The journal of pain : official journal of the American Pain Society
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Little is known about cognitive and behavioral factors that influence older adults' adjustment to chronic pain. The objective of this study was to investigate the relationship of self-efficacy for managing pain to reports of pain intensity, pain-related disability, depressive symptoms, and pain coping strategy use among 140 retirement community residents (88% female; age mean = 81.7, range 66-99 years) with chronic pain. The 8-item Arthritis Self-Efficacy Scale, modified to specify pain rather than arthritis, demonstrated good psychometric characteristics (Cronbach alpha = .89, minimal floor and ceiling effects, and validity) in this sample. Controlling for age, gender, and pain intensity, self-efficacy was associated significantly and negatively with pain-related disability and depressive symptoms (P values < .001), and positively with use of pain coping strategies previously found to be associated with better outcomes (task persistence, exercise/stretch, coping self-statements, activity pacing; P values < .05). Self-efficacy for managing pain appears to be important in the adjustment of older adults with pain. Research is needed to determine whether interventions designed to increase self-efficacy improve quality of life and prevent functional declines in this population. ⋯ Among retirement community residents (mean age of 82 years) with chronic pain, higher self-efficacy for managing pain is associated with less disability and depression and with the use of pain coping strategies related to better adjustment. This suggests the potential value of interventions to increase self-efficacy in this population.
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Although N-methyl-D-aspartate (NMDA) receptor antagonists clearly attenuate the development of tolerance to the antinociceptive effects of opioids, it is not clear whether they also alter acute opioid-induced antinociception. The present study was designed to assess NMDA/opioid interactions in C57BL/6 mice by examining various NMDA receptor antagonists of different selectivity in combination with the mu opioid receptor agonists morphine and l-methadone. A mouse hot plate procedure was used to assess the effects of morphine (0.1 to 10.0 mg/kg) and l-methadone (0.1 to 5.6 mg/kg) alone and after pretreatment with the competitive NMDA receptor antagonist LY235959 (0.1 to 1.0 mg/kg), the glycine site NMDA receptor antagonist R(+)-HA-966 (10.0 to 56.0 mg/kg), or the polyamine site and NR2B selective NMDA receptor antagonist ifenprodil (3.2 to 10.0 mg/kg). Morphine and l-methadone produced dose- and time-dependent increases in 56 degrees C hot plate latencies. At the doses tested, the NMDA receptor antagonists produced no effect on hot plate latencies. However, when these drugs were combined with morphine, latency to respond to the hot plate was significantly increased from morphine alone. Combinations of the NMDA receptor antagonist LY235959 and l-methadone produced similar increases in hot plate latencies; however, combinations of l-methadone with R(+)-HA-966 or ifenprodil did not increase hot plate latencies compared with l-methadone alone. These results suggest that a range of NMDA receptor antagonists potentiate morphine-induced antinociception, although the potentiation of l-methadone might be specific to the antagonist examined. ⋯ The inclusion of low-dose NMDA receptor antagonists to opioids might be beneficial for the treatment of acute pain by enhancing the antinociceptive effects of the opioid.
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Abnormal spontaneous firing is well described in axotomized sensory neurons and likely contributes to nerve injury-induced pain. The hyperpolarization-activated current I(h) initiates spontaneous, rhythmic depolarization in the sinoatrial node and central neurons. This study was undertaken to investigate the possible contribution of I(h) to primary afferent ectopic discharge and pain behavior in nerve-injured rats. Nerve injury was produced by tight ligation of lumbar spinal nerves (L5/6). Two weeks later, rats showed marked mechanical allodynia. Withdrawal thresholds were measured before and after administration of saline or the specific I(h) antagonist ZD7288 (1, 3, or 10 mg/kg, intraperitoneally). ZD7288 dose-dependently reversed mechanical allodynia. In a second experiment, we performed both in vivo and in vitro extracellular single unit recordings from teased dorsal root fascicles. Intravenous infusion (2.5 or 5 mg/kg) of ZD7288 during a period of 10 minutes significantly blocked ectopic discharges in vivo. Perfusion (25 to 100 mumol/L) of ZD7288 for 5 minutes in vitro almost completely blocked ectopic discharges from large myelinated fibers (Abeta) while partially suppressing ectopic discharge from thinly myelinated fibers (Adelta). We conclude from these data that in axotomized sensory neurons, a ZD7288-sensitive current contributes to spontaneous discharges in myelinated fibers. Thus, I(h) might substantially contribute to the pathophysiology of nerve injury-related neuropathic pain. ⋯ The current study investigated the mechanism of abnormal spontaneous discharges (ectopic discharges) from axotomized sensory afferents. Ectopic discharges are a main driving source of nerve injury-induced neuropathic pain. Understanding the mechanism of ectopic discharges and identifying how to control them will be useful toward developing new therapies.
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Previous studies have consistently suggested that there are sex differences in pain report, but there is no consensus regarding sex differences in the associations among psychological factors and pain report. This cross-sectional study used a novel, clinically relevant, psychophysical pain-induction technique to examine sex differences between sensory and affective pain report and sex differences in the association of depression, pain related anxiety, and catastrophizing with pain report. Patients with chronic low back pain (N = 53) were recruited from an outpatient spine clinic, and those consenting completed self-report measures of pain-related anxiety, depression, pain catastrophizing, and pain. A measure of induced low back pain was obtained by having study participants perform a protocol on the MedXtrade mark Low-Back Exercise Apparatus. Our results indicated that no sex differences were detected in psychological factors and self-reported or induced low back pain. However, the relationships between pain related anxiety and self-report of low back pain (z = 2.51, P < .05) and between pain-related anxiety and induced low back pain (z = 3.00, P < .05) were significantly stronger in men than women. These findings suggest that anxiety was linked to self-reported and induced low back pain for men, but not for women. ⋯ Results of this study suggest that pain-related anxiety has a stronger association with psychophysical and clinical reports of low back pain for men.
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We have shown previously that using recombinant adeno-associated viral vector (rAAV) to up-regulate mu opioid receptors (muORs) in dorsal root ganglia (DRGs) increases the potency of subcutaneous morphine. Here we report an improved method of introducing rAAV-muOR viral vectors into DRGs. Instead of injecting the rAAV-muOR gene directly into DRGs as shown before, the vector was introduced into the sciatic nerve of rats. Changes in muOR expression and antinociceptive effects of intrathecal morphine in rAAV-muOR rats were examined. Immunocytochemical studies showed that the transduced muORs were expressed in all types (ie, small, medium, and large) of DRG neurons. The expression of muORs in DRG neurons, quantified by Western blotting, was increased by 1.7-fold 4 weeks after the sciatic nerve injection. The up-regulation persisted for more than 6 months. The effects of intrathecal morphine on paw withdrawal latencies to heat were studied in rats inflamed with complete Freund's adjuvant. Compared with rats injected with rAAV containing the enhanced green fluorescent protein gene (rAAV-EGFP), the antinociceptive potency of intrathecal morphine in rAAV-muOR rats was significantly increased, and the effective dose (ED50) for morphine was 5.4-fold lower (rAAV-muOR: ED50 = 0.84 microg, confidence interval, 0.70-0.99 microg; rAAV-EGFP: ED50 = 4.50 microg, confidence interval, 3.55-5.86 microg). With minimum tissue damage and a large persistent increase in the opioid potency, remote nerve injection of rAAV-muOR to up-regulate muORs could be a useful therapeutic strategy for the treatment of chronic pain. ⋯ Injection of adeno-associated viral vector containing the muOR gene into the sciatic nerve produces a significant up-regulation of muORs in DRGs for up to 6 months without producing any immune responses in the injected animals. This results in a 5.4-fold increase in the potency of intrathecal morphine.