Delta Power in Sleep in Relation to Neuropsychological Performance in Healthy Subjects and Schizophrenia Patients

Department of Psychiatry and Psychotherapy, Centre for Integrative Psychiatry (ZIP), Christian-Albrechts-University School of Medicine, Niemannsweg 147, 24105 Kiel, Germany.
Journal of Neuropsychiatry (Impact Factor: 2.82). 02/2006; 18(4):529-35. DOI: 10.1176/appi.neuropsych.18.4.529
Source: PubMed


Delta power in sleep is of increasing interest because of its association with waking performance in neuropsychological tests. In schizophrenia, this link might be impaired because of a decrease in delta power in sleep and pronounced cognitive deficits. The authors analyzed delta power in sleep and neuropsychological performance in 16 patients with schizophrenia on stable medication with amisulpride and 17 healthy subjects. In healthy subjects, the authors found significant positive correlations between morning performance in declarative memory, procedural learning, and attention and delta power, especially in frontal channels. The authors interpret these results in terms of dysfunctions of thalamocortical and prefrontal networks in schizophrenia.

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    • "The number of slow-wave events or delta power during sleep in patients with SCZ has been reported to be lower (Keshavan et al., 1998; Hoffmann et al., 2000; G€ oder et al., 2006), although this is not the case in all studies (Keshavan et al., 2011). Where a specific reduction in SWA has been reported, changes have typically been limited to occipital and temporal regions (G€ oder et al., 2006) or to a missing frontal asymmetry of slow-wave counts in SCZ (Sekimoto et al., 2007). "
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    ABSTRACT: The neurophysiology of non-rapid eye movement sleep is characterized by the occurrence of neural network oscillations with distinct origins and frequencies, which act in concert to support sleep-dependent information processing. Thalamocortical circuits generate slow (0.25–4 Hz) oscillations reflecting synchronized temporal windows of cortical activity, whereas concurrent waxing and waning spindle oscillations (8–15 Hz) act to facilitate cortical plasticity. Meanwhile, fast (140–200 Hz) and brief (< 200 ms) hippocampal ripple oscillations are associated with the reactivation of neural assemblies recruited during prior wakefulness. The extent of the forebrain areas engaged by these oscillations, and the variety of cellular and synaptic mechanisms involved, make them sensitive assays of distributed network function. Each of these three oscillations makes crucial contributions to the offline memory consolidation processes supported by non-rapid eye movement sleep. Slow, spindle and ripple oscillations are therefore potential surrogates of cognitive function and may be used as diagnostic measures in a range of brain diseases. We review the evidence for disrupted slow, spindle and ripple oscillations in schizophrenia, linking pathophysiological mechanisms to the functional impact of these neurophysiological changes and drawing links with the cognitive symptoms that accompany this condition. Finally, we discuss potential therapies that may normalize the coordinated activity of these three oscillations in order to restore healthy cognitive function.
    Full-text · Article · Apr 2014 · European Journal of Neuroscience
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    • "Coherence between hippocampal and neocortical networks increases during SWS (Ji & Wilson, 2007; Sirota, Csicsvari, Buhl, & Buzsaki, 2003), and neuroimaging studies reveal relationships between brain activity during SWS and declarative memory (Chee & Chuah, 2008). Furthermore, observations of EEG power in the delta band during sleep are related to declarative memory assessed before sleep (Bodizs, Bekesy, Szucs, Barsi, & Halasz, 2001; Goder et al., 2006). Notably, during SWS, reactivation of some recently encoded memories is thought to take place, as SWS hippocampal firing patterns parallel those present during waking (Pavlides & Winson, 1989; Wilson & McNaughton, 1994), and reactivating recently learned memories via external cues during SWS benefits declarative memory (Rasch, Buchel, Gais, & Born, 2007; Rudoy, Voss, Westerberg, & Paller, 2009). "
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    ABSTRACT: Whereas patients with Alzheimer's disease (AD) experience difficulties forming and retrieving memories, their memory impairments may also partially reflect an unrecognized dysfunction in sleep-dependent consolidation that normally stabilizes declarative memory storage across cortical areas. Patients with amnestic mild cognitive impairment (aMCI) exhibit circumscribed declarative memory deficits, and many eventually progress to an AD diagnosis. Whether sleep is disrupted in aMCI and whether sleep disruptions contribute to memory impairment is unknown. We measured sleep physiology and memory for two nights and found that aMCI patients had fewer stage-2 spindles than age-matched healthy adults. Furthermore, aMCI patients spent less time in slow-wave sleep and showed lower delta and theta power during sleep compared to controls. Slow-wave and theta activity during sleep appear to reflect important aspects of memory processing, as evening-to-morning change in declarative memory correlated with delta and theta power during intervening sleep in both groups. These results suggest that sleep changes in aMCI patients contribute to memory impairments by interfering with sleep-dependent memory consolidation.
    Full-text · Article · Feb 2012 · Journal of the International Neuropsychological Society
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    • ") , and also greater cognitive improvement ( Howard et al . , 2001 ) . In schizophrenic patients , reduc - tions in SWS and delta sleep have been linked to a poor clinical outcome and impairments in cognitive func - tioning ( Görder et al . , 2006 ) . These decreases may be caused by some dysfunction on 5 - HT receptors ( Benson et al . , 1991 ) . By acting on 5 - HT 2 receptors , atypical neuroleptics such as olanzapine might improve negative , cognitive and sleep symptoms . The greater increase in SWS observed in women in our study would , therefore , reflect a greater therapeu"
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    ABSTRACT: Polysomnography abnormalities are frequent in schizophrenia and have been correlated with clinical variables. Because women with schizophrenia present a general better clinical outcome than men, we aimed to determine whether sex differences in antipsychotic-induced effects on sleep could contribute to this difference. Single oral morning doses of olanzapine (5 mg) were administered to 10 men and 10 women. Sleep variables were evaluated using traditional polysomnography Rechstschaffen and Kales criteria and all-night sleep electroencephalogram spectral analysis. Drug plasma concentrations were also measured. Significant sex-by-drug interactions were obtained in slow-wave sleep. After olanzapine, women showed an increase in slow-wave sleep, whereas men showed a decrease. We did not observe sex differences in olanzapine-induced hypnotic effects. Neither did we find any significant differences in pharmacokinetic parameters between sexes. Significant sex effects were observed in deep sleep, with women showing longer periods than men. Our results showed significant pharmacodynamic differences in olanzapine sleep effects between men and women. Further studies in clinical populations are needed to assess if these sex-based differences suggest that optimal treatment and doses should differ between men and women.
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