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The Mechanism of Cortico-Striato-Thalamo-Cortical Neurocircuitry in Response Inhibition and Emotional Responding in Attention Deficit Hyperactivity Disorder with Comorbid Disruptive Behavior Disorder

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Abstract

The neurocircuitries that constitute the cortico-striato-thalamo-cortical (CSTC) circuit provide a framework for bridging gaps between neuroscience and executive function in attention deficit hyperactivity disorder (ADHD), but it has been difficult to identify the mechanisms for regulating emotional problems from the understanding of ADHD comorbidity with disruptive behavior disorders (DBD). Research based on “cool” and “hot” executive functional theory and the dual pathway models, which are thought of as applied response inhibition and delay aversion, respectively, within the neuropsychological view of ADHD, has shed light on emotional responding before and after decontextualized stimuli, while CSTC circuit-related domains have been suggested to explain the different emotional symptoms of ADHD with or without comorbid DBD. This review discusses the role of abnormal connections in each CSTC circuit, especially in the emotion circuit, which may be responsible for targeted executive dysfunction at the neuroscience level. Thus, the two major domains – abstract thinking (cool) and emotional trait (hot) – trigger the mechanism of onset of ADHD.

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Acknowledgements

The authors thank Liqiong Huang for proofreading the final edition. This review was supported by a Project of Shanghai Municipal Health and Family Planning Commission ( 201540114), a Key Specialty Project of Shanghai Municipal Health and Family Planning Commission grant for Child Psychiatry (ZK2015B01) and a Research Project of the Shanghai Changning Health and Family Planning Commission grant (20164Y013).

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Correspondence to Weidong Ji.

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Zhu, Y., Jiang, X. & Ji, W. The Mechanism of Cortico-Striato-Thalamo-Cortical Neurocircuitry in Response Inhibition and Emotional Responding in Attention Deficit Hyperactivity Disorder with Comorbid Disruptive Behavior Disorder. Neurosci. Bull. 34, 566–572 (2018). https://doi.org/10.1007/s12264-018-0214-x

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