The journal of pain : official journal of the American Pain Society
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Although intrathecal (i.t.) administration of the alpha(2)-adrenoceptor agonist clonidine has a pronounced analgesic effect, the clinical use of clonidine is limited by its side effects. Previously, our laboratory has demonstrated that the subcutaneous injection of diluted bee venom (DBV) into an acupoint (termed apipuncture) produces significant analgesic effect in various pain animal models. The present study was designed to examine whether DBV injection into the Zusanli acupoint (ST-36) could enhance lower-dose clonidine-induced analgesic effects without the development of hypotension, bradycardia, or sedation. In the mouse formalin test, DBV injection produced a dramatic leftward shift in the dose-response curve for clonidine-induced analgesia. In a rat neuropathic pain model i.t. clonidine dose dependently suppressed chronic constriction injury (CCI)-induced mechanical allodynia and thermal hyperalgesia, and this clonidine-induced analgesic effect was significantly potentiated by apipuncture pretreatment. DBV apipuncture alone or in combination with a low dose of i.t. clonidine produced an analgesic effect similar to that of the high dose of clonidine, but without significant side effects. The analgesic effect produced by the combination of i.t. clonidine and apipuncture was completely blocked by pretreatment with an alpha(2)-adrenoceptor antagonist. These data show that DBV-apipuncture significantly enhances clonidine-induced analgesia and suggest that a combination of low dose clonidine with acupuncture therapy represents a novel strategy for pain management that could eliminates clonidine's side effects. ⋯ This study demonstrated that intrathecal clonidine-induced analgesia is significantly enhanced when it is combined with chemical acupuncture treatment. The administration of low-dose clonidine in combination with acupuncture produced a potent analgesic effect without significant side effects and thus represents a potential novel strategy for the management of chronic pain.
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This study evaluated the ability of end-of-day (EOD) ratings to accurately reflect momentary (EMA) ratings on 10 widely used pain and fatigue items. Rheumatology patients (n = 105) completed >or=5 randomly scheduled EMA assessments of each item per day as well as EOD ratings. Correlations were high between EOD and EMA ratings of the 5 pain items (r = .90 to .92) and somewhat lower for the 5 fatigue/energy items (r = .71 to .86). To examine the ability of EOD ratings to represent 1 week of EMA ratings, 7 EOD ratings were averaged and correlated with EMA (r >or= .95 for pain items, r = .88 to .95 for fatigue/energy items). Further, averaging only 3 to 5 EOD ratings achieved very high correlations with 1 week of EMA ratings. Within-subject correlations of EOD with mean daily EMA across 7 days confirmed patients' ability to provide daily ratings that accurately reflect their day-to-day variation in symptom levels. These EOD results were compared to traditional recall ratings collected in the same protocol. It was concluded (1) that EOD ratings were a better representation of EMA than were recall ratings, and (2) that EOD ratings across a reporting period can replace EMA for studies targeting average levels of pain or fatigue. ⋯ This study in chronic pain patients demonstrated that end-of-day ratings of pain are highly accurate representations of average levels of pain experience across a day; ratings of fatigue were somewhat less accurate, though still at a level that would be valid.
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This observational study aimed to determine whether pain sensitivity in patients with noncancer chronic pain, taking either methadone or morphine, is similar to patients maintained on methadone for dependence therapy, compared with a control group. Nociceptive thresholds were measured on a single occasion with von Frey hairs, electrical stimulation, and cold pressor tests. In all subjects receiving methadone or morphine, nociceptive testing occurred just before a scheduled dose. Cold pressor tolerance values in patients with noncancer, chronic pain, treated with morphine and methadone, were 18.1 +/- 2.6 seconds (mean +/- SEM) and 19.7 +/- 2.3 seconds, respectively; in methadone-maintained subjects it was 18.9 +/- 1.9 seconds, with all values being significantly (P < .05) lower than opioid-naïve subjects (30.7 +/- 3.9 seconds). These results indicate that patients with chronic pain managed with opioids and methadone-maintained subjects are hyperalgesic when assessed by the cold pressor test but not by the electrical stimulation test. None of the groups exhibited allodynia as measured using the von Frey hairs. These results add to the growing body of evidence that chronic opioid exposure increases sensitivity to some types of pain. They also demonstrate that in humans, this hyperalgesia is not associated with allodynia. ⋯ This article presents an observational study whereby the pain sensitivity of patients with chronic pain managed with opioids and opioid-maintained patients were compared with opioid-naïve patients. The results suggest that opioid use may contribute to an increase in the sensitivity to certain pain experimental stimuli.
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There is evidence that pain patients demonstrate attentional biases toward some pain-related stimuli (eg, sensory words) and not others (eg, affective words). However, whether individuals in chronic pain caused by rheumatoid arthritis (RA) also demonstrate this bias has not been investigated. Further, within the pain literature, whether these biases reflect hypervigilance or difficulty disengaging from stimuli remains contentious. The present study aimed to determine (a) whether RA patients demonstrate an attentional bias to sensory pain words; and (b) whether this bias is a result of hypervigilance or failure to disengage from the stimuli. RA patients showed a bias toward sensory words and away from threat-related words. The effect for sensory words resulted from slowed performance on incongruent trials (ie, difficulty disengaging), whereas the bias away from threat words resulted from faster responses on incongruent trials (ie, avoidance of threat). The pattern of attention biases in RA patients is very similar to those found in patients with chronic pain. At least in RA, attentional biases appear to be related to a failure to disengage from pain-related words rather than hypervigilance. ⋯ There is continued debate about whether these biases are caused by hypervigilance toward pain stimuli or difficulty disengaging from pain stimuli. This study shows that in a group of RA patients, attentional biases toward pain are caused by difficulty disengaging rather than hypervigilance.