Original Research ARTICLE

Front. Psychiatry, 09 May 2014 | doi: 10.3389/fpsyt.2014.00050

Dysfunction and dysconnection in cortical–striatal networks during sustained attention: genetic risk for schizophrenia or bipolar disorder and its impact on brain network function

imageVaibhav A. Diwadkar1*, imageNeil Bakshi1†, imageGita Gupta1, imagePatrick Pruitt1†, imageRichard White1 and imageSimon B. Eickhoff2,3
  • 1Department of Psychiatry and Behavioral Neurosciences, Wayne State University, Detroit, MI, USA
  • 2Institute of Clinical Neuroscience and Medical Psychology, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany
  • 3Institute of Neuroscience and Medicine (INM-1), Research Center Jülich, Jülich, Germany

Abnormalities in the brain’s attention network may represent early identifiable neurobiological impairments in individuals at increased risk for schizophrenia or bipolar disorder. Here, we provide evidence of dysfunctional regional and network function in adolescents at higher genetic risk for schizophrenia or bipolar disorder [henceforth higher risk (HGR)]. During fMRI, participants engaged in a sustained attention task with variable demands. The task alternated between attention (120 s), visual control (passive viewing; 120 s), and rest (20 s) epochs. Low and high demand attention conditions were created using the rapid presentation of two- or three-digit numbers. Subjects were required to detect repeated presentation of numbers. We demonstrate that the recruitment of cortical and striatal regions are disordered in HGR: relative to typical controls (TC), HGR showed lower recruitment of the dorsal prefrontal cortex, but higher recruitment of the superior parietal cortex. This imbalance was more dramatic in the basal ganglia. There, a group by task demand interaction was observed, such that increased attention demand led to increased engagement in TC, but disengagement in HGR. These activation studies were complemented by network analyses using dynamic causal modeling. Competing model architectures were assessed across a network of cortical–striatal regions, distinguished at a second level using random-effects Bayesian model selection. In the winning architecture, HGR were characterized by significant reductions in coupling across both frontal–striatal and frontal–parietal pathways. The effective connectivity analyses indicate emergent network dysconnection, consistent with findings in patients with schizophrenia. Emergent patterns of regional dysfunction and dysconnection in cortical–striatal pathways may provide functional biological signatures in the adolescent risk-state for psychiatric illness.

Keywords: attention, brain networks, schizophrenia, bipolar disorder, dynamic causal modeling abstract

Citation: Diwadkar VA, Bakshi N, Gupta G, Pruitt P, White R and Eickhoff SB (2014) Dysfunction and dysconnection in cortical–striatal networks during sustained attention: genetic risk for schizophrenia or bipolar disorder and its impact on brain network function. Front. Psychiatry 5:50. doi: 10.3389/fpsyt.2014.00050

Received: 01 November 2013; Accepted: 28 April 2014;
Published online: 09 May 2014.

Edited by:

André Schmidt, University of Basel, Switzerland

Reviewed by:

Karl Friston, University College London, UK
Paolo Brambilla, University of Udine, Italy

Copyright: © 2014 Diwadkar, Bakshi, Gupta, Pruitt, White and Eickhoff. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Vaibhav A. Diwadkar, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Suite 5B, Tolan Park Medical Building, 3901 Chrysler Drive, Detroit, MI 48201 USA e-mail: vdiwadka@med.wayne.edu

Present address: Neil Bakshi, School of Medicine, University of Michigan, Ann Arbor, MI, USA; Patrick Pruitt, Department of Neuroscience, University of Michigan, Ann Arbor, MI, USA

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