Pain
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Metastatic bone cancer causes severe pain that is primarily treated with opioids. A model of bone cancer pain in which the progression of cancer pain and bone destruction is tightly controlled was used to evaluate the effects of sustained morphine treatment. In cancer-treated mice, morphine enhanced, rather than diminished, spontaneous, and evoked pain; these effects were dose-dependent and naloxone-sensitive. ⋯ These results indicate that sustained morphine increases pain, osteolysis, bone loss, and spontaneous fracture, as well as markers of neuronal damage in DRG cells and expression of pro-inflammatory cytokines. Morphine treatment may result in "add-on" mechanisms of pain beyond those engaged by sarcoma alone. While it is not known whether the present findings in this model of osteolytic sarcoma will generalize to other cancers or opioids, the data suggest a need for increased understanding of neurobiological consequences of prolonged opioid exposure which may allow improvements in the use of opiates in the effective management of cancer pain.
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The Self-Administered Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS), an assessment tool to determine if pain is predominantly neuropathic, has not been validated in a community setting. Previously identified residents of Olmsted County, Minnesota, with chronic pain were recruited using a stratified randomization process to increase the frequency of neuropathic pain in the study sample. Subjects completed the S-LANSS in mailed and telephone formats, and underwent clinical assessment to determine if a component of their pain was neuropathic. ⋯ Compared to clinical assessment, sensitivity and specificity in the mailed S-LANSS were 57% (95% CI, 46-69%) and 69% (95% CI, 61-77%), respectively, and in the telephone S-LANSS were 52% (95% CI, 39-64%) and 78% (95% CI, 68-85%), respectively. The sensitivity and specificity of the S-LANSS in both formats were lower than the initial S-LANSS validation study. Differences in survey format and subject population could account for these differences, suggesting that the S-LANSS is best suited as a screening tool and its use to determine the prevalence of neuropathic pain in population studies should be viewed cautiously.
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It has become increasingly apparent that women suffer a disproportionate amount of pain during their lifetime compared to men. Over the past 15 years, a growing number of studies have suggested a variety of causes for this sex difference, from cellular to psychosocial levels of analysis. From a biological perspective, sexual differentiation of pain appears to occur similarly to sexual differentiation of other phenomena: it results in large part from organizational and activational effects of gonadal steroid hormones. ⋯ For clinical pain, the review is limited to a few syndromes for which there is considerable evidence for estrogenic involvement: migraine, temporomandibular disorder (TMD) and arthritis. Because estrogens can modulate the function of the nervous, immune, skeletal, and cardiovascular systems, estrogenic modulation of pain is an exceedingly complex, multi-faceted phenomenon, with estrogens producing both pro- and antinociceptive effects that depend on the extent to which each of these systems of the body is involved in a particular type of pain. Forging a more complete understanding of the myriad ways that estrogens can ameliorate vs. facilitate pain will enable us to better prevent and treat pain in both women and men.
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Cancer-related pain in outpatient adult populations remains high and has a direct effect on functional status. Factors that affect functional status have been explored separately, but the inter-relatedness of those factors has not been examined. Using a cross-sectional design, the purpose of this study was to examine the relationships between pain level, beliefs about pain, symptom distress, perceived control over pain, and functional status in 304 ambulatory cancer patients who experienced cancer-related pain within the past 2 weeks. ⋯ Patients' perceived control over pain may be an important component in pain management. The direct and mediating effects of perceived control and symptom distress suggest areas of further research. Interventions to increase knowledge and decrease barriers to pain control have the potential for increasing perceived control over pain.