Part III Externalizing Behavior Disorders Attention DeficitHyperactivity Disorder

Part III: Externalizing Behavior Disorders

Attention. Deficit/Hyperactivity Disorder Chapter 12 Joel Nigg

HISTORICAL CONTEXT In the 1930 s, it was discovered that Benzedrine (an amphetamine- like stimulant) seemed to “calm” hyperkinetic children. FDA approval was granted for Ritalin in the early 1960 s. By the 1970 s, treating inattentive and hyperactive children with stimulants began to spark controversy. Treatment rates rose markedly from 1990 to the present, attributable in part to changes in educational policy that facilitated identification of children with ADHD in the United States. Traditionally considered a disorder of childhood, by the end of the 20 th century it became clear that ADHD often persists into adolescence and adulthood.

TERMINOLOGICAL AND CONCEPTUAL ISSUES It is important to note that symptom domains are divided into distinct dimensions—in the DSM-IV: Inattentive-disorganized • Strongly associated with academic problems and a range of other impairments Hyperactive-impulsive • Associated with peer rejection and disruptive tendencies in school and at home

PREVALENCE In one national survey, a 1 -year prevalence rate for children and adolescents of 8. 5% is reported (Merikangas et al. , 2010). Among U. S. adults, the prevalence of ADHD is 4. 4% (Kessler et al. , 2006).

RISK FACTORS AND ETIOLOGICAL FORMULATIONS Within-child correlates may elucidate etiology and help explain the behavioral problems observed. Risk factors may contribute to the disorder, perhaps via these internal mechanisms. Genetic Influences on Liability to ADHD Hereditability of ADHD is likely to be around. 7. Nonshared environmental effects account for the remainder of variance in ADHD liability.

Gene × Environment Effects Environmental Risks and Triggers Specific environments • Inadequate schooling, rapid societal tempo, and family stress are contributing to an alleged increase in ADHD incidence. • Many of these sociological ideas are interesting but untested (or untestable) and some (like schooling) occur too late in development to account for ADHD onset. • Regarding other potential environmental potentiators of genetic liability, biological context, both pre- and postnatally, may be especially important

Gene × Environment Effects Mechanisms I: Neuroimaging Findings Structural findings demonstrate that on average, children with ADHD evidence a 5% reduction in overall brain volume and a 12% reduction in volume of key frontal and subcortical structures, particularly the prefrontal cortex (PFC), which is crucial to complex, planned behavior, keeping goals in mind, and overriding inappropriate responses. The most compelling evidence points to a neural circuit that links the prefrontal cortex and a subcortical region known as the striatum, a circuit thought to be important in response output control.

Gene × Environment Effects Mechansism II: Performance Studies of Neuropsychological and Cognitive Abilities Four key functional systems in the brain are implicated in ADHD: • • Nonexecutive attention and arousal Executive functioning and cognitive control Motivation and reinforcement Temporal information processing

Gene × Environment Effects Motivation, Approach, and Reinforcement Response A comprehensive review by Luman et al. (2005) concluded that ADHD is associated with: • Increased weighting of near-term over long-term (but larger) reward. • Possible positive response to high-intensity reinforcement. • Lack of physiological response (e. g. , heart rate acceleration) to potential rewards. Temporal Information Processing and Motor Control Problems in cerebellar functioning and temporal information processing could contribute to poor reinforcement learning, poor executive functioning, and even poor motor coordination.

DEVELOPMENTAL PROGRESSION Motoric hyperactivity is more pronounced in preschool, and tends to decline with time. Problems with inattention can become more pronounced with age as peers undergo rapid maturation of prefrontal cortical structures and accompanying cognitive abilities at the same time that school demands intensify.

COMORBIDITY ADHD is highly likely to exist in concert with one or more disruptive behavior disorders, this rate is about 50% for ODD and about 22% for CD (Willcutt et al. , in press). Anxiety co-occurs with ADHD, but any one anxiety disorder is seen only in a minority of cases (e. g. , 10% to 15% of children with ADHD will have a generalized anxiety disorder (Willcutt et al. , in press). About one quarter of children with ADHD meet criteria for a learning disorder.

SEX DIFFERENCES and CULTURAL CONSIDERATIONS ADHD shows a male preponderance, on the order of 2: 1 or higher but seems to drop in adolescence and adulthood (Polanczyl et al. , 2007). ADHD-related behaviors may not have the same meaning in the eyes of teachers and parents across cultural groups. It is unclear to what extent the ADHD syndrome has similar internal validity across ethnic or cultural groups. Treatment rates vary radically across nations and approaches to treatment may be different across cultural groups even within the United States (Visser, Bitsko, Danielson, & Perou, 2010).

PROTECTIVE FACTORS Tully et al. (2004) found that parental warmth moderated the effect of low birth weight on ADHD outcomes. Children exposed to multiple indicators of adversity, but who are below clinical cutoffs for ADHD symptoms, are more effective in neuropsychological response inhibition and have fewer “risk” catecholamine genotypes (Nigg, Nikolas, Friderici, Park, & Zucker, 2007). Secondary protective factors include: Stronger reading ability Absence of aggressive behavior Positive peer relations Effective parenting

FUTURE DIRECTIONS How will the phenotype best be defined, and in how will heterogeneity and specificity issues be resolved? What are the specific etiologies of the expected subgroups currently defined as having ADHD? What are key moderators of the meaning and outcome of these behaviors?