Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depressive symptoms are unspecific and occur in several psychiatric disorders. Sleep disturbances are also frequently present in depressed patients. As a consequence, it has been established that a number of modulations of the sleep-wake cycle can have an antidepressive effect. Total sleep deprivation or deprivation in the second half of the night have proven successful. The main limitation of the otherwise well tolerated treatment is the short duration of the antidepressive effect, which is mostly reversed in nearly all patients after the following night's sleep. New approaches are to shift the timing of sleep to earlier to ensure a possible longer-lasting effect. In clinical praxis the following manipulations should not be used: sleep deprivation in the first half of the night (not successful), REM-sleep deprivation (experimental setting), induced sleep prolongation (negative risk-benefit-ratio). In addition to patients with affective disorders sleep deprivation has proved relevant in patients with schizophrenia (depressed and/or with predominantly negative symptoms) and premenstrual dysphoric disorder. Very few side effects have been reported. Although many hypotheses have been tested, the mechanism of action underlying the antidepressive effect of sleep deprivation is still unknown.
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PMID:[Antidepressive therapy by modifying sleep]. 1073 Jan 1

Both major depressive disorders (MDD) and schizophrenia (SZ) have been associated with reductions in slow-wave (Stages 3 and 4) sleep, although these findings are controversial. The present study compared quantitative EEG measures of slow-wave activity (0.5-4 Hz) during non-REM (NREM) sleep among age-matched, symptomatic but unmedicated, depressed, schizophrenic and healthy control men (n=13/group). The amplitude of slow-wave activity (SWA) in the first NREM sleep period was significantly lower in both the MDD and SZ groups compared with controls. However, the time course of SWA, its accumulation and dissipation over all NREM sleep time, was abnormal in the MDD group but not in those with SZ. These findings suggest that the regulation of SWA is impaired in men with MDD but not in SZ. Thus, although those with SZ show reduced amplitude SWA in the first NREM period, there is no evidence that homeostatic regulation of SWA is impaired in this psychiatric group.
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PMID:Slow-wave activity during non-REM sleep in men with schizophrenia and major depressive disorders. 1097 60

Negative symptoms have been associated with poor response to neuroleptics, enlarged ventricles, cognitive impairment, and poor outcome in schizophrenia. These associations appear, however, to be dependent on the phase of study, suggesting that acute-phase (phasic) negative symptoms may be pathophysiologically distinct from enduring negative symptoms that persist through the residual phase. To compare correlates of enduring and phasic negative symptoms, we studied 60 drug-free schizophrenic patients (DSM-III-R and SADS/RDC) at baseline, 4 weeks after neuroleptic treatment, and assessed the 1 year outcome. We rated positive and negative symptoms at baseline and 4 weeks after treatment. At baseline, premorbid function, neuropsychological function, ventricle-brain ratio (VBR) and symptom response to an anticholinergic agent were assessed, and a two-night sleep EEG and 1mg dexamethasone suppression test (DST) were conducted. Phasic negative symptoms were defined as the change in negative symptoms (baseline to 4 weeks) and enduring negative symptoms as severity of negative symptoms at 4 weeks. Patients had varying proportions of phasic and enduring symptoms; the two did not define distinct subgroups. Phasic negative symptoms were significantly correlated with global treatment response, positive symptom treatment response, response to anticholinergic agent, baseline post-dexamethasone cortisol, and shortened REM latency. Enduring negative symptoms were significantly correlated with residual positive symptoms and global psychopathology, VBR, poor performance on neuropsychological testing, decreased slow-wave sleep, poor premorbid function, and poor 1 year outcome. These data suggest that phasic negative symptoms and enduring negative symptoms may be caused by different pathophysiological mechanisms.
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PMID:Phasic and enduring negative symptoms in schizophrenia: biological markers and relationship to outcome. 1104 37

Suicidal patients often report problems with their sleep. Although sleep-related complaints and EEG (electroencephalographic) changes have been seen widely across the spectrum of psychiatric disorders, sleep complaints such as insomnia, hypersomnia, nightmares, and sleep panic attacks are more common in suicidal patients. The subjective quality of sleep as measured by self-rated questionnaires also appears to be more disturbed in suicidal depressive patients. Sleep studies have reported various polysomnographic findings including increased REM (rapid eye movement) time and REM activity in suicidal patients with depression, schizoaffective disorder, and schizophrenia. One mechanism responsible for this possible association between suicide and sleep could be the role of serotonin (5HT). Serotonergic function has been found to be low in patients who attempted and/or completed suicide, particularly those who used violent methods. Aggression dyscontrol appears to be an intervening factor between serotonin and suicide. Additionally, agents that enhance serotonergic transmission decrease suicidal behavior. Serotonin has also been documented to play an important role in onset and maintenance of slow wave sleep and in REM sleep. CSF 5-HIAA levels have been correlated with slow wave sleep in patients with depression as well as schizophrenia. Moreover, 5HT2 receptor antagonists have improved slow wave sleep. Further studies are needed to investigate the possible role of sleep disturbance in suicidal behavior.
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PMID:Sleep and suicide in psychiatric patients. 1153 31

CEE-03-310 is a selective dopamine D1-like receptor antagonist with no appreciable binding affinity for other receptors. Although originally developed by Novo Nordisk A/S as NNC-687 for the treatment of schizophrenia, the company changed its therapeutic focus in the mid-1990s and the full rights to CEE-03-310 and several related compounds were subsequently granted to CeNeS Pharmaceuticals in 1999. CeNeS is currently investigating the drug's potential in the treatment of insomnia and alcohol dependency [340965], [382293], [401496],[416026]. A phase II, double-blind, placebo-controlled trial of CEE-03-310 demonstrated a dose-dependent enhancement of NREM sleep at the beginning of the night without any effects on the quantity of REM sleep [410739].
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PMID:CEE-03-310 CeNeS pharmaceuticals. 1202 61

Reduced REM latency is a common polysomnographic finding in patients with schizophrenia. This has been attributed to cholinergic hyperactivity secondary to increased dopaminergic tone. We studied polysomnographic sleep recordings, and morning serum prolactin levels as a measure of dopaminergic tone in 17 drug-free patients suffering from non-affective psychoses, hypothesizing that REM-latency and prolactin would correlate. A clear-cut positive correlation between prolactin and REM latency was found, as well as a negative correlation between prolactin and REM sleep. The findings may be explained by dopaminergic and secondary hypercholinergic and/or serotonergic mechanisms responsible for the regulation of REM sleep and the secretion of prolactin.
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PMID:REM sleep and prolactin in patients with non-affective psychoses. 1208 59

Sensory gating represents the nervous system's ability to inhibit responding to irrelevant environmental stimuli. In order to characterize the early development of acoustic sensory gating, suppression of auditory evoked potential component P1 (i.e. P50) in response to paired clicks was measured during REM sleep in healthy infants (1-4 months) that were without genetic risk for disrupted sensory gating function (i.e. having a relative with schizophrenia). As a group, the subjects exhibited significant response suppression. A correlation between increasing age and stronger response suppression was uncovered, even within this restricted age range. Parallel changes in sleep physiology could not be ruled out as the explanation for this change. Nevertheless, these results demonstrate that the neural circuits underlying sensory gating are functional very early in postnatal development.
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PMID:Early postnatal development of sensory gating. 1269 65

Insomnia is a common feature in schizophrenia. However, it seldom is the predominant complaint. Nevertheless, severe insomnia is often seen during exacerbations of schizophrenia, and may actually precede the appearance of other symptoms of relapse. The sleep disturbances of either never-medicated or previously treated schizophrenia patients are characterized by a sleep-onset and maintenance insomnia. In addition, stage 4 sleep, slow wave sleep (stages 3 and 4), non-REM (NREM) sleep in minutes and REM latency are decreased. The atypical antipsychotics olanzapine, risperidone, and clozapine significantly increase total sleep time and stage 2 sleep. Moreover, olanzapine and risperidone enhance slow wave sleep. On the other hand, the typical antipsychotics haloperidol, thiothixene, and flupentixol significantly reduce stage 2 sleep latency and increase sleep efficiency. Future research should address: (1) the sleep patterns in subtypes of schizophrenia patients; (2) the role of neurotransmitters other than dopamine in the disruption of sleep in schizophrenia; (3) the functional alterations in CNS areas related to the pathophysiology of schizophrenia during NREM sleep and REM sleep (brain imaging studies); (4) the short-term, intermediate-term, and long-term effects of atypical antisychotics on sleep variables.
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PMID:Sleep in schizophrenia patients and the effects of antipsychotic drugs. 1503 52

Clozapine is a widely used atypical neuroleptic in the treatment of schizophrenia; its effects on sleep have been poorly studied, sedation being one of its side effects. We present the case of hypersomnia and marked reduction of REM sleep secondary to treatment with clozapine and review existing scientific literature on the action of neuroleptics on sleep.
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PMID:[Sleep disorders with antipsychotic drugs: based on one case with clozapine]. 1504 72

The differential diagnosis of narcolepsy versus schizophrenia is sometimes complicated by similar phenomenology, particularly when hallucinations predominate. REM sleep disturbances seem fundamental in the pathophysiology of narcolepsy, and REM sleep intrusions during periods of wakefulness are often associated with hallucinations also in healthy controls and in patients with other brain disorders including schizophrenia. This study used a semistructured interview to investigate different aspects of hallucinations (frequency, modality, content, and dependence on body posture) in 148 patients with narcolepsy, 21 patients with acute exacerbation of a schizophrenic disorder, and 128 healthy subjects. About 80% of patients with narcolepsy, 81% of schizophrenics, and 37% of healthy subjects reported lifetime occurrence of hallucinations (at least once). Auditory hallucinations were reported by 81% of schizophrenic patients (narcoleptics 45%, healthy controls 9%), whereas 83% of narcoleptic patients reported visual hallucinations (schizophrenics 29%, healthy controls 19%). Kinetic hallucinations were experienced by 71% of patients with narcolepsy and 53% of healthy controls in contrast to only 5% of schizophrenics. Accordingly, the content of hallucinations differed substantially between the groups. Most hallucinations in narcoleptics but not in schizophrenics, were sleep-related and dependent on body posture. Taken together, the qualitative aspects of hallucinations in narcolepsy and schizophrenia were so different that a common underlying mechanism of hallucinations in the two conditions is unlikely. Although the clinical separation of patients with narcolepsy and schizophrenia with predominant hallucinations is sometimes difficult, clinical features including the patient's illness history, and careful psychopathological assessments can help to avoid misdiagnoses and treatment failures.
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PMID:Narcoleptic and schizophrenic hallucinations. Implications for differential diagnosis and pathophysiology. 1560 61


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