The journal of pain : official journal of the American Pain Society
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Females are disproportionately affected by irritable bowel syndrome (IBS) with menstrual cycle-dependent fluctuations in abdominal pain suggesting a role for ovarian hormones. IBS patients also exhibit greater activation of brain areas involved in pain affect such as the amygdala, yet the role of supraspinal processes in the effects of ovarian hormones on visceral pain is largely unexplored. The goal of the current study was to determine whether sex steroids act at the level of the amygdala to alter colonic pain sensitivity. Ovariectomized rats received implants on the amygdala of progesterone, estradiol, progesterone combined with estradiol, or cholesterol as a control to examine the involvement of the amygdala in ovarian hormone-mediated changes in visceral sensitivity. Visceral sensitivity was quantified as the number of abdominal contractions, a visceromotor response (VMR), in response to graded pressures of colorectal distension (CRD). Somatic sensitivity was also assessed by measuring the mechanical force required to elicit hindpaw withdrawal. Elevated levels of progesterone and/or estradiol on the amygdala heightened the responsiveness to CRD; in contrast, neither estradiol nor progesterone altered somatic sensation. Furthermore, administration of progesterone or estradiol to areas adjacent to the amygdala did not affect visceral sensitivity. Future studies will address the specific steroid receptors mediating the effects of progesterone and estradiol. ⋯ To our knowledge, this study represents the first description of a specific brain site mediating the effects of ovarian steroids on visceral sensitivity. These data also suggest that an amygdala-dependent mechanism may be responsible, at least in part, for the exacerbation of visceral symptomatology in females.
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The prevalence of pain and pain undertreatment in older persons, along with the many potential detrimental consequences of undertreated pain, pose a substantial burden to the individual, their family, and society. An accurate pain assessment is the foundation for treating pain; yet, thorough pain assessments and regular reassessments are too often neglected. Older adults typically present with multiple pain etiologies, making it all the more imperative that a comprehensive assessment is conducted. ⋯ Following an unsuccessful attempt at self-report from a nonverbal older adult, the potential causes of pain should be explored. Direct observation can then be used to identify behaviors suggestive of pain, and the patient's response to an analgesic trial can be observed. A pain behavior tool can also provide useful information suggesting the presence of pain.
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Review
Pharmacological management of persistent pain in older persons: focus on opioids and nonopioids.
Managing persistent pain is challenging, particularly in older adults who often have comorbidities and physiological changes that affect dosing and adverse effect profiles. The latest guideline issued by the American Geriatrics Society in 2009 is an important clinical resource on prescribing analgesics for older adults. This guideline helps form an evidence-based approach to treating persistent pain, along with other current endorsements, such as the relevant disease-specific recommendations by the American College of Rheumatology, the European League Against Rheumatism, and Osteoarthritis Research Society International, as well as opioid-specific guidelines issued by the American Pain Society, the American Academy of Pain Medicine, the Federation of State Medical Boards of the United States, and the American Society of Interventional Pain Physicians. ⋯ Combining analgesics that have multiple mechanisms of action with nonpharmaceutical approaches can be beneficial in providing pain relief. Nontraditional analgesics are also considered on a case-by-case basis, and a few of these options are weakly recommended. Therapies should be initiated at the lowest possible dose and slowly titrated to effect, while tailoring them to the therapeutic and side-effect responses of the individual.
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Randomized Controlled Trial Clinical Trial
Effects of lidocaine patch on intradermal capsaicin-induced pain: a double-blind, controlled trial.
This study evaluated the effects of topical lidocaine on skin sensation and on intradermal capsaicin-induced pain and hyperalgesia. A randomized, double-blinded, placebo controlled methodology was used. After baseline sensory testing, a placebo patch and a lidocaine patch were randomized to the volar aspect of the left or right forearm for 4 hours. The right forearm patch was removed, the sensory testing was repeated, and capsaicin was injected intradermally at the site. Pain scores were measured at the time of injection and every 2.5 minutes for 10 minutes followed by measurement of the hyperalgesic area to von Frey hair and stroking, flare response, and repeat sensory testing. At the completion of the testing on the right forearm, the left forearm patch was removed and the procedures described for the right forearm were repeated for the left forearm. There was a significant reduction in cool sensation, warm sensation, and touch thresholds in the lidocaine but not placebo patch arm. The lidocaine patch had no significant effect on hot pain or mechanical pain thresholds. Intradermal capsaicin resulted in a significant decrease in hot pain and mechanical pain thresholds; however, lidocaine was unable to significantly reverse the thermal or mechanical hyperalgesia induced by capsaicin. The lidocaine patch did not reduce flare area, nor areas of hyperalgesia or allodynia. This study suggests that the sodium channels and the capsaicin receptors function independently to control peripheral terminal depolarization. ⋯ The sodium channel and the transient receptor potential vanilloid 1 (TRPV1) receptor coexist on peripheral terminals of unmyelinated fibers. This study showed that activation of the TRPV1 receptor can depolarize the fibers in the presence of sodium channel blockade. This suggests that the sodium channel and TRPV1 receptor function independently in depolarizing the fibers.