The ADD Brain

As the video below shows, an ADD-affected child’s brain (left) matures in a normal pattern, but it is delayed by about three years compared to the brains of children without ADD (right). 

The delay affects the outer layer of brain, called the cortex, which enables people to focus, control impulsive behavior and remember things from one moment to the next–functions that are often challenging for children with ADD. Although the ADD brain may take longer to mature, a recent study conducted brain scans of 119 adult ADD patients and 107 “controls” (patients without ADD) found that differences in brain development “largely normalize” as children with ADD reach adulthood.

The Adult ADD Brain

While neurological differences between individuals with and without ADD may normalize over time, many adults do not simply “grow out of it.” Although most ADD brain research has focused on children, a growing number of studies have examined the neurological basis for ADD among adults.

For example, Dr. Richard Friedman, professor of clinical psychiatry at the Weill Cornell Medical College, has explored how dopamine, a neurotransmitter (or chemical messenger), affects mental and emotional function and the brain’s “reward response“–the pleasure one feels in response to certain experiences. Friedman explains that “rewards like sex, money, drugs and novel situations all cause the release of dopamine in the reward circuit of the brain…aside from generating a sense of pleasure, this dopamine signal tells your brain something like, ‘Pay attention, this is an important experience that is worth remembering.’”

Research has shown that lower dopamine receptor and transporter levels in the brains of non-medicated individuals with ADD contribute to the classic ADD symptoms of inattention and impulsivity. Researchers reported in 2009 that this could explain why “attentional deficits in individuals with ADD are most evident in tasks that are considered boring, repetitive, and uninteresting.” As Dr. Friedman argues, a “sluggish reward circuit makes normally interesting activities seem dull and would explain, in part, why people with ADD find repetitive and routine tasks unrewarding and even painfully boring.”

In addition to exploring the brain’s reward response, recent studies have used functional magnetic resonance imaging (fMRI) technology to observe differences in the brain’s “default mode network” (DMN) between individuals with and without ADD. The DMN is activated when people daydream, think about the future, or recall memories, and de-activated during more goal-oriented activities as the brain’s “task-positive network” takes over. Several fMRI studies have shown “altered patterns of activation” in the DMN when study participants perform tasks related to executive function.


A study published in mid-2014 used fMRI to compare DMN activity among adults who experienced ADD symptoms to adults whose symptoms had lessened over time. The network’s two hubs — the posterior cingulate cortex and the medial prefrontal cortex–normally work in tandem (image on far left), but among study participants with ADD symptoms, they were out of sync (middle image). As the far right image shows, adults whose ADD symptoms had lessened over time showed no difference compared to adults without an ADD diagnosis.

A larger study published in late 2015 used fMRI to compare adults with ADD who had received long-term methylphenidate (Ritalin, Concerta, Metadate, Daytrana) to treat ADD, and those who had never taken ADD medication. Researchers found that participants’ DMN failed to de-activate, regardless of whether or not they had ever taken medication.