Conduct Disorder Psychology 7936 Child Psychopathology.
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Transcript of Conduct Disorder Psychology 7936 Child Psychopathology.
Conduct DisorderPsychology 7936 Child Psychopathology
1. Overview of DSM-5 Conduct Disorder2. Neurobiological substrates3. Environmental influences4. New model of Conduct Disorder5. Treatment
DSM-IV and Conduct Disorder (CD)• Three of the following present within last 12 months and at least
one within last six months:• Aggression toward people or animals• Destruction of property• Deceitfulness or theft• Serious violations of rules• Individual must be under 18 years of ageAll 15 of the criteria from DSM-IV were carried over to the DSM-5• Severity includes a mild, moderate and severe type.(American Psychiatric Association, 2000)
Conduct Disorder in DSM-5
• A new section called “Specify if” asking if the following are present:• “A lack of prosocial emotion”• “Lack of remorse or guilt”• “Callous-lack of empathy”• “Unconcerned with performance”• “Shallow or deficient affect”
(American Psychiatric Association, 2013)
DSM-5 model of Conduct Disorder
Core features:AggressionProperty destructionDeceitfulness or theftViolation of rules
DSM-5 Schematic of Conduct Disorder
DispositionGenetic predispositionDifficult temperamentLow verbal IQPhysiological substrates
EnvironmentFamilial risk factorsCommunity risk factors
Secondary Subtypes:Limited prosocialityRemorselessCallous-lack of empathyShallow affectUnconcerned with performance
Non-specified conduct disorder
Onset of Conduct Disorder
• DSM-5 says you can have one of three onsets:• Childhood-onset: one symptom before age 10• Adolescent-onset: symptoms occur after age 10• Unspecified onset: there is not enough information
• 90% of girls appear to show first symptoms between 7-9 years of age (Keenan, et al. 2010).• Although more commonly studied in boys a similar statistic
doesn’t seem to be available.
Prevalence of Conduct Disorder
• Rates vary by gender but prevalence does increase with age (Maughan, et al., 2004).• Prevalence rate estimates based on:
1. Child Symptom Inventories for CD & ODD2. The relational aggression subscale of the Children’s Peer Relationship
Scale3. The callous/unemotional subscale of the Psychopathy Screening Device4. The Child Global Assessment Scale5. Global teacher rating6. The self-report Social Dissatisfaction Questionnaire
Prevalence of Conduct Disorder (Maughan, et al., 2004).• Childhood rates of CD:• Boys: 0.5-2.8% prevalence• Girls: <1% prevalence
• Adolescent rates of CD:• Boys: 3.2-5.4% prevalence• Girls: 1.4-3.3% prevalence
Course• At age 30 CD is associated with (Olino, Seeley, & Lewinsohn, 2010):
• Reduced marital and life satisfaction• Less family support• Incarceration
• At age 28, men who had CD by age 10 cost society 10 times more in social services than peers who didn’t have CD (Grove, et al., 2008).
• Prognosis appears to be age-of-onset related (Barker, Oliver, & Maughan, 2010). • “Early onset persistent” CD is characterized by neuropsychological deficits and
Antisociality appears to remain constant into adulthood• “Childhood limited” CD is childhood limited, Antisociality doesn’t continue into
adulthood• “Adolescent onset” is believed to be related to peer relationships with AB remitting
during early adulthood• Conduct disorder in combination with specifiers indicates a poorer prognosis.
Course continued (Burke, Loeber, & Birmaher, 2002)• The risk for Conduct Disorder is four times higher in children who have a history
of ODD.• The relationship between ODD and CD generally considered hierarchical (ODD
as a precursor to CD).• Adolescent/Late-Onset CD is more common in girls and may not be preceded by
ODD type symptoms (Burke, Loeber, & Birmaher, 2002).
1. Overview of DSM-5 Conduct Disorder2. Neurobiological substrates3. Environmental influences4. New model of Conduct Disorder5. Treatment
Genetic predisposition• Meta-analytically, it is estimated that 40-50% of antisocial behavior (AB) variance is “influenced
by genetics” (Ferguson, 2010).
• A recent study of the children of monozygotic (MZ) and dizygotic (DZ) twins found that 41% of adult twin AB is accounted for by the cumulative effect of genes (Silberg, Maes, & Eves, 2012).
Shared Variance
Heritability of Antisociality• Silberg, Maes, & Eves (2012) used structural equation modeling to estimate
heritability for antisociality, among other constructs.• The design employed children of co-twins.• 856 adult twin pairs with known zygosity participated • Antisocial behavior (AB) was measured using a structured interview asking
about physical violence, serious police contact or arrests, financial irresponsibility and erratic employment.• Conduct problems in kids were rated using the Rutter “A” Scale.• Scores correlated significantly with interview data
• Discordant twin pairs include the affected twin and unaffected twin
Children of co-twin studies use the following logic:• A: If a trait is environmentally based then children of
Monozygotic (MZ) and Dizygotic (DZ) twins will have the same rate.
• B: Higher rates of a trait in children of MZ but not children of DZ suggests genes account for at least some of the intergenerational transmission.
• C: If both children of MZ and DZ parents have the same rate of a trait then shared environmental factors are most important.
(D’Onofrio, et al., 2003)
• T1 & T2: Twin 1 and 2• S1 & S2: Are spouses of the
twins• A: Additive Genetics (heritability)• C: Shared environment (e.g.,
same parents that affect both children)
• E: Unique environmental effect (i.e., an event that happens to one child but not the other)
Heritability of Antisociality• Silberg, Maes, & Eves
(2012), found that in children of twins with AB:• 8% of AB is accounted for by shared genes
with parents• 50% was accounted for specific child genetic
make-up• 1.4% accounted for by parenting by
antisocial parents• 22% by specific environmental influences• 16% by unique environmental influences
Neurological mechanisms• Frontal lobe dysfunction
• Frontal lobe damage is associated with proactive aggression (Burke, Loeber, & Birmaher, 2002).
• Orbitofrontal damage is related to reactive/impulsive aggression (Burke, Loeber, & Birmaher, 2002).
• Children with Disruptive Behavior Disorders (DBD) have lower mean cortical thickness• M = 4.06mm (SD = 0.05) compared to
4.48mm (0.03) in controls• Children with CD have thinning in the medial
prefrontal cortex (mdPFC) (Fahim, et al., 2011).
• Abnormal functioning of the Anterior Cingulate Cortex (ACC) is also related to CD.
• The mdPFCs communicate with the cingulate to constrain affective expression, deficits in this circuit are thought to be a cause of aggression (Fahim, et al., 2011).
(Fahim, et al., 2011)
• Fahim, et al. (2011) propose the “eruption of a geyser” model of DBDs1. ODD children who tend to overact to affectively charged situations find the physiological and emotional
arousal difficult to regulate.2. These children become over-aroused and become cognitively debilitated.3. These children then respond to the situation with even more affect and therefore are less able to reduce
aggression.
• The neuroanatomic “eruption of a geyser:”1. The insula, which processes emotions (such as anger) among other things, begins the eruption in response
to environmental stimuli.2. The insula is then not assuaged by the anterior cingulate cortex/medial prefrontal cortex/orbitofrontal
cortex then DBD/CD behaviors arise as a result of emotional dysregulation.
“Eruption of a Geyser” Model
Other structures/systems implicatedAutonomic Nervous System:• Attenuated resting electrodermal activity (EDA) and heart rate
• Low baseline EDA is a predictor, in infancy, of aggressive behavior at age 3 (Baker, et. al, 2013).
• Lorber (2004) found that across 95 studies there were small effect sizes for EDA and heart rate on conduct problems.
Neurochemicals:• Elevations of serotonin in the blood is related to aggression in boys (Burke, Loeber, &
Birmaher, 2002).• An interaction between serotonin, corticotrophin-releasing factor in the brain and GABA
receptor expression (Lee, 2006).• The exact mechanism of serotonin function is not currently known (Burke, Loeber, &
Birmaher, 2002).
Other biological causes (Burke, Loeber, & Birmaher, 2002)
Neurochemicals continued• Increases in testosterone and lower salivary cortisol are related to CD.Neurotoxins:• Lead has been related to cognitive performance, attention, and
aggression.
Prenatal/Perinatal factors:
• Maternal smoking during pregnancy is a predictor of CD
• Parental drug use is predictive of CD
Callous-Unemotional Traits (Frick, et al., 2003)• A subgroup of children with CD have what are termed Callous-
Unemotional (CU) traits. These children lack empathy and remorse.• These affective deficits are an early indicator of later
psychopathic personality.• These children are more sensation seeking are less sensitive to
punishment cues and are less fearful.• Children with CD and CU traits are less associated with poor
parenting practices and low verbal IQ.
CU Traits (Frick, et al., 2003; Kahn, et al., 2012)• Children with CU traits make up 10-32% of the CD population
(based on DSM-V specifiers).• 2-7% of children without CD diagnosis met CU specifier criteria.• CD with CU appears to be more heritable (81%) than non-CU
conduct disorder.Proactive aggression• Amygdala dysfunction leads
to a lack of empathy and attenuated reaction to fear in others leading to a potential for instrumental violence.
Callous-Unemotional Traits
• Amygdala dysfunction is implicated as a cause of fearlessness and lack of empathy in children with CD and CU traits.• More specifically, the right
amygdala is hypoactive when viewing both fearful and calm faces (Viding, et. al, 2012).
Callous-Unemotional Traits
• Recent evidence suggests the right amygdala mediates the relationship between CU traits and a measure of proactive (i.e., instrumental/non-reactive) aggression (Lozier, et al., 2014).
Other evidence for amygdala dysfunction• Deficient ability to label afraid faces and body postures
(Muñoz, 2009).• Similar to those with bilateral amygdala damage (Spezio,
Huang, Castelli, & Adolphs, 2007), children high in CU traits attend less to eye-regions of faces (Dadds, et al., 2008).
CU Traits and the Amygdala
1. Overview of DSM-5 Conduct Disorder2. Neurobiological substrates3. Environmental influences4. New model of Conduct Disorder5. Treatment
Coercive exchanges• Coercion: the contingent use of aversive behavior.
• Contingent implies the connection of one event with another.
• The child acts in a specific way which causes the reaction of the parent and in turn the parent’s action causes the child’s reaction.
• The context of the family affects this as do parental beliefs.
• A) a parent asks a child to do chores B) the child reacts by screaming and running away C) the parent stops asking to help with chores D) the child is negatively reinforced and these types of interactions become more frequent.
(Patterson, 2002)
SEM Evidence for Coercive Exchanges• 5 year old boys (n = 201) and girls (n = 206) of two-parent families
• Parents participated in a structured interview, answered questionnaires, and responded to three phone interviews
• Each family was observed at home for an hour on four occasions
• Children's behavior was coded for “demand attention verbal,” “demand attention non-verbal,” “physical aggression,” “verbal negative,” and “ignore.”
• Parents behavior was coded for “criticism or verbal punishment,” “physical restraint or aggression,” and “crying or whining.”
• Child Behavior Checklist and Parent Daily Report were used as measures of parents perceptions of their child’s behavior
(Eddy, et al., 2001)
• Children were found to behave aversely an average of 8 times/hr whereas parents responded aversely 1-2 times/hr.
• On average, the boys and the girls had similar rates of aversive behavior.
• The highly aversive acting boys appeared to act aversively even when unprovoked by parents whereas girls acted aversively as a result of parental aversive behavior.
• This study found that for both boys and girls inept parental discipline accounted for 50% of the variance in child antisocial behavior.
• These results suggest that aversive behavior begins similarly for boys and girls.
(Eddy, et al., 2001)
Developmental pathways to Conduct Disorder• A developmental pathway is a course that a group
of individuals takes that differs from other groups (Loeber & Stouthamer-Loeber, 1998)
• Factor analysis of parent, teacher and child reports support the contention that aggressive behavior should be parsed by type of act (Loeber & Stouthamer-Loeber, 1998).
• Three pathways to serious conduct or delinquent behaviors (Burke, Loeber, & Birmaher, 2002).
1. Overt pathway: progressing from minor aggression to physical fighting then violence
2. Covert pathway: before age 15 behavior progresses from minor covert behaviors (e.g., fire setting) to moderate or serious forms of delinquency
3. Authority conflict pathway: before age 12 progressing from stubbornness to defiance, and authority avoidance
• Children can be on more than one pathway at a time.
(Loeber & Stouthamer-Loeber, 1998)
Intelligence is PIQ > VIQ?• The DSM-5 cites low verbal IQ as a component of Conduct Disorder.
• PIQ>VIQ means that performance IQ is generally higher than verbal IQ in children with CD.
• The majority of the literature on IQ in conduct disorder uses various forms of the Wechsler scales.
• Recently this relationship has been examined meta-analytically.
• Over 166 samples of over 20,000 subjects
WISC
• For African American samples the size of discrepancy was low (ES = 0.20)
• For White/Racially heterogeneous samples the effect size was medium (ES = 0.48)
These results suggest that while a lack of comprehensive knowledge is found, these children
aren’t less intelligent.
(Isen, 2001)
1. Overview of DSM-5 Conduct Disorder2. Neurobiological substrates3. Environmental influences4. New model of Conduct Disorder5. Treatment
DSM-5 model of Conduct Disorder
Core features:AggressionProperty destructionDeceitfulness or theftViolation of rules
DSM-5 Schematic of Conduct Disorder
DispositionGenetic predispositionDifficult temperamentLow verbal IQPhysiological substrates
EnvironmentFamilial risk factorsCommunity risk factors
Secondary Subtypes:Limited prosocialityRemorselessCallous-lack of empathyShallow affectUnconcerned with performance
Non-specified conduct disorder
New model of Conduct Disorder
Core features:AggressionProperty destructionDeceitfulness or theftViolation of rules
Secondary Subtypes:Limited prosocialityRemorselessCallous-UnemotionalShallow affectUnconcerned with performance
Non-specified conduct disorder
NeurobiologyGenetic predispositionFrontal lobe dysfunctionAmygdala dysfunctionAutonomic under-arousalIncreased blood serotonin levelsDecreased cortisol
EnvironmentFamilial risk factorsCommunity risk factorsCoercive exchangesLow verbal IQ
68-90%
10-32%
1. Overview of DSM-5 Conduct Disorder2. Neurobiological substrates3. Environmental influences4. New model of Conduct Disorder5. Treatment
APA Division 53 Treatment Recommendations• Well established: at least two large-scale independent randomized
controlled trials showing superiority over other treatments or placebo (Eyberg, Nelson, & Boggs, 2008).• Parent Management Training Oregon Model• Teach parents basic behavior modification principles • Both parents and kids are seen by the therapist for an average of 17
hours of treatment.• The exception to this is if the child is very young
APA Division 53 Treatment Recommendations• Probably Efficacious: strong research support but lacking the
independent researcher criteria (Eyberg, Nelson, & Boggs, 2008).• Individual CBT: Anger Control Training
• Designed for elementary school aged children • Children learn the social-information processing model of anger control.
• Problem-solving skills training• Designed for children ages 7-13 with disruptive behavior• Comprised of 20-25 session of about 45 minutes • Treatment is focused on children• Children are taught to identify problems, weigh options, act decisively and evaluate the
outcome• Therapist model effective problem solving skills and can use a token economy to
reinforce effective problem solving behavior
Probably efficacious Continued
• Group assertiveness training (Counselor-led & Peer-led) • Approximately 8 hours of treatment based on the verbal response model of assertiveness
• Multidimensional treatment foster care• Children are put into a foster care home for 6 to 9 months• Foster parents are trained to implement a token economy• Foster parents meet with care team weekly and report points daily• An Applied Behavior Analyst works with the child in the community to help improve
prosocial behaviors• During this treatment the biological parents are given intensive behavior analysis training
to reintegrate the child back into the home and community• Multisystemic therapy
• Provided in the family’s home for 3 – 5 months • Combines CBT, pharmacological therapy, behavior therapy, and parent training
Possibly efficacious treatments
• Possibly Efficacious: preliminary efficacy evidence with maybe one study showing superiority over placebo or multiple clinical studies lacking sufficient experimental manipulation (Eyberg, Nelson, & Boggs, 2008).• Group CBT• This one should be used cautiously because of possible iatrogenic effects
• Group Parent Management Training• Psychoeducational group delivered to more than one parent at a time
Treatment (Grove, et al., 2008)
• Overall, meta-analytically, prevention/treatment has a small effect on CD behaviors (d = .17).• Programs intended to prevent behavioral referrals had a large effect (d = 1.31)• Programs to prevent conduct problems had a small effect (d = .28)• Programs to prevent a combination of symptoms also had a small effect (d = .19)• Aggression prevention had a small effect (d = .10)• Oppositional symptom prevention was also small (d = .06)
• Effects do not seem to be related to age of intervention, when treatment evaluation occurred• The percentage of boys in the study moderates effect size of intervention as
does the type of outcome measure used (e.g., official police records vs teacher rating scale)
Potentially Harmful Treatments (PHT; Lilienfeld, 2007)• It is estimated that 3-10% of clients experience deterioration effects
from therapy• Potentially Harmful Treatment• Demonstrated harmful psychological or physical effects of clients or others
such as relatives• The harmful effect is not short lived• Harmful effects have been replicated by multiple teams of researchers
• Although opportunity cost of receiving an ineffective treatment when an efficacious one is available is harmful but it is not a criteria for a PHT
Potentially Harmful Treatments (PHT; Lilienfeld, 2007)• Probably harmful: probably produce harm in some clients
a) Randomized controlled trials replicated by at least one other teamb) Meta-analyses of RCTs for the treatment orc) Consistent and sudden incidence of low-base-rate adverse events
following therapy
• Possibly harmful: preliminary evidence showing harmful effectsa) Quasi-experimental design that have been replicated by at least one
independent team orb) Replicated single case designs
PHTs for Conduct Disorder (Lilienfeld, 2007) • Level I: Probably harmful• Scared straight programs: • Found with randomized controlled trials to exacerbate conduct
problems• Children are 1.6-1.7 more likely to recidivate after these types of
programs• Boot-camp interventions: meta-analytic evidence shows
exacerbation of CD problems• Recent meta-analysis found that 9 out of 29 studies showed a positive
effect on AB, 8 showed iatrogenic effects and 12 showed no effects
PHTs for Conduct Disorder (Lilienfeld, 2007) • Level II: Possibly harmful• Peer-group interventions: quasi-experimental evidence shows an
exacerbation of conduct problems• One study found higher levels of AB and tobacco use in adolescents who
were in a peer-group compared to adolescents whose parents were in a “parent training” group• This type of group is sometimes called “deviancy training” because
antisocial youths can reinforce each others’ behaviors in group
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