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In healthy individuals, emotions modulate pain and spinal nociception according to a valence linear trend (ie, pain/nociception is highest during negative emotions and lowest during positive emotions). However, emerging evidence suggests that emotional modulation of pain (but not spinal nociception) is disrupted in fibromyalgia and disorders associated with chronic pain risk (eg, major depression, insomnia). The present study attempted to extend this work and to examine whether women with premenstrual dysphoric disorder (PMDD), a cyclical syndrome associated with debilitating affective symptoms during the late-luteal (premenstrual) phase of the menstrual cycle, is also associated with disrupted emotional modulation of pain. To do so, an affective picture-viewing procedure was used to study emotional modulation of pain and spinal nociception in 14 women with PMDD and 14 control women during mid-follicular, ovulatory, and late-luteal phases of the menstrual cycle (verified by salivary hormone levels and luteinizing hormone tests). At each phase, mutilation, neutral, and erotic pictures were presented to manipulate emotion. During picture viewing, suprathreshold electrocutaneous stimuli were presented to evoke pain and the nociceptive flexion reflex (NFR; a physiological measure of spinal nociception). Statistically powerful linear mixed model analyses confirmed that pictures evoked the intended emotional states in both groups across all menstrual phases. Furthermore, emotion modulated pain and NFR according to a valence linear trend in both groups and across all menstrual phases. Thus, PMDD-related affective disturbance is not associated with a failure to emotionally modulate pain, suggesting that PMDD does not share this pain phenotype with major depression, insomnia, and fibromyalgia.

Trauma exposure, especially sexual assault (SA), is highly correlated with pain conditions, in that many chronic pain samples report trauma histories. However, our understanding of the mechanisms behind this relationship is limited. Previous findings from our lab suggest that SA disrupts descending pain modulation. However, to date, no study has used quantitative sensory testing (QST) to comprehensively assess the pain system in SA survivors. 41 healthy, pain-free SA survivors were matched to a group of 41 healthy, pain-free trauma exposed persons without SA (TE). These groups were compared to a group of healthy, pain-free persons with no trauma history (no-TE; N=62). QST included warm, cool, heat, cold, ischemia, and electric thresholds, and heat, cold, ischemia, and electric tolerances. The nociceptive flexion reflex (NFR) threshold was used to assess spinal nociception. Results suggested SA survivors had higher cool thresholds than the TE and no-TE groups. Moreover, SA survivors had lower cold thresholds, cold tolerances, and heat tolerances than no-TE. Surprisingly, SA survivors had higher ischemia tolerances than no-TE and TE groups. The TE group had lower heat and cold tolerances than the no-TE group. None of the other group differences were significant for any pain outcome. These findings suggest that SA is associated with greater sensitivity in A-delta fibers (cool thresholds) and hyperalgesia in response to thermal stimuli (heat, cold). However, hypoalgesia was noted in response to deep tissue pain (ischemia). By contrast, TE is primarily associated with reduced tolerance to heat and cold. These group differences are not likely due to spinal sensitization due to the lack of group differences in NFR. Future studies are needed to replicate these findings and determine whether QST responses can predict negative sequela of SA and non-SA trauma exposure.

Previous research has explored cultural differences concerning the prevalence, response, and treatment preferences of individuals experiencing pain. However, the meaning of these painful experiences has not been comprehensively examined. Research tends to generalize findings from predominantly European American samples and assume universality of their findings across cultures. Numerous studies have demonstrated a significantly higher prevalence of physical pain in Native Americans (NA) compared to non-Hispanic Whites (NHW). Because of this, it is important to consider whether our current understanding of painful experiences is indeed universal. To accomplish this, a semi-structured interview was administered to 156 NAs and 151 NHWs that asked open-ended questions related to: words used to describe physically injurious experiences, the purpose of pain, individual and culture-specific pain meaning, and words for the opposite of pain. Next, themes were generated from transcripts and two raters blind to participants’ racial/ethnic group coded transcripts for the themes. Strong agreement between raters was obtained (Kappa= .75-1.00). Chi-square analyses assessed whether the frequency of responses for themes were different between NHWs and NAs. In general, frequency of themes were similar between groups; nonetheless, a few small group differences were noted. NHWs used the word pain more often to describe physically hurtful experiences (45.3% vs. 42.1%; χ 2 [1, N=309]=4.675, p 2 [1, N=309]=7.320, p 2 [1, N=309]=13.310, p

Chronic pain results in tremendous economic and psychological burden. Thus, an ability to identify individuals at risk for chronic pain onset could be an important first step in reducing this burden. One mechanism that may contribute to pain onset is impaired descending pain inhibition. The present study examined whether the efficiency of descending inhibition (as measured by conditioned pain modulation, CPM) predicted future chronic pain onset in a sample of participants who were healthy and pain-free at the time of enrollment in OK-SNAP. Chronic pain onset was determined prospectively from follow-up surveys administered every 6-months following enrollment. Of the 139 Native American (NA) and 147 non-Hispanic white (NHW) participants enrolled, 208 (73%) responded to ≥1 follow-up. Participants were said to have developed chronic pain if they experienced persistent pain for >3 months and the pain did not remit at subsequent follow-ups (N=34, 16%). 174 persons did not develop chronic pain. CPM was assessed from painful electric stimulations delivered before and during hand/forearm submersion in 10˚C water. Pain ratings and nociceptive flexion reflexes (NFR; correlate of spinal nociception) were assessed in response to electric stimuli. CPM efficiency = change in pain/NFR. CPM of pain and NFR were entered as predictors in a logistic regression that controlled for race (NA vs. NHW), age, BMI, sex, general health, depression, anxiety, and somatization. Interactions between race and CPM efficiency were examined as well. Results found less efficient CPM of NFR (OR=6.53, 95%CI: 1.04, 40.95) and more depressive symptoms (OR=10.22, 95%CI: 1.28, 81.36) at enrollment predicted chronic pain onset. The model explained 34.5% of the variance (Nagelkerke R2=.345). Interactions of CPM variables with race were not significant. These findings imply that impaired descending inhibition of spinal nociception (NFR) may play a role in the development of chronic pain.

Sex hormones may contribute to inter- and intra-individual differences in pain by influencing emotional modulation of pain and nociception. To study this, a well-validated picture-viewing paradigm was used to assess emotional modulation of pain and the nociceptive flexion reflex (NFR; physiologic measure of nociception) during mid-follicular, ovulatory, and late-luteal phases of the menstrual cycle in healthy normally cycling women (n=40). Salivary estradiol, progesterone, and testosterone were assessed at each testing session. Emotional modulation of pain/NFR did not differ across menstrual phases, but low estradiol was associated with weaker emotional modulation of NFR (during all phases) and emotional modulation of pain (ovulatory and late-luteal phases). Given evidence that a failure to emotionally modulate pain might be a risk factor for chronic pain, low estradiol may promote chronic pain via this mechanism. However, future research is needed to extend these findings to women with disturbances of pain, emotion, and/or sex hormones.

Pain problems are more prevalent in Native Americans than in any other group in the U.S., and this might result from group differences in pain modulation. This study was designed to examine emotional modulation of pain and spinal nociception in healthy, pain-free Native Americans (n = 21) relative to non-Hispanic Whites (n = 20). To assess emotional modulation of pain and the nociceptive flexion reflex (NFR, a physiological measure of spinal nociception), participants underwent a well-validated emotional picture-viewing paradigm during which suprathreshold pain stimuli were delivered to the ankle. Compared to Whites, Native Americans reported less pleasure to erotic pictures and failed to show corrugator reactivity to mutilation pictures. Unlike Whites, Native Americans only evidenced pain inhibition in response to erotica, but no pain facilitation (disinhibition) to mutilation pictures. Emotional modulation of NFR was similar in both groups. These preliminary findings suggest that Native Americans failed to disinhibit pain, perhaps due to over-activation of pain inhibitory mechanisms. Chronic over-activation of this system could ultimately exhaust it, thus putting Native Americans at future risk for chronic pain.

Objective The aim of this study was to conduct a preliminary dismantling study of exposure, relaxation, and rescripting therapy (ERRT) for nightmares. Method Participants (N = 70) were randomized to 1 of 2 conditions: ERRT with nightmare exposure and rescripting (full protocol; EX) or ERRT without nightmare exposure and rescripting (NEX). Participants completed follow-ups at 1 week, 3 months, and 6 months posttreatment. Results Both conditions yielded statistically significant improvements with medium to large effect sizes on primary outcomes related to nightmares (i.e., nights with nightmares, nightmares per week, and nightmare severity). Both conditions also yielded statistically significant improvements on secondary outcomes with medium to large effect sizes on fear of sleep, sleep quality, insomnia severity, daytime sleepiness, posttraumatic stress disorder symptom severity, and depression severity. The conditions did not differ at any time point. Conclusions Findings indicate that ERRT with and without nightmare exposure and rescripting can significantly alleviate nightmares and related distress. The addition of nightmare exposure and rescription did not contribute incrementally to outcomes in this sample. It is possible that the dose of exposure was not sufficient to result in group differences or that the treatment components included in both conditions (i.e., psychoeducation about trauma, nightmares, and sleep; sleep habit modification; and relaxation training) may adequately treat factors that maintain nightmares for some individuals. Theoretical implications of findings are discussed. The reduction of symptoms of other conditions following this brief intervention provides further evidence for the primary role of nightmares and sleep disturbances posttrauma. (PsycINFO Database Record

Nightmares and sleep disturbances are gaining attention as targets of treatment interventions for trauma-exposed populations. Measures in trials evaluating these interventions tend to utilize proprietary measures of nightmare characteristics, which makes it challenging to compare findings across studies. The Trauma-Related Nightmare Survey is a questionnaire that was initially developed for utilization in efficacy studies of Exposure, Relaxation, and Rescripting Therapy. Preliminary examinations of the psychometric properties have demonstrated good test-retest reliability and convergent validity. The present brief report provides an updated examination of these properties and offers the first open publication of the measure for general use. Results support previous findings that the Trauma-Related Nightmare Survey demonstrates good test-retest reliability (r = .73) and moderate to strong convergent validity (rs = .44-.78) with other commonly utilized measures of sleep and mood symptoms.

Ellen L Terry, Yvette M Güereca, Satin L Martin, Jamie L RhudyDepartment of Psychology, The University of Tulsa, Tulsa, OK, USA Objectives: Prior research has shown a relationship between blood glucose levels and some forms of self-regulation (eg, executive function), with low blood glucose levels associated with impaired self-regulation. Further, engagement in self-regulation tasks depletes blood glucose. Given these relationships, the present study examined whether blood glucose is associated with another form of self-regulation, ie, descending pain modulatory processes. Methods: Forty-seven (32 female) pain-free participants were recruited and completed testing. Blood glucose was measured from finger sticks and a digital meter before and after experimental pain tests. Pain tests included the nociceptive flexion reflex (NFR) threshold to assess descending modulation of spinal nociception, but also electric pain threshold to assess perceptual pain detection. The Stroop color word naming test was also assessed before and after pain testing to examine changes in executive function. Results: Results indicated that mean blood glucose levels decreased after pain testing, but Stroop performance did not significantly change. Importantly, changes in blood glucose were correlated with NFR threshold, such that decreases in blood glucose were associated with lower NFR thresholds (reduced descending inhibition). Changes in blood glucose were unrelated to pain threshold or executive function. Conclusion: This study suggests that glucose depletion may impair performance of descending inhibitory processes, without impacting the perceptual detection of pain (pain threshold). Although findings need to be replicated, maintaining adequate glucose levels may be necessary to support inhibition of spinal nociception. Keywords: pain, nociception, glucose, descending modulation, executive function&nbsp

Shreela Palit,1 Emily J Bartley,2 Bethany L Kuhn,1 Kara L Kerr,1 Jennifer L DelVentura,1 Ellen L Terry,1 Jamie L Rhudy1 1Department of Psychology, University of Tulsa, Tulsa, OK, USA; 2Department of Community Dentistry and Behavioral Science, Pain Research and Intervention Center of Excellence, University of Florida, Gainesville, FL, USA Purpose: Premenstrual dysphoric disorder (PMDD) is characterized by severe affective and physical symptoms, such as increased pain, during the late-luteal phase of the menstrual cycle. The mechanisms underlying hyperalgesia in women with PMDD have yet to be identified, and supraspinal pain modulation has yet to be examined in this population. The present study assessed endogenous pain inhibitory processing by examining conditioned pain modulation (CPM, a painful conditioning stimulus inhibiting pain evoked by a test stimulus at a distal body site) of pain and the nociceptive flexion reflex (NFR, a spinally-mediated withdrawal reflex) during the mid-follicular, ovulatory, and late-luteal phases of the menstrual cycle. Methods: Participants were regularly-cycling women (14 without PMDD; 14 with PMDD). CPM was assessed by delivering electrocutaneous test stimuli to the sural nerve before, during, and after a painful conditioning ischemia task. Participants rated their pain to electrocutaneous stimuli, and NFR magnitudes were measured. A linear mixed model analysis was used to assess the influence of group and menstrual phase on CPM. Results: Compared with controls, women with PMDD experienced greater pain during the late-luteal phase and enhanced spinal nociception during the ovulation phase, both of which were independent of CPM. Both groups showed CPM inhibition of pain that did not differ by menstrual phase. Only women with PMDD evidenced CPM inhibition of NFR. Conclusion: Endogenous modulation of pain and spinal nociception is not disrupted in women with PMDD. Additionally, greater NFR magnitudes during ovulation in PMDD may be due to tonically-engaged descending mechanisms that facilitate spinal nociception, leading to enhanced pain during the premenstrual phase. Keywords: premenstrual dysphoric disorder, menstrual cycle, pain, conditioned pain modulation, nociception

Pain is a tremendously malleable experience, and emotions are one of many psychological factors that modulate it. This chapter examines the emotion–pain relationship and provides a motivational framework for understanding it. It is suggested that a valence-by-arousal interaction characterizes the influence of emotions on pain in healthy humans. Specifically, positively valenced emotions generally inhibit pain, with greater inhibition resulting from greater positive arousal. By contrast, negatively valenced emotions with low-to-moderate arousal facilitate pain, with greater facilitation resulting from greater negative arousal. However, negatively valenced emotions with high arousal inhibit pain. Emerging evidence suggests that a failure to emotionally modulate pain could be a risk factor for the development of chronic pain; however, additional research is needed to confirm these preliminary data.

Respiratory sinus arrhythmia (RSA) is the modulation of heart rate along with respiration. Individual differences in RSA reflect parasympathetic cardiac control. Low RSA is linked to emotional dysregulation, perhaps from an inability to modulate the parasympathetic nervous system to emotion. For the current study, pictures of varying emotional contents were presented to participants with low and high RSA. During some pictures, acoustic probes were delivered to elicit startle. Emotional responding was assessed from subjective and physiological reactions to pictures. Results suggested that low RSA participants exhibited attenuated cardiac orienting compared to high RSA participants. Startle, corrugator electromyogram, and subjective responses to pictures were similar across groups. Thus, differences in RSA account for differences in orienting to emotional pictures but not physiological–emotional responding.

Slow breathing is used as a means to reduce pain, yet the mechanisms responsible for respiration-induced hypoalgesia are poorly understood. The present study asked 30 healthy partici- pants (Mage = 21 years, Meducation = 15 years, 80% white non-Hispanic) to breathe at normal, slow (50% normal), and fast (125% normal) rates while constant-intensity, suprathreshold electric stimu- lations were delivered to the sural nerve to elicit pain and the nociceptive flexion reflex (NFR, a mea- sure of spinal nociception). Stimulations were equally balanced across inhalations and exhalations to determine whether parasympathetic activation during exhalations contributes to hypoalgesia. Respi- ration rate, heart rate variability (HRV, a measure of parasympathetic activity), heart rate, and subjec- tive arousal were assessed as manipulation checks. Slow breathing reduced pain relative to normal breathing and fast breathing, but NFR was not influenced by breathing. Further, pain and NFR did not differ between exhalations and inhalations, and changes in HRV did not correlate with changes in pain or NFR. Together, these findings suggest that respiration-induced hypoalgesia does not re- quire gating of spinal nociception or changes in parasympathetic activity. Perspective: Slow breathing reduced pain relative to normal and fast breathing. This respiration- induced hypoalgesia does not appear to be due to gating of spinal nociception or changes in para- sympathetic activity.

The menstrual cycle influences pain, with symptoms often increasing during the premenstrual (late-luteal) phase. Deficiencies in endogenous inhibition of afferent nociception at the spinal level might contribute to menstrual phase-related changes in pain. This study assessed whether conditioned pain modulation (CPM) of spinal nociception differs between mid-follicular and late-luteal phases. CPM was evoked by a blood pressure cuff affixed to the right forearm and inflated to induce ischemia in 41 healthy women during both menstrual phases. Suprathreshold electric stimuli were delivered to the left sural nerve to evoke pain and the nociceptive flexion reflex (NFR) before, during, and after forearm ischemia. Forearm ischemia produced CPM of electrocutaneous pain and NFR, but inhibition did not differ across mid-follicular and late-luteal phases. Mechanisms contributing to changes in experimental pain across mid-follicular and late-luteal phases in healthy women are not due to deficits in CPM of spinal nociception.

Motivational priming theory (MPT) and preparedness theory generate competing hypotheses about the impact of an aversive US on responses to an affective foreground. MPT predicts the aversive US will facilitate negative emotional reactions to unpleasant pictures and inhibit positive emotional reactions to pleasant pictures. Preparedness theory predicts an aversive US will increase negative emotional reactions to unpleasant pictures, but will not impact responses to pleasant pictures. The present study (N = 125) compared these competing hypotheses by assessing how noxious shocks and non-noxious noises influence responses to emotional pictures. Following each picture, participants rated how the picture made them feel using the Self Assessment Manikin. Results supported MPT - noxious USs, but not non-noxious USs, facilitated negative emotional reactions to unpleasant pictures and inhibited positive emotional reactions to pleasant pictures.

Study Objectives: Evidence supports the use of cognitive behavioral therapies for nightmares in trauma-exposed individuals. This randomized clinical trial replicated a study of exposure, relaxation, and rescripting therapy (ERRT) and extended prior research by including broad measures of mental health diffi culties, self-reported physical health problems, and quality of life. Additionally, physiological correlates of treatment-related change assessed from a script-driven imagery paradigm were examined. Methods: Forty-seven individuals were randomized to treatment or waitlist control. Results: The treatment group demonstrated improvements relative to the control group at the one-week post-treatment assessment. At the 6-month follow-up assessment, signifi cant improvements were found for frequency and severity of nightmares, posttraumatic stress disorder symptoms, depression, sleep quality and quantity, physical health symptoms, anger, dissociation, and tension reduction behaviors. Participants also reported improved quality of life. Treatment-related decreases in heart rate to nightmare imagery were correlated with improvements in sleep quality and quantity; treatment-related decreases in skin conductance to nightmare imagery were correlated with improvements in nightmare severity, posttraumatic stress disorder symptom severity, sleep quality, and fear of sleep; and treatment-related decreases in corrugator activity to nightmare imagery were correlated with improved physical health. Conclusions: Findings provide additional support for the use of ERRT in treating nightmares and related diffi culties and im

The August 2010 issue of Journal of Clinical Sleep Medicine (Vol. 6, No. 4) included an article suggesting treatment recommendations for adult nightmare disorder. Although we appreciate the work by the authors, we were left with three basic concerns about the methodology utilized and results found. First, works providing evidence for some of the treatments were not reported in the original article. Second, search methodology in the original article was not used consistently at updated time points. Third, the original article only utilized results obtained from PubMed and did not consider other databases. The current study sought to replicate the methodology and compare findings as well as expand by equalizing search methodology across updated time points. The present study expands the original efforts further by conducting article searches again on PsycINFO. Consequent changes to evidence levels and recommendations are discussed.

The nociceptive flexion reflex (NFR) is a physiological tool to study spinal nociception. However, NFR assessment can take several minutes and expose participants to repeated suprathreshold stimulations. The 4 studies reported here assessed the reliability and validity of a brief method to assess NFR threshold that uses a single ascending series of stimulations (Peak 1 NFR), by comparing it to a well-validated method that uses 3 ascending/descending staircases of stimulations (Staircase NFR). Correlations between the NFR definitions were high, were on par with test-retest correlations of Staircase NFR, and were not affected by participant sex or chronic pain status. Results also indicated the test-retest reliabilities for the 2 definitions were similar. Using larger stimulus increments (4 mAs) to assess Peak 1 NFR tended to result in higher NFR threshold estimates than using the Staircase NFR definition, whereas smaller stimulus increments (2 mAs) tended to result in lower NFR threshold estimates than the Staircase NFR definition. Neither NFR definition was correlated with anxiety, pain catastrophizing, or anxiety sensitivity. In sum, a single ascending series of electrical stimulations results in a reliable and valid estimate of NFR threshold. However, caution may be warranted when comparing NFR thresholds across studies that differ in the ascending stimulus increments. Perspective This brief method to assess NFR threshold is reliable and valid; therefore, it should be useful to clinical pain researchers interested in quickly assessing inter- and intra-individual differences in spinal nociceptive processes.

Pain catastrophizing is associated with enhanced temporal summation of pain (TS-Pain). However, because prior studies have found that pain catastrophizing is not associated with a measure of spinal nociception (nociceptive flexion reflex [NFR] threshold), this association may not result from changes in spinal nociceptive processes. The goal of the present study in healthy participants was to examine the relationship between trait (traditional) and state (situation-specific) pain catastrophizing and temporal summation of NFR (TS-NFR) and TS-Pain. A secondary goal was to replicate prior findings concerning relationships between catastrophizing and NFR threshold, electrocutaneous pain threshold, and sensory and affective ratings of electrocutaneous stimuli. All analyses controlled for depression symptoms, pain-related anxiety, and participant sex. As expected, multiple regression analyses indicated that neither trait nor situation-specific catastrophizing was associated with NFR threshold, but that situation-specific catastrophizing was associated with pain ratings. Multilevel linear growth models of TS data indicated that situation-specific catastrophizing was associated with TS-Pain but not TS-NFR. Trait catastrophizing was not related to TS-Pain or TS-NFR. Together, these results confirm prior studies that indicate that catastrophizing enhances pain via supraspinal processes rather than spinal processes. Moreover, because catastrophizing was associated with TS-Pain but not TS-NFR, caution is warranted when using pain ratings to infer temporal summation of spinal nociceptive processes.

Nightmares and sleep disturbances are thought to play a key role in the development of posttrauma problems. Research efforts have increased in an attempt to understand this association. The present study examined differences in nightmare characteristics, related psychopathology, treatment outcome, and trauma history among trauma-exposed individuals whose nightmares began before a traumatic event and those whose nightmares began after a traumatic event, while controlling for posttraumatic stress disorder status. Individuals whose nightmares began following a trauma experienced more depression and posttraumatic stress symptoms and poorer sleep quality, reported a higher number of traumatic events, and were more likely to report nightmares replicative of or similar to the trauma than those whose nightmares began before the trauma. No other between-groups differences were found for nightmare characteristics or response to treatment. This study is an important step in understanding the nature of nightmares and their relationship to traumatic events and consequences, but additional research is warranted.

Research indicates pain may be influenced by the menstrual cycle. While the mechanisms underlying these effects are unclear, it is possible that menstrual phase-related changes in endogenous pain modulation contribute. The present study used well-validated methods to study affective modulation of pain and the nociceptive flexion reflex (NFR) in healthy women during two menstrual phases (mid-follicular vs. late-luteal). Women (N = 41) tracked their menstrual phases for three complete cycles and were asked to attend two laboratory testing sessions in the second and third cycles to assess affective modulation of pain and nociception (testing order counterbalanced). Menstrual phase was assessed from daily diaries, luteinizing hormone tests, and basal body temperature. At each session, emotionally charged pictures were presented and suprathreshold electrocutaneous stimulations were delivered during and in between pictures. Subjective and physiological emotional reactions were recorded in response to each picture and pain ratings and NFRs were recorded in response to each suprathreshold stimulus. Results suggested pictures effectively manipulated emotion in both menstrual phases. Moreover, arousing unpleasant pictures enhanced pain and NFR, whereas arousing pleasant pictures inhibited pain and NFR. These modulatory effects were similar in both menstrual phases. Together, these findings suggest that affective engagement of corticospinal mechanisms does not differ across these phases of the menstrual cycle. However, future research is needed to directly assess the relationship between affective modulation of pain/nociception and inter- and intra-individual differences in ovarian hormones and to extend these findings to women who suffer from menstrual cycle-related pain (e.g., premenstrual dysphoric disorder, fibromyalgia).

Fibromyalgia syndrome (FMS) is a chronic pain disorder associated with widespread musculoskeletal pain, tenderness, and fatigue. Additionally, correlational research suggests negative affect (eg, depression, anxiety) and deficits in positive affect may contribute to FMS symptomatology. However, well-controlled, experimental research is necessary to ascertain whether patients with FMS have problems in affective processing. The present study used a well-validated picture-viewing paradigm to evoke emotional responses in 17 patients with FMS and 17 sex- and age-matched healthy control participants. Each participant viewed pleasant (erotica), neutral, and unpleasant (attack related) pictures, and abrupt white noises were delivered during two-thirds of the pictures to evoke startle eyeblinks. Appetitive and defensive responding was assessed from subjective (valence/pleasure and arousal ratings) and physiological (corrugator EMG, heart rate, skin-conductance response, startle-reflex modulation) reactions to pictures. Results suggested FMS was associated with greater defensive activation (displeasure, subjective arousal, corrugator EMG) to the unpleasant, threat-related pictures, but not deficits in appetitive activation to erotic pictures. Although preliminary, these data suggest individuals with FMS have deficits in affective processing, but this dysregulation may be limited to defensive activation. Implications for treatment and future research are discussed. Perspective Fibromyalgia is a debilitating disease associated with affective distress. Results from the present study suggest that FMS is associated with enhanced defensive activation to nonpainful threat-related stimuli, but not deficits in appetitive reactions to erotic stimuli. These findings have implications for the treatment and study of FMS.

Physiological reactions to noxious stimuli are often used to make inferences about pain, but few studies have thoroughly examined the intra- and interindividual relationships between them. In the present study (N=104), multilevel analyses was used to assess relations between physiological (nociceptive flexion reflex magnitude [NFR], blink reflex magnitude, skin conductance response [SCR], heart rate [HR]) and subjective reactions to electrocutaneous stimuli. All physiological reactions were significant predictors of ratings when entered alone, explaining 1% (SCR) to 29% (NFR) of the variance; but only NFR, blink, and HR were significant in a multivariate predictor model. Significant interindividual variability in slopes was found for blink and HR, but not NFR. A final trimmed model that included NFR, blink, and the blink random slope explained 35% of the variance in ratings.

The nociceptive flexion reflex (NFR) is a polysynaptic withdrawal reflex typically assessed from biceps femoris electromyogram (EMG) following noxious stimulation of the ipsilateral sural nerve. Electrophysiological evidence suggests the reflex is elicited following the activation of small diameter A-delta afferents. As a result, the NFR is assumed to be a categorically distinct construct that emerges from EMG activity only following nociceptor activation. Despite the widespread use of the NFR in pain research, there has been little attempt to verify the latent structure of the NFR. The present study used "coherent cut kinetics" taxometric analyses to examine whether the latent structure of biceps femoris EMG reflects the taxonic structure that would be predicted from electrophysiological evidence. To achieve this end, preliminary analyses first compared different methods of scoring NFR magnitude. Results suggested the presence of a taxon in the covariance of biceps femoris EMG and stimulus intensity that is likely to be the NFR. Furthermore, preliminary analyses suggested the best method of scoring NFR magnitude was using Cohen's d. Implications of these results are discussed.

Prior research suggests emotional picture-viewing modulates motoric (nociceptive flexion reflex), autonomic (skin conductance response, heart rate acceleration), and subjective (pain rating) reactions to noxious electrodermal stimulation. The present study sought to determine whether emotional valence and arousal contribute to nociception modulation. To do so, pictures varying in emotional content (erotica, food, neutral, loss, attack) were chosen to manipulate emotional valence (pleasant = erotic and food; unpleasant = loss and attack) and arousal (low = food and loss; moderate = erotica and attack). Pictures were presented in pseudorandom order to elicit emotional processing while noxious electric stimulations were delivered to the sural nerve. Nociceptive flexion reflex (NFR) magnitude, skin conductance response (SCR), heart rate (HR) acceleration, and subjective pain ratings to each stimulation were measured, standardized, averaged by picture content, and analyzed. Results suggested that picture-viewing explained 52% of the variance in the multivariate combination of the nociceptive reactions and modulated them in parallel. Pleasant pictures inhibited reactions, whereas unpleasant pictures enhanced them. However, only erotica and attack pictures elicited significant modulation relative to neutral pictures, suggesting arousal also contributed. An exploratory multilevel analysis also supported this conclusion. Together, these data suggest emotional control of nociceptive reactions (ECON) is associated with a valence-byarousal interaction. Implications of these findings for how emotional picture-viewing can be used to study supraspinal modulation are discussed. � 2007 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Emotionally charged facial expressions (happy, fear) served as conditioned stimuli in a differential fear conditioning procedure. Expressions were presented in pseudo-random order on a computer monitor. For half of the participants, the fear expression was paired with an aversive electric stimulation (UCS), whereas the happy expression was unpaired. The other participants had the opposite pairing. To assess the influence of conditioned fear on pain, expressions were shown again in the absence of the UCS and pain threshold was assessed during each expression. The latency of finger withdrawal from a radiant heat device was used to index pain threshold. Skin conductance response (SCR) and self-reported emotion were measured to assess fear conditioning. Consistent with preparedness theory, differential fear conditioning was only present when the fear expression was paired with the UCS. Moreover, pain threshold was only influenced by fear conditioning in persons for whom the fear expression was paired with the UCS. Specifically, finger withdrawal latencies were lower (suggesting hyperalgesia) during the fear expression than during the happy expression; an effect that was not present before CSUCS pairing. This work suggests that some stimuli are more readily associated with an aversive event and can lead to pain enhancement. Perspective: Although preliminary, these results suggest that fear-relevant environmental stimuli (including facial expressions) may provide important environmental cues during aversive events that influence the level of pain experienced.

Despite the widespread use of the nociceptive flexion reflex (NFR) paradigm in clinical and experimental pain research, there is currently no consensus on how best to define NFR threshold. Accordingly, the present studies were designed to assess the accuracy and reliability of different NFR threshold scoring criteria. Study 1 compared 13 scoring criteria in their accuracy for identifying the presence of the NFR, then generated empirically derived cut-points for the best criteria, and examined the test-retest reliability of NFR thresholds derived from these cut-points. Study 2 evaluated the replicability of these findings in an independent sample. Results from the two studies suggested that standardized peak (NFR Interval Peak z score) and mean (NFR Interval z score) biceps femoris electromyogram (EMG) activity were accurate and reliable criteria for defining NFR threshold. Acknowledging that cut-points may need to be adjusted for different research designs, graphs depicting sensitivity and specificity across a range of cut-points have been provided to facilitate researcher’s decision-making. It is hoped that the results of these studies will promote a standard NFR threshold assessment methodology, and further encourage the application of the NFR paradigm in the investigation of mechanisms and characteristics of both painful and non-painful diseases.

Prior research has found that pain catastrophizing measured before pain testing is not correlated with the nociceptive flexion reflex (NFR) threshold (a measure of spinal nociception), suggesting that catastrophizing does not alter pain through descending modulatory mechanisms. However, recent evidence suggests that in vivo catastrophizing (measured during or after pain testing) is a better predictor of pain outcomes. In the present study, NFR threshold and pain sensation ratings were assessed in 78 healthy participants by delivering electric stimulations to the sural nerve. After pain testing, participants were asked to rate their affective reaction (displeasure, arousal) to electric stimuli and to report on their pain catastrophizing. Hierarchical regression analyses controlling for participant sex, pre-experiment affect, depressive symptoms, and self-efficacy were used to predict pain-related outcomes (NFR threshold, pain sensation, displeasure ratings, arousal ratings) from in vivo catastrophizing scores. Results indicated that in vivo catastrophizing was related to pain sensation but not to NFR thresholds or arousal reactions. The relation between in vivo catastrophizing and displeasure ratings was not significant after other variables were controlled. These data support prior research suggesting that catastrophizing does not alter pain by engaging descending modulatory mechanisms. Perspective Pain catastrophizing is an important psychological predictor of pain and pain-related functioning. The present study confirms prior reports suggesting that catastrophizing does not work by engaging mechanisms that alter pain transmission in the spinal cord before the signal travels to the brain.

This study tested the prospective effects of hope on depression and anxiety using a longitudinal design. A sample of 522 college students completed self-report measures of hope, depression, and anxiety at three time points, with 1-month delays between administrations. Structural equation modeling was employed to test two cross-lagged panel models of the reciprocal effects of the Agency and Pathways components of hope on depression and anxiety. Results indicated statistically significant negative effects for the Agency component of hope on later depression but no unique effect of the Pathways component of hope on depression. Likewise, Agency showed a statistically significant negative effect on later anxiety, but again Pathways had no significant influence on anxiety. In both cases, neither depression nor anxiety demonstrated any longitudinal effects on either the Agency or Pathways components of hope. Implications of these findings are discussed, along with potential directions for future research.

Chronic nightmares pose a significant problem for many individuals affected by trauma. The present study attempts to extend current knowledge on the nature, characteristics, and associated sequelae of chronic nightmares. Data were collected from 94 trauma-exposed, treatment-seeking participants (74

Objectives History of trauma exposure is often associated with negative physical health outcomes. Better understanding of this association may have important implications for improved health and decreased health care–related costs. One possible link between trauma and poor health outcomes is the pernicious impact of sleep disturbances. In the present study, it was hypothesized that sleep quality would predict physical health symptoms above and beyond posttraumatic stress disorder (PTSD) and depression. Methods Fifty-four trauma-exposed adults participated in a randomized controlled trial for treatment of trauma-related nightmares. Physical health symptoms, depression, PTSD symptoms, and sleep quality were assessed via self-report. Results Consistent with expectations, analyses revealed sleep quality uniquely contributed to physical health symptoms above and beyond PTSD and depression symptoms. Moreover, sleep quality mediated the relationship between PTSD symptoms and physical health symptoms. Conclusions Findings suggest sleep disturbances may require specific interventions to maximize positive physical and mental health outcomes.

Individuals with high-trait anxiety frequently report decreased perceived control. However, it is unclear how these processes are instantiated at a neural level. Prior research suggests that individuals prone to anxiety may have exaggerated activity in the anterior insula and altered activity in the cingulate cortex during anticipation of aversive events. Thus, we hypothesized that anxiety proneness influences anterior insula activation during anticipation of unpredictable threat through decreased perceived control. Forty physically healthy adults underwent neuroimaging while they explored computer-simulated contexts associated either with or without the threat of an unpredictable shock. Skin conductance, anxiety ratings and blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging were used to assess responses to threat versus no threat. Perceived control was measured using the Anxiety Control Questionnaire-Revised. Mediation analysis examined how anxiety proneness influenced BOLD activity. Anticipation of unpredictable threat resulted in increased skin conductance responses, anxiety ratings and enhanced activation in bilateral insula, anterior midcingulate cortex (aMCC) and bed nucleus of the stria terminalis. Individuals with greater anxiety proneness and less perceived control showed greater activity in dorsal anterior insula (dAI). Perceived control mediated the relationship between anxiety proneness and dAI activity. Increased dAI activity was associated with increased activity in aMCC, which correlated with increased exploratory behavior. Results provide evidence that exaggerated insula activation during the threat of unpredictable shock is directly related to low perceived control in anxiety-prone individuals. Perceived control thus may constitute an important treatment target to modulate insula activity during anxious anticipation in anxiety-disordered individuals.

Research has shown that individuals who have sustained mild head injury demonstrate a slowed speed of processing that is exacerbated by fatigue/stress. We administered the Paced Auditory Serial Addition Test (PASAT) at the beginning and at the end of a 4-h experimental protocol to determine whether fatigue or a stressor would result in poorer scores for individuals who had previously sustained mild head injury. A significant improvement was found between the first and second administration for both head-injured and control subjects, but difference scores revealed a significant between-groups difference for the first of the four trials, with the head-injured participants performing worse than controls. Apparently, head-injured participants were slower to develop, as well as slower to regain, a means of efficiently processing rapidly presented information.

Background: Research suggests that the influence of gender on the processing and experience of pain is a result of several mechanisms. One mediating variable is emotion, which may modulate pain through an interaction of valence (pleasant-unpleasant) and arousal (calm-excited). Objective: This review examines whether gender differences in the experience and processing of emotion contribute to differences in the modulation and perception of pain. Methods: An English-language search of MEDLINE and PsycINFO was conducted from 1887 to May 2005. Additional literature was obtained from reference lists of articles retained in the initial search. Results: Emotion appears to influence pain through a valence-by-arousal interaction. Specifically, negatively valenced emotions with low to moderate arousal (eg, anxiety) enhance pain, whereas negatively valenced emotions with high arousal (eg, fear) reduce pain. In contrast, positively valenced emotions always reduce pain, as long as minimal arousal is achieved. Some evidence suggests that women are more sensitive than men to threat-related stimuli and thus experience more negative affect than men. This would generally lead to enhanced pain perception in women. It is also possible that women are more likely than men to experience negative affect with high arousal (intense fear) and thus pain inhibition. However, the relatively lower base rate of intense negative emotions is not likely to contribute much to gender differences in pain. Evidence also suggests that men may be more sensitive to positive events, particularly sexual/erotic stimuli, which may lead to more positive emotion-induced pain reduction in men, relative to women. Conclusions: This review suggests that gender differences in the experience of pain may arisefrom differences in the experience and processing of emotion that, in turn, differentially alter pain processing. Specifically, the system associated with negative affect may be more attuned to threatening stimuli in women, and the system associated with positive affect may be more attuned to pleasurable stimuli in men. However, there is a paucity of research directly addressing this issue; much of the research on this topic has failed to test a comprehensive model of emotion, failed to use adequate manipulation checks, or failed to use within-subject experimental designs that control for intra- and interindividual differences. Therefore, it is concluded that additional research is warranted.

Objective.—The primary objectives of the present study were to (1) contrast reproductive hormone levels and ratings of menstrual distress of female migraineurs with those of a control group in each menstrual cycle phase, (2) examine correlations between hormone levels and migraine frequency, severity, and migraine-related disability, and (3) examine correlations between menstrual distress and migraine frequency, severity, and migraine-related disability. A secondary objective was to evaluate the validity of a migraine disability measure modified to reflect 7-day recall. Background.—Further controlled, prospective study is needed regarding the temporal relationships between reproductive hormones at each stage of the menstrual cycle and fluctuations in migraine activity across the cycle. Methods.—Twenty-three women (17 with migraine, 6 control participants) completed laboratory hormone assays and measures of menstrual distress and disability at each phase of one menstrual cycle, and monitored their headache activity daily during the same cycle. Results.—The migraine group evidenced lower premenstrual luteinizing hormone and more menstrual distress symptoms at each phase of the menstrual cycle. Hormones were associated with migraine activity and disability within cycle phases, and across phases in a time-lagged manner. Menstrual distress was associated with ovulatory phase migraine activity and with migraine-related disability across the menstrual cycle. A retrospective 7-day migraine disability measure appeared to be a consistently valid index. Conclusions.—Both reproductive hormones and menstrually related distress appear to predict migraine activity and disability. These associations were evident not only for perimenstrual migraine, but also for migraine at each phase of the menstrual cycle. Ke yw ords: hormones, migraine, menstrual cycle, distress, disability Abbreviations: BBT basal body temperature, HDI headache disability inventory, LH luteinizing hormone, MDQ menstrual distress questionnaire, MIDAS migraine disability assessment, d Cohen’s effect size

Prior research indicates that exposure to fear-inducing stimuli inhibits finger withdrawal to sudden onset and high intensity radiant heat in humans. Although withdrawal latencies to intense heat are thought to reflect changes in spinal nociceptive processing, supraspinal measures are needed to determine whether pain perception is altered. The present study used gradual onset and low intensity radiant heat to induce a finger withdrawal response that depends on supraspinal processes. After baseline pain threshold tests, 57 healthy human participants were randomly assigned to 1 of 2 groups. In the fear group, participants received 3 brief shocks. In the neutral group, participants did not receive shock. Results suggest that finger withdrawal latencies to low intensity heat were increased after shock presentation, providing additional evidence that fear reduces pain on a measure that is influenced by supraspinal processes. Both self-report and physiological (skin conductance level, heart rate, and blood pressure) measures of emotion confirmed that the intended affective states were induced. Finger temperature was unaffected by emotion manipulations; thus, skin cooling does not appear to mediate increased withdrawal latencies. These findings provide additional evidence that fear not only inhibits spinal nociceptive reflexes, it also inhibits supraspinal measures of pain. Perspective From a clinical perspective, these data suggest that patients who experience intense fear in response to unpredictable threatening events will show a reduction in pain perception.

Objectives. Our laboratory has shown that electrical shocks induce fear in human participants and subsequently inhibit pain on the hand receiving shocks. The present study examined whether pain modulation is bilateral, by testing pain on the hand contralateral to the one receiving shocks. We also evaluated whether individual differences in emotional response to the shocks influenced pain modulation. Design. Following baseline tests, 61 participants were randomly assigned to one of two groups. In the shock group, participants received three surprising electrical shocks. In the control group, stimulating electrodes were removed from participants' fingers, and no shocks were presented. Both groups received two more pain threshold tests 2 and 8 minutes later. Outcome Measures. Similarly to the tail-flick test used in rodents, pain threshold was tested by measuring the latency of finger withdrawal to radiant heat. The following manipulation checks assessed the emotional state induced by shocks and the control procedure: Self-reported affect, skin conductance level (SCL), heart rate (HR), and blood pressure (BP). Results. Surprisingly, self-reported affect data indicate that some participants reacted to the shocks with humor and fear, while others reacted primarily with fear. Therefore, these groups were analyzed separately. Participants reacting with fear only exhibited hypoalgesia; however, participants reacting with mixed fear and humor showed no change in pain. This divergent effect was not mediated by arousal, because SCL, HR, and BP were similar in both shocked groups (fear only, fear + humor). Conclusions. These data suggest that fear-induced hypoalgesia occurs bilaterally. However, humor experienced concurrent with fear appears to inhibit hypoalgesia. These findings may help explain individual differences in pain following traumatic events.

Prior work indicates that exposure to fear-inducing shock inhibits finger-withdrawal to radiant heat in humans (hypoalgesia), whereas anxiety induced by threat of shock enhances reactivity (hyperalgesia; Pain 84 (2000) 65-75). Although finger-withdrawal latencies are thought to reflect changes in pain sensitivity, additional measures of pain are needed to determine whether pain perception is altered. The present study examined the impact of negative affect on visual analog scale (VAS) ratings of fixed duration thermal stimuli. One hundred twenty-seven male and female human subjects were randomly assigned to one of three emotion-induction conditions: (1) negative affect induced by exposure to three brief shocks; (2) negative affect elicited by the threat of shock without presentation; and (3) neutral affect, with no intervention. VAS ratings were tested before and after emotion-induction. Results suggest that both negative affect manipulations reduced pain. Manipulation checks indicated that the emotion-induction treatments induced similar levels of fear but with different arousal levels. Potential mechanisms for affect induced changes in pain are discussed.

Objective Sex differences in pain are well established, with women reporting greater incidence of clinical pain and heightened responsivity to experimental pain stimuli relative to men. Sex hormones (ie, estrogens, progestins, androgens) could contribute to extant differences in pain sensitivity between men and women. Despite this, there has been limited experimental research assessing the relationship between pain and sex hormones. The purpose of this study was to extend previous research and examine the association between sex hormones and nociceptive processing in healthy women. Materials and methods A total of 40 healthy women were tested during the mid-follicular, ovulatory, and late-luteal phases of the menstrual cycle (testing order counterbalanced). Salivary estradiol, progesterone, and testosterone were collected at each testing session and pain was examined from electrocutaneous threshold/tolerance, ischemia threshold/tolerance, and McGill Pain Questionnaire-Short Form ratings of noxious stimuli. Nociceptive flexion reflex threshold was assessed as a measure of spinal nociception. Results Overall, there were no significant menstrual phase-related differences in pain outcomes. Nonetheless, variability in testosterone (and to a lesser degree estradiol) was associated with pain; testosterone was antinociceptive, whereas estradiol was pronociceptive. No hormone was associated with nociceptive flexion reflex threshold. Discussion Although future research is needed to replicate and extend these findings to clinical populations (ie, chronic pain, premenstrual dysphoric disorder), results from the present study indicate that menstrual phase-related changes in sex hormones have minimal influence on experimental pain. However, individual differences in testosterone may play a protective role against pain in healthy women.

Impaired sleep enhances pain, perhaps by disrupting pain modulation. Given that emotion modulates pain, the present study examined whether emotional modulation of pain and nociception is impaired in persons with severe insomnia symptoms relative to controls. Insomnia group (n = 12) met the International Classification of Diseases, tenth revision symptoms for primary insomnia and controls (n = 13) reported no sleep impairment. Participants were shown emotionally evocative pictures (mutilation, neutral, and erotica) during which suprathreshold pain stimuli were delivered to evoke pain and the nociceptive flexion reflex (NFR; physiological correlate of spinal nociception). Emotional responses to pictures were similar in both groups, except that subjective valence/pleasure ratings were blunted in insomnia. Emotional modulation of pain and NFR was observed in controls, but only emotional modulation of NFR was observed in insomnia. Consistent with previous findings, pain modulation is disrupted in insomnia, which might promote pain. This may stem from disrupted supraspinal circuits not disrupted brain-to-spinal cord circuits.