific neck pain (CNSNP); this lack of agreement could be due to the presence of different pathophysiological mechanisms in CNSNP. ⋯ Widespread pressure pain hyperalgesia was detected in patients with CNSNP with NF, but not in patients with CNSNP with No-NF. Patients with CNSNP presented bilateral pressure pain hyperalgesia over the cervical region and a decreased cervical ROM compared to healthy controls. However, no differences were found between the 2 CNSNP groups. These findings suggest differences in the mechanism of pain processing between patients with CNSNP with NF and No-NF.