The journal of pain : official journal of the American Pain Society
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The nature of the transition from acute to chronic pain still eludes explanation, but chronic pain resulting from surgery provides a natural experiment that invites clinical epidemiological investigation and basic scientific inquiry into the mechanisms of this transition. The primary purpose of this article is to review current knowledge and hypotheses on the transition from acute to persistent postsurgical pain, summarizing literature on clinical epidemiological studies of persistent postsurgical pain development, as well as basic neurophysiological studies targeting mechanisms in the periphery, spinal cord, and brain. The second purpose of this article is to integrate theory, information, and causal reasoning in these areas. ⋯ These propose that chronic pain results from: 1) persistent noxious signaling in the periphery; 2) enduring maladaptive neuroplastic changes at the spinal dorsal horn and/or higher central nervous system structures reflecting a multiplicity of factors, including peripherally released neurotrophic factors and interactions between neurons and microglia; 3) compromised inhibitory modulation of noxious signaling in medullary-spinal pathways; 4) descending facilitatory modulation; and 5) maladaptive brain remodeling in function, structure, and connectivity. The third purpose of this article is to identify barriers to progress and review opportunities for advancing the field. This review reveals a need for a concerted, strategic effort toward integrating clinical epidemiology, basic science research, and current theory about pain mechanisms to hasten progress toward understanding, managing, and preventing persistent postsurgical pain.
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Persistent pain can lead to difficulties in executive task performance. Three core executive functions that are often postulated are inhibition, updating, and shifting. Optimism, the tendency to expect that good things happen in the future, has been shown to protect against pain-induced performance deterioration in executive function updating. ⋯ A 2 (optimism: optimism vs no optimism) × 2 (pain: pain vs no pain) mixed factorial design was conducted. Participants (N = 61) completed a shifting task once with and once without concurrent painful heat stimulation after an optimism or neutral manipulation. Results showed that shifting performance was impaired when experimental heat pain was applied during task execution, and that optimism counteracted pain-induced deterioration in task-shifting performance.
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Although depression is associated with more clinical pain complaints, psychophysical data sometimes point to hypoalgesic alterations. Studying the more reflex-like facial expression of pain in patients with depression may offer a new perspective. Facial and psychophysical responses to nonpainful and painful heat stimuli were studied in 23 patients with major depressive disorder (MDD) and 23 matched control participants. ⋯ Pain psychophysics was unaltered in MDD patients compared with healthy control participants. In conclusion, the facial expression of pain in MDD patients indicates rather hyper- than hypoalgesia, with enhanced affective pain processing. Moreover, the linkage between subjective and facial responses was much stronger in MDD patients, which may be due to a reduced influence of social display rules, which normally complicate this relationship.
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We explored causal mediation of sleep quality and perceived stress in development of painful temporomandibular disorder (TMD). Sleep quality and perceived stress were assessed at baseline and quarterly intervals thereafter in 2,737 initially TMD-free adults in the Orofacial Pain Prospective Evaluation and Risk Assessment study (OPPERA) prospective cohort study. During follow-up, incident TMD cases were classified using research diagnostic criteria. Mediation analysis was conducted using a weighted Cox proportional hazards regression model that estimated hazard ratios (HRs) and 95% confidence limits (CL) of first-onset TMD. Models determined whether: 1) poor sleep quality during follow-up mediated the effect of baseline perceived stress on first-onset TMD, and 2) perceived stress during follow-up mediated the effect of baseline poor sleep quality on first-onset TMD. In both analyses, the total effect was decomposed into natural direct and indirect effects. Poor baseline sleep quality led to heightened perceived stress that then contributed to TMD development. When the total effect of poor sleep quality (HR = 2.10, CL = 1.76, 2.50) was decomposed, 34% of its effect was mediated by perceived stress (indirect effect HR = 1.29, CL = 1.06, 1.58). The effect of perceived stress on first-onset TMD was not mediated by sleep quality. Improving sleep may avert escalation of stress, limiting effects of both factors on TMD development. ⋯ Causal mediation analysis highlights mechanisms by which poor sleep quality promotes development of TMD. First, poor sleep quality exerts a direct effect on pain. Second, it triggers a heightened perception of stress, which acts as an intermediate factor in the causal pathway between poor sleep quality and first-onset TMD pain.
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The role of various forms of social support (including the mere presence of another person) in pain has been studied in children and younger adults, but parallel studies involving older persons have not been conducted. In this investigation, older adults (N = 100) took part in a series of experimental pain tasks in each of the following conditions: alone, in the presence of a stranger, and in the presence of a family member. Indices of pain (threshold, tolerance, intensity, unpleasantness, facial expressions) and facial expressions of emotion were analyzed. ⋯ In examining sex differences, male participants reported higher pain tolerance and female participants displayed more prominent facial expressions of pain. Moreover, facial expressions of neutral states and happiness were more frequent among female participants, whereas facial expressions of anger were more frequent among male participants. Results show that the presence of others influences the experience and expression of pain in older persons.