Pain
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Temporal variations in cancer pain intensity are highly prevalent, and are often difficult to manage. However, the phenomenon is not well understood: several definitions and approaches to classification and bedside assessment of cancer breakthrough pain (BTP) have been described. The present study is a systematic review of published literature on cancer BTP to answer the following questions: which terms and definitions have been used; are there validated assessment tools; which domains of BTP do the tools delineate, and which items do they contain; how have assessment tools been applied within clinical studies; and are there validated classification systems for BTP. ⋯ Analysis of these publications indicates a range of overlapping but distinct definitions have been used to characterize BTP; 42 of the included papers presented one or more ways of classifying BTP; and while 10 tools to assess patients' experience of BTP were identified, only 2 have been partially validated. We conclude that there is no widely accepted definition, classification system or well-validated assessment tool for cancer-related breakthrough pain, but there is strong concurrence on most of its key attributes. With further work in this area, an internationally agreed upon definition and classification system for cancer-related breakthrough pain, and a standard approach on how to measure it, hold the promise to improve patient care and support research in this poor-prognosis cancer pain syndrome.
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Randomized Controlled Trial
Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism.
Clinical data have accumulated showing that relative hypocortisolism, which may be regarded as a neuroendocrinological correlate of chronic stress, may be a characteristic of some functional pain syndromes. However, it has not been clarified yet whether deregulations of the hypothalamus-pituitary-adrenal (HPA) axis may directly alter pain perception and thus be causally involved in the pathophysiology of these disorders. To test this hypothesis, we performed a randomized placebo-controlled crossover trial in N=20 healthy drug-free volunteers (median age 24yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5-13m/s impact stimuli), perceptual wind-up (9m/s impact stimuli at 1Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10N pressure stimuli for 2min). ⋯ Perceptual wind-up by contrast was reduced when cortisol synthesis was blocked (p<.05). This result is reminiscent of findings from animal studies showing a reversal of NMDA receptor activation by glucocorticoid receptor antagonists in neuropathic pain models. Our results speak in favor of a potential causal role of HPA axis alterations in pain chronicity.
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In the past two decades, functional brain imaging has considerably advanced our knowledge of cerebral pain processing. However, many important links are still missing in our understanding of brain activity in relation to the regulation of pain-related physiological responses. This fMRI study investigates the cerebral correlates of pain (rating), motor responses (RIII-reflex) and autonomic activity (skin conductance response; SCR) evoked by noxious electrical stimulation. ⋯ Additionally, trial-to-trial fluctuations of RIII-reflex and SCR (within-subjects) were proportional to shock-evoked responses in subgenual cingulate cortex (RIII), anterior insula (SCR) and midcingulate cortex (SCR and RIII). Together, these results confirm that individual differences in perceptual, motor, and autonomic components of pain reflect robust individual differences in brain activity. Furthermore, the brain correlates of trial-to-trial fluctuations in pain responses provide additional evidence for a partial segregation of sub-systems involved more specifically in the ongoing monitoring, and possibly the regulation, of pain-related motor and autonomic responses.
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This study investigated the psychometric properties of the Chronic Pain Acceptance Questionnaire (CPAQ) in a mixed chronic pain, Internet sample and sought to develop a valid and reliable short form. Questionnaires were completed by 428 respondents, comprising a sample accessed via the Internet (n=319) and a sample who completed a paper and pencil version of the measures (n=109). Using confirmatory factor analysis (CFA) the two-factor structure of the CPAQ in the Internet sample was supported, though a good model fit was only achieved following the removal of one item. ⋯ Using structural equation modelling both subscales were found to partially mediate the impact of pain severity on pain interference and emotional distress. In this model AE had stronger associations with outcomes while PW accounted for a small portion of the variance in pain interference and anxiety, but not depression. This study confirmed the two-factor structure of the CPAQ in a mixed chronic pain Internet sample and provides preliminary evidence for the psychometric soundness of the CPAQ-8.