Disorders of Childhood and Adolescence (Neurodevelopmental Disorders) 545

use of antidepressant medication and subsequent onset and hostile behavior toward authority figures that persists
of suicidal behavior remains a topic of intense debate
within the field.
Psychological treatments have proven effective in the
treatment of depression in children and adolescents. Con-
trolled studies of psychological treatment of adolescents
with depression have shown significantly reduced symp-
toms with the use of CBT (Spirito et al., 2011). Comprehen-
sive meta-analytic studies that examine the overall
effectiveness of psychological treatments for child and
adolescent depression reveal that such interventions are
effective, especially in the short term, and that such treat-
ments also seem to decrease anxiety symptoms (although
not behavior problems) in children receiving them (Weisz,
McCarty, & Valeri, 2006). Longitudinal follow-up studies
of adolescents who have been treated for depression have
shown that effective treatment can reduce the recurrence of
depression (Beevers et al., 2007). Overall, these studies sug-
gest that although depression is fairly common among
youth, effective treatments are available.
for at least 6 months. ODD is grouped into three subtypes:
angry/irritable mood, argumentative/defiant behavior,
and vindictiveness. This disorder usually begins by the age
of 8 and has a lifetime prevalence of 10 percent, with a
slightly higher rate among boys (11 percent) than girls
(9 percent) (Nock et al., 2007). Prospective studies have
found a developmental sequence from ODD to conduct
disorder, with common risk factors for both conditions.
That is, virtually all cases of conduct disorder are preceded
developmentally by ODD, but not all children with ODD
go on to develop conduct disorder within a 3-year period
(Lahey et al., 2000). The risk factors for both include family
discord, socioeconomic disadvantage, antisocial behavior
in the parents, and overlapping neural correlates (Blair
et al., 2014; Noordermeer et al., 2016).

Disruptive, Impulse-Control,
and Conduct Disorder

Anna Nahabed/123RF
15.3 Describe the presentation and prevalence of
oppositional defiant disorder and conduct disorder.
Anxiety and depressive disorders often are referred to as
“internalizing disorders” because the focus of the symp-
toms is on what is happening inside the person (i.e., abnor- Defiant, oppositional, and hostile behaviors are characteristics of
both oppositional defiant disorder and conduct disorder, although
malities in their thoughts and feelings). In contrast,
there are important differences between these two conditions.
disorders characterized by symptoms focused outside the
person, such as engagement in disruptive and impulsive
behavior, often are referred to as “externalizing disorders.” Conduct Disorder
Two of the most common externalizing disorders are oppo-
Conduct disorder (CD) is characterized by a persistent,
sitional defiant disorder and conduct disorder. Of course, many
repetitive violation of rules and a disregard for the rights of
children will act out from time to time, disobeying adults
others (see the DSM criteria box for CD). CD has a median
and getting into fights, and so it is important to distinguish
age of onset of 12 years (meaning half of those who ever
normal acting out from the more severe and persistent
develop this disorder have it by age 12) and a lifetime preva-
behaviors that can occur in those with oppositional defiant
lence of 10 percent (Nock et al., 2006). Like ODD, CD is more
disorder and conduct disorder. It also is important to dif-
common among boys (12 percent) than girls (7 percent).
ferentiate between these disorders and illegal activity
Because the combination of any 3 of the 15 symptoms listed
among youth. Juvenile delinquency is the legal term used
in the DSM criteria box can lead to a diagnosis of CD, there
to refer to violations of the law committed by minors.
is a great deal of variability in the clinical presentation of
Although youth with externalizing disorders may break
this disorder. Statistical analyses that examine how symp-
the law, breaking the law in itself does not signal the pres-
toms cluster together have revealed the presence of five
ence of one of these disorders. (See the Unresolved Issues
common subtypes of CD, with each made up of children
section at the end of this chapter.)
engaging primarily in (1) rule violations (26 percent of
those with CD), (2) deceit/theft (13 percent), (3) aggressive
Oppositional Defiant Disorder behavior (3 percent), (4) severe forms of subtypes 1 and 2
Oppositional defiant disorder (ODD) is characterized by (29 percent), and (5) a combination of subtypes 1, 2, and 3
a recurrent pattern of negativistic, defiant, disobedient, (29 percent) (Nock et al., 2006).

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 546 Chapter 15
DSM-5 Criteria for. . .
Conduct Disorder
A. A repetitive and persistent pattern of behavior in which the
basic rights of others or major age-appropriate societal norms
or rules are violated, as manifested by the presence of at least
three of the following 15 criteria in the past 12 months from
any of the categories below, with at least one criterion present
in the past 6 months:
Aggression to People and Animals
1. Often bullies, threatens, or intimidates others.
2. Often initiates physical fights.
3. Has used a weapon that can cause serious physical harm
to others (e.g., a bat, brick, broken bottle, knife, gun).
4. Has been physically cruel to people.
5. Has been physically cruel to animals.
6. Has stolen while confronting a victim (e.g., mugging,
purse snatching, extortion, armed robbery).
7. Has forced someone into sexual activity.
Destruction of Property
8. Has deliberately engaged in fire setting with the intention
of causing serious damage.
9. Has deliberately destroyed others’ property (other than
by fire setting).
Children and adolescents with CD are also frequently
comorbid for other disorders such as substance abuse dis-
order (Goldstein et al., 2006) or depressive symptoms
(Stalk et al., 2015). CD significantly increases the risk of
pregnancy and substance abuse in teenage girls and of the
later development of antisocial personality disorder and a
range of other disorders (Goldstein et al., 2006). One study
that followed more than 1,000 children for many years into
adulthood revealed that between 25 and 60 percent of peo-
ple who have a mental disorder during adulthood had a
history of CD and/or ODD during childhood or adoles-
cence (Kim-Cohen et al., 2003).
Causal Factors in ODD and CD
Our understanding of the factors associated with the
development of conduct problems in childhood has
increased tremendously in the past 20 years. Several fac-
tors are covered in the sections that follow.
A SELF-PERPETUATING CYCLE Evidence has accumu-
lated that a genetic predisposition leading to low verbal
intelligence, mild neuropsychological problems, and dif-
ficult temperament can set the stage for early-onset CD
(Simonoff, 2001). Researchers also have found strong heri-
table effects of conduct problems and antisocial behavior
across ethnically and economically diverse samples
M15_BUTC4568_18_GE_C15.indd 546
Deceitfulness or Theft
10. Has broken into someone else’s house, building, or car.
11. Often lies to obtain goods or favors or to avoid obliga-
tions (i.e., “cons” others).
12. Has stolen items of nontrivial value without confronting
a victim (e.g., shoplifting, but without breaking and
entering; forgery).
Serious Violations of Rules
13. Often stays out at night despite parental prohibitions,
beginning before age 13 years.
14. Has run away from home overnight at least twice while
living in the parental or parental surrogate home, or once
without returning for a lengthy period.
15. Is often truant from school, beginning before age 13 years.
B. The disturbance in behavior causes clinically significant impair-
ment in social, academic, or occupational functioning.
C. If the individual is age 18 years or older, criteria are not met for
antisocial personality disorder.
Source: Reprinted with permission from the Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition, (Copyright 2013). American
Psychiatric Association.
(Baker et al., 2007). The child’s difficult temperament may
lead to an insecure attachment because parents find it
hard to engage in the good parenting that would promote
a secure attachment. In addition, the low verbal intelli-
gence and mild neuropsychological deficits that have
been documented in many of these children—some of
which may involve deficiencies in self-control functions
such as sustaining attention, planning, self-monitoring,
and inhibiting unsuccessful or impulsive behaviors—may
help set the stage for a lifelong course of difficulties. In
attempting to explain why the relatively mild neuropsy-
chological deficits typically seen can have such pervasive
effects, consider the following example. Imagine a young
boy with low IQ, difficulties with attention, and poor
behavioral control. Such a boy may have difficulties
following instructions from his parents at home as well as
trouble with reading, writing, and numbers. Once in
preschool or kindergarten, the boy’s lack of preparedness
might lead to further problems focusing in class, which
could exacerbate his behavioral problems, which could
lead teachers to pull him out of class to avoid disruptions
to other students, which could in turn further delay his
learning. Over time, such a cycle could cause his initial
cognitive problems and behavioral problems to interact
with his environment in a way that perpetuates each of
these difficulties.
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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders)
AGE OF ONSET AND LINKS TO ANTISOCIAL PERSON-
ALITY DISORDER Children who develop CD at an ear-
lier age are much more likely to develop psychopathy or
antisocial personality disorder as adults than are adoles-
cents who develop CD suddenly in adolescence (Copeland
et al., 2007). The link between CD and antisocial personal-
ity is stronger among lower-socioeconomic-class children
(Lahey et al., 2005). It is the pervasiveness of the problems
first associated with ODD and then with CD that forms the
pattern associated with an adult diagnosis of psychopathy
or antisocial personality. Although only about 25 to 40 per-
cent of cases of early-onset CD go on to develop adult anti-
social personality disorder, over 80 percent of boys with
early-onset CD continue to have multiple problems of
social dysfunction (in friendships, intimate relationships,
and vocational activities) even if they do not meet all the
criteria for antisocial personality disorder. By contrast,
most individuals who develop CD in adolescence do not
go on to become adult psychopaths or antisocial personali-
ties but instead have problems limited to the adolescent
years. These adolescent-onset cases also do not share the
same set of risk factors that the child-onset cases have,
including low verbal intelligence, neuropsychological defi-
cits, and impulsivity and attentional problems.
PSYCHOSOCIAL FACTORS In addition to the genetic or
constitutional liabilities that may predispose a person to
develop CD and adult psychopathy and antisocial person-
ality, family and social context factors also seem to exert a
strong influence (Kazdin, 1995). Children who are aggres-
sive and socially unskilled are often rejected by their peers,
and such rejection can lead to a spiraling sequence of social
interactions with peers that exacerbates the tendency
toward antisocial behavior (Freidenfelt & Klinteberg,
2007). Severe conduct problems can lead to other mental
health problems as well. For instance, children who report
higher levels of conduct problems are nearly four times
more likely to experience a depressive episode in early
adulthood (Mason et al., 2004).
This socially rejected subgroup of aggressive children
is also at the highest risk for adolescent delinquency. In
addition, parents and teachers may react to aggressive chil-
dren with strong negative affect such as anger (Capaldi &
Patterson, 1994), and they may in turn reject these aggres-
sive children. The combination of rejection by parents,
peers, and teachers leads these children to become isolated
and alienated. Not surprisingly, they often turn to deviant
peer groups for companionship, at which point a good
deal of imitation of the antisocial behavior of their deviant
peer models may occur.
Investigators generally seem to agree that the family
setting of a child with CD is typically characterized by
rejection, harsh and inconsistent discipline, and parental
neglect (Frick, 1998). There is some evidence that parental
M15_BUTC4568_18_GE_C15.indd 547
547
behavior can inadvertently “train” antisocial behavior in
children—directly via coercive interchanges (e.g., mother
asks child to get ready for bed ➔ child starts whining ➔
whining annoys mother so she walks away and lets her
stay awake: here the child learns that if she whines she gets
her way, whereas the mother learns that if she backs off the
child stops whining; both behaviors are reinforced and the
child has “learned” to misbehave) and indirectly via lack
of monitoring and consistent discipline (Capaldi & Patter-
son, 1994). This all too often leads to association with devi-
ant peers and the opportunity for further learning of
antisocial behavior.
In addition to these familial factors, a number of
broader psychosocial and sociocultural variables increase
the probability that a child will develop CD and, later,
adult psychopathy or antisocial personality disorder
(Granic & Patterson, 2006) or depressive disorder (Boylan
et al., 2010). Low socioeconomic status, poor neighbor-
hoods, parental stress, and depression all appear to
increase the likelihood that a child will become enmeshed
in this cycle (Schonberg & Shaw, 2007).
Treatments and Outcomes
Approximately half of those with ODD (54 percent) and a
third of those with CD (32 percent) have received treatment
for their behavior problems (Merikangas, He, et al., 2011).
The relatively high rate of treatment is likely due to the
unavoidable problems associated with ODD, CD, and other
“externalizing” disorders in which children’s behavior
toward others is the source of concern. This is in contrast to
“internalizing” disorders like depression and anxiety, as
noted, in which children’s problems are self-focused or
“internal” and so less often noticed by others. Effective
treatments for ODD and CD focus primarily on modifying
the child’s family and broader environment as a way of
decreasing his or her problematic behavior (Kazdin, 2018).
One interesting and often effective treatment strategy
with CD is the cohesive family model (Granic & Patterson,
2006; Patterson et al., 1998). In this family-group-oriented
approach, ODD and CD are conceptualized as being rein-
forced and maintained by ineffective parenting practices. For
instance, parents can inadvertently reinforce inappropriate
behavior such as in the example in the prior section in which
the child learned to escape or avoid parental commands by
escalating her negative behavior (whining). This tactic, in
turn, increases parents’ aversive interactions and criticism.
The child observes the increased anger in his or her parents
and models this aggressive pattern. The parental attention to
the child’s negative, aggressive behavior actually serves to
reinforce that behavior instead of suppressing it. Viewing
conduct problems as emerging from such interactions places
the treatment focus squarely on the interaction between the
child and the parents (Patterson et al., 1991).
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 548 Chapter 15
Fortunately, during the past several decades, research-
ers have developed psychological treatments that have
been shown to significantly decrease ODD and CD. Alan
Kazdin, a pioneer in the development and evaluation of
treatments for child conduct problems, has shown through
a series of many studies that standard talk therapies are
not effective in treating ODD and CD. However, two psy-
chological approaches that target some of the key risk fac-
tors already mentioned do have a positive effect. Parent
management training, an approach in which the clinician
teaches the parents how to effectively prompt and rein-
force prosocial behaviors while ignoring aggressive or
antisocial behaviors, has been shown to be quite success-
ful. In addition, a separate approach in which the clinician
meets with the child to teach social problem-solving skills
(such as how to generate and perform more adaptive
responses to others) also has proven effective. The combi-
nation of these two approaches is especially successful at
decreasing child conduct problems, with effects lasting
well after treatment has ended (Kazdin, 2008b).
Given that prior research has identified many different
risk factors for CD, researchers and clinicians can use this
information to identify which children are at high risk of
developing CD and can test prevention programs designed
to decrease the likelihood of conduct problems. For
instance, the Fast Track Prevention Program identified 891
first-graders determined to be at high risk for developing
CD and randomly assigned half of them to receive 10 years
of prevention services that included training parents in
effective behavior management procedures, social skills
training for the children, and academic tutoring. The
Figure 15.4
The Fast Track Prevention Program has been shown to significantly
decrease the risk of conduct disorder. In this 2011 study, only 20
percent of at-risk children receiving this intervention went on to
develop conduct disorder by 12th grade, compared to 42 percent
of those in the control condition.
(Based on Conduct Problems Research Group, 2011, The Effects
of the Fast Track Preventive Intervention on the Development of Conduct
Disorder Across Childhood, Child Dev. 2011 Jan-Feb; 82(1): 331–345.)
0.5
Control
Intervention
0.4
0.3
0.2
0.1
0 Medical treatment of enuresis typically centers on
Grade 3 Grade 6 or Grade 9 or Grade 12 or
earlier earlier earlier
M15_BUTC4568_18_GE_C15.indd 548
results showed that children assigned to the intervention
were significantly less likely to develop CD (20 percent)
compared to children in the control condition (42 percent)
(see Figure 15.4; Conduct Problems Prevention Research
Group, 2011). Thus, although CD is associated with signifi-
cant impairment and problems later in life, such problems
are treatable and even preventable.
Elimination Disorders
15.4 List and define elimination disorders.
The childhood disorders we deal with in this section—
“elimination disorders” (enuresis and encopresis)—
involve a single outstanding symptom rather than a
pervasive maladaptive pattern.
Enuresis
The term enuresis refers to the habitual involuntary dis-
charge of urine, usually at night, after the age of expected
continence (age 5). In the DSM-5, functional enuresis is an
elimination disorder described as bed-wetting that is not
organically caused. Children who have primary functional
enuresis have never been continent; children who have
secondary functional enuresis have been continent for at
least a year but have regressed. Estimates of the prevalence
of enuresis reported in the DSM-5 are 5 to 10 percent
among 5-year-olds, 3 to 5 percent among 10-year-olds, and
1.1 percent among children ages 15 or older.
Enuresis may result from a variety of organic condi-
tions, such as genetic predisposition, disturbed cerebral
control of the bladder, or excessive production of urine
during the night (Kessel et al., 2017). Research also has
identified a number of psychological and environmental
factors that can play a role, such as: (1) failure to learn how
to inhibit reflexive bladder emptying; (2) psychological
immaturity, associated with or stemming from emotional
problems; (3) disturbed family interactions, particularly
those that lead to sustained anxiety; and (4) stressful events
(Kessel et al., 2017). For example, a child may regress to
bed-wetting when a new baby enters the family and
becomes the center of attention.
Conditioning procedures have proved to be highly
effective treatment for enuresis (Friman et al., 2008). Mowrer
and Mowrer (1938), in their classic research that is still rele-
vant today, introduced a bell-and-pad procedure in which a
child sleeps on a pad that is wired to a battery-operated bell.
At the first few drops of urine, the bell is set off, thus awak-
ening the child. Through conditioning, the child comes to
associate bladder tension with awakening.
using medications such as the antidepressant drug imipra-
mine. The mechanism underlying the action of the drug is
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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders)
Anzacare Ltd.
When combined with medication such as desmopressin, a urine
alarm (shown here) can be very effective in treating enuresis. The
child sleeps with a wetness detector, which is wired to a battery-
operated alarm in his or her undergarment. Through conditioning,
the child comes to associate bladder tension with awakening.
unclear, but it may simply lessen the deepest stages of
sleep to light sleep, enabling the child to recognize bodily
needs more effectively (Dahl, 1992). An intranasal desmo-
pressin (DDAVP) has also been used to help children man-
age urine more effectively (Rahm et al., 2010). This
medication, a hormone replacement, apparently increases
urine concentration, decreases urine volume, and therefore
reduces the need to urinate. The use of this medication to
treat children with enuresis is no panacea, however. Disad-
vantages of its use include its high cost and the fact that it
is effective only with a small subset of children with enure-
sis, and then only temporarily. Moffatt (1997) suggested
that DDAVP has an important place in treating nocturnal
enuresis in youngsters who have not responded well to
behavioral treatment methods. Keep in mind, however,
that medications by themselves do not cure enuresis and
that there is frequent relapse when the drug is discontin-
ued or the child habituates to the medication (Dahl, 1992).
Some evidence suggests that a biobehavioral approach—
that is, using the urine alarm along with desmopressin—is
most effective (Mellon & McGrath, 2000).
With or without treatment, the incidence of enuresis
tends to decrease significantly with age, but many experts
still believe that enuresis should be treated in childhood
because there is currently no way to identify which chil-
dren will remain enuretic into adulthood. Research has
identified predictors of the persistence of enuresis, such as
higher levels of child anxiety and depression both before
and after the onset of enuresis; however, such factors have
M15_BUTC4568_18_GE_C15.indd 549
549
not yet shown an ability to help researchers, clinicians,
or parents accurately predict the course of bed-wetting
(Kessel et al., 2017).
Encopresis
The term encopresis describes a symptom disorder of chil-
dren who have not learned appropriate toileting for bowel
movements after age 4. This condition, classified under
elimination disorders in DSM-5, is less common than enure-
sis; however, DSM-based estimates are that about 1 percent
of 5-year-olds have encopresis. A study of 102 cases of chil-
dren with encopresis yielded the following list of character-
istics: The average age of children with encopresis was 7,
with a range of ages 4 to 13. About one-third of children
with encopresis were also enuretic, and a large sex differ-
ence was found, with about six times more boys than girls
in the sample. Many of the children soiled their clothing
when they were under stress. A common time was in the
late afternoon after school; few children actually had this
problem at school. Most of the children reported that they
did not know when they needed to have a bowel move-
ment or were too shy to use the bathrooms at school.
Many children with encopresis suffer from constipa-
tion, so an important element in the diagnosis is a physical
examination to determine whether physiological factors
are contributing to the disorder. The treatment of encopre-
sis usually involves both medical and psychological
aspects. Several studies of the use of conditioning proce-
dures with children with encopresis have reported moder-
ate treatment success; that is, no additional incidents
occurred within 6 months following treatment (Friman
et al., 2008). However, research has shown that a minority
of children (11 to 20 percent) do not respond to learning-
based treatment approaches (Keeley et al., 2009).
Neurodevelopmental
Disorders
15.5 Summarize what is known about the
characteristics, course, and treatment of attention-
deficit/hyperactivity disorder and autism spectrum
disorder.
Neurodevelopmental disorders are a group of conditions
characterized by an early onset and persistent course that
are believed to be the result of disruptions to normal brain
development (Andrews et al., 2009; Insel, 2014). Neurode-
velopmental disorders are different from anxiety and
depression in that they must have their onset during child-
hood. These disorders differ from ODD and CD in that
they are believed to be the result of significant delays or
disruptions in brain development that persist into
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adulthood (with a few exceptions discussed next).

Although neurodevelopmental disorders are heteroge-
neous in nature, they often overlap and share common risk
factors. In this section we review some of the most com-
mon neurodevelopmental disorders.
Sabrina, a Student with ADHD
Sabrina was referred to a community clinic because of her over-
active, inattentive, and disruptive behaviors in class. She was usu-
ally very talkative and spoke out loud even when it was clear that
the teacher was delivering an important lesson. Sabrina would also

Attention-Deficit/Hyperactivity impulsively kick tables and chairs, hit other students, and even throw
things to students farther away from her. She appeared to have end-
Disorder less energy—she was perpetually in motion despite being punished
Attention-deficit/hyperactivity disorder (ADHD) is charac- by her teacher not long ago. While Sabrina was determined to be a
smart student, her grades suffered due to her behavioral problems.
terized by a persistent pattern of difficulties sustaining atten-
While she knew that some of her behaviors were unwelcome, she
tion and/or impulsiveness and excessive or exaggerated
felt “unable to control” her behaviors and impulses.
motor activity. We all have had lapses in attention or periods
of excess energy during childhood; however, in order to
meet criteria for ADHD these problems have to be numer- ADHD BEYOND ADOLESCENCE Although ADHD has
ous, persistent, and causing impairment at home, school, or long been thought of as a disorder that occurs only during
the workplace (see the DSM-5 criteria box for ADHD). childhood and adolescence, studies done in the United
Perhaps due partially to their behavioral problems, chil- States and internationally suggest that approximately half
dren with ADHD often score approximately 7 to 15 points of children with ADHD will continue to meet criteria in
lower on intelligence quotient (IQ) tests (Barkley, 1997) and adulthood (Kessler, Green, et al., 2010; Lara et al., 2009).
show deficits on neuropsychological testing that are related Interestingly, however, most cases of adult ADHD are char-
to poor academic functioning (Biederman et al., 2004). They acterized by symptoms of inattention (95 percent), whereas
often exhibit specific learning disabilities such as difficulties a much smaller percentage are characterized by hyperac-
in reading or learning other basic school subjects. Children tivity (35 percent) (Kessler, Green, et al., 2010). It is esti-
and adolescents with ADHD also are at significantly higher mated that approximately 4 percent of U.S. adults meet
risk of a range of school problems including suspension and
repeating a grade, and these effects appear to be due in large
part to disruptive behavior problems (Kessler et al., 2014). In
addition to academic problems, symptoms of ADHD also
can lead to significant social impairment. Hyperactive chil-
dren often have great difficulty getting along with their par-
ents because they often fail to obey rules. Their behavior
problems also can result in their being viewed negatively by
their peers (Hoza et al., 2005).
ADHD is fairly prevalent, occurring in approximately
9 percent of children and adolescents (Merikangas et al.,
2010). Although it is not the most prevalent disorder
among U.S. children and adolescents (specific phobia is
seen in 19 percent of youth), it is the one that is most fre-
quently diagnosed by health professionals (Ryan-Krause et Marlin Levison/ZUMA Press/Newscom

al., 2010). The reason for this difference is that parents are
much more likely to bring a child with ADHD in for treat-
ment than they are a child with a less disruptive disorder
such as specific phobia.
The rate of ADHD is much higher in boys (13 percent)
than in girls (4 percent) (Merikangas et al., 2010) and is
commonly comorbid with other externalizing disorders
such as ODD and CD (Beauchaine et al., 2010; Frick &
Nigg, 2012). ADHD is seen in cultures all around the world.
For example, one study of 1,573 children from 10 European
countries reported that ADHD symptoms are similarly rec- Although children with ADHD are at elevated risk for employment
problems later in life, most people with this disorder go on to have
ognized across all countries studied and that the children
very happy and productive careers. For instance, the award-winning
have significant impairments across a wide range of singer and actor Justin Timberlake has reported that he has struggled
domains (Bauermeister et al., 2010). with ADHD, and he’s doing pretty okay career-wise.

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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders)
DSM-5 Criteria for. . .
Attention-Deficit/Hyperactivity Disorder
A. A persistent pattern of inattention and/or hyperactivity-
impulsivity that interferes with functioning or development,
as characterized by (1) and/or (2):
1. Inattention: Six (or more) of the following symptoms
have persisted for at least 6 months to a degree that is
inconsistent with developmental level and that negatively
impacts directly on social and academic/occupational
activities:
Note: The symptoms are not solely a manifestation of
oppositional behavior, defiance, hostility, or failure to
understand tasks or instructions. For older adolescents
and adults (age 17 and older), at least five symptoms are
required.
a. Often fails to give close attention to details or makes
careless mistakes in schoolwork, at work, or during
other activities (e.g., overlooks or misses details, work
is inaccurate).
b. Often has difficulty sustaining attention in tasks or play
activities (e.g., has difficulty remaining focused during
lectures, conversations, or lengthy reading).
c. Often does not seem to listen when spoken to directly
(e.g., mind seems elsewhere, even in the absence of
any obvious distraction).
d. Often does not follow through on instructions and fails
to finish schoolwork, chores, or duties in the work-
place (e.g., starts tasks but quickly loses focus and is
easily sidetracked).
e. Often has difficulty organizing tasks and activities
(e.g., difficulty managing sequential tasks; difficulty
keeping materials and belongings in order; messy,
disorganized work; has poor time management; fails
to meet deadlines).
f. Often avoids, dislikes, or is reluctant to engage
in tasks that require sustained mental effort (e.g.,
schoolwork or homework; for older adolescents and
adults, preparing reports, completing forms, review-
ing lengthy papers).
g. Often loses things necessary for tasks or activities
(e.g., school materials, pencils, books, tools, wallets,
keys, paperwork, eyeglasses, mobile telephones).
h. Is often easily distracted by extraneous stimuli (for
older adolescents and adults, may include unrelated
thoughts).
i. Is often forgetful in daily activities (e.g., doing chores,
running errands; for older adolescents and adults, re-
turning calls, paying bills, keeping appointments).
2. Hyperactivity and impulsivity: Six (or more) of the fol-
lowing symptoms have persisted for at least 6 months to
a degree that is inconsistent with developmental level
M15_BUTC4568_18_GE_C15.indd 551
551
and that negatively impacts directly on social and
academic/occupational activities:
Note: The symptoms are not solely a manifestation of
oppositional behavior, defiance, hostility, or a failure to
understand tasks or instructions. For older adolescents
and adults (age 17 and older), at least five symptoms are
required.
a. Often fidgets with or taps hands or feet or squirms
in seat.
b. Often leaves seat in situations when remaining seated
is expected (e.g., leaves his or her place in the class-
room, in the office or other workplace, or in other situ-
ations that require remaining in place).
c. Often runs about or climbs in situations where it is
inappropriate.
(Note: In adolescents or adults, may be limited to feeling
restless.)
d. Often unable to play or engage in leisure activities quietly.
e. Is often “on the go,” acting as if “driven by a motor” (e.g.,
is unable to be or uncomfortable being still for extended
time, as in restaurants, meetings; may be experienced
by others as being restless or difficult to keep up with).
f. Often talks excessively.
g. Often blurts out an answer before a question has been
completed (e.g., completes people’s sentences; cannot
wait for turn in conversation).
h. Often has difficulty waiting his or her turn (e.g., while
waiting in line).
i. Often interrupts or intrudes on others (e.g., butts into
conversations, games, or activities; may start using oth-
er people’s things without asking or receiving permis-
sion; for adolescents and adults, may intrude into or take
over what others are doing).
B. Several inattentive or hyperactive-impulsive symptoms were
present prior to age 12 years.
C. Several inattentive or hyperactive-impulsive symptoms are
present in two or more settings (e.g., at home, school, or
work; with friends or relatives; in other activities).
D. There is clear evidence that the symptoms interfere with, or
reduce the quality of, social, academic, or occupational
functioning.
E. The symptoms do not occur exclusively during the course of
schizophrenia or another psychotic disorder and are not better
explained by another mental disorder (e.g., mood disorder,
anxiety disorder, dissociative disorder, personality disorder,
substance intoxication or withdrawal).
Source: Reprinted with permission from the Diagnostic and Statistical Manual
of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric
Association.
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 552 Chapter 15

criteria for ADHD, with higher rates

among those who are male, divorced,
and unemployed (Kessler, Adler, et al.,
2006). The association with unemploy-
ment may be due to trouble finding work,
but may also be the result of poor work
Figure 15.5 The prevalence of stimulant use increased dramatically from
the 1980s to the 1990s and remains at this higher level today. This increase is
driven by prescriptions for those 6 to 18 years old. (National Expenditure
Survey, 1987 and Medical Expenditure Panel Survey, 1996–2008).
(Based on Zuvekas, S. H., & Vitiello, B. (2012). Stimulant medication use in children: a 12-year
perspective. Am J Psychiatry, 169(2), 160–166.)

performance or absenteeism. One recent

study showed that those with ADHD 6
Age group

Number of users per 100 population

miss significantly more days of work
(years)
(approximately 22 more days each year) 5
0–5
than those without ADHD (de Graaf et
6–12
al., 2008), highlighting the long-term 4
13–18
impairment associated with this disorder. 0–18
3
CAUSAL FACTORS IN ATTENTION-
DEFICIT/HYPERACTIVITY DISORDER
2
The specific causes of ADHD have been
widely debated. As with most disorders,
1
available evidence points to both genetic
(Ilott et al., 2010; Sharp et al., 2009) and
0
social-environmental factors (e.g., prena-
1986
1987
1988
1989
1990
1991
1992
1993
1994
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
2005
2006
2007
2008
tal alcohol exposure; Ware et al., 2012).
But how do genetic variations and social- Year
environmental events produce the par-
ticular constellation of symptoms of
ADHD that we see in children and adults? Research on the
neurobiology of ADHD suggests that the answer may lie,
with ADHD, stimulant medication decreases overactivity
at least in part, in the way that the brain develops in those
and distractibility and, at the same time, increases their
with ADHD. Children with ADHD have smaller total
alertness (Konrad et al., 2004). As a result, they are often
brain volumes than those without ADHD (Castellanos
able to function much better at school (Hazell, 2007;
et al., 2002), and their brains appear to mature approxi-
Pelham et al., 2002).
mately 3 years more slowly than those without ADHD
Ritalin also seems to lower the amount of aggressive-
(Shaw et al., 2007). Interestingly, these maturational delays
ness in children with ADHD (Fava, 1997). In fact, many
are most prominent in prefrontal brain regions involved in
children whose behavior has not been acceptable in regular
attention and impulsiveness. Findings like these are excit-
classes can function and progress in a relatively normal
ing steps toward understanding this disorder, but ques-
manner when they use such a drug. In a 5-year follow-up
tions remain about how and why these differences arise.
study, Charach, Ickowicz, and Schachar (2004) reported
Answering these questions will likely lead not just to
that children with ADHD on medication showed greater
better understanding, but to the development of more
improvement in teacher-reported symptoms than non-
effective treatments.
treated children. The possible side effects of Ritalin, how-
TREATMENTS AND OUTCOMES Although hyperactiv- ever, are numerous: decreased blood flow to the brain,
ity in childhood was first described more than 100 years which can result in impaired thinking ability and memory
ago, disagreement over the most effective methods of treat- loss; disruption of growth hormone, leading to suppres-
ment continues, especially regarding the use of stimulant sion of growth in the body and brain of the child; insom-
medications such as Ritalin (methylphenidate) to treat nia; psychotic symptoms; and others. Although
young children with ADHD. Yet this approach to treating amphetamines do not cure ADHD, they have reduced the
children with ADHD has great appeal in the medical com- behavioral symptoms in about one-half to two-thirds of the
munity. Indeed, the use of stimulant medication to treat cases in which medication appears warranted. Newer vari-
ADHD has risen dramatically in recent years, with this ants of the drug, referred to as extended-release methyl-
increase occurring primarily among adolescents (see phenidate (Concerta), have similar benefits and are
Figure 15.5; Zuvekas & Vitiello, 2012). available in doses that may better suit an adolescent’s life-
Interestingly, research has shown that stimulants have style (Mott & Leach, 2004; Spencer, 2004b).
a quieting effect on children—just the opposite of what we Three other medications for treating ADHD have
would expect from their effects on adults. For children received attention in recent years. Pemoline is chemically

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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders)
very different from Ritalin (Faigel & Heiligenstein, 1996); it
exerts beneficial effects on classroom behavior by enhanc-
ing cognitive processing and has fewer adverse side effects
than Ritalin (Bostic et al., 2000; Pelham et al., 2005).
Strattera (atomoxetine), a noncontrolled treatment option
that can be obtained readily, is a U.S. Food and Drug
Administration (FDA)-approved nonstimulant medication
(FDA, 2002). Side effects include decreased appetite, nau-
sea, vomiting, and fatigue. The development of jaundice
has been reported, and the FDA (2004) has warned of the
possibility of liver damage from using Strattera. Another
drug that reduces symptoms of impulsivity and hyperac-
tivity in children with ADHD is Adderall. This medication
is a combination of amphetamine and dextroamphetamine;
however, research has suggested that Adderall provides no
advantage or improvement in results over Ritalin or
Strattera (Miller-Horn et al., 2008).
Recent studies have shown that there are long-term
benefits associated with the use of stimulants among both
children and adults with ADHD. For instance, although
those with ADHD are at significantly elevated risk of sub-
stance use disorders later in life, those who took stimulants
during childhood have a lower risk of substance use disor-
ders during adulthood (Dalsgaard et al., 2014). Moreover,
adults with ADHD are at significantly increased risk of
outcomes such as car accidents and suicide attempts; how-
ever, the risk of these outcomes is significantly reduced
when these adults are using ADHD medications (Chang
et al., 2014; Chen et al., 2014).
There have also been some reported misuses of stimu-
lant medication, particularly among college students.
Some college students share the prescription medication of
friends as a means of obtaining a “high” (Chutko et al.,
2010); however, even more frequently it is used as a study
aid. One recent meta-analysis revealed that approximately
17% of college students report using stimulant medication
that was not prescribed to them, with the most commonly
reported reasons for using it including “to concentrate bet-
ter while studying” and “to stay awake longer” (Benson
et al., 2015). Perhaps ironically given these motivations, the
same study found that stimulant misuse is associated with
lower GPA scores and higher rates of academic problems
(so lay off the stimulants if not prescribed to you by your
doctor).
Due to concerns about the use of stimulant medica-
tions with children, some parents and clinicians prefer
using psychological interventions, which also have shown
positive effects (Corcoran, 2011; Pelham & Fabiano, 2008).
The behavioral intervention techniques that have been
developed for ADHD include teaching organizational and
planning skills, techniques for decreasing distractibility
and procrastination, as well as parenting techniques
focused on providing reinforcement for adaptive child
behavior. Randomized controlled trials have shown that
M15_BUTC4568_18_GE_C15.indd 553
553
those assigned to such treatment have significantly better
outcomes than those assigned to various control condi-
tions (Fleming et al., 2015; Sprich et al., 2016).
Autism Spectrum Disorder
Autism spectrum disorder (which we refer to as “autism”)
is a neurodevelopmental disorder that involves a wide
range of problematic behaviors including deficits in lan-
guage and perceptual and motor development; defective
reality testing; and impairments in social communication.
The following case illustrates some of the behaviors that
may be seen in a child within the autism spectrum.
The Need for Routine
Daryl is 6 years old. Typically, children of this age should enjoy being
inquisitive and exploring the world in a relatively stress-free way. This
is not the case for Daryl: he rarely wants to speak to other people
and even when does, he avoids eye contact. In addition, Daryl’s par-
ents notice that he never really began to speak like a normal 3-year-
old, who usually speak back-and-forth with their parents as part of
their development. Instead, Daryl spent most of his time playing with
building blocks in his room, and the model he built was almost identi-
cal every day. He also did not show any interest in going out or meet-
ing new people, and would be very sensitive and anxious in a new
environment. When things were out of routine, like spending their
holiday abroad, Daryl would usually become noncooperative, and cry
out loud for no obvious reasons.
Autism was first described in 1943 (Kanner). It afflicts
tens of thousands of American children from all socioeco-
nomic levels and is seemingly on the rise (Fombonne,
2005). However, the reported increase in autism in recent
years is likely due to methodological differences between
studies and changes in diagnostic practice and public and
professional awareness rather than an increase in preva-
lence (Williams et al., 2006). A recent national, multi-year
study of U.S. children and adolescents reported that 2.4%
of children and adolescents meet criteria for autism (3.5%
of boys and 1.2% of girls) (Xu et al., 2018).
Autism is usually identified before a child is 30 months
of age, and diagnostic stability over the childhood years is
quite high. Lord and colleagues (2006) report that children
diagnosed with autism by age 2 tend to be similarly diag-
nosed at age 9. Recent research suggests that early signs of
problems with social communication can be detected in the
first 6 months of an infant’s life (Jones & Klin, 2014). When
scanning the world around them, developing infants from
2 to 6 months of age typically focus increasingly on the face
and especially the eyes of others. This focus allows infants
to better understand those caring for them and helps facili-
tate later social interaction. In contrast, children later diag-
nosed with autism show a significant decline in their focus
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 554 Chapter 15
DSM-5 Criteria for…
Autism Spectrum Disorder
A. Persistent deficits in social communication and social interac-
tion across multiple contexts, as manifested by the following,
currently or by history (examples are illustrative, not exhaus-
tive; see text):
1. Deficits in social-emotional reciprocity, ranging, for
example, from abnormal social approach and failure of
normal back-and-forth conversation; to reduced sharing
of interests, emotions, or affect; to failure to initiate or
respond to social interactions.
2. Deficits in nonverbal communicative behaviors used
for social interaction, ranging, for example, from poorly
integrated verbal and nonverbal communication; to ab-
normalities in eye contact and body language or deficits
in understanding and use of gestures; to a total lack of
facial expressions and nonverbal communication.
3. Deficits in developing, maintaining, and understanding
relationships, ranging, for example, from difficulties
adjusting behavior to suit various social contexts; to diffi-
culties in sharing imaginative play or in making friends; to
absence of interest in peers.
B. Restricted, repetitive patterns of behavior, interests, or activi-
ties, as manifested by at least two of the following, currently or
by history (examples are illustrative, not exhaustive; see text):
1. Stereotyped or repetitive motor movements, use of
objects, or speech (e.g., simple motor stereotypies, lining
up toys or flipping objects, echolalia, idiosyncratic
phrases).
2. Insistence on sameness, inflexible adherence to routines,
or ritualized patterns of verbal or nonverbal behavior (e.g.,
extreme distress at small changes, difficulties with transi-
tions, rigid thinking patterns, greeting rituals, need to take
same route or eat same food every day).
on the eyes of others from 2 to 6 months of age and this
decline continues until 24 months—at which point it is
approximately half the level of focus as that seen in typi-
cally developing children (see Figure 15.6; Jones & Klin,
2014). In contrast, while their attention to other people’s
eyes decreases, infants later diagnosed with autism show a
significant increase in their focus on inanimate objects,
which is double the level of typically developing children
by 24 months.
THE CLINICAL PICTURE OF AUTISTIC SPECTRUM DIS-
ORDER Children with autism show varying degrees of
impairments and capabilities. A cardinal and typical sign is
that a child seems apart or aloof from others, even in the
earliest stages of life (Hillman et al., 2007). Mothers often
remember such babies as not being cuddly, not reaching
out when being picked up, not smiling or looking at them
M15_BUTC4568_18_GE_C15.indd 554
3. Highly restricted, fixated interests that are abnormal in
intensity or focus (e.g., strong attachment to or preoc-
cupation with unusual objects, excessively circumscribed
or perseverative interests).
4. Hyper- or hyporeactivity to sensory input or unusual inter-
est in sensory aspects of the environment (e.g., apparent
indifference to pain/temperature, adverse response to
specific sounds or textures, excessive smelling or touch-
ing of objects, visual fascination with lights or movement).
C. Symptoms must be present in the early developmental period
(but may not become fully manifest until social demands
exceed limited capacities, or may be masked by learned strat-
egies in later life).
D. Symptoms cause clinically significant impairment in social,
occupational, or other important areas of current functioning.
E. These disturbances are not better explained by intellectual dis-
ability (intellectual developmental disorder) or global develop-
mental delay. Intellectual disability and autism spectrum
disorder frequently co-occur; to make comorbid diagnoses of
autism spectrum disorder and intellectual disability, social
communication should be below that expected for general
developmental level.
Note: Individuals with a well-established DSM-IV diagnosis of
autistic disorder, Asperger’s disorder, or pervasive developmental
disorder not otherwise specified should be given the diagnosis of
autism spectrum disorder. Individuals who have marked deficits
in social communication, but whose symptoms do not otherwise
meet criteria for autism spectrum disorder, should be evaluated
for social (pragmatic) communication disorder.
Source: Reprinted with permission from the Diagnostic and Statistical Manual
of Mental Disorders, Fifth Edition, (Copyright 2013). American Psychiatric
Association.
while being fed, and not appearing to notice the comings
and goings of other people.
A Social Deficit Children with autism often do not show
any need for affection or contact with others. Several stud-
ies, however, have questioned the traditional view that
children with autism are emotionally flat. These studies
have shown that children with autism do express emo-
tions and should not be considered as lacking emotional
reactions (Jones et al., 2001). Instead, some have character-
ized the seeming inability of children with autism to
respond to others as a lack of social understanding—a
deficit in the ability to attend to social cues from others.
Indeed, neuroimaging studies have revealed that children
with autism show decreased activity in the medial pre-
frontal cortex, a region associated with understanding the
mental states of others, but increased activation in the
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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders) 555

Figure 15.6
In a recent study by Jones and Klin (2014), the authors showed infants videos of humans and objects and found that chil-
dren later diagnosed with autism showed a decline in their focus on the eyes of others (choosing instead to focus on inani-
mate objects). Part (A) shows eye-gaze data from a 6-month-old later diagnosed with autism, (B) shows eye-gaze data from
a typically developing 6-month-old, (C) shows the pattern of decline for two children later diagnosed with autism, and (D)
shows the pattern of stability for two typically developing children.
Based on Warren Jones and Ami Klin, Attention to Eyes Is Present but in Decline in 2–6-Month-olds Later Diagnosed with Autism, Nature.
December 19, 2013; 504(7480), pages 427–431.

(A) (B)

Autism Spectrum Disorder Typical Development

100 100

80 80

60 60

40 40
Function time, eyes (%)

20 20

0 0
23456 9 12 15 18 24 23456 9 12 15 18 24
100 100

80 80

60 60

40 40

20 20

0 0
23456 9 12 15 18 24 23456 9 12 15 18 24
Age (months) Age (months)
(C) (D)

M15_BUTC4568_18_GE_C15.indd 555 24/09/2020 19:35

 556 Chapter 15
ventral occipitotemporal regions involved in object per-
ception (Sigman et al., 2006).
Additionally, children with autism show deficits in
attention and in locating and orienting to sounds in their
environment (Hillman et al., 2007). These children often
show an aversion to auditory stimuli, crying even at the
sound of a parent’s voice. The pattern is not always consis-
tent, however; children with autism may at one moment be
severely agitated or panicked by a very soft sound and at
another time be totally oblivious to a loud noise.
An Absence of Speech Children with autism often have
an absence or severely limited use of speech. If speech is
present, it is almost never used to communicate except in
the most rudimentary fashion, such as by saying “yes” in
answer to a question or by the use of echolalia—the par-
rot-like repetition of a few words. Whereas the echoing of
parents’ verbal behavior is found to a small degree in nor-
mal children as they experiment with their ability to pro-
duce articulate speech (e.g., Parent: “Please put your toys
away.” Child: “Toys away.”), echolalia is more common
and more persistent among children with autism
(Gernsbacher et al., 2016). Problems with speech, and with
social interactions more generally, are believed to be the
result, at least in part, to atypical organization or connec-
tivity in the brains of people with autism spectrum disor-
der. Brain-imaging studies comparing children with autism
to typically developing children show that among those
with autism, there is under-developed connectivity within
regions of the brain associated with imitating others, but
over-developed connectivity between imitation regions
and other parts of the brain (Fishman et al., 2015). More-
over, among those with autism, the greater the under-con-
nectivity within imitation regions, the greater the
symptoms of the disorder.
Self-Stimulation Self-stimulation is often characteristic of
children with autism. It usually takes the form of such
repetitive movements as head banging, spinning, and
rocking, which may continue by the hour.
Maintaining Sameness Many children with autism
become preoccupied with and form strong attachments to
unusual objects such as rocks, light switches, or keys.
When their preoccupation with the object is disturbed—for
example, by its removal or by attempts to substitute some-
thing in its place—or when anything familiar in the envi-
ronment is altered even slightly, these children may have a
violent temper tantrum or a crying spell that continues
until the familiar situation is restored. Thus children with
autism are often said to be “obsessed with the maintenance
of sameness.”
CAUSAL FACTORS IN AUTISM Autism is a complex
disorder and its precise causes are unknown. Twin and
M15_BUTC4568_18_GE_C15.indd 556
sibling studies have shown that there is a very strong heri-
table component in autism. For instance, 2 to 14 percent of
siblings of children diagnosed with autism also have the
disorder, and approximately 20 percent have some symp-
toms of the disorder (Newschaffer et al., 2007). Although
there is a clear heritable component, the exact mode of
genetic transmission is not yet understood. On one hand,
recent research has shown that hundreds of different genes
are associated with increased risk of autism, suggesting
that there are many different paths to developing this dis-
order (Robinson et al., 2014; State & Sestan, 2012). On the
other hand, research also has shown that the same genetic
variants are associated with multiple disorders. For
instance, some of the same genes that have been linked
with an increased risk of autism also increase the risk of
ADHD, schizophrenia, bipolar disorder, and depression
(Smoller et al., 2013).
Given the complexity of this picture, how will we ever
know what causes autism? Researchers are pursuing sev-
eral different avenues of research to try to answer this
question. They are trying to determine what portion of the
genetic risk is inherited (52 percent) and what portion is
due to de novo genetic mutations (3 percent). De novo muta-
tions are those that occur in the egg or sperm and are
passed on to every cell in the child’s body, despite not
appearing in the parents’ DNA. It seems that much of the
risk for autism is indeed inherited from one’s parents
(Gaugler et al., 2014). However, a significant portion of risk
also arises due to de novo mutations. This is important to
know, because as we learn about factors that increase the
likelihood of genetic mutations, we can take steps to try to
decrease their occurrence. For instance, genetic mutations
have been reported to occur at higher rates in the sperm of
older men, and there is now converging evidence that
older father age at a child’s birth is associated with
increased risk of autism (D’Onofrio et al., 2014). Findings
like these do not explain how or why such mutations
increase the risk of autism, but can be useful for the pur-
poses of family planning.
TREATMENTS AND OUTCOMES OF AUTISM The
treatment prognosis for many children with autism is poor
in part because so many people with autism are insuffi-
ciently treated (Moldin & Rubenstein, 2006). In fact, for
many years, it was generally accepted that there is no effec-
tive way to treat people diagnosed with autism. Moreover,
many children with autism are subjected to a range of fads
and “novel” approaches that have little to no support for
their effectiveness. However, in 1987, Ivar Lovaas (1987)
reported that an intensive behavioral intervention admin-
istered via one-on-one meetings with the child for over 40
hours per week for 2 years resulted in extremely positive
results. The intervention was based on both discrimina-
tion-training strategies (reinforcement) and contingent
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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders)
aversive techniques (punishment). The treatment plan typi-
cally enlists parents in the process and emphasizes teaching
children to learn from and interact with “normal” peers in
real-world situations. Of the treated children in the study
by Lovaas and colleagues, 47 percent achieved normal intel-
lectual and educational functioning, compared with only
2 percent of children in the untreated control condition.
More recent versions of this intensive behavioral
approach have continued to demonstrate success. Geraldine
Dawson and colleagues (2010) showed that toddlers
(18–30 months old) with autism who were randomly
assigned to receive the Early Start Denver Model (ESDM)
intervention displayed significant improvements in IQ (an
average of a 17-point increase), language, and adaptive
behavior as well as a decrease in symptoms of autism. The
ESDM intervention involves more than 20 hours per week of
intensive behavioral work with the child and parent(s)
focused on interpersonal exchanges, verbal and nonverbal
communication, and adult sensitivity to children’s cues.
Children receiving the ESDM intervention also showed
greater cortical activation when viewing other people’s faces
(compared to objects), which in turn was correlated with
greater improvements in the children’s social communica-
tion (Dawson et al., 2012). Although treatments like this one
are extremely time consuming, their powerful results sug-
gest that behavioral interventions can cause improvements
in people diagnosed with autism. See the Developments in
Practice box for other novel approaches to treating autism.
Ociacia/Shutterstock
Humanoid robots have some human characteristics, but not as
complex, so it doesn't overstimulate or overwhelm a child with autism.
Tic Disorders
A tic is a persistent, intermittent muscle twitch or spasm,
usually limited to a localized muscle group. The term is
used broadly to include blinking the eye, twitching the
mouth, licking the lips, shrugging the shoulders, clearing
the throat, and grimacing, among other actions. Tic disor-
ders are classified under motor disorders in DSM-5. Tics
occur most frequently between the ages of 8 and 14 (Yang
et al., 2016). In some instances, as in clearing the throat, an
individual may be aware of the tic when it occurs, but
usually he or she performs the act habitually and does not
notice it. In fact, many individuals do not even realize they
M15_BUTC4568_18_GE_C15.indd 557
557
have a tic unless someone brings it to their attention. A
cross-cultural examination of tics found a similar pattern
in research and clinical case reports from other countries
(Staley et al., 1997). Moreover, the age of onset (average 7
to 8 years old) and predominant gender (male) of cases
were reported to be similar across cultures (Turan & Senol,
2000). A recent study on the prevalence of tic disorder in
children and adolescents reported that the lifetime preva-
lence of tic disorders (TDs) is 2.6 percent for transient tic
disorder (TTD), 3.7 percent for chronic tic disorder (CTD),
and 0.6 percent for Tourette’s disorder (Stefanoff et al.,
2008). The psychological impact that tics can have on an
adolescent is illustrated in the following case.
A Vicious Cycle of Blinking and Anxiety
Jamie always wanted to be a teacher. One day, after a period of pro-
longed sadness, she visited the counseling center at her school and
said that she was thinking of giving up her plan to be a teacher. When
asked why, she said that her friends pointed out that she usually blinked
very rapidly while speaking in class. She was unaware of this habit and,
even after being told about it, was unable to tell when it took place. As a
result, she became hypervigilant and self-conscious, refusing to speak
during class discussions. This made her more tensed and lowered her
self-esteem, which increased the frequency of her blinking. Thus, a
vicious cycle was established. She began distancing herself from situa-
tions that required her to speak, including her dream to teach, to avoid
perceived embarrassment. Fortunately, the rapid blinking proved ame-
nable to treatment by conditioning and assertive training.
Tourette’s disorder, classified as a motor disorder in
the neurodevelopmental disorders section of DSM-5, is an
extreme tic disorder involving multiple motor and vocal
patterns. This disorder typically involves uncontrollable
head movements with accompanying sounds such as
grunts, clicks, yelps, sniffs, or words. Some, possibly most,
tics are preceded by an urge or sensation that seems to be
relieved by execution of the tic. Tics are thus often difficult
to differentiate from compulsions, and they are sometimes
referred to as “compulsive tics” (Dell’Osso et al., 2017). An
epidemiological study in Sweden reported the prevalence
of Tourette’s disorder in children and adolescents to be
about 0.5 percent (Khalifa & von Knorring, 2004). Approxi-
mately one-third of individuals with Tourette’s disorder
manifest coprolalia, which is a complex vocal tic that
involves the uttering of obscenities. Some people with
Tourette’s disorder also experience explosive outbursts
(Budman et al., 2000). The average age of onset for
Tourette’s disorder is 7, and most cases have an onset
before age 14. The disorder frequently persists into adult-
hood, and it is about three times more frequent among
males than among females. Although the exact cause of
Tourette’s disorder is undetermined, evidence suggests a
strong biological basis (Margolis et al., 2006). There are
many types of tics, and many of them appear to be
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Developments in Practice
Can Video Games Help Children with Neurodevelopmental Disorders?
Kids love video games. They are fun, provide
ongoing and immediate reinforcement, and are
Figure 15.7
able to engage children’s attention for hours at a In this “Happy” level of the game FaceMaze, the player (represented by the purple
face) must move through the maze eating candy pieces and has to make a
time. Many popular video games teach children
“happy” expression to remove the yellow faces blocking his path. Gordon and
how to get very good at driving cars at high colleagues (2014) showed that playing this game significantly improves the ability
speeds (Mario Kart), shooting at people (Call of to make different facial expressions in children with autism.
Duty), or both (Grand Theft Auto). Although chil- (Based on Gordon et al. 2014, Quantifying narrative ability in autism spectrum disorder: a
dren with autism often have trouble with attention computational linguistic analysis of narrative coherence, J Autism Dev Disord. 2014 Dec;
44(12):3016–25.)
and disruptive behavior, they can readily become
engrossed in the world of video games (Durkin,
2010). Researchers are now using new technol-
ogies, including video games, to help children How to Smile to Fill the Meter
Level 2 play Start
with autism to improve some of their social, cog- Smile-O-
nitive, and emotional deficits. For instance, chil- Meter
dren with autism have trouble producing
emotional expressions, which contributes to their
social communication problems. To address this,
researchers developed a Pacman-like game in
which the player has to gobble up candy, but in
order to get to the candy, the player must remove
obstacles in his or her path by producing differ-
ent facial expressions (e.g., happy, angry), which
are read by computer facial recognition software
(see Figure 15.7). Gordon and colleagues (2014)
showed that children with autism who play this
game demonstrate improvements in their facial
expressions of emotion, and in fact make them
indistinguishable in quality from those of typically
developing children.
As part of their difficulty communicating with dren demonstrated a significant increase in their use of verbal
others, children with autism often have trouble delivering compli- compliments and gestures. That is, there was a whole lotta fist
ments appropriately. This contributes to their impairment, pumping going on!
because compliments can increase the extent to which others The use of video games and newer, portable technologies
like us and want to engage with us socially. To address this, has attracted many people’s interest, but also has prompted
Macpherson, Charlop, and Miltenberger (2014) created an some important questions. For instance, research has shown that
iPad®-based video training that showed children how to compli- kids with autism tend to play video games for longer duration than
ment others. The use of portable technology allowed them to other kids, and show greater sleep problems than typically devel-
test this intervention in a real-world child setting: a kickball game! oping kids as a result (Engelhardt et al., 2013), raising concerns
They showed that when kids with autism played kickball, they about game overuse among those with autism. Although the
didn’t compliment their teammates very much at all. However, available and acceptable use of computer-based learning meth-
when they administered the intervention, which consisted of ods show promise, there are professional issues and program
showing a video of someone complimenting a teammate (e.g., research limitations that need to be more fully explored before the
saying “That was a great kick!” and doing a fist pump), the chil- full potential of this methodology is reached.

associated with the presence of other psychological disor-
ders, particularly obsessive-compulsive disorder (OCD).
Most tics, however, do not have a purely biological basis
but stem from psychological causes such as self-conscious-
ness or tension in social situations, and they are usually
associated with severe behavioral problems (Evans et al.,
2016). As in the case of the adolescent boy previously
described, an individual’s awareness of the tic often
increases tension and the occurrence of the tic.
Behavioral interventions also have been used to effec-
tively treat tics (Hollis et al., 2016). One successful pro-
gram, habit reversal training or HRT, involves several
sequential elements, beginning with awareness training,
relaxation training, and the development of incompatible

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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders) 559

responses, and then progressing to cognitive therapy and
modification of the individual’s overall style of action
(Chang, Piacentina, & Walkup, 2007). Because children
with Tourette’s disorder can have substantial family adjust-
ment and school adjustment problems, interventions
should be designed to aid their adjustment and to modify
the reactions of peers to them. School psychologists can
play an effective part in the social adjustment of the child
with Tourette’s disorder by applying behavioral interven-
tion strategies that help arrange the child’s environment to
be more accepting of such unusual behaviors.
Among medications, antipsychotic and noradrenergic
drugs are most effective for the treatment of Tourette’s and
tic disorders (Hollis et al., 2016). A common concern, how-
ever, among parents of children with these disorders is that
it can be difficult to find specialists with experience treat-
ing them, both in terms of knowing the most effective
behavioral interventions and the most effective medica-
tions to use for these conditions (Hollis et al., 2016).
academic performance in one or more school subjects such
as math, spelling, writing, or reading. Typically, these chil-
dren have overall IQs, family backgrounds, and exposure to
cultural norms and symbols that are consistent with at least
average achievement in school. They do not have obvious,
crippling emotional problems, nor do they seem to be lack-
ing in motivation, cooperativeness, or eagerness to please
their teachers and parents—at least not at the outset of their
formal education. Nevertheless, they fail, often abysmally
and usually with a stubborn, puzzling persistence.
The consequences of these encounters between children
with learning disabilities and rigid school systems can be
disastrous to these children’s self-esteem and general psy-
chological well-being, and research indicates that these
effects do not necessarily dissipate after secondary schooling
ends but continue to impact these individuals’ career adjust-
ments (Morris & Turnbull, 2007). Thus, even when learning
disorder difficulties are no longer a significant impediment,
an individual may bear, into maturity and beyond, the scars
of many painful school-related episodes of failure.

Specific Learning Disorders

15.6 Describe what is currently known about the causes
and treatment of learning disorders.
Learning disorders are delays in cognitive development in
the areas of language, speech, mathematical, or motor
skills that are not necessarily due to any demonstrable
physical or neurological defect. Of these types of problems,

Fotoksa/Shutterstock
the best known and most widely researched are a variety
of reading/writing difficulties known collectively as dys-
lexia. In dyslexia, the individual has problems in word rec-
ognition and reading comprehension; often he or she is
markedly deficient in spelling and memory (Smith-Spark
Children with learning disorders can experience deep emotional
& Fisk, 2007) as well. On assessments of reading skill, these
tension under normal learning circumstances.
persons routinely omit, add, and distort words, and their
reading is typically painfully slow.
But there is also a brighter side to this picture. High
The diagnosis of learning disorders is restricted to
levels of general talent and of motivation to overcome the
those cases in which there is clear impairment in school
obstacle of a learning disorder sometimes produce a life of
performance or (if the person is not a student) in daily liv-
extraordinary achievement. Sir Winston Churchill, British
ing activities—impairment not due to intellectual disabil-
statesman, author, and inspiring World War II leader, is
ity or to a pervasive developmental disorder such as
said to have had dyslexia as a child. The same attribution is
autism. Skill deficits due to ADHD are coded under ADHD.
made to Woodrow Wilson, former university professor and
Significantly more boys than girls are diagnosed as having
president of the United States, and to Nelson Rockefeller,
a learning disorder, but estimates of the extent of this gen-
former governor of New York and vice president of the
der discrepancy have varied widely from study to study.
United States. Such examples remind us that the “bad
Estimates suggest that 2 to 10 percent of children have a
luck” and personal adversity of having a learning disorder
learning disorder, most often classified as dyslexia (80 per-
need not be uniformly limiting—in fact, quite the contrary.
cent), with about 30 percent of children with a learning dis-
order also suffering from a comorbid disorder such as
ADHD, depression, or anxiety (Sahoo et al., 2015). Causal Factors in Learning Disorders
Children with learning disorder are initially identified Probably the most widely held view of the causes of spe-
as such because of an apparent disparity between their cific learning disorders is that they are the products of
expected academic achievement level and their actual subtle CNS impairments. In particular, these disabilities

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 560 Chapter 15
are thought to result from some sort of immaturity, defi-
ciency, or dysregulation limited to those brain functions
that supposedly mediate, for normal children, the cogni-
tive skills that children with learning disorders cannot effi-
ciently acquire. For example, many researchers believe that
language-related learning disorders such as dyslexia are
associated with a failure of the brain to develop in a nor-
mally asymmetrical manner with respect to the right and
left hemispheres. Specifically, there appears to be dysfunc-
tion in the left hemisphere’s reading network among peo-
ple with dyslexia (Richlan, 2012). Research using functional
magnetic resonance imaging (see Chapter 4) has suggested
that people with dyslexia have a deficiency of physiologi-
cal activation in the cerebellum (Richards et al., 2005).
Some investigators believe that the various forms of
learning disorder, or the vulnerability to develop them,
may be genetically transmitted. This issue seems not to
have been studied with the same intensity or methodologi-
cal rigor as in other disorders, but identification of a gene
region for dyslexia on chromosome 6 has been reported
(Schulte-Koerne, 2001). Although it would be somewhat
surprising if a single gene were identified as the causal fac-
tor in all cases of reading disorder, the hypothesis of a
genetic contribution to at least the dyslexic form of learn-
ing disorder seems promising.
Treatments and Outcomes
We do not yet fully understand the causes of learning dis-
orders, but researchers have identified treatments for these
conditions that have been shown to lead to significant
improvements in learning and academic outcomes. A
recent review of 22 different randomized controlled trials
testing treatments for reading disabilities revealed that
phonics instruction, which involves teaching children let-
ter–sound correspondence as well as how to decode and
create syllables, is associated with significant improve-
ments in reading and spelling abilities (Galuschka et al.,
2014). Although there is still much progress to be made in
terms of accurately identifying children with learning dis-
abilities and providing effective intervention, the percent-
age of students with learning disorders who go on to
Ikat Photography/Pearson Education Ltd
Dyslexia: When Your Brain Makes Reading Tricky.
M15_BUTC4568_18_GE_C15.indd 560
receive a high school diploma has been increasing over
recent years, which suggests that efforts by educators, par-
ents, and researchers in this area are starting to have a pos-
itive effect (Cortiella & Horowitz, 2014).
Intellectual Disability
15.7 Define intellectual disability and name three
known causal factors involved in its development.
Intellectual disability (also called intellectual developmental
disorder; see the Thinking Critically box) is characterized by
deficits in general mental abilities, such as reasoning, prob-
lem solving, planning, abstract thinking, judgment, aca-
demic learning, and learning from experience (APA, 2013,
p. 31). Intellectual disability is defined in terms of both
intelligence and level of performance, and for the diagnosis
to apply, these problems must begin before the age of 18. By
definition, any functional equivalent of intellectual disabil-
ity that has its onset after age 17 is considered to be “demen-
tia” rather than intellectual disability. The distinction is an
important one because the psychological situation of a per-
son who acquires a pronounced impairment of intellectual
functioning after attaining maturity is vastly different from
that of a person whose intellectual resources were below
normal throughout all or most of his or her development.
Intellectual disability occurs among children through-
out the world (Fryers, 2000). In its most severe forms, it is a
source of great hardship to parents as well as an economic
and social burden on a community. The prevalence of diag-
nosed intellectual disability in the United States is esti-
mated to be about 1 percent, which would indicate a
population estimate of some 2.6 million people. However,
prevalence is extremely difficult to pin down because defi-
nitions of intellectual disability vary considerably (Carr &
O’Reilly, 2016). Most states have laws providing that per-
sons with IQs below 70 who show socially incompetent or
persistently problematic behavior can be classified as hav-
ing an “intellectual disability” and, if judged otherwise
unmanageable, may be placed in an institution.
Initial diagnoses of intellectual disability most fre-
quently occur at ages 5 to 6 (around the time that schooling
begins for most children), peak at age 15, and drop off
sharply after that. For the most part, these patterns in age
of first diagnosis reflect changes in life demands. During
early childhood, individuals with only a mild degree of
intellectual impairment, who constitute the vast majority
of those with intellectual disability, often appear to be nor-
mal. Their below-average intellectual functioning becomes
apparent only when difficulties with schoolwork lead to a
diagnostic evaluation. When adequate facilities are avail-
able for their education, children in this group can usually
master essential school skills and achieve a satisfactory
level of socially adaptive behavior. Following the school
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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders)
DSM-5 Thinking Critically about DSM-5
What Role Should Cultural Changes Have in Developing Medical Terminology?
Along with the addition of new diagnostic categories, such as
gambling disorder and hoarding disorder, and the revision of
other earlier diagnostic criteria resulting in disorders such as dis-
ruptive mood dysregulation disorder, there have been changes to
some existing categories that are largely nominal in order to make
the terminology more appropriate with contemporary language
use and/or consistent with the forthcoming International Classifi-
cation of Diseases (ICD-11) system.
One noteworthy revision in DSM-5 is the removal of the term
mental retardation, which was used in describing individuals with
intellectual impairment in previous editions of the DSM. The term
mental retardation has come to be considered derogatory by
many. The new term, intellectual disability, has replaced mental
retardation and is becoming more commonly used by profession-
als, by the lay public, and by various advocacy groups. As noted
by the DSM-5 committee, a U.S. legal statute (Public Law
years, they usually make a more or less acceptable adjust-
ment in the community and thus lose the identity of hav-
ing an intellectual disability.
Levels of Intellectual Disability
The various levels of intellectual disability are described in
greater detail in the following sections.
MILD INTELLECTUAL DISABILITY Tests of human intel-
ligence produce IQ scores that have an average of 100 and a
standard deviation of 15. That means that most people (95
percent) receive a score somewhere between 70 and 130.
Individuals with mild intellectual disability have IQ scores
ranging from 50–55 to approximately 70 (i.e., more than two
standard deviations below the mean) and constitute by far
the largest number of those diagnosed with this condition
(see Table 15.1). Within the educational context, people in
this group are considered educable, and their intellectual lev-
els as adults are comparable to those of average 8- to 11-year-
old children. Statements such as the latter, however, should
not be taken too literally. An adult with mild disability with a
mental age of, say, 10 (that is, his or her intelligence test per-
formance is at the level of the average 10-year-old) may not
in fact be comparable to the average 10-year-old in informa-
tion-processing ability or speed. On the other hand, he or she
will normally have had far more experience in living, which
would tend to raise the measured intelligence scores.
The social adjustment of people with mild intellectual
disability often approximates that of adolescents, although
M15_BUTC4568_18_GE_C15.indd 561
561
111-256 or Rosa’s Law) has replaced the term mental retardation
with intellectual disability. At the Second Session of the 111th
Congress of the United States in 2010 the following resolution
was passed:
(b) INDIVIDUALS WITH DISABILITIES EDUCATION ACT—
(1) SECTION 601(c) (12)(C) of the Individuals with Disabilities
Education Act (20 U.S.C. 1400(c) (12)(C) is amended by striking
“having mental retardation” and inserting “having intellectual
disabilities.”
What role should cultural changes have in developing medi-
cal terminology? If a term for a psychiatric or medical condition
takes on a negative connotation in our society, should it be
changed? Or should we instead engage in public education cam-
paigns in order to change the negative connotation and stigma?
Who should make decisions about medical terminology, and
what factors should they consider?
Table 15.1 Disability Severity and IQ Ranges
Diagnosed Level of Intellectual Corresponding
Disability IQ Range
Mild disability 50–55 to approximately 70
Moderate disability 35–40 to 50–55
Severe disability 20–25 to 35–40
Profound disability Below 20–25
they tend to lack normal adolescents’ imagination, inven-
tiveness, and judgment. Ordinarily, they do not show signs
of brain pathology or other physical anomalies, but often
they require some measure of supervision because of their
limited abilities to foresee the consequences of their actions.
With early diagnosis, parental assistance, and special edu-
cational programs, the great majority of individuals with
mild intellectual disability can adjust socially, master sim-
ple academic and occupational skills, and become self-sup-
porting citizens (Maclean, 1997).
MODERATE INTELLECTUAL DISABILITY Individuals
with moderate intellectual disability have IQ scores rang-
ing between 35–40 and 50–55 and, even in adulthood,
attain intellectual levels similar to those of average 4- to
7-year-old children. Although some can be taught to read
and write a little and may manage to achieve a fair com-
mand of spoken language, their rate of learning is slow,
and their level of conceptualizing is extremely limited.
They usually appear clumsy and ungainly and suffer from
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 562 Chapter 15
AMELIE-BENOIST/BSIP SA/Alamy Stock Photo
Individuals with mild intellectual disability constitute the largest
number of those categorized as having an intellectual disability. With
help, a great majority of these individuals can adjust socially, master
simple academic and occupational skills, and become self-supporting
citizens.
bodily deformities and poor motor coordination. In general,
with early diagnosis, parental help, and adequate opportu-
nities for training, most individuals with moderate intellec-
tual disability can achieve partial independence in daily
self-care, acceptable behavior, and economic sustenance in a
family or other sheltered environment. Many also can mas-
ter routine skills such as cooking or minor janitorial work if
provided specialized instruction in these activities.
SEVERE INTELLECTUAL DISABILITY Individuals with
severe intellectual disability have IQ scores ranging from
20–25 to 35–40 and commonly suffer from impaired speech
development, sensory defects, and motor handicaps. They
can develop limited levels of personal hygiene and self-
help skills, which somewhat lessen their dependency, but
they are always dependent on others for care. However,
many profit to some extent from training and can perform
simple occupational tasks under supervision.
PROFOUND INTELLECTUAL DISABILITY Most indi-
viduals with profound intellectual disability have IQ scores
below 20–25 and are severely deficient in adaptive behav-
ior and unable to master any but the simplest tasks. Useful
speech, if it develops at all, is rudimentary. Severe physical
deformities, CNS pathology, and retarded growth are typi-
cal; convulsive seizures, mutism, deafness, and other phys-
ical anomalies are also common. These individuals must
remain in custodial care all their lives. Unfortunately, they
also tend to have poor health and low resistance to disease
and thus a short life expectancy. Severe and profound cases
of intellectual disability can usually be readily diagnosed
in infancy because of the presence of obvious physical mal-
formations, grossly delayed development (e.g., in taking
solid food), and other obvious symptoms of abnormality.
These individuals show a marked impairment of overall
intellectual functioning.
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Causal Factors in
Intellectual Disability
Some cases of intellectual disability occur in association
with known organic brain pathology (Kaski, 2000). In these
cases, the level of disability is virtually always at least
moderate, and it is often severe. Profound intellectual dis-
ability, which fortunately is rare, always includes obvious
organic impairment. In this section, we consider five bio-
logical conditions that may lead to intellectual disability,
noting some of the possible interrelationships among them.
Then we review some of the major clinical types of intel-
lectual disability associated with these organic causes.
GENETIC-CHROMOSOMAL FACTORS Genetic-chro-
mosomal factors play a much clearer role in the etiology of
relatively infrequent but more severe types of intellectual
disability such as Down syndrome (discussed in more
detail later) and a heritable condition known as fragile X
(Huber & Tamminga, 2007; Schwarte, 2008). The gene
responsible for fragile X syndrome (FMR-1) was identified
in 1991 (Verkerk et al., 1991). In such conditions, genetic
aberrations are responsible for metabolic alterations that
adversely affect the brain’s development. Genetic defects
leading to metabolic alterations may also involve many
other developmental anomalies besides intellectual dis-
ability (e.g., autism) (Vissers et al., 2016). Intellectual dis-
ability associated with known genetic-chromosomal
defects tends to be moderate to severe in nature.
INFECTIONS AND TOXIC AGENTS Intellectual disabil-
ity also can result from a wide range of conditions due to
infection, such as viral encephalitis or genital herpes
(Kaski, 2000). If a pregnant woman is infected with syphilis
or HIV-1 or if she gets German measles, her child may suf-
fer brain damage as a result.
A number of toxic agents such as carbon monoxide
and lead may cause brain damage during fetal develop-
ment or after birth (Kaski, 2000). Similarly, if taken by a
pregnant woman, certain drugs, including an excess of
alcohol (West et al., 1998), may lead to congenital malfor-
mations. And an overdose of drugs administered to an
infant may result in toxicity and cause brain damage. In
rare cases, brain damage results from incompatibility in
blood types between mother and fetus. Fortunately, early
diagnosis and blood transfusions can minimize the effects
of such incompatibility.
TRAUMA (PHYSICAL INJURY) Physical injury at birth
can result in intellectual disability (Kaski, 2000). Although
the fetus is normally well protected by its fluid-filled pla-
centa during gestation, and although its skull resists deliv-
ery stressors, accidents that affect development can occur
during delivery and after birth. Difficulties in labor due to
malposition of the fetus or other complications may irrepa-
rably damage the infant’s brain. Bleeding within the brain
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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders) 563

is probably the most common result of such birth trauma. cranial anomalies are discussed here. Table 15.2 presents
Hypoxia—lack of sufficient oxygen to the brain stemming information on several other well-known forms.
from delayed breathing or other causes—is another type of
DOWN SYNDROME First described by Langdon Down
birth trauma that may damage the brain.
in 1866, Down syndrome is the best known of the clinical
IONIZING RADIATION In recent decades, a good deal conditions associated with moderate and severe intellectual
of scientific attention has focused on the damaging effects disability. The prevalence of Down syndrome has been
of ionizing radiation on sex cells and other bodily cells and
tissues. Radiation may act directly on the fertilized ovum
or may produce gene mutations in the sex cells of either or
both parents, which may lead to intellectual disability
among offspring. Sources of harmful radiation were once
limited primarily to high-energy X-rays used in medicine
for diagnosis and therapy, but the list has grown to include
nuclear weapons testing and leakages at nuclear power
plants, among others.

MALNUTRITION AND OTHER BIOLOGICAL FACTORS

It was long thought that dietary deficiencies in protein and
other essential nutrients during early development of the
fetus could do irreversible physical and mental damage;
however, data in this area so far are inconclusive. A recent
review of observational studies that tested the association
between maternal weight/nutrition and cognitive function-
ing in their offspring, as well as experimental studies that
tested the potential benefits of providing pregnant women
with nutritional supplements (e.g., vitamins, iron, protein),

SPL/CNRI/Science Source
found no clear links between maternal nutritional status and
offspring cognitive functioning (Veena et al., 2016).

Organic Intellectual
Disability Syndromes
Intellectual disability stemming primarily from biological
causes can be classified into several recognizable clinical
types, of which Down syndrome, phenylketonuria, and
This is a reproduction (karyotype) of the chromosomes of a female
patient with Down syndrome. Note the triple (rather than the normal
paired) representation at chromosome 21.

Table 15.2 Other Disorders Sometimes Associated with Intellectual Disability

Clinical Type
No. 18 trisomy syndrome
Tay-Sachs disease
Turner’s syndrome
Klinefelter’s syndrome
Niemann-Pick’s disease
Bilirubin encephalopathy
Rubella, congenital
SOURCE: Based on American Psychiatric Association (2013); Harris (2006).
Symptoms Causes
Peculiar pattern of multiple congenital anomalies, the most common being Autosomal anomaly of chromosome 18
low-set malformed ears, flexion of fingers, small jaw, and heart defects
Hypertonicity, listlessness, blindness, progressive spastic paralysis, and Disorder of lipoid metabolism, carried by a
convulsions (death by the third year) single recessive gene
In females only; webbing of neck, increased carrying angle of forearm, Sex chromosome anomaly (XO)
and sexual infantilism; intellectual disability may occur but is infrequent
In males only; features vary from case to case, the only constant finding Sex chromosome anomaly (XXY)
being the presence of small testes after puberty
Onset usually in infancy, with loss of weight, dehydration, and progressive Disorder of lipoid metabolism
paralysis
Abnormal levels of bilirubin (a toxic substance released by red cell Often, Rh (ABO) blood group incompatibility
destruction) in the blood; motor incoordination frequent between mother and fetus
Visual difficulties most common, with cataracts and retinal problems often The mother’s contraction of rubella (German
occurring together, and with deafness and anomalies in the valves and measles) during the first few months of her
septa of the heart pregnancy

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 564 Chapter 15
reported to be 5.9 per 10,000 of the general population
(Cooper et al., 2009). It is a condition that creates irrevers-
ible limitations on intellectual achievement, competence in
managing life tasks, and survivability (Bittles et al., 2007;
Patterson & Lott, 2008). It also is associated with health
problems in later life such as pneumonia and other respira-
tory infections. The availability of amniocentesis and cho-
rionic villus sampling in expectant mothers has made it
possible to detect in utero the extra genetic material
involved in Down syndrome, which is most often the tri-
somy of chromosome 21, yielding 47 rather than the nor-
mal 46 chromosomes.
A number of physical features are often found among
children with Down syndrome, but few of these children
have all of the characteristics commonly thought to typify
this group. The eyes appear almond shaped, and the skin
of the eyelids tends to be abnormally thick. The face and
nose are often flat and broad, as is the back of the head. The
tongue, which seems too large for the mouth, may show
deep fissures. The iris of the eye is frequently speckled. The
neck is often short and broad, as are the hands. The fingers
are stubby, and the little finger is often more noticeably
Marcel Jancovic/Shutterstock
Physical features found among children with Down syndrome
include almond-shaped eyes, abnormally thick skin on the eyelids,
and a face and nose that are often flat and broad. The tongue may
seem too big for the mouth and may show deep fissures. The iris of
the eye is frequently speckled. The neck is often short and broad, as
are the hands. The fingers are stubby, and the little finger is often
more noticeably curved than the other fingers.
M15_BUTC4568_18_GE_C15.indd 564
curved than the other fingers. Although facial surgery is
sometimes tried to correct the more stigmatizing features,
its success is often limited (Roizen, 2007). Parents’ accep-
tance of their Down syndrome child is inversely related to
their support of such surgery (Katz et al., 1997).
Death rates for children with Down syndrome have
decreased dramatically in the past century. In 1919 the life
expectancy at birth for such children was about 9 years;
most of the deaths were due to gross physical problems,
and a large proportion occurred in the first year of life.
Thanks to antibiotics, surgical correction of lethal anatomi-
cal defects such as holes in the walls separating the heart’s
chambers, and better general medical care, many more of
these children now live to adulthood (Hijii et al., 1997).
Nevertheless, they appear as a group to experience an
accelerated aging process (Hasegawa et al., 1997) and a
decline in cognitive abilities (Thompson, 2003). One recent
study reported that of those with Down syndrome who
were age 60 and above, more than 50 percent had clinical
evidence of dementia (Margallo et al., 2007).
Despite their problems, children with Down syn-
drome are usually able to learn self-help skills, acceptable
social behavior, and routine manual skills that enable
them to be of assistance in a family or institutional setting
(Brown et al., 2001). Although children and adolescents
with Down syndrome show deficits in their verbal abili-
ties, language skills, and attention/executive functioning,
relative to children with other intellectual disorders, those
with Down syndrome show lower rates of other forms of
psychopathology, lower levels of family stress, and a more
cheerful and positive personality style—each of which
could serve as strengths in their everyday functioning
(Grieco et al., 2015).
Chromosomal abnormalities other than the trisomy of
chromosome 21 may occasionally be involved in the etiol-
ogy of Down syndrome. However, the extra version of
chromosome 21 is present in at least 94 percent of cases. As
we noted earlier, it may be significant that this is the same
chromosome that has been implicated in research on
Alzheimer’s disease, especially given that persons with
Down syndrome are at extremely high risk for Alzheimer’s
as they get into and beyond their late 30s (Grieco et al.,
2015; Prasher & Kirshnan, 1993).
The reason for the trisomy of chromosome 21 is not
clear, and research continues to address the potential
causes (Korbel et al., 2009), but the defect is probably
related to cognitive deficit (Kahlem, 2006) and to parental
age at conception. It has been known for many years that
the incidence of Down syndrome increases (from the 20s
on) with increasing age of the mother. A woman in her 20s
has about 1 chance in 1,000 of conceiving a Down syn-
drome baby, whereas the risk for a woman in her 40s is
more than 1 in 100 (Loane et al., 2013). As in the case of all
birth defects, the risk of having a baby with Down syn-
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 Disorders of Childhood and Adolescence (Neurodevelopmental Disorders) 565

drome also is high for very young mothers, whose repro- In the rare condition known as macrocephaly (“large-
ductive systems have not yet fully matured. Research has headedness”), for example, there is an increase in the size
indicated that the father’s age at conception is also impli- and weight of the brain, an enlargement of the skull, visual
cated in Down syndrome, with higher ages conferring impairment, convulsions, and other neurological symp-
greater risk (Andersen & Urhoj, 2017). toms resulting from the abnormal growth of glial cells that
form the supporting structure for brain tissue.
PHENYLKETONURIA In phenylketonuria (PKU), a baby
The condition known as microcephaly (“small-head-
appears normal at birth but lacks a liver enzyme needed to
edness”) is defined by a head circumference that is more
break down phenylalanine, an amino acid found in many
than three standard deviations below that of children of
foods. The genetic error results in intellectual disability only
the same age and sex and is caused by decreased growth of
when significant quantities of phenylalanine are ingested,
the cerebral cortex during infancy (as skull size during
which is virtually certain to occur if the child’s condition
infancy is determined by brain growth) (Woods, 2004). Pri-
remains undiagnosed (Grodin & Laurie, 2000). This disor-
mary microcephaly refers to decreased brain growth dur-
der, which occurs in about 1 in 12,000 births (Deb & Ahmed,
ing pregnancy, and secondary microcephaly refers to
2000), is reversible (Embury et al., 2007); however, if it is not
decreased brain growth during infancy. Children with
detected and treated, the amount of phenylalanine in the
microcephaly fall within the moderate, severe, and pro-
blood increases and eventually produces brain damage.
found categories of intellectual disability and most show
The disorder usually becomes apparent between 6 and
little language development and are extremely limited in
12 months after birth, although symptoms such as vomit-
mental capacity.
ing, a peculiar odor, infantile eczema, and seizures may
occur during the early weeks of life. Often, the first symp-
toms noticed are signs of intellectual disability, which may
be moderate to severe, depending on the degree to which
the disease has progressed. Lack of motor coordination
and other neurological problems caused by the brain dam-
age are also common, and often the eyes, skin, and hair of

Taro Yamasaki/The LIFE Images

untreated patients with PKU are very pale (Dyer, 1999).
PKU can be detected early by examining urine for the

Collection/Getty Images
presence of phenylpyruvic acid, a routine procedure in
developed countries. In addition, dietary treatment (such
as the elimination of phenylalanine-containing foods such
as diet soda or turkey) and related procedures can be used
to prevent the disorder (Sullivan & Chang, 1999). With
early detection and treatment—preferably before an infant
is 6 months old—the deterioration process can usually be In the condition known as microcephaly, decreased brain growth
during infancy leads to smaller head circumference, as shown in the
arrested so that levels of intellectual functioning may range
child above, and typically results in intellectual disability.
from borderline to normal. A few children suffer intellec-
tual disability despite restricted phenylalanine intake and
A recent review of nearly 700 cases of microcephaly
other preventive efforts, however. Dietary restriction in
revealed that the cause of the condition was identified in
late-diagnosed PKU may improve the clinical picture
approximately 60 percent of cases (von der Hagen et al.,
somewhat, but there is no real substitute for early detection
2014). Approximately half of these were caused by genetic
and prompt intervention (Pavone et al., 1993).
factors, 45 percent were the result of brain damage in utero
For a baby to inherit PKU, both parents must carry the
(e.g., due to factors such as maternal disease or birth com-
recessive gene. Thus, when one child in a family is discov-
plications), and 3 percent were caused by brain damage
ered to have PKU, it is especially critical that other children
after birth. It is important to note that the cause of micro-
in the family be screened as well. Also, a pregnant mother
cephaly is completely unknown in about 40 percent of
with PKU whose risk status has been successfully
cases, and so much additional research is needed to better
addressed by early dietary intervention may damage her
understand this condition.
at-risk fetus unless she maintains rigorous control of phe-
The condition referred to as hydrocephaly is a rela-
nylalanine intake.
tively rare disorder in which the accumulation of an abnor-
CRANIAL ANOMALIES Intellectual disability can occur mal amount of cerebrospinal fluid within the cranium
in a number of conditions that involve alterations in head causes damage to the brain tissues and enlargement of the
size and shape and for which the causal factors have not skull (Materro et al., 2001). In congenital cases, the head
been firmly established (Carr et al., 2007). either is already enlarged at birth or begins to enlarge soon

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 566 Chapter 15
thereafter, presumably as a result of a disturbance in the
formation, absorption, or circulation of the cerebrospinal
fluid. The disorder can also arise in infancy or early child-
hood following the development of a brain tumor, subdu-
ral hematoma, meningitis, or other conditions. In these
cases, the condition appears to result from a blockage of
the cerebrospinal pathways and an accumulation of fluid
in certain brain areas.
The clinical picture in hydrocephaly depends on the
extent of neural damage, which in turn depends on the age
at onset and the duration and severity of the disorder. In
chronic cases, the chief symptom is the gradual enlarge-
ment of the upper part of the head out of proportion to the
face and the rest of the body. Although the expansion of the
skull helps minimize destructive pressure on the brain,
serious brain damage occurs nonetheless. This damage
leads to intellectual impairment and to such other effects as
convulsions and impairment or loss of sight and hearing.
The degree of intellectual impairment varies, being severe
or profound in advanced cases.
Hydrocephaly can be treated by a procedure in which
shunting devices are inserted to drain cerebrospinal fluid.
With early diagnosis and treatment, this condition can usu-
ally be arrested before severe brain damage has occurred
(Duinkerke et al., 2004). Even with significant brain damage,
carefully planned and early interventions that take into
account both strengths and weaknesses in intellectual func-
tioning may minimize disability (Baron & Goldberger, 1993).
Treatments, Outcomes,
and Prevention
A number of programs have demonstrated that significant
changes in the adaptive capacity of children with intellec-
tual disability are possible through special education and
other rehabilitative measures (Berney, 2000). The degree of
change that can be expected is related, of course, to the
individual’s particular condition and level of intellectual
disability.
Parents of children with intellectual disability often
find that childrearing is a significant challenge (Glidden &
Schoolcraft, 2007). For example, recent research has shown
that learning disability is associated with a higher inci-
dence of mental health problems (Cooper & van der Speck,
2009). One decision that the parents of a child with an intel-
lectual disability must make is whether to place the child
in an institution (Gath, 2000). Most authorities agree that
this should be considered as a last resort, in light of the
unfavorable outcomes normally experienced—particularly
in regard to the erosion of self-care skills (Lynch et al., 1997)
Importantly, there are programs that exist to help peo-
ple with intellectual disability. For example, classes for
individuals with mild intellectual disability, which usually
emphasize reading and other basic school subjects,
M15_BUTC4568_18_GE_C15.indd 566
budgeting and money matters, and development of occu-
pational skills, have succeeded in helping many people
become independent, productive community members.
For children with mild intellectual disability, the question
of what schooling is best is likely to challenge both parents
and school officials. Many such children fare better when
they attend regular classes for much of the day. Of course,
this type of approach—often called mainstreaming or
“inclusion programming”—requires careful planning, a
high level of teacher skill, and facilitative teacher attitudes
(Wehman, 2003).
Classes for those with moderate and severe intellec-
tual disability usually have more limited objectives, but
they emphasize the development of self-care and other
skills—for example, toilet habits (Wilder et al., 1997)—that
enable individuals to function adequately and to be of
assistance in either a family (e.g., Heller et al., 1997) or an
institutional setting. Just mastering toilet training and
learning to eat and dress properly may mean the difference
between remaining at home or in a community residence
or being institutionalized. Programs that use applied
behavior analysis, including structured reinforcement pro-
grams that teach and strengthen adaptive behaviors, have
shown especially strong promise to effectively help those
with intellectual disability (Lloyd & Kennedy, 2014).
Currently, approximately 129,000 people with intellec-
tual disability and other related conditions are receiving
intermediate care, although many are not institutionalized.
This is considerably less than the number of residents in
treatment 40 years ago. These developments reflect both
the new optimism that has come to prevail and, in many
instances, new laws and judicial decisions upholding the
rights of people with intellectual disabilities and their fam-
ilies. A notable example is Public Law 94–142, passed by
Congress in 1975 and since modified several times
(Hayden, 1998). This statute, termed the Education for All
Handicapped Children Act, asserts the right of people with
intellectual disabilities to be educated at public expense in
the least restrictive environment possible.
During the 1970s, there was a rapid increase in alterna-
tive forms of care for individuals with intellectual disability.
These included the use of decentralized regional facilities
for short-term evaluation and training, small private hospi-
tals specializing in rehabilitative techniques, group homes
or halfway houses integrated into the local community,
nursing homes for the elderly with intellectual disability,
the placement of children with severe intellectual disability
in more enriched foster-home environments, varied forms
of support to the family for own-home care, and employ-
ment services (Conley, 2003). The past 25 years have seen a
marked enhancement in alternative modes of life for indi-
viduals with intellectual disability, rendering obsolete (and
often leading to the closing of) many public institutions
formerly devoted exclusively to this type of care.
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