1. “Defects in moral control”, independent of intellectual development Inadequacy of self-control despite seemingly adequate child-rearing or environmental stimulation Deficiencies in attention, moral consciousness, responsiveness to discipline, emotional maturity, and social conduct (e.g., lying and stealing) Increased minor physical anomalies Greater proportion of males Hereditary predisposition Still, 1902 Research Report

2. ADHD: Prevalence and Demographics Affects school-aged children – Overall prevalence 3% to 5% – Diagnosed in boys 3 to 4 times more than in girls – Unclear if prevalence is similar in other cultures Accounts for 30% to 50% of mental health referrals for children Prevalence increases as SES level declines Resulted in ~8.6 million physician-office visits in 1999 Persists in some patients into adolescence and adulthood (symptom profile may change)

3. ADHD: Diagnosis Diagnostic assessment typically prompted by academic and/or behavioral problems Diagnosis requires meeting DSM-IV criteria Clinical diagnosis requires input from parents, teachers, practitioners Specific physical tests not available Medical and neurological status evaluated

4. ADHD: DSM-IV Symptoms Six of more of the following Inattention Careless Difficulty sustaining attention in activity Doesn’t listen No follow through Can’t organize Avoids/dislikes tasks requiring sustained mental effort Loses important items Easily distracted Forgetful in daily activities

5. ADHD: DSM-IV Symptoms Six or more of the following Hyperactivity Squirms and fidgets Can’t stay seated Runs/climbs excessively Can’t play/work quietly “On the go”/ “Driven by a motor” Talks excessively Impulsivity Blurts out answers Can’t wait turn Intrudes/interrupts others

6. ADHD: Symptoms and Diagnosis Symptoms—inattention and/or hyperactivity- impulsivity – Present before age 7 years – Maladaptive and inconsistent with developmental level – Persistent (>6 months) – Impairment is present in two or more settings – Symptoms not due to other psychiatric/developmental disorders Diagnosis—DSM-IV types – Predominantly inattentive – Predominantly hyperactive-impulsive – Combined Type

7. ADHD: Social and Academic Impact Symptoms of ADHD interfere with child’s functioning at home, at school, with peers, which may include – Stress on family – Poor school performance – Classroom disruptions – Poor peer interactions Embarrassment of taking medication at school

8. ADHD: Potential Consequences As reported in 1998 NIH Consensus Statement, ADHD has been associated with – Injuries, drug abuse, antisocial behavior when in combination with conduct disorders – Increased parental frustration, marital discord, as reported with other chronic disorders – Serious burden of medical costs for families not covered by health insurance – Disproportional share of resources and attention from health care system, schools, and other social service agencies

9. ADULT ADHD Utah Criteria A. Childhood history of ADHD* 1. Fidgety, restless, always on the go, talked excessively 2. Attention deficit 3. Behavioral problem in school 4. Impulsivity 5. Overexcitability 6. Temper outbursts *Must have first two characteristics and at least two of the remaining characteristics

10. ADULT ADHD Utah Criteria – Cont’d B. Presence of ADHD in Adulthood* 1. Persistent motor hyperactivity 2. Attention deficits 3. Affective lability 4. Inability to complete tasks 5. Poorly controlled temper, explosive, short-lived outbursts 6. Impulsive behavior (distinct from manic episode) 7. Stress intolerance *Must have first two characteristics and at least two of the remaining characteristics

11. MANIFESTATIONS OF ADULT ADHD  Impaired social skills  Low self-esteem  Frequent loss of temper  More driving accidents  Difficulty organizing/finishing tasks  Anxious restlessness  Frequent job failures  Increased risk for antisocial behavior, mood disorders, substance abuse

12. ADHD: Differential Diagnosis A. Psychiatric 1. Learning disabilities 2. Conduct disorder 3. Affective disorder, depression, bipolar disorder, mania 4. Pervasive development disorder (e.g., autism) 5. Childhood schizophrenia 6. Anxiety disorders (separation anxiety, school phobia) 7. Mental retardation

14. ADHD: Differential Diagnosis B. Medical 1. Use of phenobarbital as an anticonvulsant 2. Theophylline (used in asthmatics) 3. Substance abuse (amphetamines) 4. Hyperthyroidism 5. Tourette’s syndrome

16. ADHD: Genetic Factors A. Family aggregation studies 1. First-degree relatives 2. Second-degree relatives B. Adoption Studies C. Twin Studies D. Other Genetic Hypotheses 1. Tourette’s syndrome (50% of affected individuals have elements of ADHD) 2. Mutation giving rise to generalized resistance to thyroid hormone

17. ADHD: Neuroanatomical Substrates A. Frontal Lobe Hypothesis B. Non-Dominant Frontal-Striatal Dysfunction C. Corpus Callosum - ? Decreased Splenial Area

18. ADHD: Suggested Pathophysiology Neurochemical pathways – Dopaminergic and noradrenergic implicated Structural and functional differences from non- ADHD controls – PET and MRI Scans of ADHD patients show reduced glucose metabolism in premotor cortex and superior prefrontal cortex compared to controls – Dopamine transmission Genetic forms of ADHD are associated with abnormalities at the dopamine reuptake transporter gene and the D 4 receptor gene

19. ADHD: Total Treatment Program Total Treatment Program: Recommended for maximum benefit Behavior Management: Includes strategies and methods for home and classroom environments Pharmacological Treatment: Targets underlying neurochemical causes Enhances behavior management efforts

20. ADHD: Treatment Approaches Pharmacological Intervention Parent Training Modification of Classroom Environment – Formal classification (IDEA) – “504” Accommodations Self-Control Training with Child Individual or Group Counseling Residential Treatment

21. ADHD: Unproven Therapies Removal of food additives, dyes, and flavors Removal of sugar or caffeine from diet Vitamin therapy Sensory-Integration training Avoidance of fluorescent lighting Relaxation training/biofeedback Play therapy

22. ADHD: Stimulant Treatment CNS stimulants highly effective – Reduce core symptoms of inattention, hyperactivity, and impulsivity in 75% to 90% of children with ADHD Pharmacological treatment usually involves – Methylphenidate products – Dextro-amphetamine/amphetamine products Common side effects – Insomnia, decreased appetites, dysphoric mood – Irritability, reduced motor activity – Headaches, G-I complaints – Tics – Decreased frequency of social interactions

23. ADHD: Methylphenidate Treatment Methylphenidate – Commonly prescribed medication – Formulations currently available Immediate-release Sustained-release Extended-release preparations –Taken only in the morning –Typically last between 6-12 hours depending upon dose

24. ADHD: Non-Stimulant Treatment Antidepressant Medications Tricyclic Antidepressants Used primarily for ADHD-Inattentive Type Studies have shown superior to placebo but less effective than stimulant medications Side effects: sedation, constipation, anoxeria, dry mouth, dizziness, increased pulse and BP (case reports of sudden cardiac death) SSRI’s Controlled studies to date not impressive (unless co- morbid depression is present) Some agents (e.g., fluoxetine) can increase hyperactive and or impulsive behavior

25. ADHD: Non-Stimulant Treatment Antidepressant Medications Others Buproprion – has amphetamine-like effect, useful in adult ADHD, pervasive developmental disorder

26. ADHD: Non-Stimulant Treatment Alpha-2 Agonists Clonidine Unclear if more effective in patients with greater impulsivity and behavioral dyscontrol (controlled trials equivocal) Commonly used to treat TS + ADHD Less effective than MPH in controlling inattention, distractibility Effect on cognitive and academic performance not established Side effects: sedation, motor retardation, dry mouth, dizziness Often used in combination with MPH Guanfacine Similar in action to clonidine but less sedating Controlled trials in ADHD equivocal; proven to useful in treating TS + ADHD

27. ADHD: Non-Stimulant Treatment Norepinephrine Reuptake Inhibitors Atomoxetine hydrochoride (approved 12/02) Selective NE reuptake inhibitor thought to be related to selective inhibition of the pre- synaptic norepinephrine transporter Can be dosed once or twice per day Generally well-tolerated upset stomach, decreased appetite, nausea and vomiting, dizziness, tiredness, and mood swings Cannot be taken with MAOI’s, certain SSRI’s