Pain-related emotions modulate experimental pain perception and autonomic responses

Pain 118 (2005) 306–318 www.elsevier.com/locate/pain

Pain-related emotions modulate experimental pain perception and autonomic responses Pierre Rainville*, Quoc Viet Huynh Bao, Pablo Chre´tien De´partement de Stomatologie, Faculte´ de me´decine dentaire, Universite´ de Montre´al, CP. 6128, Succ. Centre-ville, Montre´al, Que., Canada H3C 1J7 Received 10 May 2005; received in revised form 13 July 2005; accepted 18 August 2005

Abstract The effect of emotions on pain perception is generally recognized but the underlying mechanisms remain unclear. Here, emotions related to pain were induced in healthy volunteers using hypnosis, during 1-min immersions of the hand in painfully hot water. In Experiment 1, hypnotic suggestions were designed to induce various positive or negative emotions. Compared to a control condition with hypnoticrelaxation, negative emotions produced robust increases in pain. In Experiment 2, induction of pain-related anger and sadness were found to increase pain. Pain increases were associated with increases in self-rated desire for relief and decreases in expectation of relief, and with increases in arousal, negative affective valence and decreases in perceived control. In Experiment 3, hypnotic suggestions specifically designed to increase and decrease the desire for relief produced increases and decreases in pain, respectively. In all three experiments, emotion-induced changes in pain were most consistently found on ratings of pain unpleasantness compared to pain intensity. Changes in pain-evoked cardiac responses (R–R interval decrease), measured in experiments 2 and 3, were consistent with changes in pain unpleasantness. Correlation and multiple regression analyses suggest that negative emotions and desire for relief influence primarily pain affect and that pain-evoked autonomic responses are strongly associated with pain affect. These results confirm the hypothesized influence of the desire for relief on pain perception, and particularly on pain affect, and support the functional relation between pain affect and autonomic nociceptive responses. This study provides further experimental confirmation that pain-related emotions influence pain perception and painrelated physiological responses. q 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. Keywords: Experimental pain; Pain affect; Emotion Desire for relief; Hypnosis; Human

1. Introduction Pain is defined as a sensory and affective experience (Merskey and Spear, 1967; Melzack and Casey, 1968; Price, 1999). Furthermore, a separation has been proposed between primary and secondary pain affect. ‘Second stage pain affect’ encompasses negative emotions (e.g. sadness) brought about by cognitive processes underlying the elaboration of meanings and the evaluation of the significance and future implications of pain (Price, 1999). * Corresponding author. E-mail address: [email protected] (P. Rainville).

In the present study, we examine the influence of secondary affective processes related to pain on pain sensation and primary affective responses. Clinical pain correlates positively with sustained negative emotions of fear-anxiety and sadness-depression related to the pain condition, as well as anger mainly directed at oneself (Fernandez and Milburn, 1994; Fernandez and Turk, 1995; Okifuji et al., 1999; Huyser and Parker, 1999; Keefe et al., 2001). Catastrophizing and the fear of pain have been shown to contribute to pain severity, distress, and disability (Sullivan and D’Eon, 1990; Sullivan and Neish, 1998; Crombez et al., 1999; Vlaeyen and Crombez, 1999; Vlaeyen and Linton, 2000; Eccleston et al., 2001; Sullivan et al., 2001a,b).

0304-3959/$20.00 q 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.pain.2005.08.022

P. Rainville et al. / Pain 118 (2005) 306–318

However, most clinical studies are based on correlative approaches, and it is difficult to establish the direction of causality between pain and emotions. The relation between pain and emotion has been proposed particularly between pain unpleasantness and feelings of depression, anxiety, frustration, and fear in chronic pain patients (Wade et al., 1990; 1996). According to the model proposed by Price (1999) and substantiated by Wade et al. (1990, 1996), pain-related emotions (i.e. second-stage pain affect) are triggered by the immediate unpleasantness of pain (first-stage pain affect) as a function of the context and cognitive interpretation of the meaning of pain and the anticipation of future consequences. However, this model does not include a recursive effect of pain-related emotions on pain. We have previously used hypnotic suggestions specifically designed to modulate separately pain sensation intensity and the immediate unpleasantness of pain (Rainville et al., 1999) to demonstrate the role of different brain areas in those dimensions of the pain experience (Rainville et al., 1997; Hofbauer et al., 2001; Rainville, 2002). In those studies, we have found that the modulation of pain intensity produces parallel changes in pain unpleasantness while the specific modulation of pain unpleasantness could be largely independent from changes in pain sensation intensity. We also found changes in pain-evoked heart rate responses correlated to changes in pain unpleasantness. Here, we developed hypnotic suggestions to induce different emotional states related to pain (second-stage pain affect) in order to test their effects on the sensory (pain intensity) and primary affective responses (pain unpleasantness and autonomic response) evoked by experimental pain in groups of normal volunteers. We further examine the possible experiential mediators of the interaction between pain and emotions. Physiological measures were included in Experiment 2 (ECG and respiration) and 3 (ECG) to further test the hypothesized association between autonomic activity and pain unpleasantness.

307

hypnotic susceptibility (meanGSD, min–max) in Experiment 1 (5.8G3.2, 0–12), 2 (5.0G3.8, 0–12), and 3 (5.3G3.2, 0–10). All procedures were approved by the ethics committee of the University of Montreal and all subjects provided written informed consent. 2.2. Pain stimulation Pain was induced experimentally by the immersion of the hand in circulating water for 1 min. Temperature was adjusted individually (45.0–47.5 8C) in pre-experimental trials to produce pain that subjects could tolerate for 1 min and that produced pain intensity rated between 40 and 80 (numerical-visual pain scale of 0–100; Rainville et al., 1992). Stimulations were applied to one (left hand in Experiment 2) or both hands alternatively (Experiments 1 and 3) and an interval of at least 5 min separated successive trials to minimize sensitization. 2.3. Experimental procedure and measures In all three experiments, subjects were first explained the pain test and the different scales used to evaluate pain and emotion. Preexperimental tests were administered to familiarize subjects with the pain stimulus and individually establish the adequate temperature for the experiment. Two pre-hypnotic control trials were then performed and served as each subjects’ baseline. Hypnosis was then induced with the SHSS-A. The different emotional induction conditions were administered in each experiment as described below. Suggestions were formulated to induce emotional states in relation to pain (see Annex 1). In all three experiments, we also included a hypnotic relaxation condition with no specific suggestions to induce emotions as an additional control for the non-specific effect of hypnotic induction on pain. Each experimental condition was administered twice in successive trials and the order of the conditions was counterbalanced between subjects. Suggestions were given continuously for 1 min immediately before and during the stimulation. After each trial, subjects rated the intensity and the unpleasantness of pain on 0–100 scales (Rainville et al., 1992). Subjects also rated the emotions experienced using different sets of scales in each experiment (see below). Between each pair of trials performed in an emotion conditions, subjects were instructed to relax, clearing their minds of any feelings related to the prior pain experience or emotional state.

2. Methods 2.1. Subjects Three groups of healthy volunteers were recruited from students and staff at the University of Montreal. A group of 26 subjects participated in Experiment 1 (8 women and 18 men; mean age GSD: 27G9 y), 20 subjects participated in Experiment 2 (8 women and 12 men; mean age GSD: 26G7 y), and 23 subjects participated in Experiment 3 (14 women, 9 men; mean age GSD: 25G6 y). Subjects were tested for hypnotic susceptibility during the experiment using the Stanford Hypnotic Susceptibility Scale form A (SHSS-A; French translation; (Bourassa and Leclerc, 1991)). This provided an independent index of responsiveness to hypnotic suggestions but did not constitute a selection criterion. The sample included subjects with high, moderate and low

2.3.1. Experiment 1 In Experiment 1, hypnotic suggestions were specifically designed to elicit the following five states in separate trials: sadness, anger, fear, anticipation of relief, and satisfaction-pride to tolerate pain easily (see Annex 1). After each trial, subjects were asked to report all the emotions they felt during pain using an open ended list of emotional states, and to rate the overall valence of the emotions felt on a scale ranging from the most intense negative emotion (K10) to the most intense positive emotion (C10), with 0 defined as neutral. 2.3.2. Experiment 2 In Experiment 2, we selected the two most effective experimental conditions tested in Experiment 1, sadness and anger, to examine further the dimensions of emotional experience

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that best predicted changes in pain. Based on an experiential model of emotions, we further asked subjects to rate their experienced desire for relief and their expectation of relief on 0–10 scales (Price and Barrell, 1980; Price et al., 1980; Price and Barrell, 1984). Subjects also rated their felt affective valence (positive–negative), arousal (high/excited–low/calm), and perceived control (being in control–being controlled) during the stimulation using the selfassessment manikin scales (SAM; Lang, 1980). In addition to those self-report measures of pain and emotions, we monitored ECG and respiratory activity to determine whether emotion-related changes in pain were associated with changes in pain-induced physiological activity. ECG was recorded using a standard 3 leads montage. Respiration was monitored using a tension transducer attached to a strain-gage belt placed over the lower floating rib and adjusted individually in the preexperimental set up phase to produce the maximal deflection during normal breathing. Physiological activity was acquired at 1000 Hz using the MP150 system and AcqKnowledge software (Biopac Systems Inc.). Recordings were monitored online during the experiment and visually inspected off-line. Recording artifacts were identified and corrected by interpolation. Instantaneous R-R intervals were calculated from the ECG using a peak detection algorithm to detect successive R-waves and obtain a continuous R–R tachogram. The respiratory signal was smoothed using the mean of a 1-sec moving window and transformed to obtain instantaneous (cycle-by-cycle) measurements of period and amplitude. Complete physiological recordings were obtained in 19 participants (data sets were incomplete or irrecoverable in four subjects). Several dependent variables were obtained from the physiological recordings. We calculated pain-evoked changes in the mean relative amplitude and period of respiration. In addition to the mean heart rate, we derived indices of heart rate variability. High frequency RR variability is associated with parasympathetic activity, is generally associated with the amplitude of the respiratory sinus arrhythmia, and has been related to the experience of emotions (George et al., 1989; Yeragani et al., 1991; Yeragani et al., 1994; Friedman and Thayer, 1998; Rao and Yeragani, 2001). We first extracted the mean difference between consecutive R–R intervals (R–RiC1K R–Ri) to index R–R interval variability (linear index). We also performed an exact Fast Fourier Transform (FFT) analysis on 215 samples (32, 768 s) of the continuous R–R tachogram ending at the end of the 60 s pain test or pre-stimulus period. We calculated the integral of the high frequency components (0.15– 0.4 Hz) as another index of parasympathetic activity (frequencydomain index of RR variability). All analysis were performed following the guidelines of the Task force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (1996). 2.3.3. Experiment 3 In Experiment 3, we tested a new set of hypnotic suggestions to modulate specifically the desire for relief (Annex 1), one of the emotional dimension that best predicted changes in pain in Experiment 2. Subjects rated their experienced desire for relief and their expectation of relief on 0–10 scales after each trial. The ECG was also recorded throughout this experiment but only the mean RR-interval was analyzed.

2.4. Data analysis Ratings of emotions (Experiments 1–2), and desire and expectation for relief (Experiment 3) were first analyzed using repeated measures ANOVA and follow-up contrasts to verify that the target emotional states were induced by the suggestions. Twotailed P-values were adjusted using the Bonferroni correction for multiple comparisons according to the number of contrasts performed within each experiment. In each experiment, effect sizes estimates were calculated for the contrast between each emotion condition and the hypnotic relaxation control, based on the pooled SD, r-adjustment, and Hedges’ bias correction (Cohen, 1988). Pain modulation, indexed by changes from the pre-hypnotic control condition, was computed on pain intensity (INT) and unpleasantness (UNP) ratings (Experiments 1–3) and on the mean cardiac pain-responses (Experiments 1–3; change in the mean R–R interval decrease induced by pain). Correlation analyses between pain modulation indices of pain and cardiac responses were computed using Bonferroni-corrected thresholds, and followed by linear regression models. The moderating effect of hypnotic susceptibility was tested using non-parametric correlations (Spearman-rho).

3. Results 3.1. Experiment 1 3.1.1. Emotional experience The self-report measures of emotion confirmed that the hypnotic suggestions were effective to induce emotions in Experiment 1. Out of a total of 26 subjects, most subjects reported feeling the target emotional state, or experienced feelings congruent with that state, in relaxation (nZ24; e.g. well-being), sadness (nZ22; e.g. sad and discouraged), anger (nZ23; e.g. anger and frustration), fear (nZ18; e.g. fear and anxiety), anticipation of relief (nZ13; e.g. relief), or satisfaction (nZ20; e.g. satisfaction, pride or wellbeing). The mean emotional intensity rating and the results of the statistical tests comparing the experimental conditions are reported in Table 1. The mean emotional rating was close to neutral for both the pre-hypnotic control and the hypnotic relaxation condition and did not differ significantly from each other. Negative emotional states were reported in response to suggestions for sadness, anger, and fear while slightly positive emotional states were reported following suggestions for anticipation of relief and satisfaction to tolerate pain easily. The comparison of emotion intensity ratings across all conditions was highly significant (see Table 1). Anger and to a lesser extent sadness and fear produced some negative emotions relative to the pre-hypnotic control. In all three cases, the emotion felt was also more negative than the hypnotic relaxation condition although the effect of fear failed to reach significance based on the conservative Bonferroni correction. Anticipation of relief produced only small and nonsignificant increases in positive emotions relative to both

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Table 1 Results of the within-subject comparison of mean (SD) ratings of emotion and pain self-reports in Experiment 1 Dependent variable

Repeated measures ANOVA

Pre-hyp. baseline

Hypnotic relaxation

Sadness

Anger

Fear

Anticipation of relief

Satisfaction

Emotion intensity (K10 to C10) Pain Intensity (0–100) Pain Unpleasantness (0–100)

F(6,150)Z17.3 P!0.001 F(5,125)Z4.04 P!0.001 F(5,125)Z11.5 P!0.001

K0.6 (0.8)

0.5 (0.6)

K3.9ad (0.8)

K4.2bd (0.7)

K2.8ac (0.7)

1.2 (0.6)

2.8ac (0.6)

58.8 (17.0)

55.2 (21.6)

58.8 (22.9)

62.3c (20.2)

56.9 (21.6)

49.9a (20.8)

47.5bc (18.4)

45.4 (23.6)

39.7 (23.4)

59.6ad (24.4)

59.5ad (23.7)

54.5c (22.2)

33.3a (20.3)

33.9a (24.5)

a–d: Follow-up pairwise contrasts; P-corrected based on a Bonferroni correction applied for 18 contrasts (6 contrasts emotion vs control * 3 analyses). a–b: Significantly different from Pre-hypnotic (Pre-Hyp.) Baseline at a: P-uncorrected!0.05, b: P-corrected!0.05. c–d: Significantly different from Hypnotic Relaxation at c: P-uncorrected!0.05, d: P-corrected!0.05.

the pre-hypnotic and the hypnotic relaxation control. Suggestions for satisfaction produced some positive emotional states relative to both the pre-hypnotic and the hypnotic relaxation controls but these effects did not survive the conservative Bonferroni correction. Taken together, these self-report measures indicated that the hypnotic suggestions for sadness and anger produced negative emotions most consistently while suggestions for fear produced weaker negative emotions. In contrast, suggestions for satisfaction yielded some positive emotions while suggestions for anticipation of relief did not produce significant changes in emotion. 3.1.2. Effects of emotions on pain The induction of emotions produced highly significant changes in both pain intensity and pain unpleasantness, as shown in Table 1. Follow-up contrasts indicated that pain intensity decreased in anticipation of relief and satisfaction relative to the pre-hypnotic baseline. Pain intensity also increased in anger and decreased in satisfaction relative to the hypnotic relaxation condition. However, only the effect of satisfaction relative to the pre-hypnotic baseline remained significant on pain intensity after the Bonferroni correction. Pain unpleasantness increased in the negative emotion conditions, particularly in contrast to the hypnotic

relaxation condition. Effect sizes and confidence intervals confirmed the large to very large effects produced by sadness and anger on pain unpleasantness (Table 2). In contrasts, the decreases in pain observed in the positive emotion conditions did not significantly exceed those produced by hypnotic relaxation and were of only small to moderate sizes (Table 2). These results generally confirmed the increases in pain during negative emotions with the most robust effects found for sadness and anger on pain unpleasantness. 3.1.3. Relation between changes in emotion and changes in pain Trials in which subjects reported the target emotion, or an emotional congruent with that target, were included in correlation analyses testing for the effect of emotion intensity on pain modulation (i.e. changes relative to the pre-hypnotic baseline). Overall, larger increases in pain were found in response to more negative emotions across conditions. This correlation was stronger for pain unpleasantness (Pearson-R: pain unpleasantness: RZK0.76, P! 0.001; Figure 1) than pain intensity (RZK0.46, P!0.001). This effect also reached significance within emotion conditions on pain unpleasantness for sadness (RZK0.69, P!0.01), anger (RZK0.79, P!0.001), and fear

Table 2 Effect sizes (confidence interval) in Experiment 1, 2, and 3 for the contrast between each emotion conditions and the hypnotic relaxation control on pain intensity and pain unpleasantness

Experiment 1

Experiment 2 Experiment 3

Sadness Anger Fear Anticipation of relief Satisfaction Sadness Anger High Desire for Relief Low Desire for Relief High Vs Low Desire

Pain intensity

Pain unpleasantness

C0.27 (K0.28 to C0.81) C0.57 (C0.02 to C1.13) C0.11 (K0.43 to C0.66) K0.40 (K0.95 to C0.15) K0.62 (K1.17 to K0.06) C1.03 (C0.37 to C1.69) C1.35 (C0.66 to 2.04) C0.34 (K0.24 to C0.93) K0.65 (K1.24 to K0.05) C1.12 (C0.50 to C1.74)

C0.96 (0.38 to 1.53) C1.27 (0.67 to 1.86) C0.75 (0.19 to 1.31) K0.49 (K1.05 to C0.06) K0.44 (K0.99 to C0.11) C1.31 (C0.63 to C1.99) C1.57 (C0.86 to C2.28) C0.71 (C0.11 to C1.30) K1.53 (K2.19 to K0.87) C1.60 (C0.93 to C2.26)

Note: Effect sizes are considered large to very large (in bold) for standardized differences O0.80 and O1.00, respectively (Cohen, 1988).

Change in Pain Unpleasantness (Emotion-baseline)

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100.0 R2 = 0.57 Relaxation 50.0

Sadness Anger

-20.0

0.0 -10.0 0.0

10.0

20.0

Fear & Anxiety Relief

-50.0

anger relative to the hypnotic relaxation condition. Relatively stronger effects were found again on unpleasantness for both sadness and anger. Effect sizes estimates were very large for both pain intensity and unpleasantness, in both sadness and anger (Table 2).

Satisfaction

-100.0 Change in Emotion (Emotion-baseline)

Fig. 1. Correlation between changes in pain unpleasantness and changes in emotion relative to the pre-hypnotic baseline control, across the emotional conditions in Experiment 1.

(RZK0.73, P!0.01; P-values adjusted using the Bonferroni correction for 12 correlations). Partial correlations remained significant between emotion intensity and unpleasantness after accounting for changes in pain intensity (across all emotion conditions: RZK0.68, P! 0.001; within emotion conditions: sadness, RZK0.69, P! 0.01, anger, RZK0.76, P!0.001, and fear, RZK0.59, Puncorrected!0.05). In contrast, there was no residual effect of emotion on pain intensity after accounting for changes in pain unpleasantness (all P’sO0.05). Taken together, these correlations confirmed that the increase in pain observed in the negative emotion condition was related to the increase in negative emotion and that this effect was observed mainly on pain unpleasantness. 3.2. Experiment 2 3.2.1. Effects of sadness and anger on pain In Experiment 2, we re-examined the effects of sadness and anger on pain. A highly significant effect of the emotion condition was found for both pain intensity and unpleasantness, as reported in Table 3. Within-subjects contrasts indicated that pain intensity increased in both sadness and

3.2.2. Changes in experiential dimensions of emotions In order to examine the potential mediators of emotioninduced changes in pain, we examined the self-ratings of various dimensions of subjective experience (Table 3). Desire for relief showed highly significant effects with increases found in both sadness and anger relative to the hypnotic relaxation condition and the pre-hypnotic baseline. Expectation of relief decreased in both sadness and anger relative to the hypnotic relaxation condition and the prehypnotic baseline, although the contrasts with hypnotic relaxation did not survive the Bonferroni correction. Highly significant effects were also found on valence, arousal, and perceived control (Table 3). Sadness and anger produced some increases in negative valence and arousal, particularly in contrast to hypnotic relaxation. Perceived control decreased in both sadness and anger but within-subject contrasts did not reach significance after the Bonferroni correction. 3.2.3. Relation between changes in emotion and changes in pain Correlation analyses were performed to examine the relation between pain and the emotion-related variables (Padjusted using Bonferroni correction for 12 correlations, i.e. for desire for relief, expectation of relief, valence, arousal, dominance, and RR-interval by pain intensity and pain unpleasantness). Increases in pain unpleasantness, and to a lesser degree pain intensity, were associated with stronger desire for relief (UNP: RZ0.83, P!0.001; INT: RZ0.74, P!0.001) and to lower expectation of relief (UNP: RZK0.65, P!0.001; INT: RZK0.36, PZ0.07, ns). Similarly, pain increased with negative valence (UNP: RZ0.76, P!0.001; INT: RZ0.65, P!0.001) and higher arousal (UNP: RZ0.67, P!0.001; INT: RZ0.52, P! 0.001), and with decreases in perceived control (UNP:

Table 3 Results of the within-subject comparison of mean (SD) ratings of pain and emotion self-reports in Experiment 2 Dependent variable

Repeated measures ANOVA

Pre-hyp. baseline

Hypnotic relaxation

Sadness

Anger

Pain intensity Pain unpleasantness Desire for relief Expectation of relief Valence Arousal Perceived control

F(3,57)Z10.4 P!0.001 F(3,57)Z17.0 P!0.001 F(3,57)Z16.8 P!0.001 F(3,57)Z10.9 P!0.001 F(3,57)Z15.8 P!0.001 F(3,57)Z10.6 P!0.001 F(3,57)Z6.1 PZ0.001

52.8 (14.9) 37.0 (18.5) 3.7 (2.1) 8.6 (1.6) 5.1 (1.4) 2.9 (1.5) 6.2 (2.1)

49.8 (23.7) 39.2 (22.0) 4.6 (3.1) 7.7 (3.1) 4.8 (1.4) 2.7 (1.2) 5.8 (1.8)

66.0ad (22.7) 62.6bd (27.7) 7.0bd (3.0) 6.1bc (2.8) 6.9bd (1.5) 4.6ad (2.0) 4.6ac (2.3)

70.1bd (18.4) 65.4bd (24.9) 7.3bd (2.6) 6.2bc (2.7) 6.6bd (1.5) 4.8ad (2.3) 4.9ac (2.1)

a–d: Follow-up pairwise contrasts; P-corrected is based on a Bonferroni correction applied for 21 contrasts (3 contrasts emotion Vs control * 7 analyses). a–b: Significantly different from Pre-hypnotic (Pre-Hyp.) Baseline at a: P-uncorrected!0.05, b: P-corrected!0.05. c–d: Significantly different from Hypnotic Relaxation at c: P-uncorrected!0.05, d: P-corrected!0.05.

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Table 4 Stepwise regression models predicting changes in pain intensity and unpleasantness from changes in experiential dimensions of emotions in Experiment 2 Model # and dependent variable

Predictor tested

Adjusted-R2

F (P!)

Beta

T (P!)

1. Pain intensity

Desire for relief Expectation of relief (excluded) Desire for relief Expectation of relief Pain intensity Expectation of relief Desire for relief Valence Arousal Perceived control (excluded) Valence Arousal Perceived control (excluded) Pain intensity Valence Arousal Perceived control (excluded)

0.54

66.5 (0.001)

C0.74

8.16 (0.001)

0.70

67.7 (0.001)

0.84

101.2 (0.001)

0.45

23.8 (0.001)

C0.69 K0.23 C0.56 K0.31 C0.22 C0.52 C0.26

7.48 (0.001) K2.45 (0.05) 6.98 (0.001) K4.57 (0.001) 2.35 (0.05) 4.50 (0.001) 2.25 (0.05)

0.67

58.6 (0.001)

C0.57 C0.38

6.42 (0.001) 4.30 (0.05)

0.81

81.3 (0.001)

C0.51 C0.31 C0.25

6.38 (0.001) 3.89 (0.001) 3.54 (0.001)

4. Pain intensity

5. Pain unpleasantness

6. Pain unpleasantness

RZK0.53, P!0.001; INT: RZK0.47, PZ0.0025). Those effects remained significant on pain unpleasantness after accounting for changes in pain intensity (Partial correlations; all P-corrected!0.05 except for perceived control: P-uncorrectedZ0.03). In contrast, significant correlations with changes in pain intensity did not reached significance after accounting for changes in pain unpleasantness (Partial correlations; all P-correctedO0.05). This suggests that emotions produced changes in pain unpleasantness over and beyond their effects on pain intensity. Stepwise linear regression models were further tested to predict changes in pain from changes in emotions (Table 4). Models were first tested including desire for relief and expectation of relief as predictor variables. Desire for relief was the only significant variable retained by the model predicting changes in pain intensity (Model 1). In contrast, pain unpleasantness was predicted by both desire for, and expectation of, relief (Model 2). Adding pain intensity to the model predicting pain unpleasantness increased the fit of the model with all three factors contributing significantly to the effect (Model 3). Other models were tested using the SAM variables. Both pain intensity and pain unpleasantness were predicted by valence and arousal (Models 4 and 5, respectively). Again, adding pain intensity to the model predicting pain unpleasantness increased the fit of the model with intensity, valence and arousal contributing significantly to the effect (Model 6). Changes in perceived control did not contribute significantly to those models.

condition as shown in Figure 2 (Pain X Emotion: F(3,57)Z 7.02, PZ0.0004). The pain-related physiological response was calculated by subtracting the activity measured during the pain stimulus from that recorded prior to the pain stimulus on each trial to compare emotion conditions. There was no significant effect of hypnotic relaxation alone on pain-evoked responses (pre-hypnotic baseline Vs hypnotic A. Experiment 2 Changes in R-R Interval (s)

3. Pain unpleasantness

-0.06

-0.04

-0.02

0 Baseline

Sadness

Anger

Relaxation

High desire

Low desire

-0.06

-0.04

-0.02

0 Baseline

3.2.4. Changes in pain-evoked physiological responses Pain produced a highly significant decrease in the mean R–R interval (ANOVA, main effect of Pain; F(1,57)Z14.4, PZ0.001). However, this effect interacted with the emotion

Relaxation

B. Experiment 3 Changes in R-R Interval (s)

2. Pain unpleasantness

Fig. 2. Mean (GSEM) changes in the cardiac response evoked by pain (decrease in the R–R interval) in Experiment 2 (A) and 3 (B). Pain-evoked responses increase significantly during sadness, anger, and high desire for relief (see text).

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Table 5 Results of the within-subject comparison of mean (SD) ratings of emotion and pain self-reports in Experiment 3 Dependent variable

Repeated measures ANOVA

Pre-hyp. baseline

Hypnotic relaxation

High desire

Low desire

Desire for relief Expectation of relief Pain intensity Pain unpleasantness

F(3,66)Z18.4 P!0.001 F(3,66)Z3.8 PZ0.01 F(3,66)Z11.3 P!0.001 F(3,66)Z22.5 P!0.001

5.7 (2.0) 8.9 (1.5) 69.0 (14.4) 66.2 (15.9)

4.9a (2.4) 8.6 (1.8) 59.4b (15.8) 53.7b (19.7)

6.4d (2.5) 8.0ac (2.3) 62.3a (19.3) 60.5c (24.2)

3.7bd (2.3) 9.0 (1.5) 53.7bc (14.4) 41.5bd (16.8)

a–d: Follow-up pairwise contrasts; P-corrected is based on a Bonferroni correction applied for 12 contrasts (3 contrasts emotion Vs control * 4 analyses). a–b: Significantly different from Pre-hypnotic (Pre-Hyp.) Baseline at a: P-uncorrected!0.05, b: P-corrected!0.05. c–d: Significantly different from Hypnotic Relaxation at c: P-uncorrected!0.05, d: P-corrected!0.05.

relaxation; F(1,19)Z1.8, PZ0.19). Larger increases in the cardiac responses were observed in both negative emotions relative to hypnotic relaxation control (sadness: F(1,19)Z9,3, PZ0.007; anger: F(1,19)Z11.7, PZ0.003). This indicated an increase in the cardiac response to pain during sadness and anger. Pain was also associated with significant decreases in R–R interval variations (RRiC1–RRi; ANOVA, main effect of Pain F(1,57)Z10.4, PZ0.005), in the high frequency component of R–R variability (FFT analysis; F(1,57)Z12.3, PZ0.003), and in mean respiratory period (F(1,57)Z20.9, P!0.001). However, the interaction between the pain-response and the emotion conditions approached significance only on the R–R interval variations (Pain X Emotion: F(3,57)Z2.58, PZ0,051; all other P’sO0.1). These physiological variables were not considered further. Emotion-related increases in the cardiac response (i.e. decrease in R–R interval) were correlated with emotioninduced increases in pain unpleasantness and to a lesser degree in pain intensity (UNP: RZ0.59, P!0.001; INT: RZ0.48, PZ0.002). The correlation with pain unpleasantness remained significant after accounting for changes in pain intensity (Partial correlation, RZ0.38, PZ0.04) but the correlation with pain intensity was completely accounted for by changes in unpleasantness (RZ0.02, ns). The addition of cardiac pain-responses to the regression models described in Table 4 led to modest but significant (P!0.05) increases in the fit of Models 2 (adjusted-R2Z 0.72), 4 (adjusted-R2Z0.46), 5 (adjusted-R2Z0.71), and 6 (adjusted-R2Z0.82). Additional post-hoc correlation analyses between changes in cardiac responses and changes in dimensions of emotions were generally significant at P-unccorrected! 0.05. However, most correlations did not reach significance after accounting for changes in pain intensity or pain unpleasantness (Partial correlations; P’sO0.05). There was only one exception with the increase in arousal moderately or weakly correlated with increases in the cardiac painresponse both before (RZ0.55, P-uncorrected!0.00001), and after accounting for changes in pain intensity (RZ0.40, P-uncorrectedZ0.002) and unpleasantness (RZ0.27, Puncorrected!0.05).

3.3. Experiment 3 3.3.1. Changes in desire for relief In Experiment 3, we first verified the effectiveness of our hypnotic intervention to induce changes in desire for relief, the specific target of the hypnotic suggestions in this experiment. Highly significant effects of the hypnotic suggestions were found on desire for relief, as reported in Table 5. Hypnotic relaxation produced a small decrease in desire for relief compared to the pre-hypnotic baseline. The high desire condition produced increases and the low desire condition produced decreases in self-ratings of desire for relief relative to the hypnotic relaxation control. Direct comparison of high and low desire confirmed the highly significant modulation of the felt desire (F(1,22)Z34.7, P!0.00001). A modest but significant effect was also noted in ratings of expectation with a small decrease observed in the high desire condition (Table 5). However, this latter effect did not survive the Bonferroni correction. All other contrasts on expectation did not approach significance (all P-uncorrectedS0.10). These effects confirmed that our procedure induced robust changes mainly in the felt desire for relief. 3.3.2. Effects of desire for relief on pain Highly significant effects of the experimental conditions were found on pain intensity and pain unpleasantness, as reported in Table 5. Compared to the pre-hypnotic control, hypnotic relaxation produced a small but significant decrease in pain intensity and unpleasantness. Low desire for relief produced significant decreases in pain relative to both hypnotic relaxation and the pre-hypnotic baseline, with a very large effect size observed on ratings of unpleasantness (Table 2). High desire for relief produced small to moderate effects on pain intensity and unpleasantness, respectively, but those effects did not reach the Bonferronicorrected criterion for significance (Table 5). Direct contrast between the high and low desire conditions was highly significant on both pain intensity (F(1,22)Z11.1, PZ0.003) and unpleasantness (F(1,22)Z32.7, P!0.001). Those effects can be considered very large based on the effect size estimates reported in Table 2.

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3.3.3. Relation between changes in desire for relief and changes in pain In order to examine more directly the relation between pain and desire for relief, we calculated the changes between the high and low desire conditions for each dependent variable. Modulation of pain unpleasantness, and to a lesser extent pain intensity, was positively correlated to the modulation of desire for relief (Figure 3; UNP: RZ0.72, P!0.001; INT: RZ0.57, PZ0.03; P-adjusted using Bonferroni correction for six correlations, i.e. desire, expectation for relief and RR-interval by pain intensity and pain unpleasantness). The correlation with pain unpleasantness remained highly significant after removing the effect of pain intensity (Partial correlation: RZ0.56, PZ0.04). In contrast, the correlation with pain intensity did not reach significance after accounting for changes in unpleasantness (Partial correlation: RZ0.20, PO0.10, ns). Changes in pain were negatively correlated to expectation but those effects did not approach significance (UNP: RZK0.32, PO0.10; INT: RZK0.39, PO0.10). This suggests that the manipulation of desire for relief produced mainly changes in pain unpleasantness, independent of changes in expectation of relief or pain intensity. Stepwise regression model predicting changes in pain intensity and unpleasantness from changes in desire for relief and expectation confirmed that desire for relief was the main explanatory factor (UNP: adjusted-R2Z0.49, P! 0.001; INT: adjusted-R2Z0.29, PZ0.005). Forcing expectation into the models led to negligible and non-significant increases in the fit (P’sO0.10). Similarly, forcing pain intensity or pain unpleasantness in models predicting pain unpleasantness and pain intensity, respectively, produced only small increases in model fit that did not reach significance (P’sO0.05).

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3.3.4. Modulation of pain-evoked cardiac responses There was a highly significant decrease in the R–R interval during pain corresponding to the typical cardiac response to noxious stimuli (main effect of pain: F(1,54)Z 11.8, PZ0.003). However, this cardiac response varied across the experimental conditions as illustrated in Figure 2B (interaction: F(3,54)Z5.80, PZ0.002). The pain-evoked cardiac response did not vary significantly between the pre-hypnotic baseline and the relaxation condition or between the low desire condition and the prehypnotic baseline or the hypnotic relaxation control (all P’sO0.3, ns). However, the high desire condition produced a significant increase in the cardiac response compared to the hypnotic relaxation control (F(1,18)Z9.72, PZ0.03) and the low desire condition (F(1,18)Z12.11, PZ0.016; P’s adjusted for six contrasts). The modulation of the R–R responses observed in the target conditions (high minus low desire for relief) was marginally correlated to the modulation of pain unpleasantness (RZK0.51, P-uncorrectedZ0.02) but not with pain intensity (RZK0.19, P-uncorrectedZ0.43). The correlation between changes in the cardiac response and unpleasantness did not decrease after accounting for changes in pain intensity (partial correlation: RZK0.52, P-uncorrectedZ0.03). However, the inclusion of the changes in cardiac response to the regression analyses predicting changes in pain did not significantly improve the fit of models described above (see Section 3.3.3). We tested one additional stepwise regression model to predict changes in the cardiac response from experiential dimensions of pain (intensity and unpleasantness) and emotions (desire and expectation). Pain unpleasantness was the only variable contributing significantly to the model (adjusted-R2Z0.22, P!0.02).

Changes in Pain Unpleasantness (High-Low)

3.4. Moderating effect of hypnotic susceptibility

60 R2 = 0.51 50 40 30 20 10 0 -10 -20 -2

0

2

4

6

8

Changes in Desire for relief (High-Low) Fig. 3. Correlation between changes in pain unpleasantness and changes in desire for relief observed in the high and low desire conditions in Experiment 3.

In all three experiments, we secondarily examined the moderating effect of hypnotic susceptibility (SHSS-A score) on the modulation of pain produced by the emotions induced by the hypnotic suggestions. In all three experiments, a median split of the groups based on the SHSS-A score confirmed that the induction of emotions and the modulation of pain were generally more pronounced in subjects with high hypnotic susceptibility. The effect of hypnotic susceptibility was then tested statistically on the pain-related variables using correlation analyses (Spearman-rho, 2-tailed P-adjusted using Bonferroni correction for the number of bivariate correlations tested within each experiment). In Experiment 1, the increase in pain unpleasantness relative to the pre-hypnotic baseline condition observed in the negative emotion condition was correlated to the hypnotic susceptibility score (P-corrected for 10 tests, i.e. pain intensity and unpleasantness by SHSSA in the five emotion conditions: sadness rhoZ0.71, P!0.001; anger rhoZ0.45, P-uncorrectedZ0.02; fear

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rhoZ0.66, PZ0.003; anticipation of relief and satisfaction, rho’sO0.35, P-uncorrectedO0.05, ns). The correlation between the SHSS-A score and pain intensity approached significance only in fear (rhoZ0.32, P-uncorrectedZ0.03; all other P-uncorrectedO0.10). In Experiment 2, the correlations were marginally significant on pain intensity and unpleasantness in anger (intensity: rhoZ0.54, P-uncorrectedZ0.02; unpleasantness: rhoZ0.54, P-uncorrectedZ0.02) and only on unpleasantness in sadness (rhoZ0.56, P-uncorrectedZ0.01). However, subjects with higher hypnotic susceptibility also showed a stronger modulation of the cardiac response by sadness (rhoZ0.69, P-corrected for 6 testsZ0.004, anger: rhoZ 0.40, P-uncorrectedZ0.08). In Experiment 3, pain modulation in the high and low desire condition (high-low) was correlated with the SHSS-A score on pain intensity (rhoZ0.59, P-correctedZ0.01) but this effect did not reach significance on pain unpleasantness (rhoZ0.39, P-uncorrectedZ0.07, ns). Taken together these correlations are generally consistent with the interpretation that the emotions reported and the pain modulatory effects are related to the subjects’ responsiveness to hypnosis, based on an independent criterion obtained in a standard hypnotic susceptibility test.

autonomic responses. Possible mediating factors of the hyperalgesic effect of negative emotions include the increase in desire for relief and secondarily the reduction in expectation of relief, as well as the increases in negative valence and arousal.

4. Discussion 4.1. Effects of pain-related emotions on pain The experimental paradigm was developed to induce acute emotional experiences previously found to be associated with clinical pain. In Wade et al. (1990, 1996), pain-related emotions are a function of both pain unpleasantness and additional cognitive factors involved in the interpretation of pain significance and future outcomes. However, this theoretical account did not support recursive effects of pain-related emotions on pain perception. Here, the experimental manipulation of pain-related emotions allowed us to demonstrate such influence. While clinical findings have shown that higher levels of pain are generally associated with more negative emotions, the experimental approach used here further demonstrates that negative emotions related to pain increase pain.

3.5. Summary of results 4.2. Effects of emotion on pain In this study we have observed pain modulation by emotions related to pain and induced by hypnotic suggestions. Experiment 1 demonstrated robust increases in pain during the experience of sadness, anger, and some increase during fear-anxiety. Pain decreases were observed in the positive emotion conditions but these changes did not significantly exceed those produced by hypnotic relaxation alone. In negative and positive emotion conditions respectively, increases and decreases in pain were significantly correlated to the strength of the emotion experienced. In Experiment 2, we replicated the effect of sadness and anger and further demonstrated that the increases in pain were correlated to increases in desire for relief and decreases in expectation of relief, as well as increases in negative valence and felt arousal, and decreases in perceived control. In Experiment 3, hypnotic suggestions specifically designed to modulate the desire for relief produced corresponding changes in pain. In all three experiments, the effect of emotions was systematically larger on pain unpleasantness than pain intensity. Partial correlation and regression analyses confirmed that the effects of emotion on pain unpleasantness could not be fully explained by changes in pain intensity. In both experiments 2 and 3, pain-evoked cardiac responses were modulated by emotions and those changes were correlated most consistently with changes in pain unpleasantness. Taken together, those results demonstrate the effects of negative emotions mainly on pain unpleasantness and confirm a corresponding modulation of pain-evoked

In previous experimental studies, emotions have been typically produced using secondary inducers, independent of the painful stimulus used to assess pain sensitivity. In those studies, pain modulation has been observed in response to emotions and moods induced by films (Zillmann et al., 1996; Weisenberg et al., 1998), affectively charged pictures (De Wied and Verbaten, 2001; Meagher et al., 2001), music (Whipple and Glynn, 1992), taste (Lewkowski et al., 2003), odours (Marchand and Arsenault, 2002; Villemure et al., 2003), and by reading affective verbal statements (Zelman et al., 1991). Those studies have generally provided results consistent with present findings indicating that positive emotions reduce pain while negative emotions increase pain. There is one important exception to this general hyperalgesic effect of negative emotions. The effects of electric shocks (stressor) or the threat of electric shocks have been difficult to interpret, with hyperalgesia reported in the anticipation of the stressor and hypoalgesia produced following the exposure to the stressor (e.g. Rhudy and Meagher, 2000; Rhudy et al., 2004; but also see Rhudy and Meagher, 2003b). In relation to the animal literature, these findings have been suggested to reflect anxiety-induced hyperalgesia in response to the threat of electric shocks and stress or fear-induced analgesia following the prior-exposure to the shock (Rhudy and Meagher, 2000). However, those findings may also relate to a much broader diversity of emotion experienced in those

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conditions. Indeed, Rhudy and Meagher have also shown that subjects experience a variety of other emotional feelings (e.g. surprise), and use some emotional strategies such as humour in response to the threat of, or exposure to, electric shocks (Rhudy and Meagher, 2001; Rhudy and Meagher, 2003a). The specific emotional experiences evoked by the experimental manipulations have been argued to explain important parts of inter-individual variability in pain modulation.

intensity independently from the valence of the odour, while the valence of the odour affected mainly pain unpleasantness independently from the direction of attention. Those results suggest a dissociation between attention- and emotion-related mechanisms with the former affecting primarily sensory processes, and the latter affecting mainly pain affect. Here, we found that pain unpleasantness was more strongly affected by emotions than pain intensity. This is consistent with the notion that primary pain affect is more closely related to emotions.

4.3. Confounding or mediating effects of attention

4.4. Desire and expectation

Attention mechanisms may contribute to emotion-related effects (Villemure and Bushnell, 2002). The experimental studies that rely on ‘secondary inducers’ (e.g. films, pictures, etc.), or a stressor independent of the stimulus used to assess pain, introduce a competition for attention resources. In those conditions, the reduction in pain may be largely explained by a redirection of attention away from pain in favor of the emotional inducer. However, both positive and negative emotions should lead to pain reductions as a function of the distraction produced by the emotional inducer. Here, we must first emphasize that the hypnotic suggestions used were not designed to redirect the subject’s attention away from pain, even in the positive emotions conditions of Experiment 1. On the contrary, emotions were always induced in relation to pain by a reinterpretation of the pain experience and/or the direct suggestions to experience specific emotions related to pain. Second, although we cannot exclude the possibility that positive emotions induced in Experiment 1 and the induction of low desire for relief in Experiment 3 might have reduced the attention to pain, the increase in pain in the negative emotion conditions of Experiments 1 and 2 are inconsistent with a simple distraction from pain. Another possibility is that negative emotions may enhance pain-directed attention. Indeed, increases in attention to, and concern with, somatic signals have been associated with negative emotions and moods (Salovey, 1992; Arntz et al., 1994; Eccleston et al., 1997; Crombez et al., 2002; Mor and Winquist, 2002). Suggestions for negative emotions may have increased the attention allocated to pain while positive emotions and reduced desire for relief may have reduced attention to pain. Accordingly, attention may be conceived as a mediator of emotion effects rather than a confounding factor. However, this does not fully account for the stronger effects of emotions on pain unpleasantness. Attention is generally found to influence both pain sensation intensity and pain unpleasantness equally (Miron et al., 1989) or to have a stronger effect on pain intensity (Villemure et al., 2003). In the study by Villemure et al. (2003), subjects were concurrently presented heat pain stimuli with pleasant or unpleasant odours and they were instructed to attend to the thermal or olfactory stimuli in order to perform a discrimination task. The direction of attention modulated pain

The subjective desire to attain a goal and the expectation that the goal will be reached have been proposed as two critical experiential dimensions predicting emotions (Price and Barrell, 1984). In this model, avoidance goals (e.g. avoiding pain, pain relief, etc.) are associated with strong negative emotions, and possibly pain increases, when they are associated with moderate to high desires and moderate to low expectations that they can be attained. In contrast, positive emotions, and possibly pain decreases, may be experienced only when pain relief is highly desired and highly expected. Desire for relief, and expectation of relief, have been shown to affect both experimental and clinical pain, and increases in relief expectation has been positively associated with placebo analgesia (Price et al., 1980; Price et al., 1999; Vase et al., 2003). In contrast, increases in desire for relief have been associated with increases in pain (Vase et al., 2003). In Experiment 2, we found that the hyperalgesic effects of sadness and anger may be largely explained by increases in desire for relief (Table 1). Furthermore, the specific modulation of the desire for relief in Experiment 3 confirmed that changes in desire for relief leads to proportional changes in pain (Figure 3). These findings demonstrate that the experiential model of emotion predicts changes in pain induced by emotions. We should emphasize that our description of emotionrelated effects based on this experiential model is not in contradiction with other models of emotions. Indeed, we also found that pain-related emotions could be adequately described along the dimensions of valence, arousal and perceived control, according to a motivational theory of emotion (Bradley and Lang, 2000). 4.5. Emotion and pain-related autonomic responses In addition to the changes in the experiential dimensions of emotion, in pain intensity, and in pain unpleasantness, this study demonstrated that the induction of pain-related emotion produces changes in the cardiac pain-response. This demonstrates that pain reports are consistent with objective changes in physiological response. In the models proposed by Price (2000) and Rainville et al., (1999), autonomic nociceptive responses contribute mainly to the affective dimension of pain. Consistent with this possibility, cardiac responses were correlated mainly or exclusively

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with pain unpleasantness. Those changes provide the confirmatory validation of the experiential changes observed in this study and further support the strong association between autonomic responses and pain affect.

5. Conclusion There is a general agreement that emotions influence pain. However, there is only moderate consensus about the specific conditions under which those effects occur, their direction and magnitude, or their underlying mechanisms. The experimental model used here relied on hypnosis, an intervention ideally suited to target and modulate specific aspects of subjective experience. This allowed us to induce emotional states, measure the corresponding changes in various experiential dimensions, and test their effects on pain perception and pain-related physiological responses. Both the desire for, and the expectation of, relief and the valence and arousal dimensions of emotions adequately accounted for the changes in pain. However, although pain relief may adequately reflect the goal of patients in some acute pain situations, the patients’ goals may be extremely diverse in chronic pain situations. Assessing more explicitly those goals and the corresponding desire and expectation may inform about the individual underpinnings of painrelated emotions and their possible influence on pain and suffering.

Appendix A. ANNEX A.1. Suggestions in Experiment 1 (translated from French) A.1.1. Hypnotic Relaxation (Well-being) During the (next) stimulation, you will feel the pain normally. I want you to simply relax. Do not try to resist if you are beginning to feel more and more relax. Just let it happens. I only want you to relax. Do not be tensed. Relax yourself completely. Relax yourself while you are listening to my voice. My voice is the only thing you are hearing. Pay good attention to my voice and to what it says. All the muscles of your body are relaxed. A pleasant sensation of warmth and heaviness takes over your body. Your entire body seems heavy. You are relaxed. very relaxed. You continue to feel the pain but you are completely relaxed as you listen to my voice. I just want you to relax. Relax yourself completely.Relax yourself completely. A.1.2. Sadness (depression) During the (next) stimulation, you feel the pain normally but you are extremely preoccupied by the painful sensation. You would like to get rid of the pain, but you cannot. You would really like to make it stop, but it never stops. You are beginning to feel some discouragement. and maybe some sadness. You are discouraged towards this unceasing pain

and it makes you feel sad. maybe even depressed. Depressed to notice that there is no escape from this pain. You are depressed. more and more depressed. extremely depressed because there is absolutely nothing you can do to stop this pain. depressed to see that this pain never stops. You continue to feel the pain and you feel your sadness grow stronger and deeper inside you and this feeling of intense depression caused by this pain overcomes you completety. A.1.3. Anger (frustration) During the (next) stimulation, you feel the pain normally but you are extremely preoccupied by the painful sensation. You would like to get rid of the pain, but you cannot. You feel some frustration towards this situation. You would really like to make it stop, but it does not stop. You are beginning to feel some anger. Anger towards this situation that would not stop. You are angry. more and more angry. extremely angry towards this unceasing pain. You do not know why you have to experience this pain. nor the necessicity to endure this sensation. You continue to feel the pain and you feel anger grow stronger and deeper inside you and this feeling of intense anger triggered by this pain overcomes you completety. A.1.4. Fear (anxiety) During the (next) stimulation, you feel the pain normally but you are extremely preoccupied by this painful sensation. You are asking yourself if this painful sensation will ever stop. You fear this sensation will never end. that it would persist continuously. You are afraid. more and more afraid. extremely afraid of this pain. afraid of it consequences. afraid that you cannot get rid of this unceasing pain. You fear that this sensation will never end. You continue to feel the pain and you feel your fear grows stronger within your body and this feeling of intense fear trigged by this pain overcomes you completely. A.1.5. Anticipation of relief During the (next) stimulation, you feel the pain normally but you are extremely preoccupied by the painful sensation. You are asking yourself if this painful sensation will ever stop. However, you are relieved to know that this sensation will stop eventually. relieved to know that it will not persist. You are relieved. more and more relived . extremely relieved to know that this pain will cease in no time. You know this pain will stop soon. It will stop, that is for sure. You continue to feel the pain and you feel this relief grow stronger. kwowing that this pain will stop in a moment gives you a feeling of relief which overcomes you completely. A.1.6. Satisfaction (pride) During the (next) stimulation, you feel the pain normally. You feel the pain. but at the same time, you are feeling good that you are able to stand the pain. This pain could be

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like a test that you are satisfied to overcome. that is it. satisfaction is what you are feeling. You are satisfied because you are able to support the pain. you can overcome this test. you are satisfied. more and more satisfied. extremely satisfied to notice by yourself that you can easily endure this pain. You continue to feel the pain and you feel your satisfaction grow stronger and this feeling of intense satisfaction triggered by your ability to surmount this test overcomes you completely. A.2. Suggestions to increase or decrease the desire for relief (translated from French) A.2.1. Decreased desire for relief During the (next) stimulation, you feel the pain normally. You feel the pain. but at the same time, you are not very preoccupied by pain relief. A.2.2. Increased desire for relief During the (next) stimulation, you feel the pain normally. You feel the pain. but at the same time, you are extremely preoccupied by pain relief. you wish that pain ceases as soon as possible. you contibnue to feel pain normally, and you constantly think about the moment when you will be relieved, your strongest wish is that the pain stops as soon as possible. you very strongly wish for this pleasant moment when you will be relieved.

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