Articles: hyperalgesia.
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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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Dopamine is implicated in different orofacial pain-related diseases. The mechanisms underlying this invalidating pain are not yet understood. Therefore, the present study investigated if unilateral or bilateral lesions of the medial forebrain bundle (MFB) could induce a trigeminal static mechanical allodynia (SMA) comparable to that obtained after chronic construction injury of the infraorbital nerve (CCI-IoN) in rats. ⋯ Our data show that unilateral and bilateral dopamine depletion promoted trigeminal SMA comparable to that obtained after CCI-IoN. This allodynia can be alleviated by D2R activation, making D2R agonist a potential analgesic for orofacial neuropathic pain.