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
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
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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01 Jul 1984
15 citations
TL;DR: In this paper, the effects of W. 1854 on sleep and REM conditions during sleep while under treatment with W.1854 were investigated based on clinical observation, and it was shown that patients treated with W 1854 reported increased dream activity.
Abstract: Until now there has been no literature on the investigation of sleep or REM conditions during sleep while under treatment with W. 1854. The following investigation is based on the clinical observation, that patients treated with W. 1854 reported increased dream activity. In 1967 the first report was presented (1,4) on the effects of the test compound HF 1854 manufactured by Sandoz-Wander AG, Bern. It involved a special type of neuroleptic which showed no cataleptic characteristics in its pharmacological effects and which is not an apomorphine antagonist. It possesses peripheral anti-cholinergic and antiadrenergic characteristics and in this respect has a substantially stronger effect than previously known neuroleptics. In terms of arousal reaction and because of the muscle relaxing effect with decerebrized cats, a strong inhibiting effect on the reticular formation could be demonstrated in animal studies (11). Retrospective and prospective investigations in our clinic ( 2 ) showed, that in over 50% of the patients treated with this drug, a more-orless pronounced temporary increase in body temperature occurred in the first two weeks. The temperature increase is not dependent on the dosage, as long as the drug is given in amounts (150-800 mgs./day) which are antipsychotically effective. The duration of the temperature increase amounts to 4-8 days and the temperature then returns to normal even if medication is continued. Although no systematic investigations have been carried out, the general clinical impression is that a remission of psychotic symptoms coincides with the temperature increase and with the intensified dream activity.
13 citations
Journal Article•
11 citations
TL;DR: A significant correlation was noted to exist between drug-induced change inREM sleep and the per cent increase in REM sleep following PDRD.
10 citations
TL;DR: Measures of sleep disturbance and behavioral pathology were obtained over a four month period on 21 largely chronic schizophrenic patients and the value of gross but systematic sleep observation of psychiatric patients was emphasized.
8 citations