Welcome to Your Child's Brain: How the Mind Grows From Conception to College (43 page)

In many respects, the answer is yes, as demonstrated by treatability and the recent identification of genes associated with it. However, ADHD’s history—including the recency of modern conditions that brought it to the forefront of public attention—has led to a fair amount of skepticism. Definitions of ADHD have changed several times since 1980 and are not always applied consistently. According to the American Psychiatric Association’s
Diagnostic and Statistical Manual of Mental Disorders
(DSM-IV), evaluators ask whether a child “is often easily distracted by external stimuli,” “often talks excessively,” or “often blurts out answers before questions have been completed.” Most children (including Sam in his earlier years) meet at least some of these criteria. Indeed, your child may have some of these characteristics, which are common in children. However, diagnosis requires that these symptoms must exist to a degree that is considered maladaptive.

The strongest evidence that ADHD is a real disorder comes from genetics. The susceptibility to ADHD is inherited. In genetic linkage studies, ADHD has a heritability of 70–80 percent, on par with autism and greater than schizophrenia. There are dozens of identified ADHD susceptibility genes, many of which are
involved in development and are also associated with autism and schizophrenia. Indeed, ADHD brains show changes in the growth trajectories of gray and white matter compared with normal development (see
chapter 9
).

At the same time, ADHD is also a product of social and cultural pressures. Your child’s brain was originally optimized by natural selection to help him handle everyday problems, which did not include sitting in a classroom, much less resisting the attraction of a television or text message. The mismatch between evolution and civilization has not always been addressed by treatment. Long ago, children who made trouble often dropped out of school and sometimes society—think of Huckleberry Finn. Some of them ended up working on farms or drifting into crime. In most developed countries, we no longer let such children go down their own paths. Stimulant drugs and other therapies provide a means to treat such children—perhaps along with other children who do not belong in this category.

ADHD appears to be part of the natural range in attentiveness that results from generation-to-generation shuffling of the gene pool.

Attention-deficit hyperactivity disorder is misnamed; children with this condition have the capacity to pay attention, but they lack the ability to control where their attention goes. Many such children have problems with executive function, a suite of capacities that includes planning ahead, inhibiting undesirable responses, and holding information in working memory (see
chapter 13
). One consequence is that ADHD children are bad at estimating time intervals of up to a minute, missing wildly. A second area of deficit is an inability to forgo a small immediate reward in order to get a larger one that comes later. For this reason, they count future rewards less than other children do when they make decisions about what to do.

Teachers and parents may be motivated to look for ADHD by the availability of drug treatments for improving children’s ability to focus. Most prominent among these is methylphenidate. This drug was first synthesized in 1944 by the chemist Leandro Panizzon. His wife, Rita, who had low blood pressure, used the
drug to pep herself up before tennis games. In a romantic gesture, Leandro named the drug Ritaline after her—today, Ritalin. In addition to its alerting qualities, Ritalin also helps mental focus and began to be used for ADHD in the 1960s.

Ritalin’s major biological action is as a
dopamine uptake blocker
; it prevents the neurotransmitter dopamine from being taken back up into neurons after it is released by synapses, thus prolonging its action on its receptors. Neurons in the ventral tegmental area and the substantia nigra release dopamine for a wide variety of functions: to regulate movement, to signal a rewarding event, and to control attention (see
chapter 14
). Dopamine uptake blockade is also the mechanism by which cocaine and amphetamine act. When cocaine, amphetamine, or Ritalin is present, dopamine hangs around longer in brain tissue and reaches higher concentrations—thus providing a stronger signal and better control over attention.

Only a few genes related to dopamine signaling have been linked to ADHD, and these genes have only a small influence on whether children develop problems. So despite the effectiveness of Ritalin, ADHD is not necessarily caused by a dysfunction of dopamine signaling. A more plausible explanation is that developmental steps impair the brain’s ability to stay on task, with dopamine signaling as one mechanism that feeds into the circuitry. Differences in this circuitry have been probed by measuring both activity and size of key brain structures.

Distinctive patterns of brain activity are seen in ADHD children. Electroencephalography (EEG) can record electrical signals at the scalp that reflect the activation of neurons near the recording electrode, in approximate synchrony. At this broad level, brain activity oscillates at a variety of characteristic frequencies, with different frequencies becoming more prominent depending on the task at hand. For instance, the theta rhythm, which rises and falls between four and seven times per second, is active in idling brains—a signal that indicates that a person is spacing out. Higher frequencies include the alpha (eight to twelve times per second) and beta (twelve to thirty times per second) rhythms, which become more prominent in a variety of states including relaxation, inhibition of action, and alert concentration. All of these can be measured using EEG.

In children and adults with ADHD, alpha and beta rhythms are smaller in strength relative to theta rhythm than in typical children. The disparity between these rhythms occurs in ADHD children resting with their eyes open or closed, as well as when they engage in other activities such as a drawing or solving a problem. It appears that the brain rhythms associated with idling are stronger relative to those associated with other mental states in ADHD children.

PRACTICAL TIP: SPOTTING UNTRUSTWORTHY TREATMENTS

We live in an age of celebrity spokespersons. For example, the model and comic actress Jenny McCarthy is an advocate for a popular—but thoroughly disproven—connection between vaccines and autism (see
chapter 27
). How should parents react to this onslaught of advice?

There is a long list of products sold using marketing claims that are poorly supported by science. These include brain scanning to diagnose and treat ADHD, balancing exercises for dyslexia, chelation therapy for autism, and nutritional supplements to aid brain function. Unfortunately, it’s often difficult to distinguish between scientists with no financial interests and companies trying to manipulate their data to sell products.

Often a speculative treatment is based on some loosely related piece of evidence. For example, in many disorders such as autism, abnormalities are seen in the cerebellum, a structure that is traditionally associated with movement. Organizations such as the Dore Programme assert that movement exercises can alleviate all sorts of problems, including dyslexia, autism, and learning difficulties, but there is no credible peer-reviewed evidence for these sweeping claims.

When evaluating possible treatments for any problem, parents should ask this key question: is the argument for this treatment based on peer-reviewed literature or on inspirational stories? If it’s based on stories alone, there is no reliable evidence for whether the treatment works. Other warning signs for quackery are the claim of a cure for a disorder whose causes are not understood, a single treatment that is claimed to be effective for multiple different disorders, and a failure to measure improvement objectively.

A few rules of thumb can help you identify which treatments are likely to be legitimate. Treatments that work for most people should be backed up by key phrases such as “peer-reviewed study,” “controlled study,” or “control group.” When enough studies are done, meta-analyses can combine them into an even stronger form of evidence. If these elements are missing, all that is left are anecdotes—which do not guarantee that your child will obtain any benefit. Particularly if a Web site is dominated by individual testimonials or the authority of one person, watch out!

Based on these differences, it may be possible to improve function in ADHD kids’ brains without resorting to drugs. Researchers devised exercises in which EEG signals are presented to the child as a form of
neurofeedback
. In a typical regimen, the child participates in a video-game-like exercise in which rewards are given for a desirable change, for instance, a decrease in the theta rhythm or an increase in the beta-to-theta ratio.

A meta-analysis of fifteen studies indicates that neurofeedback training reduces impulsivity and inattention considerably, with an effect size of 0.7 (see
chapter 8
for a discussion of effect sizes); that’s much larger than the improvements resulting from behavior modification alone and comparable to those seen using Ritalin. The meta-analysis included randomized trials (in which kids were assigned to treatment or no-treatment groups at random) and control groups who received similar amounts of training or therapist interaction as the test group, suggesting that the improvements came from neurofeedback treatment itself as opposed to other factors.

As might be expected from the EEG findings, differences are also seen in functional brain imaging studies. In this case, though, the differences are found when entire groups of ADHD children are averaged. Imaging methods are also far more expensive than EEG. Although some advertisements claim otherwise (see
Myth: The all-powerful brain scan
), functional imaging is not reliable enough to be useful as a clinical or diagnostic tool.

On average, ADHD children show some subtle differences in brain structure from other children. Between the ages of six and nineteen, the brains of children with ADHD are 3 percent smaller on average than those of typically developing children. This difference is not uniformly distributed over all parts of the brain. The largest reductions are seen in white matter, which is made entirely of axons. White matter is reduced by 5 to 9 percent, suggesting that long-distance axons in ADHD children are narrower (and therefore slower) or reduced in number. There is also a slight thinning of the gray matter of the prefrontal and temporal cortex as well as the vermis, or central part, of the cerebellum.

One consistent finding in brain scans has been a reduction in the size of the
caudate nuclei
. These nuclei (left and right) form one component of the dorsal striatum of the basal ganglia, which communicate with many parts of the neocortex. The basal ganglia are involved in directing attention and actions, for instance, in switching from one subject or task to another. One facet of switching is updating the importance of a particular stimulus or event. In addition, the basal ganglia select desired actions and reinforce the likelihood of action in future situations. Deficits in this ability could account for the difficulty that people with ADHD have in refraining from making an automatic or immediately appealing response—for example, looking in the direction of a distracting sound or attractive event.

MYTH: THE ALL-POWERFUL BRAIN SCAN