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

Burns, John W.; Kubilus, Amanda; Bruehl, Stephen

doi:10.1016/s0304-3959(03)00298-7

Cited by 56 publications

(65 citation statements)

References 36 publications

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“…The pain-related effects of anger-in were due to the fact that those exhibiting an anger suppressive style tend to be more affectively distressed (depressed, anxious, and angry), which in turn negatively influences pain responsiveness. This finding supports prior work suggesting that statistical overlap between anger-in and general negative affect may account for many of the reported health-related effects of anger-in [9,15,36]. In contrast, while anger-out was significantly correlated with negative affect in this study, this overlap did not account for its genetically-moderated influence on pain responsiveness.…”

Section: Discussionsupporting

confidence: 83%

The mu opioid receptor A118G gene polymorphism moderates effects of trait anger-out on acute pain sensitivity

Bruehl

Chung

Burns

2008

Pain

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Both trait anger-in (managing anger through suppression) and anger-out (managing anger through direct expression) are related to pain responsiveness, but only anger-out effects involve opioid mechanisms. Preliminary work suggested the effects of anger-out on post-operative analgesic requirements were moderated by the A118G single nucleotide polymorphism of the mu opioid receptor gene. This study further explored these potential genotype X phenotype interactions as they impact acute pain sensitivity. Genetic samples and measures of anger-in and anger-out were obtained in 87 subjects (from three studies) who participated in controlled laboratory acute pain tasks (ischemic, finger pressure, thermal). McGill Pain Questionnaire (MPQ) Sensory and Affective ratings for each pain task were standardized within studies, aggregated across pain tasks, and combined for analyses. Significant anger-out X A118G interactions were observed (p's<.05). Simple effects tests for both pain measures revealed that whereas anger-out was nonsignificantly hyperalgesic in subjects homozygous for the wild-type allele, anger-out was significantly hypoalgesic in those with the variant G allele (p's<.05). For the MPQ-Affective measure, this interaction arose both from low pain sensitivity in high anger-out subjects with the G allele and heightened pain sensitivity in low anger-out subjects with the G allele relative to responses in homozygous wild-type subjects. No genetic moderation was observed for anger-in, although significant main effects on MPQ-Affective ratings were noted (p<.005). Anger-in main effects were due to overlap with negative affect, but anger-out X A118G interactions were not, suggesting unique effects of expressive anger regulation. Results support opioid-related genotype X phenotype interactions involving trait anger-out.

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Section: Discussionsupporting

confidence: 83%

The mu opioid receptor A118G gene polymorphism moderates effects of trait anger-out on acute pain sensitivity

Bruehl

Chung

Burns

2008

Pain

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“…For chronic low back pain patients, high levels of resting lower paraspinal muscle tension or large increases in lower paraspinal tension during emotional arousal appear to impact chronic pain severity (Burns et al 2003;Burns 2006b). However, Pain Catastrophizing Scale scores were not correlated significantly with resting muscle tension or with reactivity, and so further tests of mediation were inappropriate.…”

Section: Discussionmentioning

confidence: 99%

“…The anger and sadness recall procedures elicit significant muscle tension, SBP, DBP and HR reactivity (Burns et al 1997;Burns 2006b). Moreover, findings tell that both anger and sadness recall interviews elicit self-reported valence and arousal in expected directions (Burns et al 2003;Neumann and Waldstein 2001).Details of the procedures can be found in Burns (2006b). In brief, the experimenter asked a participant to recall a recent event in their life during which they experienced the relevant emotion.…”

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confidence: 87%

Pain catastrophizing, physiological indexes, and chronic pain severity: tests of mediation and moderation models

et al. 2007

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Catastrophizing about pain is related to elevated pain severity and poor adjustment among chronic pain patients, but few physiological mechanisms by which pain catastrophizing maintains and exacerbates pain have been explored. We hypothesized that resting levels of lower paraspinal muscle tension and/or lower paraspinal and cardiovascular reactivity to emotional arousal may: (a) mediate links between pain catastrophizing and chronic pain intensity; (b) moderate these links such that only patients described by certain combinations of pain catastrophizing and physiological indexes would report pronounced chronic pain. Chronic low back pain patients (N = 97) participated in anger recall and sadness recall interviews while lower paraspinal and trapezius EMG and systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were recorded. Mediation models were not supported. However, pain catastrophizing significantly interacted with resting lower paraspinal muscle tension to predict pain severity such that high catastrophizers with high resting lower paraspinal tension reported the greatest pain. Pain catastrophizing also interacted with SBP, DBP and HR reactivity to affect pain such that high catastrophizers who showed low cardiovascular reactivity to the interviews reported the greatest pain. Results support a multi-variable profile approach to identifying pain catastrophizers at © Springer Science+Business Media, LLC 2007 john.burns@rosalindfranklin.edu. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript greatest risk for pain severity by virtue of resting muscle tension and cardiovascular stress function. KeywordsPain catastrophizing; Chronic pain severity; Lower paraspinal muscle tension; Cardiovascular reactivity; Profile approachCatastrophizing about pain is linked to elevated pain severity and poor adjustment among chronic pain patients (Sullivan et al. 1995). It is defined as a tendency to rumi-nate, magnify and feel helpless about pain (Sullivan et al. 1995), and as a negative automatic appraisal of painful stimuli rooted in activation of maladaptive beliefs or pain schemas (Michael and Burns 2004;Spanos et al. 1979;Sullivan et al. 2001). Irrespective of theoretical conceptualization, only a few physiological mechanisms by which pain catastrophizing maintains and exacerbates chronic pain intensity have been explored (e.g., Edwards and Fillingim 2005).Physical and psychological stress may lead to frequent and intense, or low level but sustained muscular contractions (Sjegaard et al. 2000). This muscle activity can increase pain through ischemia and hypoxia (Fields 1987), and through changes in mechanoreceptor sensitivity (Mense 1993). Flor and colleagues (Flor et al. 1985(Flor et al. , 1991(Flor et al. , 1992 proposed a "symptom-specificity" model of chronic pain, which proposes that patients with certain kinds of musculoskeletal disorders can be distinguished from patients with other kinds of musculoskeletal disorders by substantial stres...

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“…Both anger expression and anger suppression have been linked with pain severity via various physiological mechanisms (e.g. Bruehl, Chung, Burns, & Biridepalli, 2003;Burns, Kubilus, & Bruehl, 2003;Burns, Quartana, & Bruehl, 2008). Fear of pain has been shown to be closely related to various measures of patient functioning in chronic pain (Crombez, Vlaeyen, Heuts, & Lysens, 1999;McCracken, Zayfert, & Gross, 1992), as has anxiety sensitivity (Keogh & Cochrane, 2002) and worry (Eccleston & Crombez, 1999).…”

Section: Key Practitioner Messagementioning

confidence: 99%

Basic emotion profiles in healthy, chronic pain, depressed and PTSD individuals

Finucane

Dima

Ferreira

et al. 2011

Clin Psychology and Psychoth

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ObjectivesTo compare self-reports of five basic emotions across four samples: healthy, chronic pain, depressed and PTSD, and to investigate the extent to which basic emotion reports discriminate between individuals in healthy or clinical groups. MethodsIn total, 439 participants took part in this study: healthy (N = 131), chronic pain (N = 220), depressed (N = 24) and PTSD (N = 64). Participants completed the trait version of the Basic Emotion Scale (Dalgleish & Power, 2004). Basic emotion profiles were compared both within each group and between the healthy group and each of the three other groups. Discriminant analysis was used to assess the extent to which basic emotions can be used to classify participants as belonging to the healthy group or one of the clinical groups.2 ResultsIn the healthy group, happiness was experienced more than any other basic emotion.This was not found in the clinical groups. In comparison to healthy participants, the chronic pain group experienced more fear, anger and sadness; the depressed group reported more sadness; and the PTSD group experienced all of the negative emotions more frequently. Discriminant analysis revealed that happiness was the most important variable in determining whether an individual belonged to the healthy group or one of the clinical groups. Anger was found to further discriminate between depressed and chronic pain individuals. ConclusionThe findings demonstrate that basic emotion profile analysis can provide a useful foundation for the exploration of emotional experience both within and between healthy and clinical groups. Key Practitioner Message• More frequent experiences of happiness relative to discrete negative emotions most clearly discriminate between individuals in healthy and clinical groups.More frequent anger experiences further discriminate between individuals with chronic pain and those with depression while disgust levels help discriminate between those with PTSD and depression.• More frequent experiences of high arousal negative emotions -fear, anger and disgust are characteristic of individuals with PTSD.• Fear is the most frequently experienced negative emotion in both healthy and clinical groups. Higher levels of fear compared to other discrete negative emotions are not necessarily an indicator of psychopathology. Consideration of emotional profiles more generally and the relative frequency with which happiness is experienced relative to negative emotions may be more useful in delineating between healthy individuals and those with chronic pain, depression or PTSD. 3Although emotions play an important role in psychopathology, few studies have applied models of everyday emotions to research in psychopathology. Nonetheless,

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

Cited by 56 publications

References 36 publications

The mu opioid receptor A118G gene polymorphism moderates effects of trait anger-out on acute pain sensitivity

The mu opioid receptor A118G gene polymorphism moderates effects of trait anger-out on acute pain sensitivity

Pain catastrophizing, physiological indexes, and chronic pain severity: tests of mediation and moderation models

Basic emotion profiles in healthy, chronic pain, depressed and PTSD individuals

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