Enhanced neural activity in frontal and cerebellar circuits after cognitive training in children with attention-deficit/hyperactivity disorder.

The brain is a plastic entity that can undergo dynamic changes throughout the lifespan as a result of training. Attention-deficit/hyperactivity disorder (ADHD) is commonly treated with psychostimulant medication, and the prevalence of ADHD medication prescription is a topic of heated scientific debate. In addition, cognitive training is frequently provided to patients with ADHD. Although psychostimulant effects have been thoroughly investigated, no previous studies have assessed the neural effects of cognitive training in ADHD. We applied fMRI-paradigms of response inhibition and selective attention to chart the effects of a 10-day cognitive training program in 19 unmedicated ADHD children receiving either cognitive or control training. The two resulting longitudinal datasets were analyzed using whole-brain random-effects general linear models. Although we observed no increases of activity in the control group, both fMRI-datasets revealed enhanced activity after cognitive training in neural structures closely related to ADHD pathophysiology. On the inhibition paradigm, our results indicated increases in orbitofrontal, superior frontal, middle temporal, and inferior frontal cortex. The attentional task was characterized by increased activity in the cerebellum, which correlated with improvement on in-scanner measures of attention. Our findings provide preliminary evidence that cognitive training enhances activity in neural structures typically affected by the disorder. Similar results have been obtained following methylphenidate administration, suggesting that training of cognitive functions may mimic the effects of psychostimulant medication on the brain. These findings postulate a neural account for the potency of cognitive training in ADHD, and hold clinical implications, supporting the inclusion of training programs in standard ADHD-treatment.

Differential abnormalities of the head and body of the caudate nucleus in attention deficit-hyperactivity disorder.

The aim of the study is to present a new method for the segmentation of the caudate nucleus and use it to compare the caudate heads and bodies of an attention deficit-hyperactivity disorder (ADHD) group with those of a control group. We used a 1.5-T system to acquire magnetic resonance brain scans from 39 children with ADHD, as defined by DSM-IV TR, and 39 age, handedness and IQ matched controls. The new method for caudate head and body segmentation was applied to obtain semi-automatic volumes and asymmetric patterns. Bilateral volumetric measures of the head, body, and head-body of the caudate nuclei were compared within groups and between ADHD and control groups. Although the group factor was not significant, there were first and second order interactions. The analysis of simple effects showed that the right body and right head+body of the ADHD group was significantly smaller than in the control group, although the ADHD right caudate head was bigger. No ADHD within-group caudate differences were found. Controls showed a significantly larger left caudate head and a significantly bigger caudate right body and right head+body. Our new method for segmenting the caudate nucleus detected differential abnormalities of the right caudate head and body in the ADHD group, explaining previous heterogeneous findings in the literature.

Pediatric OCD structural brain deficits in conflict monitoring circuits: a voxel-based morphometry study.

The aim of this study is to use a voxel-based morphometry protocol to compare the brains of 18 children with obsessive-compulsive disorder (OCD) with those of a healthy group matched for gender and handedness. Images were acquired with a 1.5-T MRI scanner, spatially normalized, and segmented with an optimized voxel-based morphometry protocol. OCD children presented a 5.93% reduction of gray matter (GM) total volume in comparison with control brains. We identified OCD brain volume reductions in regions that have been extensively related to action monitoring and error signaling processes. Specifically, we found decreased bilateral GM in frontal (significant after Family Wise Error (FEW), multiple comparisons correction) and cingulate regions as well as decreased white matter (WM) in bilateral frontal and right parietal (p<0.001 uncorrected). Additionally, we found a negative correlation between symptom severity and bilateral hippocampal GM-volume (p<0.001uncorrected) as well as a positive correlation between age and GM left caudate volume (p=0.037 FWE small volume corrected) in the OCD group. As a conclusion, our results point to conflict monitoring structural brain regions as primary deficits in pediatric OCD, and to striatal abnormalities as age-related deficits.