Attention-Deficit / Hyperactivity Disorder

1. Attention-Deficit/ Hyperactivity Disorder Child and Adolescent Psychopathology & Oppositional Defiant Disorder, Conduct Disorder, and Juvenile Delinquency

2. Three types • Inattentive-disorganized (314.00) • Hyperactive-impulsive(314.01) • Combined type (314.01)   • Controversy over whether impulsivity should belong to hyperactive-impulsive type or separate category

3. Assessment of ADHD • 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)

4. Prevalence 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 Attention-Deficit/Hyperactivity Disorder: National Survey of Children's Health, 2003

5. Etiological formulations • 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)

6. Etiological Formulations • Environmental Risks and Triggers • 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)

7. Environmental Risks and Triggers • Gene-environment interactions • Inflated heritability term in twin studies: experiential effects might differentially activate genetic risk   • Unknown effect size of these experiential effects

8. Environmental Risks and Triggers • Environmental risk factors: • Low birth weight (<2,500 grams) • Prenatal teratogens:   • Maternal alcohol exposure   • Maternal smoking • Postnatal exposure to toxins • (e.g., lead exposure) • Dietary insufficiencies • (Uganda experience)

9. Neural imaging findings • 5% reduction in overall brain volume • 12% reduction in volume of key frontal and subcortical structures *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. *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)

10. Neuropsychological and cognitive abilities • Attention: ability to filter information is compromised • Cognitivecontrol: strategic allocation of attention and response is compromised

11. Cognitive control • Working memory: Limited capacity system for keep something in mind while doing something else is compromised, especially spatial working memory weaknesses • Response suppression: Ability to interrupt a response during dynamic moment-to-moment behavior (e.g. check-swing) is compromised

12. Cognitive control • Set shifting: shifting one’s mental focus within a task is compromised (e.g. sorting by color or number) *Wisconsin Card Sorting task

13. Cognitive control • Task switching: alternating tasks is compromised (e.g. counting or naming objects)

14. Neuropsychological and cognitive abilities • Motivation, approach, and reinforcement response • ADHD not related to low reactive control as in psychopathy • ADHD related to weakened reinforcement - delay gradient - lose interest in reward earlier than others • Positive response to high intensity reinforcement • Lack of physiological response to potential rewards

15. Neuropsychologicaland cognitive abilities • Temporal informational processing and motor control • Faulty time perception for behavioral control • Poor time estimation • Poor time reproduction

16. Developmental Progression • Diagnosis as young as age 3 • Motoric hyperactivity more pronounced in preschool • Inattention more pronounced with age • Criteria for adolescents and adults are lacking

17. Comorbidity: ODD, CD, anxiety disorders, learning disorders • 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

18. Cultural differences • ADHD informant ratings differ cross-culturally • ADHD might consist of different systems cross-culturally • Differences in treatment cross-culturally (stimulants for minorities)

19. Protective factors •  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 

20. Future directions • Specification of heterogeneity of ADHD • Specification of etiologies of ADHD subgroups • Specification of key moderators of ADHD behaviors • Specification of long-term treatment

21. Oppositional Defiant Disorder, Conduct Disorder, Juvenile Delinquency • 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

22. Comorbidity • ODD, CD, ADHD all co-occur • ODD and CD co-occur with depression

23. Developmental trajectories of conduct problems • Childhood-onset (life-course persistent) trajectory: (5-14%) • Early neurodevelopmental deficits • Inadequate parenting and adverse social influences • Adolescent-onset (adolescence-limited) trajectory: • (10-21%) • Few conduct problems in childhood • First law breaking in adolescence • Desist from offending in early adulthood

24. Developmental trajectories of conduct problems • 3:1 Ratio of males to females for childhood onset, but 1:1 ratio for adolescent onset Not two distinct trajectories but rather a continuum for children CD children mostly childhood onset and met criteria of ODD

25. Age, sex, and prevalence • ODD more prevalent than CD during early childhood • ODD and CD have equal prevalence through adolescence • CD increase is greater in males than females • ODD more prevalent in males at all ages • Rates of delinquency peak at 16 or 17 and then decline sharply (age-crime curve)

26. Child characteristics that predict CD and delinquency • Temperament: resists control, responds to threats with negative emotions, daring sensation-seeking, low prosocial behaviors, impulsivity, lack of persistence • ODD  CD • ADHD × CD APD (moderational model)

27. Child characteristics that predict CD and delinquency • Early shyness and anxiety conduct problems • Childhood cognitive skills and language conduct problems • Lower verbal intelligence conduct problems because affect more likely to be expressed behaviorally, more frustrating for parents

28. Adolescent and Adult outcomes of childhood ODD and CD • Likelihood of other serious mental Dx in adulthood • Majority of CD children (60-70%) do not progress to 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

29. Environmental risk factors for conduct problems • 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

30. Environmental risk factors for conduct problems • 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

31. Molecular Genetics • Maltreatment × low-activity MAO-A genotype  Conduct problems • Birth weight × high-risk COMT genotype  Conduct problems

32. Summarizing dispositions to 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)

33. Fin