Attention-Deficit/Hyperactivity Disorder, or ADHD, is a neurodevelopmental condition recognized by patterns of inattention, hyperactivity, and impulsivity. These behaviors stem from differences in the brain’s development and functional pathways, not from a person’s character. The condition reflects variations in how specific brain systems form and communicate. Understanding ADHD involves looking at the brain’s chemical signaling, its physical structure, and the genetic factors that guide its construction.
The Role of Neurotransmitters
The transmission of signals between nerve cells is managed by chemical messengers called neurotransmitters. In ADHD, dopamine and norepinephrine are relevant to regulating cognitive processes like attention and motivation. Dopamine is linked to feelings of pleasure and reward, which helps in maintaining motivation for tasks. Norepinephrine is involved in modulating alertness, arousal, and the ability to focus.
A theory in the neurobiology of ADHD is that the systems regulating these chemicals are disrupted. Research indicates that individuals with ADHD may have a higher density of dopamine transporters, which are proteins that reabsorb dopamine. This increased transporter density can lead to dopamine being cleared from the space between neurons too quickly, resulting in inefficient signaling.
This inefficiency means that messages related to maintaining focus and managing impulses are not transmitted effectively. Stimulant medications used to treat ADHD work by blocking these transporters, which increases the availability of dopamine and norepinephrine. This action enhances neurotransmission, allowing for more effective communication between brain cells and illustrating the connection between these systems and ADHD symptoms.
Brain Anatomy and Executive Function
Beyond chemical signaling, the physical structure of the brain contributes to ADHD. Specific regions, particularly those in the fronto-striato-cerebellar circuits, show differences in individuals with the condition. The prefrontal cortex (PFC), a region at the front of the brain, is responsible for executive functions.
Executive functions are a set of mental skills that include:
- Planning for the future
- Organizing tasks
- Maintaining attention
- Shifting focus between activities
- Regulating impulses
The PFC is the control center for these skills. Neuroimaging studies have revealed differences in the PFC of individuals with ADHD, including reduced volume, cortical thickness, and a slower maturation timeline. This developmental delay in reaching peak cortical thickness can be between two to five years.
These structural differences are not limited to the PFC. The basal ganglia, a group of structures involved in motor control and learning, also show volumetric reductions in some individuals with ADHD. The cerebellum, traditionally associated with motor coordination, is also implicated, with some studies showing reduced volume. The cerebellum contributes to cognitive functions like attention and working memory, and alterations in this structure are linked to challenges with executive function.
Atypical Brain Network Communication
The brain operates through large-scale networks, which are collections of distinct regions that activate together. For attention, the relationship between the Default Mode Network (DMN) and the Task-Positive Network (TPN) is important. The DMN is active when the brain is at rest and is associated with internal thoughts and daydreaming. The TPN is engaged during goal-oriented activities that require concentration.
In a neurotypical brain, these two networks have a reciprocal relationship; when one is active, the other deactivates. This process is managed by the salience network, which acts as a switch, determining what information deserves attention. This mechanism allows a person to shift from internal mind-wandering to external focus when a task demands it.
A neurobiological theory of ADHD suggests that this switching mechanism is impaired. In individuals with ADHD, the DMN often remains active even when the TPN is engaged. This failure to suppress the DMN leads to interference from internal thoughts and distractibility, making it difficult to maintain focus on external tasks. Functional connectivity studies have shown weaker segregation between these systems in children with ADHD.
This “faulty switch” results in a constant pull of attention away from a task and toward unrelated thoughts. The difficulty in suppressing the DMN is linked directly to the core symptom of inattention. The competition between these networks can make it challenging to sustain the mental effort required for tasks that are tedious or lack immediate reward.
Genetic Influences on Brain Development
The origins of these differences in brain structure and function are strongly linked to genetics. ADHD is a highly heritable condition, with studies estimating its heritability at approximately 70-90%. This indicates that genetic factors play a substantial role in the likelihood of developing the disorder. Having a first-degree relative with ADHD increases the risk five- to ten-fold.
There is no single “ADHD gene”; the condition is polygenic, resulting from the combined effects of many different genes. These genes primarily influence the neurobiological systems discussed previously. For example, implicated genes are those that regulate the dopamine system, such as the dopamine transporter gene (DAT1) and the dopamine receptor D4 gene (DRD4). Variations in these genes can affect the availability of dopamine in the brain.
These genetic variations also contribute to the development of brain structures. The genes associated with ADHD risk influence the growth, maturation, and connectivity of the prefrontal cortex and other related regions. They provide the blueprint for building the neural circuits that underpin executive functions and attention regulation.