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)

Developmental cortical damage has been implicated in the basic neurobiology of schizophrenia. Adult rhesus monkeys with neonatal temporal limbic damage show a stimulus-dependent disinhibition of subcortical dopamine (DA) release. We measured dopamine D2 receptors and transporters in vivo in rhesus monkeys with neonatal and adult mesial temporal limbic lesions and control monkeys to explore further the effects of this developmental lesion on striatal DA function. All monkeys were studied with [I-123]IBZM SPECT to assess the availability of striatal dopamine D2 receptors and with [I-123]beta-CIT SPECT to measure the availability of dopamine transporters in the striatum. IBZM binding was significantly reduced in monkeys with neonatal limbic lesions. No group difference in beta-CIT binding was found. The reduction in IBZM binding was significantly correlated with subcortical dopamine release after monoaminergic prefrontal stimulation as determined with in vivo microdialysis. Our findings imply specific interactions between age at lesion and the availability of DA transporter and receptors in non-human primates, and suggest that stimulus-dependent DA activity affects the expression of DA receptors.
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PMID:Striatal dopamine receptors and transporters in monkeys with neonatal temporal limbic damage. 1023 Nov 27

The presence of disorders of eye movements is today regarded as 'the strongest candidate for a genetically transmitted biological trait marker of schizophrenic disorders' (1). The present study is based on the experience, rather than the behaviour, of one patient in a search for a method of objectifying his visual problems. This method was found to be a simple test, which demonstrates a disturbance of fixation: while one eye accommodated on the figure without vergence, the other, vergent, eye fused with the image of the related background. The disorder had been misdiagnosed as 'exophoria' in conventional ophthalmological examinations, because prevailing ophthalmological theory accepts only one mode of vision; according to the most recent researches, however, it is necessary to distinguish two complementary modes of vision--one for panorama and one for detail--which differ in their coordination of vergence and accommodation. This new bimodal theory of vision--presented here for the first time--made it possible to understand the cause of the disorder as a substitution of sighting for fixation, due either to a disinhibition of panorama vision during fixation vision, or to an interchange of ipsilateral temporal and contralateral nasal projections from the retina, both associated with a fixation disparity. After correction of the patient's fixation disparity according to an unusual method, the dissociation of the visual goals was remedied and the mental disturbances of the patient vanished.
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PMID:The somatic component of schizophrenia: a dissociation of the goals of visual attention and bifoveal fixation? 1034 Feb 97

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 sub-type of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison with other psychopathological groups is challenged as well. 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- 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:Symposium: Normal and abnormal REM sleep regulation: REM sleep in depression-an overview. 1060 97

Several neuropsychological models of schizophrenia have regarded the syndrome as a disorder of the left hemisphere. However, discrepant experimental findings have been reported. It has been proposed that the different psychopathological dimensions of the syndrome are associated with distinct patterns of hemispheric imbalance. The present study was aimed at exploring relationships of psychopathological dimensions of schizophrenia with fronto- and temporo-hippocampal functioning of either hemisphere in 42 drug-free patients with a DSM-III-R diagnosis of schizophrenia. For the negative dimension, an inverse correlation with the performance on a verbal conditional associative task was found, consistent with the presence of a left fronto-hippocampal impairment in this dimension. As to the positive dimension, our results showed a direct correlation with perseveration on a verbal self-ordered pointing task, suggesting a hyperactivation of the left-hemisphere in this dimension. The disorganisation was found to be associated with a faster execution of a spatial memory task, probably reflecting increased perceptual priming and a right temporo-hippocampal disinhibition.
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PMID:Hemispheric asymmetry and psychopathological dimensions in drug-free patients with schizophrenia. 1061 53

This study examined neurological signs as familial vulnerability factors to schizophrenia. Fifteen Chinese schizophrenic patients, 21 of their nonpsychotic siblings, and 26 healthy volunteers, matched for age, sex, and education, were assessed by using the Cambridge Neurological Inventory. Results showed that patients and their siblings had significantly higher global neurological impairment than controls. The severity of motor coordination impairment of the siblings was in between patients and controls. This may suggest either patients have higher genetic vulnerability for the neurological abnormality and schizophrenia than their nonpsychotic siblings or the disease can further worsen the preexisting neurological deficit. Disinhibition signs were similar in patients and siblings, but significantly less in controls indicating its familial nature. Extrapyramidal and sensory integration signs were similar in siblings and controls, but significantly more severe in patients, suggesting nonfamilial abnormalities. In conclusion, these findings may imply different etiological origins for different subgroups of neurological signs.
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PMID:Soft neurological signs in schizophrenic patients and their nonpsychotic siblings. 1069 36

Most of psychoactive substances abuse or dependence disorders are associated to another psychiatric disorders. Depression, anxiety and psychotic disorders are the more frequent comorbid disorders. Psychiatric comorbidity is induced by acute consumption of psychoactive agents, chronic consumption or withdrawal. Psychiatric disorders are more frequent when patient are assessed immediately after the withdrawal. Main biological factors implicated in the pathophysiology of psychiatric disorders associated to dependence disorders are: increase in norepinephrine activity, during withdrawal, activation of locus coeruleus, kinding induced by repeated withdrawals. Psychotic disorders in opiate dependent patients can be induced by withdrawals. These psychotic disorders are more often described after methadone discontinuation. Consumption of cocaine can provocate paranoid delusions. Phenylcyclidine provocates sensorial distortion or delusive disorders resembling schizophrenia. Flash backs, following withdrawal realized brief and transient psychotic disorders. They can occur up to one year after the end of the intoxication. The occurrence of depression in dependent patients is frequent. Depressed patients are at risk for suicide. Retrospective studies showed that near of 40% of the subjects died from suicide have presented alcohol or drug abuse or dependence. Withdrawal from opiates provocates depression. Clinical picture included apathy, blunting of the affects, sadness and loss of interest. Cocaine consumption provocates manic-like disinhibition at the beginning of the intoxication. Long term consumption and withdrawal increase the risk of depression.
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PMID:[Psychiatric disorders induced by drug dependence other than alcohol]. 1085 11

The present report describes the participation of nicotinic receptors (nAChRs) in controlling the excitability of local neuronal circuitries in the rat hippocampus and in the human cerebral cortex. The patch-clamp technique was used to record responses triggered by the non-selective agonist ACh and the alpha7-nAChR-selective agonist choline in interneurons of human cerebral cortical and rat hippocampal slices. Evidence is provided that functional alpha7- and alpha4beta2-like nAChRs are present on somatodendritic and/or preterminal/terminal regions of interneurons in the CA1 field of the rat hippocampus and in the human cerebral cortex and that activation of the different nAChR subtypes present in the preterminal/terminal areas of the interneurons triggers the tetrodotoxin-sensitive release of GABA. Modulation by nAChRs of GABAergic transmission, which can result either in inhibition or disinhibition of pyramidal neurons, depends both on the receptor subtype present in the interneurons and on the agonist acting upon these receptors. Not only do alpha7 nAChRs desensitize faster than alpha4beta2 nAChRs, but also alpha7 nAChR desensitization induced by ACh lasts longer than that induced by choline. These mechanisms, which appear to be retained across species, might explain the involvement of nAChRs in cognitive functions and in such neurological disorders as Alzheimer's disease and schizophrenia.
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PMID:Neuronal nicotinic receptors in synaptic functions in humans and rats: physiological and clinical relevance. 1094 40

Plasma homovanillic acid (pHVA) concentrations are considered to reflect, in part, central dopamine metabolism and thus may be of value in assessing the role of dopamine neurotransmission in schizophrenia. Furthermore, some recent studies have suggested a relationship of pHVA with symptomatology. We have undertaken a study of pHVA in a large cohort of unmedicated DSM-IV schizophrenic patients in order to assess the relationship of pHVA to various clinical parameters. pHVA in 58 drug-free patients (10.11+/-0.52 ng/ml) was significantly elevated in comparison with 62 matched control subjects (8.77+/-0.39 ng/ml). pHVA was found to be higher in patients with a more negative syndrome. No significant correlation of pHVA with overall SAPS or SANS scores was apparent in the patients although, within the SANS subscales, a significant relationship to anhedonia-asociality was apparent. Interestingly, the male drug-free patients showed a correlation of pHVA with negative symptoms defined by SANS and several SANS subscales, while females showed no significant relationship with any SANS subscales. The results may suggest that an increased dopaminergic turnover is apparent in (male) schizophrenic patients with predominantly negative symptoms, providing some support for reports that this change in neuronal activity may be related to the neuropathological abnormalities seen in the disease, which may themselves differ between males and females. Such neuronal deficits of developmental or degenerative origin may thus result in an elevation/disinhibition of central dopamine metabolism in schizophrenia.
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PMID:Plasma homovanillic acid in untreated schizophrenia--relationship with symptomatology and sex. 1128 53

Several studies have reported that patients with schizophrenia and their relatives perform poorly on antisaccade tasks and have suggested that this deficit represents saccadic disinhibition. If this proposition is correct, then varying task parameters that specifically increase the difficulty with which unwanted saccades can be inhibited should exacerbate deficits. Forty-two schizophrenia patients, 42 of their first-degree biological relatives, 21 psychotic affective disorder patients, and 38 nonpsychiatric comparison subjects were given fixation and antisaccade tasks. The introduction of distracters and the presence of visible fixation stimuli were parameters used to vary the difficulty in suppressing unwanted saccades (inhibitory load). It is known that the presence of a fixation stimulus at the time when a saccade must be inhibited results in fewer reflexive errors on antisaccade tasks. Performance on fixation tasks without (low load) vs with distracters (high load) and antisaccade tasks that had fixation stimuli still visible (low load) vs already extinguished (high load) at the time when the reflexive saccade must be inhibited was compared. The schizophrenia patients and their first-degree biological relatives showed evidence of increased saccadic disinhibition that was most pronounced during high inhibitory load conditions. These data indicate that dysfunctional inhibitory processes, at least in the oculomotor domain, are associated with the liability to schizophrenia. Results also suggest that this genetic liability may be related to dysfunctional prefrontal cortical areas that provide top-down inhibitory control over reflexive saccade generation.
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PMID:Saccadic disinhibition in schizophrenia patients and their first-degree biological relatives. A parametric study of the effects of increasing inhibitory load. 1131 52

As many World War II and Korean Conflict veterans suffering from posttraumatic stress disorder (PTSD) grow older, increasing numbers will be diagnosed with dementia. We retrospectively analyzed patients with dementia, comparing the behavioral disturbances of those with PTSD to those without PTSD. We hypothesized that due to the additive effect of the neurobiological and behavioral changes associated with PTSD and dementia, the dementia with PTSD group would show more agitation and disinhibition than the dementia without PTSD group. Sixteen patients with diagnoses of dementia and PTSD were matched on age and Mini-Mental States Examination (MMSE) scores to 16 patients with dementia without PTSD. Demographic characteristics, co-morbid diagnoses, global Assessment of Functioning (GAF), Cohen-Mansfield Agitation Inventory (CMAI), and paranoid items of Brief Psychiatric Rating Scale (BPRS) and Positive and Negative Syndrome Scale for Schizophrenia (PANSS) were assessed. The patients with diagnoses of dementia with PTSD did not differ significantly in their clinical presentation, hospital course, and condition at discharge from patients with dementia without PTSD. Chi-square analysis showed that significantly more subjects in the PTSD group were prescribed anti-depressants compared to the non-PTSD group. Interestingly, within the PTSD group, the subgroup of patients who were former prisoners of war had a significantly higher mean score for paranoia and significantly less verbal agitation. This pilot study reveals that a diagnosis of PTSD alone is not sufficient to influence behavior in veterans with dementia; however, we also present provocative results that patients with more severe trauma (POW) do have changes in their behavior.
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PMID:Contribution of PTSD/POW history to behavioral disturbances in dementia. 1133 21


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