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The Effects of Cognitive Processing Therapy + Hypnosis on Objective Sleep Quality With Posttraumatic Stress Disorder
The Effects of Cognitive Processing Therapy + Hypnosis on Objective Sleep Quality With Posttraumatic Stress Disorder
Insomnia, characterized by difficulty falling and staying asleep, is a common and debilitating symptom of posttraumatic stress disorder (PTSD) that is resistant to first-line, trauma-focused therapies. Previous research has found that sleep-directed hypnosis improves subjective sleep quality, particularly sleep onset latency, in women with PTSD. However, it cannot be assumed that improvements in subjective sleep reports correspond with objectively measured sleep improvements, because research has indicated a lack of agreement across these measures. The current study examined the effects of sleep-directed hypnosis plus cognitive processing therapy (hypCPT) on objective indices of sleep quality measured with actigraphy. Method: Forty-five women with PTSD were randomized to receive sleep-directed hypCPT or sleep and psychiatric symptom monitoring plus CPT (ssmCPT). Pre- and posttreatment, participants completed 1 week of daily actigraphy assessments of nocturnal sleep onset latency, waking after sleep onset, and total sleep time. Results: Overall improvement in objective sleep indices was not observed. Despite this, at posttreatment, treatment completers receiving hypCPT took significantly less time to fall asleep than did women receiving ssmCPT. Conclusions: More research is needed to understand and reduce the discrepancy between subjectively and objectively assessed sleep impairments in PTSD. Nevertheless, results indicate that adding sleep-directed hypnosis to trauma-focused therapy may be of some use for individuals with PTSD-related insomnia. (PsycInfo Database Record (c) 2021 APA, all rights reserved)
Clinical Impact Statement—This study examined the effects of sleep-directed hypnosis and cognitive processing therapy on objectively assessed sleep quality in women with posttraumatic stress disorder. In contrast to the severe insomnia symptoms they reported, participants exhibited relatively normal objective sleep patterns. Despite this, compared to controls, women receiving sleep-directed hypnosis tended to take less time to fall asleep at the beginning of the night. This suggests that sleep-directed hypnosis may be a promising add-on to existing trauma-focused therapies. (PsycInfo Database Record (c) 2021 APA, all rights reserved)
Insomnia, characterized by difficulty falling or staying asleep, is a common and debilitating symptom of posttraumatic stress disorder (PTSD). Indeed, between 80% and 90% of individuals with PTSD endorse clinically significant insomnia symptoms (Koffel, Khawaja, & Germain, 2016). Notably, insomnia is resistant to first-line treatments for PTSD, including cognitive processing therapy (CPT) and prolonged exposure (Belleville, Guay, & Marchand, 2011; Larsen, Fleming, & Resick, 2019). For example, a recent study found that following CPT, 74% to 80% of participants maintained clinically significant insomnia symptoms (Pruiksma et al., 2016). Such findings highlight the need for treatments that better address insomnia in the context of PTSD.
Previously, our research group examined sleep-directed hypnosis as an adjunct to CPT for PTSD (Galovski et al., 2016). Prior to CPT, participants completed 3 weeks of sleep-directed hypnosis (hypCPT) or were asked to monitor sleep and psychiatric symptoms (ssmCPT). When assessed after the sleep intervention but prior to CPT, participants receiving sleep-directed hypnosis demonstrated greater improvement than did ssmCPT participants in self-reported global sleep quality and sleep onset latency (SOL) but not total sleep time (TST). Following CPT, both conditions evidenced statistically significant improvement in global insomnia symptoms and did not differ from each other.
Despite promising effects on self-reported insomnia symptoms, it remains unknown whether adding sleep-directed hypnosis to CPT improves sleep that is objectively measured (e.g., with actigraphy). Research cannot assume that improvements in subjective sleep reports correspond with objectively measured sleep improvements, because previous research has indicated a lack of agreement across these measures (e.g., Werner, Griffin, & Galovski, 2016). Evidence supporting objectively assessed sleep impairments in PTSD has been equivocal (Koffel et al., 2016). Research using actigraphy has suggested that individuals with, versus without, PTSD experience longer SOL but are not likely to differ in number of nighttime awakenings, amount of time spent awake after initially falling asleep (waking after sleep onset [WASO]), or TST (Slightam et al., 2018). Because sleep-directed hypnosis targets SOL (Stanton, 1989), it may be particularly useful for improving the aspect of objective sleep quality that appears to be most impaired among individuals with PTSD.
This study compared the effects of sleep-directed hypnosis and symptom monitoring on objective sleep indices in women with PTSD completing CPT. Based on previous research (Galovski et al., 2016), we expected participants in both conditions to demonstrate improved SOL following treatment. However, we expected improvement to be greater for participants receiving sleep-directed hypnosis. Given previous research, significant between-groups changes over time were not expected for WASO or TST.
Data came from a larger (N = 92) randomized controlled trial comparing hypCPT and ssmCPT for female survivors of interpersonal violence with PTSD (Galovski et al., 2016). Women in the parent study were invited to participate in an auxiliary study examining objective sleep quality pre- and posttreatment. Forty-five women participated. Women opting into the study did not differ in age, race or ethnicity, PTSD symptom severity, or frequency of sleep medication use from women who declined participation (ps > .05).
Participants were at least 18 years old, had current PTSD, and endorsed PTSD-related sleep impairment (i.e., frequency and intensity score ≥3 for symptom D1 [Trouble Initiating or Falling Asleep] on the Clinician Administered PTSD Scale for DSM−IV;Blake et al., 1995). Exclusion criteria included psychosis, alcohol or substance abuse or dependence, suicidality, or a peritraumatic living situation. Psychotropic medication use was required to be stable prior to participation. Women could not receive outside trauma- or sleep-focused psychotherapy during their participation.
Participants identified as White or Caucasian (53.3%) or Black or African American (46.7%); 2.2% also identified as Hispanic or Latina. Average age was 36.16 years (SD = 11.66). Frequency of sleep medication use (Pittsburgh Sleep Quality Index; Buysse, Reynolds, Monk, Berman, & Kupfer, 1989) was as follows: 46.3% never, 7.3% less than once a week, 17.1% once or twice a week, 29.3% three or more times a week.
Objective sleep quality was assessed with actigraphy. Research has indicated that actigraphy collected over seven nights is a valid indicator of sleep compared to independent in-laboratory polysomnography (PSG; Withrow, Roth, Koshorek, & Roehrs, 2019). Actometers (Ambulatory Monitoring Inc., Ardsley, NY) were used to obtain daily assessments of SOL, WASO, and TST at pre- and posttreatment. Actigraphy measurements were collected in 30-s epochs using the proportional integrating mode, which corresponds most reliably with PSG assessments (Blackwell et al., 2008). Action W analysis software (Version 2; Ambulatory Monitoring Inc., Ardsley, NY) provided down intervals and estimates of sleep and wake parameters. The University of California—San Diego algorithm (Cole, Kripke, Gruen, Mullaney, & Gillin, 1992) was used to calculate SOL, WASO, and TST for each night of recording. Variables of interest included pre- and posttreatment means (in minutes) for SOL, WASO, and TST.
Participants were randomized to receive either hypCPT (n = 27) or ssmCPT (n = 18). Detailed descriptions of these treatment conditions can be found in Galovski et al. (2016). Briefly, participation in the ssmCPT condition began with a 3-week period of daily sleep and psychiatric symptom monitoring and included weekly phone check-ins with a study therapist. Participants in the hypCPT condition also monitored sleep and psychiatric symptoms and received three weekly, 60-min sessions of sleep-directed hypnosis. During sessions, hypnotic trance was induced using an eye fixation technique and was deepened using progressive muscle relaxation. Sessions also included guided imagery, psychoeducation, and the use of self-statements. Sessions were largely scripted. Hypnosis sessions were taped, and participants were asked to practice hypnosis on a nightly basis. Following the sleep intervention phase, all participants completed a standard CPT protocol consisting of 12 weekly, 60-min sessions (for a description, see Resick & Schnicke, 1992).
Procedures were approved by the University of Missouri—St. Louis’s Institutional Review Board. At an initial visit, inclusion or exclusion criteria, demographic characteristics, and use of sleep medication were assessed. Participants were then fitted with an actometer on their nondominant wrist and were instructed to wear it 24 hr/day for 7 days. Participants returned to the clinic within 2 weeks, at which point actigraphy data were collected by study staff. Some participants wore the actometer beyond 7 days as initially instructed. Across participants, all available actigraphy data were used in analyses (M = 6.35 days, SD = 3.01). Participants then completed either hypCPT or ssmCPT protocols followed by a second, posttreatment actigraphy assessment (M = 6.92 days, SD = 3.94).
Actigraphy data were available from 43 participants at pretreatment and 24 at posttreatment. At pretreatment, missing data were due to technical difficulties with the actometer (n = 2). At posttreatment, missing data were due to technical difficulties (n = 3) or attrition from the study (n = 18). Attrition largely occurred prior to initiating treatment, within the first five sessions of CPT, or after CPT but prior to the posttreatment actigraphy assessment. Rates of attrition did not differ by condition, χ2(1, N = 45) = .02, p = .89. Further, missingness was unrelated to age, race or ethnicity, PTSD symptom severity, or sleep medication use (ps > .05). Data were thus considered to be missing at random.
Sleep outcomes were examined using linear mixed models in SPSS 25. This approach maximized use of available data to examine differences between conditions at pre- and posttreatment. Within analyses, we used a compound symmetry covariance structure to account for within-subject correlated errors. Separate models were conducted to examine SOL, WASO, and TST. For each outcome, we first examined a main effects model, including fixed effects of time (pretreatment = 0, posttreatment = 1) and condition (ssmCPT = 0, hypCPT = 1). We then examined a model including a Time × Condition interaction term. The models’ −2 restricted log likelihood values were compared using a chi-square difference approach. In all cases, the model including the interaction term provided significantly better fit than did the main effects model (all −2 restricted log likelihooddifference > 5.91, df = 1, p < .02). Thus, the results presented below include only the models with the interaction terms. Within these models, the condition effect reflects the difference between conditions at posttreatment, the time effect reflects the slope from posttreatment to pretreatment for hypCPT participants, and the Condition × Time effect reflects the change in slope between hypCPT and ssmCPT participants.
Pretreatment, participants took an average of 19.98 min (SD = 15.84) to fall asleep and spent an average of 46.64 min (SD = 25.37) awake during the night. Average TST was 406.94 min (SD = 69.89), which is within the range of normal sleep duration for healthy adults (Fernandez-Mendoza et al., 2011).
We first examined the intent-to-treat sample (N = 45). As seen in Table 1, SOL did not change significantly for hypCPT (pretreatment: M = 14.70 min, SE = 4.24; posttreatment: M = 19.71 min, SE = 3.23) or ssmCPT (pretreatment: M = 20.48 min, SE = 4.17; posttreatment: M = 27.29 min, SE = 5.48) participants. However, at posttreatment, participants in the hypCPT condition took marginally less time to fall asleep than did participants in the ssmCPT condition. No significant effects emerged from the models examining WASO or TST (see Table 1).
This study examined treatment-related change in objectively assessed sleep among individuals with PTSD. It also examined whether sleep-directed hypnosis is a useful adjunct to CPT for addressing PTSD-related insomnia symptoms. The intervention affected SOL, particularly among treatment completers. At posttreatment, hypCPT participants fell asleep an average of 13 min faster than did ssmCPT participants. This was driven mainly by a marginally significant pre- to posttreatment increase in SOL among ssmCPT participants. Consistent with previous research (Galovski et al., 2016; Slightam et al., 2018), the intervention did not significantly alter WASO or TST.
Despite this observed difference, treatment-related change in objective sleep variables was minimal. Because objective TST prior to treatment was not impaired relative to norms for healthy adults (Fernandez-Mendoza et al., 2011), lack of improvement may reflect a ceiling effect. These results are in contrast to those in our previous research using self-reported sleep outcomes, where both conditions improved significantly in SOL and global sleep quality (Galovski et al., 2016). The discrepancy between results relying on self-reported versus objective sleep impairments is consistent with that in previous PTSD research (Slightam et al., 2018; Werner et al., 2016), as well as in sleep intervention research with other patient populations (Lund, Rybarczyk, Perrin, Leszczyszyn, & Stepanski, 2013). Elucidating reasons for a discrepancy between self-reported and objective sleep (i.e., sleep state misperception) could inform the understanding of PTSD-related insomnia symptoms (Rezaie, Fobian, McCall, & Khazaie, 2018).
Results should be considered preliminary, because the study’s sample was small and a sizable percentage of posttreatment data was missing. Though our analytic approach maximized use of available data, actigraphy was collected at only two time points, and analyses examining change over time were particularly underpowered to detect effects. The study also did not include an actigraphy assessment immediately following the sleep intervention phase of treatment. Our previous research found the strongest effects of hypCPT versus ssmCPT immediately after the sleep intervention phase and before starting CPT (Galovski et al., 2016). We expect that future investigations will see stronger effects if actigraphy assessment occurs in closer temporal proximity to the sleep-directed hypnosis intervention. Though controlling for use of sleep medication did not alter study results, data on the use of specific medications were not collected in this study.
Understanding how treatment affects objectively measured sleep is critical to addressing the often debilitating insomnia experienced by individuals with PTSD. Results of the current study suggest that CPT does not improve (and may even worsen, at least in the short term) objective sleep outcomes. Adding sleep-directed hypnosis may be of some value, though more research is needed to confirm this. Studies aimed at elucidating and reducing sleep-state misperception in individuals with PTSD may also prove useful.
By: Kimberly A. Arditte Hall
Department of Psychology and Philosophy, Framingham State University;
Kimberly B. Werner
Missouri Institute of Mental Health, University of Missouri—St. Louis
Michael G. Griffin
Center for Trauma Recovery, Department of Psychology, University of Missouri—St. Louis
Tara E. Galovski
VA National Center for PTSD, VA Boston Healthcare System, Boston, Massachusetts, and Boston University School of Medicine
Acknowledgement: This research was supported by National Center for Complementary and Alternative Medicine Grant 1R21AT004079 (principal investigator: Tara E. Galovski). The views expressed in this article are those of the authors’ and do not necessarily represent the views of the Department of Veterans Affairs or the U.S. government.
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Submitted: January 31, 2020 Revised: June 20, 2020 Accepted: August 7, 2020
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Source: Psychological Trauma: Theory, Research, Practice, and Policy. Sep 10, 2020
Accession Number: 2020-66927-001
Digital Object Identifier: 10.1037/tra0000970
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