Pain
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Clinical Trial
An experimental study of attention, labelling and memory in people suffering from chronic pain.
Cognitive-behavioural approaches to treatment have become an important part of the clinical management of chronic pain. More recent developments in cognitive-behavioural theory, based on recent developments in the understanding and treatment of health anxiety, have emphasized the importance of catastrophizing appraisals, which drive both attentional processes and behavioural responses, which in turn are believed to be crucial for the maintenance of chronic pain. The experiment conducted here investigated the responses of pain patients (n=39) and controls (n=71) to a behavioural task (prolonged squeezing a dynamometer). ⋯ Patients were found to be less able to sustain prolonged muscle tension than controls, but the effect was not evident once the distracting task was introduced; similar effects were found for discomfort. All participants subsequently recalled the squeezing task as being longer and associated with less discomfort than they had actually recorded it at the time. In the dichotic listening tasks, although patients detected the same number of words overall as controls did, they were less able to focus on the target channel (i.e. they detected more of the words included as distractors on the unattended channel).
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Migraine is a complex disease with a significant genetic background. One possible strategy to investigate the genetics of migraine is the evaluation of functional vulnerability markers or biological elementary endophenotypes in individuals with the greatest probability of developing the disorder (high-risk design). In this study the contingent negative variation (CNV) was recorded in 35 high-risk subjects with a positive family history of migraine without aura (FHP), 35 low-risk individuals without a positive family history (FHN), and 35 migraineurs (migraine without aura). ⋯ The amplitude of the iCNV correlated significantly with the relative number of subjects suffering from migraine among first- and second-degree relatives. The higher the density of affected individuals in the family, the more pronounced were the CNV abnormalities in relatives. This study provides evidence that the familial factor contributes to the abnormal amplitude, and to a lesser degree, habituation of the iCNV, and that the iCNV may be used as a functional-genetic vulnerability marker in further research of migraine genetics.
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The results of a considerable number of recent prospective studies have demonstrated that greater acute pain severity in herpes zoster patients is associated with a significantly greater risk of developing postherpetic neuralgia (PHN). Only a few studies have examined the relationships between acute pain severity and demographic characteristics and clinical features of patients with herpes zoster, however, and the results of these studies have been inconsistent. ⋯ These results demonstrate that three of the established risk factors for PHN - older age, greater rash severity, and the presence of a prodrome - are also associated with more severe acute pain assessed soon after rash onset in patients with herpes zoster. The results of this study are consistent with the recommendation that herpes zoster patients who are older, who have had a prodrome, or who have severe rash or severe acute pain should be targeted for interventions designed to prevent PHN.
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Coincident with nociception, both noxious chemical stimulation of the hind paw and chronic constriction injury (CCI) of the sciatic nerve produce an increase in protein kinase C (PKC) translocation in the spinal cord of rats. Noxious stimulus-induced PKC translocation likely depends on glutamate activity at either N-methyl-D-aspartate (NMDA) receptors or group I metabotropic glutamate receptors (mGluR1/5) in the spinal cord dorsal horn. This study compares nociceptive responses to, and the alterations in membrane-associated PKC, induced by noxious chemical stimulation of the hindpaw and CCI of the sciatic nerve, as well as their modulation by both NMDA and mGluR1/5 receptor antagonists. ⋯ In contrast, i.t. treatment with (S)-4CPG failed to significantly affect either nociceptive behaviours in the formalin test or formalin-induced increases in [3H]-PDBu binding in laminae I-II and III-VI of the lumbar spinal cord. On the other hand, i.t. treatment with either MK-801 or (S)-4CPG produced a significant reduction in mechanical and cold hypersensitivity, as well as [3H]-PDBu binding in laminae I-II and III-VI of the lumbar spinal cord, after CCI. These results suggest that while NMDA, but not mGluR1/5, receptors are involved in translocation of PKC and nociception in a model of persistent acute pain, both types of receptors influence the translocation of PKC in dorsal horn and mechanical and cold allodynia in a model of chronic neuropathic pain.
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Protein kinase A (PKA) can play a critical role in the modulation of neuronal excitability. We examined the role of PKA in the modulation of abnormal spontaneous activity (SA) originating from the chronically compressed dorsal root ganglion (CCD). The L(4) and L(5) dorsal root ganglia (DRGs) were compressed by inserting a stainless steel rod into each corresponding intervertebral foramen. ⋯ Sp-cAMPS (500 microM), a specific activator of PKA, increased the discharge rate of SA in all injured units tested, but did not trigger firing in silent neurons. Okadaic acid (0.1 microM), a protein phosphatase inhibitor, and forskolin (1 microM), an adenyl cyclase activator, each significantly increased the discharge rate of SA. These results strongly suggest that PKA modulates the SA in injured DRG neurons with myelinated axons.