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Query: UNIPROT:O75628 (REM)
 5,581 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

10 patients with moderate non-psychotic sleep disturbances were investigated polygraphically for a total of 14 nights each. These 14 nights were subdivided into 4 test series: Placebo was given during the first, Plantival plus during the second and third and placebo again during the fourth series. The results showed that wakefulness decreased after the application of Plantival plus and that there was an increase in deep sleep. These effects could be observed mainly during the first hour of sleep and disappeared gradually during the later sleeping hours. REM-phases were not influenced by the medication. Due to these observations, Plantival plus should mainly be applicated when disturbances in falling asleep and problems in sleeping continuously occur. In case interrupted sleep in the early morning hours has been found, this preparation could be applicated only in combination with other kinds of treatment.
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PMID:[Polygraphic recording of sleep under the influence of Plantival plus]. 0 47

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

Short and long term effects of sulpirid on the sleep EEG in humans were investigated in 8 patients aged 20-68 years (average 40.4) suffering from autonomic instability. In each patient seven polygraphic night sleep recording were performed. After an adaption night and two nights without medication each subject got 200-400 mg sulpirid i.m. for two days and then 300-600 mg orally for a three-week period. In both groups the short-term application of sulpirid caused a reduction of waking periods and a slight decrease of stage 3, while stage 2 was increased. In psychotic patients the long-term orally administered substance was followed by an increase of deep synchronous sleep (stage 4). As this alteration of sleep couldn't be revealed in the control group, we consider this finding as a result of the improvement of psychosis. In the patient group the amount of REM sleep was augmented during the short-term application as well as during the long-term application, where, as in the control group the amount of REM sleep decreased when sulpirid was given orally for three weeks. This result is discussed in comparison with the properties of the tricyclic antidepressant drugs and monoamine oxidase inhibitors and the clinical effects of sulpiride.
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PMID:[The influence of sulpirid on sleep. Results of polygraphic night sleep recordings (author's transl)]. 18 80

On the basis of two EEG sleep criteria, REM latency and REM activity, the authors achieved 81% accuracy in distinguishing between 47 patients with primary depression and 48 patients with secondary depression using discriminant analysis. Sleep efficiency, the percentage of delta sleep, and the percentage of REM sleep discriminated between psychotic and nonpsychotic subgroups in the group with primary depression with 75% accuracy. REM activity and intermittent nocturnal awakening accurately discriminated two subtypes of patients with secondary depression at a level of 81%. These results suggest that EEG sleep measurements can yield significant data to aid in differential diagnosis in psychiatry.
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PMID:The application of EEG sleep for the differential diagnosis of affective disorders. 20 Nov 74

At present EEG investigations in heterogenous acute schizophrenic and psychotic syndromes suggest changes in the regulating, reticulo-thalamo-cortical, functional system. One may further assume that cerebral functional changes consist of a dissociation of normally closely linked functional systems. In favor are findings in functional psychoses ("Funktionspsychosen"), also the dissociation of usually coordinated systems in normal psychologic changes during going to sleep and REM stages of dreams. A further thalamohippocampo-reticulo system which might act in parallel to the activating reticular system has become important in EEG research into psychoses. Changes here probably in part of focal EEG phenomenon localized in the temporal region. Here, too, EEG findings in schizophrenic syndromes requiring further proof emerge.
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PMID:[Electroencephalography in clinical research into psychoses (author's transl)]. 20 20

In the last decade all night EEG sleep research has attempted to delineate the sleep features most characteristics of depressive states occurring in adult life. We have reported that EEG sleep variables could be used to verify a diagnostic classification for affective syndromes. This EEG sleep generated schema significantly dichotimized each major clinical category using only two or three EEG sleep measures. REM latency and REM density were sufficient to separate out primary from secondary depressed patients. Sleep efficiency, REM sleep percent, and delta sleep percent discriminated between the psychotic and nonpsychotic subgroups in the primary depressive group. Furthermore, EEG sleep variables separated secondary depression with concurrent medical disease from secondary depression without medical disease using REM activity and intermittent nocturnal awakening as the requisite variables of discrimination. Other ongoing investigations have established that the REM intensity of the first REM period is increased in primary depression. The search for EEG sleep correlates of clinical response in depressed patients receiving tricyclic antidepressants has suggested that, the more rapid the suppression of REM sleep, the more likely that the patient will respond to tricyclic antidepressants. Finally, clinical response appears to be associated with a period of sustained elevation of REM latency.
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PMID:Application of EEG sleep for the differential diagnosis and treatment of affective disorders. 20 49

Electrographic (EEG) patterns of nocturnal sleep were investigated in young psychiatric patients during unipolar depressive episodes. EEG-sleep data was recorded in 20 non-psychotic depressed patients all under 26 years old individually matched with a normal control group. All 20 subjects slept in the laboratory for 1-3 consecutive baseline nights from 12-8:00 a.m. During a subsequent extended condition 14 in each group were allowed to sleep ad-lib. Although the mean total time asleep on baseline nights was about the same between groups (greater than 7.1 hr), the depressives had a statistically significant reduction in REM time, increased transitions into stage 1, but most especially averaged: (a) less stage 4; and (b) more stage 1. Compared with the prior eight-hour night 27/28 subjects among both groups exhibited elevated time asleep during the extended condition, but the patients' mean total 10.3 hr sleep was significantly greater by 1.5 hr than the controls (X = 8.8 hr). Sleep exceeding 9 hr on the ad-lib night was a consistent phenomenon which occurred in significantly more (11/14) young depressed patients contrasted to 4/14 control subjects. These findings indicate that young persons with primary affective disorders do not exhibit nocturnal EEG disturbances of comparable severity to most older depressed patients such as reduced time asleep, increased wakefulness or lowered slow-wave (stages 3 and 4) sleep. Although no direct evidence of symptomatic 'hypersomnia' in these patients was provided, the present results demonstrated that some young persons with clinical depression have the capacity to sleep for sustained periods.
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PMID:Electrographic analysis of the sleep cycle in young depressed patients. 21 58

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

By means of a review of genetic, biological and neurophysiological studies, we attempted to validate the DSM III-R depressive disorder categories. Genetic studies support the distinction between bipolar and recurrent major (unipolar) depression although genetic heterogeneity and variable phenotypic expressivity have been suggested in bipolar depression. Biological and neuroendocrine abnormalities in depression seem to relate more to a particular symptomatological profile than to a specific depressive subtype including the bipolar-unipolar dichotomy. For example, catecholamines and serotonin metabolism seem to reflect respectively psychomotor status and aggressiveness in depression. Using genetic and biological criteria, major depression with psychotic features is the best validated category of the four main DSM-R major depressive subclasses or specifications (psychotic, chronic, melancholic, seasonal). Psychotic depression seems to constitute the most coherent subgroup and biological abnormalities such as dexamethasone non suppression and shortened REM latency are very often observed. An important confounding variable in these biological validation studies is the severity of the depressive state. Psychotic depression is considered to be a more severe depressive subtype and also shows marked biological disturbances. Conversely, in seasonal depression, a less severe depressive subtype, CSF monoamine metabolism abnormalities, dexamethasone non suppression and shortened REM latency could not clearly be demonstrated. Genetic studies show that early onset dysthymia and cyclothymia could be part of the affective spectrum and some maintain that these two clinical entities are attenued forms of bipolar or recurrent major depression.
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PMID:[Biological psychiatry and current classifications of depressive disorders]. 186 51

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


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