In This Issue

Abnormalities in brain systems, as well as specific regions, are verified by a meta-analysis of functional magnetic resonance imaging (fMRI) studies of children and adults with attention deficit hyperactivity disorder (ADHD). The 55 studies identified by Cortese et al. (CME, p. 1038) indicate that both children and adults with ADHD have an underresponsive frontoparietal network (figure), which is involved in goal-directed executive functions. Both groups also display hyperactivation of the network underlying self-referential, or default, cognitive processes. Children in addition have abnormalities in attention-related networks, and their hyperactive somatomotor and visual systems suggest compensation for dysfunction in executive processes and in integration of external information. These compensatory systems may be an appropriate focus for therapeutic remediation efforts.

Applying the latest proposed DSM-5 criteria for autism spectrum disorder (ASD) to parent-reported symptoms yielded an ASD diagnosis for 91% of 4,453 children previously given DSM-IV clinical diagnoses of pervasive developmental disorders (PDDs)—autistic disorder, Asperger’s disorder, or PDD not otherwise specified. This rate reported by Huerta et al. (p. 1056) is substantially higher than the rate in the DSM-5 field trial, which used the first draft of the criteria. The higher sensitivity of the current draft criteria extended to children with higher cognitive functioning, girls, and children younger than 4. As noted by editorialist Tsai (p. 1009), the ability to exclude children with non-ASD conditions, e.g., language disorders or ADHD, is only slightly better with DSM-5 than with DSM-IV.

Both patients with obsessive-compulsive disorder (OCD) and their siblings, while performing a task requiring response inhibition, showed hyperactivity of a brain region involved in suppressing motor responses. The presupplementary motor area is key to rapidly resolving conflicting action plans, and de Wit et al. (p. 1100) propose this familial dysfunction as a link between genetic predisposition and OCD behavior. A reliable biological OCD trait might point toward mechanisms of the disorder and increase the homogeneity of patient groups for research.