Transcript Attention-Deficit Hyperactivity Disorder

&
Oppositional Defiant Disorder, Conduct
Disorder, and Juvenile Delinquency
Child and Adolescent
Psychopathology
1) Inattentive-disorganized (314.00)
2) Hyperactive-impulsive (314.01)
3) Combined type (314.01)
 Controversy over whether
impulsivity should belong to
hyperactive-impulsive type
or separate category
 Careful history
 Data from multiple informants (e.g., parents, teachers)
 Not normal developmental variation (e.g.,
toddlerhood)
 Rule-out diagnoses (e.g., anxiety and mood disorders,
sleep and health-related disorders, some learning disorders)
 Direct observations
 Functional impairments (e.g., at home and school, with
peers)
In U.S. population:

6.8% between ages 6-11
(although half also received
diagnosis of LD)

4.4% of adults diagnosed

5.3% of worldwide prevalence estimate
*Percent of Youth 4-17 ever diagnosed with AttentionDeficit/Hyperactivity Disorder: National Survey of Children's
Health, 2003
① Genetic influences on liability to ADHD:
 Heritability
estimated between .6 and .9
 Nonshared environmental effects are modest to
small
 Shared environmental effects are negligible
 Genome-wide scans: focus on chromosome 5
(where DA transporter gene has been mapped)
 Candidate
gene studies: DA receptor genes (e.g.
DA beta-hydroxylase gene)
② Environmental Risks and Triggers
a)
Gene-environment correlations:
 Parents who pass on ADHD genes
and also provide chaotic home
environment
 Child contributes to
counterproductive socialization
experiences
 Caregiver behavior also impacts
ADHD sx
 Transactional model: but child effects
are greater
(e.g., medication reduced mothers'
negative/controlling behaviors)
b)
Gene-environment interactions
Inflated heritability term in twin studies: experiential
effects might differentially activate genetic risk

Unknown effect size of
these experiential effects

c)
Environmental risk factors:
 Low birth weight (<2,500 grams)
 Prenatal teratogens:
o
o
Maternal alcohol exposure
Maternal smoking
 Postnatal exposure to toxins
(e.g., lead exposure)
 Dietary insufficiencies
(Uganda experience)

5% reduction in overall brain volume

12% reduction in volume of key frontal and subcortical
structures
*UQ neuroscientist, Dr Ross Cunnington of Queensland
Brain Institute (QBI) said there appears to be a biological
difference in the brain that makes some children more
susceptible to attention deficit hyperactivity disorder,
combined type (ADHD-CT) (2007)
*Neuroanatomical and functional model of attention-deficit
hyperactivity disorder developed by Arnsten et al. (1996). Lateral view
of the brain with a section of the cortex removed. Red lines represent
noradrenergic pathways and black lines indicate cortical pathways mediated
primarily by excitatory amino acids.
Attention: ability to filter information is compromised
② Cognitive control: strategic allocation of attention and
response is compromised
①
a) Working memory:
Limited capacity system
for keep something in mind
while doing something else
is compromised, especially
spatial working memory
weaknesses
b) Response suppression:
Ability to interrupt a
response during dynamic
moment-to-moment
behavior (e.g. checkswing) is compromised
c) Set shifting: shifting one’s mental focus within a task
is compromised (e.g. sorting by color or number)
*Wisconsin Card Sorting task
d) Task switching: alternating tasks is compromised
(e.g. counting or naming objects)
③ Motivation, approach, and reinforcement
response
a) ADHD not related to low reactive control as
in psychopathy
b) ADHD related to weakened reinforcement delay gradient - lose interest in reward earlier
than others
c) Positive response to high intensity
reinforcement
d) Lack of physiological response to potential
rewards
④ Temporal informational processing and motor
control
a) Faulty time perception for behavioral control
b) Poor time estimation
c) Poor time reproduction

Diagnosis as young as age 3

Motoric hyperactivity more pronounced in
preschool

Inattention more pronounced with age

Criteria for adolescents and adults are lacking
 Sex differences:

Male preponderance:
2.5:1 in childhood, 1.6:1 in adulthood

Girls are less likely to show comorbid
externalizing problems

Some impaired girls are missed by current
diagnostic criteria

Girls might have greater resistance to etiological
factors of ADHD

ADHD informant ratings differ
cross-culturally

ADHD might consist of different
systems cross-culturally

Differences in treatment crossculturally (stimulants for
minorities)

 Birth weight × lack of parental warmth  ADHD
(moderational model)

Effectiveness in neuropsychological response
inhibition

Protective factors for ADHD children:




 reading ability
absence of aggressive behavior
positive peer relations
effective parenting

Specification of
heterogeneity of ADHD

Specification of etiologies of
ADHD subgroups

Specification of key
moderators of ADHD
behaviors

Specification of long-term
treatment

Juvenile delinquency: Children who have broken a law

Conduct Disorder: 3 out of 15 antisocial behaviors within
12 months

Oppositional Defiant Disorder: 4 out of 9 disruptive
interpersonal behaviors

ODD, CD, ADHD all
co-occur

ODD and CD cooccur with depression
①
Childhood-onset (life-course persistent) trajectory:
(5-14%)
•
•
Early neurodevelopmental deficits
Inadequate parenting and adverse social influences
②
Adolescent-onset (adolescence-limited) trajectory:
(10-21%)
•
Few conduct problems in childhood
First law breaking in adolescence
Desist from offending in early adulthood
•
•
③ 3:1 Ratio of males to females for childhood onset,
but 1:1 ratio for adolescent onset
④ Not two distinct trajectories but rather a continuum
for children
⑤ CD children mostly childhood onset and met
criteria of ODD
①
ODD more prevalent than CD during early
childhood
②
ODD and CD have equal prevalence through
adolescence
③
CD increase is greater in males than females
④
ODD more prevalent in males at all ages
⑤
Rates of delinquency peak at 16 or 17 and then
decline sharply (age-crime curve)
① Temperament: resists control, responds to threats
with negative emotions, daring sensation-seeking,
low prosocial behaviors, impulsivity, lack of
persistence
② ODD  CD
③ ADHD × CD 
APD (moderational
model)
④ Early shyness and anxiety   conduct problems
  Childhood cognitive skills and  language 
 conduct problems
⑥ Lower verbal intelligence
  conduct problems
because affect more likely
to be expressed
behaviorally, more
frustrating for parents
  Likelihood of other serious mental Dx in adulthood
② Majority of CD children (60-70%) do not progress to

④
⑤
⑥
APD
 Likelihood of depression (CD  stressful life
events  depression) (mediational model)
Adolescent suicide  with CD, depression, and
substance abuse
Adult males: criminal behavior, work problems,
substance abuse
Adult females: depression, suicidal behavior, poor
physical health
 Birth weight and birth complications
 Maternal cigarette smoking and substance use
during pregnancy
 SES + lower parental education (mostly childhood
onset)
 Parental characteristics, family characteristics, and
parenting




Parental antisocial behavior and substance abuse
Low maternal IQ
Young mothers
Mother’s multiple partners and discordant relationships
 Deviant peer influence and gang membership
•
•
Almost all adolescent crime is committed with
peers
Association with delinquent peers is highly
correlated with delinquency
 Neighborhood and urbanicity: poverty and
social disorganization
 Maltreatment × low-activity MAO-A genotype

 Conduct problems
  Birth weight × high-risk COMT genotype

 Conduct problems
 Prosociality vs. callousness
 During sensation-seeking
vs. fearful inhibition
 Negative emotionality vs.
emotional stability
 Slowly developing cognitive
skills and language
(interferes with socialization
experiences)
Fin