Corrado Sandini1, Elisa Scariati2, Maria Carmela Padula2, Maude Schneider3, Marie Schaer4, Dimitri Van De Ville5, Stephan Eliez6. 1. Developmental Imaging and Psychopathology Laboratory, University of Geneva School of Medicine, Switzerland. Electronic address: corrado.sandini@unige.ch. 2. Developmental Imaging and Psychopathology Laboratory, University of Geneva School of Medicine, Switzerland. 3. Developmental Imaging and Psychopathology Laboratory, University of Geneva School of Medicine, Switzerland; Center for Contextual Psychiatry, Research Group Psychiatry, Department of Neuroscience, KU Leuven, Leuven, Belgium. 4. Developmental Imaging and Psychopathology Laboratory, University of Geneva School of Medicine, Switzerland; Stanford Cognitive and Systems Neuroscience Laboratory, Stanford University School of Medicine, Stanford, California. 5. Department of Radiology and Medical Informatics, University of Geneva, Switzerland; Institute of Bioengineering, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland. 6. Developmental Imaging and Psychopathology Laboratory, University of Geneva School of Medicine, Switzerland; Department of Genetic Medicine and Development, University of Geneva School of Medicine, Switzerland.
Abstract
BACKGROUND: 22q11.2 deletion syndrome (22q11DS) is the third-largest known genetic risk factor for the development of psychosis. Dysconnectivity has consistently been implicated in the physiopathology of psychosis. Structural covariance of cortical morphology is a method of exploring connectivity among brain regions that to date has not been employed in 22q11DS. METHODS: In the present study we employed structural covariance of cortical thickness to explore connectivity alterations in a group of 108 patients with 22q11DS compared with 96 control subjects. We subsequently divided patients into two subgroups of 31 subjects each according to the presence of attenuated psychotic symptoms. FreeSurfer software was used to obtain the mean cortical thickness in 148 brain regions from T1-weighted 3T images. For each population we reconstructed a brain graph using Pearson correlation between the average thickness of each couple of brain regions, which we characterized in terms of mean correlation strength and in terms of network architecture using graph theory. RESULTS: Patients with 22q11DS presented increased mean correlation strength, but there was no difference in global architecture compared with control subjects. However, symptomatic patients presented increased mean correlation strength coupled with increased segregation and decreased integration compared with both control subjects and nonsymptomatic patients. They also presented increased centrality for a cluster of anterior cingulate and dorsomedial prefrontal regions. CONCLUSIONS: These results confirm the importance of cortical dysconnectivity in the physiopathology of psychosis. Moreover they support the significance of aberrant anterior cingulate connectivity.
BACKGROUND: 22q11.2 deletion syndrome (22q11DS) is the third-largest known genetic risk factor for the development of psychosis. Dysconnectivity has consistently been implicated in the physiopathology of psychosis. Structural covariance of cortical morphology is a method of exploring connectivity among brain regions that to date has not been employed in 22q11DS. METHODS: In the present study we employed structural covariance of cortical thickness to explore connectivity alterations in a group of 108 patients with 22q11DS compared with 96 control subjects. We subsequently divided patients into two subgroups of 31 subjects each according to the presence of attenuated psychotic symptoms. FreeSurfer software was used to obtain the mean cortical thickness in 148 brain regions from T1-weighted 3T images. For each population we reconstructed a brain graph using Pearson correlation between the average thickness of each couple of brain regions, which we characterized in terms of mean correlation strength and in terms of network architecture using graph theory. RESULTS:Patients with 22q11DS presented increased mean correlation strength, but there was no difference in global architecture compared with control subjects. However, symptomatic patients presented increased mean correlation strength coupled with increased segregation and decreased integration compared with both control subjects and nonsymptomatic patients. They also presented increased centrality for a cluster of anterior cingulate and dorsomedial prefrontal regions. CONCLUSIONS: These results confirm the importance of cortical dysconnectivity in the physiopathology of psychosis. Moreover they support the significance of aberrant anterior cingulate connectivity.
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