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

The significance and nature of smooth pursuit impairments in schizophrenia are considered. Studies of potential artifacts show that the phenomenon is not due to medications, age, inattention, or poor motivation. Abnormal pursuit eye movements in schizophrenics consist of intrusive saccades which are present during any visually guided slow eye movements, and in some patients are related to nonvoluntary attention. These results rule out a generalized motor or oculumotor dysfunction, as well as a specific pursuit system dysfunction. The findings are consistent with a cortical dysfunction which results in saccadic disinhibition. Questions are raised for future research.
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PMID:Smooth pursuit impairment in schizophrenia--what does it mean? 684 87

The present study aimed at investigating the question whether abnormalities of sleep, especially disinhibition of rapid eye movement (REM) sleep, are already present in adolescents with primary major depressive disorder (MDD). Ten healthy controls assessed at home, 10 inpatients with MDD and 10 inpatients with schizophrenia (age range: 13-19 years) were investigated polysomnographically. REM latency was significantly shortened in MDD compared with the two other groups. Adolescents with MDD did not display disturbances of sleep continuity as typically observed in adults with major depression. The most pronounced impairment of sleep continuity was noted in schizophrenic patients. The results stress that shortened REM latency may already occur in adolescent depression.
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PMID:Sleep in adolescents with primary major depression and schizophrenia: a pilot study. 775 93

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

Disinhibition of rapid eye movement (REM) sleep (e.g. shortening of REM latency, heightened REM density) is frequently encountered in patients with a major depressive disorder (MDD). Administration of cholinomimetics prior to or during sleep leads to a more pronounced advance of REM sleep in depressed patients compared to healthy controls and patients with other psychiatric disorders. The present study tested whether the cholinergic REM induction test (CRIT) with 1.5 mg RS 86 (an orally acting muscarinic agonist) differentiates patients with MDD (n = 40) from those with schizophrenia (n = 43) and healthy controls (n = 36). The most pronounced shortening of REM latency after cholinergic stimulation occurred in patients with MDD. However, a significant number of patients with schizophrenia also displayed short REM latencies (REM latency < 25 minutes) under placebo conditions and after cholinergic stimulation. REM density measures more clearly differentiated patients with MDD from those with schizophrenia. It is concluded that a subgroup of patients suffering from schizophrenia displays signs of a muscarinic receptor supersensitivity.
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PMID:Cholinergic REM induction test: muscarinic supersensitivity underlies polysomnographic findings in both depression and schizophrenia. 793 82

It has been hypothesized that a saccade control dysfunction is one cause of a smooth pursuit eye movement (SPEM) dysfunction in schizophrenia. We studied the voluntary control of saccades in schizophrenic patients with the SPEM dysfunction using an antisaccade task. The mean error rate in the antisaccade task was significantly higher in the two schizophrenic groups with and without a SPEM dysfunction than in the normal control group. Furthermore, the schizophrenic group with the SPEM dysfunction showed significantly more errors than the schizophrenic group without the SPEM dysfunction. These findings seem to suggest a close relationship between the SPEM dysfunction and the appearance of errors which indicates an inability to inhibit reflexive saccades voluntarily in the antisaccade task. However, 4 of 10 subjects with the SPEM dysfunction showed an error rate less than the mean error rate of the schizophrenic group without the SPEM dysfunction. So, a voluntary control disorder of saccades as the main cause of the SPEM dysfunction appeared to be unlikely. An interesting finding of this study was that many schizophrenic subjects with the SPEM dysfunction showed errors with the latencies similar to those in express saccades, particularly in the rightward direction. This finding may suggest a close relationship between the SPEM dysfunction in schizophrenic patients and some pathological conditions of express saccades such as disinhibition of express saccades.
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PMID:Smooth pursuit eye movements and voluntary control of saccades in the antisaccade task in schizophrenic patients. 793 10

Abnormalities of saccades such as disinhibition have been hypothesized as one cause of smooth pursuit eye movement (SPEM) dysfunctions in schizophrenia. Thus, we studied saccadic eye movements in schizophrenics with SPEM dysfunction. Subjects were divided into three groups: 10 normal control subjects, 10 schizophrenic subjects without SPEM dysfunction and 10 schizophrenic subjects with SPEM dysfunction characterized by a cogwheel appearance. Visually guided saccades in gap and overlap paradigms (Saslow, 1967) were examined and saccadic reaction times (SRTs) were measured in all subjects. Only schizophrenics with SPEM dysfunctions tended to manifest excessive reflexive saccades, named express saccades (Fischer, 1987), in the gap paradigm. Moreover, most of them were also found to have express saccades in the overlap paradigm, whereas normal subjects and schizophrenic subjects without SPEM dysfunction did not show such phenomena under the same conditions. In particular, most express saccades in the overlap paradigm in schizophrenics with SPEM dysfunction, were found in movements to the right.
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PMID:Smooth pursuit eye movements and express saccades in schizophrenic patients. 804 22

A large number of psycholinguistic findings on how human beings store lexical information suggest the existence of associative memory, which may be characterized by a large capacity and a long duration. Its anatomical basis supposedly is, at least in part, the frontal lobes, and some of its functional characteristics have been tentatively linked to dopamine release. Working memory has a limited capacity, lasts only for seconds and is relevant for goal-directed behavior. Its anatomical basis in the frontal cortex is established and strong evidence suggests the involvement of dopaminergic pathways. Experimental evidence using several lexical decision tasks and a delayed response task is provided to demonstrate that some characteristic features of schizophrenic thinking--in particular the rapid shift of associations, the indirect relationship of associations, the overly abstract or overly concrete use of concepts, the lack of context-sensitivity and of general integrative function and intellectual capacity--can be explained in terms of an activation or disinhibition of associative memory, and of a dysfunctional working memory. The findings serve as an example of schizophrenia research in a cognitive neuroscience framework.
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PMID:The psychopathology, neuropsychology, and neurobiology of associative and working memory in schizophrenia. 821 28

Association psychology research in psychiatry dates back to Kraepelin, Aschaffenburg and C.G. Jung. Findings of the 1950s and 60s in this field suggest that semantic memory is organized in the form of a network. New results of experimental psychiatric studies indicate that schizophrenic symptoms, in particular formal thought disorders, are in part the result of an unfocussed activation or disinhibition of such associational network structures: The phenomenon of semantic priming is more pronounced in schizophrenic patients than in normals. Moreover, the phenomenon of indirect semantic priming on short stimulus onset asynchrony can be seen only in schizophrenic patients. The study of spontaneous speech further suggests the activation of structures responsible for the storage and processing of meaning. Increase in semantic priming, similar to that observed in schizophrenia, can further be observed in normal subjects on awakening from REM sleep. The findings are discussed in the framework of recent findings on the neurobiological causes of schizophrenia. They can be related structurally to an involvement of the frontal lobe, and functionally to disturbances of dopaminergic transmission. Methods such as the investigation of priming effects in lexical decision tasks, as well as concepts from the domain of cognitive neuroscience such as neural networks and the spreading activation model of lexical access, can help to bridge the gap between phenomenological psychopathology and neurobiology.
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PMID:[Associative networks, formal thought disorders and schizophrenia. On the experimental psychopathology of speech-dependent thought processes]. 847 85

Glutamatergic hypothesis stemmed from the observation of phencyclidine-induced psychosis. Phencyclidine is able to induce in healthy subjects negative and positive schizophrenic-like symptoms, as well as thought disorganization. Phencyclidine acts as an antagonist of NMDA receptor, one of the glutamatergic receptors. Experimental studies in animals have demonstrated that compartmental effect of phencyclidine is due to its action at striatal level, allowing the disinhibition of down-stream structures. The organization of the two striato-thalamocortical loops, which exert, respectively, a positive and negative retro-control on cortical activity, may explain how a glutamatergic deficiency induces both positive and negative symptoms. Positive symptoms could also be due to a secondary hyperdopaminergia, since a part of striatum, the striosomes, connected with limbic system, control the activity of dopaminergic neurons. This model validates the hypothesis that a single anomaly can lead to the different symptomatic dimensions of schizophrenia and supports the implication of basal ganglia in the expression of mental disease.
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PMID:[Glutamatergic hypothesis of schizophrenia: psychoses induced by phencyclidine and cortical-subcortical imbalance]. 852 68


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