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Abnormalities of cortical structures in adolescent-onset conduct disorder

  • Y. Jiang (a1), X. Guo (a1), J. Zhang (a1), J. Gao (a2) (a3) (a4), X. Wang (a1), W. Situ (a5), J. Yi (a1), X. Zhang (a1), X. Zhu (a1) (a6) (a7), S. Yao (a1) (a6) (a7) and B. Huang (a1) (a8) (a9)...

Abstract

Background.

Converging evidence has revealed both functional and structural abnormalities in adolescents with early-onset conduct disorder (EO-CD). The neurological abnormalities underlying EO-CD may be different from that of adolescent-onset conduct disorder (AO-CD) patients. However, the cortical structure in AO-CD patients remains largely unknown. The aim of the present study was to investigate the cortical alterations in AO-CD patients.

Method.

We investigated T1-weighted brain images from AO-CD patients and age-, gender- and intelligence quotient-matched controls. Cortical structures including thickness, folding and surface area were measured using the surface-based morphometric method. Furthermore, we assessed impulsivity and antisocial symptoms using the Barratt Impulsiveness Scale (BIS) and the Antisocial Process Screening Device (APSD).

Results.

Compared with the controls, we found significant cortical thinning in the paralimbic system in AO-CD patients. For the first time, we observed cortical thinning in the precuneus/posterior cingulate cortex (PCC) in AO-CD patients which has not been reported in EO-CD patients. Prominent folding abnormalities were found in the paralimbic structures and frontal cortex while diminished surface areas were shown in the precentral and inferior temporal cortex. Furthermore, cortical thickness of the paralimbic structures was found to be negatively correlated with impulsivity and antisocial behaviors measured by the BIS and APSD, respectively.

Conclusions.

The present study indicates that AO-CD is characterized by cortical structural abnormalities in the paralimbic system, and, in particular, we highlight the potential role of deficient structures including the precuneus and PCC in the etiology of AO-CD.

Copyright

Corresponding author

* Addresses for correspondence: S. Yao, Medical Psychological Institute, the Second Xiangya Hospital of Central South University, no. 139, Middle Renmin Road, Changsha, Hunan 410011, People's Republic of China; B. Huang, Department of Biomedical Engineering, School of Medicine, Shenzhen University, no. 3688, Nanhai Avenue, Shenzhen, Guangdong 518060, People's Republic of China. (Email: shuqiaoyao@163.com) [S.Y.] (Email: huangbs@gmail.com) [B.H.]

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