Transdiagnostic cognitive behavioral therapy for nightmares and parasomnias
ABSTRACT
Study Objectives:
This pilot study determined whether transdiagnostic cognitive behavioral therapy for parasomnias (CBTp) reduces parasomnia and activity levels during sleep in a sample of adult sleep clinic outpatients. A secondary objective was to assess whether treatment produces improvements in daytime fatigue/sleepiness, perceived cognition, mood, and depression/anxiety/stress, as well as functional impairment in work and leisure activities.
Methods:
This was a randomized controlled trial with CBTp and self-monitoring control conditions. Participants were 19 adults with a DSM 5 parasomnia disorder who received individual CBTp virtually from their homes. CBTp consisted of psychoeducation, sleep hygiene and safety instructions, relaxation training, parasomnia techniques, and relapse prevention in a 6-week manualized, structured program.
Results:
Using a repeated measures analysis of variance model, and relative to a self-monitoring control condition, results showed that CBTp produced statistically significant improvements in parasomnia frequency, severity, nocturnal activity, and sleep efficiency. There was a trend toward reduced sleep-onset latency and improved work and social adjustment. Of treated participants, 100% rated themselves as improved at study conclusion.
Conclusions:
Implications of these findings are that cognitive behavioral interventions for parasomnias are effective in lessening parasomnias. More investigation into this type of treatment is warranted.
Clinical Trial Registration:
Registry: ClinicalTrials.gov; Name: Impact of Cognitive Behavioral Therapy on Parasomnias; URL: https://clinicaltrials.gov/ct2/show/NCT04633668; Identifier: NCT04633668.
Citation:
Vincent N, Dirkse D, Giannouli E, McQuarrie A. Transdiagnostic cognitive behavioral therapy for nightmares and parasomnias. J Clin Sleep Med. 2023;19(3):499–509.
BRIEF SUMMARY
Current Knowledge/Study Rationale: This study attempted to determine whether a transdiagnostic cognitive behavioral therapy for parasomnias reduces parasomnia and activity levels during sleep. A second purpose was to assess whether treatment produced improvements in daytime fatigue/sleepiness, perceived cognition, mood, depression/anxiety/stress, and functional impairment.
Study Impact: This study demonstrated that transdiagnostic cognitive behavioral therapy for parasomnias improves parasomnia frequency, severity, nocturnal activity, and sleep efficiency. This type of intervention may be more easily disseminated given the comorbidity of parasomnias and difficulty associated with their assessment.
INTRODUCTION
Parasomnias are sleep disorders such as nightmare disorder, sleep terrors, sleepwalking, and sleep behavior disorder.1 The diagnostic criteria for non-rapid eye movement (NREM) parasomnias refer to partial amnesia for the events and more limited dream imagery; however, more recent research shows that approximately 60–90% of adults have some recall of mental experience associated with their parasomnia episode.2 Studies of both community-dwelling and treatment-seeking adults show that there is significant comorbidity of parasomnias.3 Daytime impairments among those with parasomnias range from fatigue and insomnia4 to increased rates of depression and anxiety,5,6 fear and avoidance of sleeping,7 marital stress,8 reduced productivity and academic performance,9 increased risk of cardiovascular disease,10 neurologic disorders,11 and injuries.12 A recent study of 1,500 shift workers showed that those who reported a parasomnia within the past year vs not were significantly more likely to have a history of occupational (44% vs 24%) and motor-vehicle (47% vs 24%) accidents.13 The lifetime prevalence of parasomnia disorders ranges from 7% (sleepwalking) to 67% (nightmare disorder).1,14,15
Individuals are genetically predisposed to develop parasomnias.16,17 In vulnerable individuals, NREM parasomnias may be primed by events that increase the proportion of deep NREM sleep and/or that increase arousal threshold (eg, pain, caffeine, noise, touch, stress, upper airway problems, periodic limb movements, rotating or night shift work).13,18 Alcohol may reduce the likelihood of sleepwalking through inhibition of motor activity.19 However, for people who are predisposed to NREM parasomnias and who also have sleep-disordered breathing (ie, sleep apnea, upper airway resistance syndrome), alcohol can indirectly increase the occurrence of NREM parasomnias by increasing the likelihood of breathing-related sleep disruptions.2 The degree to which obstructive apnea events and repeated desaturations may trigger NREM parasomnias may depend upon the sleep stage in which the desaturations occur.20 A variety of short- or intermediate-acting hypnotics (eg, temazepam, diazepam), beta-blockers (propranolol), mood stabilizers (lithium), some antidepressants (citalopram, amitriptyline), and nonbenzodiazepine sedatives (zolpidem) may prime an NREM parasomnia, and the strongest evidence is with zolpidem.21 For rapid eye movement parasomnias, in addition to genetics, pesticide exposure, head injury, male sex, and age increase the risk for developing idiopathic rapid eye movement sleep behavior disorder. These conditions can be primed by the abrupt withdrawal of several medications (hypnotics, selective serotonin reuptake inhibitors, tricyclic medications) and drugs (caffeine). Also, ischemic heart disease, chronic obstructive pulmonary disease, smoking, hyperarousal due to stress/threat, frank trauma, or psychiatric comorbidities increase the risk for both nightmares and rapid eye movement sleep behavior disorder.16,22,23
Treatment of parasomnias
Currently accepted interventions for parasomnias include pharmacological24–26 and psychological treatments. Psychological treatments for most of the parasomnias are lacking in development, with the notable exception of nightmare disorder. The American Academy of Sleep Medicine identified that imagery rehearsal therapy is recommended for nightmare disorder.27 Imagery rehearsal therapy is a cognitive behavioral technique that involves changing parasomnia content by creating a new set of images which reduce fear. Next, the individual rehearses a rescripted parasomnia during the daytime while awake. Other promising interventions which have been insufficiently studied include cognitive behavioral therapy (generally or focused on insomnia), eye movement desensitization and reprocessing, and exposure, relaxation, and rescripting. Additionally, there have been 2 randomized controlled trials investigating lucid dreaming on nightmares, both significantly reducing nightmare frequency.28,29 Lucid dreaming involves teaching individuals to become more aware of when they are dreaming and so to exit a nightmare when it begins or to experience the nightmare with less distress. Very notable is the lack of systematic study and review of behavioral treatments for rapid eye movement sleep behavior disorder. One exception is a study30 utilizing an alarm system which awakened the sleeper when movement out of bed was detected. Developed in the pediatric area, the most reviewed intervention for NREM parasomnias is scheduled awakening. Scheduled awakening has been used for both sleepwalking and sleep terrors.31 Scheduled awakening is a behavior strategy wherein the sleeper is briefly awakened 30 minutes before the anticipated parasomnia onset and then instructed to return to sleep. Fading of the strategy occurs after 1 week once symptoms are eliminated. With an absence of clinical trials, multiple-baseline studies show evidence of success.32 Finally, a new adaptation of an old cognitive technique, called association splitting, may also have a role in treating rapid eye movement and NREM parasomnias. Neuroscience research shows that sleep is important in emotional memory reprocessing. Association splitting involves training individuals to associate nightmare stimuli in wakefulness with less-threatening stimuli (eg, associated neutral or pleasant words). This in turns reduces the degree of distress experienced during the nightmare through habituation to provocative stimuli.33 This technique has not yet been systematically studied in sleep disorders.
In summary, parasomnias frequently co-occur and there has been a lack of systematic study of psychological treatments except for nightmare disorder. The objectives of this study were to examine the efficacy of a transdiagnostic cognitive behavioral treatment for parasomnias (CBTp) in a sample of sleep clinic outpatients. One hypothesis of the study was that those in receipt of CBTp compared to self-monitoring controls would have less-frequent and -severe parasomnias. A second hypothesis of the study was that those in receipt of CBTp, relative to self-monitoring controls, would experience more improvements in fatigue and sleepiness, perceived cognition, mood, anxiety, and stress and social and leisure role functioning.
METHODS
Design
This was a two-group (CBTp, self-monitoring control) randomized controlled pilot trial. Self-monitoring control was elected as it has been shown to have small but positive effects in reducing parasomnia frequency.34
Participants
A description of participant characteristics is found in Table 1. All participants with obstructive sleep apnea-hypopnea were receiving continuous positive airway pressure treatment with high levels of compliance. The sample was characterized by having an average of 5 parasomnia events per week (standard deviation [SD] = 3.4), with mild sleepiness, moderate fatigue, insomnia, and daytime impairment. There were several comorbid medical conditions in the sample (eg, irritable bowel syndrome, hypothyroidism, rheumatoid arthritis, migraines, endometriosis, cholesteremia, and polycystic ovary disease) which were stable during study. Using chi-square analyses and independent t tests, there were no significant differences between the treatment and self-monitoring control group on any of the demographic, sleep, or psychiatric conditions with 1 exception: scores on the Work and Social Adjustment Scale [MCBTp = 30.50, SD = 6.40, MControl = 17.00, SD = 12.18, t(13) = 2.69, P = .0] were significantly higher (reflecting less-favorable adjustment) in the CBTp than in the self-monitoring control condition. No information was collected regarding participant ethnicity or income. All participants were English-speaking. No participant had current or historical seizures or engaged in injurious or stereotypic behavior during their parasomnia.
| Variable | CBTp | Self-Monitoring Control | ||
|---|---|---|---|---|
| (n = 10) | (n = 9) | |||
| % | n | % | n | |
| Female sex | 70.00 | 7 | 88.90 | 8 |
| High school education | 100.00 | 10 | 100.00 | 9 |
| Employed | 60.00 | 6 | 33.30 | 3 |
| Married | 60.00 | 6 | 33.39 | 3 |
| Psychiatric comorbidity | 80.00 | 8 | 77.80 | 7 |
| Depressive disorder | 0 | 0 | 33.30 | 3 |
| Dysthymia | 20.00 | 2 | 44.40 | 4 |
| Generalized anxiety disorder | 50.00 | 5 | 44.40 | 4 |
| Posttraumatic stress disorder | 10.00 | 1 | 33.33 | 3 |
| Panic disorder | 0 | 0 | 22.20 | 2 |
| Social phobia | 10.00 | 1 | 11.10 | 1 |
| Obsessive compulsive disorder | 0 | 0 | 11.10 | 1 |
| Sleep | ||||
| Apnea | 20.00 | 2 | 11.10 | 1 |
| Restless legs syndrome | 10.00 | 1 | 22.20 | 2 |
| Sleepwalking | 20.00 | 2 | 22.20 | 2 |
| Sleep terrors | 40.00 | 4 | 66.60 | 6 |
| Nightmare disorder | 90.00 | 9 | 77.80 | 7 |
| REM sleep behavior | 30.00 | 3 | 0 | 0 |
| Insomnia disorder | 60.00 | 6 | 33.30 | 3 |
Inclusion
Inclusion criteria were age ≥ 18 years and with a diagnosed parasomnia from a board-certified sleep medicine physician. All participants met Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM 5) criteria for a parasomnia on the Structured Clinical Interview for DSM 5 Sleep Disorders Module.35 In addition, a disturbance of sleep at least once per week, daytime fatigue or sleepiness, and parasomnias of at least 6 months in duration were additional criteria.
Exclusion
Exclusion criteria were presence of untreated sleep apnea or narcolepsy and/or the presence of an established neurologic disorder. Each of these conditions has been associated with increased sleep fragmentation, and stimulant treatments for narcolepsy may worsen sleep. Further, participants using agents known to trigger parasomnias (eg, lithium carbonate, amitriptyline) were excluded. For participants taking benzodiazepines or prazosin, a stable dose regime for the past 4 weeks was required. Additionally, excessive alcohol consumption defined as the consumption of > 10 alcoholic beverages per week and current or prior CBT for sleep were exclusionary factors. Participants with psychiatric or other medical conditions were not excluded provided that the condition was stable and no changes in treatment occurred during the study period.
Primary end-point measures
The primary end points were parasomnia frequency, severity, and activity during sleep episode. A revised version of a gold standard measurement of sleep, the prospective Consensus Sleep Diary,36 collected information on parasomnias in addition to several other sleep domains (eg, total sleep time [TST], sleep onset latency [SOL], sleep efficiency [SE], number of nocturnal awakenings, wake after sleep onset, and sleep quality). The diary was modified for use in this study by adding 4 questions to assess the presence/absence of parasomnias. Patients were provided with a description of each parasomnia for orientation purposes. Sleep diary measures were completed daily, scored for each night, and then averaged across the recording period. Self-report scales for assessing parasomnias have been shown to have adequate reliability and validity when respondents are oriented to understand what defines these conditions.37,38 Using a convenience sample of 76 outpatients with insomnia disorder from the authors’ clinics, the 6-week test–retest reliability of parasomnia frequency using the sleep diary was .80, with an average of .82 parasomnia events per week (SD = 2.60). A subscale of the reliable and valid Nightmare Experience Scale39 measured severity of nightmares. Scores on the distress subscale range from 2 to 8, with higher scores indicating more severe and distressing nightmares.
Actigraphy was used to measure changes in activity during sleep. A Philips Respironics Actigraphy (Actiwatch Spectrum Plus, Philips, Murrysville, PA) device using solid-state piezoelectric technology was worn on the nondominant wrist each night during recording periods and sampled movement in 1-minute epochs. The wake threshold value (ie, the number of activity counts used to define wake) was set to medium sensitivity. The actigraphic device produced information pertaining to TST, SOL, number of nocturnal awakenings, wake after sleep onset, SE, and an activity count (minutes of movement during sleep). Actigraphy data correlate significantly and positively with results from polysomnography40 and with metabolic equivalence scores.41 Middle-aged nonclinical adults in supine rest have activity counts (mean [M] = 8.5, SD = 23.1) on this device which are lower than those who are sitting (M = 34.8, SD = 68.1) or standing (M = 37.8, SD = 79.3).42 Further, adults with idiopathic rapid eye movement behavior disorder have significant higher activity counts than controls.43
Secondary end-point measures
All measures had established reliability and validity. The general fatigue subscale of the Multi-Dimensional Fatigue Inventory measured fatigue.44 Scores can range from 4 to 20, and scores > 13 have been associated with chronic unwellness (eg, > 6 months of unwellness). The Epworth Sleepiness Scale measured the tendency to fall asleep.45 Scores can range from 0 to 24. The Insomnia Severity Scale46 is a 7-item measure of symptoms of insomnia. Scores can range from 0 to 28 and reduction in Insomnia Severity Scale scores > 8.4 points is evidence of moderate improvement after treatment.47 The Depression Anxiety Stress Scale is a 21-item measure of symptoms of depression, anxiety, and stress.48 Subscale scores can range from 0 to 21, with higher scores indicating more symptoms. The Work and Social Adjustment Scale49 is a 5-item scale assessing a patient’s perspectives of impaired functioning in important life domains (eg, ability to work, home management, social leisure, private leisure, maintain close relationships) attributed to sleep. Scores range from 0 to 40, with higher scores indicating more impairment. The Patient Reported Outcomes Measurement Information System v. 1 Applied Cognitive Abilities50 is a 4-item measure of perceived cognitive function. Scores range from 4 to 20 and are converted to t scores with a mean of 50 and SD = 10, and higher scores reflect less cognitive difficulty.
Satisfaction measures
The Client Satisfaction Questionnaire51 measured participants’ satisfaction with treatment. Scores range from 8 to 32, with higher scores indicating more satisfaction. The Clinical Global Improvement Scale self-report version52 assessed participants’ perceived global improvement. The Clinical Global Improvement Scale required participants to report the overall change in their parasomnia and not in any other problem such as chronic pain, depression, or anxiety. Response choices ranged from very much improved (1) to very much worse (7).
Materials
The CBTp protocol was developed by N.V., organized into six modules, to be delivered over 6 weeks, and guided by a workbook (N. Vincent, “Parasomnias,” unpublished workbook, 2020) (see Table 2).
| Module | Content | Homework |
|---|---|---|
| 1 | Education about parasomnias (eg, information about types, etiology, prevalence) and overview of treatment | Self-monitor using sleep diary and actigraphy |
| 2 | Education about sleep hygiene (regularizing sleep, minimizing noise, alcohol, smoking, caffeine, extended napping, problematic foods/liquids before bed, light exposure in sleep quarters, moderating bedroom temperature, and sleeping safely | Pick 2 sleep habits and begin modifying, improve safety in bedroom environment |
| 3 | Relaxation training (paced breathing, progressive muscle relaxation, imagery-induced relaxation, self-hypnosis for parasomnias with suggestions to remain in bed when mind becomes activated) | Pick 1 or more relaxation method and practice with daily |
| 4 | Imagery Rehearsal Therapy (eg, practicing with rehearsal of a modified nightmare/terror/sleepwalking episode with a relaxing ending), Scheduled Awakening (eg, pre-empting parasomnia by brief awakening using alarm clock), Lucid Dreaming (eg, practicing and rehearsal with identifying difference between wake and sleep), Association Splitting (eg, practicing with associating parasomnia content with a neutral or positive word) | Practice with 1 or more of these techniques, preferably at least 2 |
| 5 | Cognitive Therapy (eg, identification and correction of automatic thoughts pertaining to parasomnias that may increase arousal (eg, After a night with a parasomnia, I won’t be able to function next day), scheduled problem solving (eg, spending 15 minutes per day noting worries, possible solutions, and ways to better accept problem), downward arrow technique (eg, attempting to uncover coping strategies for the most difficult aspect of worry) | Apply 1 or more of the cognitive techniques |
| 6 | Review of concepts, evaluating progress, planning for future, relapse prevention | Decide upon most efficacious strategies and continue practicing with these |
Procedure
See Figure 1 for an illustration of the flow of participants through the study. All participants were identified and diagnosed by a board-certified sleep physician (E.G.) and referred to N.V. for behavioral treatment of parasomnias. A research assistant (A.M.) phone-screened potential participants to determine whether they met study criteria and whether they were interested in participating. Informed consent was obtained at this time. Next, participants were administered the Structured Clinical Interview for DSM-5 Sleep Disorders35 and the Diagnostic Assessment Research Tool53 and were asked for information about medical history and current medications (for sleep and any other problem). Also, participants completed a questionnaire package through Survey Gizmo consisting of study measures (ie, Multi-Dimensional Fatigue Inventory, Insomnia Severity Scale, Depression Anxiety Stress Scale, Work and Social Adjustment Scale, Patient Reported Outcomes Measurement Information System). They were asked to wear an actigraph and to complete a sleep diary, both for 7 days. Once materials were returned, participants were randomized to the intervention group (CBTp) or to a self-monitoring control group using https://www.randomizer.org/. Both groups monitored their sleep throughout the study using a sleep diary (daily), actigraphy (daily), and nightmare experience scale (weekly). The intervention group (CBTp) received 6 weekly, virtual (MS Teams) 50-minute appointments with a clinical health psychologist (N.V. or D.D.), guided by a workbook. The self-monitoring control group monitored their sleep as outlined above and had no contact with study staff. At the end of 6 weeks, the questionnaire survey was readministered, in addition to the Client Satisfaction Questionnaire and the Clinical Global Improvement Scale. The questionnaire survey, actigraph, and sleep diary were each administered during a follow-up week, 2 months after completion of the program. The study was conducted between January 2021 and April 2022 and was approved by an institutional ethical review board.
CBTp = cognitive behavioral therapy for parasomnias.
RESULTS
Of participants, 16% (n = 3 of 19) dropped out of the study (see Figure 1). The number of dropouts was not significantly different between study conditions [χ2 (1, 19) = 0.28, P = .60]. Using a series of t tests and chi-square tests, we determined that there were no significant differences between dropouts and completers on any of the study variables apart from age. Those who dropped out of the study were younger (M = 24.67 years, SD = 1.15) than completers [M = 43.06, SD = 16.91) t(17) = 4.30, P = .001].
Treatment integrity
Treatment integrity was assessed using weekly adherence questionnaires for those in the CBTp condition. No homework was assigned for week 6. The numbers of participants completing adherence checks for each week was as follows: week 1 (n = 9 of 10), week 2 (n = 9 of 10), week 3 (n = 7 of 10), week 4 (n = 7 of 9), week 5 (n = 7 of 8). Using a repeated measures analysis of variance procedure, there was no significant group, time, or interactive effect on medication use frequency throughout the study. Those in the CBTp group did not use more medication from pre- to posttreatment, nor did they initiate any new treatments for their sleep or psychiatric disorders. Of participants, the vast majority identified nightmares as the primary parasomnia and thus was the focus of treatment.
Effect of CBTp on primary end-point variables
Results from repeated measures analysis of variance in Table 3 showed that there was a significant group × time interaction for the variable of parasomnia frequency (F2, 28 = 6.85, P = .004) and a significant main effect of time (F2, 28 = 3.6, P = .05) and group (F1, 14 = 9.34, P = .009). Similarly, there was a significant group × time interaction for the variable of parasomnia distress (F2, 26 = 12.42, P = .0001), a significant effect of time (F2, 26 = 22.24, P = .0001), and a significant effect of group (F1, 13 = 4.92, P = .05). There was a significant group × time interaction for the variable of nocturnal activity (F2, 16 = 8.22, P = .003) and a significant main effect of time (F2, 16 = 4.10, P = .04) and group (F1, 8 = 5.75, P = .04). For the CBTp but not self-monitoring control group, parasomnia frequency, distress, and nocturnal activity were significantly reduced from pre- to posttreatment and between pretreatment to follow-up. Notably, the effect sizes (η2p) for each analysis were large.
| Variable | Group | Pretreatment | Posttreatment | Follow-up | η2p | |||
|---|---|---|---|---|---|---|---|---|
| M | SD | M | SD | M | SD | |||
| Parasomnia events/w | CBTp (n = 8) | 5.53 | 4.10 | 1.09 | 1.46 | 1.56 | 1.39 | .33 |
| Control (n = 8) | 5.91 | 2.74 | 7.19 | 3.99 | 6.02 | 3.16 | ||
| Parasomnia distress | CBTp (n = 7) | 7.29 | 0.95 | 4.43 | 1.81 | 4.00 | 1.83 | .49 |
| Control (n = 8) | 6.88 | 0.99 | 6.50 | 1.31 | 6.38 | 1.06 | ||
| Nocturnal activity count (actigraphy) | CBTp (n = 8) | 9.56 | 1.88 | 8.96 | 2.57 | 9.09 | 2.32 | .51 |
| Control (n = 8) | 10.73 | 2.45 | 13.36 | 3.99 | 13.17 | 5.46 | ||
Effect of CBTp on secondary end-point variables
Results from repeated measures analysis of variance in Table 4 showed that there was a nonsignificant interactive or main effect of group and time on ratings of general fatigue and sleepiness. For the variable of insomnia severity, there was a nonsignificant group × time (F2, 26 = .66, P = .52) and group effect (F1, 13 = .26, P = .62) but a significant main effect of time (F2, 26 = 6.15, P = .006) such that insomnia became less severe over time. For work and social adjustment, results showed that there was a trend toward a significant group × time interaction (F2, 16 = 3.05, P = .08) but a nonsignificant effect of group (F1, 8 = .79, P = .40) and time (F2, 16 = 1.22, P = .32). Those in the CBTp group had better adjustment over time. Finally, there were nonsignificant interactive and main effects on perceived cognitive functioning, depression, and anxiety. There was a nonsignificant interactive effect of group and time on stress but a significant main effect of time on stress (F2, 26 = 4.62, P = .02) such that participants reported less stress over time.
| Variable | Group | Pretreatment | Posttreatment | Follow-up | η2p | |||
|---|---|---|---|---|---|---|---|---|
| M | SD | M | SD | M | SD | |||
| MFI | CBTp (n = 5) | 10.80 | 3.42 | 9.00 | 3.08 | 8.40 | 4.16 | .10 |
| Control (n = 6) | 9.50 | 5.47 | 9.83 | 5.34 | 8.17 | 3.49 | ||
| ESS | CBTp (n = 7) | 11.29 | 7.13 | 7.86 | 6.57 | 8.86 | 6.23 | .07 |
| Control (n = 8) | 5.88 | 5.49 | 5.50 | 5.55 | 6.00 | 4.41 | ||
| ISI | CBTp (n = 7) | 17.14 | 6.67 | 12.14 | 6.20 | 12.71 | 4.57 | .05 |
| Control (n = 8) | 17.50 | 8.38 | 15.25 | 8.26 | 14.63 | 8.05 | ||
| WSAS | CBTp (n = 4) | 30.50 | 6.40 | 19.50 | 7.94 | 22.25 | 15.04 | .28 |
| Control (n = 6) | 17.00 | 12.18 | 20.33 | 12.64 | 17.17 | 11.69 | ||
| PROMIS | CBTp (n = 7) | 36.54 | 12.09 | 37.92 | 10.15 | 35.21 | 6.92 | .005 |
| Control (n = 8) | 39.44 | 10.24 | 40.21 | 10.79 | 37.23 | 8.08 | ||
| Depression | CBTp (n = 7) | 16.29 | 12.57 | 13.43 | 14.32 | 17.14 | 14.78 | .05 |
| Control (n = 8) | 17.75 | 9.47 | 14.00 | 9.07 | 13.75 | 9.77 | ||
| Anxiety | CBTp (n = 7) | 12.57 | 11.47 | 13.14 | 12.91 | 10.86 | 10.57 | .03 |
| Control (n = 8) | 12.75 | 9.13 | 11.75 | 7.29 | 11.88 | 11.34 | ||
| Stress | CBTp (n = 7) | 12.14 | 10.45 | 13.71 | 11.57 | 15.71 | 9.20 | .04 |
| Control (n = 8) | 26.00 | 10.42 | 22.50 | 8.67 | 21.50 | 9.78 | ||
Results in Table 5 show the impact of CBTp on sleep diary parameters. There were no significant interactive or group main effects for the sleep diary variables. The effect sizes for the group × time interactions ranged from small to large with larger effects for SOL and SE. Actigraph sleep data in Table 6 illustrate that there was a significant group × time interaction for sleep efficiency (F2, 28 = 3.31, P = .05) such that there was more improvement in the CBTp than in the self-monitoring control condition. There was a trend toward a significant group × time interaction for SOL (F2, 28 = 2.65, P = .09) such that those in CBTp condition fell asleep more quickly those in the self-monitoring control condition. There were no significant main effects of time or group for SE or SOL. There were no other significant group × time interactions for other sleep variables as measured using actigraphy, although the effect size was large for interactions involving TST.
| Variable | Group | Pretreatment | Posttreatment | Follow-up | η2p | |||
|---|---|---|---|---|---|---|---|---|
| M | SD | M | SD | M | SD | |||
| SOL | CBTp (n = 8) | 24.78 | 18.28 | 12.24 | 9.02 | 18.42 | 12.89 | .11 |
| Control (n = 7) | 47.61 | 40.49 | 54.55 | 46.24 | 53.00 | 45.15 | ||
| NOW | CBTp (n = 8) | 2.74 | 1.20 | 2.36 | 1.99 | 2.44 | 2.02 | .03 |
| Control (n = 7) | 3.43 | 1.69 | 2.28 | 0.83 | 2.80 | 0.82 | ||
| WASO | CBTp (n = 8) | 24.03 | 23.91 | 19.98 | 27.37 | 21.43 | 26.93 | .03 |
| Control (n = 7) | 57.65 | 90.70 | 43.73 | 54.37 | 39.32 | 34.39 | ||
| TST | CBTp (n = 8) | 7.68 | 1.10 | 7.91 | 0.69 | 8.04 | 0.93 | .05 |
| Control (n = 7) | 7.72 | 0.82 | 7.86 | 0.95 | 7.09 | 2.84 | ||
| SE | CBTp (n = 8) | 91.01 | 8.67 | 95.86 | 6.20 | 95.18 | 6.09 | .13 |
| Control (n = 7) | 84.35 | 13.22 | 83.23 | 13.43 | 85.41 | 11.05 | ||
| SQ | CBTp (n = 8) | 1.69 | 0.98 | 2.18 | 0.96 | 1.78 | 1.05 | .05 |
| Control (n = 7) | 1.83 | 0.68 | 1.96 | 1.00 | 1.94 | 0.73 | ||
| Variable | Group | Pretreatment | Posttreatment | Follow-up | η2p | |||
|---|---|---|---|---|---|---|---|---|
| M | SD | M | SD | M | SD | |||
| SOL | CBTp (n = 8) | 21.58 | 28.17 | 5.83 | 5.06 | 7.32 | 8.02 | .16 |
| Control (n = 8) | 12.26 | 9.23 | 20.56 | 20.76 | 11.09 | 6.77 | ||
| NOW | CBTp (n = 8) | 23.57 | 5.51 | 21.36 | 4.69 | 22.62 | 5.96 | .08 |
| Control (n = 8) | 26.56 | 10.98 | 27.05 | 7.83 | 33.45 | 10.51 | ||
| WASO | CBTp (n = 8) | 41.78 | 7.43 | 36.66 | 8.00 | 41.60 | 11.62 | .03 |
| Control (n = 8) | 48.87 | 16.63 | 50.54 | 20.61 | 58.36 | 28.70 | ||
| TST | CBTp (n = 8) | 6.88 | 0.60 | 6.97 | 1.15 | 7.33 | 1.39 | .12 |
| Control (n = 8) | 8.27 | 1.03 | 7.49 | 1.51 | 7.80 | 1.43 | ||
| SE | CBTp (n = 8) | 86.95 | 2.49 | 88.69 | 2.42 | 88.24 | 3.07 | .13 |
| Control (n = 8) | 87.55 | 4.30 | 84.11 | 8.17 | 85.04 | 4.68 | ||
Clinical significance of findings
Of those who received CBTp, 7 of 8 completed the Clinical Global Improvement Scale. Results showed that 100% rated themselves as improved, with 4 out of 7 rating themselves as much or very much improved and the remaining 3 of 7 as minimally improved. No participants rated themselves as unchanged or worsened. Of self-monitoring control participants, none rated themselves as much or very much improved, but 2 out of 8 rated themselves as minimally improved, and 6 out of 8 rated themselves as unchanged. Between 15% and 40% of participants who received CBTp were both reliably improved and had follow-up scores typical of community-dwelling adults on primary end-point variables and daytime fatigue. When normative sleep was defined as TST > 6.5 hours, SOL ≤ 30 minutes, wake after sleep onset ≤ 30 minutes, and SE ≥ 85%, 75% (n = 6 of 8) of treated participants vs 37.5% of self-monitoring controls had sleep in the normative range at the posttreatment period.
Although the study was underpowered to examine the effect of psychiatric comorbidity and parasomnia overlap on outcomes, at posttreatment 66% of those with a psychiatric disorder had reliable change in parasomnia frequency vs 50% of those without any such disorders, but this was less likely to be sustained at follow-up (where 33% with a disorder had reliable improvement vs 50% without a disorder). At posttreatment and follow-up, 80% of those with any psychiatric disorder had reliable change in parasomnia severity vs 100% of those without any such disorder. Of participants with parasomnia overlap disorders, 50% had reliable change in parasomnia frequency and severity at posttreatment and at follow-up.
DISCUSSION
The main finding of this study was that a transdiagnostic and cognitive behavioral approach to parasomnias was effective in reducing parasomnia frequency, distress, and nocturnal activity in a small sample of adult outpatients with nightmares and other parasomnias. There were medium to large (but not statistically significant) effects on fatigue and accompanying social and occupational functioning, and this occurred despite the finding that the treatment group had worse social and occupational functioning at the outset of the study. It is possible that there was more room for the CBTp group to improve as a function of regression to the mean, that the treatment was quite effective, or both. The average frequency of parasomnias at the follow-up period was once per week, and this is comparable to or better than other psychological treatment trials for parasomnias.27 Research on nightmare disorder has found that although cognitive behavioral treatments reduce parasomnias they may not eliminate them and often leave individuals with 2 or more nightmares per week.27 It is possible that a longer duration of treatment, or more emphasis on reducing insomnia, might have led to further gains. However, in a randomized controlled trial of cognitive behavioral therapy for insomnia vs waiting list,54 there was no effect of cognitive behavioral therapy for insomnia on nightmare frequency and intensity among a sample of adults with posttraumatic stress disorder.
Research shows that parasomnias often cluster, and an older study1 found that 70% of middle-aged community adults had a lifetime prevalence of ≥ 2 parasomnias. This clustering was also true of the current outpatient sleep sample in which 53% had ≥ 2 current parasomnias. It is possible that this elevated number of parasomnias led to difficulty with complete resolution of events. The small sample size did not permit us to examine whether CBTp was more effective for particular parasomnias and our sample consisted of 84% with nightmare disorder. It is possible that this treatment is less effective for those with other types of parasomnias, but future research will be needed to make this determination. The comorbidity of the sample was noteworthy (ie, 79% had a co-occurring psychiatric disorder, and 16% had co-occurring but treated sleep disorder) and it is possible that the comorbidities reduced the impact of treatment on parasomnias, although only n = 4 met criteria for posttraumatic stress disorder. The baseline sleep efficiency of this sample was comparable to other samples of participants with NREM parasomnias55 but better than samples consisting of nonparasomnia disorders (eg, posttraumatic stress disorder with insomnia disorder or insomnia disorder alone).56,57
CBTp resulted in significant improvements in sleep efficiency (and to a lesser extent sleep-onset latency) despite the presence of significant sleep and psychiatric comorbidity. These changes occurred despite no interventions aimed at sleep restriction and, at the outset, 47% (n = 9 of 19) meeting DSM 5 criteria for insomnia disorder. The average sleep efficiency of the treated group at follow-up ranged between 88% (sleep diary) to 95% (actigraphy), approximating the 90% benchmark. Scores on the Insomnia Severity Index from the treated group at posttreatment were reduced on average by 5 points and represented a medium effect. The number with objectively normative sleep based on a combination of SE, TST, wake after sleep onset, and SOL was 75% at posttreatment, which is somewhat better than that obtained in randomized controlled trials for insomnia disorder.58 Thus, CBTp resulted in moderate improvements in comorbid insomnia without the use of cognitive behavioral therapy for insomnia.
Notably, although the frequency and severity of parasomnias and level of nocturnal activity were significantly reduced in the CBTp group vs self-monitoring control, this change was not associated with significantly reduced fatigue or sleepiness. The effect sizes for the fatigue and sleepiness variables were medium to large, and so it is possible that with a larger sample these may have reached significance. It is also possible that the scales used to measure sleepiness and fatigue lacked sensitivity. Although widely used in clinical settings, the Epworth Sleepiness Scale has been critiqued for failing to show criterion validity.59 The average Epworth Sleepiness Scale score in a US population study was 8.8 (SD = 4.03),60 and we had only 15% of treated participants who achieved this level of alertness at follow-up. In contrast, fatigue scores at posttreatment and follow-up were consistent with norms for well populations (M = 8.42, SD = 3.5), and 40% of treated participants achieved a normative level of fatigue at the end of the study. Other research shows that sleepiness is not highly correlated with the number of NREM3 interruptions and more related to short sleep-onset latency and longer total sleep time.61 Thus, sleepiness may not be a consequence of NREM parasomnias but may merely reflect greater sleep pressure. Finally, it is possible that some of the medications being used to treat these parasomnias were responsible for sleepiness. Thus, CBTp may have better improved fatigue than sleepiness.
Many participants in the study had sleep-interfering behaviors such as disruption to sleep due to noise, medical conditions, and pets. Also, many participants in the study had a delayed chronotype or a tendency toward later bedtimes than is typical for the good sleeping and insomnia populations. It is possible that long-standing avoidance of sleeping resulted in later bedtimes for these patients, or that the comorbid psychiatric conditions led to later bedtimes (due to the presence of significant late-night worry/rumination). During CBTp, some patients wanted to discuss the details of their parasomnias and to speculate on what the parasomnia was trying to teach them. Patients recognized that parasomnias have much to do with their own psychology. The schematic content of parasomnias often pertained to feelings of defectiveness/shame, vulnerability to harm, dependency or incompetence, or expectations of emotional deprivation or lack of protection. Like other studies, the content of both nightmares and rapid eye movement sleep behavior disorder often pertains to interpersonal situations and had more unfortunate endings and aggressiveness.62 The content of sleep terrors often involved a feared home invader, and the content of sleepwalking often involved searching for a pet or family member. Addressing these schemas in the more complex intervention of imagery rehearsal therapy was important and required therapist involvement. Without such involvement, participants tended to rescript parasomnias in a manner that was overly alerting, too unbelievable, and/or not in alignment with the schemas underlying their parasomnias. Identifying and addressing these schemas naturally led participants to apply this approach to their waking life, which was of benefit to the individual.
Some of the qualitative feedback indicated that this was one of the first times that patients had read descriptions of their problems, about possible causes, and about behavioral solutions. This suggests that parasomnias may not be identified or discussed very frequently among referral sources. Additionally, there is little media coverage of parasomnias and the behavioral methods with which to treat them. It can be difficult for patients and providers to differentiate which symptoms are attributable to which disorders. For these reasons, a transdiagnostic approach is appealing and would allow for ease of dissemination among specialist sleep providers. However, the skill set required to conduct some of these interventions may require further training. Participant feedback suggests that this type of intervention is feasible for this patient population.
Limitations
Limitations of the study include the use of a small sample and self-report measurement of parasomnias, the latter of which is potentially problematic due to less recall of events associated with NREM sleep. The use of polysomnography for assessment of parasomnias is expensive and imperfect as parasomnias may not occur during the overnight sleep study period. Actigraphy does not rely on patient self-report and in addition to retrospective questionnaires is most used to identify parasomnias. Actigraphy is also imprecise in identifying complex parasomnia events. As a result, a multimodal approach to assessment is warranted until we have better tools to identify these conditions. The measurement of parasomnia severity used in the current study was focused on nightmares for lack of any appropriate alternatives. The field is generally lacking in reliable and validated measurement of distress associated with NREM parasomnias and community-based (and clinical) norms for measures of parasomnias, with some exceptions.37 This requires urgent action to identify the types and severity of daytime impairment attributed to these conditions. The heterogeneous sample included a variety of comorbid conditions. The role of improvement in comorbidities (particularly anxiety disorders) on the parasomnia outcomes is therefore unclear; however, existing sparse research has not shown that that treatment of psychiatric conditions improves NREM parasomnia symptoms.63 More research into mechanisms of action of CBTp is warranted.
DISCLOSURE STATEMENT
All authors have read and approved the manuscript. Work for this study was performed at the University of Manitoba. This study was funded by an internal grant from the Max Rady College of Medicine, University of Manitoba. The authors report no conflicts of interest.
ABBREVIATIONS
| CBTp | cognitive behavioral therapy for parasomnias |
| DSM | Diagnostic and Statistical Manual of Mental Disorders |
| M | mean |
| NREM | non-rapid eye movement |
| SD | standard deviation |
| SE | sleep efficiency |
| SOL | sleep onset latency |
| TST | total sleep time |
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