Neural Anomalies During Vigilance in Schizophrenia: Diagnostic Specificities and Genetic Associations

Thumbnail Image

Persistent link to this item

View Statistics

Journal Title

Journal ISSN

Volume Title


Neural Anomalies During Vigilance in Schizophrenia: Diagnostic Specificities and Genetic Associations

Published Date




Thesis or Dissertation


Impaired vigilance is a core cognitive deficit in schizophrenia and may serve as an endophenotype (i.e., mark genetic liability). We used a continuous performance task with perceptually degraded stimuli in schizophrenia patients (N=48), bipolar disorder patients (N=26), first-degree biological relatives of schizophrenia patients (N=55) and bipolar disorder patients (N =28), as well as healthy controls (N=68) to clarify whether previously reported vigilance deficits and abnormal neural functions were indicative of genetic liability for schizophrenia as opposed to a generalized liability for severe psychopathology. We also examined variation in the Catechol-O-methyltransferase gene to evaluate whether brain responses were related to genetic variation associated with higher-order cognition. Relatives of schizophrenia patients had an increased rate of misidentification of nontarget stimuli as targets when they were perceptually similar, suggestive of difficulties with contour perception. Larger early visual responses (i.e., N1) were associated with better task performance in patients with schizophrenia consistent with enhanced N1 responses reflecting beneficial neural compensation. Additionally, reduced N2 augmentation to target stimuli was specific to schizophrenia. Both patients with schizophrenia and first-degree relatives displayed reduced late cognitive responses (P3b) that predicted worse performance. First-degree relatives of bipolar patients exhibited performance deficits, and displayed aberrant neural responses that were milder than individuals with liability for schizophrenia and dependent on sex. Variation in the Catechol-O-methyltransferase gene was differentially associated with P3b in schizophrenia and bipolar groups. Poor vigilance in schizophrenia is specifically predicted by a failure to enhance early visual responses, weak augmentation of mid-latency brain responses to targets, and limited engagement of late cognitive responses that may be tied to genetic variation associated with prefrontal dopaminergic availability. Experimental results illustrate specific neural functions that distinguish schizophrenia from bipolar disorder and provides evidence for a putative endophenotype that differentiates genetic liability for schizophrenia from severe mental illness more broadly.


University of Minnesota M.A. thesis. October 2020. Major: Psychology. Advisors: Scott Sponeim, Monica Luciana. 1 computer file (PDF); iv, 44 pages.

Related to



Series/Report Number

Funding information

Isbn identifier

Doi identifier

Previously Published Citation

Suggested citation

Klein, Samuel. (2020). Neural Anomalies During Vigilance in Schizophrenia: Diagnostic Specificities and Genetic Associations. Retrieved from the University Digital Conservancy,

Content distributed via the University Digital Conservancy may be subject to additional license and use restrictions applied by the depositor. By using these files, users agree to the Terms of Use. Materials in the UDC may contain content that is disturbing and/or harmful. For more information, please see our statement on harmful content in digital repositories.