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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Self-produced tactile stimulation usually feels less tickly--is perceptually attenuated--relative to the same stimulation produced externally. This is not true, however, for individuals with schizophrenia. Here, we investigate whether the lack of attenuation to self-produced stimuli seen in schizophrenia also occurs for normal participants following REM dreams. Fourteen participants were stimulated on their left palm with a tactile stimulation device which allowed the same stimulus to be generated by the participant or by the experimenter. The level of self-tickling attenuation did not differ between REM and non-REM sleep awakening conditions, where presence or absence of an accompanying dream was not controlled for. However, for the female participants, when awakening occurred from an REM sleep dream, self-stimulation ratings were higher than for external stimulation, whereas ratings after NREM sleep unaccompanied by a dream were lower for self-stimulation than for external stimulation. These results indicate deficits in self-monitoring and a confusion between self- and externally generated stimulation accompany REM dream formation.
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PMID:The ability to self-tickle following Rapid Eye Movement sleep dreaming. 1615 89

This study aimed to investigate the relationship between measures of clinical symptom severity and sleep EEG parameters in a relatively diagnostically homogeneous group of patients with schizophrenia. We obtained sleep EEG data in 15 drug-free inpatients who met DSM-IV-R criteria for schizophrenia, undifferentiated type, with 15 age- and sex-matched normal controls over two consecutive night polysomnographic recordings. Clinical symptoms were assessed by the Positive and Negative Symptom Scale (PANSS) and Hamilton Rating Scale for Depression. Characteristic features of sleep disturbance were seen in patients with schizophrenia: profound difficulties in sleep initiation and maintenance, poor sleep efficiency, a slow wave sleep (SWS) deficit, and an increased REM density. SWS was inversely correlated with cognitive symptoms. REM density was inversely correlated with positive, cognitive, and emotional discomfort symptoms as well as PANSS total score. Our data demonstrate that drug-free patients with chronic undifferentiated type schizophrenia suffer from profound disturbances in sleep continuity and sleep architecture. Both the SWS deficit and cognitive impairment found in schizophrenics in this study may relate to similar underlying structural brain abnormalities.
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PMID:Clinical significance of sleep EEG abnormalities in chronic schizophrenia. 1637 58

The paper promotes the view that the alert brain alternates between operating in an action mode, based on frontal lobe function, and a receptive mode, involving cholinergic system activity. Their alternation forms a conversation with the environment. It is hypothesized that competition between the modes centers on control over excitability of neurons in the CA1 field of the hippocampus. Increased excitability enhances the flow of hippocampal output through the subiculum resulting in support for frontal lobe function and the action mode. Decreased excitability, on the other hand, reduces this output and that support, leading to a disconnection between frontal lobes and hippocampus. At the same time, correlated cholinergic activity enhances receptive mode processes, indicated by the occurrence of the hippocampal theta rhythm. It is suggested that the hypothesis provides a conceptual framework for considering various phenomena including REM sleep, schizophrenia, and hypnosis. In REM sleep the receptive mode remains dominant as cholinergic activity supports the hippocampal integration of experience into a composite view of reality. In schizophrenia, the action and receptive modes are not properly coordinated because of a dysfunction in anterior hippocampal output. And hypnosis might be seen as a process in which conditions and suggestions are able to induce in some people a prolonged occurrence of the receptive mode allowing a normal view of reality to be altered.
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PMID:The conversational brain: fronto-hippocampal interaction and disconnection. 1682 1

Animal models are a promising method to approach the basic mechanisms of the neurobiological disturbances encountered in mental disorders. Depression is characterized by a decrease of REM sleep latency and an increase of rapid eye movement density. In schizophrenia, electrophysiological, tomographic, pharmacological and neurochemical activities are all encountered during REM sleep. Mental retardation and dementia are characterized by rather specific REM sleep disturbances. Identification of the genetic support for these abnormalities (endophenotypes) encountered during REM sleep could help to develop specific treatments.
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PMID:The neurobiological characteristics of rapid eye movement (REM) sleep are candidate endophenotypes of depression, schizophrenia, mental retardation and dementia. 1735 Jul 44

Sleep architecture, EEG power pattern and locomotor activity were investigated in a putative animal model of schizophrenia. The model was prepared by excitotoxic damage of the ventral hippocampus on postnatal day 7 (PD 7), after which locomotor activity and electroencephalographic (EEG) sleep profile were compared between lesioned and sham operated animals respectively, at prepuberty (postnatal day PD 35) and postpuberty (PD 56). An enhancement of locomotor activity was observed in lesioned adult PD 56, but not in juvenile PD 35 rats. Spontaneous EEG/EMG recordings during 24 h showed no major differences between both groups at PD 35 and at PD 56. However, quantitative analysis of the EEG revealed an enhancement of power in delta (delta), theta (theta) and alpha (alpha) activities in lesioned animals at PD 35 during wakefulness in both light and dark phases. At PD 56, the power in the delta and theta bands was increased during the light and dark periods in both wakefulness and non-REM sleep. These findings suggest that ventral hippocampus lesion is not associated with disturbance of sleep architecture in rats, while consistent changes were observed in the dynamic of EEG slow wave frequency domain. Thus, the data indicate that neonatal lesion of ventral hippocampus did not mimic sleep abnormalities observed in schizophrenia, however this rodent model may model some EEG features seen in schizophrenia such as a frontally pronounced slowing of the slow EEG activity in delta and theta frequency bands.
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PMID:Sleep and EEG profile in neonatal hippocampal lesion model of schizophrenia. 1752 34

The pathophysiology of schizophrenia includes abnormalities in subcortical-cortical transfer of information that can be studied using REM sleep EEG spectral analysis, a measure that reflects spontaneous and endogenous thalamocortical activity. We recorded 10 patients with first-episode schizophrenia and 30 healthy controls for two consecutive nights in a sleep laboratory, using a 10-electrode EEG montage. Sixty seconds of REM sleep EEG without artifact were analyzed using FFT spectral analysis. Absolute and relative spectral amplitudes of five frequency bands (delta, theta, alpha, beta1 and beta2) were extracted and compared between the two groups. Frequency bands with significant differences were correlated with BPRS positive and negative symptoms scores. Patients with schizophrenia showed lower relative alpha and higher relative beta2 spectral amplitudes compared to healthy controls over the averaged total scalp. Analysis using cortical regions showed lower relative alpha over frontal, central and temporal regions and higher relative beta2 over the occipital region. Absolute spectral amplitude was not different between groups for any given EEG band. However, absolute alpha activity correlated negatively with BPRS positive symptoms scores and correlated positively with negative symptoms scores. Since similar results have been reported following EEG spectral analysis during the waking state, we conclude that abnormalities of subcortical-cortical transfer of information in schizophrenia could be generated by mechanisms common to REM sleep and waking.
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PMID:REM sleep EEG spectral analysis in patients with first-episode schizophrenia. 1828 May 2

Many clinical, laboratory and non-laboratory studies have examined dream content reported by patients with schizophrenia but findings have been variable and inconsistent. Using both questionnaire-based measures and laboratory REM sleep awakenings, we investigated dream content in 14 patients with schizophrenia (mean age=25.5+/-3.2 years) under atypical antipsychotic medication and 15 healthy controls (mean age=22.3+/-4.2 years). The relationship between eye movement density during REM sleep and dream content was also explored. Questionnaire data revealed that when compared to controls, patients with schizophrenia report experiencing a greater number of nightmares but no significant differences were found on other measures including overall dream recall, presence of recurrent dreams, and frequency of specific emotions. 39 dream reports were collected from each group following awakenings from REM sleep. Laboratory dream narratives from the patients were shorter and, after controlling for report length, most significant differences in dream content between the two groups disappeared with the exception of a greater proportion of unknown characters in the participant group. Patients with schizophrenia spontaneously rated their dream reports as being less bizarre than did controls, despite a similar density of bizarre elements as scored by external judges. Finally, both groups had a comparable density of rapid eye movements during REM sleep but a significant positive correlation between eye-movement density and dream content variables was only found in controls. Taken together, the findings suggest that dream content characteristics in schizophrenia may reflect neurocognitive processes, including emotional processing, specific to this disorder.
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PMID:Dream content in chronically-treated persons with schizophrenia. 1940 57

L-stepholidine, an active ingredient of the Chinese herb Stephonia, is the first compound known to have mixed dopamine D(1) receptor agonist/D(2) antagonist properties and to be a potential treatment medication for schizophrenia. In schizophrenic patients insomnia is a common symptom and could be partly related to the presumed over-activity of the dopaminergic system. To elucidate whether stepholidine modulates sleep behaviors, we observed its effects on sleep-wake profiles in mice. The results showed that stepholidine administered i.p. at doses of 20, 40 or 80 mg/kg significantly shortened the sleep latency to non-rapid eye movement (non-REM, NREM) sleep, increased the amount of NREM sleep, and prolonged the duration of NREM sleep episodes, with a concomitant reduction in the amount of wakefulness. Stepholidine at doses of 40 and 80 mg/kg increased the number of state transitions from wakefulness to NREM sleep and subsequently from NREM sleep to wakefulness. However, stepholidine had no effect on either the amount of REM sleep or electroencephalogram power density of either NREM or REM sleep. Immunohistochemistry study showed that stepholidine dose-dependently increased c-Fos expression in neurons of the ventrolateral preoptic area, a sleep center in the anterior hypothalamus, as compared with the vehicle control. These results indicate that stepholidine initiates and maintains NREM sleep with activation of the sleep center in mice, suggesting its potential application for the treatment of insomnia.
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PMID:D(1)/D(2) receptor-targeting L-stepholidine, an active ingredient of the Chinese herb Stephonia, induces non-rapid eye movement sleep in mice. 1960 96

Psychosis and dreaming have many similarities, including delusions, hallucinations, bizarre thinking and perceptual distortions. This clinical observation has lead us to hypothesize that the suprachiasmatic nucleus (SCN), a hypothalamic center regulating sleep and wakefulness, is involved in the pathogenesis of schizophrenia. Schizophrenic patients have certain sleep architecture characteristics, and distinctive biological markers suggesting abnormity of the SCN, including irregular pattern of melatonin secretion, abnormal actigraphyic studies, D1-dopamine receptors involvement in the process of entraining the SCN and vulnerability to psychotic exacerbation due to jet lag. In addition, SCN lesions in rodents are associated with pathologic day-time sleep pattern, very similar to the sleeping pattern in patients with schizophrenia. We introduce the concept of REM sleep abnormity as a possible etiological factor in development of psychosis. We hypothesize that the proposed dysfunction of the SCN may contribute to schizophrenia through several different, not necessarily mutually exclusive, mechanisms, including "REM sleep (dream) rebound" phenomenon, damaged neuronal pathways connecting SCN to the brain regions affected by schizophrenia, and the SCN dysfunction induced dysregulation of gene expression in different parts of the body, including the brain. Moreover, the influenza virus, which has been implicated in the etiology of schizophrenia, is capable of resetting the SCN, the ultimate processor of light signals, suggesting the explanation for chronological variability of incidence of schizophrenia. Future investigation of the proposed mechanisms will provide the ultimate test of our hypothesis that lesions of the suprachiasmatic nucleus play an important role in the etiology of schizophrenia.
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PMID:Schizophrenia as a possible dysfunction of the suprachiasmatic nucleus. 1974 97

Most psychiatric disorders, such as schizophrenia, mood disorders, or neurotic disorders are associated with sleep disorders of various kinds, among which insomnia is most prevalent and important in psychiatric practice. Almost all patients suffering from major depression complain of insomnia. Pharmacological treatment of insomnia associated with major depression shortens the duration to achieve remission of depression. Insomnia has been recently reported to be a risk factor for depression. In patients with schizophrenia, insomnia is often an early indicator of the aggravation of psychotic symptoms. Electroencephalographic sleep studies have also revealed sleep abnormalities characteristic to mood disorders, schizophrenia and anxiety disorders. A shortened REM sleep latency has been regarded as a biological marker of depression. Reduced amount of deep non-REM sleep has been reported to be correlated with negative symptoms of schizophrenia. Recently, REM sleep abnormalities were found in teenagers having post-traumatic stress disorder after a boat accident. Although these facts indicate that insomnia plays an important role in the development of psychiatric disorders, there are few hypotheses explaining the cause and effect of insomnia in these disorders. Here, we reviewed recent articles on insomnia associated with psychiatric disorders together with their clinical managements.
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PMID:[Insomnia associated with psychiatric disorders]. 1976 32


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