ebook_ADHD2019_engl.

The World Federation of ADHD Guide 29 turation of brain structures that mature earlier in healthy controls, and that brain maturation in ADHD may catch-up at later age. 82 This theory was developed given earlier observations that ADHD is associated with delayed maturation of cerebral cortex. Shaw et al. 83 reported that the age of attaining peak cortical thickness was 10.5 years for individuals with ADHD and 7.5 years for controls. This delay was most prominent in prefrontal regions important for control of executive functio- ning, attention, and motor planning. 83 The development of cortical surface area was delayed in ADHD, but ADHD was not associated with altered developmental trajectories of cortical gyrification. 84 Although the work reviewed above suggests that age-dependent decline in the prevalence of ADHD may be due to a late development of ADHD-associated brain structures and functions, most patients with ADHD do not show comple- te developmental “catch up”. Indeed, widespread reductions in cortical thickness have been implicated in ADHD not only in children but also in adults. Findings include both cortical thinning (superior frontal cortex, precentral cortex, inferior and superior parietal cortex, temporal pole, and medial temporal cortex 84,85 and cortical thickening (presupplementary motor area, somatosensory cortex and oc- cipital cortex). 86 Changes across age in the brains of ADHD patients are of much interest gi- ven the age dependent prevalence of ADHD. 87 Some brain volumetric alterations observed in childhood normalize with age. 88 A longitudinal MRI study found ba- sal ganglia volumes and surface area to be smaller in adolescents with ADHD compared to controls; this difference was fixed and not-progressive over age. 89 In contrast, for ventral striatal surfaces, controls showed surface area expansion with age, whereas ADHD patients experienced a progressive contraction of the surfa- ce, which may explain abnormal processing of reward in ADHD. 89 VOXEL-BASED MORPHOMETRY Voxel-based morphometry (VBM) analyses (see Box 2.2) on brain scans of adoles- cents with ADHD observed significantly smaller grey matter volume in 5 clusters located in the precentral gyrus, medial and orbitofrontal cortex, and (para)cingu- late cortices, compared to controls. 90 Unaffected siblings of the ADHD probands had also smaller volumes that were significantly different from controls in 4 of these clusters (all except the precentral gyrus). The brain areas that are smaller in ADHD are involved in decision making, motivation, cognitive control and motor functioning, all functional domains that may be affected in ADHD. The altera- tions in the unaffected siblings indicate the familiality of four of the structural brain differences, supporting their potential as endophenotypes (see above).