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Aug 3, 2015 - Geneviève Belleville, School of Psychology, Université Laval; André Marchand, Department of Psychology, Université du Québec a` Montréal; ...
Archives of Scientific Psychology 2015, 3, 93–100 DOI: http://dx.doi.org/10.1037/arc0000018

© 2015 The Author(s) 2169-3269

Archives of Scientific Psychology www.apa.org/pubs/journals/arc

Do Treatments for Panic Disorder Improve Sleep in Patients With Unexplained Chest Pain? Geneviève Belleville Université Laval

André Marchand Université du Québec a` Montréal

Julien Poitras Hôtel-Dieu de Lévis Hospital—A Université Laval Affiliated Hospital, Lévis, Canada

Alain Vadeboncoeur Montreal Heart Institute, Montreal, Canada

Jean-Marc Chauny Hôpital du Sacré-Coeur de Montréal, Montreal, Canada

Guillaume Foldes-Busque Université Laval and Hôtel-Dieu de Lévis Hospital—A Université Laval Affiliated Hospital, Lévis, Canada

Marie-Ève Pelland and Marie-Josée Lessard Université du Québec a` Montréal

Richard Fleet Hôtel-Dieu de Lévis Hospital—A Université Laval Affiliated Hospital, Lévis, Canada

Kim L. Lavoie Université du Québec a` Montréal

This article was published August 3, 2015. It was accepted under the editorial term of Harris Cooper and Gary R. VandenBos. Geneviève Belleville, School of Psychology, Université Laval; André Marchand, Department of Psychology, Université du Québec a` Montréal; Julien Poitras, Research Center of the Hôtel-Dieu de Lévis Hospital—A Université Laval Affiliated Hospital, Lévis, Canada; Alain Vadeboncoeur, Emergency Department, Montreal Heart Institute, Montreal, Canada; Jean-Marc Chauny, Research Center, Hôpital du Sacré-Coeur de Montréal, Montreal, Canada; Guillaume FoldesBusque, School of Psychology, Université Laval, and Research Center of the Hôtel-Dieu de Lévis Hospital—A Université Laval Affiliated Hospital; Marie-Ève Pelland and Marie-Josée Lessard, Department of Psychology, Université du Québec a` Montréal; Richard Fleet, Research Center of the Hôtel-Dieu de Lévis Hospital—A Université Laval Affiliated Hospital; Kim L. Lavoie, Department of Psychology, Université du Québec a` Montréal. A small portion of the data presented in this article has been previously published in abstract form: Belleville, G., Marchand, A., Lessard, M.-J., Pelland, M.-È., & Poirier-Bisson, J. (2010). Sleep disturbances in patients with chest pain and panic disorder recruited in an emergency department [Abstract]. Sleep, 33, A232. The present study reports secondary analyses of sleep data from a sample of panic disorder patients consulting an emergency department: Marchand, A., Belleville, G., Fleet, R., Dupuis, G., Bacon, S. L., Poitras, J., . . . Lavoie, K. L. (2012). Treatment of panic in chest pain patients from emergency departments: Efficacy of different interventions focusing on panic management. General Hospital Psychiatry, 34, 671– 680. Geneviève Belleville received postdoctoral scholarships from the Research Group on Agoraphobia and Panic and the Fonds de Recherche en Santé du Québec. The research was funded by a grant to André Marchand from the Canadian Institutes of Health Research (153245). The authors report no proprietary or commercial interest in any product mentioned or concept discussed in this article. This article has been published under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License (http://creativecommons.org/ licenses/by-nc/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited and the work is not used for commercial purposes. Copyright for this article is retained by the author(s). Author(s) grant(s) the American Psychological Association the exclusive right to publish the article, identify itself as the original publisher, and claim all commercial exploitation rights. Please use APA’s Online Permissions Process (Rightslink®) at http://www.apa.org/about/contact/copyright/seek-permission.aspx to request commercial reuse of this content. For further discussion on this topic, please visit the Archives of Scientific Psychology online public forum at http://arcblog.apa.org. Correspondence concerning this article should be addressed to Geneviève Belleville, École de Psychologie, Université Laval, 2325, Rue des Bibliothèques, Québec, G1V 0A6, Canada. E-mail: [email protected]

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A B S T R A C T Approximately 50% of individuals consulting emergency departments with chest pain have noncardiac or unexplained chest pain (UCP). Of those, a significant proportion suffers from panic disorder (PD), an anxiety disorder characterized by frequent and spontaneous panic attacks. The high prevalence of PD among UCP patients is thought to be caused by similarities between symptoms of cardiovascular diseases and symptoms of panic attacks, which include chest pain. The excessive preoccupation PD patients have toward physical symptoms they interpret as dangerous makes them inclined to seek help in medical settings. A vast majority of individuals with PD also report significant sleep problems, such as insomnia and nocturnal panic attacks, that is, abrupt awakenings in a state of panic. The presence of sleep disturbances in the context of an anxiety disorder is associated with more severe anxiety symptoms, greater functional impairment, greater residual symptoms and a greater risk of relapse after a successful treatment, and increased suicidal ideation. There exist efficient treatments to overcome PD, but their impact on sleep is unknown. The objective of the present study was to examine the impact of PD treatment on sleep problems. The authors also wished to assess the influence of insomnia on PD and pain severity. The results showed that, after treatment of PD, 35% of participants still had insomnia, and 20% still reported nocturnal panic attacks. Moreover, patients with greater insomnia severity also reported more intense pain. These findings highlight the importance of carefully assessing sleep in patients with PD and UCP to determine the need to directly tackle sleep problems with adequate treatments.

S C I E N T I F I C

A B S T R A C T

A significant number of patients with unexplained chest pain (UCP) have panic disorder (PD), and most individuals with PD report poor sleep, including insomnia and nocturnal panic attacks (NPA). The objective of the study was to examine the impact of treatment for PD on sleep problems and to assess the influence of pretreatment insomnia on posttreatment persistence of PD diagnosis and pain severity. Secondary analyses were conducted on sleep data collected from 42 PD patients consulting emergency departments (ED) for UCP. In this quasi-experimental design, cohorts of participants were randomly assigned to 1 of 4 conditions: (a) 7 sessions of cognitive-behavior therapy (CBT) for PD, (b) a 1-session panic management intervention, (c) pharmacotherapy, or (d) usual care. Data from clinical interviews performed by trained assistants and from self-report questionnaires were collected before and after treatment. After treatment, 35% of participants still met the diagnostic criteria for insomnia, and 20% of the sample still reported NPA. The presence of insomnia was a predictor of posttreatment pain severity (B ⫽ 1.336, SE B ⫽ .483, p ⫽ .009), regardless of the severity of pretreatment anxiety and depressive symptoms or of assignation to an active PD treatment. Treatment for PD had a small effect on sleep, and residual sleep difficulties persisted after treatment. More importantly, the presence of insomnia was a significant predictor of persistent pain after treatment. The results highlight the importance of careful assessment of sleep before and during treatment for PD in UCP patients. Keywords: panic disorder, unexplained chest pain, sleep, insomnia, nocturnal panic attacks Supplemental materials: http://dx.doi.org/10.1037/arc0000018.supp Data repository: http://dx.doi.org/10.3886/ICPSR36134.v1 (see Belleville & Marchand, 2015)

Approximately 50% of individuals consulting emergency departments (EDs) with chest pain have noncardiac or unexplained chest pain (UCP; Christenson et al., 2004). It is not uncommon for patients with UCP to have a psychiatric disorder, mostly a mood or an anxiety disorder (Wulsin, Arnold, & Hillard, 1991). One of the most frequent is panic disorder (PD), which has been found in 20% to 30% of UCP patients (Wulsin et al., 2002). The high prevalence of PD among UCP patients is thought to be caused by similarities between symptoms of cardiovascular diseases and symptoms of panic attacks, which include chest pain. The excessive preoccupation PD patients have toward physical symptoms they interpret as dangerous makes them inclined to seek help in medical settings (Pauli et al., 1991). Between 66% and 91% of individuals with PD report poor sleep (Overbeek, van Diest, Schruers, Kruizinga, & Griez, 2005). Insomnia is common, and polysomnography studies have demonstrated that patients with PD have longer sleep latency, reduced sleep efficiency, and reduced slow-wave sleep (Hauri, Friedman, & Ravaris, 1989; Mellman & Uhde, 1989; Sloan et al., 1999). PD is associated with poor sleep, even in the absence of comorbid mood or substance use disorders (Arriaga et al., 1996; Ramsawh, Stein, Belik, Jacobi, & Sareen, 2009). Nocturnal panic attacks (NPA)—abrupt awakenings in a state of panic— constitute another sleep disturbance often associated

with PD. Recurrent NPA are reported in 18% to 33% of PD patients (Overbeek et al., 2005). The presence of sleep disturbances in the context of an anxiety disorder is associated with more severe symptoms (Soehner & Harvey, 2012), greater functional impairment (Ramsawh et al., 2009), and greater residual symptoms and a greater risk of relapse after a successful treatment (Ohayon & Roth, 2003). Moreover, insomnia is associated with greater pain intensity (Okifuji & Hare, 2011), an important variable to consider when PD is treated in the context of UCP (Belleville et al., 2014). Sleep problems in PD patients can exacerbate anxiety and provoke panic attacks the following day (RoyByrne, Uhde, & Post, 1986). Sleep problems not only exacerbate PD symptoms but can also increase psychological distress and suicidal ideation (Ag˘argün & Kara, 1998). Psychotherapy (primarily cognitive– behavior therapy; CBT), pharmacotherapy (primarily selective serotonine reuptake inhibitors), or a combination of the two have been demonstrated to effectively treat approximately 80% of individuals with PD in psychiatric settings (Clum, Clum, & Surls, 1993). Despite the availability of powerful therapeutic tools for treating panic attacks and associated anxiety, the impact of PD treatment on concomitant sleep disturbances has been disappointing. The very few studies that have measured the impact of

SLEEP IN UCP PATIENTS AFTER PD TREATMENT

CBT for PD on sleep found very small effect sizes (Belleville, Cousineau, Levrier, St-Pierre-Delorme, & Marchand, 2010). The present study reports secondary analyses of sleep data from a sample of PD patients consulting an ED for UCP (Marchand et al., 2012). The objective of the mother study from which our data was drawn was to compare the efficacy of four PD treatment modalities for ED patients with UCP. The primary objective of the present study was to examine the impact of PD treatment on sleep problems in a sample of patients consulting ED with UCP and suffering from PD. We also wished to assess the influence of pretreatment insomnia diagnosis on posttreatment PD diagnosis and pain severity. Based on previous findings, we hypothesized that treatment for PD would have a favorable impact on concomitant sleep problems, but that residual sleep difficulties would remain. We also expected that a pretreatment diagnosis of insomnia would have a detrimental effect on posttreatment PD diagnosis and pain severity. These hypotheses were tested with pre- and posttreatment data collected from a quasi-experimental treatment study.

Method Participants To recruit prospective participants, we monitored the flow of patients from the ED of three hospitals in the province of Quebec, Canada: Montreal’s Sacré-Coeur Hospital, the Montreal Heart Institute, and the Hôtel-Dieu de Lévis university-affiliated hospital center. Montreal Sacré-Cœur Hospital and the Montreal Heart Institute serve an urban population, and the Hôtel-Dieu de Lévis university-affiliated hospital center serves a rural and urban population. The latter is roughly 150 miles away from the two other hospitals. The institutional review boards of the three recruitment sites approved the research protocol, in compliance with their standards and the Code of Ethics of the World Medical Association (Declaration of Helsinki). Informed consent was obtained after the nature of the study was explained. In Phase 1, we administered diagnostic interviews and assessed sleep and other symptoms in patients consulting for UCP (Belleville et al., 2014). Participation to Phase 2—a study of PD treatment in patients with UCP (Marchand et al., 2012)—was offered to participants meeting PD criteria. Participation was voluntary and there was no compensation other than receiving free treatment for PD (except for participants in the usual care condition). Patients in the usual care condition were unaware of the existence of the three other treatment conditions and signed a different consent form. Participants were French- or English-speaking Canadians who consulted an ED with UCP. Inclusion criteria for Phase 2 were (a) a primary diagnosis of PD; (b) aged 18 years or older; (c) able to speak and read French or English; and (d) nontraumatic chest pain diagnosed as highly unlikely to be of cardiac or organic origin (i.e., negative serial electrocardiogram and cardiac enzyme tests, absence of cause identifiable by radiography). Exclusion criteria were (a) presence of a major medical condition or mental disorder with psychotic features; (b) significant cognitive deficit precluding adequate participation in study procedures; (c) drug or alcohol abuse; and (d) current psychotherapy. Participants in current psychotherapy were excluded to avoid involvement in two different psychotherapies with two different therapists at the same time, which is rarely recommended. However, participants were not automatically excluded if they used a psychotropic medication that could be used in combination with paroxetine. When a potential participant reported the use of a psychotropic medication, the possibility to combine his or her current pharmacotherapy to paroxetine was ascertained by the physi-

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cians associated with the study (Julien Poitras, Alain Vadeboncoeur, and Jean-Marc Chauny). Nevertheless, participants were asked to refrain from adjusting their psychotropic medication for the duration of the study. Questions regarding medication use and involvement in psychotherapy were asked at each assessment and throughout treatment by the therapists for participants in the CBT and PM conditions and by research assistants for participants in the pharmacotherapy and usual care conditions.

Measures Semistructured clinical interviews. Anxiety Diagnostic Interview Schedule for DSM–IV. The Anxiety Diagnostic Interview Schedule for DSM–IV (ADIS-IV; DiNardo, Brown, & Barlow, 1994) is a semistructured interview that diagnoses and evaluates the severity of anxiety disorders, mood disorders, somatoform disorders, and substance use disorders according to DSMIV–TR criteria. It has been recommended for research on PD and possesses good psychometric qualities (Shear & Maser, 1994). The ADIS-IV was used to determine eligibility for the study (presence of PD) and to gather descriptive data about the sample (presence and severity of PD, and of other anxiety, mood, and substance-related disorders). To ensure the accuracy of the diagnoses, intake interviews were audiorecorded and a second evaluator, unaware of the initial diagnostic profile, listened to 30% of the interviews. Interrater reliability was 94%. Insomnia Interview Schedule. The Insomnia Interview Schedule (IIS; Morin, 1993) is a semistructured interview that uses DSM-IV diagnostic criteria for primary and secondary insomnia to collect clinical information about sleep difficulties. For the present study, three questions were added to evaluate the presence of NPA (whether or not the participant had ever experienced an NPA and if so, how many times in the past month and in the past year). The following variables were retained as outcomes measures to assess change on sleep and insomnia after PD treatment: presence of insomnia meeting DSM-IV criteria for primary or secondary insomnia, presence of NPA in the past month (yes/no), and number of NPA in the past month. The contribution of pretreatment insomnia diagnosis was also assessed as a predictor of posttreatment PD diagnosis and pain severity. Sleep diaries. To provide subjective estimates of sleep parameters, participants completed a 1-week daily sleep diary. The following parameters were derived from the sleep diaries: (a) sleep efficiency (SE; percentage of time in bed during which the participant was asleep); (b) total wake time (TWT); (c) total sleep time (TST); (d) sleep onset latency (SOL); (e) wake after sleep onset (WASO); and (f) number of nocturnal awakenings. These variables were used as outcome measures to assess change on sleep parameters after PD treatment. Questionnaires. Insomnia Severity Index. The Insomnia Severity Index (ISI; Morin, 1993) assesses sleep impairment and its daytime consequences with seven Likert-type items. The ISI has good internal consistency (␣ ⫽ .90) and is a reliable subjective measure to detect therapeutic change (Morin, Belleville, Belanger, & Ivers, 2011). The Frenchlanguage version used in the present study has been validated (Blais, Gendron, Mimeault, & Morin, 1997). ISI mean score was used as an outcome measure to assess change on insomnia symptoms after PD treatment. Dysfunctional Beliefs and Attitudes About Sleep Scale. The Dysfunctional Beliefs and Attitudes About Sleep Scale (DBAS; Morin, 1993) was developed to evaluate sleep-disruptive cognitions. The DBAS includes 30 items, each rated on a 10-point Likert scale. It has adequate internal consistency (␣ ⫽ .77 for clinical and 0.79 for

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research samples) and temporal stability (r ⫽ .83; Morin, Vallières, & Ivers, 2007). The DBAS is sensitive to several indices of clinical change following insomnia treatment (Carney & Edinger, 2006). The French-language version has previously been validated (Blais et al., 1997). DBAS mean score was used as an outcome measure to assess change on sleep-related beliefs after PD treatment. McGill Pain Questionnaire. Pain severity was measured using the short form McGill Pain Questionnaire (MPQ; Melzack, 1987). This self-report questionnaire includes 15 descriptors of pain (11 sensory and four affective) rated on a 4-point scale. A total score can be obtained from the sum of the intensity value assigned to each pain descriptors. A pain intensity index and a visual analogue scale are also available, but the data are not reported in the present paper in order to keep the results concise. The MPQ is widely used in pain research and has been extensively validated (Melzack, 1975; Melzack & Katz, 2001). A Canadian French version is available (Boureau, Luu, & Doubrere, 1992). Participants were specifically asked to rate their chest pain. Posttreatment MPQ total score was used as the predicted indicator of pain severity in the regression analyses. Anxiety Sensitivity Index. Fear of anxiety-related symptoms was measured using the Anxiety Sensitivity Index (Peterson & Reiss, 1993). This 16-item instrument has a 5-point scale that measures the tendency to attribute negative consequences to anxious symptoms. This questionnaire was selected because it is considered to be able to detect PD in patients undergoing nuclear testing for chest pain (Carter et al., 1994). The French-language version has previously been validated (Stephenson, Marchand, Lavallée, & Brillon, 1996). Its total score was used as a control of anxiety severity in the regression analyses. Beck Depression Inventory—Revised. Presence and severity of depressive symptoms were measured using the Beck Depression Inventory—revised (BDI-II; Beck, Steer, Ball, & Ranieri, 1996). This 21-item instrument evaluates the severity of symptoms in a 4-point scale and is based on the DSM–IV criteria for major depressive

Figure 1.

disorder. The BDI-II is commonly used in research and has been extensively validated. French-language version of the BDI-I has previously been validated (Gauthier, Morin, Thériault, & Lawson, 1982), and revisions were made according to the ones made on the BDI-II English version. The BDI-II total score was used as a control of depressive symptoms severity in the regression analyses.

Procedure This cohort study was conducted from November 2005 to December 2009. Research assistants were present in the three participating EDs and gathered information about the presenting problems of all entering patients. Subsequent to diagnosis of noncardiac chest pain by the emergency physician, 246 potentially eligible participants were screened for PD (see Figure 1). The ADIS-IV and the IIS were administered by graduate and advanced undergraduate psychology students, who had received an extended formation on the administration of the semistructured interviews and were closely supervised by two psychologists specialized in the assessment of sleep and anxiety disorders (Geneviève Belleville and André Marchand). Ninety-nine eligible patients with PD were informed of the nature of the study and invited to participate. Seventy-one patients agreed to participate and completed the baseline assessment. Participants were then assigned to one of four intervention conditions according to the period during which they were recruited. Conditions, rather than participants, were randomized, using a predetermined random sequence that allowed one cohort to be recruited during a 3-month period in every year of recruitment. Posttreatment assessment was conducted 14 weeks after the beginning of treatment, a period corresponding to the end of the seven biweekly sessions of CBT. Interventions. The four conditions were (a) seven sessions of biweekly brief CBT for PD; (b) a one-session PM intervention; (c) 6 months of pharmacological treatment; and (d) usual care. The brief CBT intervention protocol included information and education about

Recruitment flow. PD ⫽ panic disorder; CBT ⫽ cognitive– behavior therapy.

SLEEP IN UCP PATIENTS AFTER PD TREATMENT

chest pain and about the nature and development of PD; demystification of panic symptoms and fears associated with PD; exposure to panic symptoms; in vivo exposure to avoided situations (if applicable); and cognitive restructuring. The intervention was manual-based and participants received a treatment workbook. Therapists were seven psychologists and advanced graduate psychology students specialized in the treatment of PD. Supervision was available upon request with the researchers (Geneviève Belleville and André Marchand). All CBT sessions were audiorecorded and 30% of recordings were randomly selected for independent evaluation. Treatment integrity was determined to be 99%. The one-session PM intervention was 2 hr long. Participants in this condition received the same treatment workbook as did participants in the CBT condition, but in-session discussion was limited to education about chest pain and panic symptoms, and strategies for facing panic. The PM intervention was delivered by the same seven psychologists who delivered the CBT intervention. Participants assigned to the pharmacotherapy condition received generic paroxetine. The initial dose was 10 mg and was gradually increased to 40 mg within 4 weeks. The 40-mg dose was maintained for 4 months and then gradually reduced and ceased altogether within 4 weeks. Overall, participants took paroxetine for a total of 6 months. Treatment adherence was evaluated with pill counts and 91% of the participants were judged to be adherent. Participants in the usual care condition completed the same assessments as did the intervention groups, but received no intervention from the research team. The treating physician at the ED assumed case management. Data analysis. Prospective recruitment of participants in ED was challenging; convincing participants to complete the study’s demanding protocol was even more difficult. Consequently, our dataset had a lot of missing data, compared to that of the primary study, which reported data on 71 participants (with an intended sample size, determined by power analysis, of 84 participants; Marchand et al., 2012). Only participants with sleep data on the same measure (IIS, sleep diaries, ISI, or DBAS) in two separate evaluations were retained for the analyses presented here, resulting in a final sample of 42 participants (see Figure 1). Even using this criterion, some data were still missing. To allow the reader to navigate the incomplete dataset, sample sizes for each analysis are provided with the results.

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Pre- and posttreatment sleep variables were compared with repeated-measures analysis of covariance for continuous outcomes. The covariable was whether the participant had been assigned to an active treatment (CBT, PM, or pharmacotherapy conditions) or not (usual care condition). Categorical outcomes were compared with ␹2 tests. Effect sizes were assessed with odds ratios (with 95% confidence intervals) for categorical variables and eta squared (␩2) for continuous variables. According to Cohen (Cohen, 1988), ␩2 ⫽ .01 is a small effect, ␩2 ⫽ .06 is a medium effect, and ␩2 ⫽ .16 is a large effect. To assess the influence of insomnia on posttreatment outcome and pain severity, two sets of hierarchical multiple regression analyses were performed, with posttreatment diagnosis of PD (measured by the ADIS-IV) and pain severity (MPQ total score) as separate predicted variables. In each analysis, the same four predictors were entered as three blocks. The first block consisted of pretreatment sensitivity to anxiety and depressive symptoms. The second block was assignation to active treatment (pharmacotherapy, CBT, or PM vs. usual care). Positive outcomes on posttreatment PD diagnosis and pain severity has previously been associated with assignation to an active treatment in this sample (Marchand et al., 2012). Finally, insomnia diagnosis (as measured by the IIS) was entered as the third block.

Results Sample Description The final sample was composed of 42 participants with PD (38% women). Mean age was 41.76 years (SD ⫽ 12.37; range 19 – 81). One half of the sample was taking a psychotropic medication at the time of recruitment: 13 participants (32%) used benzodiazepines, five (12%) used antidepressants, two (5%) used a combination of benzodiazepines and antidepressants, and one (2%) used hypnotics. Nine individuals (21%) had a comorbid major depressive disorder and 20 individuals (48%) had a comorbid other anxiety disorder: 17 (41%) had agoraphobia, three (7%) had social phobia, 11 (26%) had generalized anxiety disorder, two (5%) had obsessive-compulsive disorder, seven (17%) had specific phobia, three (7%) had posttraumatic stress disorder, and none (0%) had acute stress disorder.

Table 1 Pre- and Posttreatment Sleep Data Summary data Pre NPA Insomnia

ISI (n ⫽ 33) DBAS (n ⫽ 33) TWT (n ⫽ 20) TST (n ⫽ 19) SE (n ⫽ 19) SOL (n ⫽ 20) WASO (n ⫽ 20) # Awakenings (n ⫽ 20) # NPA (n ⫽ 35)

46% (16/35) 58% (23/40)

Inferential tests Post

20% (7/35) 35% (14/40)

Effect sizes

␹2

df

p

Odds ratio

95% CI

5.641 11.018

1 1

.018 .001

3.368 2.513

[1.164, 9.744] [1.019, 6.198]

df

p

␩2

.74 .028 .038 .058 .12 .39 .29 .71 .90

.004 .146 .217 .196 .133 .042 .063 .008 .000

Pre M (SE)

Post M (SE)

Fa

11.39 (6.39) 4.43 (1.34) 87.27 (83.30) 394.49 (79.93) 82.57 (15.01) 26.79 (22.63) 27.25 (27.43) 1.52 (1.30) 2.17 (5.31)

8.91 (6.95) 3.74 (1.41) 69.78 (59.37) 416.14 (73.67) 85.73 (12.27) 25.79 (23.05) 18.62 (22.58) 1.14 (1.16) 3.11 (14.31)

.117 5.295 4.989 4.136 2.616 .782 1.213 .141 .015

1, 1, 1, 1, 1, 1, 1, 1, 1,

31 31 18 17 17 18 18 18 33

Note. DBAS ⫽ Dysfunctional Beliefs and Attitudes About Sleep; ISI ⫽ Insomnia Severity Index; NPA ⫽ nocturnal panic attacks; SE ⫽ sleep efficiency; SOL ⫽ sleep onset latency; TST ⫽ total sleep time; TWT ⫽ total wake time; WASO ⫽ wake after sleep onset; CI ⫽ confidence interval; df ⫽ degrees of freedom. a Results for the within-subject main effect (pre- to posttreatment) with one covariable (assignation to active treatment) in the model.

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Table 2 Logistic Regression Analyses Predicting Presence of Panic Disorder Posttreatment (n ⫽ 39) Variables Step 1 Pretreatment sensitivity to anxiety Pretreatment depressive symptoms Step 2 Assignation to active treatment Step 3 Pretreatment insomnia diagnosis

Nagelkerke R2

B

SE B

Odds ratio

95% CI

.016 .027

.036 .033

1.016 1.028

[.947, 1.090] [.964, 1.095]

⫺2.956**

1.057

.052

[.007, .413]

1.754

1.036

5.780

.045 .367** .454** [.758, 44.046]

Note. CI ⫽ confidence interval. ** p ⬍ .01.

Baseline sleep disturbances. At baseline, 58% (23/40) met diagnostic criteria for insomnia, and 46% (16/35) of participants reported at least one NPA within the past month (nine participants reported both insomnia and NPA). Mean ISI score (11.39; SD ⫽ 6.39) indicated an elevated prevalence of insomnia. Sleep parameters from participants’ diaries also suggested sleep difficulties, with a mean total wake time of approximately 1.5 hr and mean sleep efficiency inferior to 85% (see Table 1). Participants reported a mean 2.17 NPA in the past month. Effect of treatment on sleep. Table 1 presents pre- and posttreatment sleep data. After treatment, 14 of 40 participants (35%) still had insomnia, and seven of 35 participants (20%) still reported NPA. More precisely, 13 of 23 (57%) individuals with baseline insomnia still had insomnia after treatment, and six of 16 (38%) individuals with baseline NPA still reported NPA after treatment. Significant improvements associated with large effect sizes were observed on the DBAS, as well as on TWT. Large effect sizes were also observed on TST and SE, although those differences were not statistically significant. Only 19 participants reported sufficient data on their sleep diary to compute TST and SE, so the statistical analyses may have been underpowered. Surprisingly, the number of NPA reported in the past month increased after treatment, although the difference was not statistically significant. Large standard deviations indicated considerable individual differences. Impact of pretreatment insomnia diagnosis on posttreatment outcomes. Results from logistic regression analyses indicated that together, all three blocks (composed of pretreatment sensitivity to anxiety and depressive symptoms, assignation to active treatment and pretreatment insomnia diagnosis) accounted for 45.4% of the prediction of posttreatment PD, ␹2(4) ⫽ 15.14, p ⫽ .004 (see Table 2). The first block, composed of sensitivity to anxiety and depressive symptoms, did not significantly contribute to the model. The second block (assignation to active treatment) provided a significant 32.2% increase in R2, ␹2(1) ⫽ 10.51, p ⫽ .001. The addition of pretreatment insomnia diagnosis (third block) in the model provided an 8.7% increase in

Nagelkerke R2 that did not reach statistical significance, ␹2(1) ⫽ 3.37, p ⫽ .066. Results from hierarchical multiple regression analyses indicated that together, all three blocks (composed of pretreatment sensitivity to anxiety and depressive symptoms, assignation to active treatment and pretreatment insomnia diagnosis) accounted for 24.3% of posttreatment pain severity variance, F(5, 31) ⫽ 3.64, p ⫽ .010 (see Table 3). The blocks composed of sensitivity to anxiety, depressive symptoms, and assignation of an active treatment of PD did not significantly contribute to the model. The addition of pretreatment insomnia diagnosis (third block) in the model provided a significant 16.1% increase in accounting for pain severity variance, Finc(4, 32) ⫽ 3.89, p ⫽ .011.

Discussion The objectives of the present study were to examine the impact of treatment for PD on associated sleep problems in PD patients presenting in ED with UCP, and to explore the impact of pretreatment insomnia on panic and pain outcomes after treatment. Findings revealed significant decreases in dysfunctional beliefs and attitudes about sleep and wake after sleep, but not in insomnia severity. After treatment, 35% still met diagnostic criteria for primary or secondary insomnia, and 20% of the sample still reported NPA. Together, these results confirmed our hypothesis: treatment for PD had a small positive impact on sleep, but residual sleep difficulties persisted after treatment. This hypothesis is also supported by findings revealing changes in sleep-related beliefs and time spent awake during the night, but not in self-perceived insomnia severity: although treatment for PD will have a positive impact on some aspects of sleep, general dissatisfaction with sleep may still be reported by patients after a successful treatment of PD. A small effect of PD treatment on sleep problems was also observed in a study comparing CBT alone to combined CBT and buspirone (Bouvard, Mollard, Guerin, & Cottraux, 1997), and after an extensive 18-session CBT for PD patients (Cervena, Matousek, Prasko, Brunovsky, & Paskova, 2005).

Table 3 Multiple Regression Analyses Predicting Posttreatment Pain Severity (n ⫽ 37) Variables Step 1 Pretreatment sensitivity to anxiety Pretreatment depressive symptoms Step 2 Assignation to active treatment Step 3 Pretreatment insomnia diagnosis *

p ⬍ .05.

**

p ⬍ .01.

B

SE B



sr2

.009 ⫺.037

.024 .022

.061 ⫺.282

.062 ⫺.277

⫺.921

.490

⫺.311

⫺.311

1.336**

.483

.488**

.440

Adjusted R2

⌬R2

.022

.077

.090

.089

.243*

.161**

SLEEP IN UCP PATIENTS AFTER PD TREATMENT

It could be argued that the effect of treatment for a given disorder can be expected to be small if the baseline pathology is minimal. Indeed, in our study and in previous literature in this area, the impact of PD treatment on sleep was evaluated in individuals who did not explicitly report sleep difficulties. Still, 57% of individuals with baseline insomnia still had insomnia after treatment, and 38% of individuals with baseline NPA still reported NPA after treatment. These observations suggest that some sleep problems persist after treatment of PD. Nevertheless, future studies should assess whether the impact of PD treatment on sleep in individuals with explicit sleep problems is similar to that observed in general samples of PD patients. The presence of insomnia was a predictor of posttreatment pain severity, regardless of the severity of pretreatment anxiety and depressive symptoms or of assignation to an active PD treatment. Sleep difficulties appear to be common in patients with UCP (Jerlock, Gaston-Johansson, Kjellgren, & Welin, 2006) and, in patients presenting to ED with UCP, insomnia was associated with greater pain intensity (Belleville et al., 2014). Adding sleep management strategies to psychotherapy for UCP (Mayou et al., 1997), or for PD associated with UCP, may prove useful. There exist efficacious time-limited cognitive– behavioral interventions specifically targeting insomnia (National Institutes of Health, 2005). The efficacy of CBT for insomnia in UCP patients, either alone or in combination with a treatment targeting pain, anxiety or panic, should be assessed in future studies. Several characteristics of the study reported here may limit the generalizability of the findings. First, results were obtained from secondary analyses, and the mother study was not designed to assess sleep difficulties in PD. Consequently, our sample was restricted to PD patients with UCP recruited in ED. Second, because of the difficulty of prospectively recruiting patients with PD who were consulting primarily for chest pain (and not for panic symptoms), the sample was small, limiting the statistical power. Among the strengths of the study, insomnia was measured with validated multimethod measures (i.e., a diagnostic interview, a self-report questionnaire, and daily self-observations), and treatments were based on manuals (for psychotherapies) and protocols (for pharmacotherapy). This study is one of the very few to report on the sleep quality of patients with PD undergoing treatment.

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Received June 23, 2014 Revision received March 9, 2015 Accepted April 7, 2015 䡲