Neurobiology of ADHD: the brain basis of the disorder
Let's take a look at what is known so far about the relationship between adhd and the brain.
ADHD stands for attention deficit hyperactivity disorder, a complex clinical entity that mainly affects children and adolescents, and whose main symptoms include abnormal levels of hyperactivity, impulsivity and/or inattention.
Currently, Although ADHD is considered to be a brain disorder, the exact neurobiological mechanisms underlying the condition are unknown. underlying the condition are unknown, nor has an effective genetic marker been discovered that can be used to make a reliable diagnosis, apart from psychological testing and cognitive and behavioral assessments.
In this article we review the current state of research on the neurobiology of ADHDThe main genetic and brain imaging studies that have been performed, and the theories that attempt to explain how and why this disorder develops.
What is known about ADHD?
The Disorder by Attention Deficit Hyperactivity Disorder (ADHD) is a clinical condition diagnosed on the basis of persistent levels of hyperactivity, inattention and impulsivity.. Currently, there are no biomedical tests capable of detecting ADHD and the diagnosis is based on the observation of certain behavioral symptoms.
The lack of a physical cause or several causes to prove the existence of this disorder has generated some controversy in the scientific community and in society in general, and treatments based on psychostimulant medication for children and adolescents have been questioned. However, the effectiveness of pharmacological treatment in many cases has led researchers to suspect an underlying neurobiological etiology.
Current research on ADHD from a neurobiological point of view focuses, above all, on the theoretical framework that involves the study of the alteration of dopaminergic activity (its receptors and transporters), as well as its implications in the generation of the symptomatology of this disorder. of this disorder.
Today, among the neuroscientific community, the concept of deficit in the inhibitory control of responses continues to be handled, which is the inability of people with ADHD to control and inhibit impulses and cognitive responses, which ends up interfering with the executive functions that plan, coordinate and execute the final behaviors.
Current research on ADHD is therefore focused on finding the neurobiological mechanisms that explain the disorder and on genetic markers that serve as a reliable diagnostic basis. The following are the main theories on the neurobiology of ADHD.
Neurobiology of ADHD
There is an extensive scientific literature on the neurobiology of ADHD focused on motivational processes and motivational control. motivational processes and cognitive control in children with ADHD.. For example, behavioral reinforcement has been extensively investigated and in recent years there have been major advances in understanding the neural mechanisms involved in reinforcement processing.
It has been suggested that dopamine plays an important role in mediating cognitive reinforcement signaling. Structures that have emerged as playing a central role in the mechanisms of reinforcement learning are those innervated by dopaminergic projections of the midbrain. In fact, some of these same structures have been implicated in ADHD, since in this disorder there is an alteration in the processing of rewards.
The dopaminergic theory is based on the existence of deficits in two regions in which dopamine plays a crucial roleThe anterior cingulate, whose hypoactivation produces a cognitive deficit; and the caudate nucleus, whose overactivation generates an excess of motor behaviors, typical in subjects with ADHD.
Although there seems to be enough evidence in favor of the dopaminergic theory, research has also focused on the role of other possible candidate genes, such as the norepinephrine transporter NET1, or the dopamine receptor gene DRD1. However, for the time being no biological marker of ADHD has been detected and its diagnosis is still based on the observational method and neurocognitive evaluations.
Genetic studies
Research with relatives has consistently indicated the existence of a strong genetic contribution to ADHD. Twin studies have shown a high heritability of ADHD.. Multiple genes exerting a modest effect are likely to be involved, as no single gene has been found to play a major role to date.
Researchers have focused on studying genetic variations in the dopamine D4 receptor and the dopamine transporter DAT1, but these have been found to exert only weak effects individually and neither is necessary or sufficient for ADHD to occur. In fact, a recent review of several molecular genetic studies concluded that there were significant associations for four genes in ADHD: dopamine D4 and D5 receptors, dopamine and serotonin transporters.
All in all, there is a growing recognition among the scientific community that there is a potential interaction between genetics and genetic factors in ADHD. a potential interaction between genetics and environmental risk factors.. Without diminishing the importance of genetic factors, environmental factors that increase the risk of ADHD have also been identified, such as exposure to lead or polychlorinated biphenyls during early childhood, although their effects are not specific to ADHD.
Brain imaging studies
Severe anatomical changes in brain dimensions associated with ADHD have been observed in brain imaging studies. The most consistent finding is a reduction of the total brain size that persists into adolescenceThe reduction in the size of several brain regions, such as the caudate nucleus, the prefrontal cortex, the white matter and corpus callosum, and the cerebellar vermis.
A meta-analysis conducted in 2007 concluded that the caudate nucleus and globus pallidus, which contain a high density of dopamine receptors, were smaller in size in subjects with ADHD than in those with ADHD. in subjects with ADHD compared to control groups. In addition, decreased blood supply in regions of the striatum, as well as changes in dopamine transporter binding, have also been observed.
Cortical thickness studies have also shown changes in ADHD. A regional reduction in cerebral cortex thickness associated with the DRD4 allele has been detected.allele, which is widely associated with the diagnosis of ADHD. This cortical thinning is most evident in childhood and, to a large extent, appears to resolve during adolescence.
Alterations in the frontal and cerebellar white matter of children and adolescents with ADHD have also been detected in tractography images. On the other hand, in reinforcement and reward tasks, subjects with ADHD show a preference for immediate over delayed reinforcement. And in studies with functional magnetic resonance imaging in adolescents with ADHD it has been shown that there is a reduction of the ventral striatum when the reward is anticipated, contrary to what occurs with control subjects in which there is an activation of this brain region.
(Updated at Apr 14 / 2024)