Do symptoms of depression, anxiety or stress impair the effectiveness of cognitive behavioural therapy for insomnia? A chart-review of 455 patients with chronic insomnia.

BACKGROUND: Co-occurring insomnia and symptoms of depression, anxiety, and stress pose difficult diagnostic and treatment decisions for clinicians. Cognitive Behavioural Therapy for Insomnia (CBTi) is the recommended first-line insomnia treatment, however symptoms of depression, anxiety and stress may reduce the effectiveness of CBTi. We examined the effect of low, moderate, and severe symptoms of depression, anxiety, and stress on insomnia improvements during CBTi. METHODS: We undertook a chart-review of 455 patients (67% Female, Age M = 51.7, SD = 15.6) attending an outpatient CBTi program. Sleep diaries and questionnaire measures of insomnia, depression, anxiety, and stress symptoms were completed at pre-treatment, post-treatment and three-month follow up. We examined 1) the effect of low, moderate, and severe symptoms of depression, anxiety, and stress before treatment on changes in sleep diary and questionnaire measures of insomnia during CBTi, and 2) changes in symptoms of depression, anxiety, and stress during CBTi. RESULTS: Sleep diary and questionnaire measures of insomnia severity showed moderate-to-large improvements during CBTi (d = 0.5-2.7, all p ≤ 0.001), and were not moderated by levels of depression, anxiety or stress before treatment (all interactions p > 0.05). Symptoms of depression, anxiety, and stress improved by three-month follow-up (M improvement = 41-43%; CI = 28-54, Cohen's d = 0.4-0.7). CONCLUSIONS: Symptoms of depression, anxiety, and stress do not impair the effectiveness of CBTi. Instead, CBTi was associated with moderate-to-large improvement of depression, anxiety, and stress symptoms in patients with insomnia disorder. Clinicians should refer patients with insomnia for CBTi even in the presence of comorbid symptoms of depression, anxiety, and stress.

Does comorbid obstructive sleep apnea impair the effectiveness of cognitive and behavioral therapy for insomnia?

AIMS: Comorbid insomnia and obstructive sleep apnea (OSA) represents a highly prevalent and debilitating condition; however, physicians and researchers are still uncertain about the most effective treatment approach. Several research groups have suggested that these patients should initially receive treatment for their insomnia before the sleep apnea is targeted. The current study aims to determine whether Cognitive and Behavioral Therapy for Insomnia (CBT-i) can effectively treat insomnia in patients with comorbid OSA and whether its effectiveness is impaired by the presence of OSA. METHODS: A retrospective chart review was conducted to examine 455 insomnia patients entering a CBT-i treatment program in a hospital out-patient setting. Three hundred and fourteen patients were diagnosed with insomnia alone and 141 with insomnia and comorbid OSA. Improvements in average sleep diary parameters, global insomnia severity, and several daytime functioning questionnaires from baseline, to post-treatment, to 3-month follow-up were compared between insomnia patients with and without comorbid OSA. RESULTS: Insomnia patients with comorbid OSA experienced significant improvements in insomnia symptoms, global insomnia severity, and other daytime functioning measures during and following treatment. Furthermore, improvements were no different between patients with or without comorbid OSA. Sleep apnea presence and severity were not related to rates of insomnia-remission or treatment-resistance following treatment. CONCLUSIONS: CBT-i is an effective treatment in the presence of comorbid OSA. This information offers support for the suggestion that patients with comorbid insomnia and OSA should be treated with CBT-i prior to the treatment of the OSA.

The direction of the relationship between symptoms of insomnia and psychiatric disorders in adolescents.

BACKGROUND: This study assessed the direction of the relationship between symptoms of insomnia disorder, depression, various anxiety disorders and obsessive compulsive disorder (OCD) in adolescents after controlling for age, gender, chronotype, and outcome variable at baseline. METHODS: Data was collected in eight high schools in Adelaide, South Australia, at two time-points approximately 6 months apart. The study was completed by 318 and 255 high school students at baseline and follow-up, respectively, aged 12-18 (M=14.96, SD=1.34) in grades 7-11 at baseline. Hierarchical regression analyses were used to assess each relationship, the first model controlling for age, gender and chronotype, and the second controlling for outcome variable at baseline. RESULTS: Insomnia symptoms predicted and were predicted by symptoms of each psychiatric disorder in model 1. In model 2, insomnia symptoms predicted symptoms of depression, and vice-versa. Symptoms of insomnia also predicted symptoms of separation anxiety disorder (SAD) once SAD, but not vice-versa, in model 2. Symptoms of obsessive compulsive disorder (OCD) and social phobia (SP) predicted symptoms of insomnia disorder in model 2, but not vice-versa. Insomnia symptoms were no longer related to symptoms of other anxiety disorders in model 2. LIMITATIONS: The use of self-report measures, and potential predisposing, precipitating, perpetuating or preventative factors were not assessed. CONCLUSIONS: Symptoms of insomnia disorder are bidirectionally related to depressive symptoms independent from baseline symptoms, and unidirectionally related to symptoms of OCD and SP where OCD and SP are independent risk-factors of the development of insomnia symptoms.

The independent relationships between insomnia, depression, subtypes of anxiety, and chronotype during adolescence.

OBJECTIVES: To investigate the independent effects of depression and subtypes of anxiety on insomnia, and vice versa, and the independent effect of chronotype on insomnia, depression, and subtypes of anxiety. METHODS: In all, 318 South Australian high school students from grades 7-11 (age range, 12-18years; mean, 14.97±1.34) participated in this cross-sectional study. Validated self-report questionnaires were used to assess insomnia, depression, subtypes of anxiety, and chronotype. RESULTS: After confounder variables were controlled, insomnia predicted depression and panic disorder (PD), whereas insomnia was predicted by depression and generalized anxiety disorder (GAD). Obsessive-compulsive disorder (OCD), separation anxiety (SAD), and social phobia (SP) were not significantly related to insomnia. Eveningness predicted the models in which depression and PD predicted insomnia and vice versa. Eveningness also predicted the models in which insomnia was predicted by OCD, SAD, and SP. CONCLUSIONS: Insomnia independently predicts depression and is predicted by depression and GAD, but not by other forms of anxiety. The independent prediction of insomnia on PD is unlikely to be clinically significant. Chronotype independently predicts and hence is a risk factor for insomnia and depression, but not subtypes of anxiety. Theoretical and clinical implications are discussed.

Insertion sequence ISPst4 activates pUC plasmid replication in Pseudomonas stutzeri.

Insertion sequences (IS) are important drivers of bacterial evolution. Here, we report a previously undescribed IS element (ISPst4) in Pseudomonas stutzeri, and its unusual interaction with plasmids introduced into this species. Transformation of the pUC19 derivative plasmid pUS23 into P. stutzeri yielded ampicillin-resistant transformants in P. stutzeri, but these grew very poorly. Plasmids recovered from the transformants frequently contained insertions of the IS elements ISPst4 and ISPst5. Hybridisation analysis showed that these two IS elements were common in P. stutzeri strains, but were not found in other pseudomonads. Insertions of ISPst4 in pUS23 were found predominantly between bla and oriV, and plasmids with this type of insertion were capable of robust replication in P. stutzeri, unlike pUS23. A promoter-containing region was localised to a 74 bp NcoI-SacI fragment within ISPst4, and we postulate that this promoter drives expression of the pUC oriV in P. stutzeri. This is the first report of IS transposition directly leading to an expansion of the effective host range of a plasmid, adding a new dimension to our understanding of the relationship between plasmids and IS elements.

A Systematic Review Assessing Bidirectionality between Sleep Disturbances, Anxiety, and Depression.

STUDY OBJECTIVES: To investigate whether sleep disturbances are bidirectionally related to anxiety and depression, and thus identify potential risk factors for each problem. DESIGN: A systematic review was conducted on 9 studies (8 longitudinal, 1 retrospective) that assessed bidirectionality between a sleep disturbance, and anxiety or depression. Treatment studies were excluded, along with those solely based on clinical samples or cohorts at high risk of suffering from a sleep disturbance, anxiety and depression. Eligible studies were identified by searching PubMed, PsychINFO, Embase, and Scopus databases, and reference lists of eligible studies. Publication dates ranged from the beginning of each database to December 2011. MEASUREMENTS AND RESULTS: Syntheses of longitudinal studies suggested insomnia and sleep quality were bidirectionally related to anxiety and depression, and depression/anxiety, respectively. Childhood sleep problems significantly predicted higher levels of depression and a combined depression/anxiety variable, but not vice-versa. A one-way relationship was found where anxiety predicted excessive daytime sleepiness, but excessive daytime sleepiness was not associated with depression. CONCLUSIONS: Definitive conclusions regarding bidirectionality cannot be made for most sleep disturbances due to the small number and heterogeneity of cohort samples used across studies. Nevertheless, best available evidence suggests insomnia is bidirectionally related to anxiety and depression. Clinical and theoretical implications are discussed. CITATION: Alvaro PK; Roberts RM; Harris JK. A systematic review assessing bidirectionality between sleep disturbances, anxiety, and depression. SLEEP 2013;36(7):1059-1068.

A randomized controlled trial of intensive sleep retraining (ISR): a brief conditioning treatment for chronic insomnia.

STUDY OBJECTIVE: To investigate the effectiveness of intensive sleep retraining in comparison and combination with traditional behavioral intervention for chronic primary insomnia. PARTICIPANTS: Seventy-nine volunteers with chronic sleep-onset insomnia (with or without sleep maintenance difficulties) were randomly assigned either to intensive sleep retraining (ISR), stimulus control therapy (SCT), ISR plus SCT, or the control (sleep hygiene) treatment condition. INTERVENTION: ISR treatment consisted of 50 sleep onset trials over a 25-h sleep deprivation period. MEASUREMENTS AND RESULTS: Treatment response was assessed with sleep diary, activity monitoring, and questionnaire measures. The active treatment groups (ISR, SCT, ISR+SCT) all resulted in significant improvements in sleep onset latency and sleep efficiency, with moderate to large effect sizes from pre- to post-treatment. Wake time after sleep onset decreased significantly in the SCT and ISR+SCT groups. Total sleep time increased significantly in the ISR and ISR+SCT treatment groups. Participants receiving ISR (ISR, ISR+SCT) experienced rapidly improved SOL and TST during treatment, suggesting an advantage of rapid improvements in sleep in response to ISR. Although there were few statistically significant differences between groups on individual variables, ISR+SCT resulted in consistently larger effect sizes of change than other treatments, including questionnaire measures of sleep quality, sleep self-efficacy, and daytime functioning. The combination treatment group (ISR+SCT) showed trends to outperform other active treatment groups with fewer treatment dropouts, and a greater proportion of treatment responders with 61% reaching "good sleeper" status. Treatment gains achieved at post-treatment in the active treatment groups were largely maintained throughout follow-up periods to 6 months. CONCLUSION: This 25-hour intensive conditioning treatment for chronic insomnia can produce rapid improvements in sleep, daytime functioning, and psychological variables. Adding ISR to traditional interventions seems to result in a superior treatment response.

Intensive Sleep Retraining treatment for chronic primary insomnia: a preliminary investigation.

The aim of this study was to assess the effectiveness of Intensive Sleep Retraining, a novel, short duration behavioural therapy in treating chronic primary insomnia. Seventeen consecutive volunteers from the general public (mean age = 39.1 years), meeting selection criteria for chronic primary insomnia participated in the treatment study. The study was performed as a case replication series. Assessment involved sleep diary, actigraph and questionnaire measures of sleep and daytime functioning for a period of 2 weeks prior to, immediately after, and 6 weeks following the treatment. Treatment involved a single night of sleep deprivation, facilitating short sleep latencies (mean: 6.9 min) to a series of 50 brief nap opportunities. Following treatment, Sleep Onset Latency significantly decreased by a mean of 30.5 min (SD = 28.3), Wake Time after Sleep Onset significantly decreased by a mean of 28 min (SD = 34.0), and Total Sleep Time significantly increased by 64.6 min (SD = 45.5). Significant improvements were also seen in the daytime functioning and psychological measures of fatigue and vigour, cognitive sleep anticipatory anxiety and self-efficacy for sleep. This brief therapy was effective in improving sleep and some daytime functioning and psychological questionnaire measures. These improvements were maintained up to 2 months following the treatment weekend. Further exploration of this brief therapy is needed, with larger, randomized, placebo-controlled trials over longer follow-up periods, and in comparison to other traditional therapies for insomnia.

The Flinders Fatigue Scale: preliminary psychometric properties and clinical sensitivity of a new scale for measuring daytime fatigue associated with insomnia.

STUDY OBJECTIVES: To evaluate the psychometric properties and clinical significance of a new scale for measuring daytime fatigue associated with insomnia: The Flinders Fatigue Scale (FFS). METHODS: The 7-item FFS was used in two separate studies. Study 1 was an on-line validation study involving 1093 volunteers (mean [SD] age = 38.6 [14.7] y, 626 poor sleepers, 467 good sleepers) in a cross-sectional design; Study 2 investigated the clinical sensitivity of the FFS on 113 insomnia patients (mean [SD] age = 48.3 [15.0] y) in response to a 5-week cognitive-behavior therapy for insomnia (CBT-I) program. RESULTS: The FFS had an internal consistency of 0.91; it comprised a single factor, accounting for 67% of the total variance. Poor sleepers in Study 1 scored significantly higher than good sleepers on the FFS (p < 0.0001). In Study 2, significant reductions in FFS scores were found in response to CBT-I (p < 0.0001). These reductions in fatigue correlated with improvements on subjective sleep parameters (all p < 0.0001). The FFS showed good discriminant validity with the Epworth Sleepiness Scale. CONCLUSIONS: The Flinders Fatigue Scale is a brief, clinically sensitive measure with strong psychometric properties.

Do chronic primary insomniacs have impaired heat loss when attempting sleep?

For good sleepers, distal skin temperatures (e.g., hands and feet) have been shown to increase when sleep is attempted. This process is said to reflect the body's action to lose heat from the core via the periphery. However, little is known regarding whether the same process occurs for insomniacs. It would be expected that insomniacs would have restricted heat loss due to anxiety when attempting sleep. The present study compared the finger skin temperature changes when sleep was attempted for 11 chronic primary insomniacs [mean age = 40.0 years (SD 13.3)] and 8 good sleepers [mean age = 38.6 years (SD 13.2)] in a 26-h constant routine protocol with the inclusion of multiple-sleep latency tests. Contrary to predictions, insomniacs demonstrated increases in finger skin temperature when attempting sleep that were significantly greater than those in good sleepers (P = 0.001), even though there was no significant differences in baseline finger temperature (P = 0.25). These significant increases occurred despite insomniacs reporting significantly greater sleep anticipatory anxiety (P < 0.0008). Interestingly, the core body temperature mesor of insomniacs (37.0 +/- 0.2 degrees C) was significantly higher than good sleepers (36.8 +/- 0.2 degrees C; P = 0.03). Whether insomniacs could have impaired heat loss that is masked by elevated heat production is discussed.