Delta power in sleep in relation to neuropsychological performance in healthy subjects and schizophrenia patients.
ABSTRACT 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.
- SourceAvailable from: Alain Nicolas[Show abstract] [Hide abstract]
ABSTRACT: Schizophrenia, the most disabling of psychiatric diseases, is frequently associated with sleep disorders which nature and severity depend on the active/chronic phase and subtype of the disease. Experimentally schizophrenic patient's sleep is characterized by an increased latency and fragmentation leading to decrease of total sleep time and sleep efficiency, which are maximal during active phases of the disease and may persist during chronic phases. Several sleep architectural abnormalities have been reported. Schizophrenic patients with negative symptoms may have a decrease in duration and proportion of slow wave sleep. REM sleep disturbances (decrease in REM sleep duration, proportion and latency and lack of rebound after REM sleep deprivation) seem to be restricted to patients presenting severe positive symptoms, during acute phases. These polysomnographic changes tend to normalize under antipsychotic medication with the exception of the deficit in slow wave sleep. Finally, we found no evidence favoring an endogenous perturbation of the wake-sleep regulation in the literature. Indeed, most of the chronobiological changes previously reported were attributable to a disruption of wake-sleep behavioral patterns and to sedative side effects of medications. Further studies are necessary to characterize more precisely the hypnologic patterns of schizophrenics.Médecine du Sommeil 09/2008; 5(17).
Article: Sleep and schizophrenia.[Show abstract] [Hide abstract]
ABSTRACT: Sleep disturbance is as much a part of schizophrenic disorder as it is of affective illness. Research is cited indicating that after REM deprivation, remitted schizophrenics show an abnormally large transient increase in REM sleep and that active schizophrenics have dreams that are more bland and not as well confined to REM sleep as those of normals. The hypothesis of REM phasic-event/intrusion is reviewed, and it is suggested that regressive schizophrenic mentation and regressive sleep mentation are the result of forced intrusion of incongruous thought of affect into the normal stream of consciousness. The treatment of sleep and affective disturbances that may follow the discontinuance of neuroleptic medication is discussed. (56 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)Psychiatric Annals 07/1979; · 0.71 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Rhythmic neural network activity patterns are defining features of sleep, but interdependencies between limbic and cortical oscillations at different frequencies and their functional roles have not been fully resolved. This is particularly important given evidence linking abnormal sleep architecture and memory consolidation in psychiatric diseases. Using EEG, local field potential (LFP), and unit recordings in rats, we show that anteroposterior propagation of neocortical slow-waves coordinates timing of hippocampal ripples and prefrontal cortical spindles during NREM sleep. This coordination is selectively disrupted in a rat neurodevelopmental model of schizophrenia: fragmented NREM sleep and impaired slow-wave propagation in the model culminate in deficient ripple-spindle coordination and disrupted spike timing, potentially as a consequence of interneuronal abnormalities reflected by reduced parvalbumin expression. These data further define the interrelationships among slow-wave, spindle, and ripple events, indicating that sleep disturbances may be associated with state-dependent decoupling of hippocampal and cortical circuits in psychiatric diseases.Neuron 11/2012; 76(3):526-33. · 15.77 Impact Factor