The journal of pain : official journal of the American Pain Society
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Negative emotions (eg, tension, anxiety, fear, anger) influence acute pain recall. Given reliance on patient-provided pain reports across the care continuum, an understanding of factors that modulate pain memory processing become important to patients, clinicians, and health care organizations. The purpose of this study was to investigate the influence of negative emotions on the prediction of 6-month pain recall by using an experimental stress manipulation (speech task) + pain (forehead cold pressor) versus nonstress control + pain crossover design (n = 68). Results showed that (1) negative emotions were greater in the stress session than the nonstress session, and experienced pain levels did not differ by condition or sex; (2) the level negative emotions at the time of the pain stimuli mediated the ability of experienced pain to predict pain recall; and (3) women recalled more stress session pain than men, and nonstress pain was accurately recalled. Integrating these findings with those of others, we present a model of acute pain memory recall in which negative emotions influence pain memory processing wherein the level of experienced pain predicts short-term recall and affective state at the time of the experience becomes a powerful predictor for the long-term recall of experienced pain level. ⋯ After 6 months the level of recalled experimental pain delivered within a stressful context becomes exaggerated. Negative emotions at the time of the painful stimuli and at recall influenced the prediction of the level of recalled pain. Emotional arousal may influence how memory for pain is encoded, processed, and retrieved.
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Bone is a common metastatic site for prostate and breast cancer, and bone cancer is usually associated with severe pain. Traditional treatments for cancer pain can sometimes be ineffective or associated with side effects. Thus an increasing number of patients seek alternative therapies. In this study we investigated the analgesic effects of a soy diet on 3 experimental models of bone cancer pain. Mice were fed a diet in which the protein source was either soy or casein. After 1 week on the diet, sarcoma cells (NCTC 2472) were injected into the medullary cavity of the humeri, femur, or calcaneus. Experimenters blinded to diet of the animal assessed the pain behavior in these animals, forelimb grip force in the humerus model and paw withdrawal frequency to mechanical stimuli in the calcaneus and femur models. The effect of morphine on cancer-induced pain behavior was investigated in calcaneus and femur models. In addition, in the femur model, the effects of soy on tumor size and bone destruction were studied. The soy diet reduced secondary mechanical hyperalgesia in the femur model but had no effect on primary mechanical hyperalgesia in the calcaneus model or on movement-related hyperalgesia in the humerus model. No dietary impact was discerned in measurements of tumor size, bone destruction, and body weight in the femur model, suggesting that the soy diet had no effect on cancer growth. Morphine dose-dependently reduced hyperalgesia with no diet-based difference. These results suggest that a soy diet might provide analgesia in certain forms of hyperalgesia associated with bone cancer. ⋯ The study raises the possibility of dietary supplements influencing aspects of cancer pain. Further research will help determine if use of nutritional supplements, such as soy proteins, can reduce opioid analgesic use in chronic pain states and help minimize the side effects associated with long term use of opioids.
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The purpose of the present investigation was to determine the influence of parental hypertension history on leg muscle pain ratings during cycling exercise in African American women. Eighteen women (age, 19 +/- 2 years) with a positive family history (+PH) of hypertension and 16 (age, 19 +/- 1 years) with a negative family history (-PH) underwent maximal exercise and cold pressor testing. Maximal exercise was conducted on a cycle ergometer. Quadriceps muscle pain intensity ratings were obtained each minute during the maximal exercise test by using a category-ratio scale. The hand cold pressor test was used to determine cardiovascular reactivity. Repeated measures analysis of variance showed significantly lower pain ratings during exercise for the +PH group compared to the -PH group. Psychophysical power functions indicated that the +PH participants had significantly lower exponents for pain throughout exercise. Systolic blood pressure reactivity did not significantly predict pain ratings during exercise. Normotensive African American women with +PH of hypertension experienced less muscle pain during exercise compared to normotensive African American women with a -PH of hypertension. The results are consistent with data demonstrating reduced sensitivity to experimental pain stimuli in individuals at risk for developing hypertension and extend them to naturally occurring muscle pain produced by exercise. ⋯ African American women, a sedentary group with an elevated risk for developing hypertension and chronic pain, show the same negative relationship between +PH and pain perception as men, suggesting that central nervous system mechanisms of pain modulation are more related to family history than gender. Acute exercise provides an experimental model for manipulating naturally occurring pain in studies concerned with the association between pain and hypertension.
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Clinical Trial Controlled Clinical Trial
Intrathecal but not intravenous opioids release adenosine from the spinal cord.
Opioids increase spinal release of adenosine in rats, and analgesia from systemic and intrathecal morphine is reduced in animals by adenosine receptor antagonists. We performed 3 studies to determine whether opioid administration also induces adenosine release in humans. To determine the effect of intrathecal opioid exposure, 15 women received intrathecal fentanyl, 50 microg, or saline, and cerebrospinal fluid was sampled at 2-minute intervals for 6 minutes before surgery. In a second study, 8 healthy volunteers received intrathecal morphine, 50 microg, plus fentanyl, 50 microg, with cerebrospinal fluid sampled 20 and 60 minutes later. To determine the effect of intravenous opioid exposure, 9 healthy volunteers received intravenous remifentanil for 60 minutes, and cerebrospinal fluid was sampled before and at the end of the infusion. Adenosine concentrations were similar in the 3 studies before opioid administration. Intrathecal fentanyl or saline did not affect adenosine concentrations during the 6 minutes in the first study. Adenosine concentrations increased significantly 20 and 60 minutes after intrathecal morphine plus fentanyl was administered. In contrast, adenosine concentrations were unaffected by intravenous remifentanil. These results suggest that intrathecal but not systemic opioid analgesia in humans is associated with spinal release of adenosine. ⋯ Although the role of adenosine release in the spinal cord for opioid receptor activation in subsequent analgesia from opioids is controversial in laboratory studies, these clinical data suggest that local opioid receptor stimulation in the spinal cord of humans does release adenosine. Whether adenosine participates in analgesia from spinal opioids in humans is not known, but spinal adenosine itself is analgesic in humans, consistent with an opioid-adenosine role in analgesia.