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

Human genetic studies have directed attention to genetic imprinting in a number of syndromes involving brain dysfunction, such as Prader-Willi syndrome, Angelman syndrome, Turner's syndrome, bipolar depression and schizophrenia. Molecular genetics is providing insights into the complexity of these imprinting mechanisms, while experimental studies are revealing the differential roles that maternal and paternal genomes may play in brain development and growth.
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PMID:Genomic imprinting in the brain. 928 7

The articles that appear in this issue offer a framework of insights about the neuroanatomy of schizophrenia from three learned and creative perspectives. All three articles advance our understanding of schizophrenia from a single locus/specific "lesion" model to more advanced perspectives of neural circuit dysfunction models. Goldman-Rakic and Selemon review their own and others' work on structure-activity relationships of the frontal cortex and related working memory dysfunction. This important but sometimes cloudy and complex area is illuminated by their highly specific, informative research. Jones focuses on thalamic abnormalities hypothetically linked to abnormal oscillations in large arrays of cortical and thalamic neurons, a critically important concept in understanding the functional consequences of abnormal (thalamic) brain structure and function. Graybiel describes her interest in abnormal basal ganglia activity-dependent loops that may access the thalamus and set the tone of thalamo-cortical transmission. This view allows for us to understand the "upward" influences on basal ganglia function (and dysfunction) relevant to schizophrenia. These intriguing articles raise a number of issues that await increased data and continued integrating insights. These issues include the need for more information about (1) the developmental timing of lesions or dysfunctions; (2) the extent and regional distribution of abnormalities; (3) the relationship of brain dysfunction to clinical/cognitive abnormalities; and (4) the variable expression of brain abnormalities across the schizophrenia spectrum. These three articles and their authors are at the forefront of our expanding knowledge about the neuroanatomy of schizophrenia and how complex structural and functional deficits are expressed in individuals in the group of schizophrenias.
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PMID:Neuroanatomy of schizophrenia. 932 11

Schizophrenia is a human brain disease with well-defined symptoms and a lifelong disease course, but without a current biological explanation. Several observations implicate brain glutamatergic abnormalities in the pathophysiology of this illness. This evidence includes both human neurochemical and clinical pharmacologic data. Furthermore the psychotomimetic action of phencyclidine, the noncompetitive NMDA-sensitive glutamate receptor antagonist, suggests the association between human psychosis and NMDA receptor blockade. This paper reviews basic aspects of glutamatergic transmission in animal and human brain with particular attention to its putative role in schizophrenia. Consideration is given to other glutamate-related human brain diseases and their purported mechanisms. Evidence of glutamatergic abnormalities in schizophrenia is critically reviewed, including data using postmortem neurochemistry, in vivo human brain imaging, clinical pharmacology, and animal models. The current theoretical formulations based on these studies are articulated. We propose a "working" glutamate hypothesis of schizophrenia which postulates a diminished glutamatergic transmission in the hippocampal glutamate-mediated efferent pathways and cerebral dysfunction in the hippocampus and its target areas, especially the anterior cingulate cortex. Considerable work remains to be done in this area to formulate and test a comprehensive hypothesis.
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PMID:Schizophrenia and glutamatergic transmission. 944 80

Evidence has begun to accumulate which suggests that lack of awareness of illness in schizophrenia is related to and possibly the result of a cognitive deficit involving prefrontal cerebral dysfunction. This study further explores this relationship along with other domains of self-awareness in chronic schizophrenics and other subjects with serious mental disorders. One hundred eight schizophrenics and 21 bipolar subjects from three separate sites in Britain, Germany, and Canada were administered the Wisconsin Card Sorting Test and three measures of self-awareness. Lack of illness awareness and other domains of self-knowledge were significantly more related to poorer neuropsychological performance in schizophrenia patients than in the other subjects. The results support the hypothesis that lack of illness awareness is related to defective frontal lobe functioning as indexed by neuropsychological measures.
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PMID:Further parameters of insight and neuropsychological deficit in schizophrenia and other chronic mental disease. 945 46

Substantial verbal IQ (VIQ)-performance IQ (PIQ) discrepancies may reflect brain dysfunction. The authors examined 159 patients with schizophrenia (115 men and 44 women) or schizoaffective disorder (25 men and 19 women) and 79 normal participants (33 men and 46 women), calculated mean VIQ-PIQ discrepancy scores by sex and diagnosis, and identified persons with large VIQ-PIQ discrepancies (15-point difference in either direction). Schizophrenic/schizoaffective men had a larger mean VIQ-PIQ discrepancy than did other groups. The proportion of all patients with either VIQ > PIQ or PIQ > VIQ (17.8%) was not significantly different from that of normal participants (22.8%). However, significantly more men than women with schizophrenia exhibited a VIQ > PIQ pattern (20% vs. 3.2%). No unusual discrepancy patterns were noted among normal participants. Results were interpreted in light of theories of hemisphere dysfunction in schizophrenia.
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PMID:Sex differences in verbal IQ-performance IQ discrepancies among patients with schizophrenia and normal volunteers. 950 49

Neurological assessment was carried out on patients with schizophrenia from multiply and singly affected families, their relatives, and a normal control group (214 subjects). A systematic examination was used in which abnormal signs were divided into 'primary' and 'integrative' signs. Primary signs were elicited by a standard clinical neurological examination and included signs of focal damage to nuclei and tracts, whilst integrative signs were selected as reflecting distributed brain function. The assessments were carried out to test the hypotheses that (i) neurological abnormalities are present in schizophrenia, (ii) the pattern of abnormality is different in familial and sporadic schizophrenic subjects, and (iii) the well relatives of familial (but not sporadic) schizophrenic subjects will show neurological abnormalities. An excess of primary signs compared with the controls was demonstrated in the sporadic schizophrenic group only. Both the familial schizophrenics and their first-degree relatives (but not their sporadic counterparts) showed an increase in integrative signs. The results support the existence of different mechanisms of underlying brain dysfunction in familial and sporadic schizophrenia.
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PMID:Neurological abnormalities in familial and sporadic schizophrenia. 954 99

The past decade has seen renewed interest in the neuropathology of schizophrenia. The advent of new postmortem techniques and functional imaging, along with a greater understanding of the neuropsychology of schizophrenia, have provided many new clues to the nature of the underlying brain dysfunction in this disorder. There has also been a greater understanding of the presence of severe cognitive dysfunction among many elderly persons with schizophrenia. In this article, a series of investigations are described that seek to answer basic questions about the neuropathology of schizophrenia, in particular as it pertains to cognitive impairment. The first study describes neuropathological findings in 100 consecutively autopsied persons with schizophrenia, the majority of whom had had detailed antemortem assessments. Results from this first study prompted the conclusion that schizophrenia is not characterized by classical, histologically identifiable neuropathology. Moreover, most cases of dementia in schizophrenia are probably not the result of neuropathologically identifiable dementing illnesses. The next four studies examined chemical markers that are altered in Alzheimer's disease and some other dementing conditions and have also been suggested to be abnormal in schizophrenia: choline acetyltransferase, catecholamines and indolamines, neuropeptides, and synaptic proteins. Schizophrenia cases as a group did not show a cholinergic deficit; nor did they differ from elderly comparison cases with respect to cortical catecholamines and indolamines. Among the schizophrenia cases, however, cognitive impairment was negatively correlated with choline acetyltransferase activity. Those with cognitive impairment showed evidence of cortical noradrenergic and serotonergic deficits. Neuropeptide deficits were also present in schizophrenia, but their pattern differed from that seen in Alzheimer's disease. Increased synaptic protein activity was found in the cingulate cortex of persons with schizophrenia, and this activity was correlated with schizophrenia symptoms. From this second series of studies, it was concluded that some biological measures in schizophrenia may be related to cognitive impairment (e.g., cortical amines), whereas others may be related to diagnosis (e.g., neuropeptide deficits). In addition, synaptic organization may correlate with schizophrenia symptoms.
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PMID:Postmortem studies in schizophrenia. 971 27

Recently, with the increase in elderly population, we have had more opportunities to administer neuroleptics to elderly patients for hallucinatory delusional state, delirium, psychomotor excitement, wandering etc. However, little is known about the characteristics of the neuroleptic malignant syndrome (NMS) in elderly patients, which is the most serious side effect of neuroleptics. In this paper, we present the clinical course of five NMS patients in the presenium and senium. Case 1 was 72-year-old male who was diagnosed as having dementia of Alzheimer's type (with late onset). He showed nocturnal wandering, insomnia, and irritability. Tiapride 60 mg per day had been administered previously. Just after the addition of oxypertine 10 mg per day, NMS occurred, and he died of pneumonia a week later. Case 2 was 75-year-old male who was diagnosed as having vascular dementia. He showed insomnia, hyperactivity and wandering. He had been given levomepromazine (LPZ) 10 mg per day over a long period of time. At first, he had daily episodic fever, however, serum CPK levels did not increase at that time. A month later, all the symptoms of NMS appeared and then the patient's condition suddenly deteriorated and he died three days later. Case 3 was a 64-year-old male who was diagnosed as having dementia of Alzheimer's type (with early onset). He showed insomnia, irritability and violence. Tiapride 50-125 mg per day was administered along with oxypertine 50-115 mg per day. Almost two months later, NMS occurred. He had daily episodic fever at first, extrapyramidal symptoms and autonomic instabilities gradually increased. Soon after symptoms of NMS were completed. In this case, NMS seemed to be induced by bacterial pneumonia after long term administration of LPZ 5 mg per day. Case 4 was a 75-year-old female who was diagnosed as having dementia of Alzheimer's type (with late onset). She showed hallucinatory delusional state. Although she had autonomic instabilities just after adminstration of haloperidol 1-2 mg per day, NMS itself occurred after discontinuing the neuroleptic. Case 5 was a 61-year-old female who was diagnosed as having schizophrenia at the age of forty. She was given various neuroleptics over a period of time. The neuroimaging in SPECT showed her cerebral cortex was generally hypoactive. She had a tendency to have autonomic instabilities after the administration of relatively high potential neuroleptics. Risperidone 3-6 mg per day was administered, and almost a month later, autonomic instabilities increased and she was diagnosed as having NMS. All the patients would be able to have brain dysfunction, which suggested that such patients may be liable to NMS. In our patients, NMS occurred after the additional administration of oxypertine 10 mg per day or after long time administration of LPZ 5 mg per day. It was suggested that NMS could occur after the administration of low dose and relatively low potential neuroleptics in elderly patients. Our 3 of 5 patients showed the delayed type of NMS, which might be relatively more frequent in senior and presenior patients than in younger patients. In case 3, NMS was induced by the somatic disease (bacterial pneumonia), however in other cases, NMS was not always induced by somatic disease. Our 4 of 5 patients experienced some of the symptoms of NMS--episodic fever, extrapyramidal symptoms and autonomic instabilities--before the onset of NMS. Such symptoms may be "pre-steps" to NMS. Once NMS occurred, the patient's systemic condition tended to deteriorate acutely. Due to the fact that our 2 of 5 patients died, it was suggested that the prognosis of the NMS patients in presenium and senium tends to be much worse. It is important to find the "pre-steps" to NMS and treat them as soon as possible for better prognosis.
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PMID:[A study of neuroleptic malignant syndrome in the presenium and senium]. 974 53

Psychopathological symptoms and cognitive test performance were examined in 34 acute schizophrenic patients. The results of a clusteranalytic approach in order to distinguish groups of patients with different syndromes were disappointing. Three dimensions of negative, hallucinatory-delusional, and disorganised symptoms could be established by factor analysis. The disorganised symptom dimension showed strong and significant relations to mnestic and intellectual impairments of the patients. Hallucinatory-delusional symptoms were related to deficits in tests of visual memory and visual search. Negative symptoms were not related to cognitive impairments of the patients. The results are discussed in respect of other studies reporting correlations of schizophrenic symptoms and cognitive disturbances, and with regard to hypotheses of brain dysfunction in schizophrenia. In future research, consideration of the three main dimensions of schizophrenic symptoms could be useful to reduce the heterogeneity of schizophrenic samples.
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PMID:[Psychopathologic symptoms and cognitive test performance in schizophrenic patients]. 985 Aug 29

Almost all the neurons in the brain are influenced by the excitatory amino acid glutamate. Glutamatergic neurotransmission has been associated functionally with a number of physiological processes and with certain pathophysiological processes, including schizophrenia. Imaging studies provide indirect evidence that glutamate may be involved in schizophrenia. Positron emission tomography scanning has shown a correlation between positive symptoms of schizophrenia and abnormalities of glucose metabolism in components of the limbic system with the highest concentration of glutamate receptors. Studies with ketamine, an anaesthetic that antagonises the N-methyl-D-aspartate (NMDA) glutamate receptor, show an exacerbation or worsening of positive symptoms when this drug is administered to patients with schizophrenia. Regional cerebral blood flow studies with ketamine show that the drug produces increased blood flow in the anterior cingulate cortex, the area where high concentrations of NMDA receptors exist and where alterations in glucose metabolism seem to occur in people with schizophrenia. Diminished glutamatergic neurotransmission in the hippocampal glutamate-mediated efferent pathways and cerebral dysfunction in the hippocampus and its target areas, particularly the anterior cingulate cortex, may underlie some of the clinical manifestations of schizophrenia.
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PMID:Glutamatergic aspects of schizophrenia. 1021 Nov 34


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