European journal of pain : EJP
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Clinical Trial Controlled Clinical Trial
Pavlovian conditioning of opioid and nonopioid pain inhibitory mechanisms in humans.
Learning processes such as respondent or Pavlovian conditioning are believed to play an important role in the development of chronic pain, however, their influence on the inhibition of pain has so far not been assessed in humans. The purpose of this study was the demonstration of Pavlovian conditioning of stress-induced analgesia in humans and the determination of its opioid mediation. In a differential classical conditioning paradigm two different auditory stimuli served as conditioned stimuli and mental arithmetic plus white noise as unconditioned stimulus. ⋯ Pain tolerance was affected by naloxone whereas pain threshold was not. The data of this study show that stress analgesia can be conditioned in humans and that it is at least partially mediated by the endogenous opioid system. Learning processes also influence pain inhibitory processes in humans and this effect might play a role in the development of chronic pain.
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The aim of this study was to investigate whether pain itself or pain-related fear is crucial in eliciting attentional bias towards pain-related information in healthy individuals. The results from two successive experiments provide evidence that attentional bias does not take place as a function of pain-related fear or as a function of pain per se. Attentional bias for pain words was neither found to be related to trait variables like anxiety, depression, catastrophising, fear of pain, and pain vigilance. Implications of the results are discussed and directions for future research are provided.
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Heterotopic noxious conditioning stimulation (HNCS) has been thought to give access to the diffuse noxious inhibitory controls (DNIC) in man, which can be activated in wide-dynamic-range neurons by noxious stimulation from remote areas of the body and form the neurophysiological basis of the phenomenon 'pain inhibits pain'. The latter phenomenon suggests that the subjective experience of pain is a prerequisite for an inhibitory action. The necessity of using painful stimuli as conditioning and as test stimuli to produce inhibitory effects was investigated in the present study, using a HNCS paradigm. ⋯ However, the intensity ratings of the test stimuli indicated inhibitory effects of the conditioning stimuli also upon non-painful levels. Furthermore, non-painful heat as conditioning stimulus also appeared to be capable of decreasing the ratings of the test stimuli at painful levels. The latter two findings suggest: (i) that very strong but subjectively still non-painful stimulation can trigger pain inhibitory effects and (ii) that also subjectively non-painful stimuli are affected by inhibitory influences during HNCS.
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Some patients who have sustained whiplash injuries present with chronic widespread pain and mechanical allodynia. This single-blind, case control matched study of 43 chronic whiplash patients sought to examine psychophysical responses to non-noxious stimuli and their relationship to psychological profiles. Symptom Check List 90-R (SCL-90-R), Neck Disability Index and Shortform McGill Questionnaire were completed prior to testing. ⋯ Pain in response to non-noxious stimulation over presumably healthy tissues suggests that central mechanisms are responsible for ongoing pain in at least some whiplash patients. The additional findings of pain on punctate pressure and hyperalgesic responses to heat and cold stimuli are consistent with enhanced central responsiveness to nociceptor input. These results have important therapeutic and prognostic implications.
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The aim of this study was to investigate the influence of experimental pain intensity in the local and referred pain area on somatosensory perception thresholds in the area of referred pain. Pain was induced by intramuscular electrical stimulation of the left infraspinatus muscle in 12 healthy individuals. The stimulation corresponded to the local pain threshold ("mild local pain"), the referred pain threshold ("mild referred pain"), and a pain intensity corresponding to 2 on a 10-point category scale in the referred pain area ("moderate referred pain"). ⋯ Compared to baseline, PPTs increased bilaterally during stimulation corresponding to "mild local pain" and "mild referred pain", respectively, and a further increase was seen during "moderate referred pain". The decreased sensitivity to innocuous cold, warmth, and pressure pain was bilateral, indicating activation of endogenous net inhibitory mechanisms interacting bilaterally. We found no influence of pain intensity on somatosensory thresholds restricted to the referred pain area and light touch was the only affected modality in the referred pain area only.