ATTENTION-DEFICIT/HYPERACTIVITY DISORDER
From Masters of Pediatrics 2008 Leadership Conferences, presented by the University of Miami Miller School of
Medicine, Miami, FL
David O. Childers, Jr, MD, Chief, Section of Developmental Pediatrics, University of Florida College of Medicine,
Jacksonville
Educational Objectives
| The goal of this program is to present an overview of the diagnosis and management of attention-deficit/hyperactivity
disorder (ADHD), particularly as it relates to psychopharmacology. After hearing and assimilating this program, the
clinician will be better able to:
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 | 1. List the elements that go into a diagnosis of ADHD.
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| 2. Define the concept of receptive language age and explain its importance in diagnosis and management of
ADHD.
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| 3. Describe the long-term consequences of untreated ADHD.
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| 4. Discuss the role of psychopharmacology in the treatment of ADHD.
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| 5. Manage the side effects of medications used in treating ADHD.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the
planning committee to disclose relevant financial relationships within the past 12 months that might create any personal
conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes
quality in health care and not a proprietary business or commercial interest. For this program, the faculty and planning
committee reported nothing to disclose.
Acknowledgements
This program was recorded at the Masters of Pediatrics 2008 Leadership Conferences, held February 20-25, 2008, in
Miami Beach, FL, and sponsored by the University of Miami Miller School of Medicine. The Audio-Digest Foundation
thanks the speaker and the sponsor for their cooperation in the production of this program.
| Definition of attention-deficit/hyperactivity disorder (ADHD): neurologically based inability to attend to critical
items
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| Double-edged sword: child lacks own attention and can never get enough of another’s attention
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| Diagnosis: usually involves minimal brain dysfunction; never stand-alone diagnosis; should include diffuse pattern of biologically
based neurologic immaturities (eg, social, emotional, behavioral, learning, fine-[eg, dysgraphia] and gross-
motor function [eg, clumsiness, stress posturing]); according to Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition (DSM-IV), may be inattentive type or hyperactive/impulsive type; critical component, behavior
inappropriate for developmental level
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| Receptive language age: consists of sum total of level of developmental function; key to neurodevelopment; “internal
monologue” or “conversation in one’s head” on which judgment based; expressed as behavior modulation; determines
level of comprehension and attention (child’s attention issues cannot be determined until level of comprehension established);
involves ability to attend to things not inherently interesting; determines child’s ability to pay attention, independent
of medication
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| Executive function: basic neurologic problem in ADHD frontal lobe issue of executive function; according to model
developed by TE Brown, executive functions impaired in ADHD are activating (becoming engaged by something important),
focusing, regulating (focusing back and forth on various aspects of task), emotional regulation, memory, and
modulating and regulating behavior, based on feedback from actions
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| Brain areas governing executive function: anterior cingulate and basal ganglia—responsible for executive controls;
right frontal lobe—learning and vigilance; superior parietal lobe, thalamus, and midbrain—orientation and selective
attention; volumetric studies—children with ADHD have smaller brain structures than control children, except
for caudate nucleus; differences include frontal and temporal lobes, which are primarily responsible for executive function
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| Genetics of ADHD: multiple genes implicated by several studies; DAT gene—number of alleles may predict medication
efficacy and treatment outcomes; however, no one gene causes specific disorder or disease process; always combination
of genetic activation and environment
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| Neurotransmitters: interest in dopamine began in 1950s, when dextroamphetamine (Dexedrine) prescribed for weight
loss also proved effective against ADHD; norepinephrine, epinephrine, and serotonin also implicated, but not studied
in as much detail
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| Heritability: most cases inherited (odds ratio 0.8, with 1.0 being 100% likely); relatively rare, noninherited forms of
ADHD include those associated with extreme prematurity or fetal alcohol syndrome
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| Keys to understanding ADHD: biologically based, primary neurodevelopmental disorder resulting from central nervous
system pathology; organic, irreversible, and lifelong; sooner ADHD diagnosed, sooner adjustments can be made
in child’s environment; mild forms far more common than severe forms, but even mild cases should be treated to maximize
child’s potential; ADHD is real disorder with demonstrable genetic basis and heritability; biologic differences
reflected in smaller brain volumes, impaired executive function, and diffuse neurologic dysfunction among children
with ADHD; responsive to treatment, but medication is “Band-Aid” (cannot cure ADHD, but treatment allows child to
do well socially and academically until he or she masters behavioral interventions designed to foster self-control)
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| Intervention strategy: keys are consistency of medication and environment; genetic component suggests parents should
also be treated
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| Lifetime consequences of untreated ADHD: preschool—disruptive behavior; elementary school—academic
failure, poor socialization and self-esteem (class clown is classic manifestation); injuries; adolescence—smoking, substance
abuse, crime, car accidents; college—academic failure due to being overwhelmed from multitasking required;
adulthood—substance abuse, occupational failure (problems with sustained work environment), relationship failures;
chronic substance abuse and dependence, and frequent incarceration
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| Questions and answers: how early should pediatrician be able to recognize ADHD in office? between 12 and 18
mo of age; when child can understand novel commands (16-18 mo of age), start behavioral intervention using positive-
and negative-reinforcement model
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| PSYCHOPHARMACOLOGY OF ADHD
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| Therapeutic goal: attaining attention appropriate to child’s receptive-language age; average person’s attention span 3
min/yr of language age (plateaus at 16-18 yr of age, so average adult’s attention span slightly <1 hr)
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| Interventions: medications do not fix ADHD; “they simply provide a safety net”; must educate parents about role and
limitations of medication; school-based accommodation, including individualized education plan (IEP) “absolutely essential”;
comorbidities help determine choice of medication
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| 504 plan: derived from section 504 of Americans with Disabilities Act; allows for implementation of IEP, including classroom
accommodations to increase structure and decrease distraction (eg, preferential seating); applicable as long as not
unduly onerous for teacher, but not enforceable; however, should be attempted before psychopharmacology
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| Multimodal Treatment Study of children with ADHD (MTA study): confirmed importance of medication in
managing ADHD; 4 treatment groups—1) medication only (children managed with 31.2 mg methylphenidate [MPH]
alone); 2) intensive behavior management alone; 3) combination group (37.7 mg MPH plus intensive behavior management);
4) community resources (pediatricians prescribing 22.6 mg MPH on average); results at 14 mo—efficacy 56%,
33%, 68%, and 25% respectively; 24-mo follow-up study—efficacy had decreased to 37%, 32%, 48%, and 28% respectively;
in general—no intervention had any effect on child’s social skills, reading achievement, or on parental discipline
techniques; confounders present in follow-up study—division between groups became blurred after 14 mo; in combination
group, only 70% of children still on medication; in medication-only group, only 72% still on medication; in behavioral
management group, 38% of children had started medication; in community resources group, 62% had started
medication; overall conclusion—effects of medication less robust but persistent; medication important component in
managing ADHD
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| Central nervous system stimulants:—MPH; dextroamphetamines; assuming correct diagnosis, stimulants effective in
≥75% of cases (if one class not effective, try other); combination effective in >95% of cases; if unsuccessful and diagnosis
correct, try a different drug from first class; try long-acting medications first; if multiple trials unsuccessful, reassess
diagnosis (learning disabilities, depression, and anxiety may mimic ADHD)
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| α2 agonists: clonidine—administer qid for impulse-control form of ADHD; effective, but causes cycling and may be sedating;
guanfacine—administer bid; milder; less effective but fewer effects; associated with better compliance
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| Methods of administration: oral (pill or liquid); transdermal; prodrug form stirred into liquid for individual titration
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| Side effects: warn parents and advise them on ways to manage side effects; headaches and stomachaches—manage with
acetaminophen (eg, Tylenol); anorexia—take baseline weight and monitor weight; child doing fine as long as weight
gain consistent (when child eats less important); tics—relative contraindication (usually bother parents more than
child); short stature—cause unclear (thought to be related to insomnia); may be price for better social and academic
functioning afforded by medication; rebound phenomena—anger, irritability, moodiness; increased signs of
depression—another possible side effect; risk for sudden cardiac death—review family history before placing
child on drug; consider obtaining electrocardiography before starting child on medication
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| Follow-up: every 1 to 2 wk until child stable; start low, with schedule for titrating up, working towards predetermined
high dose; see child every 2 to 3 mo after that to verify improvement; use standardized scoring instruments, eg, Conners
Parent or Teacher Rating Scale or Vanderbilt ADHD Diagnostic Parent or Teacher Rating Scale, for medication
management; also monitor child’s weight and (if on α2 agonist) blood pressure
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| Equivalency dosing: 5 mg mixed amphetamine salt (MAS) equivalent to 10 mg MPH (not ideal starting dose for 5-yr-old)
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| Side effects of medications: considerations—appetite suppression and sleep disturbances common but manageable
through simple strategies; impact on growth velocity usually modest and most noticeable in older heavier children; etiology
of tics unclear; anorexia—in separate studies, seen in 9.7% of children taking MPH and 22% of children taking
MAS; sleep disturbances—in separate studies, seen in 7% of children taking MPH and 17% taking MAS; sleep disturbances
common in children with ADHD before ever starting medication; good sleep hygiene essential; obtain sleep
history before placing child on medication; sleep hygiene tips—bedroom; establish regular bedtime; have child drink
warm milk 30 min before bedtime; administer 1-2 mg melatonin; give child warm bath and then begin bedtime routine;
reserve bed for sleeping only (no daytime play or timeouts); if necessary, start with very late bedtime and move backward
from there until reasonable time established; problem may occur because stimulant wearing off (prescribe small
nighttime dose so child can fall asleep); tic disorders—similar whether medications used alone or in combination;
substance abuse—untreated ADHD risk factor; pharmacologic treatment may be protective; minimize potential for
abuse of ADHD medication through choice of agent and formulation (long-acting instead of short-acting); in general,
treatment associated with a significantly reduced risk for substance abuse later in life
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| Key points: suboptimal dosing produces suboptimal outcomes; a given dose of MAS does not equal same dose of MPH;
titrate any drug to maximum effect before choosing another one; appetite suppression and sleep disturbances can be
ameliorated with good interventions
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Suggested Reading
Abikoff HB et al: Methylphenidate effects on functional outcomes in the Preschoolers with Attention-Deficit/Hyperactivity
Disorder Treatment Study (PATS). J Child Adolesc Psychopharmacol 17:581, 2007; Ballas P: ADHD
and sleep deprivation in school-aged children. Curr Psychiatry Rep 10:1, 2008; Brown RT et al: Treatment of attention-deficit/hyperactivity
disorder: overview of the evidence. Pediatrics 115:e749, 2005; Brown TE: Executive
functions and attention deficit hyperactivity disorder: implications of two conflicting views. Int J Dis Dev Ed 53:35,
2006; Gilchrist RH, Arnold EL: Long-term efficacy of ADHD pharmacotherapy in children. Pediatr Ann 37:46,
2008; Greenhill LL et al: Attention deficit hyperactivity disorder in preschool children. Child Adolesc Psychiatr
Clin N Am 17:347, 2008; Heriot SA et al: Critical influences affecting response to various treatments in young
children with ADHD: a case series. Child Care Health Dev 34:121, 2008; Lollar DJ: Function, impairment, and
long-term outcomes in children with ADHD and how to measure them. Pediatr Ann 37:28, 2008; MTA Cooperative
Group: National Institute of Mental Health Multimodal Treatment Study of ADHD follow-up: 24-month outcomes
of treatment strategies for attention-deficit/hyperactivity disorder. Pediatrics 113:754, 2004; Power TJ et
al: Managing attention-deficit/hyperactivity disorder in primary care: a systematic analysis of roles and challenges.
Pediatrics 121:e65, 2008; Swanson JM et al: Effects of stimulant medication on growth rates across 3 years in the
MTA follow-up. J Am Acad Child Adolesc Psychiatry 46:1015, 2007; Wisniewska B et al: The assessment of comorbid
disorders in ADHD children and adolescents. Adv Med Sci 52 Suppl 1:215, 2007.
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