A relatively common and diffuse childhood disorder, it is a constellation of problems that become manifest in children entering school, characterised by inattentiveness, hyperactivity, poor impulse control, behaviour management problems, and a high risk of other co-morbid behaviours and academic problems. First described by Heinrich Hoffmann (1809-1894) in 1845, it was not until 1902, following the Goulstonian lectures delivered by the first British professor of paediatrics George F. Still (1861-1941) at the Royal College of Physicians in London, that it was seen as something other than arising from the effects of inadequate child rearing. It has recently been claimed, however, that the first description of the syndrome was made in 1798 by Alexander Crichton (1763-1856), the Scottish physician to the Imperial Russian Court. Since the beginning of the 20th century, it was variously referred to hyperkinesis, the hyperkinetic reaction of childhood, and hyperactivity. In 1980, the diagnosis of ADHD was formally recognized in the Diagnostic and statistical manual, 3rd edition (DSM III), the official diagnostic manual of the American Psychiatric Association. Estimates of ADHD in the school-age population range from 3% to 5%. Thus, in a classroom of 25 to 30 children, there will be at least one with ADHD. Genetic influences are indicated by the fact that ADHD runs in families (e.g., at least one-third of fathers who had ADHD have children with the syndrome), and that when one identical twin has the disorder there is an increased likelihood of the other one having it. Recent fMRI research focused on neurotransmitters in the frontal cortex has indicated that children with ADHD have a more than a two-fold increased level of glutamate (an excitatory neurotransmitter), together with a decreased level of gamma amino butyric acid (GABA, an inhibitory neurotransmitter). Lower levels of brain glucose metabolism have also been shown in such children by means of PET scans, particularly in the premotor cortex and the superior prefrontal cortex. Then there is a study of transgenic mice with duplicated neural projections from the superior colliculus to the retina. The consequence of this defect is visual hyperstimulation together with excess noradrenaline in the superior colliculus. The mice displayed a lack of behavioral inhibition, impulsiveness and a lack of the ability to understand relevant information (e.g., based on the Go/No Go test). The authors speculate that the effects of noradrenaline on the superior colliculus could lead to news ways of treating the disorder.
See Apraxia, Attention, Behavior modification, Brain (neuro-) imaging, Cognitive behavior therapy, Conduct disorder, Co-morbidity, Continuous performance task, Controlled attention, Executive function, Focused attention, Functional magnetic resonance imaging (fMRI), Frontal cortex, Gamma aminobutyric acid (GABA), Glutamate (or glutamate), Impulsivity, Go/no go test, Neurotransmitters, Norephinephrine (or noradrenaline), Obsessive-compulsive disorder, Oppositional defiant disorder (ODD), Prefrontal cortex (PFC), Prefrontal-frontal-striatal loops, Premotor cortex, Reification, Ritalin, Superior colliculus, Retina, Wisconsin Card Sorting Test (WCST)