Cognitive behaviour therapy to improve mood in people with epilepsy: a randomised controlled trial.

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Cognitive Behaviour Therapy to Improve Mood in People with Epilepsy: A Randomised Controlled Trial ab

a

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Milena Gandy , Louise Sharpe , Kathryn Nicholson Perry , Zoe d

de

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Thayer , Laurie Miller , Janet Boserio & Armin Mohamed

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The School of Psychology, University of Sydney, Sydney, Australia b

Department of Psychology, Centre for Emotional Health, Macquarie University, Sydney, Australia c

Centre for Health Research and School of Social Sciences and Psychology, University of Western Sydney, Sydney, Australia d

Institute of Clinical Neurosciences, The Royal Prince Alfred Hospital, Sydney, Australia e

Sydney Medical School, University of Sydney, Sydney, Australia Published online: 18 Mar 2014.

To cite this article: Milena Gandy, Louise Sharpe, Kathryn Nicholson Perry, Zoe Thayer, Laurie Miller, Janet Boserio & Armin Mohamed (2014) Cognitive Behaviour Therapy to Improve Mood in People with Epilepsy: A Randomised Controlled Trial, Cognitive Behaviour Therapy, 43:2, 153-166, DOI: 10.1080/16506073.2014.892530 To link to this article: http://dx.doi.org/10.1080/16506073.2014.892530

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Cognitive Behaviour Therapy, 2014 Vol. 43, No. 2, 153–166, http://dx.doi.org/10.1080/16506073.2014.892530

Cognitive Behaviour Therapy to Improve Mood in People with Epilepsy: A Randomised Controlled Trial Milena Gandy1,2*, Louise Sharpe1, Kathryn Nicholson Perry3, Zoe Thayer4, Laurie Miller4,5, Janet Boserio4 and Armin Mohamed4,5


1

The School of Psychology, University of Sydney, Sydney, Australia; 2Department of Psychology, Centre for Emotional Health, Macquarie University, Sydney, Australia; 3Centre for Health Research and School of Social Sciences and Psychology, University of Western Sydney, Sydney, Australia; 4Institute of Clinical Neurosciences, The Royal Prince Alfred Hospital, Sydney, Australia; 5Sydney Medical School, University of Sydney, Sydney, Australia Abstract. This study compared a 9-week individualised Cognitive Behaviour Therapy (CBT) programme for people with epilepsy (PWE), with a wait-list control. Fifty-nine PWE were randomised and 45 (75%) completed post-treatment outcomes. People with lower quality of life (QoL), particularly for cognitive functioning, were more likely to drop out. Analyses based on treatment completers demonstrated significant improvements on the Neurological Depressive Disorders Inventory for Epilepsy ( p ¼ .045) and Hospital Anxiety Depression Scale-Depression subscale ( p ¼ .048). Importantly, CBT significantly reduced the likelihood of clinical depressive symptoms ( p ¼ .014) and suicidal ideation ( p ¼ .005). Improvements were not observed for anxiety, QoL or maintained overtime for depression. Results suggest that CBT was effective, however, and could be improved to increase patient retention and long-term outcomes. Key words: mood; psychopathology; psychotherapy; anxiety. Received 18 November 2013; Accepted 5 February 2014 Correspondence address: Dr Milena Gandy. The School of Psychology, University of Sydney, Sydney, Australia. Tel: þ61 2 9850 4152. Fax: þ61 (0)2 9850 9911. E-mail: [email protected]

Introduction Depression is now recognised as the most common and problematic psychiatric condition experienced by people with epilepsy (PWE; LaFrance, Kanner, & Hermann, 2008). There is consistent evidence to demonstrate that the rates of depression in PWE are alarmingly high compared to the general population and other chronic illnesses (Barry et al., 2008; Beyenburg, Mitchell, Schmidt, Elger, & Reuber, 2005; Hermann, Seidenberg, & Bell, 2000). Indeed, recent international estimates suggest that between 25% and 48% of PWE met criteria for a depressive disorder (Bragatti et al., 2011; Brandt et al., 2010; de Araujo, Mazetto, da Silva, Caboclo, & Yacubian, 2011; Desai et al., 2010; Filho et al., 2008; Sanchez-Gistau et al., 2010). Many PWE also experience atypical and q 2014 Swedish Association for Behaviour Therapy

subclinical forms of depression that fail to meet formal DSM-IV criteria for depression, but are highly disruptive (Kanner, 2009a). Overall, depression in PWE is associated with numerous negative consequences, including increased suicide risk (Jones et al., 2003; Nilsson, Ahlbom, Farahmand, Asberg, & Tomson, 2002; Verrotti et al., 2008), poorer quality of life (QoL; Boylan et al., 2004; Taylor, Sander, Taylor, & Baker, 2011) and complications with epilepsy management (Barry et al., 2008; Cramer, Blum, Reed, & Fanning, 2003). Nevertheless, there still remains a lack of clear evidence regarding the most effective pharmacological and psychological treatments (e.g. Noe, Locke, & Sirven, 2011; Ramarantnam, Baker, & Goldstein, 2008) to improve depression in PWE. Cognitive Behaviour Therapy (CBT) has recently been recommended by the


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international consensus clinical practice statement for the treatment of neuropsychiatric conditions associated with epilepsy as the psychological treatment of choice for depression in PWE (Kerr et al., 2011). Despite the consensus that PWE who are depressed should be given CBT, the most recent Cochrane review concluded that there was insufficient evidence to support the efficacy of any type of psychotherapy for PWE (Ramarantnam et al., 2008). Slightly more optimistic conclusions were recently outlined by a systematic review of only CBT programmes for PWE. This review reported that CBT interventions targeting depressive symptoms showed promise and were possibly efficacious (Gandy, Sharpe, & Nicholson Perry, 2013). While these preliminary conclusions are encouraging, they were based on only three effective randomised controlled trials (RCTs), and the review highlighted the need for further trials in this area. Gandy et al. (2013) found that three of the four trials of CBT that focused specifically on depression resulted in improvements not observed in the control group. However, one of those trials targeted adolescents with recently diagnosed epilepsy (Martinovic´, Simonovic´, & Djokic´, 2006) and therefore may not be generalisable to other age groups or stages of epilepsy diagnosis (e.g. adults with a long duration of epilepsy). The second trial, the PEARLS trial, developed a comprehensive CBT programme administered over a 12month period, where therapy was delivered in the participant’s home (Ciechanowski et al., 2010). Although this trial had promising results, the use of home visits to administer therapy is expensive and therefore may not be available in most settings. The other trial adopted a more cost-effective approach, using a combination of phone and Internet-based treatment, where participants were treated in online groups (Thompson et al., 2010). As a result, it is unclear the degree to which the peer support versus CBT skills accounted for the positive findings. Further, the high drop-out rates (36%) were problematic in this trial of group therapy. Importantly, two of the most effective previous trials, both of which also reported good treatment adherence, utilised an individual therapy approach (Ciechanowski et al., 2010; Martinovic et al, 2006).

COGNITIVE BEHAVIOUR THERAPY

While these findings highlight the potential importance of CBT in the management of depressed mood in PWE, there is need for further RCTs in this area in order to confidently establish the level of effectiveness of CBT in the management of depression in PWE (Gandy et al., 2013). The aim of this study was to develop and assess the efficacy of a CBT programme for treating mood-related symptoms in adults with epilepsy post-treatment and at 3-month follow-up. We developed a 9-week manualised CBT intervention that aimed to improve depressive symptoms in the context of living with epilepsy. The present study reports the results of a RCT that compared the effectiveness of this individualised CBT treatment programme with a waitlist control (WLC) condition in a sample of adults with epilepsy. The primary outcomes were depressive symptoms, suicidal risk and rates of clinically significant depressive symptoms. We hypothesised that CBT would produce significant benefits for PWE in primary outcome variables compared to WLC. We also assessed the impact of the programme on secondary variables including anxiety and quality of life.

Methods Participants

The majority of participants were recruited from the Comprehensive Epilepsy Service at the Royal Prince Alfred Hospital (RPAH) in Sydney Australia (n ¼ 59). The remaining participants contacted us following advertisements about the study with Epilepsy Action Australia (EAA: n ¼ 7). Recruitment took place between January 2011 and December 2011. To be eligible to take part in the trial, participants had to (1) provide written informed consent, (2) have a formal diagnosis of epilepsy according to the International League Against Epilepsy (ILAE) criteria (1989) that was confirmed by their treating neurologist, (3) be between the ages of 18 and 65, (4) be of at least average range IQ as estimated by a score of $ 80 (at least low average intelligence) on the National Adult Reading Test (NART; Crawford, Parker, Stewart, Besson, & De Lacey, 1989) and (5) be fluent in English. Participants did not have to have a diagnosable depressive disorder to be eligible, as it is known that amongst PWE


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Cognitive behaviour therapy to improve mood in people with epilepsy

atypical presentations are particularly common (Kanner, 2009a). Participants were excluded if they (1) had a psychotic disorder, (2) were acutely suicidal, (3) had a severe personality disorder or (4) were about to undergo epilepsy surgery. We also excluded participants whose primary health concern and reason for seeking psychological support was related to another chronic illness (e.g. multiple sclerosis) as opposed to their epilepsy, which was considered a secondary health problem. This study had ethical approval from the Sydney South West Area Health Service Ethics Review Committee (RPAH Zone), which was ratified by the University of Sydney Ethics Committee. The trial was registered with the Australian New Zealand Clinical Trials Registry (ACTRN12609000389202). Figure 1 summarises the recruitment details of participants. Of the 66 participants who volunteered, 7 (11%) were excluded prior to randomisation. Reasons for exclusions included: other primary medical illness (n ¼ 2), acutely suicidal (n ¼ 2), no formal epilepsy diagnosis (n ¼ 1), presence of psychosis (n ¼ 1) and scheduled epilepsy surgery (n ¼ 1). The remaining 59 participants were randomised to CBT (n ¼ 31) or WLC (n ¼ 28). Attrition was significantly different between the groups ( p ¼ .014). For the CBT group, there was a higher drop-out rate (12/31 ¼ 39%), with only 19 (61%) participants completing the intervention. Factors contributing to treatment dropout are highlighted within the results and discussion. One participant completed posttreatment assessments despite not completing all sessions. Hence, data were available for 20 participants. All 19 of those who completed treatment also completed the 3-month followup. Within the WLC group, only 3 out of 28 participants (11%) dropped out at posttreatment, and a further 2 at followup (5/28 ¼ 18%). Procedure. All eligible participants were provided with an information and consent form. Those who consented completed the battery of baseline measures outlined in the Measures section. Following completion of baseline measures, participants were randomly allocated to treatment condition. A list of random numbers using the Bernoulli function was generated by an independent researcher who was not involved in the treatment or assessment

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of the participants. The set of random numbers was consecutively assigned to each new participant. Random allocation was concealed until after participants had completed the baseline data. Participants assigned to the CBT intervention completed the assessment and 9-week treatment outlined in Table 1. Participants assigned to the WLC condition completed the same set of questionnaires at the equivalent time points of 2 and 5 months following randomisation. After 5 months on the waiting list, these participants were invited to take part in the CBT intervention. Measures. Demographic and medical details. Basic demographic data were collected, including gender, age, employment status, relationship status and highest educational attainment. Medical details included medication status, presence of additional chronic illnesses, history of diagnosis and/or treatment of mental illness, and the duration of epilepsy. These medical details were confirmed by the patients’ treating neurologist and clinical nurse specialist, who also coded whether the participant had well-controlled or refractory epilepsy. The National Adult Reading Test (NART; Mathias, Bowden, & Barrett-Woodbridge, 2007). The NART is a single word reading pronunciation test used to screen for intellectual functioning (Mathias et al., 2007). Participants were given a standardised list of 50 words (e.g. simile, banal) from the NART and asked to read them aloud to the chief researcher who recorded the number of errors made. The number of errors was used to calculate the participant’s estimated Wechsler Adult Intelligence Scale-Revised Full Scale IQ score. The NART has good reliability (Bright, Jaldow, & Kopelman, 2002), and loads strongly onto general intelligence factor (Crawford et al., 1989). Scores , 80 on the NART are indicative of below average intelligence. No participants referred to the RCT were identified to be in this range. The Neurological Depressive Disorders Inventory-Epilepsy (NDDI-E; Gilliam et al., 2006). The NDDI-E is an epilepsy-specific 6item self-report depression screening measure (Gilliam et al., 2006). Participants are required to indicate how frequently they have experienced six symptoms (e.g. “everything is a struggle”) over the past two weeks on a 4point Likert scale (1 ¼ never, 2 ¼ rarely,

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Adults 18-65 years with epilepsy referred Epilepsy Action Australia (n=7)

Royal Prince Alfred Hospital (n=59)

Assessed for Eligibility (NART, assessed exclusion criteria ) Excluded (n=7) • • •

epilepsy surgery (n=1) health condition (n=2) acutely suicidal (n=2)

psychosis (n=1) not confirmed epilepsy (n=1)

• •

Remaining participants (n =59)


Baseline questionnaires (NDDI-E, HADS) RANDOMISED (= 59) WLC (n = 28)

CBT (n = 31)

Referred to therapist for detailed assessment & 8 weekly one-hour sessions Drop-out CBT (n = 12) • not contactable (n=1) • work hours (n=2) • travel difficulties (n=3) • not motivated (n=1) • health problems (n=2) • poor memory (n=1)

•

WL (n = 3) not contactable (n=3)

Post-Treatment asessment measures (NDDI-E, HADS) CBT (n=20) • completed CBT (n=19) • drop-out return (n=1)

WLC (n = 25)

Drop-out CBT (n=0) •

WLC (n=2) work commitments (n=2)

3-month Follow-up Assessment (NDD-E, HADS) CBT (n=19)

WLC (n=23)

Referred to therapist for detailed assessment & 8 weekly one-hour sessions per week

Figure 1. Recruitment flow-chart. Note. Abbreviations: CBT, Cognitive Behaviour Therapy; HADS, Hospital Anxiety Depression Scale; NART, National Adult Reading; NDDI-E, Neurological Depressive Disorders Inventory-Epilepsy; QOLIE, Quality of Life Inventory in Epilepsy; WLC, Waitlist Control.

3 ¼ sometimes and 4 ¼ always or often). The scores are summed to give a total score with a maximum of 24. Scores $ 15 are indicative of clinically significant depression and have been found to be a reliable screen for depressive

disorders in PWE (Gandy et al., 2012). Cronbach’s alpha for the NDDI-E in the current study was high (a ¼ .80). The NDDI-E contains an item that assesses the frequency of suicidal ideation (“I’d be

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Table 1. Session by session content of CBT programme Session

CBT component

1 2

Assessment, introduction to treatment, CBT formulation of presenting problem Education about epilepsy and mood difficulties, managing lifestyle factors in epilepsy, e.g. seizure triggers & medication, problem-solving training Behavioural maintaining cycles in depression and reversing via behavioural activation Behavioural maintaining cycles in anxiety (avoidance) and reversing via exposure techniques Cognitive aspects of mood difficulties, identifying unhelpful thinking and cognitive distortions Cognitive challenging, behavioural experiments Assertive communication training Identifying life values and targeting the enmeshment between self-identity and epilepsy Review of programme, relapse prevention

3 4


5 6 7 8 9

Note. CBT, Cognitive Behaviour Therapy.

better off dead”) over the past two weeks. This item was analysed separately in order to specifically assess current suicidal ideation. The Hospital Anxiety Depression Anxiety Scale (HADS; Zigmond & Snaith, 1983). The HADS is a 14-item measure of symptoms of depression (HADS-D; 7 items) and anxiety (HADS-A; 7 items) for patients who are physically ill (Zigmond & Snaith, 1983). There are three comprehensive reviews relating to the validity and clinical use of the HADS (Bjelland, Dahl, Haug, & Neckelmann, 2002; Christoph, 1997; Spinhoven et al., 1997). In the current data-set, internal consistency was acceptable for the HADS-D (a ¼ .81) and HADS-A (a ¼ .76). The Quality of Life Inventory in Epilepsy-31 (QOLIE-31; Cramer et al., 1998). The QOLIE31 produces a total health-related QoL (HRQoL) score based on the assessment of seven subscales: emotional well-being (5 items, a ¼ .75), social function (5 items, a ¼ .69), energy/fatigue (4 items, a ¼ .77), cognitive function (6 items, a ¼ .83), seizure worry (5 items, a ¼ .86), medication effects (3 items, a ¼ .72), overall QoL (2 items, a ¼ .21) and one question about overall health status. Raw scores are converted to a 0–100 range with higher scores indicating better HRQoL. All QoL subscales had acceptable Cronbach alpha levels, except for the two-item overall QoL scale, which was excluded from further individual analysis. In the current data-set, the total QoL score had good internal consistency (a ¼ .81) and was used in the majority of analyses.

The CBT intervention. This CBT treatment was modelled on previous CBT manuals for depression in other illness groups with confirmed treatment efficacy (Sharpe, Allard, & Sensky, 2008; Sharpe, Sensky, Timberlake, Allard, & Brewin, 2001; Sharpe, Sensky, Timberlake, Ryan, & Allard, 2003). The CBT components were tailored towards treating depressive symptoms in the context of living with epilepsy. We also incorporated treatment components to address the common occurrence of comorbid anxiety and depression in PWE, as has been recommended by Kanner (2009b) and Kanner et al. (2012). Treatment was carried out at the University of Sydney Psychology Clinic. It involved a 1 –2-hour therapist-client assessment session and subsequently 8-weekly, individualised, 1hour therapist-client sessions. Each session included a home-based practical task to be completed between sessions that were reviewed at the beginning of the next session. For instance, following Session 3 participants were requested to practice behaviour activation by scheduling time for both peasant and achievement-based activities during their week. Sessions were tailored to the individual patient’s needs based on a cognitive behaviour formulation of their presenting epilepsyrelated mood problems. That is, the programme included an assessment interview, which aimed to understand the person’s beliefs and behaviours relating to their epilepsy and their individual treatment goals. We included a session of psychoeducation, including identifying the triggers for seizures


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(where relevant). The cognitive components of the programme taught participants the relationships between their thoughts, feelings and behaviours. Participants learned to identify unhelpful thoughts and skills for challenging these (including thought challenging and behavioural experiments). In addition, we included a single session on anxiety, which focused on identifying situations that patients avoided and developing hierarchies to help them achieve particular goals relating to these situations. In addition, we included a communication session to help participants think about ways in which to communicate with others about their illness. The programme also helped identify the patient’s values and set goals to allow them to live a valued life with epilepsy rather than feeling that they were defined by the illness. The final session involved relapse prevention. A description of the therapy components is provided in Table 1. As many PWE complain of memory difficulties (Hall, Isaac, & Harris, 2009; Helmstaedter & Kurthen, 2001), all CBT sessions were designed in a way to optimise retention of skills. This involved using a number of written handouts, reviewing material learnt in the past sessions each week and tape-recording each session for the patients to review between sessions. The treatment was delivered by postgraduate Doctorate level intern psychologists under the supervision of senior clinical psychologists (who had at least 10 years experience). All therapists and their supervisors attended a one-day workshop on the use of the treatment manual. During therapy, a strict adherence checklist was completed by all therapists, who also attended weekly supervision with senior clinical psychologists, who had been specifically trained for the project. Analysis. The power analysis was based on the median effect size of CBT treatments reported in a systematic review of CBT interventions for depression in PWE (ES ¼ .86; Gandy et al., 2013). According to G-power, 20 participants per group were needed to give 98% power at a .05 level of significance (source: G-power). All analyses were conducted using IBM SPSS Statistics Software Version 20, utilising twotailed p values. The distribution of data was inspected for normality. A series of t-tests were conducted to determine whether there were significant


differences between CBT and WLC groups at baseline. x 2 tests were used for categorical data. Covariates were included on the basis of those variables that both (a) differed significantly between the groups at randomisation and (b) were correlated with changes in the primary or secondary outcomes. A series of t-tests and x 2 analyses were conducted to determine whether there were any significant differences in demographic, medical, mood or psychosocial baseline measures between those participants who completed post-treatment assessments or dropped out of the trial. The major analyses consisted of a series of group (CBT vs WLC) X time (pre- vs post OR pre- vs 3-month follow-up) ANOVAs to determine whether CBT produced changes in symptoms on our primary outcomes (depression indices) that were greater than those in the WLC group at post-treatment and at 3-month follow-up. Similar analyses were conducted for the secondary outcomes (QoL, anxiety symptoms). In addition, we wanted to assess for clinical, as well as statistical, significance of change. Therefore, we categorised participants according to whether or not they fell above the clinical cut-off for depression on the NDDI-E ($ 15). x 2 analyses comparing those in the CBT group and WLC group for the proportion who met criteria before and after treatment were conducted at post-treatment and at 3-month follow-up. The size of the treatment effect was assessed using Cohen’s d standardised effect sizes, which were calculated for within- and betweengroup changes, based on the pooled standard deviation. Standard criteria for small (.02), medium (.05) and large (.08) were used (Cohen, 1992).

Results Descriptive data for the final sample (n ¼ 45) and those participants within the CBT intervention group (n ¼ 20) and the WLC group (n ¼ 25) are summarised in Table 2. There were no significant differences between completers in CBT and WLC groups for any demographic, epilepsy or outcome variables at baseline. However, there was a significant difference in the gender distribution for those initially allocated to CBT (n ¼ 31) versus WLC (n ¼ 28), with fewer women allocated

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Table 2. Demographics and epilepsy characteristics of CBT and WLC groups


Characteristic

CBT (n ¼ (20) n (%)

WLC (n ¼ (25) n (%)

Female 10 (50%) 19 (76%) Male 10 (50%) 6 (24%) Current partner (married, cohabiting, dating) 13 (65%) 14 (56%) No current partner (single, divorced or widowed) 7 (35%) 11 (44%) Secondary school/vocational education 12 (60%) 11 (44%) Tertiary education 8 (40%) 14 (56%) Employed/student 10 (50%) 19 (76%) Unemployed/retired/homemaker 10 (50%) 6 (24%) Focal epilepsy 14 (70%) 21 (79%) Generalized epilepsy 6 (30%) 4 (16%) Refractory 9 (45%) 13 (52%) Well-controlled 11 (55%) 12 (48%) Anti-depressant medication 3 (15%) 4 (16%) Anti-anxiety medication 1 (5%) 1 (4%) Previous mental illness 13 (65%) 10 (40%) Clinical range NDDI-E ($15) 11 (80%) 16 (64%) Mean (SD;Range) Age (years) 41 (12; 19 – 66) 38 (13; 20 – 63) NART (estimated IQ) 104 (10; 84 – 118) 106 (10; 81 – 122) Number of AEDs 2 (.8;0– 4) 2 (1;1– 4) Common types of AEDs taken n (%) n (%) Keppra 9 (45%) 12 (48%) Tegretol 4 (20%) 7 (28%) Epilim 8 (40%) 7 (28%) Lamictal 4 (20%) 7 (28%) Duration of epilepsy (years) 15 (13;.5– 37) 12 (9;.5– 32) NDDI-E 16 (4; 10 – 21) 16 (4; 8 – 22) HADS-Depression 5 (4.0; 0 – 13) 6 (4; 0 – 17) HADS-Anxiety 8 (4; 0 – 17) 8 (4; 2 – 19) QOLIE-31Total 54 (12; 34 – 72) 46 (16; 15 – 79)

x 2 (1) or t(43) p value .07 .38 .22 .07 .22 .43 .63 .70 .09 .38 .42 .45 .14

.39 .83 .73 .70 .06

Note. AEDs, antiepileptic drugs; CBT, Cognitive Behaviour Therapy; HADS, Hospital Anxiety Depression Scale; NART, National Adult Reading; NDDI-E, Neurological Depressive Disorders Inventory-Epilepsy; QOLIE-31, Quality of Life Inventory in Epilepsy; SD, standard deviation; WLC, waitlist control

to CBT, (x 2[1, n ¼ 59] ¼ 4.38, p ¼ .04). Similarly, more participants randomised to the WLC were taking a greater number of antipileptic drugs (AEDs) (t [57] ¼ 2.14, p ¼ .04) than those in the CBT group. However, the most common AEDs types (e.g. Keppra, Epilim, Tegretol and Lamictal) taken by the two groups were comparable. Furthermore, neither gender ( p . .51) nor the number of AED taken ( p . .63) was significantly associated with the change in outcome measures following treatment. Hence, the need to control for these factors did not arise.

Drop-out analysis

The only outcome measure to significantly differ between completers versus drop-outs was QoL. Those who dropped out of the RCT

had significantly poorer QoL at baseline compared to those who remained in the RCT (t[57] ¼ 2 2.33, p ¼ .023). On closer inspection of the QoL sub-scales, it was those who reported poorer cognitive functioning on the QOLIE-31subscale who were more likely to drop out (t[57] ¼ 2 3.04, p ¼ .004).

Post-treatment analysis

Means and effect sizes for outcome measures pre- and post-treatment are displayed in Table 3.

Primary outcomes

For depression scores on the NDDI-E, there were no main effects for time (F[1,43] ¼ .633, p ¼ .431) or group (F[1,43] ¼ 1.506, p ¼ .226), but there was a significant group by time

Pre-treatment mean (SD)

4.58 (3.59) 5.5 (5.26) 6.11 (2.96) 7.45 (3.78) 59.64 (14.30) 2 .33 (2 .94 to .30) 49.35 (20.74) 2 .02(2.57 to .54)

4.05 (3.70) 6.32 (4.64)

6.8 (2.90) 7.48 (4.20)

58.38 (11.83) 46.40 (18.21)

.48 (2 .16 to 1.10) .13 (2 .43 to .68)

.26 (2 .37 to .88) 2 .11 (2 .67 to .44)

.58 (2 .07 to 1.20) 2 .47 (2 1.02 to 2.10)

1.47 (.84) 1.69 (1.04)

1.30 (.57) 1.96 (.89)

.38 (2 .26 to 2 .99) 2 .16 (2 .72 to .39)

Pre-to post-treatment CBT (n ¼ 20) WLC (n ¼ 25)

14.11 (3.70) 15.55 (3.76)

3-Month follow-up mean (SD)

14.30 (3.40) 16.48 (3.81)

Post-treatment mean (SD)

2 .23 (2.84 to 2 .38) 2 .20 (20.81 to .41)

2 .86 (2 1.46 to 2.23) 2 .53 (2 1.12. to 07)

2 .39(2 1.02 to .25) 2 .18(2 .74. to 39)

.76 (.14 to 1.36)

.57(2 .06 to 1.18)

2 .39 (21.00 to .23)

2 .39 (2.99 to .23)

Follow-up CBT (n ¼ 19) WLC (n ¼ 23)

2 .60 (2 1.19 to 2.01)

Post-treatment CBT (n ¼ 20) WLC (n ¼ 25)

.67 (.01 to 1.30) 2 .18(2.77 to .41) .15 (2 0.42. to .71)

.13 (2 .50 to .76) 0 (2.56 – .57)

.28 (2 .36 to .91) 2 .14 (2070 to .43)

.41 (2 .23 to 1.04) .09 (2 .48 to .66)

Pre to follow-up CBT (n ¼ 19) WLC (n ¼ 23)

Between group effect size Cohen’s d (95%: CI range)

Gandy et al.

Note. CBT, Cognitive Behaviour Therapy; CI, confidence interval; HADS-A, Hospital Anxiety Depression Scale-Anxiety subscale; HADS-D, Hospital Anxiety Depression Scale-Depression subscale; NDDI-E, Neurological Depressive Disorders Inventory-Epilepsy; QOLIE-31, Quality of Life Inventory in Epilepsy; SD, standard deviation; WLC, waitlist control. Guideline for Cohen d effect size interpretation: small (.02), medium (.05) and large (.08).

NDDI-E CBT 15.65 (3.76) WLC 15.88 (3.52) NDDI-E suicide item CBT 1.70 (.80) WLC 1.56 (.82) HADS-D CBT 5.10 (4.28) WLC 5.52 (8.84) HADS-A CBT 8.45 (3.93) WLC 8.00 (3.69) QOLIE-31 CBT 54.45 (12.32) WLC 46.07 (15.92)

Measure group

Within group effect size Cohen’s d (95%: CI range)

Table 3. Outcome measure means and effect sizes for pre- and post-treatment and 3-month follow-up


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interaction resulting in a medium-sized effect of treatment (F[1,43] ¼ 4.279, p ¼ .045, d ¼ .60). x 2 analyses also revealed that there were significantly fewer people within the clinical depression range in the CBT group following treatment compared to WLC (x 2[1, n ¼ 45] ¼ 6.00, p ¼ .014). For suicide risk scores on the NDDI-E, there was no main effect for group (F[1,43] ¼ 1.50, p ¼ .188) or for time (F[1,43] ¼ .00, p ¼ 1), but there was a significant group by time interaction resulting in a large effect of treatment (F[1,43] ¼ 8.79, p ¼ .005, d ¼ 0.86), favouring CBT. Similarly for depression scores on the HADS-D, there were no main effects for time (F[1,43] ¼ .076, p ¼ .785) or group (F[1,43] ¼ 1.237, p ¼ .272), but again there was a significant group by time interaction resulting in a medium effect of treatment (F[1,43] ¼ 4.140, p ¼ .048, d ¼ .53).

Secondary outcomes

For anxiety scores on the HADS-A, there was a significant main effect for time only (F [1,43] ¼ 4.130,p ¼ .048), indicating overall improvement for both groups. For QoL, there was a significant main effect for group only, indicating that the CBT group had better QoL (F[1,43] ¼ 575.778, p # .001). These differences were not significant at baseline, although there was a trend in that direction (t[43] ¼ 2 1.935, p ¼ .060), but differences between the two groups were evident at post-treatment (t[43] ¼ 2 2.542, p ¼ .015) with QoL significantly higher in the CBT groups.

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group by time interaction (F[1,40] ¼ 2.95, p ¼ .094, d ¼ 0.23). For depression on the HADS-D, there were no main effects or significant group by time interaction (F [1,40] ¼ .352, p ¼ .556, d ¼ .20).

Secondary outcomes

For HADS-A scores, there was a significant main effect of time (F[1,40] ¼ 7.892, p ¼ .008), but no main effects for group (F[1,40] ¼ .239, p ¼ .628) and no significant group by time interaction (F[1,40] ¼ 3.05, p ¼ .089). For QoL, there was a significant main effect of time (F[1,40] ¼ 4.725, p ¼ .036) and group favouring CBT (F[1,40] ¼ 4.178), p ¼ .048), but no group by time interaction (F[1,40] ¼ .21, p ¼ .652).

Intention-to-treat analysis

The findings of an intention-to-treat analysis, using the last-observation carried forward method, were consistent with the completers analysis apart from the total NDDI-E scores, which failed to reach significance ( p ¼ .057).

Discussion

Means for outcome measures pre-treatment and 3-month follow-up and effect sizes are displayed in Table 3.

The aim of this study was to assess the effectiveness of a 9-week CBT intervention tailored towards improving depression in adults with epilepsy. In support of our hypothesis, CBT resulted in significant improvements in all primary outcome measures compared to WLC at post-treatment. However, while between group comparisons resulted in medium-tolarge effect sizes at post-treatment, these differences were not maintained at 3-month follow-up. In addition, there were no significant group differences for our secondary outcome measures of QoL and anxiety.

Primary outcomes

Depression

Three-month follow-up analysis

For depression on the NDDI-E, there was a significant main effect of time (F[1,40] ¼ 4.86, p ¼ .033), but no group by time interaction (F [1,40] ¼ 2.34, p ¼ .134, d ¼ .39), or main effect for group (F[1,40] ¼ .788, p ¼ .380). There was no longer a significant difference between participants within the clinical range for depression on the NDDI-E (. 15) between CBT and WLC ( x 2 [1, n ¼ 42] ¼ .554, p ¼ .390). For the suicide item on the NDDI-E, there was no main effects, nor a

The fact that all four of our primary outcome measures revealed changes between the CBT programme and the WLC in the short term is encouraging. Importantly, the significant difference in the proportion of participants scoring in the clinical range on the NDDI-E and changes in suicidal ideation is particularly noteworthy given the high rates and negative consequence of depression and suicide risk in this population (Barry et al., 2008; Fiest et al., 2013). Our findings provide support for the


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use of CBT for depression in PWE as has recently been suggested in the international consensus guidelines for treatment for PWE (Kerr et al., 2011). Furthermore, they support preliminary conclusions of a recent systematic review that CBT tailored towards depression is likely efficacious (Gandy et al., 2013). A particular disappointment of the trial was the failure of the medium-to-large effect sizes of our depression measures to remain at follow-up. At first glance, this may appear to indicate that the improvements made in the CBT group during the treatment were not well maintained. However, closer examination of the effect sizes (Table 3) reveals a more complex pattern of results. That is, while there are medium-to-large between-group effect sizes over the treatment period, this is not only due to improvements in the CBT group, but also deterioration in the WLC group. Indeed, the within-group effect sizes on NDDI-E for the CBT group are very similar at post-treatment (d ¼ .38) and followup (d ¼ .41). However, they reflect small-tomoderate effect sizes. As a result, the between group results perhaps give an overly optimistic view of the efficacy of CBT in the short term, but an overly pessimistic view of the efficacy in the long term. What could account for this pattern of results? Firstly, examination of the means indicates that depressive symptoms unexpectedly deteriorated and then subsequently improved in the WLC. The 5-month followup was the time point where the WLC participants were offered an appointment for the CBT intervention. Anecdotally, many of the patients reported being disappointed by having been allocated to the WLC condition and it is possible that allocation to the WLC group resulted in disappointment, but the subsequent offer of treatment led to some increased hopefulness for the future which, in turn, may have improved depressed mood. Previous studies using lengthy wait-list periods (i.e. 6 months) have also found that there appears to be an improvement in mood at the point that the WLC participants are offered treatment (e.g. Sharpe & Schrieber, 2012). Secondly, the lack of betweengroup differences at the 3-month followup may have been the result of a lack of retention of CBT skills over time or failure to expand on gains. As many PWE experience

difficulties with their memory (Elger, Helmstaedter, & Kurthen, 2004; Vingerhoets, 2006), the intervention was designed to help facilitate the retention of CBT skills during the treatment phase. However, no provision was made to ensure patients retained and utilised CBT skills following treatment. This may have been facilitated by the use of booster sessions. Indeed, two previous CBT trials to report significant long-term effects on depression outcomes have utilised forms of booster sessions, including 5– 10-minute phone calls monthly over a 12-month period post-treatment (Ciechanowski et al., 2010), and monthly sessions for 4 months posttreatment (Martinovic´ et al., 2006).

Anxiety

In our CBT programme, we attempted to incorporate components that addressed the frequent comorbidity of symptoms of depression and anxiety in PWE. Despite this, our CBT trial did not find significant improvements in anxiety symptoms compared to WLC. Analyses revealed that there was also a significant main effect for anxiety symptoms at both post-treatment and follow-up, indicating anxiety symptoms improved over time for both groups. As the CBT intervention was primarily focused on improving depression in PWE, the treatment components may have been insufficient to make significant changes in anxiety symptoms. In general, the nature and treatment of anxiety in PWE remains unclear and understudied, despite the fact that it might be just as prevalent and disabling as depression (Beyenburg et al., 2005; Kanner, 2011). Future research into the nature and treatment of anxiety in PWE is therefore imperative.

Quality of life

The CBT intervention also failed to result in significant improvements in QoL compared to WLC. These findings are consistent with two other CBT RCTs, which despite finding significant effects of their intervention on depression outcomes, failed to find significant improvements in overall QoL compared to controls (Ciechanowski et al., 2010; Thompson et al., 2010). The lack of improvements in QoL within our trial may have been a result of the restricted range of QoL in our intervention sample following drop out of participants with significantly lower QoL. There was a non-


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significant difference in QoL scores between groups at baseline that remained at posttreatment, as evidenced by the findings of a significant main effect of group. Furthermore, the lack of change in QoL may be related to the intervention components. Although depression contributes to a large proportion of the variance of QoL in PWE, there may be other determining factors that this intervention did not specifically target. For instance, Chaytor and collegues (2011) suggest that CBT is more likely to result in significant improvements in QoL if it takes into consideration not only mood difficulties, but also functional problems associated with epilepsy. These include unemployment, cognitive impairment, seizures, social support and side-effects of medication.

Limitations and future research

Despite careful attention to the methodology in designing this trial, there are a number of limitations, which restrict the generalisability of the findings. Firstly, the trial is small and likely to be under-powered to find small-tomedium effect sizes. In order to ensure that the power of the trial was not further compromised, multiple comparisons were not controlled for and as such the findings should also be interpreted cautiously. Because we did not have the presence of a depressive disorder as an inclusion criteria, some participants had low levels of depressive symptoms to begin with and hence smaller effect sizes are likely. We chose not to have depressive disorders as an inclusion criteria because it is well recognised that patients with epilepsy are prone to atypical or subclinical presentations (Kanner, 2009a), but nonetheless this has statistical implications about the likely effect sizes. Our trial also experienced a high drop-out rate of participants (25%). While these high drop-out rates were comparable to previous CBT trials for PWE (e.g. Thompson et al., 2010) they were notably higher than other trials in this area (e.g. Ciechanowski et al., 2010). Notably, previous CBT trials, in particular those utilising group therapy based approaches, have reported sporadic attendance of their intervention which has led to questions of whether all participants received a sufficient dose of treatment (Gandy et al., 2013). Thus, the strength of

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our individual therapy CBT trial was the fact that treatment completers completed all 9 weeks of treatment, which ensures that a sufficient dosage of treatment was administered. When we assessed whether those participants who dropped out of the study systematically differed from those who remained in the trial, we found drop-out was related to poorer QoL, in particular that related to the cognitive functioning subscale of the QOLIE-31. Participants who dropped out reported greater difficulties in the areas of reasoning, memory and concentration. However, it is unclear whether these findings relate to subjective or objective complaints (Hall et al., 2009). Future CBT trials may benefit from formal cognitive assessment and greater provisions for these issues. For instance, while the treatment included aids for the retention of skills during treatment, such as providing recordings of sessions, these may have been insufficient for PWE with more severe memory impairments. On the other hand, if it is the case that memory complaints are largely subjective, then efforts could be made to address these concerns through cognitive challenging techniques in order to retain these participants within therapy and improve therapeutic outcomes. Furthermore, future trials may benefit from the use of a motivational scale to assess whether the level of participant motivation is associated with drop-out and/or changes in either the treatment or the WLC group. It is possible that the use of graduate students as clinicians contributed to the dropout rates, but participants also cited a number of practical barriers, work commitments, and health and travel restrictions. These results do suggest that although the type of home-visits used in the PEARLS trial may be expensive (Ciechanowski et al., 2010), these distance delivered therapies may be one way to minimise drop-out. Future research would benefit from the investigation of cost-effective distance delivered therapies, including individualised Internet CBT that have been found to be effective in other chronic health populations, including chronic pain (e.g. Dear et al., 2013).

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Conclusions We assessed the effectiveness of a 9-week CBT intervention to improve depression in adults with epilepsy. Compared to a WLC, CBT resulted in both statistical and clinical improvements on four outcome measures of depression and suicide risk in the short term. The medium-to-large differences between groups were, however, not maintained at the 3-month follow-up. These findings suggest that future trials may benefit from the use of booster sessions to ensure retention of CBT skills. Furthermore, CBT did not improve anxiety or QoL. Future CBT trials may benefit from specifically targeting these domains more directly, such as expanding interventions to account for broader functional impairment of PWE. We experienced a high drop-out rate of participants in our trial, which resulted in a small sample size. Future trials may benefit from addressing barriers to treatment attendance, including assessment of cognitive functioning and offering alternative treatment delivery formats.

Acknowledgements Dr Milena Gandy was supported by the generous scholarships of the National Health Research Council of Australia and the Molly McDonnell Foundation of the Epilepsy Society of Australia for this research. Prof. Louise Sharpe is supported by an NHMRC Senior Research Fellowship. We would also like to thank Epilepsy Action Australia for advertising the study and providing seizure diaries for participants.

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