Effect of neuroleptic treatment on polysomnographic measures in schizophrenia

Taylor, Stephan F.; Tandon, Rajiv; Shipley, James E.; Eiser, Alan S.

doi:10.1016/0006-3223(91)90004-6

Cited by 56 publications

(26 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In healthy controls, 10-mg olanzapine increased the REM latency but decreased REM sleep time (16)(17)(18) via an antagonistic effect on muscarinic cholinergic receptors. Previous studies have not found a significant increase in REM latency in schizophrenic patients receiving haloperidol (27), but acute administration of olanzapine to schizophrenics produced a significant increase in REM density (30). The anticholinergic effects of olanzapine may predict the decrease of REM activity and REM density in electroencephalogram sleep records.…”

Section: Discussionmentioning

confidence: 95%

A double-blind comparison of the effect of the antipsychotics haloperidol and olanzapine on sleep in mania

Moreno¹,

Hanna²,

Tavares³

et al. 2007

Braz J Med Biol Res

View full text Add to dashboard Cite

The effects of haloperidol and olanzapine on polysomnographic measures made in bipolar patients during manic episodes were compared. Twelve DSM-IV mania patients were randomly assigned to receive either haloperidol (mean ± SD final dosage: 5.8 ± 3.8 mg) or olanzapine (mean ± SD final dosage: 13.6 ± 6.9 mg) in a 6-week, double-blind, randomized, controlled clinical trial. One-night polysomnographic evaluation was performed before and after the haloperidol or olanzapine treatment. Psychopathology and illness severity were rated respectively with the Young Mania Rating Scale (YMRS) and the Clinical Global Impressions -Bipolar version (CGI-BP). There was a significant improvement in the YMRS and CGI-BP scores at the end of the study for both groups. Mixed ANOVA used to compare the polysomnographic measures of both drugs demonstrated significant improvement in sleep measures with olanzapine. In the olanzapine group, statistically significant time-drug interaction effects on sleep continuity measures were observed: sleep efficiency (mean ± SEM pre-treatment value: 6.7 ± 20.3%; after-treatment: 85.7 ± 10.9%), total wake time (pre-treatment: 140.0 ± 92.5 min; aftertreatment: 55.2 ± 44.2 min), and wake time after sleep onset (pretreatment: 109.7 ± 70.8 min; after-treatment: 32.2 ± 20.7 min). Conversely, improvement of polysomnographic measures was not observed for the haloperidol group (P > 0.05). These results suggest that olanzapine is more effective than haloperidol in terms of sleeppromoting effects, although olanzapine is comparatively as effective as haloperidol in treating mania. Polysomnography records should provide useful information on how manic states can be affected by psychopharmacological agents.

show abstract

Section: Discussionmentioning

confidence: 95%

A double-blind comparison of the effect of the antipsychotics haloperidol and olanzapine on sleep in mania

Moreno¹,

Hanna²,

Tavares³

et al. 2007

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…Subchronic treatment of patients suffering from schizophrenia with typical antipsychotics increases TST and sleep efficiency and reduces sleep latency in most of the studies but leaves percentage sleep stage 2 and REM unchanged (Taylor et al 1991;Wetter et al 1996;Maixner et al 1998). …”

Section: Discussionmentioning

confidence: 97%

Sleep-promoting properties of quetiapine in healthy subjects

et al. 2004

View full text Add to dashboard Cite

The aim of this study was to investigate the effects of quetiapine, an atypical antipsychotic, on polysomnographic sleep structure and subjective sleep quality. This double-blind, placebo-controlled, randomized cross-over study investigated the polysomnographic sleep structure and subjective sleep quality of 14 healthy male subjects given placebo, quetiapine 25 mg or quetiapine 100 mg. Volunteers were studied 3 times for 3 consecutive nights (N0, adaptation; N1, standard sleep conditions; N2, acoustic stress) 4 days apart. Treatment was administered orally 1 h before bedtime on nights 1 and 2. Quetiapine 25 mg and 100 mg significantly improved sleep induction and continuity under standard and acoustic stress conditions. Increases in total sleep time, sleep efficiency, percentage sleep stage 2 and subjective sleep quality were seen. A significant increase in periodic leg movements during sleep was observed with quetiapine 100 mg. The sleep-improving properties of quetiapine may be important in counteracting different aspects of psychopathology in schizophrenia and other disorders. These sleep-inducing and sleep-modifying properties are probably related to quetiapine's receptor-binding profile, including its antihistaminergic, antidopaminergic and antiadrenergic properties. Other mechanisms might be relevant as well and further investigation is required.

show abstract

“…Considering known cholinergic effects on REM latency and other sleep measures Gillin and Sitaram 1984), these data are consistent with the hypothesis of increased cholinergic activity in schizophrenia and its implication in the production of negative symptoms. In related studies (Taylor et al 1991;Maixner et al 1998;Tandon 1997), we observed that polysomnographic measures partially normalized following antipsychotic treatment (with neuroleptics, clozapine, and risperidone). Assuming that increased cholinergic activity partly underlies polysomnographic abnormalities in schizophrenia at drug-free baseline, these data may indicate a trend for increased cholinergic activity to partially normalize with neuroleptic therapy (Figure 1) (Tandon and Greden 1989;Tandon et al 1990a).…”

Section: In Vivo Measurement Of Central Cholinergic Activitymentioning

confidence: 99%

The Cholinergic System in Schizophrenia Reconsidered: Anticholinergic Modulation of Sleep and Symptom Profiles

Tandon

Taylor

DeQuardo

et al. 1999

Neuropsychopharmacology

View full text Add to dashboard Cite

Receptors, Cholinergic; Receptors, muscarinic; Parasympathetic nervous system; Sleep, REM; Symptoms, positive; Symptoms, negative The dopamine (DA) hypothesis has dominated biochemical and pharmacological research on schizophrenia for about two decades. Although pharmacological data implicate increased DA activity in the pathogenesis of positive symptoms of schizophrenia, there is minimal association with negative symptoms (Crow 1980;Andreasen and Olsen 1982;Angrist et al. 1980). The poorly elucidated pathogenesis of negative symptoms and the unique properties of the atypical antipsychotic clozapine (Jibson and Tandon 1998) have encouraged a reappraisal of the role of the DA system in schizophrenia. Newer approaches to evaluating neurochemical abnormalities in schizophrenia include consideration of other neurotransmitter systems. Models of DA-serotonin (Meltzer 1989), DA-glutamate (Carlsson and Carlsson 1990), DA-acetylcholine (Tandon and Greden 1989), and DA-norepinephrine (van Kammen et al. 1990) interactions have been proposed. Although these models still accord DA a significant role in schizophrenia pathophysiology, they suggest that altered balance between DA and one (or more) of these other neurotransmitter systems may be the principal neurochemical abnormality related to the production of schizophrenic symptoms. Some of the earliest pharmacological treatments for schizophrenia included cholinergic agents (Cohen et al. 1944;Collard et al. 1946;Pfeiffer and Jenney 1957), and in the 1970s, several investigators suggested that cholinergic activity may be reduced in schizophrenia (Friedhoff and Alpert 1973;Janowsky et al. 1973;Davis et al. 1975;Singh and Kay 1979). There was no direct evidence of altered cholinergic functioning in schizophrenic patients, however, and pharmacological trials with cholinergic agents were generally ineffective (Rowntree et al. 1950;Gerlach et al. 1977;Davis and Berger 1978). With few exceptions (Johnstone et al. 1983;Singh et al. 1987), cholinergic mechanisms were increasingly considered irrelevant to the pathophysiology of schizophrenia and discussed predominantly with reference to the treatment of undesirable extrapyramidal side effects of neuroleptics (Richelson 1984). Indirect evidence from several lines of research, however, suggests that the cholinergic system may differentially influence positive and negative symptoms in schizophrenia (Tandon and Greden 1989).We and others have been conducting various studies to evaluate the role of the cholinergic system in schizophrenia, based on a primary hypothesis that DA-acetylcholine (ACh) interactions are of central importance in the production of positive and negative symptoms of schizophrenia (Tandon and Greden 1989;Tandon and Greden 1991). Based on available data and on observations of the course of positive and negative symptoms during the acute phase of the illness (Donlon and Blacker 1973;Docherty et al. 1978;Tandon et al. 1990a), we posited a role for disruption in DA-ACh balance in the expression of positive and negat...

show abstract

Effect of neuroleptic treatment on polysomnographic measures in schizophrenia

Cited by 56 publications

References 18 publications

A double-blind comparison of the effect of the antipsychotics haloperidol and olanzapine on sleep in mania

A double-blind comparison of the effect of the antipsychotics haloperidol and olanzapine on sleep in mania

Sleep-promoting properties of quetiapine in healthy subjects

The Cholinergic System in Schizophrenia Reconsidered: Anticholinergic Modulation of Sleep and Symptom Profiles

Contact Info

Product

Resources

About