Search

Introduction Insufficient sleep increases pain sensitivity in healthy individuals. Additionally, extending sleep (eg, increasing nocturnal sleep time or adding a mid-day nap) has been shown to restore pain sensitivity to baseline levels in sleep deprived/restricted individuals. Whether sleep extension can reduce pain sensitivity beyond baseline levels in non-sleep restricted/deprived individuals remains unknown. Methods In a sample of 27 healthy, pain-free, normally-sleeping individuals (17 males, mean age ∼24 yrs), we examined the impact of five nights of sleep extension on pain sensitivity. Pain threshold (elapsed time until the participant reported pain) and pain tolerance (total time the participant kept the hand submerged in the cold water) were measured using the Cold Pressor Task. Furthermore, we assessed the extent to which self-reported sleep amount in relation to the minimal subjective sleep requirement for adequate performance (sleep credit) was associated with pain sensitivity changes. Results On average individuals slept almost 2 extra hours per night. Our results indicate that sleep extension increases pain tolerance beyond baseline levels. However, sleep extension did not impact pain threshold. We also found that individuals with a smaller sleep credit (ie, those who habitually obtain less sleep than they feel they need) experienced greater increases in pain tolerance after extending sleep. Conclusions The present findings suggest that sleep extension may increase pain tolerance but not pain threshold in healthy individuals who normally sleep the recommended amount. Our findings also support the idea that sleep credit may be a strong indicator of sleep debt in the context of pain sensitivity.

Adverse childhood experiences (ACEs) can have long-term impacts on a person's mental health, which extend into adulthood. There is a high prevalence of ACEs among service members. Further, service members also report frequently experiencing disrupted sleep. We hypothesized that disrupted sleep may serve a mechanistic function connecting ACEs to functional impairment and poorer mental health. In a cross-sectional sample (n = 759), we found evidence for an indirect effect of ACEs on mental health outcomes through disrupted sleep. In a different sample using two time-points (n = 410), we found evidence for an indirect effect of ACEs on changes in mental health outcomes and functional impairment during a reset period, through changes in disrupted sleep during the same period. Implications, limitations and future research directions are discussed.

This study explored attention and interpretation biases in processing facial expressions as correlates of theoretically distinct self-reported anger experience, expression, and control. Non-selected undergraduate students (N = 101) completed cognitive tasks measuring attention bias, interpretation bias, and Spielberger's State-Trait Anger Expression Inventory (STAXI-2). Attention bias toward angry faces was associated with higher trait anger and anger expression and with lower anger control-in and anger control-out. The propensity to quickly interpret ambiguous faces as angry was associated with greater anger expression and its subcomponent of anger expression-out and with lower anger control-out. Interactions between attention and interpretation biases did not contribute to the prediction of any anger component suggesting that attention and interpretation biases may function as distinct mechanisms. Theoretical and possible clinical implications are discussed.

STUDY OBJECTIVES: Aggression, substance misuse, and other health risk behaviors are common among combat veterans. We examined whether sleep quality and quantity predict the association between combat exposure, post-traumatic stress symptoms, and adverse health-related behaviors. METHODS: Soldiers (N = 2420) from a brigade combat team completed surveys assessing combat experiences, and psychological and behavioral health factors, approximately 3 months following deployment to Afghanistan in 2011. RESULTS: Respondents were 93.5% male; 73% were age 18–29 years old. The response rate was 80% (3076/3832); 94% (2876/3076) of the soldiers who attended the recruitment briefings consented to participate in this research. Complete data were available across the variables used in this study for up to 2420 soldiers. Sleep continuity disturbance accounted for the association of combat exposure with post-traumatic stress symptoms and aggression, alcohol use, and risky behavior. Moreover, for soldiers who reported sleep duration of

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.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.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.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.

Generalized dysfunction of the nociceptive system has been hypothesized to be an important pathophysiologic process underlying temporomandibular disorder (TMD) pain. Studies have not identified sensitization to painful stimuli administered prospectively across consecutive days among participants with TMD with chronic pain. We attempted to isolate an empirically derived laboratory-based marker of sustained mechanical pain sensitization. We examined whether this index accounted for variance in prospective assessments of clinical TMD pain. Participants were women with a clinical diagnosis of chronic TMD (n = 30) and healthy female controls (n = 30). Pain thresholds were assessed using digital algometry 4 times at 12-hour intervals over 48 consecutive hours and clinical TMD pain via follow-up telephone assessments. Sustained mechanical pain sensitization, defined by statistically significant linear decrements in pressure pain thresholds across the consecutive testing sessions, discriminated chronic TMD and control participants. An index of sustained sensitization at the masseter accounted for unique variance in clinical TMD pain over the subsequent 3-month assessment period, even controlling for mean pain threshold and baseline pain severity. These preliminary findings highlight discriminant and predictive validity characteristics of a novel marker of protracted pain sensitization among women with chronic TMD pain. Perspective A laboratory-based and empirically defined marker of sustained mechanical pain sensitization over the course of days with acceptable discriminant and predictive validity was identified. This marker may represent a clinically useful marker of chronic TMD pain in women.

Objective To characterize the indirect associations of combat exposure with post-deployment physical symptoms through shared associations with post-traumatic stress disorder (PTSD), depression and insomnia symptoms. Methods Surveys were administered to a sample of U.S. soldiers (N = 587) three months after a 15-month deployment to Iraq. A multiple indirect effects model was used to characterize direct and indirect associations between combat exposure and physical symptoms. Results Despite a zero-order correlation between combat exposure and physical symptoms, the multiple indirect effects analysis did not provide evidence of a direct association between these variables. Evidence for a significant indirect association of combat exposure and physical symptoms was observed through PTSD, depression, and insomnia symptoms. In fact, 92% of the total effect of combat exposure on physical symptoms scores was indirect. These findings were evident even after adjusting for the physical injury and relevant demographics. Conclusion This is the first empirical study to suggest that PTSD, depression and insomnia collectively and independently contribute to the association between combat exposure and post-deployment physical symptoms. Limitations, future research directions, and potential policy implications are discussed.

Objectives To investigate the effects of caffeine on psychomotor vigilance and sleepiness during sleep restriction and following subsequent recovery sleep. Methods Participants were N = 48 healthy good sleepers. All participants underwent five nights of sleep satiation (time-in-bed [TIB]: 10 hours), followed by five nights of sleep restriction (TIB: 5 hours), and three nights of recovery sleep (TIB: 8 hours) in a sleep laboratory. Caffeine (200 mg) or placebo was administered in the form of chewing gum at 08:00 am and 12:00 pm each day during the sleep restriction phase. Participants completed hourly 10-minute psychomotor vigilance tests and a modified Maintenance of Wakefulness Test approximately every 4 hours during the sleep restriction and recovery phases. Results Caffeine maintained objective alertness compared to placebo across the first 3 days of sleep restriction, but this effect was no longer evident by the fourth day. A similar pattern of results was found for Maintenance of Wakefulness Test sleep latencies, such that those in the caffeine group (compared to placebo) did not show maintenance of wakefulness relative to baseline after the second night of restriction. Compared to placebo, participants in the caffeine condition displayed slower return to baseline in alertness and wakefulness across the recovery sleep period. Finally, the caffeine group showed greater N3 sleep duration during recovery. Conclusions Caffeine appears to have limited efficacy for maintaining alertness and wakefulness across 5 days of sleep restriction. Perhaps more importantly, there may be recovery costs associated with caffeine use following conditions of prolonged sleep loss.

Objectives. We characterized trends in mental health services utilization and stigma over the course of the Afghanistan and Iraq wars among active-component US soldiers. Methods. We evaluated trends in mental health services utilization and stigma using US Army data from the Health-Related Behavior (HRB) surveys from 2002, 2005, and 2008 (n = 12 835) and the Land Combat Study (LCS) surveys administered to soldiers annually from 2003 to 2009 and again in 2011 (n = 22 627). Results. HRB and LCS data suggested increased mental health services utilization and decreased stigma in US soldiers between 2002 and 2011. These trends were evident in soldiers with and without posttraumatic stress disorder (PTSD), major depressive disorder (MDD), or PTSD and MDD. Despite the improving trends, more than half of soldiers with mental health problems did not report seeking care. Conclusions. Mental health services utilization increased and stigma decreased over the course of the wars in Iraq and Afghanistan. Although promising, these findings indicate that a significant proportion of US soldiers meeting criteria for PTSD or MDD do not utilize mental health services, and stigma remains a pervasive problem requiring further attention.

BackgroundEfficacy of pre-trauma prevention for post-traumatic stress disorder (PTSD) has not yet been established in a randomized controlled trial. Attention bias modification training (ABMT), a computerized intervention, is thought to mitigate stress-related symptoms by targeting disruptions in threat monitoring. We examined the efficacy of ABMT delivered before combat in mitigating risk for PTSD following combat.MethodWe conducted a double-blind, four-arm randomized controlled trial of 719 infantry soldiers to compare the efficacy of eight sessions of ABMT (n = 179), four sessions of ABMT (n = 184), four sessions of attention control training (ACT; n = 180), or no-training control (n = 176). Outcome symptoms were measured at baseline, 6-month follow-up, 10 days following combat exposure, and 4 months following combat. Primary outcome was PTSD prevalence 4 months post-combat determined in a clinical interview using the Clinician-Administered PTSD Scale. Secondary outcomes were self-reported PTSD and depression symptoms, collected at all four assessments.ResultsPTSD prevalence 4 months post-combat was 7.8% in the no-training control group, 6.7% with eight-session ABMT, 2.6% with four-session ABMT, and 5% with ACT. Four sessions of ABMT reduced risk for PTSD relative to the no-training condition (odds ratio 3.13, 95% confidence interval 1.01–9.22, p < 0.05, number needed to treat = 19.2). No other between-group differences were found. The results were consistent across a variety of analytic techniques and data imputation approaches.ConclusionsFour sessions of ABMT, delivered prior to combat deployment, mitigated PTSD risk following combat exposure. Given its low cost and high scalability potential, and observed number needed to treat, research into larger-scale applications is warranted. The ClinicalTrials.gov identifier is NCT01723215.

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.

Suppression of anger may be linked to heightened pain report and pain behavior during a subsequent painful event among chronic low back patients, but it is not clear whether these effects are partly accounted for by increased physiological reactivity during suppression. Chronic low back pain patients (N = 58) were assigned to Suppression or No Suppression conditions for a "cooperative" computer maze task during which a confederate harassed them. During baseline and maze task, patients' lower paraspinal and trapezius muscle tension, blood pressure and heart rate were recorded. After the maze task, patients underwent a structured pain behavior task (behaviors were videotaped and coded). Results showed that: (a) Suppression condition patients revealed greater lower paraspinal muscle tension and systolic blood pressure (SBP) increases during maze task than No Suppression patients (previously published results showed that Suppression condition patients exhibited more pain behaviors than No Suppression patients); (b) residualized lower paraspinal and SBP change scores were related significantly to pain behaviors; (c) both lower paraspinal and SBP reactivity significantly mediated the relationship between Condition and frequency of pain behaviors. Results suggest that suppression-induced lower paraspinal muscle tension and SBP increases may link the actual suppression of anger during provocation to signs of clinically relevant pain among chronic low back pain patients.

Objective. The study of anger suppression and risk for cardiovascular disease has relied predominately on inspection of correlations between trait anger-in and cardiovascular risk factors and disease. This approach tells us little about whether inhibitory processes have anything to do with outcomes, and cannot speak to whether suppression of anger per se affects cardiovascular parameters. Drawing on the broader emotion regulation literature, we examined the effects of experimentally induced anger and general negative emotion in the context of expressive and experiential suppression on cardiovascular responses to initial and subsequent laboratory stressors. Design. Of all participants, 201 healthy participants were randomly assigned to one of six conditions formed by crossing emotion (anxiety, anger) and suppression (experiential, expressive, control) conditions. Methods. Participants completed a mental arithmetic task with anxiety or anger induction under their respective suppression manipulation instructions, and subsequently were exposed to a cold pressor task. Systolic blood pressure (SBP), diastolic blood pressure, and heart rate values were obtained for each experimental epoch. Results. More robust SBP responses to the initial stressor were evidenced for those in the expressive versus the control condition. In response to the subsequent stressor, those in the experiential suppression condition showed the most pronounced SBP responses, suggesting pronounced delayed effects of this type of suppression. Effects of suppression on SBP reactivity were indistinguishable across anxiety and anger conditions. Conclusion. Effortful suppression of negative emotion has immediate and delayed consequences for stress-induced cardiovascular reactivity. Theoretical and clinical significance of these findings are discussed.

We examined whether people who tend to catastrophize about pain and who also attempt to regulate negative thoughts and feelings through suppression may represent a distinct subgroup of individuals highly susceptible to pain and distress. Ninety-seven healthy normal participants underwent a 4-min ischemic pain task followed by a 2-min recovery period. Self-reported pain and distress was recorded during the task and every 20 s during recovery. Participants completed the Pain Catastrophizing Scale and the White Bear Suppression Inventory. Repeated measures multiple regression analysis (using General Linear Model procedures) revealed significant 3-way interactions such that participants scoring high on the rumination and/or helplessness subscales of the Pain Catastrophizing Scale and who scored high on the predisposition to suppress unwanted thoughts and feelings reported the greatest pain and distress during recovery. Results suggest that pain catastrophizers who attempt to regulate their substantial pain intensity and distress with maladaptive emotion regulation strategies, such as suppression, may be especially prone to experience prolonged recovery from episodes of acute pain. Thus, emotion regulation factors may represent critical variables needed to understand the full impact of catastrophic appraisals on long-term adjustment to pain.

To examine whether high trait anger-out chronic low back (CLBP) patients would show exceptionally large symptom-specific lower paraspinal (LP) responses, compared with healthy nonpatients, during pain induction, a subsequent mental stressor, and recovery when they were urged to suppress awareness of pain and suffering.CLBP patients (n = 93) and nonpatients (n = 105) were assigned randomly to one of four attention strategy conditions for use during pain induction: sensory-focus, distraction, suppression, or control. All participants underwent a cold pressor, and then performed mental arithmetic. They completed the anger-out (AOS) and anger-in (AIS) subscales of the Anger Expression Inventory.General Linear Model procedures were used to test Attention Strategy Condition x Patient/Nonpatient Status x AOS (or AIS) x Period interactions for physiological indices. Significant interactions were found such that: a) high trait anger-out patients in the Suppression condition seemed to show the greatest LP reactivity during the mental arithmetic followed by the slowest recovery compared with other conditions; b) high trait anger-out patients and nonpatients in the Suppression condition seemed to show the slowest systolic blood pressure recoveries compared with other conditions.Results extend previous work by suggesting that an anger-out style moderates effects of how attention is allocated during pain on responses to and recovery from a subsequent mental stressor. Results provide further evidence that trait anger-out and trait anger-in among CLBP patients are associated with increased LP muscle tension during and after pain and mental stress.

We examined whether "state" anger regulation-inhibition or expression-among chronic low back pain (CLBP) patients would affect lower paraspinal (LP) muscle tension following anger-induction, and whether these effects were moderated by trait anger management style.Eighty-four CLBP patients underwent harassment, then they regulated anger under one of two conditions: half expressed anger by telling stories about people depicted in pictures, whereas half inhibited anger by only describing objects appearing in the same pictures. They completed the anger-out and anger-in subscales (AOS; AIS) of the anger expression inventory.General Linear Model procedures were used to test anger regulation condition by AOS/AIS by period interactions for physiological indexes. Significant three-way interactions were found such that: a) high trait anger-out patients in the inhibition condition appeared to show the greatest LP reactivity during the inhibition period followed by the slowest recovery; b) high trait anger-out patients in the expression condition appeared to show the greatest systolic blood pressure (SBP) reactivity during the expression period followed by rapid recovery.Results implicate LP muscle tension as a potential physiological mechanism that links the actual inhibition of anger following provocation to chronic pain severity among CLBP patients. Results also highlight the importance of mismatch situations for patients who typically regulate anger by expressing it. These CLBP patients may be at particular risk for elevated pain severity if circumstances at work or home regularly dictate that they should inhibit anger expression.

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.

OBJECTIVE The purpose of this study was to test an experimental model of the effects of sleep continuity disturbance on sleep architecture and positive mood in order to better understand the mechanisms linking insomnia and depression. DESIGN Participants were randomized to receive 3 consecutive nights of sleep continuity disruption via forced nocturnal awakenings (FA, n = 21), or one of two control conditions: restricted sleep opportunity (RSO, n = 17) or uninterrupted sleep (US, n = 24). SETTING The study was set in an inpatient clinical research suite. PARTICIPANTS Healthy, good-sleeping men and women were included. MEASUREMENT AND RESULTS Polysomnography was used to measure sleep architecture, and mood was assessed via self-report each day. Compared to restricted sleep opportunity controls, forced awakenings subjects had significantly less slow wave sleep (P < 0.05) after the first night of sleep deprivation, and significantly lower positive mood (P < 0.05) after the second night of sleep deprivation. The differential change in slow wave sleep statistically mediated the observed group differences in positive mood (P = 0.002). CONCLUSIONS To our knowledge, this is the first human experimental study to demonstrate that, despite comparable reductions in total sleep time, partial sleep loss from sleep continuity disruption is more detrimental to positive mood than partial sleep loss from delaying bedtime, even when controlling for concomitant increases in negative mood. With these findings, we provide temporal evidence in support of a putative biologic mechanism (slow wave sleep deficit) that could help explain the strong comorbidity between insomnia and depression.

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.

Anger and aggression are among the most common issues reported by returning service members from combat deployments. However, the pathways between combat exposure and anger and aggression have not been comprehensively characterized. The present study aimed to characterize the relationship between trait anger, combat exposure, post-deployment PTSD, and aggression. U.S. Army soldiers (N = 2,420) were administered anonymous surveys assessing combat exposure, current PTSD symptoms and aggression, as well as trait anger items 3 months after returning from deployment to Afghanistan. PTSD symptom levels were related to aggression at higher levels of trait anger, but not evident among soldiers who had lower levels of trait anger. The pathway from combat exposure to PTSD, and then to aggression, was conditional upon levels of trait anger, such that the pathway was most evident at high levels of trait anger. This was the first study to our knowledge that concurrently modeled unconditional and conditional direct and indirect associations between combat exposure, PTSD, trait anger, and aggression. The findings can be helpful clinically and for developing screening protocols for combat exposed Soldiers. The results of this study suggest the importance of assessing and managing anger and aggression in soldiers returning from combat deployment. Anger is one of the most common complaints of returning soldiers and can have debilitating effects across all domains of functioning. It is imperative that future research efforts are directed toward understanding this phenomenon and developing and validating effective treatments for it.

Chronic pain may be related to cardiovascular disease (CVD) risk. The current study examined whether persistent bodily pain was related to cardiovascular disease risk factors, whether these effects were moderated by body mass index (BMI), and, if not, whether chronic pain accounted for unique variance in CVD risk factors. Participants were women (N = 2,135) in the Study of Women's Health Across the Nation. A high pain frequency variable (high pain in 0 through 4 assessments) was coded to reflect the frequency of high levels of bodily pain across the first 3 years of the study. Six CVD risk factors and BMI were measured at follow-up year 3. High pain frequency and BMI were correlated significantly with risk factors, although effects for the former were small. Hierarchical multiple regressions revealed high pain frequency × BMI interactions for 5 of 6 CVD risk factors. Dissecting the interactions revealed a similar pattern across 4 risk factors: for women with normal BMI, there was a "dose-response" in which increasing frequency of high pain revealed increasingly worse CVD risk factor levels, whereas for women with obese BMI, high pain frequency was unrelated to risk factors. For obese women, increasing frequency of high pain was associated with higher blood glucose. Although BMI is a well-established CVD risk factor, evaluation of CVD risk level may be improved by considering the incidence of persistent pain, particularly in normal weight women (BMI < 25 kg/m(2)) lower BMI.

To determine whether patients with a painful myofascial temporomandibular disorder (TMD) have diminished nocturnal heart rate variability (HRV), a marker of autonomic nervous system (ANS) dysfunction, relative to healthy, pain-free controls.Participants with myofascial TMD and healthy, pain-free volunteers underwent nocturnal polysomnography studies during which HRV indices were measured. Multiple linear regression analyses were used to determine whether TMD status exerted unique effects on HRV.Ninety-five participants (n = 37 TMD; n = 58 controls) were included in the analyses. The TMD group had a lower standard deviation of R-R intervals (89.81 ± 23.54 ms versus 107.93 ± 34.42 ms, P ⋜ .01), a lower root mean squared successive difference (RMSSD) of R-R intervals (54.78 ± 27.37 ms versus 81.88 ± 46.43 ms, P.01), and a lower high frequency spectral power (2336.89 ± 1224.64 ms² versus 2861.78 ± 1319 ms², P = .05) than the control group. The ratio of the low-frequency (LF) to the high-frequency (HF) spectral power was higher in the TMD group (2.47 ± 2 versus 1.38 ± 0.65, P.01). The differences in RMSSD (91.21 ms versus 112.03 ms, P = .05) and LF:HF ratio (0.71 versus 0.32, P.01) remained significant after controlling for age and psychological distress.Myofascial TMD patients revealed lower nocturnal HRV than healthy, pain-free controls. Further research should focus on processes that address this ANS imbalance, which may potentially lead to effective therapeutic interventions.

Suppression of anger is linked to subsequent pain intensity among chronic low back patients, but it is not clear whether anger regulation style (trait anger-out, anger-in) moderates these effects or if aroused anger accounts for links between anger regulation style and pain.Chronic low back pain patients (N=58) were assigned to Suppression or No Suppression conditions for a task with harassing confederate and then underwent structured pain behavior procedures. Spielberger Anger Expression Inventory tapped trait anger-out (AOS) and anger-in (AIS).Regressions tested Emotion Regulation condition × AOS and AIS effects on outcomes. AOS was related to grimacing and sighing for Suppression condition patients. AIS was related negatively to guarding and bracing for Suppression condition patients. Anger report partly mediated effects for AOS and AIS.Anger regulation style moderated effects of state anger suppression on subsequent pain behaviors, effects that were partly explained by aroused anger.

In this issue of Sleep Medicine, Chung et al. [1] report on associations between sleep-related parameters and pain in participants with an acute major depressive episode. The authors highlight the growing recognition of the active role that sleep plays in the trajectory of both depression and clinical pain. Chung et al. found that compared to baseline, sleep was correlated more robustly with pain at three months (i.e., following pharmacotherapy for depressive symptoms) and that baseline wake after sleep onset time and changes in total sleep time correlated with changes in pain. These data provide momentum for future studies to determine whether prophylactic sleep-specific interventions can diminish pain above and beyond traditional pharmacotherapy or behavioral interventions for depression. This said, the ability of sleep to explain pain in this study was somewhat modest. Anxiety symptoms emerged consistently as the most robust correlate of pain in both the cross-sectional and prospective analyses. On one hand, these data suggest that hybrid interventions targeting sleep in addition to mood/anxiety disturbances hold promise for ameliorating pain comorbid with depression. On the other hand, the analytical approach was data-driven (i.e., stepwise regressions). Hence, the unique proportion of variance in pain at baseline and 3 months, as well as changes in pain, accounted for by sleep disturbance above and beyond anxiety and depressive symptoms, were not ascertained. Future investigations should prioritize entry of covariates in multivariate analyses based on theory-driven hypotheses (i.e., hierarchical multivariate analysis) versus the strength of zero-order correlations. Chung et al.’s finding that actigraphic measure of sleep, i.e., wake after sleep onset time and total sleep time emerged as significant correlates of pain in major depression, is promising. This is one of first studies to examine sleep-pain interactions in depression using actigraphy. It should be emphasized, however, that the validity of actigraphy to measure sleep continuity in depression has not been adequately established (2;3). Specifically, actigraphy directly measures movement and not sleep. Motoric agitation and/or retardation are features of depression, which potentially confound actigraphy algorithms derived predominantly from healthy normal sleeper samples. Pain is experienced by the majority of clinically depressed patients (4), but few longitudinal studies have sought to treat or identify potentially modifiable risk factors of pain in depression, a major void in the literature. As Chung et al. highlight, this gap is surprising because pain occurring in the context of depression is related to poorer treatment response, increased healthcare utilization and suicidality. It is also surprising because the high co-occurrence of sleep disruption, pain, depressive symptoms and anxiety has long been recognized. Seeking to understand idiopathic pain disorders, syndromes in which clear evidence of peripheral insult is often lacking, early psychodynamically-influenced theories went so far as to conceptualize these conditions as variants of a masked depressive illness (5). This conceptualization has since been criticized as lacking empirical support (6). With the development of modern neuroimaging techniques and advances in the neuroscience of pain (7), it is becoming increasingly evident that sleep-wake systems, affect regulation, and pain processing mechanisms share a common neurobiological substrate providing the groundwork for interactions between sleep, pain, and affect (8;9). As one example, well defined opioidergic descending pain inhibition circuits in the medullary brainstem are under serotoneric and noradrenergic control (10;11). These pain inhibitory mechanisms are often impaired in chronic pain disorders (12–14), though, to our knowledge, they have yet to be studied in the context of major depression. We have experimentally demonstrated that sleep disruption in healthy females reduces the efficacy of these endogenous analgesic systems (15). In addition to the well established role of serotonergic and noradrenergic reuptake inhibitors (SNRIs) in treating depression(16) and anxiety (17), studies which demonstrate the efficacy SNRIs as analgesics for chronic pain syndromes are rapidly accumulating (18;19). It is interesting that in the Chung et al. study, SNRIs and tricyclic antidepressants were not associated with differences in pain symptoms over time. Recent work, however, has demonstrated the efficacy of duloxetine to ameliorate pain in depressed older adults (20). Unraveling the shared and unique neurobiological underpinnings of sleep, pain and affect is likely to yield novel and critical insights into the functions of sleep and the pathophysiology of chronic pain, anxiety and depressive disorders. If prior research and Chung et al.’s work is any indication, this pursuit might prove akin to solving the riddle of the sphinx, as the nexus of sleep, pain, and affect poses many seeming contradictions once the surface is broken. In healthy subjects, for example, sleep deprivation induces hyperalgesia (21), depressed mood (22), and spontaneous pain (23). Similarly, negative mood induction augments sensitivity to laboratory pain tests (7). Reduced REM latency is a heritable risk factor for depression (24), and this polysomnographic marker has been linked to enhanced pain sensitivity in healthy controls (25). Clinical depression, however, is often associated with hypoalgesia (7), and a substantial number of depressed patients respond to sleep deprivation with dramatic improvements in mood coupled with hyperalgesia (26)—changes that reverse after recovery sleep (27). The mythical sphinx guarding the entrance to Thebes asked, “Which creature in the morning goes on four legs, at mid-day on two, and in the evening upon three, and the more legs it has, the weaker it be?” Of all people, Oedipus, fresh from killing his father, solved the riddle by answering it, “Man—who crawls on all fours as a baby, then walks on two feet as an adult, and then walks with a cane in old age” (27). Perhaps the seeming contradictions in the pain, sleep, depression triangle will be similarly resolved by considering the development of these interactions over time in both clinical and healthy samples. Chung et al’s. data suggest that these relationships may change or strengthen over time., i.e., the inverse relationship between sleep quality and pain, for example, strengthened considerably at three months, relative to baseline, possibly an unmasking due the waning of depressive symptoms with treatment. Similar “unmasking effects” have been observed in depressed participants undergoing quantitative sensory testing using a pharmacologic challenge (28). Ultimately, there is much to be gained in conducting more systematic and intensive research that incorporates polysomnography and quantitative sensory testing to map the developmental trajectory of these symptoms over longer periods of time while simultaneously assessing changes in candidate neurobiological mechanisms. Until then, interpretations of sleep, pain and affect interactions place us all at risk of being devoured by the sphinx.

Considerable evidence has linked catastrophizing to pain responses, and recent experimental pain research has suggested that situational catastrophizing, measured during or immediately after laboratory pain procedures, is strongly related to pain ratings of standardized noxious stimuli. However, given that most experimental pain protocols involve “static” assessments of pain ratings and catastrophizing at a single time point, the direction by which these factors may affect each other remains unclear. Does catastrophizing influences one's subsequent pain responses or do individual differences in the perceived severity of pain lead to differential rates of catastrophizing? Little is known regarding the course of these variables. Using a cross-lagged panel analysis, we evaluated whether changes in situation-specific catastrophizing preceded changes in laboratory-induced pain responses, or vice versa, during tonic capsaicin pain stimulation. Topical application of a 10% capsaicin cream was applied to the dorsal aspect of the nondominant hand of 38 healthy participants. Situation-specific catastrophizing and pain ratings were obtained at Early (0 to 15 minutes), Mid (15 to 30 minutes), and Final (30 to 35 minutes) periods during capsaicin pain. Analyses revealed that Early-to-Mid changes in catastrophizing ratings prospectively accounted for unique variance in subsequent Mid-to-Final changes in pain ratings, whereas Early-to-Mid changes in pain ratings did not account for unique variance in Mid-to-Final changes in catastrophizing ratings. That is, participants who showed the largest initial increases in catastrophizing reported the greatest subsequent increases in pain. Controlling for the reported change in stress did not affect this pattern of results. These findings provide empirical evidence that a situation-specific catastrophizing process might precede and contribute to subsequent increases in pain experience. Limitations of the present study and possible future research directions are discussed. Perspective The present study adds to a growing literature on prospective associations between catastrophizing and pain. These results provide initial evidence, in healthy individuals, that changes in catastrophizing may precede changes in pain response.

An increasing number of prospective studies suggest a bi-directional association between the pain and sleep quality. Few of these investigations have controlled for synchronous correlations, an important source of extraneous variance in lagged associations, which may have confounded conclusions of prior investigations. Despite high rates of insomnia in temporomandibular joint disorders (TMD), no studies have examined temporal associations between naturalistic fluctuations in insomnia and pain in TMD. We conducted cross-lagged panel analysis to examine reciprocal temporal associations between 1-month changes in insomnia symptom severity and self-reported pain over 3 months among 53 TMD patients. This rigorous analytic strategy represents a comprehensive method to explore possible reciprocal temporal associations between insomnia and pain that controls for both auto- and synchronous correlations. Analyses revealed that initial-month increases in insomnia were associated with next-month increases in average daily pain, but not vice versa. The direction of the effect was such that initial-month increases in insomnia symptom severity were associated with next-month increases in average daily pain. These data suggest that naturally occurring fluctuations in insomnia symptom severity are prospectively associated with fluctuations in daily pain experience for persons with TMD. Potential mechanisms by which insomnia might influence pain in TMD and therapeutic implications of these findings are discussed.

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.

Objective: Previous work suggests that elevated trait anger-out exacerbates pain responses in part through endogenous opioid dysfunction. The authors examined whether this opioid dysfunction affects not only perceived pain intensity, but also emotional responses to being hurt. Design: 79 chronic low back pain (LBP) patients and 46 healthy controls received opioid blockade (8 mg naloxone i.v.) and placebo in randomized, counterbalanced order in separate sessions. During each session, participants sequentially experienced finger pressure pain and ischemic forearm pain tasks, with emotional state assessed at baseline and postpain. Main Outcome Measures: Blockade effects indexing opioid modulation of emotional reactivity were derived by subtracting placebo from blockade condition emotional reactivity. Results: Significant Participant Type X Anger-Out interactions on blockade effects indicated that in LBP participants but not in controls, greater anger-out was associated with deficient opioid modulation of anxiety, anger, and fear reactivity to noxious stimulation. Across participant types, greater anger-in was associated with impaired opioid modulation of anxiety and fear reactivity. Anger-in opioid effects were partially due to overlap with general negative affect. Conclusions: Opioid dysfunction associated with trait anger-out may affect not only perceived pain intensity, but also pain-related suffering in individuals with chronic pain conditions. Implications for understanding the health effects of anger management styles are discussed.

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.

In the present study, we examined whether experimentally-manipulated attentional strategies moderated relations between pain catastrophizing and symptom-specific physiological responses to a cold-pressor task among sixty-eight chronic low back patients. Patients completed measures of pain catastrophizing and depression, and were randomly assigned to sensory focus, distraction or suppression conditions during a cold pressor. Lumbar paraspinal and trapezius EMG, and cardiovascular responses to the cold pressor were assessed. Attentional strategies moderated the relation between pain catastrophizing and lumbar paraspinal muscle, but not trapezius muscle or cardiovascular responses. Only for participants in the suppression condition was catastrophizing related significantly to lumbar paraspinal muscle responses. Depressed affect did not account for this relation. These findings indicate that 'symptom-specific' responses among pain catastrophizers with chronic low back depend on how they attend to pain-related information. Specifically, it appears that efforts to suppress awareness of pain exaggerate muscular responses near the site of injury.

In support of cognitive processing models, emotional expression appears to reduce associations between intrusions and psychological distress. Past research has focused primarily on the role of the expression of negative emotion, or emotion in general, in cognitive processing and adjustment. In the present study, we examined the role of both positive and negative emotional expressivity on relations between intrusions and both distress and avoidance among 93 individuals diagnosed with and treated for cancer. We hypothesized stronger negative associations between intrusive thoughts and both distress and avoidance for those individuals lower in positive or negative expressivity. Results generally supported hypotheses with regard to relations of intrusions and distress in association with positive expressivity. Negative expressivity, however, moderated relations between intrusions and distress, but not intrusions and avoidance. These findings underscore the importance of examining the impact of individual differences in negative, as well as positive, emotional expression on cognitive processing and psychological adjustment.