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)

Sleep disturbances in psychoses can mean hypo- as well as hypersomnia. In 90% of endogenous depressed patients sleep disturbances were seen, mostly as hyposomnia. In the group of schizophrenic psychotic patients only 30% had sleep disturbances. With polygraphical investigations in endogenous depressed patients a shortening of REM-latency and a disturbed sleep profile, in schizophrenic psychoses a shortened REM-rebound and a reduced amount of stages 3 and 4 were found. The treatment of choice for depressions are antidepressive drugs and sleep deprivation, for schizophrenic psychoses neuroleptic drugs. This treatments improved subjective and objective sleep disturbances with psychopathological remission at the same time. So far, only hypothetical considerations do exist about the relationship between psychopathology and sleep disturbances. It is suspected that etiological relations exist between depression and desynchronization of central sleep mechanisms and between schizophrenia and special disturbances of REM-sleep and stage 3 and 4.
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PMID:[Sleep problems and their treatment in psychosis (author's transl)]. 4 23

The functions and dysfunctions of slow wave sleep and of REM sleep and its associated dreams have a tremendous significance in understanding the psychosomatic model of illness and in establishing preventive strategies. Ten patients suffering from a variety of psychosomatic illnessess spent 3-4 nights sleeping at the Dream Laboratory. A psychiatric evaluation was carried out and those suffering from schizophrenia, severe depression, acute stage of physical illness and organic deficits were not accepted for the study. It was postulated that increased psychosomatic 'penetrance' as measured by poverty of fantasy life, feelings of helplessness, absence of dream reports, vacant and contrived emotional expression and poor psychological mindedness would be correlated with psychological test results (IPAT anxiety Scale and Zung Depression Rating Scale), manifest dream content analysis and particular REM and stage 4 deficit. The higher psychosomatic 'penetrance' in our study was not found in all patients with a psychosomatic diagnosis but rather in those patients suffering from ulcerative colitis. The degree of 'penetrance' was related to specific physiological, psychological and interpersonal parameters. Based on these findings a spectrum of clinical and physiological criteria of selection for particular therapeutic intervention was presented.
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PMID:An integrative model for the treatment of psychosomatic disorders. The place of sleep and dreams revisited. 19 60

The monoaminergic innervation of the rat prefrontal cortex arises from well-defined mesencephalic nuclei, with noradrenergic (NE) neurons located in the locus coeruleus, dopaminergic (DA) neurons located in the ventral tegmental area, and serotonergic (5-HT) neurons originating in the raphe nuclei. Specific destruction of the NE bundle was found to induce morphological (i.e., sprouting) as well as metabolic (i.e., changes in rate of DA utilization) modifications of mesocortical DA neurons, suggesting that these two catecholaminergic systems have functional interactions within the prefrontal cortex. This was substantiated by experiments showing that DA afferents modulate the sensitivity of cortical post-synaptic beta-adrenergic receptors and that, reciprocally, NE neurons control the sensitivity of cortical D1 receptors. Behavioural and pharmacological data have further indicated that the stimulation of cortical alpha-1 adrenergic receptors inhibits cortical DA transmission at D1 receptors. Secondly, we have attempted to analyze how such interactions between neuromodulatory systems may be related to the development of mental diseases such as schizophrenia. On the basis of studies in the literature describing the effects produced by the ingestion of hallucinogenic drugs or data collected regarding REM sleep, it is postulated that two modes of brain functioning exist: analogical and cognitive. Each mode is characterized by differences in the relative activities of NE, DA and 5-HT neurons. At birth, during REM sleep, and following the ingestion of hallucinogens, the mode of brain functioning is essentially analogical; in contrast, both analogic and cognitive modes are postulated to coexist in the awake state. Oscillations between these two modes are under the control of monoaminergic systems on which an increase in cortical DA release favours the cognitive processing mode, whereas intermittent activations of NE neurons would switch the brain into the analogical mode of processing. It is proposed that schizophrenic patients with "positive" symptoms suffer from an abnormal preponderance of the analogical mode while awake, whereas "negative" symptoms are due to the excessive presence of the cognitive mode. Although pure biological deficits cannot be excluded, these dysfunctions could be related to the absence of particular environmental variables early in the development of these patients. This condition is probably required to establish normal regulatory control of monoaminergic neuronal activity.
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PMID:NE/DA interactions in prefrontal cortex and their possible roles as neuromodulators in schizophrenia. 135 42

To study the effects of neuroleptic therapy on sleep EEG variables in schizophrenia, as well as the clinical correlates of these variables, we performed polysomnographic (PSG) studies on 14 schizophrenic inpatients before and during neuroleptic therapy. Sleep continuity measures improved after 3 weeks of neuroleptic therapy, showing decreased sleep latency and improved sleep efficiency. REM latency increased with treatment, although half the patients continued to exhibit REM latencies less than 60 min. Other sleep stages and measures of REM sleep (density, activity, number of periods) did not appear to change with neuroleptic treatment. At baseline, REM latency had strong negative correlations with BPRS and SANS scores, but with 3 weeks of such treatment, this association disappeared. Further work is needed to distinguish direct medication effects from the effects of the changing clinical state on PSG measures.
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PMID:Effect of neuroleptic treatment on polysomnographic measures in schizophrenia. 168 17

The authors present their experience with a number of drugs which are not antiepileptics nor antipsychotic drugs but influence the cholinergic and noradrenergic system and glucose and protein metabolism of neurons. Their efficiency in severe epileptics with psychic changes is about 60%. Standard epileptic treatment, mono- and polytherapy, failed completely in these patients. To the authors' "modulating" and "nootropic" therapy applies the same what applies to stereotactic treatment of epilepsy, i.e. that treatment must be started before the epileptic or psychotic process becomes chronic. Epileptogenesis is divided into the following stages: 1. insulation of the brain and development of a lesion (trauma, asphyxia, infection), 2. A. latency, an epileptic focus develops in the lesion, 2. B. latency, secondary and tertiary epileptic foci develop, in particular in the corpus amygdaloideum, hippocampus and fronto-orbital area and from there frequently also psychic changes arise, 2. C. the focus acts also on the thalamo-cortical reverbation circle and gradually "teaches" it epileptic discharges which sometimes can be followed on the EEG, although this stage is still in the latent period, i.e. clinically inapparent. 2. D. modulating structures of the stem fail, REM, i.e. paradox sleep, diminishes. Because these stages resemble those in the development of some psychoses, the psychogenesis of this epileptogenesis is similar; in schizophrenia the deepest stage of NONREM sleep declines. In this stage of epilepsy the inhibitory protective influence of noradrenergic, serotoninergic and dopaminergic (?) systems disappears. The 3rd stage is manifestation of clinical attacks or psychotic behaviour which may be enhanced by some provocation, e.g. alcohol, sleep deprivation, psychic stress, which influence emotivity and the sleep profile. With regard to these stages (insulation, latency, manifestation) treatment should be provided. In the 1st and 2nd stage "nootropic and modulating" treatment should be administered to a greater extent.
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PMID:[Nonstandard therapy of epileptics and psychotics]. 182 17

Based on the implication of increased muscarinic ACh activity in the production of negative symptoms, the association of decreasing cholinergic activity with positive symptoms, and the covariance of positive and negative symptoms in the psychotic phase of schizophrenia, a model of (DA) dopaminergic/(ACh) cholinergic interactions in schizophrenia was recently formulated. It suggests that DA/ACh balance is of central importance in schizophrenic pathophysiology and that muscarinic ACh activity increases in an attempt to maintain this balance in the face of increasing DA activity that occurs in the psychotic phase of the illness. The model further suggests that the muscarinic system exerts a damping influence on the emergence of positive symptoms associated with DA hyperactivity, but that this compensatory increase in muscarinic activity is accompanied by an intensification of negative symptoms. In the present study, we tested two important postulates of this model. We tested the prediction that muscarinic activity is increased in schizophrenia by comparing the effect of biperiden, an antimuscarinic M-1 agent, on REM latency in 12 drug-free schizophrenic inpatients and matched normal controls. We found that biperiden caused a smaller increase in REM latency in schizophrenic patients, suggesting that muscarinic activity is increased in schizophrenia. We tested the prediction that an anticholinergic agent would increase positive symptoms and decrease negative symptoms by studying the effect of 8 mg of biperiden/day for 2 days on positive and negative symptoms (assessed by the BPRS) in 30 medication-free schizophrenic inpatients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscarinic cholinergic hyperactivity in schizophrenia. Relationship to positive and negative symptoms. 200 53

Forty-five patients who met Research Diagnostic Criteria (RDC) for secondary depression were assessed by St. Louis criteria, and by demographic, illness history, REM latency and dexamethasone suppression test measures. Fully one-third of the RDC secondary sample met St. Louis criteria for primary depression; only age at onset and length of illness discriminated St. Louis primary from secondary depression. RDC depressed patients secondary to alcoholism were compared to those secondary to nonsubstance abuse disorders (excluding schizophrenia). The subgroup with a history of alcoholism reported less severe depression and were preponderantly male. Neither dexamethasone response nor REM latency differentiated the RDC secondary subtypes. Little support was found to validate separation of the RDC secondary subtypes studied.
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PMID:Secondary depression: a comparison among subtypes. 295 9

There are correlations between schizophrenia and the limbic seizure system on the one hand and the manic-depressive or bipolar syndromes and the generalized seizure system on the other hand, which are theoretically related to the different (although overlapping) neural substrates underlying the two major syndromes of psychosis. Evidence is reviewed that indicates that in ECT-responsive depression (with both bilateral and unilateral nondominant ECT) the modus operandi hinges on right-hemispheric neural events. At the same time the relevance of the complex interactions existing between limbic and generalized seizures, REM suppression, right limbic epilepsy and REM activation is discussed as well as the role of carbamazepine in these interactions.
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PMID:[Cerebral mechanisms of the efficacy of electroshock therapy]. 345 May 4

Electroencephalographic (EEG) sleep characteristics of young, never-medicated, nonschizoaffective schizophrenics were compared with the EEG sleep of patients with major depressive disorders (delusional and nondelusional) and with that of healthy controls. Schizophrenics had decreased sleep continuity comparable to delusional depressives. Slow-wave sleep percent was similar to that seen in healthy controls, as was the intranight temporal distribution of EEG delta activity. However, schizophrenics showed diminished delta counts per minute of non-rapid eye movement (NREM) sleep and a decreased total delta wave count. In contrast, depressives showed diminished slow-wave sleep percent compared with controls, greatly decreased delta activity (more so than did the schizophrenics), and an altered temporal distribution of delta activity, as evidenced by a shift of delta activity from the first to the second NREM period. Minutes of slow-wave sleep in the schizophrenics was inversely correlated with the severity of negative symptoms independent of the effects of age and the presence of depression. The schizophrenics showed normal REM latency and first REM period duration, in contrast to the depressives. These findings, reviewed in the historical context of sleep physiologic studies of schizophrenia over the past 30 years, suggest that young, never-medicated schizophrenics do not show the characteristic constellation of abnormalities in the first NREM-REM cycle seen in patients with major depression. However, decreased slow-wave sleep should be investigated as a possible marker for negative symptoms in schizophrenia.
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PMID:Electroencephalographic sleep in young, never-medicated schizophrenics. A comparison with delusional and nondelusional depressives and with healthy controls. 380 May 82

Few studies on schizophrenia with respect to the circadian alteration of the sleep-wake rhythm have been reported. We made a comparative study of the sleep-wake rhythm between chronic inpatient schizophrenics with a relatively bed-prone daily life and normal subjects under the conditions of absolute bed-rest to elucidate the chronobiological features of schizophrenia. The sleep-wake rhythm of the schizophrenics differed from that of the normals in two points: A significant difference was observed in the decrease of Stage 4 during their nocturnal sleep compared with the normal subjects, becoming conspicuous with the increasing lapse of time during sleep. The distribution and amount of their REM sleep in the morning were markedly low and the latency of their REM sleep was also prolonged. These facts suggested that the smooth slide of the sleep-wake rhythm was somewhat disturbed in the schizophrenics and that they were, therefore, in a state of hyperarousal despite their bed-prone life.
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PMID:Chronobiological comparison of sleep-wake rhythm between chronic schizophrenia and normal control. 383 28


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