Sleep disturbances in patients with schizophrenia : impact and effect of antipsychotics.
TL;DR: It appears possible that the high-potency drugs exert their effects on sleep in schizophrenic patients, for the most part, in an indirect way by suppressing stressful psychotic symptomatology.
Abstract: Difficulties initiating or maintaining sleep are frequently encountered in patients with schizophrenia. Disturbed sleep can be found in 30–80% of schizophrenic patients, depending on the degree of psychotic symptomatology. Measured by polysomnography, reduced sleep efficiency and total sleep time, as well as increased sleep latency, are found in most patients with schizophrenia and appear to be an important part of the pathophysiology of this disorder. Some studies also reported alterations of stage 2 sleep, slow-wave sleep (SWS) and rapid eye movement (REM) sleep variables, i.e. reduced REM latency and REM density. A number of sleep parameters, such as the amount of SWS and the REM latency, are significantly correlated to clinical variables, including severity of illness, positive symptoms, negative symptoms, outcome, neurocognitive impairment and brain structure. Concerning specific sleep disorders, there is some evidence that schizophrenic patients carry a higher risk of experiencing a sleep-related breathing disorder, especially those demonstrating the known risk factors, including being overweight but also long-term use of antipsychotics. However, it is still unclear whether periodic leg movements in sleep or restless legs syndrome (RLS) are found with a higher or lower prevalence in schizophrenic patients than in healthy controls. There are no consistent effects of first-generation antipsychotics on measuresof sleep continuity and sleep structure, including the percentage of sleep stages or sleep and REM latency in healthy controls. In contrast to first-generation antipsychotics, the studied atypical antipsychotics (clozapine, olanzapine, quetiapine, risperidone, ziprasidone and paliperidone) demonstrate a relatively consistent effect on measures of sleep continuity, with an increase in either total sleep time (TST) or sleep efficiency, and individually varying effects on other sleep parameters, such as an increase in REM latency observed for olanzapine, quetiapine and ziprasidone, and an increase in SWS documented for olanzapine and ziprasidone in healthy subjects. The treatment of schizophrenic patients with first-generation antipsychotics is consistently associated with an increase in TST and sleep efficiency, and mostly an increase in REM latency, whereas the influence on specific sleep stages is more variable. On the other hand, withdrawal of such treatment is followed by a change in sleep structure mainly in the opposite direction, indicating a deterioration of sleep quality. On the background of the rather inconsistent effects of first-generation antipsychotics observed in healthy subjects, it appears possible that the high-potency drugs exert their effects on sleep in schizophrenic patients, for the most part, in an indirect way by suppressing stressful psychotic symptomatology. In contrast, the available data concerning second-generation antipsychotics (clozapine, olanzapine, risperidone and paliperidone) demonstrate a relatively consistent effect on measures of sleep continuity in patients and healthy subjects, with an increase in TST and sleep efficiency or a decrease in wakefulness. Additionally, clozapine and olanzapine demonstrate comparable influences on other sleep variables, such as SWS or REM density, in controls and schizophrenic patients. Possibly, the effects of second-generation antipsychotics observed on sleep in healthy subjects and schizophrenic patients might involve the action of these drugs on symptomatology, such as depression, cognitive impairment, and negative and positive symptoms. Specific sleep disorders, such as RLS, sleep-related breathing disorders, night-eating syndrome, somnambulism and rhythm disorders have been described as possible adverse effects of antipsychotics and should be considered in the differential diagnosis of disturbed or unrestful sleep in this population.
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University of Freiburg1, University of Bergen2, Northumbria University3, University of Oxford4, Stavanger University Hospital5, Karolinska Institutet6, University of Copenhagen7, Paris Descartes University8, University of Parma9, National Institutes of Health10, University of Antwerp11, University of Bucharest12, Frederiksberg Hospital13
TL;DR: In this article, a European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia.
Abstract: This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia. The guideline is based on a systematic review of relevant meta-analyses published till June 2016. The target audience for this guideline includes all clinicians involved in the management of insomnia, and the target patient population includes adults with chronic insomnia disorder. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to grade the evidence and guide recommendations. The diagnostic procedure for insomnia, and its co-morbidities, should include a clinical interview consisting of a sleep history (sleep habits, sleep environment, work schedules, circadian factors), the use of sleep questionnaires and sleep diaries, questions about somatic and mental health, a physical examination and additional measures if indicated (i.e. blood tests, electrocardiogram, electroencephalogram; strong recommendation, moderate- to high-quality evidence). Polysomnography can be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders), in treatment-resistant insomnia, for professional at-risk populations and when substantial sleep state misperception is suspected (strong recommendation, high-quality evidence). Cognitive behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (strong recommendation, high-quality evidence). A pharmacological intervention can be offered if cognitive behavioural therapy for insomnia is not sufficiently effective or not available. Benzodiazepines, benzodiazepine receptor agonists and some antidepressants are effective in the short-term treatment of insomnia (≤4 weeks; weak recommendation, moderate-quality evidence). Antihistamines, antipsychotics, melatonin and phytotherapeutics are not recommended for insomnia treatment (strong to weak recommendations, low- to very-low-quality evidence). Light therapy and exercise need to be further evaluated to judge their usefulness in the treatment of insomnia (weak recommendation, low-quality evidence). Complementary and alternative treatments (e.g. homeopathy, acupuncture) are not recommended for insomnia treatment (weak recommendation, very-low-quality evidence).
1,076 citations
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TL;DR: It is proposed that brain disorders and abnormal sleep have a common mechanistic origin and that many co-morbid pathologies that are found in brain disease arise from a destabilization of sleep mechanisms.
Abstract: Sleep and circadian rhythm disruption are frequently observed in patients with psychiatric disorders and neurodegenerative disease. The abnormal sleep that is experienced by these patients is largely assumed to be the product of medication or some other influence that is not well defined. However, normal brain function and the generation of sleep are linked by common neurotransmitter systems and regulatory pathways. Disruption of sleep alters sleep-wake timing, destabilizes physiology and promotes a range of pathologies (from cognitive to metabolic defects) that are rarely considered to be associated with abnormal sleep. We propose that brain disorders and abnormal sleep have a common mechanistic origin and that many co-morbid pathologies that are found in brain disease arise from a destabilization of sleep mechanisms. The stabilization of sleep may be a means by which to reduce the symptoms of--and permit early intervention of--psychiatric and neurodegenerative disease.
864 citations
13 Dec 2017
TL;DR: This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia.
810 citations
Cites background from "Sleep disturbances in patients with..."
...Monti and Monti (2004; Monti et al., 2017) and Cohrs (2008) concluded that sedating antipsychotics increase total sleep time and the amount of slow-wave sleep in patients with schizophrenia....
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TL;DR: An overview of existing literature on the relation between poor sleep and aggression, irritability, and hostility is given and individual variation within these neurobiological systems may be responsible for amplified aggressive responses induced by sleep loss in certain individuals.
323 citations
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TL;DR: The question is: can the early and adequate treatment of insomnia prevent depression, and current understanding about sleep regulatory mechanisms with knowledge about changes in physiology due to depression are linked.
294 citations
Cites background from "Sleep disturbances in patients with..."
...With respect to AP even less evidence is available—studies are available investigating the effects of AP on sleep in schizophrenia [154] and in insomnia [155, 156]....
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References
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TL;DR: The finding that clinical doses of CPZ cause mild sedation, and enhanced SW sleep without any significant modification of REM, sleep, indicates that CPZ has features which may recommend it as a standard hypnotic.
Abstract: The aim of this study was to examine human physiological sleep profiles, including the amount and distribution of electroenoephalographic (EEG) stages of sleep, variations in specific frequency bands in the EEG spectrum and certain phasic phenomena such as movement arousals, sigma spindles and rapid eye movements, following oral administration of a moderate dose (150 mg) of chlorpromazine (CPZ) to 12 young male volunteers. At this dose level the drug had few systematic effects on sleep, although it did reduce the latency of onset of stage REM and the number of movement arousals, while increasing the amount of slow-wave (SW) sleep. These effects persisted during the post-medication recovery night, but at no time was there any systematic change in the total amount or percent of REM sleep, the duration of the REM-to-REM cycle, the average length of REM episodes or the density of rapid eye movements during stage REM. Frequency analysis of EEG revealed that CPZ produced a trend toward increased fast (beta) activity recorded from pre-central placements during stage REM, and reduced density of sigma spindles in stage 2 sleep. Thus, for the most part, a single moderate dose of CPZ left the tonic, phasic and sequential properties of the sleep cycle unaltered. These results confirm previous investigations showing that for small to moderate clinical doses, CPZ invariably enhances SW sleep and reduces the frequency of movement arousals. On the other hand, the effect of the drug on stage REM apparently depends on dose. Small doses potentiate REM sleep or accelerate its onset, whereas larger doses either reduce stage REM or leave it unaffected. Several authors have pointed out that most hypnotic agents cause substantial alterations of the sleep profile, and that their withdrawal can cause profound disruption of sleep and marked clinical disturbance. It also has been suggested that there exists a relation between drug dependency and the degree of initial REM suppression caused by a drug. The finding confirmed by the present study that clinical doses of CPZ cause mild sedation, and enhanced SW sleep without any significant modification of REM, sleep, indicates that CPZ has features which may recommend it as a standard hypnotic.
20 citations
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TL;DR: Sleep quality improved on mesoridazine (10 mg nightly) but there was diminution of zest and freshness 20 min after rising and daytime concentration and anxiety were rated as not affected either by administration or withdrawal.
Abstract: 1 Mesoridazine, a phenothiazine of short half-life, and potentially useful as an hypnotic, has here been investigated using volunteers of late middle age. 2 The electrophsiological recording of all-night sleep was studied in seven subjects for a 7-week period during which ther received mesoridazine (10 mg nightly) for 3 weeks. The drug reduced the frequency of transitions into wakefulness and stage 1 (drowsiness) and reduced the time spent in stage 1; there was a withdrawal rebound. Mesoridazine increased REM sleep above baseline levels and a rebound fall below baseline occurred on withdrawal. The drug did not alter the amount of stage 3 + 4 slow wave sleep. 3 Subjective self-ratings were assessed in a 6-week study of sixteen subjects. Sleep quality improved on mesoridazine (10 mg nightly) but there was diminution of zest and freshness 20 min after rising. Daytime concentration and anxiety were rated as not affected either by administration or withdrawal.
18 citations
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TL;DR: Delusion formation is correlated significantly with a change in score of eight individual items from the Early Signs Scale (ESS), which forms the Warning Signals Scale (WSS), which is acceptable to patients, manageable for clinicians, and has a high degree of predictive validity and reliability.
17 citations
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TL;DR: All-night polysomnography performed in patients with neuroleptic-induced akathisia displayed a pattern of leg movement activity during sleep similar to healthy individuals and depressed patients, and eight of nine patients with NIA exhibited 10− to 40-second bursts of increased leg muscle tone before sleep onset.
Abstract: To investigate nocturnal leg movement activity and other polysomnographic features in patients with neuroleptic-induced akathisia (NIA), all-night polysomnography was performed in nine patients with NIA and compared with nine healthy individuals and eight unmedicated patients with depression. Patients with NIA displayed a pattern of leg movement activity during sleep similar to healthy individuals and depressed patients. In addition, eight of nine patients with NIA exhibited 10- to 40-second bursts of increased leg muscle tone before sleep onset. Although the significance of this finding is unclear, it is possible that it may be a pathophysiological correlate of NIA.
17 citations
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TL;DR: REM sleep measures demonstrated positive and negative correlations with cognition and memory measures, depending on when REM occurred after sleep onset, which should test whether phasic REM sleep regulation at the beginning of the night plays a compensatory role for neuropsychological dysfunction in schizophrenics.
15 citations