[Structural and functional neuroanatomy of attention-deficit hyperactivity disorder (ADHD)].

INTRODUCTION: Attention-deficit hyperactivity disorder (ADHD) is a common and impairing neuropsychiatric disorder with preschool onset. ADHD occurs in approximately 3-9% of the childhood population. There is a much higher incidence rate in boys who are around three times more likely than girls to be diagnosed. Approximately 30-60% of individuals diagnosed with ADHD in youth have symptoms that persist into adulthood. LITERATURE
FINDINGS: Three subtypes of the disorder have been proposed in the current clinical view of ADHD: inattentive, hyperactive-impulsive and combined type. Numerous problems are associated with ADHD: poor academic performance, learning disorders, subtle cognitive deficits, conduct disorders, antisocial personality disorder, poor social relationships, and a higher incidence of anxiety and depression symptoms into adulthood. Researchers have emphasized poor behavioural inhibition as the central impairment of the disorder. From the neuropsychological viewpoint, impairment of the "hot" affective aspects of executive functions, like behavioural inhibition and attention and the more cognitive, "cool" aspects of executive functions like self-regulation, working memory, planning, and cognitive flexibility, are often reported by studies on ADHD. The hot executive functions are associated with ventral and medial regions of the prefrontal cortex (including the anterior cingulated cortex) and named "hotbrain" and the cool executive functions are associated with the dorsolateral prefrontal cortex and are called "coolbrain". DISCUSSION: Convergent data from neuroimaging, neuropsychology, genetics and neurochemical studies consistently point to the involvement of the frontostriatal network as a likely contributor to the pathophysiology of ADHD. This network involves the lateral prefrontal cortex, the dorsal anterior cingulate cortex, the caudate nucleus and putamen. Moreover, a growing literature demonstrates abnormalities affecting other cortical regions and the cerebellum. The exploratory brain regions of interest in which abnormalities have been identified, but that were not predicted by cognitive models of ADHD, are the temporal lobe, parietal lobe, occipital lobe and lateral ventricles. Anatomical studies suggest widespread reductions in volume throughout the cerebrum and cerebellum, while functional imaging studies suggest that affected individuals activate more diffuse areas than controls during the performance of cognitive tasks. More precisely, reductions in volume have been observed in the total cerebral volume, the prefrontal cortex, the basal ganglia (striatum), the dorsal anterior cingulate cortex, the corpus callosum and the cerebellum. Furthermore, hypoactivation of the dorsal anterior cingulate cortex, the frontal cortex and the basal ganglia (striatum) have also been reported. The paradigms mostly used in functional magnetic resonance imaging (fMRI) are tasks of motor inhibition, interference and attention such as the go/no-go, "stop-signal" and the Stroop.
CONCLUSION: This review provides an overview of the main imaging studies that investigated the neurobiological substrate of ADHD. Some guidelines for future functional magnetic imaging studies are also suggested.