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Biomedical subjects

Stephen Bruehl

Publications and source records attributed to Stephen Bruehl.

31 records · Page 2Linked to original sources

The association between anger expression and chronic pain intensity: evidence for partial mediation by endogenous opioid dysfunction.

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.

Adult↗

Do changes in cognitive factors influence outcome following multidisciplinary treatment for chronic pain? A cross-lagged panel analysis.

Changes in maladaptive cognitions may constitute therapeutic processes of multidisciplinary pain programs. A cross-lagged panel design was used to determine whether (a) early-treatment cognitive change predicted late-treatment outcome index change, but not vice versa; and (b) these effects remained significant with depression change controlled. Ninety chronic pain patients, in a 4-week multidisciplinary program, completed measures of catastrophizing, pain helplessness, depression, pain, interference, and activity level at pre-, mid-, and posttreatment. With depression changes controlled, early-treatment catastrophizing and pain helplessness changes predicted late-treatment outcome index changes, but not vice versa; early-treatment depression changes predicted late-treatment activity changes, but not vice versa. Findings advance understanding of pain treatment process and suggest that negative cognition changes may indeed affect improvements in treatment outcome.

Adaptation, Psychological↗

Predicting total knee replacement pain: a prospective, observational study.

To describe the natural history of pain after total knee arthroplasty and to identify factors predicting excessive postoperative pain, we used a prospective, observational study assessing clinical and radiographic variables preoperatively and at 1, 3, 6, and 12 months after knee replacement. Data sources included the visual analog pain scale and other measures of patient health, psychologic state, and component reliability. Regression analyses were conducted to identify specific factors predictive of postoperative pain, controlling for inequality of variables, and confirmed using regression diagnostics. For 116 patients (149 knees; mean age, 66 years; 55.2% women), significant pain was reported by 72.3%, 44.4%, 22.6%, 18.4%, and 13.1%, respectively. No intergroup differences existed for anesthesia, weight, age, or gender. Patients with greater preoperative pain had more postoperative pain, used more home therapy, and postoperative manipulations. Preoperative depression and anxiety were associated with heightened pain at 1 year. Pain after knee replacement resolves quickly, declining to approximately (1/2) by 3 months. However, one in eight patients report moderate to severe pain 1 year after surgery despite an absence of clinical or radiographic abnormalities. Development of office-based preoperative screening tools and interventions for these patients may reduce postoperative costs and improve patient-perceived outcomes.

Adult↗

Complex regional pain syndrome: are there distinct subtypes and sequential stages of the syndrome?

This study tested for evidence supporting the clinical lore of three sequential stages of complex regional pain syndrome (CRPS) and examined the characteristics of possible CRPS subtypes. A series of 113 patients meeting IASP criteria for CRPS underwent standardized history and physical examinations to assess CRPS signs and symptoms in four domains identified in previous research: pain/sensory abnormalities, vasomotor dysfunction, edema/sudomotor dysfunction, and motor/trophic changes. K-Means cluster analysis was used to derive three relatively homogeneous CRPS patient subgroups based on similarity of sign/symptom patterns in these domains. The resulting CRPS subgroups did not differ significantly regarding pain duration as might be expected in a sequential staging model. However, the derived subgroups were statistically-distinct, and suggested three possible CRPS subtypes: (1) a relatively limited syndrome with vasomotor signs predominating, (2) a relatively limited syndrome with neuropathic pain/sensory abnormalities predominating, and (3) a florid CRPS syndrome similar to "classic RSD" descriptions. Subtype 3 showed the highest levels of motor/trophic signs and possible disuse-related changes (osteopenia) on bone scan, despite having directionally the briefest pain duration of the three groups. EMG/NCV testing suggests that Subtype 2 may reflect CRPS-Type 2 (causalgia). Overall, these results are consistent with limited previous work that argues against three sequential stages of CRPS. However, several distinct CRPS subtypes are suggested, and these could ultimately have utility in targeting treatment more effectively.

Adult↗

Anger and pain sensitivity in chronic low back pain patients and pain-free controls: the role of endogenous opioids.

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.

Acute Disease↗

The relationship between resting blood pressure and acute pain sensitivity in healthy normotensives and chronic back pain sufferers: the effects of opioid blockade.

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.

Acute Disease↗

Psychological differences between reflex sympathetic dystrophy and non-RSD chronic pain patients.

This study examined possible psychological differences between Reflex Sympathetic Dystrophy (RSD) and non-RSD chronic pain patients. Unlike the few previous studies in this area, this study controlled statistically for age and pain duration differences across diagnostic groups, and included a non-RSD limb pain control group. Subjects were a consecutive series of 34 RSD, 50 non-RSD limb pain (Limb), and 165 low back pain (LBP) patients presenting for treatment at the Rush Pain Center. Analyses revealed that RSD patients reported more somatization and phobic anxiety on the Brief Symptom Inventory than LBP patients. RSD patients also reported greater coping with pain through diverting attention than LBP patients did on the Coping Strategies Questionnaire. Comparisons between the RSD and Limb groups revealed no significant differences with the exception of somatization scores. The relationship between distress and pain severity was found to be stronger in RSD and Limb patients than in LBP patients. These results provide partial support for clinical assumptions that RSD patients are more psychologically dysfunctional than other chronic pain patients. However, these conclusions do not generalize across all comparison groups. The fact that RSD and non-RSD limb pain patients were quite similar on nearly all measures suggests that sympathetic mediation of pain is not the source of these psychological differences.

Adaptation, Psychological↗

Do endogenous opioids mediate the relationship between blood pressure and pain sensitivity in normotensives?

Elevated resting blood pressure is associated with decreased pain sensitivity in both animals and humans. Recent evidence suggests that this relationship may be mediated by endogenous opioid peptides in hypertensives, but the precise mechanism has not been investigated in normotensives. We examined the effect of opioid receptor blockade with naloxone on the relationship between resting blood pressure and pain sensitivity in normotensive humans. Sixteen young adults were given cold pressor and handgrip challenges after treatment with either naloxone or saline in a placebo-controlled, within-subject design. Multiple regression procedures indicated that resting systolic blood pressure was a significant predictor of cold pain ratings even after the effects of naloxone were statistically controlled. The interaction between systolic blood pressure and opioid blockade was non-significant. These data suggest that the relationship between resting blood pressure and pain sensitivity in normotensive humans is mediated, at least in part, by non-opioid mechanisms.

Adolescent↗

Two brief interventions for acute pain.

This study evaluated two brief (3-5 min) interventions for controlling responses to acute pain. Eighty male subjects were randomly assigned to 1 of 2 intervention groups (Positive Emotion Induction (PEI) or Brief Relaxation (BR)) or to 1 of 2 control groups (No-instruction or Social Demand). The PEI focused on re-creating a pleasant memory, while the BR procedure involved decreasing respiration rate and positioning the body in a relaxed posture. All subjects underwent a 60-sec finger pressure pain trial. Analyses indicated that the PEI subjects reported lower ratings of pain, fear, and anxiety, and experienced greater finger temperature recovery than controls. The BR procedure resulted in greater blood pressure recovery, but did not alter ratings of pain or emotion relative to controls. Further research is needed to explore the clinical use of the PEI for acute pain management.

Acute Disease↗

The relationship between pain sensitivity and blood pressure in normotensives.

Hypertension has been found to be related to decreased sensitivity to painful stimuli. The current study explored whether this relationship extends into the normotensive range of blood pressures. Resting blood pressures were assessed in 60 male normotensives. Subjects then underwent a 1 min finger pressure pain stimulation trial. Pain ratings were inversely related to resting systolic blood pressure. This relationship was unrelated to emotional state or coping styles. Multiple regression analyses indicated that over one-third of the variance in pain ratings can be accounted for by resting blood pressure, coping style, and emotional state.

Adaptation, Psychological↗

Endogenous opioids and chronic pain intensity: interactions with level of disability.

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

Adult↗

Prevalence of clinical hypertension in patients with chronic pain compared to nonpain general medical patients.

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.

Adult↗

Anger management style and hostility among patients with chronic pain: effects on symptom-specific physiological reactivity during anger- and sadness-recall interviews.

OBJECTIVES: We examined whether anger-in, anger-out, and hostility predicted symptom-specific muscle tension reactivity during anger induction (but not sadness induction) among patients with chronic low back pain (CLBP). For patients with CLBP, relevant muscles are the lower paraspinals (LPs). Anger-in x hostility and anger-out x hostility interactions were tested to determine whether particularly reactive groups of patients could be identified with a multivariable profile approach. METHODS: Ninety-four patients with CLBP underwent anger recall (ARI) and sadness recall (SRI) interviews, whereas LP and trapezius electromyography and systolic blood pressure, diastolic blood pressure, and heart rate were recorded. They completed anger-in, anger-out, hostility, and trait anger measures. RESULTS: Hierarchical regressions were used to test anger-in x hostility and anger-out x hostility interactions for physiological changes during the ARI and SRI. A significant anger-in x hostility interaction was found for LP change during the ARI (but not SRI) such that high anger-in/high hostility patients evinced the greatest reactivity. Effects for trapezius reactivity were nonsignificant. Significant anger-in x hostility interactions were also found for systolic blood pressure and diastolic blood pressure changes during the ARI such that high anger-in/low hostility patients showed the smallest changes. The anger-out x hostility interaction for diastolic blood pressure change during ARI was also significant such that high anger-out/low hostility patients showed the smallest changes. All effects remained significant with trait anger controlled. CONCLUSIONS: A multivariable profile approach may help identify especially vulnerable patient groups. Patients with CLBP who tend to suppress anger and are cynically hostile may be more likely to experience high levels of muscle tension near the site of pain and injury during anger, but not during sadness, than other groups.

Adaptation, Psychological↗