Phillip J. Quartana

Pain catastrophizing: a critical review

Pain catastrophizing is conceptualized as a negative cognitive–affective response to anticipated or actual pain and has been associated with a number of important pain-related outcomes. In the present review, we first focus our efforts on the conceptualization of pain catastrophizing, highlighting its conceptual history and potential problem areas. We then focus our discussion on a number of theoretical mechanisms of action: appraisal theory, attention bias/information processing, communal coping, CNS pain processing mechanisms, psychophysiological pathways and neural pathways. We then offer evidence to suggest that pain catastrophizing represents an important process factor in pain treatment. We conclude by offering what we believe represents an integrated heuristic model for use by researchers over the next 5 years; a model we believe will advance the field most expediently.

Anger inhibition and pain: conceptualizations, evidence and new directions

Anger and how anger is regulated appear to affect acute and chronic pain intensity. The inhibition of anger (anger-in), in particular, has received much attention, and it is widely believed that suppressing or inhibiting the verbal or physical expression of anger is related to increased pain severity. We examine theoretical accounts for expecting that anger inhibition should affect pain, and review evidence for this claim. We suggest that the evidence for a link between trait anger-in (the self-reported tendency to inhibit anger expression when angry) and acute and chronic pain severity is quite limited owing to a number of factors including a inadequate definition of trait anger-in embodied in the popular anger-in subscale of Spielberger’s Anger Expression Inventory, and a strong overlap between trait anger-in scores and measures of general negative affect (NA). We argue that in order to determine whether something unique to the process of anger inhibition exerts direct effects on subsequent pain intensity, new conceptualizations and approaches are needed that go beyond self-report assessments of trait anger-in. We present one model of anger inhibition and pain that adopts elements of Wegner’s ironic process theory of thought suppression. Findings from this emerging research paradigm indicate that state anger suppression (suppression manipulated in the laboratory) may indeed affect sensitivity to subsequent painful stimuli, and we outline potentially productive avenues of future inquiry that build on this model. We conclude that although studies employing correlational designs and self-reports of trait anger-in have not upheld the claim that anger inhibition affects pain severity, evidence from studies using new models suggests that actually inhibiting anger expression during a provocative event may increase perceived pain at a later time.

Painful consequences of anger suppression.

The authors experimentally examined the effects of anger suppression on pain perception. On the basis of ironic process theory, they proposed that efforts to suppress experiential or expressive components of anger may paradoxically enhance cognitive accessibility of anger-related thoughts and feelings, thereby contaminating perception of succeeding pain in an anger-congruent manner. Participants were randomly assigned to nonsuppression or experiential or expressive suppression conditions during mental arithmetic with or without harassment. A cold-pressor task followed. Results revealed that participants instructed to suppress experiential or expressive components of emotion during harassment not only reported the greatest pain levels, but also rated the anger-specific dimensions of pain uniquely strong. Results suggest that attempts to suppress anger may amplify pain sensitivity by ironically augmenting perception of the irritating and frustrating qualities of pain.

Cognitive dimensions of anger in chronic pain

Anger has long been recognized as an integral part of pain experience [1,19]. Reviews highlight the deleterious effect of anger on social, clinical, and functional outcomes [9,22,32]. Anger has been discussed as an aversive emotional state ranging from mild irritation to fury [25], and comprising specific cognitive attributions and action tendencies [21,34]. Anecdotal and empirical data suggest that anger is commonplace among chronic pain sufferers [32]. In their 2003 review, Greenwood et al. [22] identified anger as an important target of research and behavioral management; since that review, research has highlighted biopsychosocial mechanisms through which anger may affect pain experience [5,9,33]. However, to date, no systematic line of research has addressed the cognitive dimensions of anger in chronic pain. We believe that elucidating these facets of anger in pain sufferers might strengthen the empirical foundation for more effective treatment. Although not exhaustive, the current review highlights potential sources of anger among pain sufferers by drawing on conceptualizations from existing social psychological theory and newly evolving lines of research. On this basis, we discuss the role of anger in treatment settings, and possible frameworks for research and intervention.

Evidence for indirect effects of pain catastrophizing on clinical pain among myofascial temporomandibular disorder participants: the mediating role of sleep disturbance.

Summary Pain catastrophizing was associated with greater sleep disturbance, and both pain catastrophizing and pain‐related rumination indirectly affected clinical pain and pain‐related interference through alterations in sleep. ABSTRACT Sleep disturbance and pain catastrophizing are important mediators of the chronic pain experience. To date, these factors have not been considered concurrently despite compelling theoretical rationale to do so. In the present study, we examined whether pain catastrophizing not only has direct effects on clinical pain and pain‐related interference, but also indirect effects through its association with sleep disturbance. We evaluated this hypothesis using a cohort (n = 214) of myofascial temporomandibular disorder participants using a statistical bootstrapping technique recommended for tests of indirect effects. Results suggested that pain catastrophizing was associated with greater sleep disturbance, and that a significant portion of variance in clinical pain severity and pain‐related interference attributable to pain catastrophizing was mediated by sleep disturbance. Supplementary analyses revealed that the rumination component of catastrophizing seemed to be indirectly related to clinical outcomes through sleep disturbance. No evidence for indirect effects was observed for helplessness and magnification components. These results suggest that rumination about pain may contribute to clinical pain indirectly through alterations in sleep. Prospective studies are needed to examine lagged associations between these constructs. These findings have important theoretical and clinical implications. Critically, interventions that reduce pain catastrophizing may concurrently improve sleep and clinical pain.

Chronic Pain and Opioid Use in US Soldiers After Combat Deployment

Chronic Pain and Opioid Use in US Soldiers After Combat Deployment Chronic pain affects a quarter of people seeking primary health care.1,2 Opioid medications are prescribed for chronic pain, but recently, rates of opioid use and misuse have ballooned, leading to significant numbers of overdose-related hospitalizations and deaths.3 The prevalence of chronic pain and opioid use assoc iated w ith deployment is not well known, despite large numbers of wounded service members. To our knowledge, this is the first study to assess chronic pain prevalence and opioid use in a non– treatment-seeking, active duty infantry population following deployment.

Threat-Related Attention Bias Variability and Posttraumatic Stress

OBJECTIVE Threat monitoring facilitates survival by allowing one to efficiently and accurately detect potential threats. Traumatic events can disrupt healthy threat monitoring, inducing biased and unstable threat-related attention deployment. Recent research suggests that greater attention bias variability, that is, attention fluctuations alternating toward and away from threat, occurs in participants with PTSD relative to healthy comparison subjects who were either exposed or not exposed to traumatic events. The current study extends findings on attention bias variability in PTSD. METHOD Previous measurement of attention bias variability was refined by employing a moving average technique. Analyses were conducted across seven independent data sets; in each, data on attention bias variability were collected by using variants of the dot-probe task. Trauma-related and anxiety symptoms were evaluated across samples by using structured psychiatric interviews and widely used self-report questionnaires, as specified for each sample. RESULTS Analyses revealed consistent evidence of greater attention bias variability in patients with PTSD following various types of traumatic events than in healthy participants, participants with social anxiety disorder, and participants with acute stress disorder. Moreover, threat-related, and not positive, attention bias variability was correlated with PTSD severity. CONCLUSIONS These findings carry possibilities for using attention bias variability as a specific cognitive marker of PTSD and for tailoring protocols for attention bias modification for this disorder.

Pain Catastrophizing and Salivary Cortisol Responses to Laboratory Pain Testing in Temporomandibular Disorder and Healthy Participants

UNLABELLED Pain catastrophizing is an important variable in the context of acute and chronic pain. The neurophysiological correlates of pain catastrophizing, however, have not been rigorously evaluated. We examined the relationship between trait-pain catastrophizing and morning salivary cortisol levels before and following a 45-minute laboratory pain-testing session in healthy, pain-free (n = 22), and temporomandibular disorder (TMD) participants (n = 39). We also examined whether TMD patients evidenced generalized hyperalgesia and hypercortisolism. Pain catastrophizing was associated with a flattened morning salivary cortisol profile in the context of pain testing, irrespective of pain status. Cortisol profiles did not differ between healthy and TMD participants. TMD was associated with mechanical hyperalgesia only at the masseter. These data are the first to show an association between pain catastrophizing and elevated salivary cortisol profiles in the context of standardized experimental pain testing. These findings in both healthy individuals and those with chronic orofacial pain suggest that aberrant adrenocortical responses to pain may serve as a neurophysiologic pathway by which pain catastrophizing enhances vulnerability for development of chronic pain and maintains and/or exaggerates existing pain and associated morbidity. PERSPECTIVE Neurophysiological mechanisms by which pain catastrophizing is related to acute and chronic pain recently have come under empirical study. Understanding of these mechanisms has the unique potential to shed light on key central-nervous-system factors that mediate catastrophizing-pain relations and therapeutic benefits associated with changes in catastrophizing and related cognitive processes.

Effects of anger suppression on pain severity and pain behaviors among chronic pain patients: evaluation of an ironic process model.

OBJECTIVE Evidence for links between anger inhibition or suppression and chronic pain severity is based mostly on studies with correlation designs. Following from ironic process theory, we proposed that attempts to suppress angry thoughts during provocation would increase subsequent pain intensity among chronic low back pain (CLBP) patients, and do so through paradoxically enhanced accessibility of anger. DESIGN CLBP patients (N = 58) were assigned to suppression and nonsuppression conditions while performing a computer maze task with a harassing confederate. A structured pain behavior task (SPBT) followed. MAIN OUTCOME MEASURES Self-reported anger, anxiety, and sadness following maze task. Self-reported pain severity and number of observed pain behaviors during SPBT. RESULTS Patients told to suppress during provocation: (a) reported greater anger following the maze task, reported greater pain intensity during the SPBT, and exhibited more pain behaviors than patients not suppressing; (b) postmaze anger levels significantly mediated group differences on pain behaviors. CONCLUSION Attempts by CLBP patients to suppress anger may aggravate pain related to their clinical condition through ironically increased feelings of anger.

Anger management style moderates effects of emotion suppression during initial stress on pain and cardiovascular responses during subsequent pain-induction

Background: Suppression of emotion, anger in particular, may be linked to heightened pain intensity during a subsequent painful event, but it is not clear whether an individual’s anger management style (trait anger-out or trait anger-in) moderates effects on pain intensity and cardiovascular responses during pain.Purpose: To determine whether (a) trait anger-out and/or trait anger-in moderate effects of Emotion-Induction (anger, anxiety)×Emotion Suppression (nonsuppression, experiential, expressive) manipulations during mental arithmetic on pain intensity and cardiovascular responses during and following a cold pressor pain task, such that “mismatch” relationships emerge (preferred anger management style is discrepant from situation demands), and (b) general emotional expressivity accounts for these effects.Method: Healthy nonpatients (N=187) were assigned to 1 of 6 conditions for a mental arithmetic task. Cells were formed by crossing 2 Emotion-Induction (anxiety, anger)×3 Emotion Suppression (non-suppression, experiential, expressive) conditions. After mental arithmetic, participants underwent a cold pressor followed by recovery. Systolic blood pressure (SBP), diastolic BP (DBP), heart rate (HR), and pain intensity ratings were recorded. Spielberger Anger Expression Inventory tapped anger management style.Results: General Linear Model procedures tested Emotion-Induction×Emotion Suppression×Anger-Out or Anger-In (continuous)×Period (baseline, cold pressor, recovery) effects on pain intensity, SBP, DBP, and HR. A 4-way interaction emerged for pain intensity: Only for those in the anger-induction/experiential suppression condition, anger-out was related significantly to pain recovery. Three-way interactions emerged for SBP and DBP: Only for those in expressive suppression condition, anger-out was related significantly to SBP during and following cold pressor and to DBP following cold pressor. General emotion expressivity did not account for anger-out effects.Conclusions: A mismatch situation may apply for high anger-out people who suppress emotion in a certain circumstance and thus may suffer greater discomfort and physiological responsiveness to subsequent pain than high anger-out people not having to suppress.