Articles: hyperalgesia.
-
Tissue damage and pain can lead to a change in the stimulus/response characteristics of the nociceptive system. Hyperalgesia has been described in experimental pain states and some clinical conditions, but has not been investigated in osteoarthritis (OA). We sought to establish the presence of hyperalgesia at the thumb in subjects with OA of the hand and to explore any relationship between sensitivity to extrinsic stimuli and the experience of clinical pain. ⋯ OA in the hands is associated with cutaneous and deep hyperalgesia to thermal and mechanical stimuli. Increased levels of continuous pain are associated with more pronounced hyperalgesia. The associations of movement pain suggest the contribution of central mechanisms in the stimulus/response changes accompanying movement pain.
-
It has been reported that mu-opioid receptor activation leads to a sustained increase in glutamate synaptic effectiveness at the N-methyl-D-aspartate (NMDA) receptor level, a system associated with central hypersensitivity to pain. One hypothesis is that postoperative pain may result partly from the activation of NMDA pain facilitatory processes induced by opiate treatment per se. The authors tested here the effectiveness of the opiate analgesic fentanyl for eliciting a delayed enhancement in pain sensitivity. ⋯ Fentanyl activates NMDA pain facilitatory processes, which oppose analgesia and lead to long-lasting enhancement in pain sensitivity.
-
Several lines of evidence suggest that secondary hyperalgesia to punctate mechanical stimuli arises from central sensitization to the input from primary afferent nociceptors. Conventional C-fiber nociceptors respond to heat stimuli and yet heat hyperalgesia is absent in the region of secondary hyperalgesia. This evidence suggests that the central sensitization to nociceptor input does not involve heat sensitive nociceptors. ⋯ However, touch threshold and pain to pinching stimuli were not significantly altered. The intradermal capsaicin injection led to the development of a similar degree of secondary hyperalgesia at both the vehicle and capsaicin treatment areas. These results indicate that capsaicin insensitive nociceptive afferents play a dominant role not only in normal mechanical pain but also in secondary hyperalgesia to noxious mechanical stimuli.
-
Complex regional pain syndromes (causalgia and RSD) can be relieved by blockade of the sympathetic efferent activity. The mechanisms of sympathetically maintained pain (SMP) are unclear. So far an adrenergic interaction between sympathetic vasoconstrictor neurons and nociceptors has been proposed. Alternatively, a cholinergic coupling of sympathetic sudomotor neurons and nociceptors is possible. ⋯ Cutaneous sympathetic sudomotor activity does not influence capsaicin induced pain and mechanical hyperalgesia.
-
Exp Clin Psychopharmacol · Feb 2000
Randomized Controlled Trial Clinical TrialA clinical laboratory model for direct assessment of medication-induced antihyperalgesia and subjective effects: initial validation study.
Analgesic medications are often tested in clinical laboratory studies by observing their ability to reduce the pain produced by noxious stimuli presented to healthy skin. These medications may then be used clinically to reduce disease-related hyperalgesia. ⋯ Results demonstrate that ultraviolet (UV) light induces hyperalgesia, commonly prescribed analgesic medications reduce UV-induced hyperalgesia, and this UV-induced hyperalgesia model can be used to assess the time course of a medication's antihyperalgesia effects. Coupled with participant-rated measures of drug liking and mood, this model may prove useful for predicting the clinical efficacy and side-effect profile of novel analgesic medications in cost-efficient and statistically powerful laboratory studies.