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Dual-stream information processing proposes that reasoning is composed of two interacting processes: a fast, intuitive system (Stream 1) and a slower, more logical process (Stream 2). In non-patient controls, divergence of these streams may result in the experience of conflict, modulating decision-making towards Stream 2, and initiating a more thorough examination of the available evidence. In delusional schizophrenia patients, a failure of conflict to modulate decision-making towards Stream 2 may reduce the influence of contradictory evidence, resulting in a failure to correct erroneous beliefs.
Delusional schizophrenia patients and non-patient controls completed a deductive reasoning task requiring logical validity judgments of two-part conditional statements. Half of the statements were characterized by a conflict between logical validity (Stream 2) and content believability (Stream 1).
Patients were significantly worse than controls in determining the logical validity of both conflict and non-conflict conditional statements. This between groups difference was significantly greater for the conflict condition.
The results are consistent with the hypothesis that delusional schizophrenia patients fail to use conflict to modulate towards Stream 2 when the two streams of reasoning arrive at incompatible judgments. This finding provides encouraging preliminary support for the Dual-Stream Modulation Failure model of delusion formation and maintenance.
We sought to explore whether obstetric complications (OCs) are more likely to occur in the presence of familial/genetic susceptibility for schizophrenia or whether they themselves represent an independent environmental risk factor for schizophrenia.
The presence of OCs was assessed through maternal interview on 216 subjects, comprising 36 patients with schizophrenia from multiply affected families, 38 of their unaffected siblings, 31 schizophrenic patients with no family history of psychosis, 51 of their unaffected siblings and 60 normal comparison subjects. We examined the familiality of OCs and whether OCs were commoner in the patient and sibling groups than in the control group.
OCs tended to cluster within families, especially in multiply affected families. Patients with schizophrenia, especially those from multiply affected families, had a significantly higher rate of OCs compared to normal comparison subjects, but there was no evidence for an elevated rate of OCs in unaffected siblings.
Our data provides little evidence for a link between OCs and genetic susceptibility to schizophrenia. If high rates of OCs are related to schizophrenia genes, this relationship is weak and will only be detected by very large sample sizes.
P300 wave anomalies correlate with genetic risk for schizophrenia and constitute a plausible endophenotype for the disease. The COMT gene is thought to influence cognitive performance and to be a susceptibility gene for schizophrenia. Unlike two previous studies, we found no significant influence of the COMT gene on P300 amplitude or latency in 189 individuals examined. The well-supported role of the COMT gene both in dopamine catabolism as well as in prefrontal cognition makes a strong theoretical case for the influence of COMT Val158Met polymorphism on P300 endophenotypes. However, the available neurophysiologic evidence suggests that any such association, if present, must be very subtle.
Prospective longitudinal investigations are needed to identify causal processes leading to schizophrenia. However, there is presently no cost-effective way to identify children who are at risk of developing schizophrenia spectrum disorders.
The present study tested the feasibility of screening community samples to identify children, aged 9-12 years, who experience a triad of putative antecedents of schizophrenia identified in previous research, including: (1) speech and/or motor development lags/problems; (2) social, emotional, or behavioural problems; and (3) psychotic-like-experiences. 3410 children and 796 caregivers completed questionnaires.
12.3% of boys and 8.0% of girls displayed the antecedent triad. Consistent with schizophrenia incidence data, children of African-Caribbean origin presented elevated risk for the antecedent triad relative to white British children. Preliminary results from event-related potential recordings in children presenting the triad (n=14; mean age: 11 years, 4 months; mean IQ: 111) and in control children experiencing none of the antecedents (n=9; mean age: 11 years, 6 months; mean IQ: 109), indicate brain function abnormalities in triad children. The amplitude of the error-related negativity (Ne/ERN) component elicited by erroneous responses to NoGo trials in a Go/NoGo task, relative to correct responses to Go trials, was reduced in children experiencing the triad (controlling for age and IQ). Similar reduction in Ne/ERN in adults with schizophrenia is thought to indicate deficits in patients’ internal monitoring of behaviour.
Questionnaire screening of community samples of children for the putative antecedents of schizophrenia is feasible. Accuracy of identification will be established only by follow-up studies.