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

Antipsychotic drugs provide effective relief from hallucinations but do not improve, and may even induce, other symptoms of schizophrenia. Tardive dyskinesia, which is often associated with intellectual impairment, is generally attributed to chronic therapy with antipsychotic drugs. However, the possible contribution of medication to cognitive impairment is not easily dissociated from the underlying progression of the disease. Recently evidence has accumulated from studies performed in patients and experimental monkeys that augmentation of catecholamine function may improve performance on certain cognitive tasks. Further investigation of the role of catecholamines in cognition is warranted in order to assist development of antipsychotic drugs with fewer undesirable effects and entirely new approaches to therapy for cognitive impairment in schizophrenia.
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PMID:Cognitive impairment in schizophrenia: how experimental models using nonhuman primates may assist improved drug therapy for negative symptoms. 790 32

The treatment of psychotic illness has long been inextricably associated with society's view in general on social deviance. In medieval times, psychotic individuals were contained within the community, a situation which still prevails in many developing countries. Aggregation of such patients in asylums followed the increasing industrialization of communities in the nineteenth century, when the ability of the disadvantaged of all kinds to survive was greatly jeopardized. The twentieth century has seen a gradual reversal of this process, as attitudes towards mentally ill people have become a little more enlightened and liberal. However, the swing against the great lunatic asylums of the last century has proceeded at such an administrative rate that our patients are again in danger of succumbing medically and economically within our communities. It is common to see desperately poor and damaged psychotic individuals on our streets. The advent of neuroleptics was a major factor in the change from a custodial to an ostensibly rehabilitative approach in the treatment of schizophrenia. However, classic neuroleptics have a long list of well-recognized side effects such as affective and cognitive impairment that lead to poor treatment compliance, psychiatric relapse and social decompensation, the state of affairs of our street psychotics. Treatments that lessen the probability of this unfortunate process are desperately needed. The introduction of new neuroleptic drugs with favourable side effect profiles is to be welcomed as a major step in increasing the quality of life of our patients, both in hospital and functioning in the community.
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PMID:Neuroleptic-induced deficit syndrome. Historical introduction. 791 52

Cognitive dysfunction may underlie some of the psychopathology of schizophrenia as well as contribute to impaired social and vocational function in this disorder. Chronic treatment with typical neuroleptics has been reported to produce only minimal improvement in and may impair cognitive function in schizophrenia. We have studied the effect of clozapine, an atypical antipsychotic drug, on cognitive function in 36 patients with treatment-resistant schizophrenia. In addition, patients with non-treatment-resistant schizophrenia were randomly assigned to clozapine (N = 24) or typical neuroleptics (N = 23). Cognitive function in the treatment-resistant schizophrenia group was studied after 6 weeks and 6 months of treatment, while the non-treatment-resistant patients were also studied at 12 months of treatment. Clozapine treatment improved several domains of cognitive function, especially attention and verbal fluency in both treatment-resistant schizophrenia and non-treatment-resistant schizophrenia. On the other hand, typical neuroleptic treatment produced minimal improvement in cognitive function. The effect of clozapine on some tests of attention and verbal fluency was significantly greater than that of typical neuroleptic treatment in non-treatment-resistant schizophrenia. These data suggest that clozapine treatment was superior to typical neuroleptics in improving cognitive function in schizophrenia. The possibility that this is related to normalization of dopaminergic function by clozapine is discussed.
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PMID:Effects of clozapine on cognitive function in schizophrenia. 796 82

Research has suggested that poor insight in patients with schizophrenia is associated with poorer treatment compliance and outcome. Little is known about the etiology of poor insight. Poor insight has been attributed to a willful preference for illness, a psychological defense, and cognitive impairments. To test the hypothesis that poor insight is related to enduring cognitive deficits, the performance of 29 patients with schizophrenia and impaired insight and 63 patients with schizophrenia and unimpaired insight was compared on repeated administrations of the Wisconsin Card Sorting Test. Results indicate that subjects with impaired insight demonstrate consistently poorer performance over a period of 1 year than subjects with unimpaired insight. When the effects of IQ were partialled out, subjects with impaired insight made significantly more perseverative errors and achieved fewer categories correct, a pattern of performance deficits identified with neuropsychological dysfunction in schizophrenia. These results support the hypothesis that cognitive impairment may underlie poor insight in schizophrenia.
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PMID:Insight and cognitive impairment in schizophrenia. Performance on repeated administrations of the Wisconsin Card Sorting Test. 796 75

We tested 54 nonpsychotic first degree relatives of 23 schizophrenic probands and 18 control subjects matched for age and education on several neuropsychological tests. The tests were selected to assess overall intellectual ability or because previous work indicated that they are particularly sensitive measures of cognitive dysfunction in schizophrenic patients. The relatives of schizophrenic patients performed significantly worse than the control subjects on tests of verbal fluency and on Trailmaking, part B. Each of these tests contributed unique variance to the discrimination between groups. The groups did not differ significantly on the number of perseverative errors on the Wisconsin Card Sorting Test, Wechsler Adult Intelligence Scale-Revised block design or vocabulary, or Trailmaking, part A. Eight relatives who met DSM-III-R criteria for schizotypal personality disorder were more impaired than the remaining 46 relatives on letter fluency, but otherwise their performance was similar to that of nonschizotypal relatives. These data suggest that close relatives of schizophrenic patients may have subtle neuropsychological impairments that are not necessarily associated with clinical symptoms of schizophrenia spectrum disorders.
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PMID:Performance of nonpsychotic relatives of schizophrenic patients on cognitive tests. 799 26

Two cases of basal ganglia calcification involving the globus pallidus are presented. Both patients had cognitive dysfunction, temporal lobe-like symptoms (including amnestic state, perceptual distortions, or complex visual hallucinations), and myoclonus. Patient 1 manifested depression, auditory hallucinations, anxiety, paranoia, and postural tremor; patient 2 manifested multifocal dystonia with dystonic tremor. These cases supplement other reports of psychotic features and dementia associated with pallidal pathology. Additionally, the phenomena encountered in these cases are considered in light of recent advances in our understanding of basal ganglia functional pathways. These cases afford a potential pathophysiological window to the possible role of the globus pallidus in these neuropsychiatric conditions. In concert with other recent findings, these cases suggest specific pathway involvement in hallucinations, paranoia, depression, myoclonus, and dystonia. Further research will indicate if these pathways play a role in schizophrenia, mood disorders, and anxiety disorders.
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PMID:Neuropsychiatric disorders, myoclonus, and dystonia in calcification of basal ganglia pathways. 801 2

The issue of progressive cognitive decline in patients with schizophrenia has been debated. We performed a cross-sectional study of patients with chronic schizophrenia, aged from 18 to 69 years, in order to address this issue. The patients included in this study passed a rigorous screen for any comorbid condition with an adverse impact on central nervous system function. We assessed intellectual deterioration with a battery of neuropsychological tests known to be sensitive to cognitive impairment in progressive dementia. No evidence of accelerated intellectual decline was found. No significant differences were found between the five age-derived cohorts (18-29, 30-39, 40-49, 50-59, and 60-69 years of age) on the Mini-Mental State Examination, Dementia Rating Scale, or other tests sensitive to dementia. While performance on the Boston Naming Test significantly declined with age, this was mainly due to age rather than duration of illness. However, it is important to note that mean performances on the majority of the tests were abnormal across all cohorts studied. These results suggest that intellectual function does not markedly decline during the adulthood of patients with schizophrenia. The course of schizophrenia is more consistent with a static encephalopathy than a dementing disorder.
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PMID:Is there cognitive decline in schizophrenia? A cross-sectional study. 803 38

We examined social problem solving in schizophrenia. Twenty-seven schizophrenic patients in an acute hospital, 19 patients with bipolar disease, and 17 demographically matched nonpatient controls were tested on an empirically developed problem-solving battery that assessed the ability to generate solutions to problems, the ability to evaluate the effectiveness of solutions, and the ability to implement solutions in a role-playing format. Schizophrenic Ss were impaired on all 3 problem-solving domains compared with the nonpatient controls, but bipolar Ss were equally impaired. Several alternative explanations for these findings were considered. The most compelling hypothesis is that the deficits resulted from different factors: cognitive impairment for schizophrenic Ss and acute illness for bipolar Ss. However, longitudinal studies are required to determine whether problem-solving deficits in schizophrenic patients persist during periods of remission. Implications for rehabilitation strategies are discussed.
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PMID:Evaluation of social problem solving in schizophrenia. 804 May 6

Epidemiological studies suggest an apparent protective effect of cigarette smoking on the risk of Parkinson's disease. There is also a report suggesting that patients with Parkinson's disease who smoke are less likely to develop dementia. I investigated the relationship of smoking to the severity of cognitive functions and presence of drug-induced parkinsonism in a group of 111 neuroleptic-treated chronic institutionalized schizophrenic patients. Patients who smoked had significantly less cognitive impairment (p < .02) and a lower prevalence of drug-induced Parkinsonism (p < .02) compared to nonsmokers. These findings suggest that cigarette smoking may protect against the development of dementia and drug-induced Parkinsonism in schizophrenia.
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PMID:Cigarette smoking: effects on cognitive functions and drug-induced parkinsonism in chronic schizophrenia. 806 38

The literature on the putative association between cognitive dysfunction in schizophrenia and the presence of tardive dyskinesia is critically reviewed, focusing on potential artifacts and specific relationships to a particular topography of involuntary movements. These issues are exemplified via a study of cognitive function in 64 schizophrenic patients, in which impaired cognitive flexibility was identified as the primary measure distinguishing those with tardive orofacial dyskinesia. The significance of such an association with cognitive dysfunction is considered in relation to competing hypotheses of organic vulnerability to vs. state marker for this movement disorder.
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PMID:Cognitive dysfunction in schizophrenia: organic vulnerability factor or state marker for tardive dyskinesia? 810 22


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