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Part III: Externalizing Behavior Disorders

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Gene Environment Effects. Motivation, Approach, and Reinforcement Response. A comprehensive review by Luman et al. (2005) concluded that ADHD is associated with: – PowerPoint PPT presentation

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Title: Part III: Externalizing Behavior Disorders


1
Part III Externalizing Behavior Disorders
2
Attention-Deficit/Hyperactivity Disorder
  • Chapter 12
  • Joel Nigg

3
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.

4
TERMINOLOGICAL AND CONCEPTUAL ISSUES
  • It is important to note that symptom domains are
    divided into distinct dimensionsin 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

5
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).

6
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.

7
  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

8
  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.

9
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

10
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.

11
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.

12
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.

13
SEX DIFFERENCES and CULTURAL CONSIDERATIONS
  • ADHD shows a male preponderance, on the order of
    21 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).

14
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

15
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?
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