Effects of anxiety sensitivity on anxiety and pain during a cold pressor challenge in patients with panic disorder

BEHAVIOUR RESEARCH AND THERAPY

PERGAMON

Behaviour Research and Therapy 37 (1999) 313±323

E€ects of anxiety sensitivity on anxiety and pain during a cold pressor challenge in patients with panic disorder Norman B. Schmidt *, Je€rey H. Cook Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, USA

Abstract Fear of anxiety symptoms, or anxiety sensitivity (AS), has been extensively studied in anxiety disorders and more recently has been linked to other psychopathological conditions including pain. Asmundson and colleagues have suggested that AS may act as a risk factor for chronic pain and several studies have demonstrated an association between AS, avoidance behaviors and pain. The present study assessed whether AS levels would be predictive of pain and anxiety during a brief pain induction task. Clinical participants meeting DSM-IV criteria for panic disorder (n = 22) were age and sex matched with nonclinical controls (n = 22) and exposed to a 2-min cold pressor challenge. Diagnostic status and AS were signi®cantly predictive of pain and anxiety during the cold pressor task. Moreover, AS appears to mediate the relationship between diagnostic status and pain. However, AS appears to be only indirectly associated with pain through its contribution to anxiety. # 1999 Elsevier Science Ltd. All rights reserved.

1. Introduction Anxiety sensitivity (AS) refers to the extent to which an individual believes that symptoms of anxiety or arousal can have harmful consequences (Reiss & McNally, 1985). Individual di€erences in AS are hypothesized to emerge from the combined in¯uences of genetic variation along with any number of experiences that ultimately lead to the acquisition of beliefs about the potentially aversive consequences of arousal (Reiss & Havercamp, in press). Such experiences may include hearing others express fear of such sensations, receiving * Corresponding author. Present address: Department of Psychology, The Ohio State University, 245 Townshend Hall, 1885 Neil Arenne Mall, Columbus, OH 43210-1222, USA. Tel.: (614) 292-2687; Fax: (614) 688-8261; E-mail: [email protected] 0005-7967/99/$ - see front matter # 1999 Elsevier Science Ltd. All rights reserved. PII: S 0 0 0 5 - 7 9 6 7 ( 9 8 ) 0 0 1 3 9 - 9

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misinformation about the harmfulness of certain sensations, witnessing a catastrophic physical event such as a heart attack and so forth. There is accumulating evidence for AS as a risk factor for anxiety and anxiety disorders from both experimental studies (Donnell & McNally, 1990) as well as prospective studies (Maller & Reiss, 1992; Schmidt, Lerew, & Jackson, 1997). Although the vast majority of research concerning anxiety sensitivity has centered on the anxiety disorders, researchers have recently begun to examine the role of AS in other conditions including pain. Exploration of relationships between anxiety and pain has been spurred by ®ndings suggesting that there is a high degree of co-morbidity between chronic pain and anxiety disorders (Asmundson, Jacobson, Allerdings, & Norton, 1996). Individuals with chronic pain tend to be more anxious that non-clinical populations (Craig, 1994) and patients with panic disorder patients frequently report signi®cant and persistent pain (Schmidt & Telch, 1997). The work of Asmundson and colleagues (Asmundson & Taylor, 1996; Asmundson et al., 1996; Asmundson, Kuperos, & Norton, 1997) suggests that AS may play a role in the onset and or maintenance of chronic pain vis a vis fear of pain and avoidance behaviors. Asmundson suggests that since AS marks an individual's general propensity to develop fears, it may amplify a speci®c tendency to develop fear of pain. Fear of pain, in turn, increases pain related escape/avoidance behaviors which have been proposed as important mechanisms of pain maintenance (Fordyce, 1976; Letham, Slade, Troup, & Bentley, 1983; Philips, 1987). More speci®cally, negative expectancies regarding the harmfulness of pain are ampli®ed by AS, causing avoidance behaviors, and these avoidance behaviors lead to deconditioning (e.g. muscular atrophy, reduction in activity and weight gain). Deconditioning leads to increased pain which heightens avoidance and exacerbates negative expectancies regarding pain (Asmundson, Norton, & Norton, in press). Thus, AS is believed to be a key factor in the maintenance of pain and disability through its action of enhancing the reciprocal relationship between fear and avoidance. To date, studies have relied fairly exclusively on comparisons among AS and diagnostic status or self-report measures assessing general levels of pain. Laboratory induction of pain provides an important complementary methodology of exploring this relationship. The present study used a laboratory paradigm (2 min exposure to a cold pressor) to assess the relationship between AS and pain. The principal research questions included: (1) are patients with panic disorder more subjectively and physiologically reactive to a cold pressor compared to nonclinical controls? (2) Does AS predict subjective and physiological reactivity to the cold pressor? (3) Does AS mediate any relationship between diagnostic status and reactions to the cold pressor? Consistent with previous work indicating that patients with panic disorder typically show subjective but not physiological di€erences from nonclinical controls to biological challenges and cold pressor stress (Holt & Andrew, 1989; Stein & Asmundson, 1994; Telch, Ilai, Valentiner, & Craske, 1994), we predicted that patients would have relatively greater subjective (i.e. anxiety and pain) but not physiological reactivity to the cold pressor. Moreover, we expected that the level of AS would predict subjective responding and that AS would mediate the relationship between diagnostic status and subjective responding.

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2. Method 2.1. Participants 2.1.1. Clinical sample The clinical sample included 22 participants who met the following criteria: (a) principal DSM-IV diagnosis of panic disorder, (b) no change in medication type or dose during the past eight weeks, (c) no evidence of serious suicide intent, (d) no evidence of current substance abuse, (e) no evidence of current or past schizophrenia or bipolar disorder, (f) no medical history of respiratory disease, renal disease, heart disease, epilepsy, or stroke and (g) between the ages of 18 and 65. Diagnostic assessment was based on a structured diagnostic interview using the SCID-I/P (First, Spitzer, Gibbon, & Williams, 1994). Interviews were conducted by advanced graduate students in clinical psychology with extensive training in SCID administration and scoring. Each interview was reviewed by a licensed clinical psychologist during weekly sta€ meetings. 20% of the videotaped SCID interviews are randomly selected for reliability analysis in our laboratory and consistently indicate very high overall interrater reliability (k = 0.84). Medication status and medical history were assessed by the project physician based on a semistructured clinical interview. Of the patients, 54% met diagnostic criteria for agoraphobia and 27% had at least one additional current co-occurring diagnosis. In this sample, 27% were taking benzodiazepines, 9% were taking antidepressants and 23% are taking a combination of both benzodiazepines and antidepressant medication. Consistent with Roth et al. (1992), analyses indicated that medication status did not predict subjective or physiological response to the cold pressor ( p's>0.05). 2.1.2. Nonclinical sample Each patient was matched with a nonclinical control participant for age and sex (n = 22). Nonclinical participants were recruited from the greater Washington metropolitan area and were initially phone screened to determine their interest and eligibility. Nonclinical participants also completed a SCID interview for Axis I disorders and medical history assessment. Eligibility requirements for nonclinical controls included: (1) no current or lifetime psychiatric condition and (2) no medical history of respiratory disease, renal disease, heart disease, epilepsy, stroke, or any other condition that might a€ect the experimental procedure. 2.2. Self-report measures 2.2.1. Anxiety Sensitivity Index (ASI) The ASI is a 16-item questionnaire that measures fear of anxiety symptoms (Peterson & Reiss, 1992). Each item assesses concern about the possible negative consequences of anxiety symptoms. The ASI has demonstrated adequate internal consistency (Telch, Shermis, & Lucas, 1989) and test±retest reliability (Maller & Reiss, 1992).

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Moreover, the ASI appears to tap fear of anxiety symptoms as opposed to state or trait anxiety (see McNally, 1994). 2.2.2. Pain and anxiety rating scales During the cold pressor task, pain and anxiety ratings were assessed using two Visual Analog rating scales (VAS) ranging from 0 (`none') to 10 (`unbearable'). 2.2.3. Discomfort Intolerance Scale (DIS) The ability to tolerate pain and discomfort was assessed using the Discomfort Intolerance Survey (DIS). The DIS is a ®ve-item, self-report questionnaire, in which participants respond to questions such as ``I am more sensitive to physical discomfort compared to most people'' on a scale ranging from 0,``Not at all like me'', to 6, ``Extremely like me''. The scale has satisfactory test±retest validity over 12 weeks (r = 0.78) and adequate internal consistency (a coecient = 0.77). 2.3. Physiological measures Heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) were monitored using a Critikon Dinamap Vital Signs Monitor (Critikon, Tampa, FL). 2.4. Procedure After participants were interviewed with the SCID, they completed the self-report measures. Participants were then seated in a comfortable reclining chair throughout the remainder of the assessment that including a 10 min baseline period in which their heart rate and blood pressure were monitored. Participants were then exposed to a 2 min cold pressor challenge. VAS ratings were made at baseline and at 1 and 2 min. Hemodynamic measures were made at 2 min intervals during baseline (and averaged for analytic purposes) and at 1 min intervals during the cold pressor. Anxiety increases blood ¯ow to skeletal muscles, reduces blood ¯ow near the skin (Guyton & Hall, 1996) and could confound pain ratings by di€erentially in¯uencing nioception in clinical participants (i.e. due to higher levels of state anxiety). To control for the e€ects of peripheral vasoconstriction, we utilized a novel cold pressor procedure. Rather than submerging a limb in ice water, we used a chemical cold compress placed over the participant's throat because this area is less likely to show anxiety-related reductions in blood ¯ow compared to a hand or foot (Guyton & Hall, 1996). The cold pressor, which measured 12  6  1 inch, was placed on the participant's throat and held in place for 120 s. Participants were informed that the test could be discontinued at any time at their request and all but two clinical participants were able to complete the 2 min test. Participants were given the following instructions prior to the cold pressor: We are going to do a brief assessment of cold tolerance as a measure of your tolerance of physical sensations. I will be placing a cold pack on your throat area for 2 min. This test is not dangerous in any way but it may bring on uncomfortable sensations. If the feelings

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become too uncomfortable, you can take the cold press o€. At the 1 min mark, I will ask you to make ratings using the following scale, at 2 min, you will make additional ratings. Participants were instructed to use enough force to keep constant contact, but not enough to impede normal breathing. The temperature of the ice pack is comparable to that of ice water cold pressor (48C) used in other studies (Roth et al., 1992).

3. Results 3.1. Di€erences between groups at baseline t-tests were used to determine whether experimental participants displayed higher scores on subjective and hemodynamic measures at baseline. Consistent with expectation, patients reported higher ASI scores (t(43) = 8.16, p < 0.001) and anxiety ratings (t(43) = 4.84, p < 0.001). There were no di€erences in pain ratings (all participants rated pain at 0) but patients reported higher levels of discomfort intolerance (t(43) = 2.95, p < 0.01). Patients showed some relative elevations in HR and SBP but these did not reach statistical signi®cance (HR (t(43) = 1.54, p > 0.05; SBP (t(43) = 1.46, p > 0.05); DBP (t(43) = 0.094, p > 0.05)). Table 1 displays means and standard deviations and intercorrelations for the primary dependent measures at baseline. Table 1 Correlations and descriptive statistics of primary measures Nonclinical control ASI Panic disorder ASI 0.0 DIS 0.16 ARS 0.41 HR 0.16 SBP 0.15 DBP 0.10 M S.D.

29.6 10.2

DIS

ARS

HR

SBP

DBP

M

S.D.

0.06 0.0 ÿ 0.09 0.17 0.07 ÿ 0.07

0.09 0.47* 0.0 0.23 ÿ0.24 ÿ0.24

ÿ 0.24 ÿ 0.02 ÿ 0.24 0.0 ÿ 0.25 0.11

0.11 ÿ 0.31 ÿ 0.17 ÿ 0.14 0.0 0.76**

ÿ 0.13 ÿ 0.17 ÿ 0.23 0.25 0.67** 0.0

8.41 15.8 0.18 64.3 114.0 68.1

6.71 6.41 0.50 9.50 14.62 8.94

21.6 6.4

1.86 1.55

68.9 10.6

120.7 15.9

67.9 10.2

Correlations and descriptive statistics for patients with panic disorder are found in the lower quadrant of the table, correlations and descriptive statistics for nonclinical controls are located in the upper quadrant of the table.ASI: Anxiety sensitivity Index, DIS: Discomfort Intolerance Scale, ARS: Anxiety Rating Scale from the Visual Analog Scale, HR: heart rate, SBP: systolic blood pressure, DBP: diasystolic blood pressure. Note that the pain rating scale is not included due to no variation (all participants rated 0 at baseline).*Correlation is signi®cant at the 0.05 level (two-tailed).**Correlation is signi®cant at the 0.01 level (two-tailed).

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3.2. Cold pressor task Hemodynamic response to the cold pressor challenge task were assessed using 2 (patient vs control; between groups)  3 (assessment periods; within groups) mixed factorial ANOVA to assess the e€ects of diagnostic status, time and their interaction. Where signi®cant main e€ects and signi®cant interactions were found, only the interaction e€ects are interpreted. These analyses yielded no main e€ects for group or time and no group by time interactions for any hemodynamic measure ( p's>0.05). These ®ndings are generally consistent with other challenge studies examining physiological reactivity, including studies using a cold pressor task (Roth et al., 1992; Stein & Asmundson, 1994), which show comparable reactivity between patients with panic disorder and controls. Subjective responding to the cold pressor task were analyzed similarly1. A signi®cant group by time interaction was observed for pain ratings (F(1, 40) = 5.27, p < 0.05) with no group di€erences at baseline but patients reporting greater pain at 1 and 2 min time points relative to controls (see Fig. 1). Evaluation of anxiety ratings also indicated a signi®cant group by time interaction e€ect (F(1, 39) = 5.20, p < 0.05). Evaluation of the form of the interaction indicates a similar pattern to that found for pain ratings. Multiple regression analyses were used to examine the relationship between anxiety sensitivity and responding to the cold pressor task. ASI scores were signi®cantly associated with pain ratings at both 1 min (F(1, 42) = 5.82, p < 0.05, standardized b = 0.35) and 2 min (F(1, 40) = 11.40, p < 0.005, standardized b = 0.47). The ASI also predicted anxiety ratings at 1 min (F(1, 42) = 28.1, p < 0.001, standardized b = 0.30) and 2 min (F(1, 40) = 24.10, p < 0.01, standardized b = 0.46). In contrast, the ASI was not signi®cantly predictive of hemodynamic reactivity measures ( p's>0.05). Ratings of discomfort intolerance were not signi®cantly predictive of any subjective or physiological measure ( p's>0.05). Analysis of whether AS mediates the relationship between diagnostic status and psychological responses to the cold pressor task was tested through a series of regression analyses in accordance with the Baron and Kenny (1986) methodology. Mediation requires demonstrating a signi®cant relationship between the mediating variable and the criterion variable with a simultaneous reduction in the e€ect of the predictor variable on the criterion variable. Regression analyses are displayed in Table 2 and generally suggest that the ASI mediates the relationship between diagnostic status and subjective responding to the cold pressor. In each equation, there is a signi®cant reduction in the amount of variance accounted for by diagnostic status such that it no longer is a signi®cant predictor of the criterion after accounting for the e€ects of the ASI. It is also interesting to consider whether anxiety sensitivity exerts a direct e€ect on the experience of pain or whether its relationship with pain is due to anxiety (and vice versa). To evaluate these relationship, we used a covariance strategy to assess predictive speci®city (see 1

A main e€ect for time attests to the integrity of the cold pressor and indicates a signi®cant increase in pain over time, (F(1, 40) = 34.13, p < 0.001). Univariate tests indicated a signi®cant increase between baseline and 1 min (t(43) = 11.14, p < 0.001), baseline and 2 min (t(41) = 11.33, p < 0.001) and between 1 and 2 min (t(41) = 5.46, p < 0.001).

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Fig. 1. Patients with panic disorder display di€erentially greater pain reactivity to a cold pressor stimulus over time. A similar pattern of ®ndings is evidenced for anxiety ratings. Table 2 Regression analyses testing mediation e€ects of anxiety sensitivity on the relationship between diagnostic status and pain and anxiety ratings Dependent variable

Independent variable(s)

b

t ratio

p value

ASI 1 min 2 min 1 min 2 min

(1) diagnostic status (2) diagnostic status

0.78 0.39 0.39 0.54 0.55

8.16 2.72 2.69 4.16 4.15

< 0.001 < 0.05 < 0.05 < 0.001 < 0.001

1 min pain

(3a) diagnostic status ASI

0.30 0.12

1.27 0.51

± ±

2 min pain

(3b) diagnostic status ASI

0.05 0.44

0.19 1.86

± 0.07

1 min anxiety

(3c) diagnostic status ASI

0.10 0.57

0.51 2.94

± < 0.01

2 min anxiety

(3d) diagnostic status ASI

0.01 0.70

0.05 3.68

± < 0.005

pain pain anxiety anxiety

b = standardized beta weight. Note that diagnostic status was separately regressed on each dependent variable in steps one and two, but in step three diagnostic status was simultaneously regressed with ASI scores. Absolute ratings of both pain and anxiety were used instead of reactivity ratings.

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Schmidt, Lerew, & Joiner, 1998). Two regression equations were constructed. The assumption of homogeneity of covariance was tested and met (cf. Joiner, 1994). For the ®rst equation, with minute 1 (or minute 2) pain scores as the dependent variable, baseline pain scores were entered into the equation ®rst thereby creating a residualized change variable. Next, minute 1 (or minute 2) anxiety scores were inserted into the equation to control for changes in anxiety. Finally, ASI scores were entered into the equation. This approach allows for the examination of the relation of anxiety sensitivity to pain symptoms beyond the e€ects of anxiety symptoms. For the second equation, a similar approach was taken, except that minute 1 (or minute 2) anxiety scores served as the dependent variable, baseline anxiety scores were entered into the equation ®rst, minute 1 (or minute 2) pain scores were entered next and, ®nally, ASI scores were entered. This allows for the assessment of the relationship between anxiety sensitivity to anxiety beyond the e€ects of pain. Results indicated that anxiety sensitivity was speci®cally related to anxiety but not pain. The ASI was a signi®cant predictor of anxiety change scores beyond pain at minute 1 (F(1, 41) = 4.11, p < 0.05, standardized b = 0.28) and minute 2 (F(1, 40) = 5.21, p < 0.05, standardized b = 0.32). ASI scores were not related to pain scores beyond changes in anxiety at minute 1 (F(1, 41) = 0.88, p > 0.05, standardized b = 0.20) or minute 2 (F(1, 40) = 1.34, p > 0.05, standardized b = 0.22).

4. Discussion The main purpose of the present report was to evaluate the role of anxiety sensitivity in the generation of both anxiety and pain during exposure to a painful stimulus. Consistent with previous work (Roth et al., 1992), patients with panic disorder showed increased subjective distress, in terms of reports of anxiety and pain, to a cold pressor. Anxiety sensitivity was also signi®cantly related to both anxiety and pain. Interestingly, anxiety sensitivity outperformed another self-report measure designed to assess pain tolerance and anxiety sensitivity appears to mediate the relationship between group status and subjective responses (both pain and anxiety) to the cold pressor. The strength of this mediational e€ect increases with time, with the ASI's e€ect being greater at the 2 min, rather than the 1 min, point for both pain and anxiety. Had the cold pressor been conducted over a longer interval, we would expect that the relationship between anxiety sensitivity and these outcomes to be even stronger. Does anxiety sensitivity predict pain vis a vis its association with anxiety or is anxiety sensitivity somehow directly related to the experience of pain? Covariance analyses controlling for the e€ects of anxiety suggest that anxiety sensitivity is only associated with pain through its association with anxiety. The reverse does not hold, however, in that anxiety sensitivity is directly associated with changes in anxiety regardless of the e€ects of pain. These analyses indicate that anxiety sensitivity may potentiate sensations of pain in some patients with panic disorder when they experience anxiety. Anecdotally, this is consistent with reports from some patients who complain that a panic attack is physically painful beyond simply being a terribly frightening and physically uncomfortable experience.

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This data is also consistent with a considerable literature suggesting that anxiety is associated with pain (Leventhal & Everhart, 1979; Gross & Collins, 1981; Weisenberg, 1987). More speci®cally, Weisenberg, Aviram, Wolf, and Raphaeli (1984) have proposed that anxiety that is relevant to the pain-inducing stimulus will exacerbate pain whereas anxiety that is irrelevant to pain will reduce pain. For example, dental phobics, relative to controls, show no di€erences in pain tolerance to arm shock but signi®cant di€erences to tooth shock (Klepac, McDonald, Hauge, & Dowling, 1980). Likewise subjects given anxiety producing information about a cold pressor report greater pain to the cold pressor than those given anxiety producing information about other (irrelevant) tasks (Absi & Rokke, 1991). Individuals with high anxiety sensitivity, who are likely to perceive any source of arousal as threatening, should be more likely to perceive a cold pressor as threatening thereby leading to a greater experience of pain. These ®ndings also impact the proposed pathways delineated by Asmundson and colleagues regarding the interrelationships between anxiety sensitivity and pain. This previous work suggests that anxiety sensitivity may contribute to pain vis a vis its relationship with fear of pain. The present report suggests an additional role for anxiety sensitivity which may lead to increased pain simply by placing the individual at increased risk for experiencing anxiety. These pathways are potentially complimentary and additional work may reveal other relationships between anxiety sensitivity and pain. The present ®ndings are somewhat at odds with one other report investigating the relationship between anxiety sensitivity and pain. No relationship was found between anxiety sensitivity and discomfort/pain associated with loud noise bursts in a sample of undergraduate women (Stewart & Pihl, 1994). This discrepancy may be due to a variety of factors including di€erences in stressors, pain measurement, and sample such that further work is needed to clearly determine the relationship between AS and the experience of pain. Questions may be raised about the generalizability of the ®ndings due to the use of a novel cold pressor task. Application of a chemical cold compress applied to the neck region has not been used in experimental paradigms as far as we can ascertain. This procedure has not been directly validated by comparison with the standard immersion technique, although the general pattern of ®ndings (e.g. signi®cant increase in pain over time) is consistent with other studies using a standardized cold pressor with panic disorder (Roth et al., 1992). We suggest that this novel cold pressor may be useful in controlling for state-related vasoconstriction due to anxiety and should be considered by investigators who are evaluating populations that may show signi®cant di€erences in anxiety. It is possible that anxious responding to the cold pressor was due to the placement of the ice pack (i.e. across the throat) rather than from the painful sensations produced by the cold pressor. Some additional data suggests otherwise. If responding was simply due to placement, we would expect that fear of choking would be predictive of subjective response to this task. To test this, a series of regression analyses was performed using an item from the Agoraphobic Cognitions Questionnaire (Chambless, Caputo, Bright, & Gallagher, 1984) that assesses choking fears (item number 5)2. The choking fears item was not signi®cantly associated with pain or anxiety ratings. 2

Participants completed the Agoraphobic Cognitions Questionnaire as part of another protocol not reported here.

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Anxiety sensitivity appears to be an important variable a€ecting the experience of pain in patients with panic disorder. One clinical rami®cation of this ®nding with anxiety patients who are disposed to experience pain in the context of anxiety (Schmidt & Telch, 1997) is to educate them about this linkage to assuage fears of increased pain. In addition, cognitive behavioral techniques e€ectively reduce anxiety sensitivity is this population (Schmidt, Trakowski, & Staab, 1997) which should reduce the fear and avoidance of pain in individuals su€ering from both anxiety and pain disorders.

Acknowledgements This research was supported by USUHS Grant RO72CF. The opinions or assertions contained herein are the private ones of the authors and are not to be construed as ocial or re¯ecting the views of the Department of Defense or the Uniformed Services University of the Health Sciences.

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