@article{ref1,
title="Impulsive aggression and response inhibition in attention-deficit/hyperactivity disorder and disruptive behavioral disorders: findings from a systematic review",
journal="Neuroscience and biobehavioral reviews",
year="2018",
author="Puiu, Andrei A. and Wudarczyk, Olga and Goerlich, Katharina S. and Votinov, Mikhail and Konrad, Kerstin and Turetsky, Bruce and Herpertz-Dahlmann, Beate",
volume="90",
number="",
pages="231-246",
abstract="BACKGROUND: Although impulsive aggression (IA) and dysfunctional response inhibition (RI) are hallmarks of attention-deficit/hyperactivity disorder (ADHD) and disrupted behavioral disorders (DBDs), little is known about their shared and distinct deviant neural mechanisms. AIMS AND METHODS: Here, we selectively reviewed s/fMRI ADHD and DBD studies to identify disorder-specific and shared IA and RI aberrant neural mechanisms. <br><br>RESULTS: In ADHD, deviant prefrontal and cingulate functional activity was associated with increased IA. Structural alterations were most pronounced in the cingulate cortex. Subjects with DBDs showed marked cortico-subcortical dysfunctions. ADHD and DBDs share similar cortico-limbic structural and functional alterations. RI deficits in ADHD highlighted hypoactivity in the dorso/ventro-lateral PFC, insula, and striatum, while the paralimbic system was primarily dysfunctional in DBDs. Across disorders, extensively altered cortico-limbic dysfunctions underlie IA, while RI was mostly associated with aberrant prefrontal activity. <br><br>CONCLUSION: Control network deficits were evidenced across clinical phenotypes in IA and RI. Dysfunctions at any level within these cortico-subcortical projections lead to deficient cognitive-affective control by ascribing emotional salience to otherwise irrelevant stimuli. The clinical implications of these findings are discussed.<br><br>Copyright © 2018. Published by Elsevier Ltd.<p /> <p>Language: en</p>",
language="en",
issn="0149-7634",
doi="10.1016/j.neubiorev.2018.04.016",
url="http://dx.doi.org/10.1016/j.neubiorev.2018.04.016"
}