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)

103 patients were admitted for the first time to the psychiatric hospital (Institute of Psychiatry and Neurology in Warsaw) between 1976-1983 and received a research diagnosis of schizophrenia (in accordance with the ICD-9 criteria). The course and clinical pattern of the illness were analyzed at a follow-up in 65 patients-rehospitalized in the 5th year from their first admission and in 10 patients not rehospitalized during catamnestic period. As regards the clinical pattern analysis, it was focussed on negative symptoms occurrence, as assessed using the Andreasen Scales (SANS). The quality of remission was evaluated. The data obtained from the case reports were statistically tested and the results were presented in the tables according to the research questions. The occurrence of negative symptoms (affective blunting, alogia, apathy, anhedonia, attention) at first hospitalization had no relation to the quality of the remission at the five-year follow-up.
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PMID:[Negative symptoms with relation to the remission in the early stage of schizophrenic psychosis]. 954 86

Anhedonia and psychomotor slowing in schizophrenia have been attributed to a dysfunction of dopaminergic neurotransmission. To differentiate between disease and drug-induced negative symptoms, we examined eight drug-free and eight neuroleptic-treated schizophrenic patients. Positive and negative symptoms and extrapyramidal side effects were assessed using standardized rating scales (PSAS, AMDP, SANS). 'Reaction time' and 'motor speed' were measured using a computer-aided system and striatal dopamine D2/D3 receptor availability was assessed using [I-123]IBZM SPECT. Psychomotor reaction time, parkinsonism, affective flattening and avolition were increased in treated patients relative to the untreated cohort and were negatively correlated with dopamine D2/D3 receptor availability. Significant positive correlations were found between parkinsonism and affective flattening and between psychomotor slowing and avolition. Positive symptoms were not significantly associated with striatal IBZM binding. These findings support the hypothesis that neuroleptic-induced dopamine D2/D3 blockade in the striatum can mimic certain negative symptoms, such as affective flattening and avolition, and indicates that psychomotor testing may be helpful in differentiating between disease and drug-induced negative symptoms.
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PMID:Psychomotor slowing, negative symptoms and dopamine receptor availability--an IBZM SPECT study in neuroleptic-treated and drug-free schizophrenic patients. 963 33

In neuropsychological vulnerability research the visual backward masking task, the Span of Apprehension, the degraded stimulus Continuous Performance Test (dsCPT), and the Wisconsin Card Sorting Test have been described as putative indicators for the predisposition to develop negative (schizophrenic) symptoms. The present study assesses the stability of the association between neuropsychological tests and negative symptoms by examining clinically improved patients. The interdependence between the four cognitive measures and clinical symptomatology was examined in 31 patients with DSM III-R and ICD-10 schizophrenia suffering predominantly from negative symptoms. Backward masking performance was related to affective flattening and anxiety-depression. False alarm rate on dsCPT was associated positively with affective flattening and hallucinations, and negatively with avolition. Card sorting preseverative errors correlated negatively with anhedonia, non-preservative errors correlated positively with avolition. Correlations notwithstanding, the data provide evidence in support of the relative independence of neuropsychological functions and negative symptoms in clinically improved schizophrenics.
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PMID:Relations between neuropsychological vulnerability markers and negative symptoms in schizophrenia. 969 61

This study examines the relationship between anhedonia and the trait dimensions of positive affect (PA) and negative affect (NA) in schizophrenia. The relationship between poor social functioning in schizophrenia and these individual differences in affectivity is also examined. Schizophrenia outpatients (n = 37) and normal controls (n = 15) were assessed at a baseline evaluation and again approximately 90 days later. Consistent with the hypothesized decrease in hedonic capacity in schizophrenia, patients reported significantly greater physical and social anhedonia and less PA than controls. However, the schizophrenia group also reported significantly greater NA and social anxiety than did controls. In support of the dispositional view of these individual differences in affectivity, trait measures demonstrated test-retest reliability, and group differences between the schizophrenia group and controls were stable over the 90-day followup period. Within the schizophrenia group, physical and social anhedonia were comparably negatively correlated with trait PA; however, social but not physical anhedonia was significantly positively correlated with NA and social anxiety. Poor social functioning in the schizophrenia group was associated with greater physical and social anhedonia and greater NA and social anxiety. Alternatively, greater trait PA was related to better social functioning. These findings indicate that schizophrenia is characterized by both low PA and elevated NA and that these affective characteristics are a stable feature of the illness. The results also suggest important links between affect and social functioning in schizophrenia.
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PMID:Anhedonia, positive and negative affect, and social functioning in schizophrenia. 971 33

The objective of this study was to study the relationship of poor functioning, cognition, and psychopathology in bipolar mood disorder. The authors assessed 36 patients with bipolar mood disorder (23 VA, 13 community) for the presence of psychopathology, cognitive deficits, and psychosocial impairment. The authors assessed psychopathology using screening and follow-up questions based on the schedule for affective disorder and schizophrenia, lifetime version (SADS-L), schedule for the assessment for negative symptoms (SANS), and schedule for the assessment of positive symptoms (SAPS), and psychosensory features using the "Profile of Psychomotor Symptoms." They tested cognitive functioning in the following domains: 1) general intelligence and language, 2) verbal and visual memory, and 3) visuospatial functioning. They also assessed psychosocial functioning using a structured scale to assess maladjustment and an impairment rating scale. Patients with bipolar disorder showed significant impairment compared to age equivalent normals in several cognitive domains. Anhedonia was related to memory deficits. Memory deficits were also associated with poor psychosocial functioning. This study demonstrates that nondemented, asymptomatic patients with bipolar disorder exhibit substantial cognitive deficits that are associated with poor functioning, and anhedonia and avolition best predict this outcome.
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PMID:Cognitive deficits, psychopathology, and psychosocial functioning in bipolar mood disorder. 974 10

College undergraduates (n = 34) identified by deviant scores (at least 1.96 SD above the mean) on the Revised Social Anhedonia (SocAnh) Scale (M. Eckblad, L. J. Chapman, J. P. Chapman, & M. Mishlove, 1982) were compared with control participants (n = 139) at an initial assessment and at a 10-year follow-up evaluation. Twenty-four percent of the SocAnh group were diagnosed with schizophrenia-spectrum disorders at the follow-up compared with only 1% of the control group, despite the fact that there had been no such difference between the groups at the initial assessment 10 years earlier. The SocAnh group exceeded the control group on severity of psychotic-like experiences and had poorer overall adjustment at the follow-up but not at the initial assessment. The groups did not differ on mood symptoms or substance-use disorders. Thus, the SocAnh Scale, unlike the Perceptual Aberration and Magical Ideation Scales, appears to identify individuals at specific risk for future development of schizophrenia-spectrum disorders.
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PMID:Social anhedonia as a predictor of the development of schizophrenia-spectrum disorders. 983 Feb 43

Individuals who scored high on Perceptual Aberration-Magical Ideation Scales (Per-Mag; n = 90), the Social Anhedonia Scale (SocAnh; n = 39), and control participants (n = 89) were administered saccadic refixation (prosaccade) and saccadic suppression (antisaccade) tasks. Eye movements were scored in terms of error rates and latency. None of the groups differed in terms of their performance on the prosaccade task. Both the Per-Mag (p < 0.01) and SocAnh (p < 0.05) groups exceeded the controls in terms of mean antisaccade errors. The high-risk groups did not differ from each other. Eighteen of the Per-Mag individuals and 10 of the SocAnh individuals displayed deviant antisaccade performance. These findings are particularly interesting in light of suggestive evidence that antisaccade task deficits may serve as a marker of susceptibility to schizophrenia. It is hypothesized that the individuals who scored aberrantly on the Chapman scales and displayed antisaccade performance deficits are most likely to be at risk for the development of psychosis.
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PMID:Antisaccade task performance in questionnaire-identified schizotypes. 998 52

Recent brain imaging studies suggest that schizophrenia may be related to abnormally high amphetamine-induced dopamine release. It is known that repeated use of amphetamine may cause paranoid psychosis and persisting stereotypies. The biochemical background for these signs and symptoms has not been clarified. In this study, positron emission tomography and [11C]raclopride were used to determine central D2-dopamine receptor density (Bmax) and apparent affinity (K(D)app) in Cynomolgus monkeys before and after 14 days of treatment with d-amphetamine sulphate (2 mg/kg/day; s.c.). One day after withdrawal from amphetamine, K(D)app was increased, suggesting [11C]raclopride competition with elevated concentration of dopamine. At 7 and 14 days after withdrawal, there was a 19-26% decrease in Bmax but no change in K(D)app as compared to baseline. Although this study was performed on two monkeys only, there was thus no support for the view that chronic intermittent hyperactivity of the dopamine system may be related to an upregulation of striatal D2-dopamine receptors. Repeated administration of amphetamine may, rather, cause a long-lasting downregulation of the D2-receptor density, which may be a neurochemical correlate to the abnormal movements, anhedonia, anxiety, and depression seen in psychostimulant abusers.
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PMID:Changes in striatal D2-receptor density following chronic treatment with amphetamine as assessed with PET in nonhuman primates. 1002 13

Previous studies have shown that anhedonia characterizes the deficit syndrome of schizophrenia. Anhedonia is also one of the main symptoms of the depressive state. The purpose of this study was to examine the relationships between anhedonia and depression in the deficit syndrome of schizophrenia. Self-evaluations of anhedonia and depression were performed by three groups of subjects (32 deficit schizophrenics, 32 major depressives, 35 healthy subjects) matched for sociodemographic variables. Deficit schizophrenics and major depressives are more anhedonic than controls, but there is no difference between the two study groups. Contrarily to what is evidenced for major depressives and for healthy subjects, the depressive symptomatology correlates with anhedonia in deficit schizophrenics. When deficit schizophrenics are dichotomized into depressed versus non-depressed patients, no difference is observed concerning anhedonia. These results suggest that anhedonia in the deficit syndrome of schizophrenia has no specificity but appears independent of coexisting depression and covaries with several characteristics of depression (retardation, cognitive distortions). Our results support the hypothesis that the deficit syndrome of schizophrenia could constitute a non-depressive mood disorder.
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PMID:Anhedonia in the deficit syndrome of schizophrenia. 1036 31

The dopaminergic reward system is activated by primary rewarding factors such as food, sexual activity and parental care. Its activation enhances the occurrence of behaviors which induced the stimulation of dopaminergic neurotransmission. Indications of a dysfunction of the dopaminergic reward system are found in major depression, schizophrenia, and addictive disorders. It has been hypothesized that dysfunction of the dopaminergic reward system is associated with anhedonia, the inability to experience pleasure. However, animal studies indicate that a reduction of central dopaminergic neurotransmission is associated with a decrease in incentive salience of reward-indicating stimuli and not with anhedonia per se. Sensitization of dopaminergic neurotransmission, on the other hand, seems to induce cue-dependent craving in addicted patients. In schizophrenia, phasic, stimulus-dependent dopamine release in the striatum may play a role in the abnormal attribution of salience to previously neutral stimuli.
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PMID:[Anhedonia--a general nosology surmounting correlate of a dysfunctional dopaminergic reward system?]. 1040 34


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