Handbook of Clinical Neurology, Vol.

174 (3rd series)

Chapter 3

Attention deficit hyperactivity disorder

1
Department of Psychology, Syracuse University, Syracuse, NY, United States
2
Department of Psychiatry, Virginia Commonwealth University Medical Center, Richmond, VA, United States

Abstract
Many authors have contributed to the description of attention deficit/hyperactivity disorder (ADHD) for
the two last centuries. In this chapter, we review the current diagnostic criteria, epidemiology, and history
of ADHD. The different phenotypes (predominantly inattentive, predominantly hyperactive/impulsive, or
combined) and diagnostic process are detailed. The DSM-5 includes the three phenotypes that begin before
age 12, are present in at least two settings, and cannot be explained by another condition. Theoretical
underpinnings and biological and environmental etiologies reported in the latest literature are discussed.
There are many comorbidities associated with ADHD, which are associated with an increase in the neg-
ative impact on everyday life. Treatment decisions involve a complex interaction between child’s age,
symptom severity levels, comorbidities, functional impairments, and parents’ preferences. Medication
(psychostimulant and nonstimulant) and psychosocial (mainly behavioral parent training) treatments as
well as school-based interventions are described.

INTRODUCTION
Pasamanick, 1959), and Stella Chess and difficult
The clinical syndrome of inattention and hyperactivity- temperament (Chess et al., 1960).
impulsivity dates back nearly 250 years to chapters on ADHD symptoms generally emerge in childhood,
disorders of attention in medical textbooks by Weikard negatively impact functioning, especially in the aca-
in 1775 (Barkley and Peters, 2012) and later by Crichton demic and social domains, and have a chronic course
in 1798 (Palmer and Finger, 2001). Now termed atten- (APA, 2013). Most children with ADHD (67%) have a
tion deficit/hyperactivity disorder (ADHD), this clinical coexisting psychiatric and/or development disorder
syndrome is defined by impairing symptoms of inatten- (Larson et al., 2011). They are also at risk for numerous
tion and/or hyperactivity-impulsivity that begin before adverse health and medical outcomes across the lifespan,
age 12, are present in two or more settings, and cannot including accidental injuries, suicide, obesity, type 2 dia-
be better explained by another condition (e.g., anxiety) betes, smoking, excess alcohol use, impaired sleep, poor
(APA, 2013). Others who have contributed to the nutrition, limited exercise, dental trauma and caries, and
categorization of the clinical syndrome of inattention coronary heart disease (Nigg, 2013; Barkley, 2015).
and hyperactivity-impulsivity include Bourneville and Consequently, they are twice as likely to die in child-
l’enfant instable (Bourneville, 1897), George Still and hood, nearly five times as likely to die by midlife
defect of moral control (Still, 1902), Henri Wallon (Dalsgaard et al., 2015), and have a 12.7-year reduction
and l’enfant turbulent (Wallon, 1925), Knobloch and in life expectancy if their disorder persists to adulthood
Pasamanick’s minimal brain damage (Knobloch and (Barkley and Fischer, 2019).

*Correspondence to: Kevin M. Antshel, Ph.D., Professor of Psychology, Department of Psychology, Syracuse University, 802
University Avenue, Syracuse, NY 13244, United States. Tel: +1-315-443-9450, Fax: +1-315-443-4085, E-mail: [email protected]
38 K.M. ANTSHEL AND R. BARKLEY
In the United States, ADHD is the most common the DSM-III, ADHD was labeled attention deficit disor-
psychiatric disorder in children, with approximately der, with or without hyperactivity (APA, 1980). In 1987,
11% of children aged 4–17 having an ADHD diagnosis it attained its present characterization (ADHD), and in
(Visser et al., 2014). Outside of the United States, pedi- 1994, with the publication of the DSM-IV, ADHD
atric prevalence estimates of ADHD are lower (5%) was further specified into three subtypes: inattentive,
(Polanczyk et al., 2007), possibly explained by environ- hyperactive/impulsive, and combined. In the DSM-5
mental factors and American educational laws, which (APA, 2013) the age of onset criterion in the diagnosis
provide school-based services for youth with ADHD. of ADHD changed from age 7 to age 12, and the symp-
The diagnostic identification rates of ADHD have tom threshold for diagnosis in individuals older than
increased significantly in the United States in the past 17 dropped from 6 symptoms to 5 symptoms.
20 years (Visser et al., 2014). Potential reasons for this
increase include increased awareness as well as several
public policy changes during the period: federal special
ADHD theories
education law was changed to include ADHD as a qual-
ifying condition in a category called “Other Health Within the past 25 years, several theories have been
Impaired,” Medicaid was reauthorized and included developed to explain ADHD. The two most influential
ADHD as a condition that was reimbursable for pro- theories are Barkley’s executive functioning theory
vider evaluation and treatment, and supplemental secu- and Sonuga-Barke’s dual-pathway model. Barkley’s
rity income law was amended to include ADHD as a executive functioning theory (Barkley, 1997, 2012)
qualifying condition (Hinshaw, 2018). proposes that deficient inhibition is a central and de-
While most children with ADHD will not retain their fining feature of ADHD. Inhibition refers to three
full ADHD diagnosis into adulthood, the majority will overlapping yet somewhat distinct and separately mea-
demonstrate impairing ADHD symptoms in adulthood surable processes: (1) inhibiting the initial prepotent
(Faraone et al., 2006). In the United States, 4.4% of (dominant) response to an event so as to create a delay
adults meet criteria for ADHD (Kessler et al., 2006) in responding; (2) interrupting an ongoing response that
while lower adult ADHD prevalence rates (1.4%– is proving ineffective and thereby permitting a delay in
3.6%) are reported for the rest of the world (Fayyad and reevaluation of the decision to continue respond-
et al., 2017). Given its high prevalence and associated ing; and (3) protecting the self-directed (executive)
impairments, it is not surprising that ADHD is consid- responses that will occur within these delays as well
ered a major public health issue in the United States with as the goal-directed behavior they generate from
between $143 and $266 billion in societal costs associ- disruption by competing events and responses (interfer-
ated with ADHD each year (Doshi et al., 2012). ence control or resistance to distraction) (Barkley,
Sex differences exist in ADHD diagnostic prevalence. 1997, 2012). Poor behavioral inhibition leads to
In child and adolescent psychiatric clinics, up to 80% of secondary impairments in four executive functions: work-
ADHD cases are male. In both clinically referred samples ing memory, internalization of speech, self-regulation of
and population studies, it is more prevalent in males, with affect-motivation-arousal, and reconstruction.
a male-to-female sex ratio of 4:1 in clinical studies and The dual-pathway model (Sonuga-Barke, 2002)
2.4:1 in population studies (Polanczyk et al., 2007). posits that ADHD is the result of dysfunction in one or
Males are more likely to have hyperactive-impulsive both of two distinct biological pathways: the dopami-
symptoms and thus get referred for treatment (Larsson nergic mesocortical and mesolimbic systems. The meso-
et al., 2011). In adult psychiatric clinics the proportion cortical pathway dysfunction is similar to Barkley’s
of males is 50% (Kooij et al., 2010). This adult equilibra- response inhibition model and conceptualizes ADHD
tion is likely due to females self-referring for ADHD as a disorder of self-regulation of thoughts and actions
treatment more often than males and women having that stems from inhibitory dysfunction. The mesolimbic
the inattentive presentation, which is more likely to pathway dysfunction suggests that ADHD has a delay-
persist than hyperactivity (Hinshaw, 2018). averse motivational style with acquired cognitive defi-
cits. This shortened delay-reward gradient engenders
discounting of future rewards and a clear preference
History
for immediate rewards. This preference for immediacy
Prior to 1980, ADHD was called minimal brain dys- can be moderated by social factors (e.g., response of
function, hyperactive/hyperkinetic syndrome, and others to impatient behaviors). Similar to the deficient
hyperactive reaction of childhood. It was not until inhibitory pathway, the principal focus of the delay-
1980, with the publication of the DSM-III, that inatten- averse pathway is impulsivity; other ADHD symptoms
tion became a defining and central feature of ADHD. In (inattention, hyperactivity) emerge as a means to reduce
 ATTENTION DEFICIT HYPERACTIVITY DISORDER 39
delay in situations where it is unavoidable (Sonuga- with the combined presentation are typically diagnosed
Barke, 2002). Both pathways lead to ADHD symptoms in early elementary school (age 7 or 8) while those with
and associated impairments in the quality and quantity of the predominantly inattentive presentation are diagnosed
task engagement. A third pathway, which involves tem- in late elementary school (age 10 or 11) (Polanczyk
poral processing deficits leading to difficulties with tim- et al., 2010).
ing, time discrimination, and time reproduction, has been
added (Sonuga-Barke et al., 2010).
Diagnostic process
In children and adolescents the diagnostic process
PHENOTYPIC DIAGNOSIS
typically involves a clinical interview with the child
By definition, ADHD is a persistent and cross-situational and parents as well as obtaining collateral information
pattern of impairing inattentive and/or hyperactive- from teacher(s) (Pelham Jr. et al., 2005). Multiple
impulsive symptoms that cannot be better explained by validated rating scales exist, including the Conners
another condition. DSM-5 diagnostic criteria for ADHD ADHD Rating Scales, the ADHD Rating Scale-5,
include the presence of more than six symptoms of inat- and the Vanderbilt Scales. The age of the child needs
tention and/or hyperactivity-impulsivity and functional to be considered in the diagnostic process as symptoms
impairments associated with these symptoms that persist can change over time. Hyperactivity in children often
for longer than 6 months. Examples of inattentive symp- becomes restlessness in adolescents (Subcommittee on
toms include often failing to pay close attention to details Attention-Deficit/Hyperactivity Disorder et al., 2011).
or frequently making careless mistakes and regularly External distractibility in childhood can become internal
avoiding or being reluctant to engage in tasks that require distractibility in adolescence. Inattention is the most
sustained attention. Examples of hyperactive-impulsive enduring ADHD symptom. No neurologic, genetic,
symptoms include often fidgeting and squirming and neuropsychologic, or behavioral tests have sufficient
frequently interrupting others. Several symptoms must positive and negative predictive power to accurately
be present before age 12 and occur in two or more classify ADHD with sufficient success to recommend
settings (e.g., school, home). Finally, alternative ex- them for clinical diagnosis (Pliszka, 2007). However,
planations (e.g., anxiety, depression) for the symptoms cognitive/neuropsychologic assessment can be helpful
of inattention and/or hyperactivity-impulsivity and asso- in specifying the phenotype, deciphering some dif-
ciated functional impairments must be excluded. Ex- ferential diagnoses, guiding families, and providing
ecutive dysfunction and emotional dysregulation valuable information for interventions (Molitor and
commonly occur in ADHD. Nonetheless, neither is part Langberg, 2017).
of the DSM-5 criteria. For most children and adolescents with ADHD, these
The DSM-5 includes three ADHD presentations: pre- attention and inhibition difficulties are manifested pri-
dominantly inattentive, predominantly hyperactive- marily in settings requiring self-restraint, persistence,
impulsive, and combined. In previous editions of the and a high level of concentration for relatively uninter-
DSM, these categories were termed “subtypes.” In esting activities (Subcommittee on Attention-Deficit/
DSM-5, this has been changed to presentations to Hyperactivity Disorder et al., 2011). Thus most youth
emphasize the developmental variability in presenta- with ADHD can exert self-control during high interest
tions (APA, 2013). For example, a child with the com- tasks (e.g., video games) yet struggle appreciably in tasks
bined presentation may become an adolescent who that are not of interest.
meets criteria for the predominantly inattentive presen- Diagnosing ADHD in adolescents can be more chal-
tation. There exists vast heterogeneity both between lenging than diagnosing it in children. Children are
and within ADHD presentations. For example, 168 often more carefully supervised by parents and one
distinct symptom combinations exist for the combined teacher. However, in adolescents, multiple teachers
presentation. Girls are more likely to be diagnosed are involved and parents typically have less contact
with the predominantly inattentive presentation while with them than with children. Thus parents may be less
boys are more likely to be diagnosed with the com- well positioned to provide information about adolescent
bined presentation (Larsson et al., 2011). peer interactions and social relationships. Diagnosing
Hyperactive-impulsive symptoms predominate in ADHD is also more complex when considering that
young children (under age 5), while the hyperactive- adolescents with ADHD typically underestimate the
impulsive presentation occurs most often in preschool level of their ADHD symptoms and the amount of
children. Inattentive symptoms become more apparent impairment (Hoza et al., 2013).
in middle childhood and adolescence and persist more Most youth with ADHD will meet criteria for another
readily into adulthood (Willcutt et al., 2012). Children DSM-5 psychiatric condition. The most common
40 K.M. ANTSHEL AND R. BARKLEY
comorbidities include oppositional defiant disorder/con- meta-analysis in 20,183 ADHD cases and 35,191 con-
duct disorder, learning disorders, anxiety disorders, and trols, including children and adults from 12 datasets,
mood disorders (Wilens et al., 2002). ADHD is also reported genome-wide significant hits in 12 independent
comorbid with intellectual disabilities, autism spectrum loci that include genes involved in neurodevelopmental
disorders, and tic disorders, yet less often due to the processes, such as FOXP2 (Demontis et al., 2019). Con-
lower base rates of these conditions. The high preva- trary to other mental disorders with high genetic load
lence of comorbid conditions complicates the diagnos- (e.g., intellectual disability and autism spectrum disor-
tic process as symptoms of inattention and der), no single gene with major risk ratio has been
hyperactivity are common to many of these comorbid reported in ADHD. Polygenic risk scores for ADHD pre-
conditions (e.g., anxiety, mood disorders). ADHD dict inattention and hyperactivity-impulsivity symptoms
comorbidity also changes over the lifespan. In child- in the general population (Martin et al., 2015).
hood, oppositional defiant disorder, conduct disorder, Neurologically, ADHD is associated with a 3%–5%
learning disorders, and anxiety disorders are the most reduction in total brain volume, largely due to reduced
common comorbidities; in adolescence and adulthood, gray matter (Castellanos et al., 2002). Reductions in
comorbid substance use disorders, mood disorders, the right globus pallidus, right putamen, caudate nucleus,
and personality disorders increase in prevalence. and cerebellum are the most consistent structural
While not part of the ADHD diagnostic evaluation, neuroimaging findings (Hoogman et al., 2017). Hypo-
deficits in multiple cognitive domains are often observed activation of frontostriatal and frontoparietal attention
in children with ADHD. Working memory, inhibitory networks and hyperactivation of the default mode net-
control, temporal information processing, and response work are consistent findings in the ADHD functional
time variability deficits are often observed (Frazier brain imaging literature (Cortese et al., 2012). Delayed
et al., 2004) and can serve as treatment targets. About maturation of the cerebral cortex, especially in the
half of the children with ADHD will perform below aver- prefrontal regions, has also been consistently reported
age on psychometric tests of executive functioning (Shaw et al., 2007). Children whose ADHD diagnosis
(Willcutt et al., 2005). Nonetheless, when parent and remitted over time have a slower rate of frontal and pari-
teacher report of the child’s day-to-day deployment of etal cortical thinning from childhood to adulthood com-
executive skills are considered, the prevalence rates of pared with those who maintained their ADHD diagnosis
executive dysfunction increase significantly (Barkley (Shaw et al., 2013). Atypical brain activity has also
and Murphy, 2010). Children with ADHD also demon- been reported using EEG, most often increased power
strate reward processing and overestimate the magnitude of low frequency activity during resting state (Kitsune
of proximal relative to distal rewards (Scheres et al., et al., 2015).
2008). It is not known if cognitive dysfunction causes
ADHD symptoms or is better considered as an outcome
of the core ADHD symptoms.
Environmental
Maternal smoking and alcohol use during pregnancy,
ETIOLOGY premature birth, low birth weight, and exposure to
environmental toxins have all been identified as environ-
Biological
mental risk factors for ADHD (Scassellati et al., 2012).
In many ways, ADHD is an exemplar of the diathesis- Primary prevention strategies for ADHD reduction often
stress model of psychopathology. Genetic diatheses are focus on maternal health during pregnancy (e.g., elimi-
clear with heritability coefficients between 0.70 and nating smoking, alcohol, and drug use in pregnancy,
0.80 (Larsson et al., 2014). A child with ADHD increases reducing maternal stress). Most of these risk factors exert
the risk for ADHD in other first-order relatives (parents, only a small effect. The combination of multiple environ-
siblings) by 5–10-fold (Biederman et al., 1995). mental and biological risk factors, as is often the case,
Genome-wide association studies (GWAS) data indi- likely surpasses a certain ADHD threshold, leading to
cates that numerous common genetic variants account the development of impairing ADHD symptoms
for 40% of the heritability of ADHD (Cross-Disorder (Faraone et al., 2015).
Group of the Psychiatric Genomics Consortium, 2013). Impulsivity is strongly heritable. Impulsive children
Candidate gene studies have identified dopamine, nor- tend to reside in less structured homes, gravitate toward
adrenaline, serotonin, and neurite outgrowth systems as high-risk contexts, and are driven to further impulsivity
being associated with ADHD (Gizer et al., 2009). by positive responses from peers. This transactional
A meta-analysis of ADHD linkage studies confirmed a cascade exemplifies an evocative gene–environment
locus on chromosome 16 (Zhou et al., 2008). A GWAS interaction (Beauchaine et al., 2017).
 ATTENTION DEFICIT HYPERACTIVITY DISORDER 41
TREATMENT AND INTERVENTION not increase the risk for substance abuse in adulthood
(Chang et al., 2014).
Treatment decisions often involve a complex interaction
For multiple reasons, treatment adherence to medica-
between child age, symptom severity levels, functional
tion is higher in children than in adolescents. The rate of
impairments, and parent preferences. With the exception
failure to adhere to treatment with stimulants may be as
of preschool children (under age 6), the most common
high as 20%–65% (Adler and Nierenberg, 2010). There
evidence-based treatment is a combination of medication
are multiple factors contributing to poor adherence,
and psychosocial/nonpharmacologic approaches. For pre-
including perceived stigma, denial, externalization of
school children, medication is not a front-line ADHD
the problem, unwanted side effects (headaches, emo-
management strategy and is typically initiated only after
tional blunting, etc.), the cost of the medication, as well
psychosocial approaches (behavioral parent training
as the fact that ADHD symptoms (e.g., forgetfulness)
(BPT)) have failed (Subcommittee on Attention-Deficit/
may directly contribute to poor adherence (Adler and
Hyperactivity Disorder et al., 2011). While medication
Nierenberg, 2010).
and nonmedication interventions may improve outcomes,
Nonstimulant treatments include atomoxetine, a
children and adolescents with ADHD are typically not
selective noradrenaline reuptake inhibitor, and clonidine
“normalized” in their functioning (Shaw et al., 2012).
and guanfacine, a2-adrenergic agonists. Atomoxetine
increases the availability of synaptic norepinephrine,
especially in the prefrontal cortex. One of the advantages
Medication treatments
of atomoxetine (and other nonstimulants) is the absence
Both stimulant and nonstimulant medications reduce of a potential for abuse, which makes it a preferred agent
ADHD symptoms in children. Stimulants (amphetamine in situations where this can be a concern. Atomoxetine
and methylphenidate) are more efficacious than nonsti- tends to be well tolerated; headaches, nausea, and loss
mulants (atomoxetine, guanfacine, and clonidine) and of appetite are the most common side effects. Guanfacine
are associated with large effect sizes for reducing ADHD is an a2-adrenergic agonist with some selectivity for the
symptoms (Faraone and Buitelaar, 2010). Approxi- 2A postsynaptic receptors. Guanfacine and other a2 ago-
mately 70%–80% of children with ADHD will respond nists increase noradrenergic brain activity, yet also serve
positively to a stimulant. Methylphenidate and amphet- to regulate glutaminergic transmissions. Clonidine, a
amine both block the dopamine transporter. Amphet- similar agent, is also frequently used; however, it is less
amine additionally promotes the release and reverse selective at the level of 2A receptors. Both guanfacine
transport of dopamine. As a result the synaptic availabil- and clonidine have similar side effects, including somno-
ity of norepinephrine and dopamine is increased. Both lence, dry mouth, hypotension, and constipation, and
methylphenidate and amphetamine are available in mul- both have FDA-approved long-acting versions.
tiple formulations, including immediate and extended Presently, it is not possible to reliably predict how a
release. Due to the short elimination half-lives, extended child will respond to stimulant or nonstimulant medica-
release formulations are more often prescribed because tion treatment for ADHD. While medication can be use-
one daily dose is usually sufficient for treating symptoms ful for reducing ADHD symptoms, the effectiveness of
throughout the day. Both medications generally require medication for improving functional outcomes is less
adjustments in doses (including when doses are taken) robust (Evans et al., 2018). It is for this reason that psy-
to maximize effectiveness. chosocial treatments are recommended in addition to
The most common side effects of stimulants are pharmacotherapy.
reduced appetite and initial insomnia. Cardiovascular
side effects (e.g., increased blood pressure) are usually
Psychosocial treatments
of no clinical significance and routine EKG screening
prior to stimulant use is needed only in those with posi- Psychosocial interventions are recommended for those
tive family or personal cardiac history (Subcommittee on children and adolescents who have psychiatric comorbid-
Attention-Deficit/Hyperactivity Disorder et al., 2011). ities or continued functional impairments despite medica-
Adolescents with ADHD and conduct disorder are at tion treatments (Subcommittee on Attention-Deficit/
increased risk for diverting their stimulant medication Hyperactivity Disorder et al., 2011). Nonmedication
(giving the medication to a friend) and should be care- treatments generally consist of dietary, behavioral, or neu-
fully monitored (Pliszka, 2007). Adults with ADHD, rocognitive interventions. Of the three categories, dietary
especially those with substance abuse histories, are also interventions are the least studied or convincing. Pres-
at increased risk for overusing or misusing their own ently, only supplementation with free fatty acids is associ-
stimulant medications (Bjerkeli et al., 2018). Nonethe- ated with ADHD symptom reduction, albeit with small
less, the use of medication in children with ADHD does and unreliable effect sizes (Stevenson et al., 2014).
42 K.M. ANTSHEL AND R. BARKLEY
Behavioral interventions are the most well-studied non- and self-regulation interventions (DuPaul et al., 2014).
medication treatment and associated with the largest effect Behavioral interventions at school seek to understand
sizes for improving functioning (Evans et al., 2018). Oper- the function of the child’s behavior, generally subsumed
ant conditioning and social learning models generally pro- under one of four categories: (1) escape or avoidance of a
vide the foundation for techniques used in most behavioral nonpreferred activity, (2) gaining attention, (3) gaining
interventions. In preschool and elementary school-aged access to preferred materials, or (4) sensory stimulation
children, behavioral interventions are generally delivered (Cooper et al., 2007). School-based interventions then
directly to parents via BPT. Incentives, token economy aim to reinforce a socially appropriate replacement
systems, and planned ignoring of attention-seeking behav- behavior that serves the same underlying function as
iors are central elements of most BPTs. The outcomes the disruptive behavior.
include improved quality of parenting and reduced disrup- Academic interventions for students with ADHD can
tive behaviors (Evans et al., 2018). Parents with ADHD include computer-assisted instruction, explicit instruc-
themselves engage in less positive and more harsh and tion, peer tutoring, and educational accommodations
lax parenting behaviors and are particularly in need of via an individualized education plan or a 504 accommo-
BPT interventions (Johnston and Mash, 2001). Positive dation plan. Finally, self-regulation interventions teach
parenting practices (high warmth and strong limit setting) students to self-monitor and identify/record their target
can protect young children with ADHD from peer conflicts behaviors (e.g., inattention). Compared with behavioral
in childhood (Healey et al., 2011). interventions, academic and self-regulation interventions
Teachers are also typically targeted in preschool and have weaker effect sizes (DuPaul et al., 2014).
elementary school-aged children and complete daily
report cards for parents to review and integrate into exist-
ing reward programs at home (DuPaul et al., 2014). For
CONCLUSIONS
adolescents with ADHD, cognitive behavioral and orga-
nizational skills training can be beneficial toward ADHD is defined by impairing symptoms of inattention
improving academic functioning (Langberg et al., and/or hyperactivity-impulsivity that begin before age
2012; Sprich et al., 2016). 12, are present in two or more settings, and cannot be
Social functioning impairments are one of the more better explained by another condition (e.g., anxiety).
treatment-resistant affected outcomes in children with The DSM-5 includes three ADHD presentations: pre-
ADHD (Shaw et al., 2012). Traditional, clinic-based dominantly inattentive, predominantly hyperactive-
social skills training programs have yielded inconsistent impulsive, and combined. While most children with
effects (de Boo and Prins, 2007). These programs typi- ADHD will not retain their full ADHD diagnosis into
cally focus on improving children’s knowledge of social adulthood, the majority will demonstrate impairing
skills and couple that with in-session practice. Generali- ADHD symptoms in adulthood. In both clinically re-
zation to real-world settings (e.g., school, athletic events) ferred samples and population studies, ADHD is more
is often a challenge. Alternative approaches to improving prevalent in males, with a male-to-female sex ratio of
social functioning have centered on involving parents and 4:1 in clinical studies and 2.4:1 in population studies.
teachers and teaching them how to provide children with In children and adolescents the ADHD diagnostic
in vivo reminders during real-world peer interactions process typically involves a clinical interview with the
(Mikami et al., 2014). child and parents as well as obtaining collateral infor-
Neurocognitive interventions such as neurofeedback mation from teacher(s). No neurologic, genetic, neurop-
training and working memory training have less sychologic, or behavioral tests have sufficient positive
research support than behavioral interventions. The and negative predictive power to accurately classify
research that does exist is limited by the nonblinded ADHD with sufficient success to recommend them for
nature of the studies as well as the limited carryover clinical diagnosis. However, cognitive/neuropsychologic
effects associated with the interventions (Evans et al., assessment can be helpful in specifying the phenotype,
2018). Moreover, physical activity has been studied deciphering some differential diagnoses, guiding
as a means of reducing ADHD symptoms. While that families, and providing valuable information for interven-
research literature is still developing, there are multiple tions. Most youth with ADHD will meet criteria for
studies that report positive effects from antecedent another DSM-5 psychiatric condition. The most common
exercise for children with ADHD (Hoza et al., 2016). comorbidities include oppositional defiant disorder/
conduct disorder, learning disorders, anxiety disorders,
and mood disorders. The high prevalence of comorbid con-
School-based interventions
ditions complicates the diagnostic process as symptoms of
Three categories of intervention are used to support stu- inattention and hyperactivity are common to many of these
dents with ADHD. These include behavioral, academic, comorbid conditions (e.g., anxiety, mood disorders).
 ATTENTION DEFICIT HYPERACTIVITY DISORDER 43
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