Transcript Child and Adolescent Psychopathology

Part III: Externalizing
Behavior Disorders
AttentionDeficit/Hyperactivity
Disorder
Chapter 12
Joel Nigg
HISTORICAL CONTEXT
 In the 1930s, it was discovered that Benzedrine (an amphetamine-
like stimulant) seemed to “calm” hyperkinetic children.
 FDA approval was granted for Ritalin in the early 1960s.
 By the 1970s, 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
20th 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:
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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:
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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?