Abstract:In a randomized controlled trial, we evaluated the efficacy of cognitive-behavioral treatment for insomnia to improve sleep and daytime symptoms, and to reduce relapse in recovering alcohol dependent (AD) participants. Seventeen abstinent AD patients with insomnia (6 women, mean age 46.2 ± 10.1 years) were randomized to 8 sessions of cognitive behavioral treatment for insomnia for AD (CBTI-AD, n=9) or to a behavioral placebo treatment (BPT, n=8). Subjective measures of sleep, daytime consequences of insomnia a… Show more
“…Commonly reported phenomena include shortened sleep onset latency (MacLean and Cairns 1982; Roehrs et al 1999; Williams, MacLean, and Cairns
1983; Stone 1980; Scrima et al 1982) and increased SWS in the first half of the
night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al
1972; Chan et al 2013; MacLean and Cairns 1982; Prinz et
al. 1980; Feige et al 2006; Arnedt, Rohsenow, et al 2011). REM sleep is suppressed, with a
longer latency to REM sleep and decreased REM sleep in the first half of the night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al
1972; Chan et al 2013) or across the whole
night (Van Reen, Jenni, and Carskadon 2006; Williams, MacLean, and Cairns 1983; Roehrs et al 1999; Rundell et al
1972; Roehrs, Yoon, and Roth 1991; Arnedt, Rohsenow, et al 2011).…”
Section: 0 Acute Effects Of Alcohol On Sleepmentioning
confidence: 99%
“…1980; Feige et al 2006; Arnedt, Rohsenow, et al 2011). REM sleep is suppressed, with a
longer latency to REM sleep and decreased REM sleep in the first half of the night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al
1972; Chan et al 2013) or across the whole
night (Van Reen, Jenni, and Carskadon 2006; Williams, MacLean, and Cairns 1983; Roehrs et al 1999; Rundell et al
1972; Roehrs, Yoon, and Roth 1991; Arnedt, Rohsenow, et al 2011). In the second half of the
night, sleep is disrupted, with increased wakefulness and/or stage 1 sleep.…”
Section: 0 Acute Effects Of Alcohol On Sleepmentioning
Alcohol acts as a sedative that interacts with several neurotransmitter systems
important in the regulation of sleep. Acute administration of large amounts of alcohol
prior to sleep leads to decreased sleep onset latency and changes in sleep architecture
early in the night, when blood alcohol levels are high, with subsequent disrupted, poor
quality sleep later in the night. Alcohol abuse and dependence are associated with chronic
sleep disturbance, lower slow wave sleep, and more rapid eye movement sleep than normal,
that last long into periods of abstinence and may play a role in relapse. The chapter
outlines the evidence for acute and chronic alcohol effects on sleep architecture and
sleep EEG, evidence for tolerance with repeated administration, and possible underlying
neurochemical mechanisms for alcohol’s effects on sleep. Also discussed are sex
differences as well as effects of alcohol on sleep homeostasis and circadian regulation.
Evidence for the role of sleep disruption as a risk factor for developing alcohol
dependence is discussed in the context of research conducted in adolescents. The utility
of sleep evoked potentials in the assessment of the effects of alcoholism on sleep and the
brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a
series of questions that need to be answered to determine the role of sleep and sleep
disturbance in the development and maintenance of problem drinking and the potential
beneficial effects of the treatment of sleep disorders for maintenance of abstinence in
alcoholism.
“…Commonly reported phenomena include shortened sleep onset latency (MacLean and Cairns 1982; Roehrs et al 1999; Williams, MacLean, and Cairns
1983; Stone 1980; Scrima et al 1982) and increased SWS in the first half of the
night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al
1972; Chan et al 2013; MacLean and Cairns 1982; Prinz et
al. 1980; Feige et al 2006; Arnedt, Rohsenow, et al 2011). REM sleep is suppressed, with a
longer latency to REM sleep and decreased REM sleep in the first half of the night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al
1972; Chan et al 2013) or across the whole
night (Van Reen, Jenni, and Carskadon 2006; Williams, MacLean, and Cairns 1983; Roehrs et al 1999; Rundell et al
1972; Roehrs, Yoon, and Roth 1991; Arnedt, Rohsenow, et al 2011).…”
Section: 0 Acute Effects Of Alcohol On Sleepmentioning
confidence: 99%
“…1980; Feige et al 2006; Arnedt, Rohsenow, et al 2011). REM sleep is suppressed, with a
longer latency to REM sleep and decreased REM sleep in the first half of the night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al
1972; Chan et al 2013) or across the whole
night (Van Reen, Jenni, and Carskadon 2006; Williams, MacLean, and Cairns 1983; Roehrs et al 1999; Rundell et al
1972; Roehrs, Yoon, and Roth 1991; Arnedt, Rohsenow, et al 2011). In the second half of the
night, sleep is disrupted, with increased wakefulness and/or stage 1 sleep.…”
Section: 0 Acute Effects Of Alcohol On Sleepmentioning
Alcohol acts as a sedative that interacts with several neurotransmitter systems
important in the regulation of sleep. Acute administration of large amounts of alcohol
prior to sleep leads to decreased sleep onset latency and changes in sleep architecture
early in the night, when blood alcohol levels are high, with subsequent disrupted, poor
quality sleep later in the night. Alcohol abuse and dependence are associated with chronic
sleep disturbance, lower slow wave sleep, and more rapid eye movement sleep than normal,
that last long into periods of abstinence and may play a role in relapse. The chapter
outlines the evidence for acute and chronic alcohol effects on sleep architecture and
sleep EEG, evidence for tolerance with repeated administration, and possible underlying
neurochemical mechanisms for alcohol’s effects on sleep. Also discussed are sex
differences as well as effects of alcohol on sleep homeostasis and circadian regulation.
Evidence for the role of sleep disruption as a risk factor for developing alcohol
dependence is discussed in the context of research conducted in adolescents. The utility
of sleep evoked potentials in the assessment of the effects of alcoholism on sleep and the
brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a
series of questions that need to be answered to determine the role of sleep and sleep
disturbance in the development and maintenance of problem drinking and the potential
beneficial effects of the treatment of sleep disorders for maintenance of abstinence in
alcoholism.
“…7 Although there is a paucity of rigorous controlled designs, preliminary studies of CBTi in comorbid disorders have demonstrated positive outcomes for both sleep variables and clinical symptoms across a range of diagnoses, including depressive disorders, posttraumatic stress disorder, alcohol dependence, and psychosis. [17][18][19][20][21] Despite the burgeoning literature on mindfulness-based insomnia interventions, particularly in relation to chronic illness, 22,23 there is a dearth of evidence for psychological therapies for insomnia outside of CBTi, particularly in the context of comorbid psychiatric difficulties.…”
Section: S C I E N T I F I C I N V E S T I G At I O N Smentioning
Study Objectives: Poor sleep quality, particularly insomnia, has been identifi ed as a frequent problem among individuals with mental health diffi culties. Comorbid sleep diffi culties adversely affect quality of life and functioning, and have been associated with the causation and maintenance of a number of psychiatric disorders, as well as increasing the risk of relapse. The study objectives were to ascertain clinician knowledge related to insomnia, investigate sleep quality among service users in a community mental health setting in the UK, and evaluate service provision of evidence-based interventions for sleep diffi culties. Methods: A cross-sectional design was used. Nineteen clinicians completed a questionnaire on their clinical practice. Seventy-three service users completed the Pittsburgh Sleep Quality Index and provided self-report data on interventions received and associated satisfaction. Results: Clinical staff demonstrated defi cits in knowledge of insomnia symptomatology. Sixty-four percent (95% CI 54% to 74%) of service users were identifi ed as poor sleepers on the PSQI. Sixty-one percent of poor sleepers had not been offered support for sleep diffi culties. The most common support received was prescribed psychotropic medication (32%). Cognitive behavioral therapy was the intervention rated as most helpful but was only received by 6%. Conclusions: This study highlights inadequacies in providing evidence-based interventions for sleep diffi culties. Key recommendations include training clinicians in the identifi cation of sleep diffi culties and provision of evidencebased interventions, provision of cost-effective transdiagnostic group interventions, and formalizing assessment and treatment pathways for service users with sleep diffi culties.
“…The trial involved 60 abstinent patients with alcohol dependence, who were assigned to either a CBT-I condition with individual therapy sessions or a self-help condition, in which sleep problems were addressed by telephone support through a therapist, or a waiting list control condition (n = 20 each). In a similar vein, Arnedt et al observed in a pilot RCT, in which 17 abstinent patients with alcohol dependence received either eight sessions of CBT-I modified for alcohol dependence or a placebo treatment, a total relapse rate of 47 %, with no significant group differences [2].…”
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