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)

Three relatively clear-cut diagnostic groups, namely primary major depressive disorder-endogenous subtype (PRI MDD-E), primary anxiety disorder with no depression (PRI ANX), and normal controls as well as two additional patient groups with mixed or coexisting anxious/depressive diagnoses were studied. Clinical assessment was made by routine psychiatric interview, Schedule of Affective Disorder and Schizophrenia (SADS) research interview, and obtaining family history of MDD. Subjects underwent both routine 'baseline' sleep EEG polygraphic arecoline, a muscarinic, cholinergic agonist infused during sleep. Cholinergic sensitivity was assessed by measuring the time to induction of REM sleep after arecoline infusion. In addition, a subgroup of MDD patients underwent pupillographic testing. Peripheral alpha-adrenergic responsivity was measured by the magnitude of pupillary mydriatic response after local ocular instillation of phenylephrine. Successful separation (83% correct classification) of the 'pure' groups (PRI MDD-E, PRI ANX, and normal) was achieved by discriminant function analysis of sleep EEG variables. Compared to PRI ANX and normal groups, patients with PRI MDD-E had supersensitive cholinergic REM-induction response, shorter REM latency, increased first REM density and REM percent. Separation of the PRI ANX and normal groups was by intermittent awake time, delta sleep percent, and total REM density. Classification of the mixed anxious/depressive groups was next attempted using the discriminant coefficients derived from the above analysis of 'pure' groups. We found that the presence of absence of family history of MDD in patients with mixed diagnosis offered the best prediction of classification into PRI MDD-E and PRI ANX groups, respectively. MDD patients with coexisting panic disorder were significantly subsensitive to phenylephrine-induced mydriasis compared to MDD patients without anxiety.
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PMID:Acetylcholine and alpha 1-adrenergic sensitivity in the separation of depression and anxiety. 650 19

The authors measured the middle ear muscle activity during REM sleep of normal subjects (N = 13) and patients with schizophrenia (N = 11), schizoaffective disorder (N = 8), or major depressive disorder (N = 10). The rates of middle ear muscle activity for 5 schizophrenic patients were higher than the highest rates of the other groups. The patients with major depressive disorder had normal rates, and the rates of those with schizoaffective disorder were below normal. Within the schizophrenic patients, high middle ear muscle activity could not be directly attributed to background sleep disturbances, age, anxiety, depression, or diagnostic subtype.
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PMID:Middle ear muscle activity during REM sleep in schizophrenic, schizoaffective and depressed patients. 713 99

Most of the previous research reporting abnormalities of rapid re-fixation eye movements (saccades) in patients with schizophrenia has used patients receiving neuroleptic medication. In this study non-neuroleptically medicated schizophrenics were compared with other psychiatric patients using a variety of saccadic paradigms to determine the specificity of saccadic dysfunction. The patient groups consisted of schizophrenics (N = 18), bipolar affectives (N = 18), anxiety neurotics (N = 10) and normal controls (N = 31), none of whom had received neuroleptic medication for the preceding 6 months. Four behavioural paradigms, reflexive, predictive, remembered and ANTI were used to elicit saccades. The primary abnormality in the schizophrenic group was a significantly increased rate of distractibility in the ANTI (saccades made towards the target rather than in an opposite direction) and REM (saccades made prior to the imperative cue) paradigms. The major neuropsychological variable predictive of these errors was Wisconsin card sort perseverative errors. These data, in conjunction with findings from previous neurological research, would seem to provide converging evidence towards dysfunction of prefrontal cortex in schizophrenia.
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PMID:Saccadic abnormalities in psychotic patients. I. Neuroleptic-free psychotic patients. 748 Apr 27

The generating mechanism of the electroencephalogram (EEG) points to the hypothesis that EEG signals derive from a nonlinear dynamic system. Hence, the unpredictability of the EEG might be considered as a phenomenon exhibiting its chaotic character. The essential property of chaotic dynamics is the so-called sensitive dependence on initial conditions. This property can be quantified by calculating the system's first positive Lyapunov exponent, L1. We calculated L1 for sleep EEG segments of 13 schizophrenic patients and 13 control subjects that corresponded to sleep stages I, II, III, IV and REM (rapid eye movement), as defined by Rechtschaffen and Kales, for the lead positions Cz and Pz. During REM sleep, for both electrode positions, the principal Lyapunov exponent L1 was significantly increased in schizophrenic patients compared with control subjects. This finding points to altered nonlinear brain dynamics during REM sleep in schizophrenia.
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PMID:Nonlinear analysis of sleep EEG data in schizophrenia: calculation of the principal Lyapunov exponent. 756 48

1. The efficacy of butoctamide hydrogen succinate (BAHS) was compared with that of nitrazepam on the basis of the polysomnograms and the subjective assessments. 2. Twelve healthy male students were divided into three groups consisting of 4 subjects each with were administered BAHS 600 mg, nitrazepam 5 mg, and BAHS 600 mg + nitrazepam 5 mg, respectively. 3. Polygraphic recordings were made for 8 consecutive nights for each subject, and the polysomnograms were evaluated by computerized automatic analysis using the interval histogram method. 4. An inert placebo was administered on the first 3 nights and on the seventh and eighth nights, and the test article regimen was administered on the fourth, fifth and sixth nights. 5. The test articles and the placebo were administered orally at 22:30 hr, and the recording of polysomnograms was started at 23:00 hr and ended at 8:00 hr the next morning. 6. The subjects were requested to fill out the subjective assessment of sleep before falling asleep and after arising the next morning. 7. BAHS increased REM sleep and decreased stage 2 sleep significantly; however, it failed to affect stage 1, 3 or 4 sleep. 8. Nitrazepam increased significantly the total sleep time and stage 2 sleep but decreased significantly the stage 3 sleep and decreased slightly the stages 1, 4 and REM sleep. 9. The combined treatment with BAHS and nitrazepam did not alter the sleep parameters except for increasing the total sleep time. 10. No obvious changes were observed in the subjective assessments after administration of the drugs. 11. These findings suggest that BAHS results in a unique sleep pattern different from benzodiazepines, and that BAHS may be suitable for treating insomnia in elderly patients and those with drug abuse, manic-depressive illness or schizophrenia.
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PMID:Stimulatory effect of butoctamide hydrogen succinate on REM sleep in normal humans. 762 90

Cholinergic neurons of the pedunculopontine nucleus (Ch5) and laterodorsal tegmental nucleus (Ch6) monosynaptically activate dopamine neurons of the substantia nigra, zona compacta (A9), and ventral tegmental area (A10) via muscarinic and nicotinic receptors. Ch5 cells and Ch6 cells are inhibited by local injections of muscarinic agonists, suggesting the presence of autoreceptors. This review advances the hypothesis that the psychotogenic effects of antimuscarinics are triggered by disinhibition of Ch5 and Ch6 cells via their autoreceptors, and that these effects are distinct from the memory-blocking effects of antimuscarinics mediated through the Ch1-Ch4 projections to the forebrain. Neuroleptic and antiparkinson agents with antimuscarinic effects selectively block m1 muscarinic receptors, whereas psychotogenic antimuscarinics are nonselective. In rats, scopolamine injected near Ch5 cells facilitates rewarding brain stimulation and induces locomotion and stereotypy, apparently via activation of dopaminergic systems. Systemically administered scopolamine induces locomotion and stereotypy via muscarinic receptors near Ch5 cells. Ch5 activation and Ch6 activation may be a causal factor in some forms of schizophrenia. Some schizophrenics show early-onset REM sleep, a condition that can result from Ch5 and Ch6 cholinergic activation of the pontine reticular formation. Schizophrenics with early-onset REM, or visual hallucinations, show more severe positive symptoms and negative symptoms. Ch5 cells and Ch6 cells have been found in twice-normal numbers in a few brains of schizophrenics. Several genetic and onset factors for schizophrenia that may be linked to Ch5 cells are considered, as well as treatment strategies based on inhibition of Ch5 cells and Ch6 cells, or blockade of their terminals.
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PMID:Role of tegmental cholinergic neurons in dopaminergic activation, antimuscarinic psychosis and schizophrenia. 776 84

Abnormalities of REM sleep, i.e. shortening of REM latency, lengthening of the duration of the first REM period and heightening of REM density, which are frequently observed in patients with a Major Depressive Disorder (MDD), have attracted considerable interest. Initial hopes that these aberrant patterns of sleep constitute specific markers for the primary/endogenous subtype of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison to other psychopathological groups is also challenged. Demographic variables like age and sex exert strong influences on sleep physiology and must be controlled when searching for specific markers of depressed sleep. It is still an open question whether abnormalities of sleep are state-markers or trait-markers of depression. Beyond baseline studies, the cholinergic REM induction test (CRIT) indicated a heightened responsitivity of the REM sleep system to cholinergic challenge in depression compared with healthy controls and other psychopathological groups, with the exception of schizophrenia. A special role for REM sleep in depression is supported by the well known REM sleep suppressing effect of most antidepressants. The antidepressant effect of selective REM deprivation by awakenings stresses the importance of mechanisms involved in REM sleep regulation for the understanding of the pathophysiology of depressive disorders. The positive effect of total sleep deprivation on depressive mood which can be reversed by daytime naps, furthermore emphasizes relationships between sleep and depression. Experimental evidence as described above instigated several theories like the REM deprivation hypothesis, the 2-process model and the reciprocal interaction model of nonREM-REM sleep regulation to explain the deviant sleep pattern of depression. The different models will be discussed with reference to empirical data gathered in the field.
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PMID:[Depression and sleep--the status of current research]. 783 18

A dramatic increase in REM sleep time at the expense of slow wave sleep has been reported in patients on clozapine monotherapy (5). It is now suggested that this effect of clozapine on the sleep pattern could be due to a dissociation of the NREM/REM sleep cycle, and that the epileptogenic EEG abnormalities induced by clozapine in daytime recordings (2) would represent a dose-dependent activation on NREM sleep mechanism during wakefulness. The implications of this theory in relation to the concept of schizophrenia are discussed.
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PMID:The secret of clozapine: to sleep while awake? 783 9

CSF diazepam-binding inhibitor-like immunoreactivity (DBI-LI) and polysomnography were studied in 28 drug-free male schizophrenic (DSM-III-R) patients. They underwent a three-night polysomnography evaluation and a lumbar puncture. CSF DBI-LI correlated positively with REM latency, the REM latency/2d nonREM period ratio and stage-4% sleep, and negatively with stage-1% sleep. CSF DBI-LI did not correlate significantly with duration of sleep or sleep latency. CSF DBI-LI during haloperidol treatment did not correlate significantly with sleep EEG measures. The results of this first study of the relationship between endogenous DBI and sleep in humans suggest that physiological effects of DBI other than interactions with the BZD/GABAA receptor complex may explain its positive effects on sleep. However, the absence of similar sleep data in normal subjects precludes us from establishing a specific relationship between DBI and sleep in schizophrenia.
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PMID:CSF levels of diazepam-binding inhibitor correlate with REM latency in schizophrenia, a pilot study. 788 20

Sleep variables and psychiatric symptoms were investigated in 6 male chronic schizophrenic outpatients. The patients were being treated with benzodiazepine (BZD) hypnotics for more than 8 weeks, and BZDs were replaced with zopiclone (ZPC) 15 mg/day. Polysomnographic examinations, subjective sleep assessments and BPRS scoring were performed during BZD therapy and at the end of 8 weeks of ZPC therapy. The doses of neuroleptics and anticholinergic agents remained fixed throughout the study. The amount of slow-wave sleep (SWS) was markedly small and that of stage 1 sleep was moderately large during BZD therapy. The amount of stage 1 was smaller and that of stage 2 was larger during treatment with ZPC than BZDs. There were no significant change in the amount of SWS between the treatment. Half of the patients exhibited a sleep-onset REM period (SOREMP) during ZPC therapy. Both total BPRS score and negative symptom score were lower during treatment with ZPC than BZDs. These results suggest that ZPC may be more beneficial in treating schizophrenic insomnia than BZD hypnotics and that reduced SWS and SOREMP may be partly involved in the pathophysiology of schizophrenia.
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PMID:Effects of zopiclone on sleep and symptoms in schizophrenia: comparison with benzodiazepine hypnotics. 791 46


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