Attention Deficit/Hyperactivity Disorder

Attention deficit/hyperactivity disorder (ADHD) is one of the most com-monly diagnosed

psychiatric problems in children. About 5% of children are diagnosed with ADHD, although its

true prevalence is hard to estimate given that the diagnostic definition of ADHD is under

constant refinement. Children and adults with this disorder have great difficulty with cognitive-

control processes such as planning, organizing their time, keeping attention focused on a task,

and inhibiting responses to distracting stimuli. ADHD symptoms are especially evident in

settings that require the exercise of self-control. For example, ADHD children can sit still for

hours when they are actively engaged in playing interactive video games, but they have trouble

paying attention in school, where they must sit for long periods and pay attention to less

captivating information. Given these problems, it is not surprising that students with ADHD are

at elevated risk for academic under-achievement (Martinussen & Major, 2011).

Most researchers and clinicians believe that ADHD involves dysfunction in the prefrontal cortex

and its cortical and subcortical connections (Solanto, Arnsten, & Castellanos, 2000), including

connections to the cerebellum and the basal ganglia. The fact that ADHD patients have difficulty

sustaining a behavior or thought over a delay is consistent with the data reviewed earlier showing

that prefrontal cortical cells play a critical role in regulating thought and behavioral output

through their sustained firing over delays, in the absence of external input. Structural

neuroimaging of children with ADHD shows that they have a smaller right prefrontal cortex, the

region associated with spatial attention and working memory. Functional-brain-imaging stud-ies

have shown evidence of decreased prefrontal activity in ADHD, while diffusion tensor imaging

has indicated weaker prefrontal white matter con-nections (Arnsten, 2006; Castellanos &

Tannock, 2002).
 Behavioral research suggests that working memory in particular is impaired in patients with

ADHD. People with ADHD show marked deficits in mental calculations that require use of

working memory (Schweitzer et al., 2000). As with schizophrenia, current medications for

ADHD act in part by altering dopamine function in the cortex. The most common treatments for

ADHD, such as Ritalin (also known as methylphenidate), are stimulants that either increase

dopamine release or block its reuptake at synapses. Unfortunately, the effects of these

medications are temporary, and the behavioral problems often reappear after 3 or 4 hours.

There is strong evidence for frontal dysfunction in ADHD, but is the frontal cortex the origin

of the attentional and cognitive control problems in people with ADHD? Some investigators

have suggested that frontal-cortex dysfunction, and the associated working-memory and

attentional problems, are actually the consequence of deficits in other subcortical structures,

espe-cially the basal ganglia (Volkow, Wang, Fowler, & Ding, 2005, 2007). The basal ganglia,

as described in Chapters 5 and 8, are critically involved in skill learning and action selection. If

the origins of ADHD are in the basal ganglia, not the frontal lobes, why do stimulants improve

working memory and reduce symptoms of ADHD? One view is that people with ADHD have

“noisy” basal ganglia that sometimes send inappropriate signals to the prefrontal cortex, resulting

in distractible behavior, while at other times the basal ganglia do not signal the prefrontal cortex

when appropriate, resulting in perseveration or inattention (Volkow et al., 2005).

How and why do stimulant medications remediate the attentional prob-lems in people

with ADHD? One possibility is that stimulant medications increase the saliency of the basal

ganglia signal to the prefrontal cortex by increasing extracellular dopamine in the striatal region

of the basal gan-glia (Volkow et al., 2004, 2005). This hypothesis is consistent with studies

(reviewed in Chapter 5) describing a key role for dopamine in the basal ganglia (as well as in the
frontal lobes). Recent brain-imaging studies have argued that increased but inefficient activity in

the prefrontal cortex, found during certain task conditions in children with ADHD, may serve a

compen-satory function for dealing with noisy input from the basal ganglia (Sheridan, Hinshaw,

& D’Esposito, 2010).

Medications are not the only treatment for ADHD. Behavioral training methods may also

offer some relief. Several studies have shown that train-ing children with ADHD over the course

of several weeks to improve their working memory during certain tasks results not only in an

improvement on the tasks but also in a reduction in core symptoms of inattention and hyper-

activity (Klingberg et al. 2005; Beck, Hanson, Puffenberger, Benninger, & Benninger, 2010).

Thus, working-memory training appears promising as an intervention for improving cognitive

functioning and ADHD symptoms.

Like schizophrenia, ADHD is a heritable psychiatric disorder (which therefore tends to

run in families), and scientists are hot on the trail of the genetic bases for this heritability. Recent

research has identified some of the genes believed to be linked to ADHD. Like some of the genes

associated with schizophrenia, these ADHD genes regulate the function of dopamine in the brain

(Durston, 2010). Future research will hopefully identify the genes more clearly, discover how

they relate to the behavioral problems of ADHD, and thus provide us with clues for developing

more effective treatments. Advances in diagnosis are also sorely needed: studying mental

illnesses like schizophre-nia and ADHD is difficult because of the lack of clear disease markers,

lack of uniformly applied diagnostic criteria, and the growing realization that these disorders are

highly heterogeneous, with each patient sharing some but not all symptoms with others in the

same diagnostic category.

 Interim Summary

■ Working-memory impairments become apparent in people with schizophrenia during attempts

to maintain a large number of items over a temporal delay, an activity that requires functions

associated with the dorsolateral prefrontal cortex. In contrast, functions attributed to the

ventrolateral prefrontal cortex seem relatively unimpaired; thus, performance on phonological or

visuospatial memory tasks, and on memory tasks involving only minimal delays or few items,

appears normal.

■ People with ADHD show deficits in mental calculations that require use of working memory.

■ Neuroimaging of people with ADHD indicates that they have a smaller prefrontal cortex as

well as noisy input signals from the basal ganglia that prevent the basal ganglia from accurately

indicating what is or is not important to attend to.

Copyright | Worth Publishers | Learning and Memory | Edition 2 | Printed from www.chegg.com