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© The Author(s) 2018. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. Introduction: Schizophrenia and schizotypal personality disorder (SPD) lie on a single spectrum of mental illness and converging evidence suggests similarities in the etiology of the 2 conditions. However, schizotypy is a heterogeneous facet of personality in the healthy population and so may be seen as a bridge between health and mental illness. Neural evidence for such a continuity would have implications for the characterization and treatment of schizophrenia. Based on our previous work identifying a relationship between symptomology in schizophrenia and abnormal movement-induced electrophysiological response (the post-movement beta rebound [PMBR]), we predicted that if subclinical schizotypy arises from similar neural mechanisms to schizophrenia, schizotypy in healthy individuals would be associated with reduced PMBR. Methods: One-hundred sixteen participants completed a visuomotor task while their neural activity was recorded by magnetoencephalography. Partial correlations were computed between a measure of PMBR extracted from left primary motor cortex and scores on the Schizotypal Personality Questionnaire (SPQ), a self-report measure of schizotypal personality. Correlations between PMBR and SPQ factor scores measuring cognitive-perceptual, interpersonal and disorganization dimensions of schizotypy were also computed. Effects of site, age, and sex were controlled for. Results: We found a significant negative correlation between total SPQ score and PMBR. This was most strongly mediated by variance shared between interpersonal and disorganization factor scores. Conclusion: These findings indicate a continuum of neural deficit between schizotypy and schizophrenia, with diminution of PMBR, previously reported in schizophrenia, also measurable in individuals with schizotypal features, particularly disorganization and impaired interpersonal relations.

Background: In patients with schizophrenia, distributed abnormalities are observed in grey matter volume. A recent hypothesis posits that these distributed changes are indicative of a plastic reorganization process occurring in response to a functional defect in neuronal information transmission. We investigated the structural covariance across various brain regions in early-stage schizophrenia to determine if indeed the observed patterns of volumetric loss conform to a coordinated pattern of structural reorganization.Methods: Structural MRI scans were obtained from 40 healthy adults and 41 age, gender and parental socioeconomic status matched patients with schizophrenia. Volumes of grey matter tissue was estimated at regional level across 90 atlas-based parcellations. Group level structural covariance was studied using a graph theoretical framework.Results: Patients had distributed reduction in grey matter volume, with high degree of localized covariance (clustering) compared to controls. Patients with schizophrenia had reduced centrality of anterior cingulate and insula but increased centrality of the fusiform cortex, compared to controls. Simulating targeted removal of highly central nodes resulted in significant loss of the overall covariance patterns in patients compared to controls. Conclusion: Regional volumetric deficits in schizophrenia are not a result of random, mutually independent processes. Our observations support the occurrence of a spatially interconnected reorganization with systematic de-escalation of conventional ‘hub’ regions. This raises the question of whether the morphological architecture in schizophrenia is primed for compensatory functions, albeit with a high risk of inefficiency.