Part I of this blog summarized what I’ve been reading about the most extensive body of research on the ADHD brain, which has focused on apparent anomalies in the dopamine system. A number of researchers theorize that the brain’s processing of dopamine encodes our predictions of future rewards for current behaviors and that ADHD reflects a systemic deficiency, which leads to Reward Prediction Error. The result is that people with ADHD are more likely to favor behaviors (e.g., inattention, impulsivity) based on an immediate sense of reward even when a deferred reward is likely to be greater.
The dopamine system is not the only part of the brain being studied in the search to explain ADHD. Researchers have been exploring other regions, discovering other anomalies, and arriving at other hypotheses.
Cortical Thickness
For many years, there has been a debate among neuroscientists as to whether ADHD arises from permanent differences in the brain or temporary variations associated with delays in its development. An intriguing contribution to this debate came from a study first reported in 2007 by Philip Shaw, MD and his colleagues at the NIMH Child Psychology Branch. These scientists conducted brain imaging among 446 children of varying ages, including 223 who had been diagnosed with ADHD and 223 who had not. With each child, they meticulously measured the thickness at more than 40,000 points along the cerebral cortex, the outer layer of gray matter that surrounds the rest of the brain. Most of the children were imaged at least twice over a period of several years. The cortex performs a great many functions that include planning, organizing, analyzing, regulating emotions, controlling behavior, solving problems, using language, making decisions, and processing signals from our sensory organs.
The cortical measurements revealed a growth pattern in which the subjects’ cortices gradually thickened until they reached a peak thickness and then became thinner, presumably as the brain pruned away neurons that were no longer needed. This pattern appeared to occur to the same degree and in the same sequence among all the children studied. However, it did not always occur at the same times. On average, the cortices of the neurotypical subjects reached peak thickness when they were 7.5 years old. Among the ADHD children the peak occurred considerably later at 10.5 years. The study also determined that this delay was prominent in the prefrontal brain regions that support attention, planning, and impulse control. Based on these findings, the researchers hypothesized that ADHD derives not from permanent variations in the ADHD brain but, rather, from delays in its cortical development that may resolve over time. One implication of this finding is that many people hindered by ADHD in childhood might reasonably expect their symptoms to diminish during and after adolescence. This is the experience reported by half or more of ADHD adults, including me.
But Wait…There’s More
The study described above is only one of many that have sought to explain ADHD in terms of specific brain regions or structures. Below are thumbnail sketches of several others.
• In 2014, science writer Anne Trafton reported on study conducted by MIT’s McGovern Institute of Brain Research, which found an association between ADHD and the brain’s default mode network, ten cortical regions that appear to be active when people are at wakeful rest and not focused on what is happening around them. Specific parts of the network account for specific types of thoughts that include musings about the past, the future, other people, and one’s self. Researchers determined that among ADHD children, two important parts of the default network – the posterior cingulate cortex and the medial prefrontal cortex – were not working with each other in synchronized fashion. They also found that, among adults who had been diagnosed with ADHD but no longer exhibited its symptoms, the asynchrony had disappeared. Based on these findings, they suggested that that the ADHD may be associated with brain regions that are working “out of sync.” It does make intuitive sense that ADHD might have something to do with parts of the brain activated during unfocused thinking.
• Researchers at England’s Cambridge University reported in 2013 on research that led them to question dopamine dysfunction as a major factor in ADHD. They based their conclusion on imaging studies showing that, in comparison to a control group, an ADHD group had no difference in dopamine activity. What that group did have was less brain matter overall.
• A 2002 study reported on imaging research that identified the part of the brain most active while subjects were completing a cognitive task. Among a control group it was the anterior cingulate cortex; among an ADHD group the active area was in the fronto-striato-thalamic network. The researchers hypothesized that ADHD may have something to do with the performance of cognitive tasks in regions other than those generally utilized by neurotypical brains.
• The American Journal of Psychiatry reported in 2009 on brain mapping research which indicated that, in comparison to controls, a group of ADHD boys exhibited differences in the size and shape of certain brain areas. They determined that the ADHD boys had a larger posterior putamen, smaller basal ganglia, and shape differences in specific parts of the basal ganglia. The functions of the basal ganglia include control of voluntary movements, procedural learning, and routine behaviors. A particularly intriguing finding was that none of the anomalies observed among the ADHD boys appeared in a group of ADHD girls who had also participated in the study. This may help explain why ADHD is less often diagnosed in girls and less likely to involve problems with impulse control. It may also suggest that boy ADHD and girl ADHD are different conditions that present in similar ways.
• Several studies have shown that the amount of gray matter in the caudate nucleus – a part of the basal ganglia that is associated with motor and impulse control as well as multiple cognitive functions – was significantly smaller in a sample group of ADHD children than among the controls. Based on reports of participants’ parents, the same ADHD group also had higher levels of hyperactive and impulsive behavior. A more recent study suggested that this anomaly also characterized a group of adults who had been diagnosed with ADHD.
• Other imaging studies have reported that in comparison with controls, ADHD children exhibited smaller frontal and temporal lobes, reduced connectivity in the brain’s white matter, and a greater volume of gray matter in two areas of the cortex. It may be that ADHD is associated with these differences.
• An fMRI study reported by Joel Nigg, Ph.D. in 2017 indicated that children with ADHD appeared to exhibit performance deficiencies in the frontal-parietal lobes believed to be part of our “attention network.” Nigg also described studies suggesting that in young ADHD brains certain axon fibers may not be fully developed, which could also account for under-performance in the attention network.
• In early 2018, a group of researchers at Baltimore’s Kennedy Krieger Institute and Johns Hopkins University School of Medicine published a brain imaging study of preschool children who had been diagnosed with ADHD. According to this research, the test subjects exhibited less than normal cortical volume in several areas of the brain, including the bilateral frontal, parietal, and temporal lobes. The study concluded that ADHD may be associated with anomalous brain structure or development.
Thus far, this blog has divided the research aimed at solving the ADHD riddle into two general streams: one focused on the dopamine system and the second looking at other brain structures. Before drawing any conclusions about either, it might be helpful to consider two more research streams that attempt to identify not differences in the ADHD brain but their origins. Those are explored Part III.
