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This study addresses the relationship between trait impulsivity and inhibitory control, two features known to be impaired in a number of psychiatric conditions. While impulsivity is often measured using psychometric self-report questionnaires, the inhibition of inappropriate, impulsive motor responses is typically measured using experimental laboratory tasks. It remains unclear, however, whether psychometrically assessed impulsivity and experimentally operationalized inhibitory performance are related to each other. Therefore, we investigated the relationship between these two traits in a large sample using correlative and latent variable analysis. A total of 504 healthy individuals completed the Barratt Impulsiveness Scale (BIS-11) and a battery of four prepotent response inhibition paradigms: the antisaccade, Stroop, stop-signal, and go/no-go tasks. We found significant associations of BIS impulsivity with commission errors on the go/no-go task and directional errors on the antisaccade task, over and above effects of age, gender, and intelligence. Latent variable analysis (a) supported the idea that all four inhibitory measures load on the same underlying construct termed "prepotent response inhibition" and (b) revealed that 12% of variance of the prepotent response inhibition construct could be explained by BIS impulsivity. Overall, the magnitude of associations observed was small, indicating that while a portion of variance in prepotent response inhibition can be explained by psychometric trait impulsivity, the majority of variance remains unexplained. Thus, these findings suggest that prepotent response inhibition paradigms can account for psychometric trait impulsivity only to a limited extent. Implications for studies of patient populations with symptoms of impulsivity are discussed.

The ability to inhibit inappropriate responses and suppress irrelevant information is a core feature of executive control. In this study, we provide a detailed analysis of prepotent response inhibition and interference in patients with schizophrenia. To further test the role of genetic factors and subclinical schizophrenia-like traits, we additionally studied clinically unaffected, first-degree relatives of schizophrenia patients and assessed dimensions of schizotypy in both relatives and healthy controls. Inhibition and interference control were assessed using a battery comprising the antisaccade, Stroop, stop signal, go/no-go, flanker, and Simon tasks. Schizophrenia patients differed from both relatives and controls in making more errors on the antisaccade task and having longer response times on the Stroop task, especially the incongruent condition. Patients also had general, that is, condition independent, increases in reaction times on the go/no-go and flanker tasks and made more errors on the flanker and Simon tasks, suggesting general performance impairments independent of inhibitory demand. Relatives were characterized by hypometric antisaccade amplitude gain despite normal prosaccades, suggesting a selective deficit in non-standard sensorimotor transformations. Schizotypy was correlated with inhibitory performance across a number of tasks in both relatives and controls. Generally, these effects were independent of verbal intelligence levels. Overall, the findings point to rather selective impairments of inhibitory control in the schizophrenia spectrum and confirm a previously observed deficit in antisaccade spatial accuracy as an endophenotype of schizophrenia.

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ObjectiveIn the present study the relationship between behavioural adjustment following cognitive conflict and schizotypy was investigated using a Stroop colour naming paradigm. Previous research has found deficits with behavioural adjustment in schizophrenia patients. Based on these findings, we hypothesized that individual differences in schizotypy, a personality trait reflecting the subclinical expression of the schizophrenia phenotype, would be associated with behavioural adjustment. Additionally, we investigated whether such a relationship would be explained by individual differences in neuroticism, a non-specific measure of negative trait emotionality known to be correlated with schizotypy.Methods106 healthy volunteers (mean age: 25.1, 60% females) took part. Post-conflict adjustment was measured in a computer-based version of the Stroop paradigm. Schizotypy was assessed using the Schizotypal Personality Questionnaire (SPQ) and Neuroticism using the NEO-FFI.ResultsWe found a negative correlation between schizotypy and post-conflict adjustment (r = −.30, p<.01); this relationship remained significant when controlling for effects of neuroticism. Regression analysis revealed that particularly the subscale No Close Friends drove the effect.ConclusionPrevious findings of deficits in cognitive control in schizophrenia patients were extended to the subclinical personality expression of the schizophrenia phenotype and found to be specific to schizotypal traits over and above the effects of negative emotionality.

Converging evidence from pharmacological investigations, genetic association studies and schizophrenia research indicates an important influence of the dopamine system on sensorimotor gating as measured by prepulse inhibition (PPI) of the acoustic startle response. In particular, D2 receptor agonists have been shown to disrupt PPI in humans and rodents. In the present study, we investigated the associations of two functional DRD2 related single nucleotide polymorphisms (rs4648317 and rs1800497, the latter also known as DRD2/ANKK1 Taq1A) with PPI in two independent healthy human samples (overall n=197; Munich n=101; London n=96). Taq1A is a prominent marker of striatal D2 receptor signalling and was therefore hypothesized to impact on PPI. In line with our hypothesis, we report here reduced PPI levels in individuals with higher striatal D2 receptor signalling as indicated by the Taq1A genotype. Meta-analysis across both samples confirmed this finding. In contrast, an association between rs4648317 and PPI found in the Munich sample could not be confirmed in the London sample. Overall, the present study helps to bridge the gap between pharmacological manipulations of PPI and molecular genetics of the dopaminergic system.

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