ABSTRACT

Attention-deficit/hyperactivity disorder (ADHD) is one of the most common childhood dis­orders referred to mental health professionals. ADHD, a complex neurodevelopmental disorder, is seen in approximately 3-7% of school-aged children, with higher rates found among boys than girls (6 :1 in clinical settings, 3:1 in community settings) in the United States (e.g., Barkley, 1998; Pastor & Reuben, 2002). In a review of estimates over a four-year period, Rowland, Leswesne, and Abramowitz (2002) found that prevalence rates varied substantially, based on presenting symptoms, assessment approaches used, and setting in which the child was evaluated. Furthermore, lack of consensus on what constitutes a core set of symptomol-ogy for ADHD children complicates the screening and assessment process (e.g., Brown et al., 2001; Elia, Ambrosini, & Rapoport, 1999). Researchers contend that a coherent set of symp­toms and causal factors does not exist, and this disorder represents a heterogeneous group of separate disorders (Neul, Applegate, & Drabman, 2003). For example, Goodman and Poillion (1992) identified 69 separate characteristics of ADHD, with 38 associated causes.Etiological considerations focus on neurobiological differences, heredity, and environ­mental influences as causal agents of ADHD (e.g., Barkley, 1998; Pearl, Weiss, & Stein, 2001). Brain differences between ADHD children and controls represent the most widely researched and theorized variable (DuPaul & Stoner, 2004). Tannock (1998) reported that the fronto-striatal networks and the prefrontal cortex showed anomalies (i.e., smaller quantities of dopamine and norepinephrine in the prefrontal cortex) among ADHD samples. The prefrontal cortex controls behavior inhibition and responses to environmental stimuli, two essential variables of ADHD symptomatology. Tannock asserted that the causes of these neurobiolog­ical abnormalities may center on genetic, hormonal, and/or environmental factors.ADHD has the highest rate of hereditability among children with emotional and behav­ioral disorders (Pearl et al., 2001). Research has suggested that a genetic component exists in approximately 80% of ADHD cases. Moreover, research on “clusters” of ADHD in families

provides further evidence for the hereditary influence (Johnston & Mash, 2001). However, it is unknown whether the high rates of ADHD among relatives are due to heritability factors or shared environments among individuals who are related. Research has found that environ­mental toxins such as poor nutrition, lead poisoning, smoking during pregnancy, and prenatal exposure to drugs or alcohol may be related to the development of ADHD symptoms and impairments (e.g., Mick, Biederman, Faraone, Sayer, & Kleinman, 2002; Mick, Bieder-man, Prince, Fischer, & Faraone, 2002). However, environmental toxins affect only symptom severity and do not cause the disorder (e.g., DuPaul & Stoner, 2004; Rowland et al., 2002).The evaluation process is also guided by theoretical models of ADHD that focus on how deficits in behavior inhibition lead to impairments in brain functioning and subsequent emo­tional and behavioral difficulties (e.g., Barkley, 1997; Logan, 1994; Quay, 1988; Schachar, Tannock, & Logan, 1993). A child’s failure to inhibit responses to stimuli triggers maladap­tive reactions that can culminate in ADHD symptoms and impairments. The DSM IV-TR (2000; DSM-IV-TR) describes ADHD as a “persistent pattern of inattention and/or hyper-activity-impulsivity that is more frequently displayed and more severe than is typically observed in individuals at a comparable level of development” (p. 85). This description does not capture the complex brain functions and emotional and behavioral difficulties of those with ADHD. For example, Bronowski (1967, 1977) argued that inhibition and how language is internalized affect children’s working memory and responses to stimuli in the environment. Language skills create an ability to think intuitively about the past and future and modulate responses to the environment based on that information.Based on Bronowski’s work (1967, 1977) and Fuster’s theory of prefrontal function (1989, 1995), Barkley (1997) proposed a hybrid model of ADHD that details inhibition and its complex impact on executive functions (i.e., working memory, internalization of speech, self-regulation of affect-motivation-arousal, and reconstitution). He outlined three activities inherent in the behavioral inhibition process (i.e., the ability to inhibit initial response, the ability to stop an ongoing response, and skill in controlling interference) and proposed that the four executive functions depend largely on successful enactment of these activities. The inability to control responses, in turn, leads to manifestations of ADHD symptomatology. ADHD symptoms are described as the failure to inhibit task-irrelevant responses, execute goal-directed persistence, incorporate feedback from the environment, re-engage in tasks fol­lowing disruption, and control behavior through internally represented information (Barkley, 1997). Thus, disinhibition can negatively affect children’s attention, motor control, impul­sivity, and emotional and behavioral development.This chapter provides an overview of the assessment practices for children and adoles­cents with ADHD. The comorbidity and differential diagnosis of ADHD and ADHD-related disorders are presented. A description of some of the major cognitive/neuropsychological and social/emotional assessment approaches used with this population is offered. Finally, a case study is presented to illustrate the application of these measures with an ADHD child.