Electroencephalographic sleep abnormalities in schizophrenia: Relationship to positive/negative symptoms and ventricular enlargement

Tandon, Rajiv; Shipley, James E.; Greden, John F.

doi:10.1016/0920-9964(89)90116-3

Cited by 29 publications

(55 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Both of these sets of findings are consistent with the hypothesis of increased cholinergic activity in schizophrenia. Baseline polysomnographic abnormalities in schizophrenia also indicate increased cholinergic activity in schizophrenia (Tandon et al 1992b;Gillin et al 1973). …”

Section: Polysomnographic Evidence For Increased Cholinergic Activitymentioning

confidence: 99%

“…All polygraph records were scored visually according to modified Rechtschaffen-Kales criteria (Rechtschaffen et al 1968) by raters blind to diagnosis. Further details of the sleep methodology are available in a prior publication (Tandon et al 1992b). The sleep EEG variables included sleep continuity, sleep architecture, and REM sleep indices.…”

Section: Sleep Eeg Study: Effects Of Biperiden On Polysomnographic Mementioning

confidence: 99%

“…To investigate possible sleep EEG abnormalities in schizophrenia, we recorded sleep EEG in 20 drug-naive schizophrenic patients, 20 drug-free but previously medicated schizophrenic patients, and 15 normal controls (Tandon et al 1992b). We observed that both drug-naive and previously medicated schizophrenic patients had significantly greater impairment of sleep continuity and shorter REM latency when compared to controls.…”

Section: Treatment Of Negative Symptoms Of Schizophrenia With Trihexymentioning

confidence: 99%

See 2 more Smart Citations

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

Section: Polysomnographic Evidence For Increased Cholinergic Activitymentioning

confidence: 99%

Section: Sleep Eeg Study: Effects Of Biperiden On Polysomnographic Mementioning

confidence: 99%

Section: Treatment Of Negative Symptoms Of Schizophrenia With Trihexymentioning

confidence: 99%

See 1 more Smart Citation

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

show abstract

“…Cortical deafferentiation is produced by ascending brainstem cholinergic projections activated under conditions of reduced perceptual input, resulting in a failure of the brainstem to deactivate. 79 During sleep, this would occur due to the suppression of external signals (eg, eyes closed), resulting in intrinsic sensory excitability. Deafferentiation is also a prominent model of hallucinations in disorders of sensory pathways such as eye disease, where it is thought to occur because of the loss of incoming sensory input in the visual sensory pathways.…”

Section: Similarities In Brain Functions and Systemsmentioning

confidence: 99%

What Is the Link Between Hallucinations, Dreams, and Hypnagogic–Hypnopompic Experiences?

Waters

Blom²,

Dang‐Vu

et al. 2016

SCHBUL

View full text Add to dashboard Cite

By definition, hallucinations occur only in the full waking state. Yet similarities to sleep-related experiences such as hypnagogic and hypnopompic hallucinations, dreams and parasomnias, have been noted since antiquity. These observations have prompted researchers to suggest a common aetiology for these phenomena based on the neurobiology of rapid eye movement (REM) sleep. With our recent understanding of hallucinations in different population groups and at the neurobiological, cognitive and interpersonal levels, it is now possible to draw comparisons between the 2 sets of experiences as never before. In the current article, we make detailed comparisons between sleep-related experiences and hallucinations in Parkinson's disease, schizophrenia and eye disease, at the levels of phenomenology (content, sensory modalities involved, perceptual attributes) and of brain function (brain activations, resting-state networks, neurotransmitter action). Findings show that sleep-related experiences share considerable overlap with hallucinations at the level of subjective descriptions and underlying brain mechanisms. Key differences remain however: (1) Sleep-related perceptions are immersive and largely cut off from reality, whereas hallucinations are discrete and overlaid on veridical perceptions; and (2) Sleep-related perceptions involve only a subset of neural networks implicated in hallucinations, reflecting perceptual signals processed in a functionally and cognitively closed-loop circuit. In summary, both phenomena are non-veridical perceptions that share some phenomenological and neural similarities, but insufficient evidence exists to fully support the notion that the majority of hallucinations depend on REM processes or REM intrusions into waking consciousness.

show abstract

“…Reduced REM sleep latency has been attributed to cholinergic hyperactivity secondary to increased dopaminergic tone in schizophrenia [20]. The most striking finding in the sleep recording was the high amount of deep sleep (SWS: 41.8%, S4 sleep: 26.1%).…”

Section: Resultsmentioning

confidence: 99%

Increased deep sleep in a medication-free, detoxified female offender with schizophrenia, alcoholism and a history of attempted homicide: Case report

et al. 2004

View full text Add to dashboard Cite

BackgroundPsychiatric sleep research has attempted to identify diagnostically sensitive and specific sleep patterns associated with particular disorders. Both schizophrenia and alcoholism are typically characterized by a severe sleep disturbance associated with decreased amounts of slow wave sleep, the physiologically significant, refreshing part of the sleep. Antisocial behaviour with severe aggression, on the contrary, has been reported to associate with increased deep sleep reflecting either specific brain pathology or a delay in the normal development of sleep patterns. The authors are not aware of previous sleep studies in patients with both schizophrenia and antisocial personality disorder.Case presentationThe aim of the present case-study was to characterize the sleep architecture of a violent, medication-free and detoxified female offender with schizophrenia, alcoholism and features of antisocial personality disorder using polysomnography. The controls consisted of three healthy, age-matched women with no history of physical violence. The offender's sleep architecture was otherwise very typical for patients with schizophrenia and/or alcoholism, but an extremely high amount of deep sleep was observed in her sleep recording.ConclusionsThe finding strengthens the view that severe aggression is related to an abnormal sleep pattern with increased deep sleep. The authors were able to observe this phenomenon in an antisocially behaving, violent female offender with schizophrenia and alcohol dependence, the latter disorders previously reported to be associated with low levels of slow wave sleep. New studies are, however, needed to confirm and explain this preliminary finding.

show abstract

Electroencephalographic sleep abnormalities in schizophrenia: Relationship to positive/negative symptoms and ventricular enlargement

Cited by 29 publications

References 0 publications

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

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

What Is the Link Between Hallucinations, Dreams, and Hypnagogic–Hypnopompic Experiences?

Increased deep sleep in a medication-free, detoxified female offender with schizophrenia, alcoholism and a history of attempted homicide: Case report

Contact Info

Product

Resources

About