Primera Parte*

The DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders, fourth Edition, text Revision) defines attention-deficit/hyperactivity disorder (ADHD) as a disorder usually first diagnosed during infancy. Its essential feature is a persistent pattern of inattention and/or hyperactivity-impulsivity that is more frequent and severe than typically observed in individuals at a comparable level of development. It produces a significant impairment in social, academic, or occupational functioning. The prevalence of ADHD among the general population is between 5-10% in children and adolescents, and 1.2% to 7.3% in adults. In clinical samples, the prevalence in adults is higher: 16.80%. Less than 10% of the children diagnosed with ADHD reached a total functional remission when they became adults. Subjects with ADHD have a higher risk of suffering personality disorders and substance abuse. This disorder has a genetic basis. About 80% of the variance is explained by genetics. Some of the genes implied in this disorder are the dopamine transporter, the dopamine receptor 4, the beta-hydroxilase enzyme, the adrenergic receptor α2, the serotonin transporter and the serotonin receptor 1B. Environmental factors such as parental nicotine consumption during pregnancy, low birth weight, perinatal problems, parental psychiatric disorders, social adversity, and low parental education are related to a higher risk for ADHD. Several studies have shown that there are morphological brain abnormalities in subjects with ADHD. Structures like frontal lobe, cerebellar hemispheres and vermis, callosum splenium, cingulate anterior cortex and right caudate, are smaller in subjects with ADHD compared with healthy subjects. On the other hand, regarding the response to stimulants, studies with positron emission tomography (PET), among other techniques, suggest that the dopamine and noradrenergic systems play a role in the pathophysiology of ADHD. From 1990 to date, there are 41 morphological studies in ADHD, published in English, reporting volumetric abnormalities. However, the results are contradictory, so definitive conclusions about the brain structures being involved in ADHD remain unclear.