Supplemental Materials
Treating Insomnia Improves Mood State, Sleep and Functioning in Bipolar Disorder: A
Pilot Randomized Controlled Trial
by A. G. Harvey et al., 2015, Journal of Consulting & Clinical Psychology
http://dx.doi.org/10.1037/a0038655
Supplementary Description of CBTI-BP
CBTI-BP. During a treatment development phase, we found that the unique features of sleep in
bipolar disorder necessitated modifications to CBT-I, including the addition of elements from
Interpersonal and Social Rhythms Therapy (IPSRT), Chronotherapy and Motivational
Interviewing, as follows and as described in several publications (Harvey, 2008, 2009, 2011;
Harvey & Li, 2009): (1) To minimize risk of mood episode relapse from sleep deprivation, time
in bed was restricted to no less than 6.5 hours. A carefully devised safety plan ensured safe
implementation. Also, basic stimulus control instructions (e.g., ‘only go to bed when sleepy’)
were sometimes modified to reduce risk of engagement in goal-seeking and/or rewarding
behaviors (Johnson, 2005) that could further reduce sleep opportunity. (2) Relative to CBT-I, a
heavier emphasis was placed on circadian/rhythm education to provide the rationale and the
motivation for the behavioral adjustments required to reduce variability in bed and wake times.
Elements from IPSRT were added to regularize daily rhythms, which build upon regular bed and
wakeup times. (3) A focus on establishing wind-down and wake-up routines was needed,
emphasizing appropriate exposure to dark/light given the sensitivity to light cues in bipolar
disorder (Barbini et al., 2005; Benedetti, Colombo, Barbini, Campori, & Smeraldi, 2001; Sit,
Wisner, Hanusa, Stull, & Terman, 2007). (4) A novel strategy, the ‘brisk wake-up’, targeted
extended sleep inertia (2-3 hours+). CBTI-BP also used activity scheduling and goal setting to
reinforce getting out of bed. (5) Features of delayed sleep phase were common and required
behavioral adjustments to adapt to earlier bedtimes, attempted in small systematic shifts (e.g.,
20-30 min earlier bedtime each week) to ensure mastery. (6) Achieving these changes required
the extensive use of MI and other behavior change strategies [e.g., emphasizing choice over
control (Keller, Harlam, Loewenstein, & Volpp, 2011) and goal setting (Pearson, 2012)]. (7) The
CBT-I approach to dysfunctional beliefs about sleep was adapted to the clinical realities of
bipolar disorder. For instance, sleep deprivation in bipolar disorder (unlike primary insomnia)
can be dangerous because it can trigger a manic episode. (8) Patients with bipolar disorder are
anxious about their sleep, in part because they are aware that sleep loss can herald mood episode
relapse (Harvey et al., 2005). As anxiety is antithetical to sleep (Espie, 2002), we target bedtime
worry, rumination and anxiety. (9) We considered and taught the potential value of a therapeutic
sleep extension (or ‘dark therapy’) procedure (Barbini et al., 2005) if a participant develops
manic symptoms, and of exposure to natural sources of light if a participant develops symptoms
of depression. (10) The LIFE chart is reviewed to develop skills and strategies for the different
sleep problems experienced over the course of bipolar disorder (e.g., hypomania, depression,
reduced sleep need, delayed phase). An individualized decision tree provides guidance and
adaptations for each kind of sleep problem.
CBTI-BP treatment components are described below.
Functional analysis/case formulation and goal setting. Sleep-related behaviors and consequences
are assessed before bed (e.g., bedtime routine), during the night (e.g., cell phone left on), on
waking (e.g., sleepiness, lethargy) and during the day (e.g., caffeine use). Specific goals are
identified.
Motivational interviewing (MI). MI (Miller & Rollnick, 2002) is a method which emphasizes
accepting the patient as an individual, avoiding argumentation, giving lectures or ultimatums and
focuses on the process of eliciting and shaping language in favor of change (i.e. change talk). MI
also includes regular straightforward reviews of perceived pros and cons of change, recognizing
that many sleep-incompatible/interfering behaviors are rewarding.
Sleep and circadian education includes definitions, environmental influences (particularly light),
circadian and social rhythms (following IPSRT) and the tendency toward delayed sleep phase.
Sleep inertia is defined and normalized (Tassi & Muzet, 2000). We address the role of sleep
disturbance in mood regulation and as a prodrome of mood episode relapse.
Behavioral components. 1) Stimulus control (Bootzin, 1972), one of the most effective treatment
components of CBT-I (Morin et al., 2006), focuses on regularizing the sleep-wake cycle and
strengthening associations between the bed and sleep (Bootzin, 1972), as well as regularizing
daytime rhythms (e.g., setting regular meal and wake-up times) (Frank, 2005). 2) Restricting
time in bed (Spielman, Saskin, & Thorpy, 1987) is derived from observations that excessive time
in bed perpetuates insomnia and increased homeostatic drive improves sleep. We limit time in
bed to the actual time slept, and gradually increase it back to an optimal sleep time. In order to
avoid sleep deprivation for safety, time in bed is never less than 6.5 hours. 3) Regularizing sleepwake times. IPSRT principles are utilized to regularize sleep and wake times and avoid naps
(Frank, 2005). These techniques promote consistent sleepiness in the evening and enable patients
with a tendency toward eveningness to progressively move their bedtime forward by 20-30
minutes per week (small enough that the circadian system can adapt). 4) Wind-down. Patients
need assistance to devise a ‘wind-down’ of 30-60 minutes in which relaxing, sleep-enhancing
activities are introduced, in dim light conditions. This helps the circadian phase advance in
patients who are evening-types, and maintains entrainment (Wyatt, Stepanski, & Kirkby, 2006).
A central issue is restricting the use of interactive electronic media (internet, cell phones, MP3
players). MI and behavioral experiments are used to facilitate voluntarily choosing an electronic
curfew. 5) Wake-up. Individualized wake-up plans draw on IPSRT principles, and include: not
hitting snooze, opening the curtains to let sunlight in, and making the bed so the incentive to get
back in is reduced.
Cognitive components. 1) Challenging unhelpful beliefs about sleep is important (J. D. Edinger,
W. K. Wohlgemuth, R. A. Radtke, G. R. Marsh, & R. E. Quillian, 2001) and common in bipolar
disorder (Harvey et al., 2005). They include: ‘the TV helps me fall asleep’ and ‘medication is the
only factor that contributes to my feeling drowsy’. Guided discovery and individualized
experiments test the validity and utility of the beliefs (Harvey, Sharpley, Ree, Stinson, & Clark,
2007; Ree & Harvey, 2004). 2) Patients with bipolar disorder are anxious about their sleep, in
part because they know that sleep loss can herald a mood episode relapse (Harvey et al., 2005).
As anxiety is antithetical to sleep onset (Espie, 2002), we use individualized strategies to reduce
bedtime worry, rumination and vigilance including cognitive therapy, diary writing, or a
scheduled ‘worry period’.
Daytime coping. A commonly held belief is that the only way one can feel less tired in the day is
to sleep more. Hence, an experiment is devised to allow the patient to experience the energy
generating effects of activity (Ree & Harvey, 2004) and develop a list of ‘energy generating’ and
‘energy sapping’ activities to better manage daytime tiredness.
Relapse prevention. The goal is to consolidate gains and prepare for setbacks using an
individualized summary of learning and achievements. The therapist and patient develop a
decision tree and menu of options for managing the range of sleep problems that may be
experienced during the course of bipolar disorder mood episodes.
Online Supplement
List of Patient Medications
Antidepressants
Name
Generic
bupropion
sertraline
citalopram
paroxetine
fluoxetine
escitalopram
venlafaxine
amitriptyline
clomipramine
nortriptyline
trazodone
mirtazapine
Antipsychotics
Name
Generic
quetiapine
aripiprazole
ziprasidone
risperidone
olanzapine
haloperidol
Anxiolytics
Name
Generic
clonazepam
lorazepam
alprazolam
buspirone
Hypnotics
Name
Generic
Brand
Wellbutrin
Zoloft
Celexa
Paxil
Prozac
Lexapro
Effexor
Elavil
Anafranil
Aventyl,
Pamelor
Desyrel,
Oleptro
Remeron
Brand
Seroquel
Abilify
Geodon
Risperdal
Zyprexa
Haldol
Brand
Klonopin
Ativan
Xanax
Buspar
Brand
N
10
4
3
3
3
1
3
1
1
1
Dose (mg)
Mean (SD)
163.75 (82.17)
100 (54.01)
163.75 (82.17)
16.67 (5.77)
31.67 (10.41)
10
75.00 (64.95)
50
75
10
6
45.83 (32.31)
1
50
N
14
8
7
4
3
1
Dose (mg)
Mean (SD)
140.63 (110.04)
13.06 (11.92)
85.71 (41.7)
7.25 (8.77)
6.67 (2.89)
25
N
7
6
1
2
Dose (mg)
Mean (SD)
.80 (.61)
.71 (8.07)
.25 (.25)
31.25 (26.52)
Range
.25-2
.5-.75
.5-.75
12.5-50
N
Dose (mg)
Mean (SD)
Range
Range
75-300
25-150
20-40
10-20
20-40
37.5-150
10-100
Range
25-400
2-30
40-160
1-20
5-10
zolpidem
temazepam
eszopiclone
Mood Stabilizers
Name
Generic
lamotrigine
valproic acid
lithium carbonate
gabapentin
Ambien
Restoril
Lunesta
11
6
1
7.72 (3.94)
24.00 (8.22)
2
Brand
Lamictal
Depakote
Eskalith,
Lithonate
Neurontin
N
15
8
7
Dose (mg)
Mean (SD)
185.00 (80.07)
990.63 (911.63)
878.57 (292.77)
1
1800
.375-12.5
15-30
Range
100-400
250-3000
450-1350
Note. Doses are means of minimum and maximum reported by participants pretreatment. Tricyclic,
trazodone, and mirtazapine doses suggested hypnotic use. In addition, 6 patients had quetiapine doses of
less than 100 mg/d, suggesting hypnotic use. In 5 cases, likely erroneously reported doses were
reinterpreted to most plausible values (e.g. olanzapine reported at 100 mg/d reinterpreted as 10 mg/d.
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