Disruptive behaviour disorders (DBDs) are common and severe developmental disorders include conduct disorder (CD) and oppositional defiant disorder (ODD). They are characterized by aggressive and antisocial behaviours associated with violations of social rules (e.g. thefts and violent behaviour) and are considered a predictor of antisocial/borderline personality disorder and substance abuse (Schutter et al. Reference Schutter, van Bokhoven, Vanderschuren, Lochman and Matthys2011). Also, they are more common in boys than in girls and are associated with a lower quality of life (Bot et al. Reference Bot, de Leeuw den Bouter and Adriaanse2011). High comorbidity is usually observed with attention deficit hyperactivity disorder (ADHD) (Spencer, Reference Spencer2006; Bellani et al. Reference Bellani, Moretti, Perlini and Brambilla2011). It should be noted that DBD children and preadolescents with comorbid ADHD show higher use of mental health services than those with mood or anxiety disorders and that ODD diagnosis is associated with the highest likelihood of the use of services at the age of 14–15 years (Ezpeleta et al. Reference Ezpeleta, Granero, de la Osa and Domènech2009). Recently, interest was addressed to a sub-group of DBDs with the so-called callous-unemotional traits (i.e. reduced empathy and guilt, poor emotional response), which may be associated with increased risk of antisocial outcomes (Marsh et al. Reference Marsh, Finger, Mitchell, Reid, Sims, Kosson, Towbin, Leibenluft, Pine and Blair2008; De Brito et al. Reference De Brito, Mechelli, Wilke, Laurens, Jones, Barker, Hodgins and Viding2009).

Several functional magnetic resonance imaging (fMRI) studies have been conducted so far to explore the biological bases of DBDs (Table 1). Specifically, adolescents with DBD exposed to emotional pictures (i.e. negative/painful situations and fearful/sad faces) showed enhanced activation of amygdala, striatum, mid-cingulate and orbitofrontal cortex (OFC) (Herpertz et al. Reference Herpertz, Huebner, Marx, Vloet, Fink, Stoecker, Shah, Konrad and Herpertz-Dahlmann2008; Decety et al. Reference Decety, Michalska, Akitsuki and Lahey2009; Passamonti et al. Reference Passamonti, Fairchild, Goodyer, Hurford, Hagan, Rowe and Calder2010) and reduced activation of anterior cingulate cortex (ACC) (Sterzer et al. Reference Sterzer, Stadler, Krebs, Kleinschmidt and Poustka2005). Also, they had reduced functional connectivity between amygdala and medial prefrontal cortex (Marsh et al. Reference Marsh, Finger, Mitchell, Reid, Sims, Kosson, Towbin, Leibenluft, Pine and Blair2008; Decety et al. Reference Decety, Michalska, Akitsuki and Lahey2009). In two studies, reduced activation of amygdala was instead observed in DBD adolescents with high callous-unemotional traits (Marsh et al. Reference Marsh, Finger, Mitchell, Reid, Sims, Kosson, Towbin, Leibenluft, Pine and Blair2008; Jones et al. Reference Jones, Laurens, Herba, Barker and Viding2009). Interestingly, a reduced activation of amygdala, insula and PFC was also present in response to angry faces in CD (Passamonti et al. Reference Passamonti, Fairchild, Goodyer, Hurford, Hagan, Rowe and Calder2010). Such functional abnormalities are consistent with structural alterations showing volume reduction of amygdala, hippocampus, insula, OFC, dorsomedial PFC, temporal cortex and caudate nucleus, particularly in CD children (Huebner et al. Reference Huebner, Vloet, Marx, Konrad, Fink, Herpertz and Herpertz-Dahlmann2008; Fairchild et al. Reference Fairchild, Passamonti, Hurford, Hagan, von dem Hagen, van Goozen, Goodyer and Calder2011). However, increased sizes of medial OFC and dorsal ACC, with preserved amygdala and insula morphometry, have also been found in boys with callous-unemotional traits and conduct problems (De Brito et al. Reference De Brito, Mechelli, Wilke, Laurens, Jones, Barker, Hodgins and Viding2009).

Table 1.

fMRI studies in DBDs using affective stimuli

ACC, anterior cingulate cortex; ADHD, attention deficit hyperactivity disorder; AO, adolescent-onset; CD, conduct disorder; CUT, high callous-unemotional traits; EO, early-onset; HS, healthy subjects; MCC, midcinguale cortex; ODD, oppositional defiant disorder; OFC, orbitofrontal cortex; PFC, prefrontal cortex.

Based on the imaging literature briefly summarized above, a dysfunctional network including amygdala, PFC, striatum and insula may underlie affective dysregulation reported in subjects with DBD. In this context, preliminary findings suggest that DBD patients with callous-unemotional traits, particularly those with CD, may represent a specific sub-group with peculiar functional and structural brain maturation. Future fMRI studies should explore whether such abnormalities are specific to CD or ODD (Barker et al. Reference Barker, Tremblay, van Lier, Vitaro, Nagin, Assaad and Séguin2011) and whether they persist over time during development. They should also further investigate the role of callous-unemotional traits for brain development in these children and should differentiate the specific features of DBD and ADHD (Rubia, Reference Rubia2011).