Pain
-
Numerous clinical studies have reported successful relief of chronic pain with sensory thalamic stimulation. However, even with the extensive use of sensory thalamic stimulation as a clinical tool in the relief of chronic pain, the results are still inconsistent. This discrepancy could probably be explained by the fact that the majority of these studies are case reports or retrospective analyses, which have often used imprecise pain measurements that do not allow a rigorous statistical evaluation of pain relief. ⋯ On the other hand, neither thalamic nor placebo stimulation affected air puff and visual ratings, suggesting that the effect applies specifically to pain and hence is not caused by a general change in attention. The level of paresthesia elicited during the placebo manipulation was also directly correlated with the degree of placebo pain relief. These results suggest that thalamic stimulation produces a small but significant reduction in pain perception, but that a significant placebo effect also exists.
-
Chronic pain interrupts behaviour, interferes with functioning, and may affect a person's identity: their sense of self. We tested whether loss of role and personal attributes and current and past self-concept differentiation, predicted adjustment as indexed by measures of depression. Chronic pain patients (n=80) completed measures of pain (MPQ), disability (PDI), depression and anxiety (BDI, HADS). ⋯ Multiple regression analyses revealed that after controlling for demographic and clinical differences, role and attribute loss predicted depression scores. There was no evidence that depression was associated with past self-concept differentiation. The results are discussed with reference to the methodology used and the relevance of self-identity to understand adjustment to chronic pain.
-
Reduced habituation to experimental pain in migraine patients: a CO(2) laser evoked potential study.
The habituation to sensory stimuli of different modalities is reduced in migraine patients. However, the habituation to pain has never been evaluated. Our aim was to assess the nociceptive pathway function and the habituation to experimental pain in patients with migraine. ⋯ Moreover, while the N1-P1 amplitude showed a significant habituation in CS after hand stimulation, it did not change across repetitions in MO patients. In conclusion, no functional impairment of the nociceptive pathways, including the trigeminal pathways, was found in either MO or CTTH patients. But patients with migraine had a reduced habituation, which probably reflects an abnormal excitability of the cortical areas involved in pain processing.
-
In male rats, carrageenan (CAR)-induced inflammation or exposure to a selective protein kinase C epsilon (PKC epsilon ) agonist (psi epsilon RACK) produces prolongation of the hyperalgesia induced by a subsequent exposure to an inflammatory mediator, a phenomenon referred to as hyperalgesic priming. Since many chronic inflammatory conditions are sexually dimorphic, we tested the hypothesis that hyperalgesic priming is sexually dimorphic. Prior injection of CAR or psi epsilon RACK produced a prolongation of the hyperalgesia induced by a subsequent injection of prostaglandin E(2), from less than 3 h to greater than 24 h, but only in male rats. ⋯ While gonadectomy in males had no effect on CAR and psi epsilon RACK induced hyperalgesic priming, female phenotype was observed following implantation of estrogen in males. Thus, mechanisms mediating the development of hyperalgesic priming produced by inflammation are suppressed by estrogen. This regulation of priming by estrogen appears to occur at or downstream of the activation of PKC epsilon.