Abnormal Psychology

Childhood Disorders 661

disorder have smaller brains than do children and adolescents without the disorder,

and the defi cit in size is particularly marked in the frontal lobes (Schneider, Retz

et al., 2006; Sowell et al., 2003; Valera et al., 2007). Indeed, particular parts of

the frontal lobes have been shown to be smaller in adults with ADHD (Durston et

al., 2004; Hesslinger et al., 2002). However, the anatomical abnormalities are not

restricted to the frontal lobes. Parts of the temporal lobes are smaller than normal

in children and adolescents who have the disorder (Sowell et al., 2003), as are por-

tions of the corpus callosum, the basal ganglia, and the cerebellum (Castellanos et

al., 2002; Schrimsher et al., 2002; Valera et al., 2007). The cerebellar defi cit is par-

ticularly interesting because this brain structure is crucial to attention and timing; in

fact, the smaller this structure, the worse the symptoms of ADHD are (Castellanos

et al., 2002; Mackie et al., 2007).

Some of the brain differences between people who have ADHD and those

who do not may actually arise because the brain has attempted to compensate for

the impaired regions. Perhaps critically, at least some of the differences found in the

brains of children—notably those in the basal ganglia—do not persist into adult-

hood (Castellanos et al., 2002; Schneider et al., 2006). This fi nding is consistent

with the fact that over half of the children who are diagnosed with ADHD do not

meet the diagnostic criteria when they become adults (Schneider et al., 2006).

Regarding brain function, the research results indicate that ADHD is not a result

of impaired functioning in any single brain area, but rather emerges from how different

areas interact. As the anatomical abnormalities would suggest, neuroimaging studies

have revealed many patterns of abnormal brain functioning in people who have ADHD

(Rubia et al., 2007; Stevens, Pearlson, & Kiehl, 2007; Vance et al., 2007). In general,

neural structures involved in attention, including portions of the frontal and parietal

lobes, tend not to be activated as strongly (during relevant tasks) in people with this

disorder as in people without it (e.g., Stevens, Pearlson, & Kiehl, 2007; Schneider et al.,

2006; Vance et al., 2007). However, virtually every lobe in the brains of individuals

with ADHD has been shown not to function normally during tasks that draw on their

functions (e.g., Mulas et al., 2006; Schneider et al., 2006; Vance et al., 2007).

In addition, abnormal brain functioning can infl uence the autonomic nervous

system (see Chapter 2): ADHD (and some types of conduct disorder) has been as-

sociated with unusually low arousal in response to normal levels of stimulation

(Crowell et al., 2006), a response that could explain some of the stimulation-seeking

behavior seen in individuals with this disorder. That is, these people could engage in

stimulation-seeking behavior in order to obtain an optimal level of arousal.

ADHD and Neural Communication

The overall pattern of diffi culties that characterizes ADHD suggests problems with

multiple neurotransmitters that are involved in coordinating and organizing cogni-

tion and behavior. For one, dopamine apparently does not function effectively in

the brains of people with this disorder (Volkow et al., 2007). This malfunction may

arise for any of various reasons, including too few of the relevant receptors or prob-

lems in removing dopamine from the synapse (Swanson et al., 2007). But dopamine

functioning is not the only issue: Imbalances in serotonin and norepinephrine may

also contribute to the disorder (Arnsten, 2006; Gainetdinov et al., 1999; Waldman

& Gizer, 2006), and the activity of other neurotransmitters may also be disrupted

(Pattij & Vanderschuren, 2008). Given the number of brain areas that are involved,

it is not surprising that problems with multiple neurotransmitters are likely to be

associated with the disorder.

ADHD and Genetics

Genes may be one reason why people with ADHD have abnormal brain systems and

disrupted neural communication. Indeed, not only does this disorder runs in families,

but also parent and teacher reports indicate that it is highly correlated among mo-

nozygotic twins (with correlations ranging from 0.60 to 0.90). In addition, a large

set of data reveals that this disorder is among the most heritable of psychological dis-

orders (Martin et al., 2006; Stevenson et al., 2005; Waldman & Gizer, 2006).

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