Citation

Puiu AA, Wudarczyk O, Goerlich KS, Votinov M, Konrad K, Turetsky B, Herpertz-Dahlmann B. Neurosci. Biobehav. Rev. 2018; 90: 231-246.

Affiliation

Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, Medical Faculty, RWTH Aachen University, Aachen, Germany. Electronic address: bherpertz@ukaachen.de.

Copyright

(Copyright © 2018, Elsevier Publishing)

DOI

10.1016/j.neubiorev.2018.04.016

PMID

29689282

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.

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.

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.

Copyright © 2018. Published by Elsevier Ltd.

Language: en

Keywords

ADHD; DBDs; cingulate cortex; control; emotional salience; fMRI; impulsive aggression; paralimbic system; prefrontal cortex; response inhibition; sMRI; top-down