Striatal abnormalities and spontaneous dyskinesias in non-clinical psychosis

BackgroundAccumulating evidence suggests that individuals experiencing non-clinical psychosis (NCP) represent a critical group for improving understanding of etiological factors underlying the broader psychosis continuum. Although a wealth of evidence supports widespread neural dysfunction in formal psychosis, there has been little empirical evidence to inform our understanding of putative vulnerability markers or brain structure in NCP. In this study, we examined the neural correlates of spontaneous movement abnormalities, a biomarker previously detected in NCP that is linked to abnormalities in the striatal dopamine.MethodsWe screened a total of 1285 adolescents/young adults, and those scoring in the upper 15th percentile on a NCP scale were invited to participate; 20 of those invited agreed and these individuals were matched with healthy controls. Participants were administered a structural scan, clinical interviews, and an instrumental motor assessment.ResultsThe NCP group showed elevated force variability and smaller putamen (but not caudate), and there was a significant relationship between motor dysfunction and striatal abnormalities for the sample. Elevated force variability was associated with both higher positive and negative symptoms, and there was a strong trend (p = .06) to suggest that smaller left putamen volumes were associated with elevated positive symptoms.ConclusionsThe results are among the first to suggest an association between neural structure and a risk marker in NCP. Findings indicate that vulnerabilities seen in schizophrenia also characterize the lower end of the psychosis spectrum.