Transcript Attention-deficit/hyperactivity disorder

ATTENTIONDEFICIT/HYPERACTIVITY
DISORDER
Puja Patel
PGY5 Pediatric Neurology
Nov 6, 2013
Epidemiology
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Overall prevalence 2-18%
School age children 8-10%most common
neurobehavioral disorder of childhood
More common in boys than girls
 Male
 4:1
to female ratios:
for predominantly hyperactive type
 2:1 for predominantly inattentive type
Clinical Features
2 categories of core symptoms:
 Hyperactive and impulsive behaviors occur together
 Inability
to sit still or inhibit behavior
 Observed by age 4, peaks age 7-8, then hyperactive
symptoms decline but impulsive symptoms persist
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Inattention
 Reduced
ability to focus attention, reduced speed of
cognitive processing and responding
 Apparent at 8-9 years old, usually lifelong
Diagnostic Criteria
DSM-5
 Age <17 years: ≥6
symptoms in 1 or both
categories
 Age ≥17 years, ≥5
symptoms of in 1 or both
categories
 Present > 1 setting
 Persist > 6mo
 Present before age 12
 Inconsistent with
developmental level child
 Impair functioning
 Exclude psychiatric
disorders
DSM-4 vs DSM-5
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New overall diagnostic category
 Neurodevelopmental
disorders (DSM-5) vs Disorders
usually first diagnosed in infancy, childhood and
adolescence (DSM-4)
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ADHD across lifespan
 Not
only a disorder of childhood
 Adding new examples to apply criteria across lifespan
 Lower age cutoff for diagnosis in adults
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Age of onset changed from 7 to 12
Removal of PDD/ASD from exclusion criteria
 Allows
for diagnosis of ADHD with comorbid PDD/ASD
Changes from subtypes to
presentations: DSM-4 vs DSM-5
DSM-4
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Combined subtype
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 Inattention
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+
hyperactive-impulsivity
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DSM-5
Predominantly
inattentive type
Predominantly
hyperactive-impulsive
type
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Combined presentation
Predominantly inattentive
 6 inattentive and 3-5
hyperactive/impulsive
symptoms
Inattentive (restrictive)
 6 inattentive and no more
than 2
hyperactive/impulsive
symptoms
Predominantly
hyperactive/impulsive
Prevalence distribution of DSM-4
subtypes
Etiologies
Genetic factors account for ~80% of etiology
 Twin studies demonstrate concordance as high as
92% in monozygotic twins and 33% in dizygotic
twins
 5-6x higher risk of first degree relatives affected
 Genes that may play a role:
 DA
and serotonin-Rs and transporters
 DA beta-hyroxylase
 Glutamate-R
Etiologies
Mixed reviews on environmental factors:
 Maternal factors
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Smoking, prenatal alcohol, lead, viral infections
Perinatal/early life risk factors
Premature infants with BW<1500gm
 Striatum and cingulate-cortical loop vulnerable to ischemia
induced release of glutamate
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Post-natal risk factors
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Cerebral trauma/infections, thyroid dysfunction, toxins,
nutritional deficiencies
Genetic factor likely basic cause; environmental factor
probably secondary, acting as a trigger
Comorbid disorders
Prevalence of comorbid disorders for
children with ADHD vs those without
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Larson et al, 2007
Primary vs
secondary
ADHD subtype
specific
comorbidities
Evaluation

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Keep in mind diagnostic criteria for ADHD
Evaluate medical/neurologic/developmental
disorders
 Hearing/visual
impairment, genetic/metabolic, sleep
d/o, seizures, med effects, learning disabilities,
language d/o
 FHx similar behaviors
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Evaluate for emotional/social stressors
 Screen
for psychiatric conditions
 Substance abuse in adolescents
Evaluation
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Behavior rating scales to be completed > 2 informants

ADHD specific (narrow-band): focus directly on core symptoms
 Sensitivity and specificity>90%
 Conners and the ADHD Rating Scale IV for preschoolers
 Vanderbilt for children ≥4 years
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Broadband scales: Assess variety of behavioral symptoms
 Less sensitive and specific
 Can help identify coexisting conditions
Educational evaluation mandated by schools in US
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Core symptoms in classroom
Neuropsych testing (IQ and academic) to eval learning d/o
Treatment
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Preschool children (4-5yo)
 Behavior
therapy administered by parent or teacher
 Addition of medication (stimulant) if fails behavioral
therapy
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School age children (6-11yo) and adolescents (1218yo)
 Medication
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+ behavioral therapy
Treat coexisting conditions concurrently with ADHD
Behavior therapy
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Modifications in physical and social environment using
rewards and nonpunitive consequences
Positive reinforcement, time-out, token economy
 Small reachable goals
 Keep organized: maintaining daily schedule,
charts/checklists
 Keep on task: minimum distractions, limiting choices
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School based interventions
Qualifications for special ed/IEP/accommodations under
section 504
 Tutoring/resource room support
 Classroom modifications
 Extended time to complete tasks

Pharmacologic Treatments
Stimulants first line
 Methylphenidate (Ritalin), dexmethylphenidate
(focalin), amphetamine (adderall)
 NE and DA reuptake inhibitor/releasing agent
 Advantages: rapid onset of action, safe, long and
short-acting forms approved in children<6
 SEs: appetite suppression, retard growth trajectory,
insomnia, mood lability, rebound, tics, psychosis,
abuse potential, sudden cardiac death (rare)
Pharmacologic Treatments
Non-stimulants
 Atomoxetine (straterra)
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NE reuptake inhibitor
Adv: no abuse potential
Disadv: less effective than stimulants, decrease dose if use with
P450 inhibitors
SEs: somnolence, GI symptoms, decreased appetite, SI (rare),
hepatitis (rare)
Alpha-2 adrenergic agonists (not FDA approved)
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Guanfacine (tenex), clonidine (catapres)
Adv: no abuse potential, helpful if coexisting sleep or tic disorders
Disadv: less effective than stimulants
SEs: somnolence, dry mouth, hypotension, orthostasis
Treatment considerations
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Monitor treatment response
Drug holidays not routinely recommended
 Consider
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if aberrant growth trajectory, excessive SEs
Stopping medications
 Consider
if stable symptoms
 Time appropriately
 Stimulant medications and atomoxetine do not need
taper
 Taper alpha-2-adrenergic agonists
Prognosis
30-60% continue to manifest appreciable symptoms
into adult life
 Impaired academic functioning
 especially
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for inattentive or combined types
Some data suggests decreased rate of employment,
lower job status and poor job performance
Increased risk for incurring intentional or
unintentional injury
Increased risk for antisocial personality disorder in
adulthood
References
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Dalsgaard S. Attention-deficit/hyperactivity disorder (ADHD). Eur Child Adolesc
Psychiatry. 2013 Feb;22 Suppl 1:S43-8
Daughton JM, Kratochvil CJ. Review of ADHD pharmocotherapies: advantages,
disadvantages, and clinical pearls. J Am Acad Child Adolesc Psychiatry
2009;48(3):240-8
Klein RG et al. Clinical and functional outcome of childhood attentiondeficit/hyperactivity disorder 33 years later. Arch Gen Psychiatry
2012;69(12):1295-303
Larson K et al. Patterns of Comorbidity, Functioning, and Service Use for US children
with ADHD, 2007. Pediatrics 2011; 127(3):462-70
Millichap JG. Etiological Classification of Attention-Deficit/Hyperactivity Disorder.
Pediatrics 2008;121(2): 358-65
Wolraich M et al. ADHD: Clinical Practice Guideline for the Diagnosis, Evaluation,
and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and
Adolescents. Pediatrics 2011 Nov;128(5):1007-22
UpToDate, “ADHD in children and adolescents,” 2013
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Clinical Features and Evaluation; Epidemiology and Pathogenesis; Overview of treatment
and Prognosis; Treatment with Medications