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OBJECTIVE: Elevated trait anger (TRANG; heightened propensity to experience anger) is associated with greater pain responsiveness, possibly via associations with deficient endogenous opioid analgesia. This study tested whether acute anger arousal moderates the impact of TRANG on endogenous opioid analgesia. METHODS: Ninety-four chronic low back pain (LBP) participants and 85 healthy controls received opioid blockade (8 mg of naloxone) or placebo in a randomized, counterbalanced order in separate sessions. Participants were randomly assigned to undergo either a 5-minute anger recall interview (ARI) or a neutral control interview across both drug conditions. Immediately after the assigned interview, participants engaged sequentially in finger pressure and ischemic forearm pain tasks. Opioid blockade effects were derived (blockade minus placebo condition pain ratings) to index opioid antinociceptive function. RESULTS: Placebo condition TRANG by interview interactions (p values < .05) indicated that TRANG was hyperalgesic only in the context of acute anger arousal (ARI condition; p values < .05). Blockade effect analyses suggested that these hyperalgesic effects were related to deficient opioid analgesia. Significant TRANG by interview interactions (p values < .05) for both pain tasks indicated that elevated TRANG was associated with smaller blockade effects (less endogenous opioid analgesia) only in the ARI condition (p values < .05). Results for ischemic task visual analog scale intensity blockade effects suggested that associations between TRANG and impaired opioid function were most evident in LBP participants when experiencing anger (type by interview by TRANG interaction; p < .05). CONCLUSIONS: Results indicate that hyperalgesic effects of TRANG are most prominent when acute anger is aroused and suggest that endogenous opioid mechanisms contribute.

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BACKGROUND: Elevated resting blood pressure (BP) and spontaneous baroreflex sensitivity (BRS) are associated with hypoalgesia to acute pain. These associations are significantly altered in chronic pain. We investigated whether degree of wind-up (marker for central sensitization) is similarly influenced by BP and BRS, and whether these associations are altered by chronic pain. METHODS: BP and BRS (sequence method) were assessed in 30 healthy and 26 chronic back pain subjects who then completed a standardized thermal stimulation protocol to assess wind-up. This protocol was performed under placebo and alpha-2 adrenergic (ADRA2) blockade with yohimbine in counterbalanced order to test for the influence of ADRA2 mechanisms. RESULTS: 1) In healthy controls, higher systolic BP was associated with lower wind-up (P < 0.05) but this was reversed in chronic pain subjects (P < 0.05); 2) higher BRS was associated with lower wind-up in healthy controls (P < 0.05) but not in the chronic pain group; 3) higher systolic BP was associated with lower BRS only in the chronic pain group (P < 0.05); and 4) ADRA2 receptor blockade did not significantly affect wind-up. CONCLUSIONS: These findings suggest that hypoalgesia associated with elevated resting BP and BRS in healthy individuals involves both diminished central sensitization (reflected in wind-up) and enhanced descending inhibition. The presence of chronic pain significantly alters the nature of these interactions. The reversal of normal interactions between overlapping systems modulating cardiovascular systems and pain in chronic pain patients may shift the healthy buffering of BP and heart rate toward instability and eventual higher BP and cardiovascular morbidity.

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Psychological and behavioral factors can exacerbate the pain and dysfunction associated with complex regional pain syndrome (CRPS) and could help maintain the condition in some patients. Effective management of CRPS requires that these psychosocial and behavioral aspects be addressed as part of an integrated multidisciplinary treatment approach. Well-controlled studies to guide the development of a psychological approach to CRPS management are not currently available. A sequenced protocol for psychological care in CRPS is therefore proposed based on available data and clinical experience. Regardless of the duration of the condition, all CRPS patients and their families should receive education about the negative effects of disuse, the pathophysiology of the syndrome, and possible interactions with psychological/behavioral factors. Patients with acute CRPS (<6-8 weeks) may not need additional psychological care. All patients with chronic CRPS should receive a thorough psychological evaluation, followed by cognitive-behavioral pain management treatment, including relaxation training with biofeedback. Patients making insufficient overall treatment progress or in whom comorbid psychiatric disorders/major ongoing life stressors are identified should additionally receive general cognitive-behavioral therapy to address these issues. The psychological component of treatment can work synergistically with medical and physical/occupational therapies to improve function and increase patients' ability to manage the condition successfully.

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Previous work has suggested that positive associations between trait anger (TRANG) and pain sensitivity are due to dysfunctional endogenous opioid analgesic systems. In this study, we examined whether TRANG is associated with impaired opioid modulation of blood pressure (BP) recovery. A total of 46 pain-free normotensive controls and 69 normotensive chronic low back pain (LBP) sufferers received opioid blockade (8 mg naloxone i.v.) or placebo in randomized, counterbalanced order in separate sessions. During each, participants underwent a 1-min finger pressure pain task followed by an ischemic forearm pain task. Opioid blockade impaired post-pain BP recovery in controls but not LBP participants (ps < .001). In controls, low TRANG was associated with blockade-induced recovery impairments, with no blockade effect in high TRANG participants. In LBP participants, blockade did not alter recovery regardless of TRANG (interaction ps < .05). Results support dysfunctional opioid modulation of BP recovery in healthy high TRANG controls and further suggest chronic pain-related impairments in opioid-mediated cardiovascular recovery.

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A family history of chronic pain has previously been linked to increased incidence of spontaneous acute pain and risk for chronic pain. Mechanisms underlying these associations are unknown, although similar effects on both acute and chronic pain suggest that central endogenous analgesic system differences may be relevant. This study tested whether a positive parental chronic pain history (PH+) was associated with impaired endogenous opioid analgesic responses to acute pain. Seventy-three chronic low back pain patients (LBP) and 46 pain-free controls received opioid blockade (8mg naloxone i.v.) and placebo blockade (saline) in randomized, counterbalanced order in separate sessions. During each, subjects participated in a 1-min finger pressure pain task followed by an ischemic forearm pain task, providing pain intensity ratings during and immediately following each task. To assess opioid analgesic function, blockade effects were derived by subtracting placebo from blockade condition pain responses. Placebo condition analyses indicated that both PH+ subjects and LBP subjects reported greater acute pain sensitivity than respective comparison groups (p's<.05). Multivariate analyses indicated that, beyond any influence of current chronic pain status, PH+ subjects failed to exhibit any endogenous opioid analgesia to acute ischemic pain, whereas PH- subjects elicited effective opioid analgesia (p<.05). A significant multivariate PHxSubject Type interaction (p<.05) indicated that opioid analgesic impairments were most prominent in PH+ LBP subjects. Similar analyses for finger pressure pain blockade effects were nonsignificant (p>.10). The possible heritability of endogenous opioid analgesic dysfunction observed in individuals with a positive parental chronic pain history remains to be investigated.

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OBJECTIVES: In healthy individuals, elevated blood pressure is associated with diminished acute pain sensitivity. These cardiovascular/pain regulatory system interactions appear altered in patients with chronic pain; elevated blood pressure is associated with increased acute and chronic pain responsiveness. If these alterations reflect failure of overlapping systems modulating pain and blood pressure, it was expected that prevalence of clinical hypertension would be increased in the chronic pain population. METHODS: A retrospective review was conducted on randomly selected records of 300 patients with chronic pain (Pain) evaluated at a tertiary care pain center and 300 nonpain internal medicine (Medicine) patients seen at the same institution. RESULTS: Results revealed that 39% of the Pain group was diagnosed with clinical hypertension, compared with 21% of the Medicine group (P < 0.001). Analyses by sex revealed similar group differences in males (P < 0.05) and females (P < 0.001), although the difference in females was double in magnitude compared with males. In contrast to more frequent male hypertension in the general population and the Medicine sample, females were more often diagnosed with hypertension (41.2%) than males (35.6%) in the Pain group. Similar group differences were obtained for antihypertensive use (P < 0.001). Stepwise logistic regression in the Pain group revealed that chronic pain intensity was a significant predictor of hypertensive status independent of the effects of age, race/ethnicity, and parental hypertension (P < 0.05). DISCUSSION: These results suggest that chronic pain may be associated with increased risk of hypertension. Factors that may underlie this association are discussed.

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Endogenous pain regulatory system dysfunction appears to play a role in the maintenance of chronic pain. An important component of the pain regulatory process is the functional interaction between the cardiovascular and pain regulatory systems, which results in an association between elevated resting blood pressure (BP) and diminished acute pain sensitivity. This BP/pain sensitivity relationship is proposed to reflect a homeostatic feedback loop helping restore arousal levels in the presence of painful stimuli. Evidence is emerging that this normally adaptive BP/pain sensitivity relationship is significantly altered in chronic pain conditions, affecting responsiveness to both acute and chronic pain stimuli. Several mechanisms that may underlie this adaptive relationship in healthy individuals are overviewed, including endogenous opioid, noradrenergic, and baroreceptor-related mechanisms. Theoretical models are presented regarding how chronic pain-related alterations in the mechanisms above and increased pain facilatory system activity (central sensitization) may contribute to altered BP/pain sensitivity interactions in chronic pain. Clinical implications are discussed.

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OBJECTIVE: To test whether endogenous opioid antinociceptive system dysfunction evidenced in response to acute pain stimuli is associated with increased clinical pain intensity in chronic pain sufferers, and to determine whether this association is moderated by disability level. DESIGN: A double-blind, placebo-controlled, randomized crossover design. Subjects underwent laboratory acute finger pressure pain stimulation and ischemic pain stimulation under placebo and under opioid blockade with naloxone. The primary independent measures, reflecting degree of endogenous opioid antinociception, were opioid Blockade Effects derived to reflect the change elicited by naloxone in pain intensity ratings for the acute pain tasks. High and Low Disability groups were derived based on Pain Disability Index scores to allow examination of the influence of disability level on the relationship between Blockade Effects and chronic pain intensity. SUBJECTS: Twenty-eight chronic low back pain sufferers. OUTCOME MEASURE: Seven-day diary ratings of overall chronic pain intensity based on McGill Pain Questionnaire-Short Form total scores. RESULTS: Greater daily chronic pain intensity was associated with greater placebo acute pain sensitivity in the laboratory (P < 0.05). Positive Blockade Effects (ie, presence of opioid analgesia) were associated as expected with lower placebo-condition acute pain sensitivity in the laboratory (P < 0.05). In main effects analyses, Blockade Effects were not associated significantly with daily chronic pain intensity. This absence of overall main effects was accounted for by significant opposing interactions between disability level and Blockade Effects (P < 0.05). Negative Blockade Effects (ie, absence of endogenous opioid analgesia to acute pain) in the High Disability group were associated with greater daily chronic pain intensity, consistent with the hypothesized effects of chronic pain-related opioid dysfunction. In contrast, Positive Blockade Effects (ie, effective opioid analgesia to acute pain) were associated with higher daily chronic pain intensity in the Low Disability group. CONCLUSIONS: These results suggest that endogenous opioid antinociceptive system dysfunction may contribute to elevated acute and chronic pain sensitivity among more disabled chronic pain patients. Among less disabled patients, chronic pain may serve as a primer producing up-regulated opioid antinociceptive responses to acute pain

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Recent work suggests that an expressive anger management style (anger-out) is associated with elevated acute pain sensitivity due to endogenous opioid antinociceptive dysfunction. We tested the hypothesis that this opioid dysfunction mediates the previously reported positive association between anger-out and chronic pain intensity. To assess endogenous opioid antinociception in the laboratory, 71 subjects with chronic low back pain received opioid blockade (8 mg naloxone i.v.) or placebo in counterbalanced order in separate sessions. During each, subjects participated in a 1-min finger pressure pain task followed by an ischemic forearm pain task, providing acute pain ratings on the McGill Pain Questionnaire-Short Form (MPQ) immediately following each task. Subjects also completed a 7-day chronic pain diary based on the MPQ between laboratory sessions. To index opioid antinociceptive function, blockade effects were derived, subtracting placebo from blockade condition pain ratings. Greater anger-out was associated with both smaller blockade effects (suggesting impaired opioid antinociception) and greater chronic pain intensity, and blockade effects were inversely associated with chronic pain intensity. Sequential hierarchical regressions suggested that opioid dysfunction partially mediates the positive association between anger-out and total MPQ chronic pain intensity. Inclusion of blockade effects in the first step of the regression resulted in a decrease from 7 to 3% in chronic pain variance accounted for by anger-out. Opioid dysfunction did not mediate the positive association between anger-in and chronic pain. These results provide preliminary support for the hypothesis that the positive association between anger expression and chronic pain intensity is mediated by opioid antinociceptive system dysfunction.

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We hypothesized that preoperative emotional distress and pain intensity would predict the occurrence of signs and symptoms of complex regional pain syndrome (CRPS) following total knee arthroplasty (TKA). Depression (Beck Depression Inventory, BDI), anxiety (State Trait Anxiety Inventory, STAI), pain (McGill Pain Questionnaire-Short Form, MPQ), and signs/symptoms meeting IASP criteria for CRPS were assessed preoperatively, and at 1-, 3-, and 6-months postoperatively in 77 patients undergoing TKA. The prevalence of subjects fulfilling CRPS criteria was 21.0% at 1 month, 13.0% at 3 months, and 12.7% at 6 months postoperative. Higher preoperative scores on the STAI predicted positive CRPS status at 1-month follow-up (P<0.05), with a similar non-significant trend for preoperative BDI scores (P<0.10). Diagnostic sensitivity for the STAI was good (0.73), with moderate specificity (0.56). Neither measure predicted CRPS at later follow-up (P>0.10). Greater preoperative pain intensity predicted positive CRPS status at 3-month (MPQ-Sensory and MPQ-Affective; P<0.01) and 6-month (MPQ-Sensory) follow-up (P<0.01), but not at 1-month (P>0.10). Diagnostic sensitivity was high (0.83-1.00), with moderate specificity (0.53-0.60). Post-TKA patients with CRPS were more depressed at 1-month follow-up (P<0.05) and more anxious at 6-month follow-up (P<0.05) than patients with ongoing non-CRPS pain (all other comparisons non-significant, P>0.10). Overall, results indicate that CRPS-like phenomena occur in a significant number of patients early post-TKA; however, it is not associated with significantly greater complaints of postoperative pain. There appears to be a modest utility for preoperative distress and pain in predicting CRPS signs and symptoms following TKA, although false positive rates are relatively high.

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Research has shown that the anger management styles of both anger-in (suppression of anger) and anger-out (direct verbal or physical expression of anger) may be associated with elevated chronic pain intensity. Only the effects of anger-out appear to be mediated by increased physiological stress responsiveness. Given the catecholamine-sensitive nature of pain mechanisms in complex regional pain syndrome (CRPS), it was hypothesized that anger-out, but not anger-in, would demonstrate a stronger relationship with chronic pain intensity in CRPS patients than in non-CRPS chronic pain patients. Thirty-four chronic pain patients meeting IASP criteria for CRPS and 50 non-CRPS (predominantely myofascial) limb pain patients completed the McGill Pain Questionnaire-Short Form (MPQ), the Anger Expression Inventory (AEI), and the Beck Depression Inventory (BDI). Analyses revealed no diagnostic group differences in mean scores on the anger-in (AIS) and anger-out (AOS) subscales of the AEI, or on the BDI (values of P>0.10). Results of general linear model analyses revealed significant AOS x diagnostic group interactions on both the sensory (MPQ-S) and affective (MPQ-A) subscales of the MPQ (values of P<0.05). In both cases, higher AOS scores were associated with more intense chronic pain in the CRPS group, but with less intense pain in the non-CRPS limb pain group. Inclusion of BDI scores as a covariate did not substantially alter the AOS x diagnostic group interactions, indicating that these AOS interactions were not due solely to overlap with negative affect. Although higher AIS scores were associated with elevated MPQ-A pain intensity as a main effect (P<0.05), no significant AIS x diagnostic group interactions were detected (values of P>0.10). The AIS main effect on MPQ-A ratings was accounted for entirely by overlap with negative affect. Results are consistent with a greater negative impact of anger-out on chronic pain intensity in conditions reflecting catecholamine-sensitive pain mechanisms, presumably due to the association between anger-out and elevated physiological stress responsiveness. These results further support previous suggestions that anger-in and anger-out may affect pain through different mechanisms.

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Resting blood pressure is inversely correlated with acute pain sensitivity in healthy normotensives. This study tested: (1) whether endogenous opioid activity is necessary for this adaptive relationship to occur, (2) whether this relationship is altered in chronic low back pain (LBP), and (3) whether endogenous opioid dysfunction underlies any such alterations. Fifty-one pain-free normotensives and 44 normotensive chronic LBP sufferers received opioid blockade (8 mg naloxone i.v.) or placebo blockade (saline) in randomized, counterbalanced order in separate sessions. During each session, subjects participated in a 1-min finger pressure (FP) pain task followed by an ischemic (ISC) forearm pain task. Among pain-free normotensives, elevated resting systolic (SBP) and diastolic (DBP) blood pressure were associated with significantly higher ISC pain thresholds (P values <0.05). Elevated SBP was also associated with significantly lower FP pain ratings (P<0.05). Opioid blockade had no significant effect on the BP-pain relationships detected (P values >0.10). In combined groups analyses, a significant subject typexSBP interaction (P<0.005) was found on ISC pain threshold: elevated SBP was associated with higher pain threshold in pain-free controls, but with lower pain threshold in LBP subjects. Although subject typexBP interactions on FP and ISC pain ratings were not significant, inclusion of LBP subjects in these analyses resulted in the overall relationship between BP and pain sensitivity becoming positive (P values <0.05). Opioid blockade exerted no significant main or interaction effects in these combined groups analyses (p values >0.10). Higher DBP was associated with greater clinical pain intensity among the LBP subjects (P<0.001). Overall, these results suggest: (1) endogenous opioids do not mediate the inverse relationship between resting blood pressure and acute pain sensitivity in pain-free normotensives; (2) the BP-pain sensitivity relationship is altered in chronic pain, suggesting dysfunction in pain regulatory systems, and (3) these alterations are not related to opioid dysfunction.

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The experience of anger (i.e. trait anger) and anger management style (i.e. anger-in, anger-out) are related to sensitivity to acute and chronic pain stimuli, although underlying mechanisms are unknown. This study tested whether anger variables are associated with impaired endogenous opioid antinociceptive activity, and whether these relationships differed between chronic pain patients and healthy normals. Forty-three chronic low back pain (LBP) sufferers and 45 pain-free normals received opioid blockade (8 mg naloxone i.v.) or placebo blockade (saline) in randomized, counterbalanced order in separate sessions. During each session, subjects participated in a 1-min finger pressure pain task followed by an ischemic forearm pain task (maximum duration 5 min), providing pain intensity ratings during and immediately following each task. As a measure of opioid antinociceptive function, drug effects were derived by subtracting placebo from blockade condition pain ratings. Multivariate general linear model analyses indicated that anger-out, but not anger-in, had significant main effects on both finger pressure drug effects (P < 0.05) and ischemic task drug effects (P < 0.05). As hypothesized, high anger-out scores were associated with an absence of opioid analgesia during the acute pain tasks; low anger-out scores were associated with effective opioid analgesia. A similar non-significant trend was noted for trait anger on finger pressure drug effects (P < 0.06). Anger-out x LBP/normal interactions were non-significant, suggesting that links between anger-out and drug effects were similar for patients and normals. Controlling for depression did not eliminate the significant relationship between anger-out and drug effects. Findings suggest that anger-in and anger-out affect pain sensitivity through different mechanisms: only the effects of anger-out may be mediated by endogenous opioid dysfunction.

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