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Psychosomatic Medicine 68:786-793 (2006)
© 2006 American Psychosomatic Society

ORIGINAL ARTICLES

Anger Management Style and Hostility Among Patients With Chronic Pain: Effects on Symptom-Specific Physiological Reactivity During Anger- and Sadness- Recall Interviews

John W. Burns, PhD, Stephen Bruehl, PhD and Phillip J. Quartana, MS

From the Rosalind Franklin University of Medicine and Science, North Chicago, Illinois (J.W.B., P.J.Q.); and Vanderbilt University School of Medicine, Nashville, Tennessee (S.B.).

Address correspondence and reprint requests to John W. Burns, PhD, Department of Psychology, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Rd., North Chicago, IL 60064. E-mail: john. burns{at}rosalindfranklin.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objectives: We examined whether anger-in, anger-out, and hostility predicted symptom-specific muscle tension reactivity during anger induction (but not sadness induction) among patients with chronic low back pain (CLBP). For patients with CLBP, relevant muscles are the lower paraspinals (LPs). Anger-in x hostility and anger-out x hostility interactions were tested to determine whether particularly reactive groups of patients could be identified with a multivariable profile approach.

Methods: Ninety-four patients with CLBP underwent anger recall (ARI) and sadness recall (SRI) interviews, whereas LP and trapezius electromyography and systolic blood pressure, diastolic blood pressure, and heart rate were recorded. They completed anger-in, anger-out, hostility, and trait anger measures.

Results: Hierarchical regressions were used to test anger-in x hostility and anger-out xhostility interactions for physiological changes during the ARI and SRI. A significant anger-in x hostility interaction was found for LP change during the ARI (but not SRI) such that high anger-in/high hostility patients evinced the greatest reactivity. Effects for trapezius reactivity were nonsignificant. Significant anger-in x hostility interactions were also found for systolic blood pressure and diastolic blood pressure changes during the ARI such that high anger-in/low hostility patients showed the smallest changes. The anger-out x hostility interaction for diastolic blood pressure change during ARI was also significant such that high anger-out/low hostility patients showed the smallest changes. All effects remained significant with trait anger controlled.

Conclusions: A multivariable profile approach may help identify especially vulnerable patient groups. Patients with CLBP who tend to suppress anger and are cynically hostile may be more likely to experience high levels of muscle tension near the site of pain and injury during anger, but not during sadness, than other groups.

Key Words: anger management style • hostility • symptom-specific reactivity • chronic pain

Abbreviations: CLBP = chronic low back pain; EMG = electromyography; AOS = anger-out scale; AIS = anger-in scale; Ho = Cook-Medley Hostility scale; TAS = Trait Anger scale; ARI = anger recall interview; SRI = sadness recall interview; LP = lower paraspinal muscles; SBP = systolic blood pressure; DBP = diastolic blood pressure; HR = heart rate.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHOD
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Anger and hostility are implicated in the development and maintenance of chronic pain (1). Whereas patients with various chronic pain disorders are characterized by high levels of trait anger and hostility, many findings implicate anger management style—primarily the pronounced tendencies to suppress or express angry feelings—as a particularly robust determinant of chronic pain severity (2–5). That anger management style is related to pain appears consonant with current conceptualizations of emotion regulation indicating that the particular ways in which emotions are handled will affect physical health (e.g., (6)). The tendency to suppress anger (anger-in), on the one hand, was noted by Engel (7) to be a typical attribute of pain-prone patients, and empiric studies (8–11) suggest that anger-in is more prevalent among patients with chronic pain than among nonpatients. Furthermore, the more patients report suppressing anger (4,9) and hostility (3), the more poorly they adjust to chronic pain and the more poorly they respond to pain treatment (12). The tendency to express anger (anger-out), on the other hand, is also related negatively to chronic pain adjustment. Bruehl et al. (2) and Burns et al. (3) reported that anger-out was related to pain severity and interference as a result of pain among patients with chronic pain. One limitation of extant research, however, is that few mechanisms have been proposed to explain how anger management style and hostility are related to the exacerbation of chronic pain.

Research suggests that physical and psychological stress can lead to frequent and intense or low level but sustained muscular contractions (13). Such muscle activity may in turn increase pain through ischemia and hypoxia (14) and through changes in mechanoreceptor sensitivity (15). Flor and colleagues (16–18) proposed a "symptom specificity" model of chronic pain founded on notions of individual response specificity (19), which holds that patients with particular musculoskeletal disorders can be distinguished from patients with other musculoskeletal disorders and from healthy individuals by substantial stress-induced tension in muscles near the site of pain or injury. Moreover, general autonomic arousal may not necessarily differentiate groups with different kinds of musculoskeletal pain from each other or from healthy people. Patients with chronic low back pain (CLBP), therefore, can be expected to show stress-induced muscular responses specific to this disorder. That is, patients with CLBP should selectively show exaggerated contraction of muscles of the low back (i.e., lower paraspinals [LP]). Findings support symptom specificity models for patients with CLBP (16–18,20–23) and for people with neck and shoulder pain (24,25). Moreover, Burns and colleagues (20,26) found that LP reactivity to psychological stress was related to reports of everyday chronic pain severity among patients with CLBP, whereas the trapezius muscle—a site distal from the site of pain or injury—and cardiovascular reactivity were not. Lundberg et al. (24) reported that supermarket cashiers with trapezius myalgia and substantial neck and shoulder pain exhibited higher levels of trapezius muscle tension during work than cashiers without pain. Although current research has not shown that patterns of abnormal muscle tension cause chronic pain conditions, extant results suggest that frequent or sustained stress-induced tension of muscles specific to a disorder may at least maintain or aggravate pain from existing chronic pain conditions.

Anger management style and hostility are related to individual differences in physiological reactivity to stress (e.g., (27–29)). Although most research has focused on cardiovascular components of sympathetic nervous system reactivity, we (30) adapted Flor’s symptom specificity model and hypothesized that one mechanism by which anger dimensions may be related to increased chronic pain severity is through muscle contraction near the site of pain or injury. In the case of CLBP, anger and hostility should affect primarily LP reactivity rather than tension in other muscle groups. Burns (30) found preliminary support for this notion in that anger-out, anger-in, and hostility were related significantly to LP reactivity during anger recall, whereas these anger variables were not related significantly to trapezius muscle reactivity. To date, these findings have not been replicated. Furthermore, the question of whether relationships among anger-related variables and muscle tension reactivity are most robust during anger in particular has not been adequately explored.

In the present study, further analyses of data collected by Burns (26) were performed to determine whether anger management style and hostility predict symptom-specific responses during the induction of anger and/or sadness. Patients with CLBP participated in separate interview procedures to induce angry and sad moods while measures of blood pressure, heart rate, and electromyography of LP and trapezius muscles were collected. According to the symptom specificity model, it was expected that anger management style and hostility would be related significantly to changes in LP muscle tension, but not to changes in trapezius muscle tension. However, because anger and hostility have been linked to laboratory-induced and ambulatory cardiovascular reactivity in several studies of healthy normal subjects (31) for reviews, see (32,33)), it was expected that anger management style and hostility would also be related to blood pressure and heart rate changes among patients with CLBP.

Two additional issues were addressed in the current study. First, anger management style and hostility appear to predict cardiovascular reactivity most consistently during anger provocation (e.g., (28,29,34–36)). According to this trait x situation approach, it may be expected that trait anger variables would predict LP reactivity best during a situation in which anger was elicited. Indeed, in Burns (30), anger management style and hostility were related significantly to LP reactivity elicited during an anger recall interview but not during a mental arithmetic task. Thus, in the current study, we expected the anger variables to significantly predict LP reactivity during the anger recall interview but not during the sadness recall interview. Second, anger suppression and expression, as styles of anger management, can be distinguished from hostility (37), which is defined as an attitude of cynical mistrustfulness, resentment, and interpersonal antagonism (38). Given these conceptual distinctions, we argued previously (3,28,30) that people may be classified into hostile and nonhostile anger management groups by considering interactions among anger management styles and hostility. This "multivariable" profile approach permits taking into account simultaneously the effects on physiological reactivity of combinations of expressive or suppressive anger management styles and a cynically mistrustful and antagonistic attitude. Results of Burns (30) suggest that only patients with CLBP who were hostile anger suppressors (i.e., those high on anger-in and high on hostility) showed substantial LP reactivity during anger recall. Examining interactions among anger management and attitude factors may help identify particularly vulnerable profiles—such as people who suppress anger born of a cynically hostile outlook—that would go unnoticed if such variables were considered individually (e.g., (39)). Thus, in the present study, we explored the effects of "anger-in x hostility" and "anger-out x hostility" interactions on physiological reactivity.


   METHOD
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
Participants were 94 patients with CLBP recruited through advertisements and postings at pain clinics between October 2002 and December 2003. All procedures and forms were approved by our Institutional Review Board. Participants were paid $40. Exclusion criteria were: a) any current cardiovascular disorder; b) current use of medications that affect cardiovascular function (i.e., beta blockers); c) chronic pain stemming from malignant conditions (i.e., cancer); d) current alcohol or substance abuse problems; e) a history of psychotic or bipolar disorders; f) daily use of narcotic analgesic medication; and g) inability to understand and speak English well enough to participate in the anger and sadness recall interviews. Inclusion criteria were: a) musculoskeletal pain of the lower back stemming from degenerative processes, muscular or ligamentous strain, or disk herniation as determined by a neurosurgeon or neurologist; and b) pain duration of at least 6 months. Women comprised 53.2% (n = 50) of the sample. Further demographic information appears in Table 1.


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  		TABLE 1. Sample Characteristics (N = 94)

 

Design Overview
Patients underwent both anger- and sadness-induction manipulations (see subsequently) with interview order counterbalanced. Resting baseline periods preceded each interview. Blood pressure, heart rate, and trapezius and LP muscle tension (i.e., electromyography [EMG]) were assessed during baselines and interviews.

Measures
Recording Electromyography
EMG activity was recorded from left and right lower paraspinals (L2–L4) and left and right trapezius muscles. Silver/silver chloride 8-mm electrodes were spaced 15 mm apart for bipolar recording as recommended by Fridlund and Cacioppo (40). Sites were prepared with vigorous alcohol abrasion. Interelectrode impedance was kept below 10 k{Omega}. Bioamplifiers with bandpass filters (Coulbourn Instruments) were used to record EMG. Raw EMG signals were amplified by a factor of 100,000. The sampling rate was 10/sec, and signals were passed through narrow bandpass filters (100–250 Hz). A narrow bandpass was used to increase the specificity of signals from target muscles. Signals were integrated and "smoothed" with contour-following and cumulative integrators (Coulbourn Instruments). Following recommendations by Fridlund and Cacioppo (40), the time constant for integration was 100 ms. Data were collected by a dedicated computer through A/D conversion using Wingraph software.

Recording Cardiovascular Indices
Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were measured with a Dinamap 1846 SX Monitor (Johnson & Johnson Medical Inc.). This instrument assesses blood pressure with the oscillometric technique. Readings were obtained about every 60 seconds during baselines and interviews. Data were collected by a dedicated computer through A/D conversion using Wingraph software.

Cook-Medley Hostility Scale
Hostility was measured with the Cook-Medley Hostility Scale (Ho (41)), which was derived from items of the Minnesota Multiphasic Personality Inventory. Results of construct validity studies suggest that the scale taps an attitude of cynical mistrustfulness, resentment, and interpersonal antagonism (38). Psychometric properties of the Ho scale appear adequate (38).

Anger Management Style
The tendencies to suppress and express anger were assessed with the Anger Expression Inventory (37). This inventory has subscales that measure anger-in (Anger-in Subscale [AIS]) and anger-out (Anger-out Subscale [AOS]) for which Spielberger et al. (37) reported adequate internal consistency coefficients.

Trait Anger
The Spielberger Trait Anger Scale (TAS (42)) was used to tap the dispositional tendency to experience anger. Scores on the TAS reflect primarily the frequency and magnitude of angry episodes. Anger-out, anger-in, and hostility also assess anger dimensions. In the event of significant AOS, AIS, or Ho effects on physiological reactivity, we controlled for TAS scores to determine whether the observed effects were due uniquely to anger management style and/or hostility or were instead largely explained by an underlying proclivity to become angry.

Emotion-Induction Interviews
Participants engaged in 5-minute semistructured interviews during which they described recent events that had elicited anger or sadness. The anger recall (ARI) and sadness recall (SRI) interviews were used to evoke the target emotions. The procedure was adapted from the "stress interview" procedure developed by Dimsdale et al. (43). The interview procedures invoke significant cardiovascular reactivity (44,45) and trapezius and LP muscle reactivity (20) and elicit self-reported valence and arousal in expected directions (45,46).

Participants were asked to recall a recent event during which they experienced the relevant emotion. The participant briefly described the event so that the experimenter could determine the appropriateness of the event for the target emotion. The participant then was told to describe the event in detail and to focus on angry or sad thoughts and feelings. The experimenter guided the participant to concentrate on and speak about the most emotion-invoking aspects of the event with requests, probes, and reflections. During the interviews, the experimenter was never hostile, avoided badgering, and did not raise questions that might implicate the participant’s character in contributing to his or her misfortune.

Procedure
For participants reporting use of opioid-based medication, they were asked not to take these substances on the day of their appointments. Participants were randomly assigned to ARI/SRI or SRI/ARI orders. On arriving at the laboratory, the participant was screened, signed an informed consent form, and was seated upright in a comfortable chair. The blood pressure cuff and electrodes were attached, and the participant then sat quietly for 10 minutes while resting EMG, SBP, DBP, and HR readings were taken. Instructions were then given for the first recall interview (either anger or sadness), and it began. After 5 minutes, the participant was stopped. Another 10-minute resting baseline began. Instructions were then given for the remaining recall interview (either anger or sadness) and it began. After 5 minutes, the participant was stopped, the blood pressure cuff and electrodes were removed, and the participant was debriefed.

Data Reduction and Analyses
For LP and trapezius EMG, readings from left and right sites were summed and averaged. First and second baseline values for EMG, SBP, DBP, and HR were defined as the mean of readings taken during the last 3 minutes of each 10-minute resting baseline period. Anger-induction and sadness-induction values for EMG, SBP, DBP, and HR were defined as the mean of readings taken during the 5-minute interviews.

As reported in Burns (26), within-subject analyses of variance revealed that both ARI and SRI elicited significant baseline to interview increases in physiological arousal across all indices. Moreover, baseline to interview changes were not significantly affected by order of interview presentation (26). See Table 2 for means and standard deviations (SDs) of baselines, ARI, and SRI values. For the current study, baseline to interview standardized (Z-score) residualized change scores (for each emotion induction manipulation) served as dependent variables and were computed by regressing interview values on the preceding baseline values for each physiological index. Following recommendations of Aiken and West (47), AOS, AIS, and Ho scores were centered on respective means before computing interaction terms. Two-way interaction terms were computed by multiplying relevant factors. To illustrate with AIS, regressions proceeded by entering AIS and Ho terms in the first step and the AIS x Ho interaction term in the second step. Regressions with significant two-way interactions were repeated with TAS scores entered in the first step to examine effects of anger management style beyond those of trait anger. For significant two-way interactions, simple slopes for Ho scores at different hypothetical "levels" of AIS or AOS scores were computed and tested for statistical significance following procedures in Aiken and West (47). Finally, two-way interactions were graphically depicted for hypothetical AIS, AOS, or Ho scores (see subsequently).


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  		TABLE 2. Means (standard deviations) of Electromyography and Cardiovascular Values

 


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Zero-Order Correlations
Correlation coefficients were generated among AIS, AOS, and Ho scores on the one hand and residualized change scores for the physiological indexes on the other (see Table 3). Few significant relationships were found, which is not inconsistent with results from meta-analyses indicating reliable but small effects between traits and reactivity (e.g., (32,33)). Of note, correlations between AOS scores and SBP reactivity were negative, an effect we reported previously with emotion recall interviews (45) and which may be attributed to allowing anger expressors an opportunity to actually express their anger (see subsequently).


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  		TABLE 3. Zero-Order Correlations

 

Lower Paraspinal Reactivity
The AIS x Ho interaction was significant (p < .05) for LP reactivity during the ARI (see Table 4). Controlling for TAS scores and a dummy-coded opioid medication variable (0 = do not use opioid medication; 1 = use opioid medication) did not influence this effect. Simple slopes for Ho scores at different "levels" of AIS scores (–1 SD and +1 SD from mean) were computed and tested for statistical significance. The simple slope for Ho at "high" AIS scores was significant (t = 3.51; p < .05), whereas the slope for Ho scores at "low" AIS scores was nonsignificant (t = –0.8; p > .10). The interaction was also depicted by solving the regression equation for hypothetical AIS and Ho values (–1 SD and +1 SD from means) as described by Aiken and West (47). Predicted LP reactivity values are displayed in Figure 1. Results suggest that patients with CLBP who reported both high anger-in and high hostility exhibited greater LP muscle tension increases than patients characterized by other profiles.


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  		TABLE 4. Summary of Hierarchical Regressions: AIS x Ho and AOS x Ho

 

Figure 121
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  		Figure 1. AIS x Ho for LP {Delta} during ARI. AIS hypothetical values = ±1 SD from centered sample mean. Ho hypothetical values = ±1 SD from centered sample mean. LP {Delta} = residualized change scores. AIS = Anger-in scale; Ho = Cook-Medley Hostility scale; LP = lower paraspinal muscles; SD = standard deviation.

 

The AIS x Ho interaction was nonsignificant (t <1) for LP reactivity during the SRI. The main effects for AIS and Ho scores, as shown in Table 3, were also nonsignificant (t’s <1).

The AOS x Ho interaction was nonsignificant (t’s <1.3; p’s >.10) for LP reactivity during both the ARI and SRI.

Trapezius Reactivity
The AIS x Ho and AOS x Ho interactions were nonsignificant for trapezius reactivity during both the ARI and SRI (t’s <1). These null results coupled with significant anger-in and hostility effects on LP reactivity provide evidence for a symptom specificity model.

Systolic Blood Pressure Reactivity
The AIS x Ho interaction was significant for SBP reactivity during both the ARI and SRI (see Table 4). Again, controlling for TAS scores and opioid medication use did not alter these effects. Simple slopes for Ho scores at different "levels" of AIS scores were computed and tested for statistical significance. The simple slope for Ho at "high" AIS scores (+1 SD from mean) scores was significant (t = 10.11; p < .05) for SBP reactivity during the ARI, whereas the slope for Ho scores at "low" AIS scores (–1 SD from mean) was nonsignificant (t = –2.06; p > .10). Interactions were depicted as described previously. The pattern of predicted SBP reactivity values was similar across the ARI and SRI, and only the former are displayed in Figure 2. Results suggest that patients who reported both high anger-in and high hostility exhibited modestly high SBP increases, but patients high on anger-in but low on hostility were distinguished by markedly low SBP reactivity.


Figure 221
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  		Figure 2. AIS x Ho for SBP {Delta} during ARI. AIS hypothetical values = ±1 SD from centered sample mean. Ho hypothetical values = ±1 SD from centered sample mean. SBP {Delta} = residualized change scores. AIS = Anger-in scale; Ho = Cook-Medley Hostility scale; SBP = systolic blood pressure; SD = standard deviation.

 

The AOS x Ho interactions were nonsignificant for SBP reactivity during both interviews (t’s <1.5; p’s >.10).

Diastolic Blood Pressure Reactivity
The AIS x Ho interaction was significant for DBP reactivity during the ARI (see Table 4) but not during the SRI (t = 1.3; p > .10). Controlling for TAS scores and opioid medication use did not change this effect. Simple slopes were computed and tested for statistical significance. The simple slope for Ho at "high" AIS scores (+1 SD from mean) scores was significant (t = 10.68; p < .05), but the slope for Ho scores at "low" AIS scores (–1 SD from mean) was nonsignificant (t = –1.88; p > .10). The interaction was depicted as described previously (see Fig. 3). Results suggest that, similar to effects for SBP, patients who reported high anger-in and high hostility evinced high DBP reactivity, but again, the high anger-in but low hostility patients were distinguished by rather low DBP increases.


Figure 321
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  		Figure 3. AIS x Ho for DBP {Delta} during ARI. AIS hypothetical values = ±1 SD from centered sample mean. Ho hypothetical values = ±1 SD from centered sample mean. DBP {Delta} = residualized change scores. AIS = Anger-in scale; Ho = Cook-Medley Hostility scale; DBP = diastolic blood pressure; SD = standard deviation.

 

The AOS x Ho interaction was also significant for DBP reactivity during the ARI (see Table 4) but not during the SRI (t = 1.8; p < .08). This effect, too, was not affected by controlling for either TAS scores or opioid medication use. Again, simple slopes were computed and tested for statistical significance. The simple slope for Ho at "high" AOS scores (+1 SD from mean) scores was significant (t = 11.84; p < .05), but the slope for Ho scores at "low" AOS scores (–1 SD from mean) was nonsignificant (t = –0.25; p > .10). The interaction was depicted as described previously (see Fig. 4). Results appear to indicate that whereas high anger-out and high hostility patients were distinguished by somewhat high DBP reactivity; the high anger-out but low hostility patients were clearly distinguished by prominently low DBP reactivity.


Figure 421
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  		Figure 4. AOS x Ho for DBP {Delta} during ARI. AOS hypothetical values = ±1 SD from centered sample mean. Ho hypothetical values = ±1 SD from centered sample mean. DBP {Delta} = residualized change scores. AOS = Anger-out scale; Ho = Cook-Medley Hostility scale; DBP = diastolic blood pressure; SD = standard deviation.

 

Heart Rate Reactivity
The AIS x Ho (t’s <1.7; p’s >.10) and AOS x Ho (t’s <1) interactions were nonsignificant for HR reactivity during both interviews.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
We proposed that one mechanism by which anger management style and hostility may be related to increased pain severity among patients with CLBP is through effects on stress-induced muscle tension near the site of pain or injury. Following trait x situation formulations, trait variables tapping dimensions of anger were expected to predict such symptom-specific reactivity most reliably during a situation in which anger in particular was aroused. Finally, we argued that anger management style and hostility traits can be profitably examined in multivariable profiles to identify especially vulnerable patient groups. Thus, patients who tend to suppress anger that stems from a cynical and hostile attitude toward the actions and motives of others were expected to exhibit the greatest symptom-specific reactivity. Hypotheses were largely supported.

Inspection of hypothetical values in Figure 1 suggests that patients with CLBP who tend to suppress anger and are characterized by a pronounced hostile attitude showed greater LP muscle tension increases during anger than patients described by other anger-in/hostility configurations. People described by other profiles appeared to exhibit comparable levels of LP reactivity. In addition, all main and interaction effects for trapezius reactivity were nonsignificant. Taken together, these findings provide support for the symptom specificity model of anger management style and chronic pain. Patients with CLBP who suppress anger that arises from hostile attributions, mistrust, and the like may be distinguished from other patients by a propensity to experience large increases in LP muscle tension during anger arousal. Tension in muscles distant from the site of pain or injury—trapezius muscles of the shoulder—were not differentially affected by anger-in/hostility profiles. Results replicate and extend those reported by Burns (30). Thus, well-documented links between trait anger-in measures and pain severity may be in part the result of a tendency for (hostile) anger-suppressing patients to evince muscle tension increases near the site of pain or injury, one process that may in turn ignite or aggravate painful episodes.

It must be emphasized that results isolated a particularly vulnerable patient group with CLBP of hostile anger suppressors, and so may help to integrate findings suggesting that patients with chronic pain are characterized by greater anger suppression and hostility than healthy people. Hostile people are generally prone to experience anger (38). Suppressing anger stemming from resentment, perceived slights, longstanding grudges, and so forth may require more effort than suppressing simple transient anger. This notion is supported by comparing the relatively small LP changes of nonhostile anger suppressors (high anger-in/low hostility) with the large increases exhibited by the hostile anger suppressors.

Moreover, consistent with a trait x situation approach, the susceptibility to experience exaggerated LP tension among hostile anger suppressors was revealed only during the anger arousal of the ARI. Although the SRI induced significant physiological reactivity, including LP tension, this variability was not predicted significantly by anger management style or hostility. It may be the case that only to the extent that hostile anger suppressors encounter anger-eliciting events will they exhibit large LP tension increases and so run the risk of spurring on pain severity. Moreover, from a transactional standpoint (48), it may be that hostile patients with CLBP perceive and even instigate a great many angering events and so lay the physiological foundation for frequent bouts of pain and suffering.

Hostile anger suppressors also showed relatively high SBP and DBP during anger arousal. Much prior work using a variety of methodological and statistical approaches points toward the tendency to express anger and/or hostility as more reliably related to stress-induced cardiovascular reactivity than suppressed anger (27,28,34,36,49,50). Two points need be raised. First, most of the research implicating expressed anger/hostility as a chief determinant of cardiovascular reactivity was based on healthy individuals. Put simply, as clinical anecdote and empiric findings suggest, suppression of anger may represent a factor more crucial in determining psychological and physical adjustment for patients with chronic pain than for healthy people. Second, a matching hypothesis may pertain. As argued by Engebretson et al. (50), physiological arousal during and after anger arousal may be influenced by whether the opportunity to express in a given situation matches an individual’s preferred anger management style. Thus, anger expressors may benefit from an opportunity to express anger, whereas suppressors may find expression of anger quite unpleasant. The ARI may represent an anger-eliciting task that, by its very nature, encourages expression. In Burns et al. (45) and here, we found AOS scores were correlated negatively with SBP reactivity during the ARI, whereas in both the previous study and here, AOS scores were not related significantly to SBP during the SRI. These findings support the notion that the ARI represents a "matching situation" for anger expressors. Conversely, anger suppressors, particularly hostile ones, may find the ARI a mismatch situation and so show heightened reactivity. In either event, the degree to which hostile anger suppressors represent an especially vulnerable subset of patients with CLBP should be pursued.

Although anger-out interacted with hostility to significantly affect only DBP reactivity during the ARI, the nature of the interaction is noteworthy. AOS scores and SBP reactivity during the ARI were related modestly and negatively, and the effect for DBP was in the same direction, although it was not statistically significant. Inspection of values depicted in Figure 4 suggests that only nonhostile anger expressors showed low DBP reactivity to anger arousal, whereas the hostile anger expressors showed DBP reactivity somewhat above the mean. Following the matching hypothesis explicated previously, results suggest that only nonhostile anger expressors benefited fully from the opportunity to express anger, whereas their hostile anger expressor counterparts did not. When people express or speak about anger that is not fueled by deep-seated resentment, bitterness, and cynicism, physiological arousal may be minimized, whereas giving voice to anger steeped in hostility may produce the opposite.

Although too much importance should not be placed on this finding short of replication, it is fair to say that these results combined with those for the anger-in x hostility profiles strongly support the potential importance of examining multivariable profiles rather than keeping exclusively to an approach described by multiple, single-variable analyses. For both anger expression and suppression, relationships to health-related outcome variables may further depend on whether the patient is also hostile. In short, the development of potentially pathogenic patterns of physiological reactivity may not only be a matter of how anger in general is regulated. Such problematic physiological responses may depend on whether a person’s anger—suppressed or expressed—tends to arise in the context of cynical and antagonistic interpretations of people’s behavior, words, and assumed motives. Such anger—suppressed or expressed—may not easily resolve because of the strong and inflexible attitudes that spawn and maintain it.

Some limitations of the present study should be delineated. First, as reported in Burns (26), patients with CLBP showed greater LP reactivity during the ARI than during the SRI. The somewhat smaller variability in LP values found in the SRI may have mitigated against finding significant anger-out or anger-in x hostility interactions. Thus, the situation-specific effects we observed may have been to some extent an artifact of this lower variability. Second, although emotion recall interviews may possess verisimilitude, the procedure still represents a laboratory procedure. We can only infer that hostile anger suppressors respond to anger provocation in daily life with symptom-specific LP reactivity. Ambulatory studies such as those that have linked hostility to blood pressure reactivity induced by everyday stressors (31,51) are needed to fill this inferential gap.

To sum, results imply that patients with CLBP who typically suppress anger that may arise from a cynical, mistrustful, and generally negative perception of the actions and intentions of others may be physiologically reactive to anger-provoking events. To the extent that stress-induced increases in LP muscle tension do indeed aggravate chronic low back pain (20,26), patients characterized by the hostile anger suppressor profile may be susceptible to episodes of pain and suffering after anger arousal. Also, to the extent that excessive blood pressure reactivity may signal dysfunction in endogenous inhibitory systems such as endogenous opioids (2), hostile anger suppressors may be vulnerable to painful episodes through deficits in other mechanisms that provide stress-induced analgesia. Finally, the multivariable profile approach may allow a full appreciation of the complexity of conducting successful psychosocial interventions (e.g., cognitive–behavioral therapy) for the most vulnerable subsets of patients with CLBP. To reduce physiological reactivity and thereby relieve pain to some extent, not only must patients learn to constructively express anger (e.g., (52)), but must do so in the context of altering characteristic attitudes (e.g., (53)), which hold that the very people to whom one should express anger and frustration are inherently untrustworthy.

We gratefully acknowledge the encouragement and generosity of Kenneth Lofland, PhD, and the help and cooperation of the staff at the Pain & Rehabilitation Clinic of Chicago, without which this study would not have been possible.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 

This research was supported in part by grants NS37164 from the National Institute of Neurological Disorders and Stroke (John W. Burns, PhD), MH071260 from the National Institute of Mental Health (John W. Burns, PhD, and Stephen Bruehl, PhD), NS046694 from the National Institute of Neurological Disorders and Stroke (Stephen Bruehl, PhD), and by grant F31 NS051200-01A1 from the National Institute of Neurological Disorders and Stroke (Phillip J. Quartana, MS).

DOI:10.1097/01.psy.0000238211.89198.e4


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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