The Brain and AD/HD

By J. Mark Bade

January, 2011

In thisthird article in 2e Newsletter’s series on the brain, we’ll look at the nature of AD/HD and how it reflects the structure, function, and development of the brain in a twice-exceptional child.


AH/HD is a disorder defined by specific behavioral characteristics. It is also a spectrum disorder, where characteristics and symptoms may be more pronounced or less. The main symptoms associated with AD/HD are:

  • The inability to focus or sustain attention
  • A high activity level (difficulty staying still)
  • Difficulty controlling impulses (acting without thinking about what the result will be).

Depending on which symptoms are strongest, an individual may be diagnosed with one of the following three common types of AD/HD:

  1. Predominantly Inattentive. Children with this diagnosis have a hard time staying focused. Organizing and finishing tasks are challenging for them. So, too, are paying attention to details and following instructions. (Note that the term AD/HD is applied to this subtype even though hyperactivity is not present.)
  2. Predominantly Hyperactive/Impulsive. Children with this diagnosis find it hard to sit still for long and to control their impulses. They typically fidget and talk more than others. When young, they may run, jump, or climb constantly. These individuals feel restless and often display impulsive behaviors such as interrupting others, being unable to wait their turn, or grabbing things from other people.
  3. Combined Type. Children with this diagnosis display symptoms of the other two subtypes.

The underlying mechanisms and treatments of the three types may vary.

Attention and Action

Attending to something requires an interplay among a variety of cerebral components. First, a child must be alert enough to pay attention. The brain’s reticular activating system (RAS) plays a part in this, as you’ll read later.

Next, a child must be able to process incoming information, which involves focusing on the information source and filtering out extraneous information. Several areas of the brain play a big part in processing.

Then executive functions come into play — the ability to plan and organize. Again, specific brain structures facilitate executive functioning, which is heavily dependent on attention and working memory.

Finally, an individual must be able to hold interest and sustain attention in anticipation of a reward. This ability is at least partly a function of the brain’s limbic system, covered later in this article.

A Short Detour: Neurotransmitters

The brain’s “thinking” structure is composed of neurons along with supporting glial cells. Neurons perform much of the processing in the brain; and they, in turn, depend on chemical neurotransmitters to transfer signals from neuron to neuron. This transferring process facilitates memory, sensory input, decisions, and other brain functions.

A neurotransmitter may excite the neighboring neuron, causing the neuron to transmit a signal; or inhibit it, discouraging transmission of a signal. Furthermore, neurons have different types of receptors for different neurotransmitters.

Three types of neurotransmitters appear to be involved in AD/HD:

  • Norepinephrine (NE, also called noradrenaline), which is mostly excitatory
  • Dopamine (DA), which can be excitatory or inhibitory
  • Glutamate, which is excitatory. 

Alertness and the Reticular Activating System

We mentioned earlier that part of attention is alertness, which depends on the brain’s reticular activating system (RAS). The RAS, which consists of structures in the brain stem along with connections to the cortex and body, helps regulate involuntary functions like heartbeat and respiration. In addition, it regulates alertness. A malfunctioning RAS may lead to difficulty in learning, to memory problems, and to poor self-control. Some researchers say that some types of AD/HD may be caused by a lack of norepinephrine in the RAS, and that stimulants increase the level of this chemical in the RAS. Stimulants also increase both norepinephrine and dopamine in the frontal lobes.

According to The AD/HD Information Library, “The Reticular Activating System plays a significant role in determining whether a person can learn and remember things well or not.” Also affected: whether a person is impulsive or self-controlled, whether a person has high or low motor activity levels, and whether a person is highly motivated or bored easily.

Brain Differences in Children with AD/HD

The Cortex and Prefrontal Cortex  

The cortex of the brain is the outermost layer of the cerebrum, the dominant part of the brain. The frontal lobe is one section of the cortex, in the front of the brain; and the prefrontal cortex (PFC) is the forward-most part of the frontal lobe. The frontal lobe (also called the frontal cortex) plays a role in the ability to filter out distractions while paying attention.  

In typical children, a task requiring sustained attention shows increased activity in the frontal lobes, as shown by imaging devices. But in children with AD/HD, the images are different. Not only are the frontal lobes likely to be smaller, fMRI studies also show that this area may be less active. 

The brain’s frontal lobes are involved with executive functions such as attention, impulse control, the ability to behave in appropriate ways, and judgment. In a 2010 study, researchers claimed to have located the brain’s impulse control center in the frontal lobes, noting how training to constrain impulsive behaviors led to changes in that particular part of the brain. Researchers focusing on one part of the frontal lobes, the prefrontal cortex (PFC), have noted that it can differ in size, depending on whether a child has AD/HD. In children with AD/HD, the right side of the PFC, an area supposedly involved in attention and inhibition of responses, may be 5 to 10 percent smaller.

Besides a smaller prefrontal cortex, two areas of the inner forebrain related to the prefrontal cortex may also be smaller in children with AD/HD. These areas, both part of the basal nuclei, are the caudate nucleus and the globus pallidus. The two are involved in motor control and learning. According to some sources, a defect in the pathway that connects the PFC, caudate nucleus, and globus pallidus may cause symptoms of AD/HD. Imaging studies indicate that these areas may be less active in children who have the disorder.

Additional recent research has shown other brain differences as well in children with AD/HD. For example, measures taken of brain waves show that signals from the frontal cortex to other parts of the brain are not transmitted optimally in individuals who have AD/HD. For example, when given a task of attention involving vision, children with AD/HD do not show alertness that would be expected in the visual areas of their brains.

Some research indicates that there may be differences in the rate of brain development in some children with AD/HD. Their cortices may develop more slowly than in typical children. A 2007 study showed that the prefrontal cortex was thinner in AD/HD children than in others at some ages, thickening and maturing three years later than normal. Because the PFC is heavily involved in attention and behavior inhibition, the delayed maturation of this brain area may explain why some children “grow out” of AD/HD.  

Other Areas of the Brain    

Two brain structures help us hold interest and attention. One is the nucleus accumbens, part of the brain’s basal nuclei, which are connected to the frontal lobe. The nucleus accumbens is the center of reinforcement and triggers the release of dopamine as part of the body’s reward system. According to researchers, the nucleus accumbens “maintains levels of motivation when a person starts a task and continues to maintain motivation until the task is completed.” These researchers found that the part of the brain in which the nucleus accumbens is found, the ventral striatum, is smaller in children with AD/HD. 

The other part of the brain involved in keeping on task is the limbic system, which includes parts of the cortex but also other, deeper brain structures. The limbic system is also closely connected to the basal nuclei. An overactive limbic system can lead to hyperactivity; an underactive limbic system may lead to a type of AD/HD some clinicians call “limbic AD/HD,” characterized by apathy, low energy, and possibly depression. (Some clinicians differentiate more than the three types of AD/HD listed at the start of this article.)

There are two parts of the limbic system which may be structurally different in children with AD/HD. One is the hippocampus, which is involved in spatial awareness and memory formation. The hippocampus is larger in children with AD/HD. The other part of the limbic system is the amygdala, which is involved in learning, memory, and emotions. The amygdala is smaller in children with AD/HD; and connectivity between the amygdala and the PFC has been shown to be poor in AD/HD, possibly detracting from impulse control and goal direction.

Working memory plays an important role in attention control. The seat of working memory is an area of the brain called the basal medial forebrain, located in the frontal lobe.  Because working memory is a component of executive functioning, those who have problems with working memory also have problems with attention control.

Another brain area different in children with AD/HD is the cerebellum, in the rear of the brain. The cerebellum, which coordinates body movements and balance, is 5 to 10 percent smaller in children with AD/HD.  

Neurotransmitters, Meds, and AD/HD

Traditional research has postulated that AD/HD is associated with lower levels of the neurotransmitter dopamine in relevant parts of the brain. Researchers think that AD/HD stimulant medications block the re-uptake of neurotransmitters like dopamine. Re-uptake is the absorption of a neurotransmitter by the neuron that originally produced and released the neurotransmitter. Reducing the re-uptake increases the level of a neurotransmitter between synapses, changing the balance and allowing more “normal” brain responses. Stimulant medicines thus have the net result of increasing brain activity in the frontal lobes, thereby having an effect on executive functioning. (Interestingly, some studies show that dopamine levels rise less in response to Ritalin in AD/HD subjects than in typical subjects.)

But researchers are beginning to look at the overall relationship and ratios among multiple neurotransmitters as opposed to focusing on individual ones in explaining or treating AD/HD. For example, some research shows that small doses of stimulants affect norepinephrine levels in the prefrontal cortex more than they do dopamine levels. However they work, AD/HD stimulant meds do increase alertness and help children filter non-relevant input. The non-stimulant AD/HD medicine Strattera (atomoxetine), on the other hand, works by increasing norepinephrine in the frontal-cortical area, assisting executive functioning.

Finally, it’s known that the neurotransmitter glutamate is important for the functioning of the prefrontal cortex and for communication between the PFC and other parts of the brain. Dopamine and NE can enhance the action of glutamate.  


Research shows us that AD/HD is real. We can see differences in the brains of individuals who are diagnosed with it. What can be done? The most widely accepted interventions currently in use are:

  • Meds to address chemical issues, as we’ve noted earlier in this article
  • Psychotherapy
  • Education and training: education about strengths, weaknesses and ways to compensate, and training in the skills that are lacking (planning, organizing, etc.).

Among other brain-based options gaining more attention and being researched are:

  • Working memory training to take advantage of neuroplasticity, which is starting to show promise in the research
  • Neurofeedback, discussed on page 7 of this issue of 2e Newsletter.

We thank pediatric neuropsychologist Paul Beljan, PsyD, ABPdN, ABN, of Scottsdale, Arizona, for reviewing a draft of this article. Any remaining inaccuracies are the responsibility of 2e Newsletter.

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