The journal of pain : official journal of the American Pain Society
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Multicenter Study Clinical Trial
Initial Psychometric Properties of the Pain Care Quality Survey (PainCQ).
This study examined the psychometric properties of the Pain Care Quality (PainCQ) survey, a new instrument to measure the quality of nursing and interdisciplinary care related to pain management. Hospitalized medical/surgical oncology patients with pain from 3 states completed the 44-item version of the PainCQ survey following completion of a nursing shift. Interdisciplinary items were evaluated over the entire hospital stay; nursing care was evaluated during the previous shift. The sample included 109 patients ranging in age from 20 to 84 (mean = 53.09). The sample was 58.7% female, 88% non-Hispanic white. Principal Axis Factoring with an oblimin rotation was used as factors were correlated. Two scales resulted. The PainCQ-Interdisciplinary scale included 11 items representing 2 constructs and explaining 47.1% of shared item variance: partnership with the health care team (k = 6 items; α = .85) and comprehensive interdisciplinary pain care (k = 5 items; α = .76). The PainCQ-Nursing scale measured three constructs and explained 60.8 % of shared item variance: being treated right (k = 15 items; α = .95), comprehensive nursing pain care (k = 3 items; α = .77), and efficacy of pain management (k =4 items; α = .87). Results supported the internal consistency reliability and structural validity of the PainCQ survey with 33 items. ⋯ This article presents the psychometric properties of a new tool to measure interdisciplinary and nursing care quality related to pain management from the patient's perspective. This tool can be used for research and as a clinical performance measure to monitor and improve quality of care and patient outcomes.
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Central sensitization is one form of long-term plasticity in the central nervous system. Sustained activation of primary sensory fibers supplying dorsal horn can induce long-lasting increases in the discharge amplitude of primary afferent synapses. This is similar to the long-term potentiation that occurs in many other CNS regions. Drugs that limit the short-duration wind-up component of central sensitization include sodium channel blockers, NMDA antagonists, fast-acting opioids and the calcium-channel ligands gabapentin and pregabalin (S-3-(aminomethyl)-5-methylhexanoic acid). Pregabalin, like gabapentin, binds selectively to the Ca(V)α₂δ auxiliary subunit of presynaptic voltage-gated calcium channels. The conformational changes induced by this binding inhibit abnormally intense neuronal activity by reducing the synaptic release of glutamate and other neurotransmitters. Recent identification in animal models of increased Ca(V)α₂δ protein expression in chronic pain, allodynia, and hyperalgesia have drawn additional interest to drugs that bind the Ca(V)α₂δ site. Experimental studies with animal models and healthy human volunteers have shown that pregabalin reduces nociceptive responses, particularly in conditions involving central sensitization. Since these actions occur with relatively modest effects on physiological and cognitive functions, pregabalin may be an important consideration in the pharmacotherapy of otherwise difficult-to-treat pain syndromes. ⋯ This focus article discusses how the central nervous system plasticity phenomenon, central sensitization, is established in the induction and maintenance of chronic pain, allodynia, and hyperalgesia. In addition, it explores the neurophysiologic actions of the calcium-channel ligands gabapentin and pregabalin in limiting pathological manifestations of central sensitization.
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Emerging evidence suggests that some individuals with regional pain disorders go on to develop chronic widespread pain (CWP). However, the mechanism behind this transition and the nature of risk factors that predispose a person to develop CWP remain to be elucidated. The purpose of this study was to describe the frequency with which participants with chronic back or neck pain develop CWP and to determine the risk factors associated with this development. In a sample of 512 individuals, we found that nearly a quarter (22.6%) of subjects who presented with regional back or neck pain in 2001/2002 had developed CWP by 2007. Logistic regression indicated that 7 factors were associated with the transition to CWP: moderate or severe pain intensity, female gender, history of abuse, family history of CWP, severe interference with general activity, having 1 or more central sensitivity syndromes, and using more pain management strategies. History of abuse was not significant in multivariate analysis. Notably, number of depressive symptoms endorsed, pain duration, age, body mass index, number of medication classes used, and receipt of disability benefits were not significantly associated with this transition. ⋯ This study offers insight into risk factors associated with the development of CWP. This information not only offers clues as to the mechanism behind the expansion of pain sensitivity from a regional pain locus to a widespread pain disorder but also provides insight as to how clinicians might mitigate this transition.
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Research has largely ignored the systematic examination of physicians' attitudes towards providing care for patients with chronic noncancer pain. The objective of this study was to identify barriers and facilitators to opioid treatment of chronic noncancer pain patients by office-based medical providers. We used a qualitative study design using individual and group interviews. Participants were 23 office-based physicians in New England. Interviews were audiotaped, transcribed, and systematically coded by a multidisciplinary team using the constant comparative method. Physician barriers included absence of objective or physiological measures of pain; lack of expertise in the treatment of chronic pain and coexisting disorders, including addiction; lack of interest in pain management; patients' aberrant behaviors; and physicians' attitudes toward prescribing opioid analgesics. Physician facilitators included promoting continuity of patient care and the use of opioid agreements. Physicians' perceptions of patient-related barriers included lack of physician responsiveness to patients' pain reports, negative attitudes toward opioid analgesics, concerns about cost, and patients' low motivation for pain treatment. Perceived logistical barriers included lack of appropriate pain management and addiction referral options, limited information regarding diagnostic workup, limited insurance coverage for pain management services, limited ancillary support for physicians, and insufficient time. Addressing these barriers to pain treatment will be crucial to improving pain management service delivery. ⋯ This article demonstrates that perceived barriers to treating patients with chronic noncancer pain are common among office-based physicians. Addressing these barriers in physician training and in existing office-based programs might benefit both noncancer chronic pain patients and their medical providers.
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Sex differences in the processing and experience of emotion exist. The present study examined whether sex differences in emotion lead to sex differences in affective modulation of pain and spinal nociception (assessed by nociceptive flexion reflex, NFR). Participants were healthy men (n = 47) and women (n = 73). Prior to affective modulation testing, electrocutaneous pain sensitivity was assessed (NFR threshold, pain threshold, pain tolerance). Affective modulation of pain and NFR was then assessed by presenting pictures that vary in emotional valence and arousal (mutilation, attack, death, neutral, families, adventure, erotica) during which suprathreshold electrocutaneous stimulations were delivered. Subjective emotional reactions were assessed after every picture, and nociceptive reactions were assessed after every suprathreshold stimulus. Results indicated women had greater pain sensitivity and also responded more negatively to attack pictures and less positively to erotic pictures. But despite these differences, affective modulation of pain/NFR was not moderated by sex: erotic pictures inhibited pain/NFR and mutilation pictures enhanced pain/NFR. Together, this implies subjective emotional experience does not completely mediate picture-evoked modulation of pain/NFR, a supposition that was further supported by exploratory analyses that demonstrated picture-evoked modulation of pain/NFR was present even after controlling for intra- and inter-individual differences in emotional reactions to pictures. Implications and limitations of these findings are discussed. ⋯ Evidence suggests that women are more sensitive to experimental and clinical pain, but the mechanisms contributing to these sex differences are poorly understood. Affective processes are known to play a role in regulating pain signaling and pain experience; therefore, the present study examined whether sex differences in affective experience contribute to sex differences in pain. Results indicate that in healthy individuals affective processes may not contribute to sex differences in pain.