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

Based on a review of the literature, the article deals with the major biological markers of schizophrenia. Recent developments in molecular biology have shown a possible association between schizophrenia and various HLA markers (A1, A2, A9, A10, A28, B27, BW16), and a linkage--in several families--between the disease and some polymorphisms of chromosome 5. On the other hand, chromosome X might also be involved. Neuropathological abnormalities have often been found in the brains of schizophrenics, such as cellular alterations in the basal ganglia and the limbic structures. Investigations by means of CT-scan and Magnetic Resonance Imaging have pointed out an enlargement of cerebral ventricles and/or an atrophy of frontal areas, especially amongst patients with prominent negative symptoms. The dopaminergic hypothesis of schizophrenia reposes on the major following facts: the therapeutic efficiency of neuroleptics (dopaminergic antagonists); a positive correlation between plasma homovanillic acid (metabolite of dopamine) concentration and the severity of schizophrenic illness; a higher density of dopaminergic D2-receptors (revealed by Positron Emission Tomography thanks to specific radioligands), particularly in the striatum; and an abnormal plasmatic growth-hormone response to apomorphine (dopaminergic agonist). Central noradrenergic dysfunctions might also occur in paranoid schizophrenia, as underlined by higher cerebrospinal fluid levels of norepinephrine, and a lack of decrease of plasma 3-methoxy-4-hydroxy-phenylglycol (MHPG, metabolite of norepinephrine) after clonidine (alpha-2-adrenergic agonist) dispensation. Nevertheless, in patients with predominating negative symptoms, this is a trouble in serotoninergic functions which has been suggested. In the field of immunology, some findings such as alteration in lymphocytes populations (T4/T8, CD5), anti-cerebral auto-antibodies, abnormal lymphocytes responses to mitogens, decreased production of interleukin-2, have lead to two main hypotheses: autoimmunity and immunologic incompetence. On the other hand, electrophysiological studies have shown a hypovariability of alpha-rythm on the EEG; a lower amplitude of the component P300 from visual evoked potentials; sleep disorders such as a shorter rapid eye movement sleep latency and a decreased total slow-wave sleep percent; irregular smooth pursuit eyes-movements; an electrodermal response according to either the hyper-responder either the non-responder type. At last, troubles in sensory integration, motor coordination and attention have also been demonstrated. All those many findings outline the heterogeneity of schizophrenic disorders.
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PMID:[Biological markers in schizophrenia]. 830 20

Schizophrenia is characterized by a variety of cognitive dysfunctions. Information-processing dysfunctions differ between clinical subtypes such that nonparanoid schizophrenia patients attend less than paranoid schizophrenia patients to connotative or contextual aspects of stimuli. The positive and negative symptom dimensions are also associated with distinct cognitive deficits. In general, positive symptoms are related to auditory-processing deficits and negative symptoms to visual/motor dysfunctions. The interaction of frontal and septohippocampal brain systems, and failures of information-processing automaticity and self-monitoring, have been proposed as the bases of positive symptoms. Negative symptoms are thought to arise from abnormalities in the complex interactions of frontal and striatal systems. Recent theoretical analyses have recommended a focus on the cognitive and neuropsychological analysis of specific symptoms (e.g., hallucinations and delusions) instead of on the more heterogeneous symptom clusters or dimensions. Studies of specific symptoms indicate that patients with hallucinations have deficits in discriminating the source of information. Delusions have been related to abnormal inference processes as well as abnormal perceptual experiences. Studies should now examine the links between information-processing abnormalities and symptoms over time, as the latter change, within the framework of explicit, disconfirmable theoretical models.
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PMID:Relations of symptoms to cognitive deficits in schizophrenia. 832 33

The production of association word to stimulus words, which was found to be correlated with conceptual disorganization, as clinically measured by the Brief Psychiatric Rating Scale, was developed as a quantifiable measure of formal thought disorder. Associative word production in patients with affective psychoses (acute episodes of mania or schizoaffective disorder) was found to be higher in a statistically significant manner than in patients with acute episode of paranoid schizophrenia. The production of associative words in the two groups of acutely psychotic patients was significantly higher than in normal subjects, unipolar depressed, or residual schizophrenic patients. These quantitative differences reflected qualitative differences in the pattern of the production of word associations. Indeed, while patients with paranoid schizophrenia showed a sinusoidal-like type of oscillation in associative word production, patients with affective psychoses were characterized by exponential-like phases in associative word production. Associative word production may thus serve as a simple quantitative test for differentiating formal thought disorder in acute psychoses between patients with mania and patients with schizophrenia.
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PMID:Word associative production in affective versus schizophrenic psychoses. 871 Oct 78

This study assesses the different approaches to treating patients with schizoaffective and paranoid schizophrenia in remission. Individualized treatment of 220 outpatient schizophrenia patients was conducted for 4 years. The choice of treatment was based on the course of the disease and the frequency of relapses. The influence of changes in treatment on the patterns of relapses is presented. The results of this prospective followup open study were evaluated by comparing data received during our research with data from the two preceding 4-year periods and with data from the control group. Compared with routine methods, special treatment tactics led to a significantly decreased frequency of relapses in patients with frequent relapses (p < 0.001). In patients with rare relapses, full cessation of treatment did not lead to increasing mean frequency of relapses. Treatment in remission should be based on the peculiarities of the course of disease, specifically, frequency of relapses, type of schizophrenia, and presence or absence of positive psychopathological signs in remission.
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PMID:Maintenance medication for schizophrenia and schizoaffective patients. 874 95

Monoamine oxidases (MAO) A and B, which are encoded by two distinct genes located on the human X chromosome, are both involved in the oxidative metabolism of dopamine. Decreased levels of platelet MAO-B activity has been reported in patients with schizophrenia and genetic variation in MAO activity had been proposed as a significant factor in the etiology of this disease. We carried out an association study using two intragenic polymorphisms within the MAO-A and MAO-B genes in 110 schizophrenic patients and 87 control subjects. For each polymorphic marker, no significant difference in allelic frequencies was observed between patients and controls. Nevertheless, a trend toward an association between allele 1 of the MAO-B gene and paranoid schizophrenia was found. Our results do not support the hypothesis that inherited variants of MAO genes might play a major role in a genetic predisposition to schizophrenia. Since several previous reports found a low MAO-B platelet activity in patients with paranoid schizophrenia, the identification of polymorphisms related to enzyme activity would be useful.
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PMID:Association study between schizophrenia and monoamine oxidase A and B DNA polymorphisms. 880 32

Different conditions of magical thinking have been analyzed. A formation of the proportion "realistic thinking - magical thinking" in paranoid schizophrenia has been discussed and the characteristic features of magical thinking in schizophrenia have been indicated.
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PMID:[Magical thinking in healthy people and in schizophrenia]. 884 7

In the light of the heterogeneous literature on disturbances of body image in schizophrenic patients, we examined body schema, body concept and body cathexis, their changes during hospital treatment and their correlations with psychopathology in 38 patients with acute paranoid schizophrenia. The image-marking method according to Askevold, the Body Distortion Questionnaire, a visual-analogue scale on body cathexis and psychopathometric scales were applied. Body schema was also investigated in 27 healthy controls. On average, patients underestimated the size of their lower extremities, indicating a centralized body schema. They accurately assessed proximal fixed points. Underestimation was significantly correlated with anxiety, overestimation with grandiosity. Body schema and body concept were relatively independent from each other and from body hallucinations. Disturbances of body perception were reduced significantly, but not completely, during the time from admission to discharge. The results confirm and clarify some findings in the literature on a distorted perception of body size and support theories on body perception in schizophrenia.
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PMID:[Body image of patients with acute paranoid schizophrenia. A follow-up study]. 892

Previous research has suggested that schizophrenics exposed to influenza in the second trimester have more delusions of jealousy, delusions of reference and suspiciousness. We therefore hypothesised that the risk-increasing effect of in utero exposure to influenza would be particularly demonstrable in paranoid schizophrenia. We studied patients with an ICD diagnosis of schizophrenia in England and Wales who were born each month between 1923 and 1965 (N = 17,247. Chi-square test for trend showed that an increase in influenza exposure level during the fifth month of gestation was accompanied by an increase in the proportion of patients with paranoid schizophrenia. However, logistic regression analysis including sex, seasonality and birth period in the model resulted in the loss of any significant association between in utero exposure to influenza and the development of paranoid schizophrenia, the loss of this significance being mainly accounted for by birth period. Therefore, the association in utero exposure to influenza and subsequent development of paranoid schizophrenia we hypothesised was not supported by our data.
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PMID:Maternal exposure to influenza and paranoid schizophrenia. 932 42

During stages of remission, patients with paranoid schizophrenia seldom show severe attentional or information-processing dysfunctions, except in cases of long-term chronicity. The diagnostic specificity of four putative psychological vulnerability indicators of schizophrenia - the Span of Apprehension, the degraded stimulus Continuous Performance Test (dsCPT), the degraded stimulus visual backward masking task and the Wisconsin Card Sorting Test (WCST) - was examined in a group of patients with paranoid schizophrenia. Since no single test seems to identify all patients, the use of a combination of measures may be a useful strategy. Accordingly, the four tests were administered to 18 paranoid schizophrenic patients, 18 depressed patients and 18 normal subjects. Paranoid schizophrenic patients could be distinguished from normal subjects primarily on the basis of their performance on the backward masking task and secondarily by the dsCPT and the WCST. Paranoid schizophrenic and depressed patients could be differentiated to some extent by their performance on an information-mask condition of the backward masking task. Thus, of the four measures studied, only the degraded stimulus backward masking appeared to be a specific indicator of paranoid schizophrenia.
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PMID:Paranoid schizophrenia: non-specificity of neuropsychological vulnerability markers. 933 1

80 patients aged 14-60 years with progredient paranoid schizophrenia which began alcohol abuse after the first attack of the disease were observed. The peculiarities of both clinical manifestations and course of alcoholism and schizophrenia were analysed in age aspect. The patients were divided into 3 groups according to age: 14-20, 21-40 and 41-60 years. It was established that alcohol abuse in schizophrenia does not cause any further increase of alcoholic symptomatology and had not the phased development as in alcoholism, i.e. alcohol abuse does not cause typical alcoholic disease. Alcoholism, which is symptomatic in schizophrenic patients, can change, however, the clinical picture of psychosis. It can cause atypical and soft course of the disease or, on the contrary, development of decompensation in remission and increase of psychic defect.
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PMID:[Symptomatic alcoholism and remissions in schizophrenia in light of a 20-year catamnesis]. 941 May 98


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