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

The search for morphological clues to the etiology of schizophrenia has led to widespread application of computed tomography (CT) scans in the examination of patients. These investigations have resulted in numerous reports over the past several years of brain atrophy and increased ventricle-brain ratios (VBR), suggestive of neuronal tissue damage, associated with the disorder. Altered activity of cellular antioxidant systems have been implicated in the neuronal cell loss that is associated with degenerative diseases of the central nervous system (CNS), but this phenomenon has not been investigated with respect to functional disorders like schizophrenia. A search for such a relationship in schizophrenics with evidence of brain atrophy has been initiated by measuring the activity of the important antioxidant enzyme glutathione peroxidase (GPx) in blood samples from a population of chronic schizophrenics and age- and sex-matched nonschizophrenic mental patients as controls. A strong negative correlation has been found between GPx activity in both isolated platelets and erythrocytes and CT scan measures of brain atrophy and VBR in the schizophrenics, but not in the control population, which exhibited comparable CT scan abnormalities. These observations suggest a unique relationship of GPx to the mechanism of tissue damage in the schizophrenics.
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PMID:Glutathione peroxidase and CT scan abnormalities in schizophrenia. 366 87

The development of and the results from a prospective longitudinal study of children of schizophrenic mothers are presented. The presented studies have been guided by a diathesis-stress model of psychopathology and data analyses relied on the paradigm that schizophrenics and schizotypes share genetic liability to schizophrenia, but that the former, in addition, suffer from environmental insult. This paradigm, hypothetically formulated by Paul Meehl (21) proved especially fruitful in the etiological inferences made in this study. The results indicate that schizophrenia is, to some degree, genetically transmitted and that schizotypes share this genetic vulnerability with schizophrenics. Schizophrenia may be conceptualized as an environmentally complicated schizotypal personality disorder. Deleterious environmental influences identified in this study are obstetric complications probably resulting in central brain atrophy as measured by the CT-scans. In addition, future schizophrenics experienced disrupted childhood conditions as measured here by the amount of institutional rearing during the first five years of life. Fathers of the high risk children were more frequently mentally disturbed than fathers of the low risk children. The presence of a schizophrenia spectrum disorder in the father significantly increased a risk for such disorder in the high risk offspring. Continuity of psychopathological deviance in the form of subtle formal thought disorder and defective emotional contact was demonstrated for the schizophrenics and schizotypes from childhood into adulthood. This suggests that such symptoms are central to schizophrenic psychopathology and that schizophrenia is a development and not a disease which affects people without forewarning.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risk factors in the development of schizophrenia: contributions from a study of children of schizophrenic mothers. 372 Mar 63

Recent evidence suggests that cerebral atrophy with cognitive deficits is associated with negative schizophrenic symptoms, including poverty of speech and speech content. This report investigates the relationship between specific measures of neuropsychological dysfunction and four major indices of associative thought disorder in schizophrenia, to ascertain whether neuropsychologically impaired schizophrenics show more associative disturbance than neuropsychologically intact schizophrenics. Twenty neuropsychologically intact and 12 impaired schizophrenics, rigorously diagnosed by the Research Diagnostic Criteria, were administered the Luria-Nebraska Neuropsychological Battery. These two groups of schizophrenics were compared on a continuous word-association test, which included two nonverbal and two verbal measures of associative disturbance. The neuropsychologically impaired schizophrenics had slower reaction times (p less than .05), but did not differ from the neuropsychologically intact schizophrenics on the verbal measures. Results indicated a stronger relationship between neuropsychological functions and the nonverbal dimensions (p less than .02), than with the verbal measures. This challenges the assumption that a left hemisphere abnormality in schizophrenia is particularly associated with cognitive disturbance, and suggests that neuropsychologically impaired schizophrenics may show greater potential for negative schizophrenic symptoms.
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PMID:Neuropsychological dysfunction in schizophrenia. Relation to associative thought disorder. 399 19

The study population consisted of 1010 in patients and 81 control subjects. Patients suffering from schizophrenia, cerebral atrophy of unknown origin, dementia, depression, mental retardation, and ethanol-induced brain deterioration (alcoholics) were skin tested with 25 micrograms of S-100 protein and neuron-specific enolase isolated from fresh human brain. Evaluation of delayed skin hypersensitivity reactions at 24 hr revealed a high incidence of positive responses to S-100 protein: heavy alcoholism, 96.8%; depression, 94.1%; cerebral atrophy, 92.6%; dementia, 91.2%; schizophrenia, 87.7%; and mental retardation, 69.4%. The incidence of positive reactions to neuron-specific enolase in schizophrenics was 91.6%. Of 58 control subjects tested with S-100 protein, 6.8% were positive, whereas of 23 normal individuals tested with neuron-specific enolase, 6.4% developed mild skin reactions. These data suggest a close relationship between delayed hypersensitivity to neural tissue antigens and immunopsychiatric diseases, and they imply that cell-mediated immune mechanisms are involved in the pathogenesis of certain mental disorders.
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PMID:Neural tissue hypersensitivity in psychiatric disorders with immunologic features. 400 35

The clinical presentation of three patients with meningiomas at different frontal sites is described. They had been ill for 3, 25, and 43 years before the tumour was demonstrated radiologically. Apathy, incontinence, dementia, and fits were seen in association with middle and superior frontal lesions, and may be mistaken for symptoms of involutional depression or presenile cerebral atrophy. In contrast, excitement and hallucinosis were seen in association with a basal frontal lesion, and may mimic psychotic syndromes like hypomania and schizophrenia, particularly if the tumour encroaches on the third ventricle and adjacent structures. Irreversible loss of myelin and axons in the frontal areas of brain surrounding the tumour may have contributed to the clinical picture of the syndrome shown by these patients.
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PMID:Three cases of frontal meningiomas presenting psychiatrically. 496 22

We studied, in a "blind" and quantitative fashion, the density of cerebellar Purkinje cells in 17 adult cases of Huntington's disease (HD), 17 patients with other movement disorders, 17 with schizophrenia, and 23 normal controls. There was a highly significant reduction in Purkinje cell density in HD compared with any of the other three groups. A much smaller difference in neuronal density between patients with other movement disorders and normal controls was barely significant. Eight of the 17 HD patients and only 1 of the other 57 subjects had Purkinje cell density less than 50% of the mean for the normal controls. The low density of Purkinje cells in HD could not be attributed to aging, seizures, or cause of death, nor was it merely a part of a generalized brain atrophy. The loss of large Purkinje cells suggests that the neuronal loss in HD may not be restricted to small and medium-size neurons.
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PMID:Reduced Purkinje cell density in Huntington's disease. 620 75

Recently, increased brain and spinal fluid (CSF) norepinephrine (NE), and a decreased cAMP response to prostaglandin E1 (PgE1) stimulation of platelet NE sensitive adenylcyclase were observed in some schizophrenic patients. Low CSF dopamine-beta-hydroxylase (DBH) activity was related to brain atrophy, whereas high plasma DBH was associated with tardive dyskinesia. Increased NE (in brain and CSF) and 3-methoxy-4-hydroxy-phenylglycol (MHPG) levels and decreased plasma DBH activity in the brain were associated with a diagnosis of paranoid schizophrenia. Impaired NE transmission in schizophrenia may relate to disturbances in the autonomic nervous system, deficits in attention and information processing and to an impaired ability to deal with stress. Although pharmacological studies have suggested a major role for dopamine (DA) in schizophrenic psychosis, this review indicates the need for further exploration of the NE system. Future studies should address the relationship with DA, the autonomic nervous system (ANS), cerebral blood flow, brain metabolism, stress response, negative and prodromal symptoms.
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PMID:Impaired noradrenergic transmission in schizophrenia? 632 3

Psychiatric patients (208 with cerebral atrophy, 46 with dementia, 82 with depression and 481 with schizophrenia) with control subjects (56 normal individuals and patients with neurosis) were skin-tested with human S-100 brain protein, soluble fraction from the brain and liver protein. The local Arthus and delayed hypersensitivity reactions were read at 4-6 hr and at 24 hr respectively. The great majority of tested psychiatric patients developed positive Arthus and delayed skin reactions to S-100 protein and soluble brain protein fraction. A small number of control subjects responded to those antigens. The results obtained suggest that there is a correlation between local cutaneous sensitivity to neurotissue antigens and psychiatric diseases, and that both humoral and cell-mediated immunity are involved in the pathogenesis and development of cerebral atrophy, dementia, depression and schizophrenia.
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PMID:Schizophrenia and other psychiatric diseases: evidence for neurotissue hypersensitivity. 644 13

Focal microdegenerative changes in the nuclei of the ansa peduncularis and the septum pellucidum are present in most cases of presenile and senile dementia, Parkinson's disease and schizophrenia (7,8). These nuclei interconnect and have extensive synaptic connections with the areas of the brain recently shown to contain non-cytopathic reovirus antigen and reovirus-like particles in the normal adult (9,10). The reovirus-involved regions closely approximate the overall pattern of the topography of brain atrophy in Alzheimer's dementia and Parkinson's disease. Mechanisms are suggested whereby mutant defective reovirus present in all adult human brains is responsible or related to the major forms of chronic mental illness including the common types of dementia and schizophrenia.
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PMID:Reovirus and the pathogenesis of some forms of chronic mental illness. 704 35

To confirm and extend previous observations concerning the correlation between cell-mediated immunity and psychiatric diseases, 511 patients with schizophrenia, cerebral atrophy, dementia, and mental retardation, and 32 control subjects and 27 control patients were skin-tested with human brain S-100 protein and human liver protein: 70.2-93.1% of tested psychiatric patients developed positive skin hypersensitivity reactions to S-100 protein, while 2.8-20.7% of patients reacted to liver protein. Of control subjects, 6.2-7.4% responded to S-100 protein, and 7.4-9.4% to liver protein. The findings indicate that cell-mediated immune processes may be involved in brain mechanisms underlying cerebral atrophy, depression, dementia, schizophrenia, and mental retardation.
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PMID:Delayed skin hypersensitivity reactions to human brain S-100 protein in psychiatric patients. 710 20


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