Pain
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Acceptance of chronic pain entails that an individual reduce unsuccessful attempts to avoid or control pain and focus instead on participation in valued activities and the pursuit of personally relevant goals. Recent research suggests that pain-related acceptance leads to enhanced emotional and physical functioning in chronic pain patients above and beyond the influence of depression, pain intensity, and coping. In these studies, acceptance was measured using the Chronic Pain Acceptance Questionnaire (CPAQ). ⋯ The present study sought to further refine the CPAQ by examining its factor structure and evaluating the relations of these factors to other indices of pain-related distress and disability. Although a previously demonstrated factor structure of the CPAQ was generally supported, only factors assessing (a) the degree to which one engaged in life activities regardless of the pain and (b) willingness to experience pain had adequate reliability and validity and were significantly related to the other measures of patient functioning. A revised version of the CPAQ is suggested.
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Chronic pain and depression are two of the most common health problems that health professionals encounter, yet only a handful of epidemiological studies have investigated the relationship between these conditions in the general population. In the present study we examined the prevalence and correlates of major depression in persons with chronic back pain using data from the first cycle of Canadian Community Health Survey in a sample of 118,533 household residents. The prevalence of chronic back pain was estimated at 9% of persons 12 years and older. ⋯ The rate of major depression increased in a linear fashion with greater pain severity. In logistic regression models, back pain emerged as the strongest predictor of major depression after adjusting for possible confounding factors such as demographics and medical co-morbidity. The combination of chronic back pain and major depression was associated with greater disability than either condition alone, although pain severity was found to be the strongest overall predictor of disability.
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Comparative Study
Cholinergic modulation of nociceptive responses in vivo and neuropeptide release in vitro at the level of the primary sensory neuron.
Muscarinic acetylcholine receptors (mAChRs) have been widely reported as pharmacological targets for the treatment of pain. However, most of these efforts have focused on CNS mAChRs and their role in modulating nociception at the level of the spinal cord. The present study examines the contribution of peripheral mAChRs in trigeminal nociceptive pathways using a combination of in vivo and in vitro approaches. ⋯ Finally, combined in situ hybridization/immunofluorescence demonstrated that m2 mRNA was present in 20% of trigeminal ganglion neurons between 30 and 60 microm in diameter and that 5-9% of these also expressed CGRP or VR1 immunoreactivity. These results show that activation of peripheral M2 receptors produces antinociception in vivo and the inhibition of nociceptor activity in vitro. While histological analyses at the level of the trigeminal neuronal cell bodies leave open the question of whether the effects of M2 agonists are direct or indirect, these data indicate that primary sensory neuronal M2 receptors may represent a viable peripheral target for the treatment of pain and inflammation.
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Comparative Study
Novel mechanism of enhanced nociception in a model of AIDS therapy-induced painful peripheral neuropathy in the rat.
To elucidate the underlying mechanisms involved in AIDS therapy-induced peripheral neuropathy, we have developed a model of nucleoside analog reverse transcriptase inhibitor-induced painful peripheral neuropathy in the rat, using 2',3'-dideoxycytidine (ddC), 2',3'-dideoxyinosine (ddI) and 2',3'-didehydro-3'-deoxythymidine (d4T), AIDS chemotherapeutic drugs that are also components of AIDS highly active anti-retroviral therapy. Administration of ddC, ddI and d4T produced dose-dependent mechanical hypersensitivity and allodynia. Peripheral administration of inhibitors of protein kinase A, protein kinase C, protein kinase G, p42/p44-mitogen-activated protein kinase (ERK1/2) and nitric oxide synthase, which have demonstrated anti-hyperalgesic effects in other models of metabolic and toxic painful peripheral neuropathies, had no effect on ddC-, ddI- and d4T-induced hypersensitivity. ⋯ Intradermal or spinal injection of intracellular calcium modulators (TMB-8 and Quin-2), which had no effect on nociception in control rats, significantly attenuated and together eliminated ddC and suramin-induced mechanical hypersensitivity. In electrophysiology experiments in ddC-treated rats, C-fibers demonstrated alterations in pattern of firing as indicated by changes in the distribution of interspike intervals to sustained suprathreshold stimuli without change in mechanical activation thresholds or in number of action potentials in response to threshold and suprathreshold stimulation. This study provides evidence for a novel, calcium-dependent, mechanism for neuropathic pain in a model of AIDS therapy-induced painful peripheral neuropathy.