Neural Abnormalities in Early-Onset and Adolescence-Onset Conduct Disorder
Abstract
Context: Conduct disorder (CD) is characterized by severe antisocial behavior that emerges in childhood (early-onset CD [EO-CD]) or adolescence (adolescence-onset CD [AO-CD]). Early-onset CD is proposed to have a neurodevelopmental basis, whereas AO-CD is thought to emerge owing to social mimicry of deviant peers. However, this developmental taxonomic theory is debated after reports of neuropsychological impairments in both CD subtypes. A critical, although unaddressed, issue is whether these subtypes present similar or distinct neurophysiological profiles. Hence, we investigated neurophysiological responses to emotional and neutral faces in regions associated with antisocial behavior (ie, the amygdala, ventromedial prefrontal cortex, insula, and orbitofrontal cortex) in individuals with EO-CD and AO-CD and in healthy control subjects. Objective: To investigate whether EO-CD and AO-CD subjects show neurophysiological abnormalities. Design; Case-control study. Setting: Government research institute, university department. Participants: Seventy-five male adolescents and young adults aged 16 to 21 years, including 27 with EO-CD, 25 with AO-CD, and 23 healthy controls. Main Outcome Measure: Neural activations measured by functional magnetic resonance imaging while participants viewed angry, sad, and neutral faces. Results: Comparing angry vs neutral faces, participants with both CD subtypes displayed reduced responses in regions associated with antisocial behavior compared with controls; differences between the CD subtypes were not significant. Comparing each expression with fixation baseline revealed an abnormal (increased) amygdala response to neutral but not angry faces in both groups of CD relative to controls. For sad vs neutral faces, reduced amygdala activation was observed in EO-CD relative to AO-CD and control participants. Comparing each expression with fixation revealed hypoactive amygdala responses to sadness in individuals with EO-CD relative to AO-CD participants and controls. These findings were not accounted for by attention-deficit/hyperactivity disorder symptoms. Conclusions: Neurophysiological abnormalities are observed in both CD subtypes, contrary to the developmental taxonomic theory of CD. Additional amygdala hypofunction in relation to sad expressions might indicate why EO-CD is more severe and persistent than AO-CD.
Additional Information
© 2010 American Medical Association. Submitted for Publication: July 13, 2009; final revision received November 11, 2009; accepted December 14, 2009. This study was supported by project grant 083140 (Drs Goodyer and Fairchild) and grant 077029 (Dr Rowe) from the Wellcome Trust; Medical Research Council project code U.1055.02.001.00001.01 (Dr Calder); and the Betty Behrens Research Fellowship at Clare Hall in Cambridge University (Dr Passamonti). This research was completed within the National Institute of Health Research Collaboration for Leadership in Applied Health Research and Care for Cambridgeshire and Peterborough. Author Contributions: Dr Passamonti had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. We thank our participants, their parents, and their teachers for taking part in the study. Giuseppina Morganti, PGCE, provided help with the reference section. The Cambridge Youth Offending Service, the schools, and pupil referral units helped with participant recruitment. Financial Disclosure: None reported.Attached Files
Published - yoa90116_729_738.pdf
Accepted Version - emss-34885.pdf
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Additional details
- PMCID
- PMC4471104
- Eprint ID
- 101554
- Resolver ID
- CaltechAUTHORS:20200225-135944388
- 083140
- Wellcome Trust
- 077029
- Wellcome Trust
- U.1055.02.001.00001.01
- Medical Research Council (UK)
- Betty Behrens Research Fellowship
- Created
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2020-02-26Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field