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Although most agree that emotion can alter pain, little well-controlled research has been conducted to examine this issue. The present review provides psychological and physiological rationales for considering the influence of emotion on pain, followed by an overview of recent work in this area. We

Considerable animal research suggests that exposure to noxious and nonnoxious fear-inducing stimuli can produce hypoalgesia. Although this effect is thought to generalize across species, only a few studies have examined the pain modulatory effects of nonnoxious fear-eliciting stimuli in humans. The present study examined whether exposure to a series of loud noise bursts would produce a fear-related hypoalgesia in male and female human subjects. Both subjective and physiologic measures (skin conductance level, heart rate) indicated that noise exposure resulted in fear, sympathetic arousal, and decreased pain reactivity in women (n = 20). In contrast, men (n = 20) did not experience fear or physiologic arousal, but reacted with surprise and increased pain reactivity. These findings provide additional evidence that hypoalgesia is mediated by fear and physiologic arousal. Although future studies should directly manipulate surprise, it appears that surprise without fear and physiologic arousal might enhance pain processing.

Major depressive disorder (MDD) is associated with risk for chronic pain, but the mechanisms contributing to the MDD and pain relationship are unclear. To examine whether disrupted emotional modulation of pain might contribute, this study assessed emotional processing and emotional modulation of pain in healthy controls and unmedicated persons with MDD (14 MDD, 14 controls). Emotionally charged pictures (erotica, neutral, mutilation) were presented in 4 blocks. Two blocks assessed physiological-emotional reactions (pleasure/arousal ratings, corrugator electromyography (EMG), startle modulation, skin conductance) in the absence of pain and 2 blocks assessed emotional modulation of pain and the nociceptive flexion reflex (NFR, a physiological measure of spinal nociception) evoked by suprathreshold electric stimulations. Results indicated pictures generally evoked the intended emotional responses; erotic pictures elicited pleasure, subjective arousal, and smaller startle magnitudes, whereas mutilation pictures elicited displeasure, corrugator EMG activation, and subjective/physiological arousal. However, emotional processing was partially disrupted in MDD, as evidenced by a blunted pleasure response to erotica and a failure to modulate startle according to a valence linear trend. Furthermore, emotional modulation of pain was observed in controls but not MDD, even though there were no group differences in NFR threshold or emotional modulation of NFR. Together, these results suggest supraspinal processes associated with emotion processing and emotional modulation of pain may be disrupted in MDD, but brain to spinal cord processes that modulate spinal nociception are intact. Thus, emotional modulation of pain deficits may be a phenotypic marker for future pain risk in MDD.

Fibromyalgia (FM) is characterized by widespread pain, as well as affective disturbance (e.g., depression). Given that emotional processes are known to modulate pain, a disruption of emotion and emotional modulation of pain and nociception may contribute to FM. The present study used a well-validated affective picture-viewing paradigm to study emotional processing and emotional modulation of pain and spinal nociception. Participants were 18 individuals with FM, 18 individuals with rheumatoid arthritis (RA), and 19 healthy pain-free controls (HC). Mutilation, neutral, and erotic pictures were presented in four blocks; two blocks assessed only physiological-emotional reactions (i.e., pleasure/arousal ratings, corrugator EMG, startle modulation, skin conductance) in the absence of pain and two blocks assessed emotional reactivity and emotional modulation of pain and the nociceptive flexion reflex (NFR, a physiological measure of spinal nociception) evoked by suprathreshold electric stimulations over the sural nerve. In general, mutilation pictures elicited displeasure, corrugator activity, subjective arousal, and sympathetic activation, whereas erotic pictures elicited pleasure, subjective arousal, and sympathetic activation. However, FM was associated with deficits in appetitive activation (e.g., reduced pleasure/arousal to erotica). Moreover, emotional modulation of pain was observed in HC and RA, but not FM, even though all three groups evidenced modulation of NFR. Additionally, NFR thresholds were not lower in the FM group, indicating a lack of spinal sensitization. Together, these results suggest that FM is associated with a disruption of supraspinal processes associated with positive affect and emotional modulation of pain, but not brain-to-spinal cord circuitry that modulates spinal nociceptive processes.

Objectives Understanding the relationship between the menstrual cycle and pain can contribute significantly to our knowledge of pain processing in women. Many early studies suggested that pain sensitivity was enhanced during the luteal phase of the menstrual cycle relative to the follicular phase; however, these studies were often limited by small sample sizes, lack of ovulation verification, focus on a single pain modality, inadequate assessment of menstrual cycle regularity, and low-powered statistical methods. The current study was designed to address these limitations and examine the difference in pain processing between the mid-follicular (days 5 to 8) and late-luteal (days 1 to 6 preceding menses) phases. Methods Forty-one healthy, regularly cycling women attended testing sessions that measured pain sensitivity from mechanical pain threshold, electrocutaneous pain threshold/tolerance, and ischemia pain threshold/tolerance, as well as McGill Pain Questionnaire qsensory and affective ratings of electric and ischemic stimuli. Electrocutaneous stimulation was also used to assess nociceptive flexion reflex threshold, a physiological measure of spinal nociception. Results When analyses were limited to data collected only in the targeted menstrual phases (N=30), results indicated no menstrual phase effect on any pain outcome (all P's>0.05), with the exception of lower electrocutaneous pain thresholds during the late-luteal phase. No outcomes differed by menstrual phase in the full sample (N=41). This indicates nociceptive responding varies little between the mid-follicular and late-luteal phases. Discussion The present study suggests that experimental pain processing does not significantly differ between the mid-follicular and late-luteal phases of the menstrual cycle in healthy women. This implies hormonal variation across these 2 phases (ie, progesterone) has a minimal effect on subjective and physiological responses to pain.

OBJECTIVES Anxiety sensitivity (AS) is the fear of anxiety-related sensations and its perceived harmful consequences. AS is associated with enhanced pain and worsened pain outcomes, suggesting it is a contributing factor in acute and chronic pain. However, the mechanisms that mediate the relationship between AS and pain are currently unknown. This study assessed the relationship between AS and 2 measures of spinal nociceptive processes (ie, nociceptive flexion reflex and temporal summation of nociceptive flexion reflex) and measures of subjective pain. This allowed us to determine whether AS engages descending cerebrospinal processes to facilitate pain signaling at spinal levels. METHODS AS was assessed in healthy men and women using the Anxiety Sensitivity Index-Revised. Then pain processing was assessed from electric pain threshold, nociceptive flexion reflex threshold, temporal summation of pain, temporal summation of nociceptive flexion reflex, and McGill Pain Questionnaire sensory and affective pain ratings. Associations among variables were assessed using Winsorized correlations (a robust and statistically powerful analytic method). RESULTS AS was positively associated with sensory pain ratings, affective pain ratings, and temporal summation of pain, but was unrelated to all other outcomes. DISCUSSION Given that AS was not significantly associated with measures of spinal nociception, these results suggest that AS may exert its influence on pain processing at the supraspinal, rather than the spinal level.

Emotion can modulate pain and spinal nociception, and correlational data suggest that cognitive-emotional processes can facilitate wind-up-like phenomena (ie, temporal summation of pain). However, there have been no experimental studies that manipulated emotion to determine whether within-subject changes in emotion influence temporal summation of pain (TS-pain) and the nociceptive flexion reflex (TS-NFR, a physiological measure of spinal nociception). The present study presented a series of emotionally charged pictures (mutilation, neutral, erotic) during which electric stimuli at 2 Hz were delivered to the sural nerve to evoke TS-pain and TS-NFR. Participants (n = 46 healthy; 32 female) were asked to rate their emotional reactions to pictures as a manipulation check. Pain outcomes were analyzed using statistically powerful multilevel growth curve models. Results indicated that emotional state was effectively manipulated. Further, emotion modulated the overall level of pain and NFR; pain and NFR were highest during mutilation and lowest during erotic pictures. Although pain and NFR both summated in response to the 2-Hz stimulation series, the magnitude of pain summation (TS-pain) and NFR summation (TS-NFR) was not modulated by picture-viewing. These results imply that, at least in healthy humans, within-subject changes in emotions do not promote central sensitization via amplification of temporal summation. However, future studies are needed to determine whether these findings generalize to clinical populations (eg, chronic pain).

Despite growing support for the use of imagery rescripting to treat posttraumatic nightmares (PTNMs), its underlying mechanisms have not been examined. This secondary data analysis piloted the proposal that modification of posttraumatic cognitions is a mechanism of change when using a manualized PTNM imagery rescripting intervention. Significant linear reductions in posttraumatic cognitions were observed from baseline through 6-month follow-up evaluations. Change in total negative cognitions was significantly correlated with change in posttraumatic stress disorder symptoms. Initial amount of change in subscale scores also predicted the amount of distal change observed at the 6-month follow-up. These findings provide preliminary evidence that trauma-related cognitions may improve over time as a result of imagery rescripting.

Temporal summation of pain (TS-pain) is the progressive increase in pain ratings during a series of noxious stimulations. TS-pain has been used to make inferences about sensitization of spinal nociceptive processes; however, pain report can be biased thereby leading to problems with this inference. Temporal summation of the nociceptive flexion reflex (TS-NFR, a physiological measure of spinal nociception) can potentially overcome report bias, but there have been few attempts (generally with small Ns) to standardize TS-NFR procedures. In this study, 50 healthy participants received 25 series of noxious electric stimulations to evoke TS-NFR and TS-pain. Goals were to: 1) determine the stimulation frequency that best elicits TS-NFR and reduces electromyogram (EMG) contamination from muscle tension, 2) determine the minimum number of stimulations per series before NFR summation asymptotes, 3) compare NFR definition intervals (90-150ms vs. 70-150ms post-stimulation), and 4) compare TS-pain and TS-NFR when different stimulation frequencies are used. Results indicated TS-NFR should be elicited by a series of three stimuli delivered at 2.0Hz and TS-NFR should be defined from a 70-150ms post-stimulation scoring interval. Unfortunately, EMG contamination from muscle tension was greatest during 2.0Hz series. Discrepancies were noted between TS-NFR and TS-pain which raise concerns about using pain ratings to infer changes in spinal nociceptive processes. And finally, some individuals did not have reliable NFRs when the stimulation intensity was set at NFR threshold during TS-NFR testing; therefore, a higher intensity is needed. Implications of findings are discussed.

The present study examined whether a moderately aversive abdominal threat would lead to greater enhancement in affect- and pain-related defensive responding as indexed by the acoustic startle reflex (ASR) and nociceptive flexion reflex (NFR) in women compared to men. We also predicted sex differences in threat-related autonomic arousal measured by skin conductance responses (SCRs) to acoustic startle and noxious sural nerve stimulation. Unpredictable threat was manipulated by alternating 30-second safe ("no abdominal stimulation will be given") and threat ("abdominal stimulation may occur at anytime") periods. The experiment consisted of 2 blocks, each containing 4 safe and 4 threat periods in which the ASR or NFR was randomly probed 9-21 seconds following period onset. Unpredictable abdominal threat potentiated both ASR and NFR responses compared to periods signaling safety. SCRs to acoustic startle probes and noxious sural nerve stimulation were also significantly elevated during the threat vs safe periods. No sex differences in ASR or startle-evoked SCRs emerged. However, nociceptive responding was moderated by sex; females showed significant increases in NFR magnitudes across both safe and threat periods compared to males. Females also showed greater threat-potentiated SCRs to sural nerve stimulation than males. Our findings indicate that both affect- and pain-related defense and arousal systems are strongly influenced by threat of an aversive, unpredictable event, a situation associated with anticipatory anxiety. Females, compared to males, showed greater nociceptive responding and pain modulation when exposed to an unpredictable threatening context, whereas affect-driven ASR responses showed no such sex differentiation.

The short allele of the serotonin transporter gene (5-HTTLPR) is associated with greater negative emotionality. Given that emotion modulates pain, short allele carriers (s-carriers) may also demonstrate altered pain modulation. The present study used a well-validated emotional picture-viewing paradigm to modulate pain and the nociceptive flexion reflex (NFR, a measure of spinal nociception) in 144 healthy genotyped participants. As expected, pain/NFR responses were largest during unpleasant pictures and smallest during pleasant pictures. However, relative to l/l-carriers, s-carriers demonstrated greater pain inhibition during pleasant pictures and greater pain facilitation during unpleasant pictures. Neither emotional modulation of NFR nor NFR threshold was associated with 5-HTTLPR polymorphisms. Results also indicated that men who were s-carriers had a higher pain threshold and tolerance than other participants. Taken together, our results indicate 5-HTTLPR polymorphisms may influence pain modulation at the supraspinal (not spinal) level; however, the influence on pain sensitivity may be sex-specific.

Sex differences in the processing and experience of emotion exist. The present study examined whether sex differences in emotion lead to sex differences in affective modulation of pain and spinal nociception (assessed by nociceptive flexion reflex, NFR). Participants were healthy men (n = 47) and women (n = 73). Prior to affective modulation testing, electrocutaneous pain sensitivity was assessed (NFR threshold, pain threshold, pain tolerance). Affective modulation of pain and NFR was then assessed by presenting pictures that vary in emotional valence and arousal (mutilation, attack, death, neutral, families, adventure, erotica) during which suprathreshold electrocutaneous stimulations were delivered. Subjective emotional reactions were assessed after every picture, and nociceptive reactions were assessed after every suprathreshold stimulus. Results indicated women had greater pain sensitivity and also responded more negatively to attack pictures and less positively to erotic pictures. But despite these differences, affective modulation of pain/NFR was not moderated by sex: erotic pictures inhibited pain/NFR and mutilation pictures enhanced pain/NFR. Together, this implies subjective emotional experience does not completely mediate picture-evoked modulation of pain/NFR, a supposition that was further supported by exploratory analyses that demonstrated picture-evoked modulation of pain/NFR was present even after controlling for intra- and inter-individual differences in emotional reactions to pictures. Implications and limitations of these findings are discussed. Perspective Evidence suggests that women are more sensitive to experimental and clinical pain, but the mechanisms contributing to these sex differences are poorly understood. Affective processes are known to play a role in regulating pain signaling and pain experience; therefore, the present study examined whether sex differences in affective experience contribute to sex differences in pain. Results indicate that in healthy individuals affective processes may not contribute to sex differences in pain.

Cognitive-behavioral treatments (CBTs) that target nightmares are efficacious for ameliorating self-reported sleep problems and psychological distress. However, it is important to determine whether these treatments influence objective markers of nightmare-related fear, because fear and concomitant physiological responses could promote nightmare chronicity and sleep disturbance. This randomized, controlled study (N=40) assessed physiological (skin conductance, heart rate, facial electromyogram) and subjective (displeasure, fear, anger, sadness, arousal) reactions to personally relevant nightmare imagery intended to evoke nightmare-related fear. Physiological assessments were conducted at pretreatment as well as 1-week, 3-months, and 6-months posttreatment. Results of mixed effects analysis of variance models suggested treatment reduced physiological and subjective reactions to nightmare imagery, gains that were generally maintained at the 6-month follow-up. Potential implications are discussed.

The Emotional Controls of Nociception (ECON) paradigm involves the presentation of emotionally-charged pictures during which painful stimuli are delivered. Across several ECON studies, unpleasant pictures enhanced pain and nociception, whereas pleasant pictures inhibited pain and nociception. However, at this time it is unknown whether emotional valence (unpleasant, neutral, pleasant) influences the habituation or sensitization of pain responses that occurs within a testing session. Indeed, ECON assumes that emotional valence modulation of pain is consistent throughout testing; otherwise the interpretation of valence modulation (unpleasant > neutral > pleasant) could be threatened. To address this issue, the present study (N = 120) presented 108 pictures that varied in emotional valence. During and in between pictures, 52 suprathreshold electrocutaneous stimuli were delivered to evoke pain, the nociceptive flexion reflex [NFR], and pain-evoked skin conductance response [SCR]. Mixed effects ANOVAs verified that within-subject changes in pain responses were influenced by stimulus repetition (NFR and SCR habituated, pain ratings sensitized) and emotional valence (responses were highest during unpleasant pictures, intermediate during neutral pictures, and lowest during pleasant pictures). However, habituation/sensitization slopes were unaffected by emotional valence, thus indicating emotional valence modulation was consistently observed throughout the testing session. These results provide additional validation for the ECON paradigm and suggest that the circuit responsible for emotional modulation of pain and nociception is less susceptible to habituation or sensitization than the circuits responsible for responses to suprathreshold shocks.

The nociceptive flexion reflex (NFR) has been used as a psychophysiological tool to study spinal nociceptive processes in numerous clinical and experimental studies. Despite widespread use of the NFR, few attempts have been made to empirically test and compare different scoring criteria to detect the presence/absence of the reflex. The present studies were conducted to address this issue. Study 1 (N=56 healthy participants) examined the reliability of 15 different scoring criteria that were examined in a previous report. Study 2 (N=73 healthy participants) extended this work by examining normalized scoring criteria based on biceps femoris activity unrelated to noxious stimulation (reference contraction, maximal contraction). In both studies, receiver operating characteristics (ROCs) analyses were used to evaluate and compare different scoring methods. The results indicate that a number of different criteria were acceptable for defining an NFR threshold based on the area under the ROC curve and its statistical significance; however, NFR Interval z score [(NFR Interval Mean-baseline mean)/baseline SD] emerged as the scoring criterion with the greatest accuracy and with cut-points that are reliable across samples. These findings support the application of a common NFR scoring criterion to enhance direct comparison of results across different research laboratories and study samples.

Existing evidence indicates that pain catastrophizing is associated with enhanced pain reports and lower pain threshold/tolerance levels, but is not significantly related to nociceptive flexion reflex (NFR) threshold in healthy and clinical pain samples. This suggests pain catastrophizing may modulate pain threshold at a supraspinal level without influencing descending modulation of spinal nociceptive inputs. To examine this issue further, the present study assessed NFR threshold, electrocutaneous pain threshold, and electrocutaneous pain tolerance, as well as subjective ratings of noxious stimuli in a sample of 105 healthy adults. Pain catastrophizing was assessed prior to testing using traditional instructions and after pain testing with instructions to report on cognitions during testing (situation-specific catastrophizing). As expected, NFR threshold was correlated with pain sensitivity measures, but uncorrelated with both measures of catastrophizing. Although situation-specific catastrophizing was correlated with some pain outcomes, neither catastrophizing measure (traditional or situation specific) moderated the relationship between NFR and pain sensitivity. These findings confirm and extend existing evidence that catastrophizing influences pain reports through supraspinal mechanisms (eg, memory, report bias, attention) without altering transmission of spinal nociceptive signals. Perspective Assessing catastrophic thoughts related to a specific painful event (situation-specific catastrophizing) provides important additional information regarding the negative cognitions that influence pain-related processes. However, neither situation-specific nor traditionally measured pain catastrophizing appear to enhance pain by engaging descending controls to influence spinal nociceptive processes.

Dysregulation of supraspinal pain modulation may contribute to chronic pain, including head/face pain. Our laboratory has shown that emotional picture-viewing reliably modulates subjective and physiological pain responses to noxious extracranial (sural nerve) stimulation, suggesting this is a valid method of studying supraspinal modulation. However, to study head/face pain, it is important to determine whether responses evoked by trigeminal stimulation are also modulated. In the present study (34 healthy participants), emotionally-charged pictures (unpleasant, neutral, pleasant) were presented during which painful trigeminal stimulations were delivered during and in between pictures. Autonomic responses to each shock (pain-evoked HR acceleration, pain-evoked skin conductance response [SCR]) were recorded. Consistent with research on extracranial pain, autonomic responses were larger during unpleasant pictures and smaller during pleasant pictures, with linear trends explaining 23% of the variance in pain-evoked HR and 35% of the variance in pain-evoked SCR (ps

Script-driven imagery was used to assess nightmare imagery-evoked physiological-emotional reactivity (heart rate, skin conductance, facial electromyogram, subjective ratings) in trauma-exposed persons suffering from chronic nightmares. Goals were to determine the efficacy of nightmare imagery to evoke physiological-emotional reactivity, correlates (mental health, nightmare characteristics) of reactivity, and consequences (sleep and health problems) of reactivity. Nightmare imagery resulted in significant reactivity relative to control imagery. No mental health variable (posttraumatic stress disorder status, depressive symptoms, dissociation) or nightmare characteristic (months experienced, frequency, similarity to trauma) was associated with reactivity level. However, nightmare imagery-evoked autonomic responses were associated with greater sleep disturbance and reported health symptoms, even when nightmare frequency was controlled. These results suggest nightmare-related autonomic reactions may contribute to sleep and health disturbance.

Pain catastrophizing is associated with enhanced pain and pain-related outcomes. Unfortunately, the mechanisms underlying the catastrophizing-pain relationship are poorly understood. Given evidence suggesting significant relationships among catastrophizing, emotion, and pain, it is possible that catastrophizing may alter nociception and pain through affective processes. Research has shown that emotionally charged pictures (erotica, neutral, threat/attack scenes) manipulate emotional valence (positive affect vs negative affect) and modulate physiological and subjective nociceptive reactions (pleasure-induced inhibition, displeasure-induced facilitation). Using this methodology, the present study addressed 2 questions: (1) Does pain catastrophizing moderate affective reactions to standard emotional stimuli (eg, augmented negative affect)? and (2) Does pain catastrophizing moderate the relationship between emotion and nociception (eg, augmented displeasure-induced facilitation)? Erotic, neutral, and attack pictures were presented to 53 participants who rated their emotional responses. During pictures, noxious electric stimulations were delivered to evoke nociceptive reactions (nociceptive flexion reflex, skin conductance response, heart rate acceleration, subjective pain). Results suggest that pain catastrophizing did not moderate emotional reactions to standardized picture stimuli, nor did catastrophizing moderate the influence of emotion on nociceptive reactions. This suggests that catastrophizing does not influence pain indirectly through emotional processes. Perspective Pain catastrophizing is commonly associated with negative emotions and maladaptive responses to pain. The current study provides evidence indicating catastrophizing does not alter pain and nociception indirectly via emotional processes.

Pain may be a barrier or a negative outcome of initiating and maintaining an exercise program in elderly patients. The purpose of this study was to examine the role of pain in a program designed to increase walking for exercise in 181 veteran primary care patients (60 - 80 years). Self-reported physical activity (min-walked per week) and pain were assessed at baseline, 6, and 12 months. Walking for exercise increased over time without significant changes in pain. Analyses suggested that baseline pain was not a barrier to initiating or maintaining a walking exercise program, nor did increased walking influence reports of pain. These results suggest that patients can be encouraged to engage in physical activity, even if they are currently suffering from pain.

Research suggests affective picture-viewing modulates subjective and physiological reactions to noxious stimulation (pain report, heart rate acceleration, skin conductance response, nociceptive flexion reflex). Because the nociceptive flexion reflex (a spinal reflex) is modulated by picture-viewing, this suggests affective processes are able to modulate afferent nociception at spinal levels. This highlights the importance of assessing nociceptive reactivity from physiological measures mediated at different levels of the neuraxis (spinal vs. supraspinal) to help elucidate the mechanisms associated with pain regulation. The present study examined whether affective pictures modulate eyeblink reactions (a supraspinal reflex) to noxious stimulation. Healthy men and women (N=23) were recruited from the psychology subject pool to participate. Pictures (attack, loss, neutral, food, erotica) that manipulated affective valence and arousal were presented and noxious electrodermal stimulations were delivered to the sural nerve. Picture duration (500-ms vs. 6-s) was also manipulated, balanced across picture content. Results suggested affective valence and arousal contributed to the modulation of eyeblinks. Eyeblinks were larger during highly arousing unpleasant pictures (attack) than highly arousing pleasant pictures (erotica), but low arousal pictures (loss, food) did not lead to significant modulation. Affective modulation was independent of picture duration or the perceived painfulness of noxious stimulation. This study suggests eyeblink reactions can serve as a supraspinal outcome in procedures used to study affective modulation of pain and nociception.

Headache is a chronic disease that occurs with varying frequency and results in varying levels of disability. To date, the majority of research and clinical focus has been on the role of biological factors in headache and headache-related disability. However, reliance on a purely biomedical model of headache does not account for all aspects of headache and associated disability. Using a biopsychosocial framework, the current manuscript expands the view of what factors influence headache by considering the role psychological (i.e., cognitive and affective) factors have in the development, course, and consequences of headache. The manuscript initially reviews evidence showing that neural circuits responsible for cognitive-affective phenomena are highly interconnected with the circuitry responsible for headache pain. The manuscript then reviews the influence cognitions (locus of control and self-efficacy) and negative affect (depression, anxiety, and anger) have on the development of headache attacks, perception of headache pain, adherence to prescribed treatment, headache treatment outcome, and headache-related disability. The manuscript concludes with a discussion of the clinical implications of considering psychological factors when treating headache.

Research suggests that emotion modulates spinal nociception and pain; however, there is limited evidence that other objective, nociceptive reactions are modulated. This study examined the impact of affective picture-viewing on autonomic reactions (skin conductance response, heart rate acceleration) resulting from noxious electric stimulations to the sural nerve. Pictures varying in affective valence (unpleasant, neutral, pleasant) were presented during which noxious stimulations were delivered. Skin conductance response and short-latency heart rate acceleration following each stimulation was calculated and averaged by picture valence. Results suggested that autonomic reactions were modulated in parallel. Specifically, reactions were smaller during pleasant pictures than unpleasant pictures, although unpleasant pictures did not result in significant facilitation relative to neutral pictures. The valence linear trend explained 26% of the variance in the multivariate combination of the reactions, suggesting emotion does modulate autonomic reactions to nociception. These results suggest that SCR and HR acceleration are outcomes that can be assessed together with NFR and pain report during picture-viewing to study affective modulation of spinal (NFR), supraspinal (SCR, HR acceleration), and subjective (pain report) nociceptive reactions.

Recent evidence suggests that emotional picture-viewing is a reliable method of engaging descending modulation of spinal nociception. The present study attempted to replicate these findings and determine the effect of noxious stimulus predictability. Participants viewed pictures from the International Affective Picture System (IAPS), during which pain and nociceptive flexion reflexes (NFR) were elicited by electric shocks delivered to the sural nerve. For half of the participants ( n = 25) shocks were preceded by a cue (predictable), whereas the other half received no cue (unpredictable). Results suggested emotion was successfully induced by pictures, but the effect of picture-viewing on the NFR was moderated by the predictability of the shocks. When shock was unpredictable, spinal nociception (NFR) and pain ratings were modulated in parallel. Specifically, pain and NFR magnitudes were lower during pleasant emotions and higher during unpleasant emotions. However, when shocks were predictable, only pain was modulated in this way. NFRs from predictable shocks were not altered by pictures. Further, exploratory analyses found that pain ratings, but not NFRs, were lower during predictable shocks. These data suggest emotional picture-viewing is a reliable method of engaging descending modulation of spinal nociception. However, descending modulation could not be detected in NFRs resulting from predictable noxious stimuli. Although preliminary, this study implies that separate mechanisms are responsible for emotional modulation of nociception at spinal vs. supraspinal levels, and that predictable noxious events may disengage modulation at the spinal level. The current paradigm could serve as a useful tool for studying descending modulation.

This study was designed to examine the effect of emotion on the nociceptive flexion reflex and pain ratings. To do so, 28 participants viewed pictures varying in emotional valence (unpleasant, neutral, pleasant) and electric stimulations were delivered during and in between pictures. Biceps femoris EMG resulting from the stimulations was used to quantify the nociceptive flexion reflex (spinal nociception), and pain ratings to the stimulations were used as an evaluative measure of supraspinal nociception. Manipulation checks suggested that pictures effectively manipulated emotion. Moreover, nociceptive flexion reflex magnitudes and pain ratings were modulated in a parallel manner. Specifically, viewing unpleasant pictures enhanced the nociceptive flexion reflex and pain, whereas viewing pleasant pictures inhibited the reflex and pain. Analyses suggested that emotional valence, but not arousal, mediated the effects of pictures.

Objective and methods Two experiments examined the impact of viewing unpleasant, pleasant, and neutral photographic slides on cold-pain perception in healthy men and women. In each experiment, participants viewed one of three slide shows (experiment 1 = fear, disgust, or neutral; experiment 2 = erotic, nurturant, or neutral) immediately before a cold-pressor task. Skin conductance and heart rate were recorded during the slide shows, whereas visual analog scale ratings of pain intensity and unpleasantness thresholds and pain tolerance were recorded during the cold-pressor task. Results Viewing fear and disgust slides decreased pain intensity and unpleasantness thresholds, but only the fear slides decreased pain tolerance. In contrast, viewing erotic, but not nurturant, slides increased pain intensity and unpleasantness threshold ratings on the visual analog scale in men, whereas neither nurturant nor erotic slides altered pain tolerance. Conclusions These results are consistent with a motivational priming model that predicts that unpleasant affective states should enhance pain and that pleasant affective states should attenuate it.

Animal studies suggest that fear inhibits pain whereas anxiety enhances it; however it is unclear whether these effects generalize to humans. The present study examined the effects of experimentally induced fear and anxiety on radiant heat pain thresholds. Sixty male and female human subjects were randomly assigned to 1 of 3 emotion induction conditions: (1) fear, induced by exposure to three brief shocks; (2) anxiety, elicited by the threat of shock; (3) neutral, with no intervention. Pain thresholds were tested before and after emotion induction. Results suggest that findings from animal studies extend to humans: fear resulted in decreased pain reactivity, while anxiety led to increased reactivity. Pain rating data indicated that participants used consistent subjective criteria to indicate pain thresholds. Both subjective and physiological indicators (skin conductance level, heart rate) confirmed that the treatment conditions produced the targeted emotional states. These results support the view that emotional states modulate human pain reactivity.