Neurobiology Of ADHD: The Brain Bases Of This Disorder
The acronym ADHD stands for attention deficit hyperactivity disorder, a complex clinical entity that primarily affects children and adolescents, and whose main symptoms include abnormal levels of hyperactivity, impulsivity and/or inattention.
At the moment, Although ADHD is considered a brain disorder, the exact neurobiological mechanisms are unknown that underlie this condition, nor has an effective genetic marker been discovered that serves to make a reliable diagnosis, apart from psychological tests and cognitive and behavioral evaluations.
In this article we review the current state of research on the neurobiology of ADHD the main genetic and brain imaging studies that have been carried out, and the theories that try to explain how and why this disorder develops.
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 that demonstrate 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 that there is an underlying neurobiological etiology.
Current research on ADHD from a neurobiological point of view focuses, above all, on the theoretical framework that implies study the alteration of dopaminergic activity (its receptors and transporters), as well as its implications in the generation of symptoms of this disorder.
Today, among the neuroscientific community, the concept of deficit in inhibitory response control continues to be used, which is the inability that people with ADHD have to control and inhibit impulses and cognitive responses, which ends up interfering with cognitive functions. executives that plan, coordinate and execute final behaviors.
Current research on ADHD is therefore focused on finding the neurobiological mechanisms that explain the disorder and genetic markers that serve as a reliable diagnostic basis. Let’s see below what the main theories are about the neurobiology of ADHD.
Neurobiology of ADHD
There is an extensive scientific literature on the neurobiology of ADHD focused on motivational processes and cognitive control in children with this disorder For example, behavioral reinforcement has been widely researched and in recent years there have been great advances in understanding the neural mechanisms involved in processing reinforcement.
It has been suggested that dopamine plays an important role as a mediator in the cognitive reinforcement signal. The structures that have emerged to play a central role in reinforcement learning mechanisms are those innervated by dopaminergic projections from the midbrain. In fact, some of these same structures have been implicated in ADHD, since in this disorder there is an alteration in reward processing.
The dopaminergic theory is based on the existence of deficits in two regions in which dopamine plays a crucial role: the 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 appears to be plenty of 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, at the moment no biological marker of ADHD has been detected and its diagnosis continues to be based on the observational method and neurocognitive evaluations.
Research with family members has consistently indicated a strong genetic contribution to ADHD. Twin studies have shown a high heritability of this disorder It is likely that multiple genes exerting a modest effect are involved, as to date no single gene has been found to play a critical role.
Researchers have focused on studying genetic variations in the dopamine D4 receptor and the dopamine transporter DAT1, but it has been found that individually they only have weak effects 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, and dopamine and serotonin transporters.
However, there is growing recognition among the scientific community that there is a potential interaction between genetics and environmental risk factors Without diminishing the importance of genetic factors, environmental factors have also been identified that increase the risk of ADHD, such as exposure to lead or polychlorinated biphenyls during early childhood, although their effects are not specific to ADHD.
Brain imaging studies
In brain imaging studies, serious anatomical changes in brain dimensions associated with ADHD have been observed. The most consistent finding is a reduction in overall brain size that persists into adolescence and the 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 carried out in 2007 concluded that The caudate nucleus and globus pallidus, which contain a high density of dopamine receptors, were smaller in subjects with ADHD compared to the control groups. In addition, decreased blood flow to 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 the thickness of the cerebral cortex associated with the DRD4 allele has been detected, which is widely related to the diagnosis of ADHD. This cortical thinning is most evident in childhood and, to a large extent, appears to resolve during adolescence.
In tractography images, alterations have also been detected in the frontal and cerebellar white matter of children and adolescents with ADHD. On the other hand, in reinforcement and reward tasks, a preference for immediate over delayed reinforcement is observed in subjects with ADHD. And in studies with functional magnetic resonance imaging in adolescents with ADHD it has been shown that there is a reduction in the ventral striatum when the reward is anticipated, contrary to what happens with control subjects in whom there is an activation of this brain region. .
