Emotional processing and panic

Behaviour Research and Therapy 42 (2004) 1271–1287 www.elsevier.com/locate/brat

Emotional processing and panic Roger Baker a,b, Jane Holloway b, Peter W. Thomas c, Sarah Thomas a, Matthew Owens b,
a

Dorset Research and Development Support Unit, Poole Hospital NHS Trust, Cornelia House, Poole, Dorset BH15 2JB, UK b Research Department, St Ann’s Hospital, Dorset Healthcare NHS Trust, Poole, Dorset BH13 7LN, UK c Dorset Research and Development Support Unit and Institute of Health and Community Studies, Bournemouth University, Poole Hospital NHS Trust, Cornelia House, Poole, Dorset BH15 7LN, UK Received 3 September 2002; received in revised form 15 July 2003; accepted 16 September 2003

Abstract In this paper Rachman’s concept of emotional processing was extended and a model highlighting the psychological operations underpinning processing was specified. Using this model, the aim was to investigate, by means of a questionnaire, whether patients with panic disorder (n ¼ 50) have more emotional processing difficulties than two samples of healthy controls (London, n ¼ 406; Aberdeen, n ¼ 125). The panic disorder group did have significantly more emotional processing difficulties than the control groups, showing a marked tendency to control feelings of anger, unhappiness and anxiety. Three emotional processing dimensions distinguished the panic from the control groups: greater control of emotional experiences (‘smothering’ or ‘bottling up’ emotions), greater awareness of feelings and more difficulties in labelling emotions. The authors hypothesise that emotional processing deficits act as a vulnerability factor for developing panic attacks. # 2003 Elsevier Ltd. All rights reserved. Keywords: Emotional processing; Emotions; Emotional control; Panic disorder

1. Introduction The concept of emotional processing was first introduced by Rachman in 1980 who put it forward as a promising explanatory concept with particular relevance and application to the anxiety


Corresponding author. Tel.: +44-1202-492137. E-mail address: [email protected] (M. Owens).

0005-7967/$ - see front matter # 2003 Elsevier Ltd. All rights reserved. doi:10.1016/j.brat.2003.09.002

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disorders. In 2001, Rachman restated the concept and applied it to post-traumatic stress disorder. Rachman used the term emotional processing to refer to the way in which an individual processes stressful life events. He defined emotional processing as: ‘‘a process whereby emotional disturbances are absorbed, and decline to the extent that other experiences and behaviour can proceed without disruption’’ (p. 51). He noted that, for the most part, people successfully process the majority of aversive events that occur in their lives. Indeed, if individuals were unable to absorb or ‘‘process’’ emotional disturbances, then they would operate at a constantly high level of arousal with so much intrusion from their feelings that it would be difficult to concentrate on the daily tasks of living. Rachman argued that if emotional experiences were incompletely absorbed or processed then certain direct signs of this failure would appear; for example, the return of fears, obsessions and intrusive thoughts. Furthermore, he proposed that excessive avoidance or prolonged and rigid inhibition of negative emotional experiences would prevent their reintegration and resolution. This may not matter for smaller everyday hassles which are part of normal experience, but could result in disturbances of behaviour and experience if the person experiences more serious negative life events. Based upon clinical and experimental observations Rachman (1980) proposed that fear reduction in the anxiety disorders came about through successful emotional processing and that appropriate exposure to affect-eliciting stimuli during therapy would aid processing. Foa and Kozak (1986) further elaborated upon the mechanisms for change and asserted that successful emotional processing resulted from the modification of information contained in the memory structures underlying fear emotions. In his initial formulation, Rachman described unwanted and emotionally powerful phenomena that intrude into consciousness such as intrusive thoughts, flashbacks, nightmares and the return of phobic anxiety as being indicators of inadequate emotional processing. Given that panic attacks also initially occur suddenly and unexpectedly, with a range of different sensations intruding into consciousness en bloc, they would appear to provide a particularly powerful sign of incomplete emotional processing. In the clinical domain, researchers have recognised and attempted to highlight the importance of emotional arousal and engagement during therapy in order to promote better emotional processing and therapeutic change (Greenberg & Safran, 1987; Samoilov & Goldried, 2000; Teasdale, 1999; Teasdale & Barnard, 1993). Various researchers have delineated factors that may promote or impede emotional processing and developed theories that have important clinical implications for this (e.g. Kelley, Lumley, & Leisen, 1997; Lang, Cuthbert, & Bradley, 1998; Shear & Weiner, 1997; Traue & Pennebaker, 1993). However, the role of emotions has been somewhat neglected and overlooked in modern conceptualisations of panic disorder, which is surprising given that panic essentially involves powerful emotions. Current theories of panic have tended to focus primarily on cognitive factors (Beck & Clark, 1997; Beck & Emery, 1985; Chambless & Goldstein, 1981; Clark, 1986, 1988, 1996; McNally, Riemann, Louro, Lukach, & Kim, 1992; Reiss, 1991). Clinical observations and experimental evidence nevertheless suggest that an individual’s characteristic emotional style may have an important role to play in the aetiology and maintenance of panic attacks.

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Numerous studies have indicated that adverse life events or prolonged stress through problematic interpersonal relationships occur in the months preceding the emergence of initial panic attacks (e.g. Barlow, 1988; Breier, Charney & Heninger, 1986; Chambless & Goldstein, 1981; Faravelli & Pallanti, 1989; Goldberg, 1988; Manfro, Otto, McArdle, Worthington III, Rosenbaum, & Pollack, 1996; Rapee, Litwin, & Barlow, 1990; Shear & Weiner, 1997). Despite obvious antecedents, panic sufferers rarely spontaneously perceive a connection between these events and the initial onset of panic. The failure of these individuals to link severe life events or problematic relationships to their current difficulties may be a reflection of an inadequate style of processing emotion. Panic patients often fail to link physical sensations to emotional states arising from life events and in general they have difficulties in identifying feelings and distinguishing them from bodily sensations (Cox, Swinson, Shulman, & Bourdeau, 1995; Marchesi, Brusamonti, & Maggini, 2000). Guidano (1987) has proposed that because agoraphobic patients often believe they are able to control their emotions they have a tendency to interpret any physical sensations not under their direct control as a symptoms of illness, rather than being emotional in nature. Berg, Shapiro, Chambless and Ahrens (1998) and Williams, Chambless and Ahrens (1997) have also found that a fear of losing control of a range of emotions (anger, depression and positive emotions) appears to be linked to a greater fear of bodily sensations. Clinically, many therapists propose that education/explanation to patients about their bodily sensations is a key part of therapy (e.g. McFadyen, 1989; Rapee & Barlow, 1989; Weekes, 1973; Zane, 1989). In therapy, explanations are often offered to show how physical sensations are related to anxiety or other affects, and how the patient’s condition is psychologically based and not a physical disorder, such as a heart attack or madness. For some patients this proves to be a startling revelation; others are never fully convinced about the psychological nature of their symptoms. In therapy, case studies, and autobiographies panic sufferers seem to describe or demonstrate a range of difficulties with emotions (Baker, 1989; Baker, 2003) as has been noted by numerous therapists (e.g. Chambless & Goldstein, 1981; Shear & Weiner, 1997; Vermilyea, 1990). Examples include: 1. A fear of any strong feelings: Mr. B., a panic sufferer RB treated, explained his fear of crying: ‘‘I allow myself to feel something in myself like sadness, crying. I go so far down. It’s bubbling in my eyes and I try to stop it and shake off what I am feeling. I don’t like starting because I get really hysterical. The last time I did that I ended up punching in a wall.’’ 2. Lack of awareness of emotions: One panic sufferer who had lost the love and inheritance of his mother through the actions of a jealous brother described taking flowers to the family grave, putting them on his mother’s grave but stamping on his brother’s grave and saying ‘‘get down’’. RB suggested he might be angry with his brother to which he sweetly smiled that he had never borne anyone any ill will. 3. Suppressing feelings: Miss R. described how she suppressed feelings: ‘‘I feel butterflies in my tummy and feel I want to cry. Then I suppress my feelings. I take a great big breath, hold it in, tense myself or put my mind onto something else-take the dog out for a walk, do the housework. I say ‘don’t be so b. . . stupid, pull yourself together’’’. 4. Control of emotions: Mrs. S., towards the end of therapy explained, ‘‘Before, I wanted everything to be perfect-nearly every day I was wanting to stay on this happy level all the time. I

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didn’t want to appear out of control to anyone else-angry, unhappy. I’m not going to let this bother me-this ‘nothing bothers me’ exterior. Now I’ve come to the regrettable conclusion that ups and downs are normal’’. Baker (2001) formalised these clinical observations and research findings in an emotional processing model that specifies some of the psychological operations that may impede processing. The model adopts a systems approach whereby a negative emotional experience is regarded as an input that needs to be consciously or unconsciously registered as a prerequisite for emotional experience. The operations include cognitive appraisal, labelling emotions, linking them to events, awareness of emotions and sensations, and control of the experience and expression of emotions. This model is not incompatible with current biological or cognitive conceptualisations of panic disorder, but rather, it complements and extends existing accounts by adding an emotional information processing dimension. It derives primarily from a psychological therapy perspective and is conceptually closest to psychodynamic and experiential models of emotion such as Bucci’s Multiple Code Theory, (1997a, b) and Epstein’s Cognitive-Experiential Self Theory (1998). Successful emotional processing is likely to involve a range of cognitive, behavioural, physiological and emotional processes such as exposure and habituation (Hunt, 1998; Rachman, 1980), appraisal and reappraisal (Lazarus, 1999), insight (Kuiken, Cary, & Nielsen, 1987), restructuring of cognitive and emotion schemas (Bucci, 1997a; Foa & Kozak, 1986), disclosure and catharsis (Bohart, 1980; Traue & Pennebaker, 1993). Using this model as a basis for emotional processing, the aims of the study were to investigate whether patients with panic disorder have more emotional processing difficulties than a healthy control group, and if they do, to investigate what types of difficulties are present. Rachman’s (1980; 2001) definition of ‘emotional processing’, which was described earlier, is the working definition of emotional processing utilised in this paper.

2. Method 2.1. Participants 2.1.1. Panic disorder cohort Referral letters to the Clinical Psychology Department at the Royal Cornhill Hospital, Aberdeen were scrutinised by two clinical psychologists, not involved in this study, and patients were selected if panic attacks were the primary focus of the letter. After an assessment interview, patients were asked to complete a battery of self-report assessments measuring various aspects of anxiety. This information was used in conjunction with the interview to establish a more accurate diagnosis of panic disorder. The interviews were conducted by a clinical psychologist with a research psychologist sitting in on one third of the interviews to provide independent assessment. Those fulfilling DSM IIIR criteria for panic disorder were included in the study. Patients with limited panic attacks or additional psychiatric diagnoses were excluded. Of the 50 panic disorder patients recruited, 48 had complete data sets and have been included in the analysis.

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Nineteen were diagnosed with panic disorder without agoraphobia and 29 with panic disorder with agoraphobia. 2.1.2. Aberdeen controls One hundred and ninety-seven individuals from the Aberdeen University Psychology Department volunteer panel were sent a questionnaire pack by mail. One hundred and twenty-three returned the pack (62% return rate). 2.1.3. London controls Anonymised data for 406 individuals who had completed the Courtauld Emotional Control Scale for Pettingale, Watson and Greer (1984) were provided as part of the analysis in the current study. This effectively represented a second control group, different in terms of time, place, and investigator from the Aberdeen sample. Table 1 provides data regarding the age and gender of these samples. There were significant age differences between the groups (F ð2; 555Þ ¼ 72:1; p < 0:001). Bonferroni post-hoc analysis revealed that the Aberdeen controls were significantly older than the panic group (p < 0:001) and London controls (p < 0:001) and that there were no differences between the panic group and London controls (p ¼ 0:51). Whilst there were fewer males (32%) to females (68%) overall, the proportion of males to females between the three groups was not significantly different (v2 ¼ 1:4; df ¼ 2; p ¼ 0:50). 2.2. Assessments A preliminary model describing the operations involved in emotional processing helped to determine what was to be measured (Baker, 2001). At the time a specific instrument assessing emotional processing was not available, thus, a validated measure of emotional control was used as it closely related to some aspects of emotional processing (Courtauld Emotional Control Scale, Watson & Greer, 1983). Additional items were also devised by the author to tap into other emotional processing operations suggested by the model. 2.2.1. Courtauld Emotional Control Scale (CECS: Watson & Greer, 1983) This 21-item self-report questionnaire asks individuals how they typically respond to three emotions: anger, feeling unhappy and feeling anxious. It normally yields four scores: control of anger (7–28), unhappiness (7–28), anxiety (7–28), and a total control score (21–84). For the purposes of the current study, two other scores were devised by regrouping items in terms of Table 1 Panic disorder cohort and control groups; age and gender Group

Panic Aberdeen London

Age

N

Mean

SD

37.3 51.4 34.5

12.5 13.8 13.7

48 123 387

Missing

0 0 19 Total

Gender Male (%)

Female (%)

12 (25%) 38 (31%) 135 (33%) 185 (32%)

36 (75%) 84 (69%) 271 (67%) 391 (68%)

N

Missing

48 122 406 576

0 1 0 1

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Baker’s hypothesised emotional processing operations. These were control of emotional experience (6–24), and control of emotional expression (15–60). Higher scores represented greater degrees of control. Walker (1990) has recommended the CECS for use in anxiety research because it seems to tap an independent dimension from other scales and is independent of social desirability response bias. 2.2.2. Other measures of emotion Twelve items were devised by the author to cover different aspects of emotional processing, using a similar format to the CECS. These included two items covering the awareness and labelling of emotional feelings, four items covering the person’s constructs about having and expressing positive and negative emotional feelings and six items asking the person to rate how frequent and intense feelings of anger, unhappiness and anxiety were. These latter six items were included to test whether the emotional control items of the CECS were really measuring a control dimension rather than just the frequency and intensity of emotions. 2.2.3. Symptom based assessments Several standardised self-report assessment scales were used to help clarify diagnosis and to act as a further test of whether the CECS was measuring an independent dimension of control, or merely reflected degree and type of symptomatology. They were: The DelusionsSymptoms-States Inventory (Bedford & Foulds, 1978), The Body Sensations Questionnaire and the Agoraphobic Cognitions Questionnaire (Chambless, Caputo, Bright, & Gallaher, 1984), and The Fear Questionnaire (Marks & Mathews, 1979). 2.3. Procedure 2.3.1. Panic disorder cohort Two to three weeks after completing the diagnostic interview and the symptom-based assessments, patients were given the CECS along with the additional emotional items and asked to return them in a stamped addressed envelope. 2.3.2. Aberdeen controls The entire Aberdeen University Psychology Department volunteer panel (n ¼ 197) were sent the CECS with the additional emotional items, and the symptom based assessments along with a cover letter explaining the nature of the study and a stamped addressed envelope. One hundred and eighteen participants completed the CECS and 109 completed the additional questions assessing emotional processing. 2.3.3. London controls Numerical data on the London sample (n ¼ 406) were sent by post from Dr. Watson to the author. The London sample completed the CECS only. 3. Results Data analysis was carried out using Statistica ’99 Edition and SPSS Version 11.0. The critical p-value was set at 0.05. Precision of estimated mean differences was summarized using 95%

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Confidence Intervals (CI). In order to ensure that the panic patients and panic patients with agoraphobia were a cohesive group they were compared on each outcome measure. There were no significant differences between them. 3.1. Courtauld Emotional Control Scale Analyses of variance (ANOVAs) were carried out with Group (panic, London and Aberdeen controls) as the independent factor and the CECS subscales and total score as the dependent variables. Analyses of covariance (ANCOVAs) were subsequently carried out to take account of age and gender differences. Post-hoc analyses using Bonferroni’s correction were conducted for significant overall group differences to identify their source. Box and whisker plots indicating the range of Total Emotional Control scores for each of the three groups are shown in Fig. 1. There were highly significant differences between the groups (F ð2; 556Þ ¼ 31:3; p < 0:001). The panic group had significantly higher Emotional Control scores than the Aberdeen (p < 0:001) and London controls (p < 0:001). The Aberdeen control group also controlled their emotions significantly more than the London control group (p ¼ 0:01). When age and gender differences were taken into account these differences remained significant. In terms of mean scores (controlling for age and gender) the mean difference between the panic group and Aberdeen controls was 10.2 points (95% CI 6.0, 14.3) and between the panic group and London controls 13.4 points (95% CI 9.9, 16.8). Between the Aberdeen and London controls the difference was 3.2 points (95% CI 0.6, 5.9). Table 2 shows the mean scores for each subscale of the CECS unadjusted and adjusted for age and gender. There were significant group differences for Control of Anger (F ð2; 557Þ ¼ 18:5; p < 0:001), Control of Unhappiness (Fð2; 557Þ ¼ 23:14; p < 0:001), and Control of Anxiety (F ð2; 559Þ ¼ 22:51; p < 0:001). In each case the panic group controlled their anger, unhappiness and anxiety significantly more than the London (all p < 0:001) and Aberdeen controls (all p < 0:05) and the Aberdeen controls controlled their anger (p < 0:001), unhappiness (p ¼ 0:02) and anxiety (p ¼ 0:02) significantly more than the London controls. When age and gender differences were taken into account the mean difference between the panic

Fig. 1. Box plot of total emotional control scores (CECS).

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Table 2 Mean scores for each subscale of the CECS (higher scores, more control), unadjusted (line 1) and adjusted for age and gender (line 2) CECS scales Control of anger Mean (SD) and CI Mean (SD) (age and gender) Control of unhappiness Mean (SD) and CI Mean (SD) (age and gender) Control of anxiety Mean (SD) and CI Mean (SD) (age and gender) Total control Mean (SD) and CI Mean (SD) (age and gender)

Panic

Aberdeen

London

and CI

19.1 (4.7) 17.8, 20.5 18.9 (5.8) 17.1, 20.6

17.1 (4.5) 16.2, 17.9 16.4 (8.7) 14.7, 18.1

15.4 (4.5) 14.9, 15.8 14.9 (11.0) 13.7, 16.0

and CI

21.2 (4.1) 20.0, 22.4 19.6 (5.5) 18.0, 21.2

18.1 (4.3) 17.3, 18.9 15.7 (8.3) 14.1, 17.3

16.8 (4.4) 16.4, 17.3 15.0 (10.3) 14.0, 16.1

and CI

21.6 (4.8) 20.2, 23.0 21.0 (5.8) 19.3, 22.7

18.5 (4.5) 17.6, 19.4 17.3 (8.7) 15.6, 19.1

17.1 (4.5) 16.7, 17.6 16.3 (11.0) 15.1, 17.4

and CI

62.0 (11.4) 58.7, 65.3 59.7 (14.0) 55.6, 63.8

53.5 (11.4) 51.3, 55.7 49.5 (20.9) 45.3, 53.6

49.3 (10.9) 48.2, 50.4 46.3 (26.3) 43.6, 49.0

group and London controls for their Control of Anger was 4.0 points (95% CI 2.6, 5.4) p < 0:001; for Control of Unhappiness 4.6 points (95% CI 3.2, 5.9) p < 0:001, and for Control of Anxiety 4.7 points (95% CI 3.3, 6.1) p < 0:001. The mean difference between the panic group and Aberdeen controls for their Control of Anger was 2.5 points (CI 0.8, 4.1) p ¼ 0:003; for Control of Unhappiness 3.9 points (CI 2.4, 5.5) p < 0:001 and for Control of Anxiety 3.6 points (CI 2.0, 5.3) p < 0:001. Finally, between the Aberdeen and London controls the difference between the groups on the Control of Anger subscale was still significant when age and gender differences were taken into account p ¼ 0:006, mean difference of 1.5 points (CI 0.4, 2.7), but no longer significant for their Control of Unhappiness, mean difference of 0.6 (CI 0.1, 1.2) p ¼ 0:7 ns, and Control of Anxiety, mean difference of 1.1 (CI 0.02, 2.2) p ¼ 0:15 ns. 3.2. Other measures of emotional processing (panic cohort and Aberdeen controls only) Independent samples t-tests were used to compare the panic group and Aberdeen controls on the additional emotional processing items and items relating to the control of emotional experience and expression from the CECS. Data for these items had not been collected for the London controls. When the assumptions of these tests appeared to be violated the p-values were compared with those from the Mann–Whitney U-test to check whether they were similar. ANCOVAs were subsequently carried out to take account of age and gender differences. Means, standard deviations and critical p-values for the additional emotional processing items are shown in Table 3, along with age and gender adjusted mean difference scores between the groups. The panic group showed significantly greater awareness of feelings (p < 0:001), significantly poorer ability to label emotions (p < 0:001), and significantly greater control of emotional experience (p < 0:001) and expression (p < 0:001). Their constructs about having and expressing emotions did not differ from the control group, although when age and gender differences were accounted for, the panic group did regard it as more appropriate to have negative feelings

a

1.4 2.1 1.5 2.2 17.5 44.8 2.2 2.7 3.0 2.8 3.0 3.3

1–4 1–4 1–4 1–4 6–24 15–60 1–4 1–4 1–4 1–4 1–4 1–4

1.4 (0.6) 1.8 (0.7) 1.6 (0.6) 2.2 (0.7) 13.7 (4.3) 40.0 (7.7) 1.9 (0.6) 1.7 (0.6) 1.8 (0.7) 2.5 (0.7) 2.1 (0.8) 2.1 (0.8)

3.1 (0.7) 1.6 (0.8)

Aberdeen mean (SD)

0.5 (0.2, 0.8) <0.001 0.4 (0.1, 0.7) <0.001 0.1 (0.2, 0.3) 0.50 0.3 (0.1, 0.6) 0.02 0.1 (0.4, 0.1) 0.36 0.1 (0.2, 0.4) 0.44 4.6 (2.8, 6.3) <0.001 6.2 (3.1, 9.3) <0.001 0.2 (-0.04 , 0.4) 0.09 0.9 (0.7, 1.2) <0.001 1.2 (0.9, 1.5) <0.001 0.3 (0.03, 0.5) 0.07 0.8 (0.5, 1.2) <0.001 1.2 (0.9, 1.5) <0.001

0.83a 0.11a 0.19a 0.65a <0.001 <0.001 0.005 <0.001a <0.001a 0.01 <0.001 <0.001

Mean diff (CI) and P-value (age and gender adjusted)

<0.001a <0.001a

P-value (unadjusted)

Confirmed with non-parametric Mann–Whitney U-test. In all other cases parametric assumptions were met.

(0.6) (0.8) (0.7) (0.8) (4.2) (7.7) (0.7) (0.8) (0.7) (0.7) (0.9) (0.7)

3.6 (0.6) 2.2 (0.9)

1–4 1–4

Awareness of feelings Labelling emotions Constructs. It is right to. . . Have positive feelings Have negative feelings Express positive feelings Express negative feelings Control of emotional experience (CECS) Control of emotional expression (CECS) Frequency of anger Frequency of unhappiness Frequency of anxiety Intensity of anger Intensity of unhappiness Intensity of anxiety

Panic mean (SD)

Score range

Emotional processing dimensions

Table 3 Emotional processing dimensions

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(p ¼ 0:02). In terms of frequency and intensity of anger, unhappiness and anxiety, not surprisingly the panic group reported significantly greater amounts. With regards to anger, there were no differences between the groups in their reported frequency or intensity when age and gender differences were accounted for. 3.3. Panic group predictors Stepwise logistic regression was performed to see which of the emotional processing dimensions best distinguished the panic group from Aberdeen controls. The following dimensions were entered into the analysis: Awareness of Feelings, Control of Emotional Experience (CECS), Control of Emotional Expression (CECS), Believing it Right to Have Negative Emotions and Labelling Feelings. These dimensions had previously been found to differ between the panic group and Aberdeen control group in the age and sex-adjusted analyses. Three of these dimensions best distinguished between the groups. These were: Awareness of Feelings, OR ¼ 2:94 (1.53, 5.66), p ¼ 0:001; Control of Emotional Experience, OR ¼ 1:20 (1.09, 1.33), p < 0:001, and Labelling Feelings, OR ¼ 2:21 (1.37, 3.58), p ¼ 0:001. Odds ratios for variables had they been included, singularly, in the final model are as follows: Believing it Right to Have Negative Feelings, OR ¼ 1:5 (CI 0.8, 2.6), p ¼ 0:1; Believing it Right to Have Positive Feelings, OR ¼ 1:6 (CI 0.8, 3.3), p ¼ 0:2; OR ¼ 0:6 (CI 0.3, 1.1), p ¼ 0:08; Believing it Right to Express Positive Feelings, OR ¼ 0:9 (CI 0.4, 1.8), p ¼ 0:7, and Control of Emotional Expression, OR ¼ 1:0 (CI 0.9, 1.1), p ¼ 0:9. 3.4. Is emotional control being measured? (panic cohort and Aberdeen controls only) In order to test whether the differences between groups on emotional control items of the CECS were really measuring control, and not number, intensity, and frequency of negative emotions, a series of Analyses of Covariance were performed. Using the CECS Total score as the dependent measure and with Group (panic, Aberdeen) as the independent factor of primary interest, each of Frequency of Emotion, Intensity of Emotion, number of Anxiety symptoms (DSSI), and number of Depression symptoms (DSSI) were included as covariates in separate models, each model also adjusting for age and gender. The unadjusted mean difference in total CECS between the panic and Aberdeen groups was 8.4 (CI 4.5, 12.4), Fð1; 153Þ ¼ 18:1; p < 0:001. This main effect of group remained throughout each separate ANCOVA analysis: number of Depressive symptoms (DSSI), 9.3 (CI 3.8, 14.8), F ð1; 143Þ ¼ 11:0; p ¼ 0:001; Total Frequency of Emotion, 9.0 (CI 3.9, 14.1), F ð1; 148Þ ¼ 12:3; p < 0:001; Total Intensity of Emotion, 8.9 (CI 3.9, 13.9), F ð1; 148Þ ¼ 12:6; p ¼ 0:001; number of Anxiety symptoms (DSSI), 7.5 (CI 1.6, 13.4), F ð1; 142Þ ¼ 6:3; p ¼ 0:01. A forward stepping approach, with age and gender entered into the model, was employed using Frequency of Emotion, Intensity of Emotion, Anxiety, and Depression as covariates. At each step, the model remained significant. With all covariates entered into the model, the adjusted mean difference in Total CECS scores between the panic and Aberdeen groups was 7.5 (CI 1.3, 13.7), Fð1; 138Þ ¼ 5:7; p ¼ 0:01. The differences between the groups in the control of emotions were not, therefore, simply a reflection of differences in

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frequency and intensity of emotion, anxiety or depressive symptoms, or any combination of these. 3.5. Is emotional control independent of panic disorder? (panic cohort and Aberdeen controls only) Three measures used in the study represent important aspects of panic disorder: The Fear Questionnaire, the Agoraphobic Cognitions Questionnaire (ACQ), and the Bodily Sensations Questionnaire (BSQ). Means and standard deviations (in parentheses) on these measures for the panic group were as follows: the Fear Questionnaire ¼ 36:1 ð19:2Þ; ACQ ¼ 28:9 ð10:2Þ; and BSQ ¼ 32:0 ð15:0Þ. In the Aberdeen group, the Fear Questionnaire ¼ 13:5 ð10:7Þ; ACQ ¼ 16:6 ð6:3Þ; and BSQ ¼ 6:1 ð6:9Þ. To investigate the possibility of a relationship between each of ACQ, BSQ, and the Fear Questionnaire with Total CECS scores, Pearson’s correlations were calculated. All correlations in the panic group were positive but small and not statistically significant (ACQ : r ¼ 0:22; p ¼ 0:18; BSQ : r ¼0.13, p=0.43; The Fear Questionnaire: r ¼ 0:21; p ¼ 0:19). In the Aberdeen control group, there was a weak negative correlation with BSQ (r ¼ 0:06; p ¼ 0:52), and a weak positive correlation with ACQ (r ¼ 0:15; p ¼ 0:12). The only statistically significant, but small, correlation was between Total CECS and the Fear Questionnaire (r ¼ 0:21; p ¼ 0:03). In order to test whether the emotional control effect can be explained as part of panic disorder or as an independent dimension, an ANCOVA model was used with Total CECS as the dependent variable and Group (panic and Aberdeen) as the independent factor of primary interest. The Fear Questionnaire, ACQ and BSQ were used as covariates and entered into separate models. The unadjusted mean difference in total CECS between the panic and Aberdeen groups was 8.4 (CI 4.5, 12.4), Fð1; 153Þ ¼ 18:1; p < 0:001. With age and gender also entered into the model the main effect of group remained with ACQ (6.6 (CI 1.4, 11.7), F ð1; 139Þ ¼ 6:4; p ¼ 0:01), BSQ (8.9 (CI 2.4, 15.4), F ð1; 139Þ ¼ 7:4; p < 0:01), and the Fear Questionnaire (5.5(CI 0.2, 10.8), F ð1; 141Þ ¼ 4:2; p ¼ 0:04). A forward stepping approach found the effect to remain with BSQ and ACQ entered (7.2 (CI 0.8, 13.5), F ð1; 136Þ ¼ 5:0; p ¼ 0:03), but did not remain significant when the Fear Questionnaire was entered into the model (5.8 (CI 0.7, 12.2), F ð1; 134Þ ¼ 3:1; p ¼ 0:08). Thus, the statistical significance of the difference in total control of emotion between the panic and control group remained when controlling for age, gender, avoidance, agoraphobic cognitions, and bodily sensations separately, and was lost only when all these variables were entered as covariates. The mean difference was reduced from 8.4 to 5.8, a 31% reduction. As the psychometric scores together almost amount to a diagnosis of panic disorder, which is the main distinction between the two groups, this suggests that the emotional control effect is robust. 4. Discussion The results would appear to confirm the hypothesis that panic disorder patients have more emotional processing difficulties than non-patient normal controls. The differences between the groups were statistically significant at very high levels. They were also clinically substantial: for instance, the panic disorder group had mean total emotional control scores 20% higher than the

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London control group. Pettingale, Watson and Greer had previously argued for a relation between the control of emotions and the development of cancer based on an 8% difference in a study involving a breast cancer cohort and the (same) London control sample. When the total emotional control score was analysed in terms of the control of specific emotions, it was found that the panic disorder group controlled feelings of anger, unhappiness, and anxiety significantly more than the control groups. They also showed greater control of their emotional experiences (‘‘smothering’’ or ‘‘bottling up’’ of feelings) and greater control of the expression of their feelings (keeping quiet about or hiding feelings from others) compared to the Aberdeen controls. Further analysis also indicated that the control of emotions was not just an artefact of anxiety or depressive symptoms, intensity and frequency of emotion, phobic avoidance, agoraphobic cognitions or bodily sensations, but represented an independent dimension. These findings suggest that the control of emotions is not just related to panic/anxiety symptoms, but is broader (see also Williams et al., 1997; Berg et al., 1998). The additional emotional processing items devised by the first author allowed a more detailed understanding of the different dimensions of emotional processing and the types of deficits that might occur in panic disorder. It was found, for example, that the panic disorder group showed significantly greater awareness of their feelings and more uncertainty in labelling strong emotions. Overall, the panic patients did not appear to differ in their attitudes about whether it is right to have and express emotions, although they did regard it as more appropriate to have negative feelings. Possible confounding factors such as age and gender were controlled for in the analysis of the data. An attempt was made to determine which of the emotional processing dimensions best distinguished the panic group from Aberdeen controls. It would appear that the panic group control their emotional experiences more, have greater awareness of feelings and find it more difficult to label strong emotions. The hypothesis that poor emotional processing precedes and contributes to the development of panic attacks was not directly tested in this study. Only a prospective research design could properly address this question. The findings might be interpreted as showing that emotional difficulties occur after panic attacks have started, i.e. excessive emotional control follows rather than contributes to panic. However, some findings do point towards emotional processing acting as a precursor or vulnerability factor for panic. In particular, the panic group were significantly more uncertain about the identity of strong emotional feelings (‘labelling’) compared to the control group. This concurs with previous research examining alexithymia where it was found that panic patients had difficulties in identifying feelings and distinguishing them from bodily sessions (Cox, Swinson, Shulman, & Bourdeau, 1995; Marchesi, Brusamonti, & Maggini, 2000). One would expect the ability to accurately label emotions to be part of normal emotional development rather than a sequel to having panic attacks. In further support of the vulnerability position is the research carried out by Williams et al. (1997) and Berg et al. (1998). They found that college students with no prior history of panic attacks who reported greater fear of losing control of their emotions, including anger and positive emotions, became more anxious after laboratory induced panic sensations than those less concerned with emotional control. These findings were seen to lend support to Chambless and Goldstein’s (1981) assertion that panic prone individuals are distressed by feelings of emotional

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Fig. 2. The role of emotional processing in the emergence of the first panic attack.

uncontrollability and Guidano’s (1987) proposal that patients regard any physical sensation beyond their personal control as a symptom of illness. Fig. 2 presents a proposed model for the role of emotional processing in the emergence of initial panic attacks. Failure of emotional processing is seen as one predisposing factor, amongst other genetic, physical and psychosocial factors. It is suggested that the emotional processing mechanisms involved in the development of panic are poor identification of emotional feelings (labelling), over-control of emotional experience and avoidance/control of the expression of emotion. If emotional feelings are incorrectly labelled they would be experienced as somatic sensations without an overall identity and it would thus be difficult to link them accurately with the triggering event(s). In normal circumstances, this style of processing would not be detrimental. However, in the face of a serious stressor or stressors (e.g. separation, death of partner, trapped in relationship), this type of emotional processing style could not adequately reduce the level of arousal generated by the stressor, nor lead to the effective understanding, removal or resolution of the stressor. Over months, this high level of physiological arousal could trigger the fight/ flight reaction, which constitutes the first panic attack (Baker, 2003; Barlow & Cerney, 1988). Once a panic attack occurs one would expect the sort of cognitive and behavioural mechanisms well described by Clark (1986); Margraf and Ehlers (1989), and Marks (1987) (i.e. appraisals of danger, fear of fear cycles and avoidance behaviour) to set in, leading to the development of a more complicated chronic condition. This vulnerability model complements and does not contradict a current cognitive understanding of what happens after panic attacks first occur. It is also consistent with Ehlers et al.’s (1988) and Clark’s (1988) views that panic prone individuals focus on and misinterpret bodily sensations fearfully and may attempt to avoid many emotion-related stimuli. The difference is that we propose that these characteristics are part of a general pre-existing emotional processing style that inhibits adequate processing of stressful life events.

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The emotional processing model has potential in the following four areas: Explanations about aetiology. It offers a testable explanation of why certain individuals should experience panic attacks when faced with psychosocial stressors, while others faced with the same stressors do not panic. Developing cognitive approaches. Research in cognitive processing (e.g. Beck, Stanley, Averill, Baldwin, & Deagle, 1992; McNally, Riemann, Louro, Lukach, & Kim, 1992), cognitive models (Teasdale, 1988) and cognitive therapy (e.g. Beck, 1985, 1988; Salkovskis, Clark, & Hackman, 1991) in panic is extensive. Rachman (2001), in his most recent formulation, even prefers the term ‘cognitive emotional processing’. Emotional processing adds an important emotional dimension to cognitive explanations. Improving therapy. It offers new elements to the therapy of panic. It would be possible to develop a focused programme of emotional understanding for panic sufferers, which could be used to enhance current psychological therapy programmes. A number of programmes already exist, such as emotional focusing (Gendlin, 1996), emotion focused therapy (Greenberg & Paivio, 1997), and narrative therapy (Pennebaker & Seagal, 1999) so this approach is quite feasible. Preventing relapse. If panic sufferers can generally learn more effective ways of processing emotions during therapy, this may help to prevent relapse when those inevitable life stresses occur again in the future (Weekes, 1989). It could offer a long-term advantage over current cognitive treatment approaches.

One of the limitations of this research is that we only compared panic disorder patients to normal participants so are unable to demonstrate whether the effect is specific to panic disorder or might be somewhat broader. Further studies are required to test for the presence, or absence of similar emotional control deficits in other anxiety conditions, and indeed in other psychological disorders. A differing pattern of emotional processing deficit has been found in colorectal cancer (Lothian, 2003). In this study, the measurement of emotional processing was limited by the lack of a psychometrically validated scale when the study was conducted. The closest relative was a validated measure of emotional control (CECS), used along with additional items to capture other aspects of emotional processing. Although this scale has been favourably reviewed (e.g. Walker, 1990) it is only one scale of one type (self-report). What is required is for studies to use differing types of emotional measurement and to utilise a properly constructed psychometric measure of emotional processing. An emotional processing scale has been developed in Dorset and used in a range of medical and psychiatric conditions (Baker et al., 2002). Such a measure should assist future research in emotional processing. The differences between panic patients and the control groups were large both statistically and clinically, indicating that the control of emotions is relevant to panic and that the emotional processing model is worthy of further investigation.

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Acknowledgements We would like to thank Drs. Maggie Watson and Steven Greer for allowing the authors to access their data. We would also like to thank Claire Fyvie, Malcolm McFadyen, Liz Hall, Julie Sinclair and Juliana MacLeod for their help with diagnosis, screening and commenting on earlier drafts of this paper.

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