1998
DOI: 10.1001/archpsyc.55.5.443
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Delta Sleep Deficits in Schizophrenia

Abstract: Delta sleep deficits that occur in schizophrenia may be related to the primary pathophysiological characteristics of the illness and may not be secondary to previous neuroleptic use. Automated sleep quantification by means of period amplitude and power spectral analyses can complement the use of conventional visual scoring for understanding electrophysiological abnormalities in psychiatric disorders.

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Cited by 170 publications
(41 citation statements)
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“…These findings are consistent with the benefit of dipyridamole association to 20 mg/day haloperidol for the treatment of schizophrenia, which was proposed to be due to adenosine-dopamine interactions [7], although we have recently claimed that as haloperidol practically abolishes dopaminergic neurotransmission, adenosine-glutamate interactions would be more likely to account for its therapeutic effect [20]. Moreover, the pattern of sleep alterations observed in schizophrenia [21], although severer, are qualitatively very similar to the alterations induced by the adenosine antagonist caffeine in healthy subjects [22]. Further speculating, given the seizure-threshold-regulating role of adenosine, impaired adenosinergic activity could underlie the connection between schizophrenia and seizures [23].…”
Section: Discussionsupporting
confidence: 83%
“…These findings are consistent with the benefit of dipyridamole association to 20 mg/day haloperidol for the treatment of schizophrenia, which was proposed to be due to adenosine-dopamine interactions [7], although we have recently claimed that as haloperidol practically abolishes dopaminergic neurotransmission, adenosine-glutamate interactions would be more likely to account for its therapeutic effect [20]. Moreover, the pattern of sleep alterations observed in schizophrenia [21], although severer, are qualitatively very similar to the alterations induced by the adenosine antagonist caffeine in healthy subjects [22]. Further speculating, given the seizure-threshold-regulating role of adenosine, impaired adenosinergic activity could underlie the connection between schizophrenia and seizures [23].…”
Section: Discussionsupporting
confidence: 83%
“…EMs have been counted visually or scored by computerized EM detection software. In AP-naive and unmedicated patients, visual and computerized scoring find no difference in REM sleep EM activity between patients who are schizophrenic and control subjects [13][14][15][16][17].…”
Section: Objective Assessmentmentioning
confidence: 90%
“…Many studies have examined this issue [13,14,16,[18][19][20][21][22][23][24], and the majority report significantly shorter REMLs in schizophrenics relative to healthy controls. Heterogeneity between patient samples and methodologic differences, including prior exposure to AP treatment, may explain the lack of consistency among these findings.…”
Section: Objective Assessmentmentioning
confidence: 99%
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“…N3, or slow wave sleep (SWS), is characterized by large delta (.5– 4Hz) waves. Medicated and APD-naïve SZ patients as well as first-degree relatives show N3 abnormalities including reduced duration and delta power (24-27). REM sleep abnormalities, usually decreased REM latency or increased REM density (rapid eye movements per minute) are also reported (25, 26, 28) but neither N3 nor REM abnormalities are consistently observed (28, 29) and meta-analyses have not revealed systematic differences in SZ compared with healthy or psychiatric controls (17, 21).…”
Section: Sleep Abnormalities In Szmentioning
confidence: 99%