Slow-wave sleep and ventricular size: a comparative study in schizophrenia and major depression

Lauer, Christoph; Krieg, Jürgen-Christian

doi:10.1016/s0006-3223(97)00342-9

Cited by 27 publications

(10 citation statements)

References 53 publications

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“…Eine Verminderung des Deltaschlafs wurde in vielen Untersuchungen [16, 20 -27] beschrieben. Andere Untersuchungen fanden wiederum keine Verminderung des NONREM-Schlafes Stadium IV [12,19,28,29]. Eine Erklärung hierfür lässt sich möglicherweise in methodischen Unterschieden finden.…”

Section: Störungen In Den Verschiedenen Schlafphasenunclassified

“…untersuchten, während die anderen Studien vorwiegend jüngere Probanden aus der Gruppe der 20-bis 40-Jährigen schlafpolygrafisch ableiteten [10, 12, 19, 27 -29]. Nur in der Untersuchung von Forest et al [29] und Ganguli et al [10] wurde der Schlaf über 2 Nächte im Schlaflabor abgeleitet, während die restlichen Studien die Schlafpolygraphie nach einer Eingewöhnungsnacht ableiteten [11,12,19,27,28]. Eine automatische Deltawellen-Analyse fand nur in 2 Untersuchungen statt [10,23].…”

Section: Schlafuntersuchungen Bei Noch Nie Neuroleptisch Behandelten unclassified

“…Eine automatische Deltawellen-Analyse fand nur in 2 Untersuchungen statt [10,23]. Bei der Auswertung der Schlafuntersuchungen fand sich bei 4 Untersuchun-gen eine Verlängerung der Wachzeit nach dem Einschlafen [10,12,19,28] (bei 2 Studien [11,27] keine Angaben diesbezüglich). Die Schlafeffizienz war im Vergleich zu den gesunden Probanden in 2 Untersuchungen signifikant erniedrigt [12,19] und die echte Schlafzeit (TST = Schlafphasen abzüglich der Wachphasen) war im Mittel in den 7 Studien um 54 min (13 -79 min) gegenüber den Kontrollprobanden erniedrigt.…”

Section: Schlafuntersuchungen Bei Noch Nie Neuroleptisch Behandelten unclassified

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Schlafstörungen bei schizophrenen Erkrankungen

Staedt

Hauser²,

Gudlowski³

et al. 2010

Fortschr Neurol Psychiatr

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Difficulties initiating and maintaining sleep as well as circadian rhythm disorders are very common in schizophrenia. Sleeping disorders occur as early signs of the first manifestation of illness as well as early signs of relapse. They bear a relation to positive symptoms and disorganisation of thought. Polysomnographic investigations with schizophrenic patients typically demonstrate a prolonged sleep-onset latency and a decrease in sleep efficiency and slow wave sleep. In particular, distortions of deep sleep can affect neocortical plasticity and cognition negatively. The considerable sleeping disorders are often not sufficiently taken into account in clinical routine. Particularly older antipsychotic medication like Haloperidol can affect the circadian and sleep-wake rhythms negatively. Therefore, pathophysiological changes of sleep within the scope of schizophrenic disorders and their potential implications are discussed in this outline. Regarding therapy, psychoeducative approaches are discussed as well as the administration of antipsychotic medication in accordance with the recommendations of sleep medicine professionals.

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Section: Störungen In Den Verschiedenen Schlafphasenunclassified

Section: Schlafuntersuchungen Bei Noch Nie Neuroleptisch Behandelten unclassified

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Schlafstörungen bei schizophrenen Erkrankungen

Staedt

Hauser²,

Gudlowski³

et al. 2010

Fortschr Neurol Psychiatr

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“…In Dbp knockout mice (11), as well as in schizophrenia (3,13,26) and depression (5,16), the duration of sleep time cycles and the consolidation of sleep episodes are reduced [i.e., decreased slow wave sleep (SWS)]. Since several lines of evidence suggest that enhanced dopamine activity reduces SWS (8,14,23), and PCP as well as METH are known to increase cortical dopaminergic activity, this raises the possibility that dopamine is capable of modulating cortical Dbp levels.…”

Section: Modeling Psychosis: Cortical Effects Of Acute Lsd Pcp and mentioning

confidence: 99%

Evaluation of common gene expression patterns in the rat nervous system

Kaiser

Nisenbaum

2003

Physiological Genomics

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In the postgenomic era, integrating data obtained from array technologies (e.g., oligonucleotide microarrays) with published information on eukaryotic genomes is beginning to yield biomarkers and therapeutic targets that are key for the diagnosis and treatment of disease. Nevertheless, identifying and validating these drug targets has not been a trivial task. Although a plethora of bioinformatics tools and databases are available, major bottlenecks for this approach reside in the interpretation of vast amounts of data, its integration into biologically representative models, and ultimately the identification of pathophysiologically and therapeutically useful information. In the field of neuroscience, accomplishing these goals has been particularly challenging because of the complex nature of nerve tissue, the relatively small adaptive nature of induced-gene expression changes, as well as the polygenic etiology of most neuropsychiatric diseases. This report combines published data sets from multiple transcript profiling studies that used GeneChip microarrays to illustrate a postanalysis approach for the interpretation of data from neuroscience microarray studies. By defining common gene expression patterns triggered by diverse events (administration of psychoactive drugs and trauma) in different nerve tissues (telencephalic brain areas and spinal cord), we broaden the conclusions derived from each of the original studies. In addition, the evaluation of the identified overlapping gene lists provides a foundation for generating hypotheses relating alterations in specific sets of genes to common physiological processes. Our approach demonstrates the significance of interpreting transcript profiling data within the context of common pathways and mechanisms rather than specific to a given tissue or stimulus. We also highlight the use of gene expression patterns in predictive biology (e.g., in toxicogenomics) as well as the utility of combining data derived from multiple microarray studies that examine diverse biological events for a broader interpretation of data from a particular microarray study.

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“…Interestingly, neuroimaging studies have revealed neuro-anatomic correlates of sleep disturbance in depression and schizophrenia, showing that schizophrenics present slow wave deficits and frontal cortical volume loss; 16 depressed patients show higher absolute cerebral glucose metabolic rate than healthy subjects, and blunted activation of limbic structures (amygdala, anterior cingulate) during REM sleep compared to wakefulness. 17 Certainly, we must be cognizant that many drugs can damage brain areas and neural pathways in sleep maintenance.…”

Section: Introductionmentioning

confidence: 99%

Dopaminergic Neurogenetics of Sleep Disorders in Reward Deficiency Syndrome (RDS)

Blum¹,

Oscar‐Berman

Badgaiyan

et al. 2014

J Sleep Disorders Ther

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It is well-known that sleep has a vital function especially as it relates to prevention of substance-related disorders as discussed in the DSM-V. We are cognizant that certain dopaminergic gene polymorphisms have been associated with various sleep disorders. The importance of “normal dopamine homeostasis” is tantamount for quality of life especially for the recovering addict. Since it is now know that sleep per se has been linked with metabolic clearance of neurotoxins in the brain, it is parsonomiuos to encourage continued research in sleep science, which should ultimately result in attenuation of sleep deprivation especially associated with substance related disorders.

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Slow-wave sleep and ventricular size: a comparative study in schizophrenia and major depression

Cited by 27 publications

References 53 publications

Schlafstörungen bei schizophrenen Erkrankungen

Schlafstörungen bei schizophrenen Erkrankungen

Evaluation of common gene expression patterns in the rat nervous system

Dopaminergic Neurogenetics of Sleep Disorders in Reward Deficiency Syndrome (RDS)

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