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Biomedical subjects

Stephen Bruehl

Publications and source records attributed to Stephen Bruehl.

At least 19 recordsLinked to original sources
PubMed2007

Trait anger expressiveness and pain-induced beta-endorphin release: support for the opioid dysfunction hypothesis.

The anger management styles of anger-in (inhibition) and anger-out (direct expression) are positively associated with pain responsiveness. Opioid blockade studies suggest that hyperalgesic effects of trait anger-out, but not those of trait anger-in, are mediated in part by opioid analgesic system dysfunction. The current study tested the opioid dysfunction hypothesis of anger-out using an alternative index of opioid function: pain-induced changes in plasma endogenous opioids. Plasma beta-endorphin (BE) was assessed at rest and again following exposure to three laboratory acute pain tasks (finger pressure, ischemic, and thermal) in 14 healthy controls and 13 chronic low back pain (LBP) subjects. As expected, acute pain ratings correlated positively with measures of anger-in (both groups) and anger-out (LBP group; p's<.05). Greater pain-induced increases in BE were associated with significantly lower pain ratings in both groups (p's<.05). Hierarchical multiple regression indicated that greater anger-out significantly predicted smaller pain-induced BE increases (p<.05). Subject type did not moderate this association (p>.10). Anger-in did not display significant main or interaction effects on pain-induced BE changes (p's>.10). The significant association between anger-out and BE release partially mediated the hyperalgesic effects of anger-out on pain unpleasantness, and was not attenuated by statistical control of general negative affect. This suggests unique associations with expressive anger regulation. Elevated trait anger-out therefore appears to be associated with opioid analgesic system dysfunction, whether it is indexed by responses to opioid blockade or by examining circulating endogenous opioid levels. Possible "statextrait" interactions on these anger-related opioid system differences are discussed.

Acute Disease↗
PubMed2006

Anger expression and pain: an overview of findings and possible mechanisms.

A tendency to manage anger via direct expression (anger-out) is increasingly recognized as influencing responses to pain. Elevated trait anger-out is associated with increased responsiveness to acute experimental and clinical pain stimuli, and is generally related to elevated chronic pain intensity in individuals with diverse pain conditions. Possible mechanisms for these links are explored, including negative affect, psychodynamics, central adipose tissue, symptom specific muscle reactivity, endogenous opioid dysfunction, and genetics. The opioid dysfunction hypothesis has some experimental support, and simultaneously can account for anger-out's effects on both acute and chronic pain. Factors which may moderate the anger-out/pain link are described, including narcotic use, gender, and genetic polymorphisms. Pain exacerbating effects of trait anger-out are contrasted with the apparent pain inhibitory effects of behavioral anger expression exhibited in anger-provoking contexts. Conceptual issues related to the state versus trait effects of expressive anger regulation are discussed.

Acute Disease↗
PubMed2006

Parental history of chronic pain may be associated with impairments in endogenous opioid analgesic systems.

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.

Adult↗
PubMed2006

Anger regulation style, postoperative pain, and relationship to the A118G mu opioid receptor gene polymorphism: a preliminary study.

Greater trait anger-out is associated with elevated pain responsiveness. Previous work suggests this effect may be mediated by deficient endogenous opioid analgesia, possibly reflecting diminished opioid receptor sensitivity. The A118G single nucleotide polymorphism (SNP) of the mu opioid receptor gene influences both opioid receptor sensitivity and clinical responsiveness to opioid analgesics. Therefore, this study tested whether this SNP either mediated or moderated the effects of anger-out on postsurgical pain outcomes. Forty-eight patients undergoing coronary artery bypass graft surgery provided genetic samples, and completed measures of anger-out and postsurgical pain. Postsurgical opioid analgesic use was also recorded. Anger-out was positively associated with postsurgical pain ratings (p < 0.05). Anger-out was not associated with A118G SNP status (p > 0.10), suggesting the latter is unlikely to mediate anger-out's pain-related effects. A significant anger-out x A118G interaction was observed on analgesic use (p < 0.05), due to a much stronger positive relationship between anger-out and analgesic demands in patient with the A118G SNP (b = 0.53) than those with the wild-type receptor (b = 0.07). These results suggest that the A118G SNP may moderate but not mediate the effects of anger-out on postoperative pain responses.

Adult↗
PubMed2006

Psychological and behavioral aspects of complex regional pain syndrome management.

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.

Behavior Therapy↗
PubMed2006

Trait anger and blood pressure recovery following acute pain: evidence for opioid-mediated effects.

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.

Acute Disease↗
PubMed2005

Anger management style, opioid analgesic use, and chronic pain severity: a test of the opioid-deficit hypothesis.

Anger management style is related to both acute and chronic pain. Recent research suggests that individuals who predominantly express anger (anger-out) may report heightened chronic pain severity due in part to endogenous opioid antinociceptive dysfunction. If exogenous opioids serve to remediate opioid deficits, we predicted that regular use of opioid analgesics by chronic pain patients would alter these relationships such that anger-out would be related to chronic pain severity only among opioid-free patients. For 136 chronic pain patients, anger management style, depression, anxiety, pain severity, and use of opioid and antidepressant medication was assessed. Results of hierarchical multiple regressions to predict chronic pain severity showed: (a) a significant Anger-out x Opioid use interaction such that high Anger-out was associated with high pain severity only among patients not taking opioids; (b) controlling for depressed affect and anxiety did not affect this association; (c) the Anger-out x Antidepressant use interaction was nonsignificant; (d) Anger-in did not interact with use of any medication to affect pain severity. Results are consistent with an opioid-deficit hypothesis and suggest that regular use of opioid medications by patients high in anger expression may compensate for an endogenous opioid deficit, and mitigate the effects of elevated anger expression on chronic pain intensity.

Adaptation, Psychological↗
PubMed2005

Stages of change in readiness to adopt a self-management approach to chronic pain: the moderating role of early-treatment stage progression in predicting outcome.

Relative readiness to assume a self-management approach to chronic pain can be conceptualised as a stage model. Although both initial stage (precontemplation, action) and changes in attitudes reflecting stage orientation have been shown to predict treatment outcome, the joint contributions of these factors need to be examined. Sixty-five chronic pain patients, participating in a 4-week multidisciplinary pain program, completed the Pain Stages of Change Questionnaire (PSOCQ), subscales of the Multidimensional Pain Inventory, and the Beck Depression Inventory at pre-, mid- and post-treatment. Patients were assigned to stage group (precontemplation or action) based on whether their Precontemplation or Action subscale scores were highest. Results showed that: (a) stage group interacted with pre- to mid-treatment Precontemplation subscale changes to predict mid- to late-treatment pain severity and interference changes such that precontemplation attitude decreases were related to reduced pain and interference only among patients who were already action stage at pre-treatment; (b) stage group interacted with pre- to mid-treatment Action subscale changes to predict mid- to late-treatment interference and activity changes such that action attitude increases were related to reduced interference and increased activity only among patients at the action stage at pre-treatment; (c) pre- to mid-treatment decreases in depression did not account for these effects. Results suggest that any advantage enjoyed by patients with predominant action attitudes at pre-treatment may be enhanced by consolidating a pain self-management approach during treatment. In contrast, late-treatment gains of patients initially taking a predominant precontemplation stance were unaffected by their degree of early-treatment attitude changes.

Adult↗
PubMed2005

How accurate are parental chronic pain histories provided by offspring?

Previous work suggests possible relationships between offspring-reported parental history of chronic pain (CP) and offsprings' personal chronic pain experience. This study examined reliability of offsprings' reports of parental CP history based on direct comparison with confirmed parental reports. Participants included 108 male and female college students who completed a questionnaire assessing presence/absence and locations of any past or present CP lasting greater than 3 months. Information on maternal and paternal CP history was obtained using a similar questionnaire based both on offspring reports and on reports provided directly by offsprings' parents (for 75 participants). Results indicated relatively high sensitivity (0.79-0.94) but modest specificity (0.55-0.63) for offspring reports of parental CP history, and a tendency to overestimate the incidence of CP in both parents. Significant (Ps<0.001) but moderate inter-rater reliability was noted for judgments of parental CP history (kappas=0.41-0.53). Reliability generally decreased when offspring were asked to report on specific locations of parental CP. Offspring-reported parental CP history predicted (Ps<0.05) presence and number of locations at which offspring reported having personally experienced CP, consistent with previous studies. Results indicated that these relationships were not mediated by social desirability, negative affect, or catastrophizing cognitions. In contrast to results for offspring-reported data, confirmed parental CP history reports failed to predict offsprings' personal CP history. These results raise questions as to the validity of previous findings of relationships between family pain history and individuals' own experience of CP.

Adult↗
PubMed2005

Current diagnosis and therapy of complex regional pain syndrome: refining diagnostic criteria and therapeutic options.

Complex regional pain syndrome is a clinically challenging entity both in terms of accurate diagnosis and effective treatment. Complex regional pain syndrome is a post-traumatic painful neurologic syndrome involving the somatosensory, sympathetic and often the somatomotor systems. This complex condition consists of local neurogenic inflammation out of proportion to injury; severe pain in the skin, subcutaneous tissues and joints; and a central hyperexcitability that is often compounded with a sympathetic component. The syndrome is multifaceted manifesting both central and peripheral neurologic pathophysiology, frequently including a prominent psychosocial component. The wide array of possible patient presentations and antecedent pathologies also complicate successful treatment. To further add to the clinical challenges of complex regional pain syndrome, the epidemiology and natural history of complex regional pain syndrome are only partially known; evidence concerning complex regional pain syndrome treatment has grown slowly, due in large part to the vagaries of diagnosis; and research data--when they are available--are difficult to interpret. Thus, in spite of our evolving understanding of this neurologic disorder, in many cases complex regional pain syndrome remains difficult to diagnose and treat successfully.

Causalgia↗
PubMed2004

Interactions between the cardiovascular and pain regulatory systems: an updated review of mechanisms and possible alterations in chronic pain.

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.

Adaptation, Physiological↗
PubMed2004

Anger management style, blood pressure reactivity, and acute pain sensitivity: evidence for "Trait x Situation" models.

BACKGROUND: Anger management style is related to acute and chronic pain, but it is not clear whether anger arousal is needed for these associations to emerge or whether physiological mechanisms mediate these links. PURPOSE: "Trait x Situation" models were examined to determine whether relationships between anger-out and pain and anger-in and pain depended on anger provocation's preceding pain induction and whether pain sensitivity variance explained by anger management style overlapped with variance in harassment-induced blood pressure reactivity. METHODS: Healthy individuals (N = 53) underwent either mental arithmetic with harassment and then a cold pressor (MA/CP) or vice versa (CP/MA). The Spielberger Anger Expression Inventory assessed anger-out using the Anger-Out subscale (AOS) and anger-in using the Anger-In subscale (AIS). RESULTS: AOS x Order and AIS x Order interactions for pain tolerance emerged, such that (a) AOS was related negatively to tolerance among MA/CP participants, whereas AOS and tolerance were not related in CP/MA; (b) AIS was related positively to tolerance in MA/CP, whereas AIS was related negatively to tolerance in CP/MA; and (c) tolerance variance accounted for by AOS in MA/CP overlapped substantially with tolerance variance accounted for by diastolic blood pressure reactivity. CONCLUSIONS: Findings support the notion that anger management style affects pain and are consistent with evidence that deficient endogenous opioid functioning may be one mechanism through which anger-out is linked to both pain sensitivity and cardiovascular stress reactivity, a connection that appears most reliably when anger is provoked.

Adaptation, Psychological↗
PubMed2004

Increased systemic catecholamines in complex regional pain syndrome and relationship to psychological factors: a pilot study.

We have demonstrated that subjects with complex regional pain syndrome (CRPS) have asymmetric venous pool plasma concentrations of norepinephrine (NE) when affected and unaffected limbs are compared, with most demonstrating decreased NE levels in the affected limb. This pilot study explored whether systemic venous plasma catecholamine levels in CRPS subjects with sympathetically maintained pain (SMP) differ from those found in healthy volunteers. We also explored whether catecholamine levels were correlated with scores on psychometric measures of depression, anxiety, and personality. Venous blood samples from 33 CRPS/SMP patients (from unaffected limbs) and 30 healthy control subjects were assayed for plasma NE and epinephrine (E) concentrations. Plasma NE levels were significantly higher in the CRPS group (P < 0.001). Statistical comparisons of E levels across groups did not achieve significance (P < 0.06), although 52% of CRPS/SMP patients had E levels exceeding the 95% confidence interval based on control data. Significant positive correlations were found between E levels and scores on the Beck Depression Inventory and Scales 1, 3, and 6 on the Minnesota Multiphasic Personality Inventory-2 (all P < 0.05). This preliminary work suggests that increased NE and E levels in CRPS/SMP patients may result from the pain of CRPS, consequent affective distress, or both. Alternatively, our findings could reflect premorbid adrenergic hyperactivity caused by affective, endocrine, or other pathology, which might predispose these individuals to develop the syndrome. Definitive studies are needed to examine these hypotheses in detail.

Adult↗
PubMed2003

Prospective examination of pain-related and psychological predictors of CRPS-like phenomena following total knee arthroplasty: a preliminary study.

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.

Aged↗
PubMed2003

Differential effects of expressive anger regulation on chronic pain intensity in CRPS and non-CRPS limb pain patients.

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.

Adult↗
PubMed2003

Emotion induction moderates effects of anger management style on acute pain sensitivity.

Anger management style (AMS) is related to both acute and chronic pain intensity. Recent work suggests that an anger expressive AMS in particular may influence acute pain, and that this effect may be most pronounced during anger provocation. The present study examined whether AMS was related to subsequent pain sensitivity without regard to prior emotion induction, only when a strong negative emotion was evoked, or only when anger was provoked. Sixty-four healthy normals partook in semi-structured interviews in which they recalled and verbally described an event in which either anger, sadness, or joy was elicited. They then underwent a cold pressor pain task. Results of hierarchical multiple regressions showed that an anger expressive AMS was related positively to pain threshold only for participants in the anger-recall condition, and that this effect was largely accounted for by their low SBP reactivity during emotion induction. An anger suppressive AMS was related positively to increases in self-reported pain severity, irrespective of emotion-induction condition, and this effect was not accounted for by reactivity in any cardiovascular index. Results extend those of previous studies by illuminating the potential importance of behavioral anger expression for individuals prone to express anger in modulating their reactivity and pain sensitivity. Findings suggest that the detrimental effects of an anger expressive style on pain sensitivity may be ameliorated under conditions in which behavioral anger expression occurs. Results are discussed in terms of recent work suggesting that an expressive AMS is associated with endogenous opioid dysfunction in the absence of behavioral anger expression.

Acute Disease↗