11 NeurodevelopmentalDisordersBowdenimagesiStockThinksto.docx

11 NeurodevelopmentalDisorders
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Chapter Objectives
After reading this chapter, you should be able to do the
following:
• Explain how developmental psychology contributes to our
understanding of psychological disorders
among children and adolescents.
• Describe the main psychological disorders first observed in
childhood and adolescence.
• Explain the effects of a childhood disorder on other family
members.
• Describe how childhood and adolescent disorders can be
treated.
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306
Understanding Developmental Psychopathology Section 11.1

11.1 Understanding Developmental Psychopathology
It is stressful for any family when one member has a
psychological disorder; it is especially
stressful when the affected person is a child. Children are
changing constantly. Unfortu-
nately, because of disease, genetics, or traumatic experiences
(to name just three possible
factors), some children find the road to adulthood full of
obstacles. Unless they are helped,
such children are at risk for psychological disorders. In addition
to the at-risk children, their
parent(s) and/or caregivers are also at risk. To gain a better
picture of children’s issues, and
those of their caregivers, we will examine the members of the
University Hospital Parent Sup-
port Group. This group was organized by psychologist Stuart
Berg. Its members are parents
of children under treatment for psychological disorders. Let’s
look at Part 1 of the support
group’s case study.
Case Study: Support Group: Part 1
Parent Support Group Transcript
DR. BERG: My name is Stuart Berg. I am a clinical
psychologist working here at University
Hospital. I want to welcome each of you to this first support
group meeting. I know some of
you, and I will look forward to meeting and working with all of
you in the weeks to come.
The goal of this support group is to help you help your children
and yourselves. You are all
here because you have a child in treatment and because you
indicated an interest in mutual
support. Although these meetings will be unstructured, they do

have a goal—to help you
cope with having a child who has a psychological disorder.
Some of the issues we discuss will
be practical: how to access government assistance programs,
how to find a babysitter, how
to get your child to the dentist. Because some parents whose
children develop psychological
disorders feel guilty and ashamed, as if they were the cause of
their child’s problems, we will
also try to educate ourselves about what causes psychological
disorders in children and what
we can do about them. Because this is our first meeting, I
thought it might be a good idea to
go around and have each of you introduce yourself to the others.
Let’s begin on my left.
JOHN CHENEY: My name is John Cheney. I am a doctor, a
radiologist, in this hospital. My son,
Eddie, has autism. He is eight. I have no other children. I just
couldn’t handle any more.
INGRID CHENEY: I am Ingrid Cheney, John’s wife. I do not
work. My life is looking after Eddie.
PASQUALE ARMANTI: My name is Pasquale Armanti. I am a
builder here in town. In fact, my
company built this hospital. My wife, Francesca, couldn’t have
children. We adopted Paolo
when he was a baby. My life hasn’t been the same since. He has
been in trouble since he could
walk and nothing—
FRANCESCA ARMANTI (interrupting her husband): You are
always picking on him. You never
wanted Paolo. You always rejected him. Even when he was
little, you spanked him—

PASQUALE ARMANTI (interrupting his wife): Lighten up!
Listen to yourself. Who are you
kidding? Paolo is out of control. He needs discipline.
DR. BERG: Perhaps we should get back to this later. Let’s
move on.
KAREN BEASLEY: I’m Karen. Karen Beasley. I’m 19 years
old. I’m here on my own because
my boyfriend Eric left us a few months ago. It’s just me and
Michelle now. Michelle is four,
and she won’t talk. She won’t hug me or let me hug her. She
just stays in her room. Sometimes
she watches TV; other times she just cries. Sometimes she hurts
herself by banging her head
(continued)
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307
Section 11.1 Understanding Developmental Psychopathology
Children who have oppositional defiant disorder are frequently
in trouble at school, are argu-
mentative and angry, and sometimes are vindictive. They may
use temper tantrums to get
their way (APA, 2013). According to the APA, they may
deliberately ignore adult rules, argue

repeatedly with adults, and feel a lot of anger and resentment.
About 12% of children qualify
for this diagnosis, with males slightly surpassing females in
prevalence (Mash & Wolfe, 2016).
Typically, the disorder presents by age eight (Mash & Wolfe,
2016).
Diagnosing psychological disorders in children is not easy
because behavior that is appro-
priate to one developmental stage may not be appropriate to
another. For example, wetting
the bed is considered normal in many 1-year-olds but not in a
10-year-old. To understand
whether a child’s behavior is “abnormal,” we need to know
what behaviors are “normal” for
children at different stages of development. Studying abnormal
behavior in its developmental
context is the goal of the specialty area of clinical psychology
known as developmental psy-
chopathology (refer to Chapter 1 for a definition of
psychopathology).
The goal of those working in this field is to identify, as early in
life as possible, the risk fac-
tors for psychological disorders, and much of the work in this
field focuses on childhood
temperament.
against the wall. But even when she is hurting herself, she
won’t let me comfort her. I don’t
have a job. I never finished high school. Lately I’ve become fat.
I’m dieting, but it doesn’t
help. I’ve been running, and even that doesn’t work. That’s
me—a fat girl with no money, no
boyfriend, and a kid who won’t talk.

CELIA BEROFSKY (to Karen): How did you get into this
mess? A baby at 15, abandoned at 19.
And what makes you think you are fat? You’re nothing but skin
and bones.
KAREN BEASLEY: I am? But I feel fat.
DR. BERG (addressing Celia): Perhaps you can introduce
yourself ?
CELIA BEROFSKY: I am Celia Berofsky, and this is my
husband, Michael.
MICHAEL BEROFSKY: Hi.
CELIA BEROFSKY: My son Gordon won’t go to school. When
we force him to go, he won’t
talk to anyone. I know this is just a phase that he will grow out
of. Michael thinks so, too. Our
psychologist suggested that we come to this group, but I don’t
think we will be members
long.
DR. BERG: Thanks, everyone, that was good. Perhaps one of
you could start off the discussion
by telling us about your experiences and the problems you are
encountering. Everyone
should feel free to ask questions. Now, who wants to start?
PASQUALE ARMANTI: I’ll start. I am used to talking about
Paolo. According to the
psychologists at school and Dr. Gale, our private psychologist,
Paolo has attention-deficit/
hyperactivity disorder. But this is not his only diagnosis. For a
long time, they told me he had
an oppositional defiant disorder, and he also supposedly has a

conduct disorder. Once they
suspected Tourette’s disorder. I wonder if anyone knows what is
wrong with Paolo. Maybe
he’s just a difficult kid.
See appendix for full case study.
Case Study: Support Group: Part 1 (continued)
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308
Section 11.1 Understanding Developmental Psychopathology
Temperament and Behavior
All children display a characteristic temperament (Sayal, Heron,
Maughan, Rowe, & Ramchan-
dani, 2013). Easy children have regular patterns of elimination,
eating, and sleeping. They
adapt readily to new environments, and, even when they are
distressed, their emotional reac-
tions are usually mild. Slow-to-warm-up children take longer to
adapt to new situations than
easy children, but they eventually adjust. Like easy children,
their emotional reactions are
mild. Difficult children are another matter. They are slow to
adapt to new situations, and they
have intense, usually negative, emotional reactions (such as
tantrums).

Difficult children are at risk for developing
psychological disorders later in childhood
and as adults (Sayal et al., 2013). They are
particularly prone to develop “acting out”
or externalizing disorders, which involve
behaviors that annoy or threaten others
(Sayal et al., 2013). Of course, not all diffi-
cult children develop psychological disor-
ders, nor do all easy and slow-to-warm-up
children avoid them. Some members of the
latter groups will develop internalizing
disorders, such as depression and anxiety,
in which symptoms are directed inward.
Whether children develop a psychological
disorder depends on the fit between their temperaments and
their environments (Sayal et
al., 2013).
As an introduction to developmental psychopathology, we will
look briefly at elimination
disorders.
Elimination Disorders
In the DSM–5, elimination disorders are included in their own
chapter rather than in the
chapter on neurodevelopmental disorders (American Psychiatric
Association [APA], 2013),
but since these disorders occur during childhood, we will
discuss them here. Researchers of
all theoretical orientations agree that elimination disorders are
most likely to occur when
toilet training is harsh or inconsistent, especially when a child
is resistant. “Difficult” children,
especially those with conduct disorders (described later in this
chapter) and those who are in

psychiatric institutions or in sheltered care, have a particularly
hard time with toilet training
(Mash & Wolfe, 2016; Park et al., 2013).
Children who do not toilet train successfully by the usual age
(or developmental level, if they
have an intellectual disability) are diagnosed as having enuresis
(poor control of urination),
encopresis (poor control of defecation), or, in rare cases, both.
Enuresis typically occurs at
night (nocturnal enuresis), but it can occur during the day
(diurnal enuresis). Children must
be at least 5 years old to be diagnosed with enuresis. About 10%
of children between the ages
Ziggy_mars/iStock/Thinkstock
There are three types of temperament in chil-
dren: easy, slow-to-warm-up, and difficult.
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309
Section 11.2 Conduct Disorder
of 5 and 16 are bed-wetters, but as the child ages the problem
becomes less common (Fri-
man, 2008). More recent data note the prevalence as between
5% to 10% among 5-year-olds,
3% to 5% among 10-year-olds, and 1% among children aged 15
years or older (APA, 2013).

Encopresis is diagnosed when a child is older than four years,
or developmentally equivalent
to four years old, and affects about 1% of five-year-olds (APA,
2013). It is often the cause of
chronic constipation that is unrelated to medical or functional
causes (Olaru et al., 2016).
Elimination disorders occur more often in boys than in girls and
seem to run in families (APA,
2013). Although this implicates biology in their etiology,
elimination disorders are also linked
to stressful life situations such as a parent’s death (Johnson et
al., 2006). Behavioral therapy
is usually successful for enuresis and may help encopresis. It is
frequently supplemented with
cognitive therapy and antidepressants. Sometimes desmopressin
(DDAVP), an antidiuretic, is
given to treat enuresis (Mash & Wolfe, 2016).
11.2 Conduct Disorder
Many children have mild temper tantrums and can be
argumentative. Although this sort of
behavior rarely presents a serious interpersonal problem,
children who commit violent acts
of aggression, such as hitting, biting, and kicking, may develop
a conduct disorder. Learning
the difference between aggression, which harms others, and
assertiveness, which is neces-
sary for effective functioning in society, is an important part of
growing up. (See the appendix
to read Part 2 of the parent support group case study.)
The main DSM–5 diagnostic criteria for conduct disorder also
apply to antisocial personal-
ity disorder. The main difference between the two disorders is
age. In theory, an adult may

be given the diagnosis of conduct disorder, but in practice,
antisocial personality disorder is
used for individuals over age 18, whereas conduct disorder is
applied to people under 18.
The DSM–5 distinguishes three conduct disorder subtypes:
childhood-onset (before age 10);
adolescent-onset (for those who are older than age 10 when the
characteristic behaviors first
appear); and unspecified onset, when criteria are met to
diagnose conduct disorder (but it
is unclear if the onset of the first symptom was before or after
age 10). Three severity speci-
fiers may also be applied: mild (behavior causes little harm),
moderate (stealing, but little
violence), and severe (when the person displays many criterion
behaviors and causes consid-
erable harm to others).
In community settings, conduct disorder is more common among
boys (14.1%) than girls
(3.8%), but the ratio is more equal in clinical settings (Costello,
Mustillo, Erkanli, Keeler, &
Angold, 2003). Higher estimates may include children who live
in threatening, high-crime
neighborhoods and engage in aggressive antisocial behavior as
part of gangs. For most such
children, antisocial behavior may not be a sign of a
psychological disorder but simply a way of
life. There is consistent evidence of a genetic basis for conduct
disorder (Silberg, Moore, & Rut-
ter, 2015). Precisely what is inherited that causes conduct
disorder remains unclear though.
One theory is that people with conduct disorder are chronically
underaroused. To make up
for this, they are always seeking excitement. When their
environment lacks socially accept-

able opportunities for excitement, they may turn to antisocial
behaviors (Mann et al., 2017).
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310
Section 11.2 Conduct Disorder
Although genetics may predispose children to conduct
disorders, it is not the whole story. The
concordance rate for conduct disorders among identical twins is
less than 100%, so environ-
ment must also play a role. One place to look for environmental
influence is in faulty family
relationships. Studies have consistently focused on parent-child
relationships, conflict and
hostility within the family, and marital problems between
parents as causes of conduct disor-
der (Silberg et al., 2015). However, these troublesome family
interactions could just as easily
be the result of having a child with a conduct disorder.
In addition to family dynamics, some theo-
rists attribute conduct disorders to drug
abuse and social factors such as poverty
and exposure to community violence and
aggressive and criminal peers and models
(Mash & Wolfe, 2016). Still, others empha-
size how extra parental and teacher atten-
tion can reinforce antisocial behavior

(Ahmadi-Kashani & Hechtman, 2014). Of
course, parental neglect, exposure to anti-
social models, and the reinforcement of
antisocial behavior are not mutually exclu-
sive; many children experience all three
(Ahmadi-Kashani & Hechtman, 2014).
Whatever the cause(s) of conduct disorders,
the outlook is poor for those whose disor-
der is first diagnosed in childhood (Mash &
Wolfe, 2016). Many such children go on to be diagnosed with
antisocial personality disorder
(Mash & Wolfe, 2016). The relationship between age of onset
and prognosis is similar for both
sexes, although females are less likely than males to develop
antisocial personality disorder
as adults (Black, 2015).
Children with conduct disorders may also have learning
disorders such as a specific learning
disorder with impairment in reading, often called dyslexia
(APA, 2013; Erford, Bardhoshi,
Ross, Gunther & Duncan, 2017). More than one third of boys
and one half of girls with conduct
disorder also display attention-deficit/hyperactivity disorder, or
ADHD, which is described
in the next section (Waschbusch, 2002). It is possible that these
learning disorders may be
one of the causes of conduct disorders. Specifically, children
who continuously fail at school
may feel humiliated because other children ridicule them. To
win respect and ease the pain of
repeated failure, such children may act out. While trying to
control this disorderly behavior,
teachers may inadvertently reinforce it by giving disruptive
children extra attention. Eventu-
ally, antisocial behavior becomes a well-rewarded habit.

Although this hypothesis is plau-
sible, keep in mind that it is based on a correlation between
conduct and specific learning
disorders. It is equally possible that the causal mechanism goes
the other way around. Con-
duct disorders may cause specific learning disorders, perhaps by
interfering with study time.
It is also possible that conduct and learning disorders both
result from the same cause. For
example, both may result from distractibility—the main
symptom of ADHD.
Olga_sweet/iStock/Thinkstock
Learning disorders may be a direct cause of
conduct disorder. Children who fail at school
may experience a sense of humiliation and act
out as a response.
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311
Section 11.3 Attention-Deficit/Hyperactivity Disorder (ADHD)
11.3 Attention-Deficit/Hyperactivity Disorder (ADHD)
Attention-deficit/hyperactivity disorder (ADHD) is a
psychological disorder that typically
begins in childhood. It is characterized by long spells of
inattention, hyperactivity, and/or
impulsivity. It can be difficult to properly diagnose and assess
(Müller et al., 2011). The notion

for the disorder originated with the work of Alfred Strauss and
his colleagues (see Strauss &
Kephart, 1955). Their goal was to identify childhood behaviors
that could be used to diagnose
brain damage in ambiguous cases (when there were no clear-cut
signs of neurological impair-
ment). Because children with brain damage were often very
active, they argued that hyper-
activity (a term they did not define) is a sign that a child is
brain damaged. To get around the
problem that hyperactive children did not show any hard signs
of brain damage, the concept
of minimal brain damage (or dysfunction) was introduced
(Strother, 1973). These children
were said to be hyperactive, impulsive, distractible, and
emotionally unstable. They had short
attention spans, perceptual-motor deficits, poor coordination,
and learning disorders.
Despite the many attempts to refine these criteria, the DSM–5
diagnostic criteria remain
problematic. For instance, clinicians do not know how much
fidgeting is “excessive” for chil-
dren at different stages of development. Moreover, children
behave differently depending on
the context. Some children have attentional problems at school,
whereas at home they sit and
watch television for hours. Because norms are unavailable for
many attentional behaviors
and because behavior depends on context, parents, teachers, and
clinicians often fail to agree
about which children suffer from ADHD (Müller et al., 2011).
According to the Centers for Disease Control and Prevention,
ADHD is more common among
boys (13.2%) than girls (5.6%). This may reflect a genuine sex

difference or a social bias. That
is, girls may not be diagnosed with ADHD because they rarely
cause the discipline problems
that lead to teacher intervention. This may also be because girls
tend to present with more
inattention than boys, who typically present with more
hyperactive and/or impulsive symp-
toms (Mash & Wolfe, 2016). Although the gender difference in
ADHD prevalence may provide
clues to its etiology, until recently many studies included only
boys (Skogli, Teicher, Ander-
sen, Hovik, & Øie, 2013). The DSM–IV (APA, 1994) field trials
established that the inclusion
of a “predominantly inattentive” subtype might identify
substantially more girls affected by
ADHD (Skogli et al., 2013).
Because ADHD counts as a disability, it qualifies children for
special treatment under the
Americans With Disabilities Act (1990, 2008). Parents may
actually want their children to be
diagnosed with ADHD if this means they will receive special
services in school.
Lead poisoning, brain damage, birth defects, food additives, and
too much sugar in the diet
have all been blamed at one time for “causing” ADHD, but none
of these supposed causes has
found strong empirical support (Riley, Carson-DeWitt, &
Knight, 2016). There is evidence that
the problem runs in families. Children whose parents have
ADHD are more likely to develop it
(APA, 1994, 2000, 2013). Among monozygotic twins, when one
twin is diagnosed with ADHD,
the other is more likely to receive the same diagnosis than if he
or she were a dizygotic twin

(Riley et al., 2016). Although these data suggest that
inheritance contributes to ADHD, even
for identical twins, the concordance rate is less than 100%. In
other words, genetics produces
a disposition to ADHD, but environmental factors also play a
role. Most research efforts have
gone into treatment, specifically the use of stimulant drugs to
control the symptoms of ADHD.
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312
Section 11.4 Tourette’s Disorder
The most commonly used stimulants are methylphenidate
(Ritalin), dextroamphetamine
(Dexedrine), and a mixture of several amphetamines (Adderall).
Stimulants can have dra-
matic effects. After only a few doses, children who are
constantly on the go calm down and
focus their attention. Because stimulants produce a dramatic
calming effect in children with
ADHD, some writers have argued that a “paradoxical” calming
response to stimulant drugs is
diagnostic all by itself. In other words, if stimulant drugs lead
to less hyperactivity and dis-
tractibility, then the child probably has ADHD. In reality, the
response of people with ADHD
is not paradoxical; it is not even unusual. Stimulants improve
everyone’s ability to concen-

trate (Hoffman, 2009; Procyshyn, Bezchlibnyk-Butler, &
Jeffries, 2017). However, despite
the effects of methylphenidate on attention and behavior, it is
not clear whether the drug
improves academic achievement (Hale et al., 2011). It does
decrease the core symptoms of
ADHD and makes children more manageable (Riley et al.,
2016).
A drawback to the use of stimulants is the likelihood of
unpleasant side effects, although
for most people they are not severe (Procyshyn et al., 2017;
Riley et al., 2016). Side effects
include sleeplessness, irritability, loss of appetite, and growth
retardation. Taking drugs may
also affect a child’s self-concept. Children may learn to
externalize responsibility for their
behavior (“I can’t control myself, so I must take medicine”).
Externalizing responsibility could
make children less responsive to learning self-control (Molina
& Musich, 2016). Skepticism
about stimulant treatment has almost as long a history as
stimulant treatment itself (Hoff-
man, 2009). In practice, the appropriate treatment for ADHD is
not an either-or choice. Many
children with ADHD receive a combination of stimulants,
cognitive therapy, and behavioral
therapy, as well as various forms of special education
(Hoffman, 2009).
Behavioral therapy has been well researched and appears to be
quite effective in treating ADHD,
especially when combined with stimulants (Riley et al., 2016)
Typically, behavioral therapy
will focus on training teachers and parents to reward attention
and self-control in the child or

pupil; this is often done while using a token economy system.
Research has also revealed that
combined stimulant and behavior modification treatment will
eventually lead to lower levels
of medication required (Hale et al., 2011). In sum, research
indicates that stimulants, either
alone or with behavior modification therapy, are the most
effective treatment approaches for
ADHD. (See the appendix to read Part 3 of the parent support
group case study.)
11.4 Tourette’s Disorder
Tourette’s disorder is characterized by strange utterances
(swearing, barking) and multiple
motor tics (sudden repetitive but irregular movements). The
DSM–5 also includes other tic
disorders (chronic motor or vocal tic disorders, provisional tic
disorder) that have some, but
not all, of the symptoms of Tourette’s disorder. Unlike those for
many psychiatric diagnoses,
the criteria for Tourette’s disorder have hardly changed from
Tourette’s original description.
The criteria include vocal and motor tics that are generally
chronic (although tic-free periods
can occur).
Like most childhood disorders, Tourette’s disorder occurs more
often in boys than in girls
(Amiri, Fakhari, Golmirzaei, Mohammadpoorasl, & Abdi, 2012;
APA, 2013). It begins with
facial tics, usually blinking or sniffing. In serious cases, it
progresses to neck and shoulder
jerking, head banging, arm flinging, and other peculiar
movements. Sometimes, the tics
are self-destructive (head banging, for instance). Odd
verbalizations are always part of the

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313
Section 11.4 Tourette’s Disorder
disorder. People with Tourette’s may sniff, bark, or, in some
cases, shout obscenities (a symp-
tom known as coprolalia; APA, 2013). As already noted, tics
come and go, and old ones are
replaced by new ones (Ludolph, Roessner, Münchau, & Müller-
Vahl, 2012).
People with Tourette’s disorder can consciously inhibit their
tics for brief periods, although
this requires considerable effort. Because they can inhibit their
symptoms at least part of the
time and because their tics disappear during sleep, people with
Tourette’s were long consid-
ered to have a psychological disorder (Shapiro, Shapiro, Bruun,
& Sweet, 1978). Symptoms
such as coprolalia were explained as either displaced aggression
or the expression of poorly
“defended” id impulses. Psychotherapy designed to uncover the
unconscious conflicts caus-
ing Tourette’s disorder did not meet with much success
(Shapiro, Shapiro, Young, & Fein-
berg, 1998), and attention shifted to the neurochemistry of the
illness (Ludolph et al., 2012).
The discovery that small doses of haloperidol (Haldol), a

dopamine-suppressing drug used to
treat schizophrenia, suppresses Tourette’s symptoms in many
people has led to the hypoth-
esis that those with Tourette’s may have an excess of dopamine
(Ludolph et al., 2012). Further
evidence for this hypothesis comes from the finding that drugs
that increase dopamine levels,
such as L-dopa (which is used in the treatment of Parkinson’s
disease), tend to increase the
severity of tics.
An important finding is that Tourette’s disorder seems to be a
genetically transmitted domi-
nant trait (Prakash, Singh, Bhat, Srivastava, & Gupta, 2015).
This is why people with Tourette’s
disorder often have relatives who also have tic disorders
(Prakash et al., 2015). They also
have a high frequency of relatives with obsessive-compulsive
disorder and ADHD, and many
people with Tourette’s disorder have these other disorders as
well (Prakash et al., 2015).
Several writers have remarked on the substantial similarities
between people with Tourette’s
disorder and people who stutter (Abwender et al., 1998; Pauls,
Leckman, & Cohen, 1993).
Both have facial tics and odd grimaces, particularly when they
are in emotionally arousing
situations, and both may be helped by haloperidol, risperidone
(Risperdal), and ziprasidone
(Geodon) (Budman, 2014; Procyshyn et al., 2017). Coprolalia,
surely the most peculiar symp-
tom of Tourette’s disorder, has also been noted among patients
with aphasia and schizo-
phrenia (Lenneberg, 1967). It has been noted that stress worsens
coprolalia and the other
symptoms of Tourette’s disorder. In other words, Tourette’s

disorder, like practically all other
psychological disorders, has both a genetic-physiological and a
psychological component.
Estimates are that Tourette’s disorder occurs in 0.3% of
children aged 6–17 years in the
United States. In addition, about 0.6% children meet criteria for
Tourette’s, suggesting that
the disorder is underdiagnosed (Cologonari & Rockmore, 2017).
Every time a television show
or magazine article discusses Tourette’s, many people with
Tourette’s symptoms consult their
doctors. Some of these people say that they have suffered from
the symptoms all of their lives
without knowing that their condition had a name.
Haloperidol remains the most common treatment for Tourette’s
syndrome. Unfortunately,
people often discontinue treatment because of the drug’s side
effects, which, ironically,
include a movement disorder similar to Parkinson’s. Other side
effects include tardive dys-
kinesia (involuntary movements of the tongue, face, mouth, or
jaw), and grogginess, blurred
vision, and dry mouth (Vallerand & Sanoski, 2017). For those
who need treatment in addition
to drugs (or who reject drugs because of their side effects),
behavior therapy and cognitive-
behavioral therapy have been used to help people relax and to
deal with the interpersonal
and social problems caused by having a tic disorder (Cologonari
& Rockmore, 2017). See the
accompanying Highlight.
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314
Section 11.5 Separation Anxiety Disorder
11.5 Separation Anxiety Disorder
Separation anxiety disorder appears in
the anxiety disorders chapter in the DSM–5,
but because it is the most common anxiety
disorder in children younger than age 12
years (APA, 2013), we will discuss it here.
The disorder is characterized by devel-
opmentally inappropriate and excessive
anxiety concerning separation from home
or from those to whom the individual is
attached. Consider the case of 10-year-old
Gordon Berofsky. At home, playing com-
puter games, Gordon seems to be a normal
boy, but he has significant problems. He typ-
ically refuses to attend school, and when he
does, he will not talk to his bus driver, the
other children, or his teachers. Gordon has
been seen by two psychologists and a psy-
chiatrist and has received several diagnoses,
as his mother relates in Part 4 of the support
group case study (see the appendix).
Highlight: Living With a Special Needs Child
According to Autism Speaks (http://www.autismspeaks.org), it
costs about $60,000 per
year to raise a child with autism spectrum disorder. Presently

there is no cure. One question
to consider is whether you think you could raise a child with
autism spectrum disorder,
Tourette’s, or some other neurodevelopmental disorder. This
might seem like an unfair
question, but it is one that anyone contemplating future
parenthood needs to be considered,
especially since there is no prenatal test for autism spectrum
disorder. Do you think you can
answer this question honestly?
Even for those who think that $60,000 a year doesn’t seem like
a lot, keep in mind that this
is an average, and it doesn’t take into account the extra time and
energy required to raise
a child with special needs. One parent may need to give up a
successful career to take care
of the child. Sometimes one or both parents are just not able to
handle the special needs.
Although some disorders respond well to therapy and/or
medication, autism spectrum
disorder is one that, in general, does not respond as well. There
is no medication specifically
to treat autism spectrum disorder (though we will discuss
risperidone as an adjunct therapy
later in this chapter).
Child-rearing is not easy, and raising a special needs child
requires a lot of extra care and
effort. Being honest with yourself is crucial to ensuring that a
special needs child can receive
proper care.
Exactostock-1527/SuperStock
Children suffering from separation anxiety
experience severe distress at the thought

of separating from home or close family
members. Younger children typically
encounter a mild uneasiness about separation
or attending school, yet if the symptoms occur
to a greater degree, they may be diagnosed
with early-onset separation anxiety disorder.
get83787_11_c11_305-324.indd 314 2/16/18 4:50 PM
http://www.autismspeaks.org
315
Section 11.6 Autism Spectrum Disorder
It is important to take into account developmental level when
considering a diagnosis of sep-
aration anxiety disorder. It is normal for young children to be
more uneasy about separation
than older children. It is unclear whether a relationship exists
between separation anxiety
disorder in children and the development of panic disorders in
adolescence and adults, but
studies have shown a poor prognosis; many children who have
separation anxiety go on to
develop adult anxiety disorders (Cooper-Vince, Emmert-
Aronson, Pincus & Comer, 2013).
As school is children’s primary social venue, it is not surprising
that the school context is a
significant source of distress for children and adolescents with
separation anxiety disorder

(Cooper-Vince et al., 2013). It seems to occur equally often in
boys and girls and is most likely
to occur at transition points—entry to elementary school or at
the beginning of junior or
senior high school. Children who refuse to go to school need
not have difficulty with school-
work. Some may fear evaluation; others fear mixing with new
children and may suffer from
a social phobia or avoidant personality disorder. Some school
refusers may fear bullying or
ridicule. However, for children like Gordon, the term school
phobia is misleading. It is not the
fear of school that motivates Gordon to stay home; it is the fear
of separation from his mother.
Gordon’s physical symptoms are an excuse to avoid school.
Children like Gordon are different
from truants, who skip school without their parents’ knowledge
to do something they like
better, such as go to the beach or a ball game (Haight, Kearney,
Hendron, & Schafer, 2011).
Gordon skips school to stay home, and his parents know all
about it.
There are many possible causes for separation anxiety. In some
cases, a child may have expe-
rienced separation from his or her parents through death or,
more often, divorce. In other
cases, separation anxiety may arise from overprotectiveness.
Parents who worry excessively
about harm coming to their child once the child is outside of
their immediate purview com-
municate their anxiety to their child, who learns to fear
separation. Children are likelier to
have an anxiety disorder if a parent has one (Hughes, Furr,
Sood, Barmish, & Kendall, 2009).

Staying home is reinforcing because it not only reduces anxiety
but also offers secondary
rewards, such as maternal attention. Refusal to go to school and
separation anxiety disorder
make a dangerous combination. Children who show both signs
may develop other anxiety
disorders (Cooper-Vince et al., 2013).
11.6 Autism Spectrum
Disorder
Autism spectrum disorder is the most seri-
ous psychopathological condition occurring
in childhood. It is marked by poor interper-
sonal relationships and communication skills,
and repetitive/stereotyped behavior. At one
time, this disorder was referred to as child-
hood schizophrenia, but it is now clear that it
is different from schizophrenia. It is not asso-
ciated with hallucinations or delusions, and
the children do not develop schizophrenia
when they grow up. Previously classified in
KatarzyynaBialasiewicz/iStock/Thinkstock
Autism spectrum disorder is character-
ized by poor social interactions, impaired
communication, and odd motor behaviors.
Parents notice unusual behavior before age
three and often report their child’s lack of
responsiveness.
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316
the DSM–IV–TR as pervasive developmental disorders, autism
spectrum disorder now consti-
tutes a separate category of psychological disorder in the DSM–
5 (APA, 2013). Autism is now
classified on a spectrum, ranging from some impairment to
severe impairment. Table 11.1
summarizes the diagnostic criteria for the disorder.
Not every child with autism spectrum disorder (also referred to
as autism throughout the
remainder of the chapter) has an intellectual disability.
Percentages of children with autism
and an intellectual disability have been estimated to range from
25% to 80%; one researcher
claimed that this prevalence is overstated (Edelson, 2006). The
association between intellec-
tual disabilities and autism is not the result of common causes;
rather, the presence of both
makes it more likely that both disorders will be diagnosed
(Skuse, 2007).
John and Ingrid Cheney were both 27 years old when their son,
Eddie, was born. Neither John
nor Ingrid knows of any mental illness in their families,
although Ingrid’s brother had a devel-
opmental language disorder as a child. As you can see from Part
5 of the parent support group
case study, Eddie’s problems became apparent early in life, and
his behavior reflects almost
all of the diagnostic criteria for autism spectrum disorder (see

the appendix).
Diagnosis
The DSM–5 notes that symptoms of autism spectrum disorder
typically are noticed from ages
12 to 24 months, but they may be seen earlier than 12 months if
the symptoms are severe,
or after 24 months if the symptoms are more subtle (APA,
2013). Autistic behaviors are so
unusual that most parents notice something is “wrong” well
before the child reaches age two.
The first sign is the child’s lack of responsiveness. Eddie was
typical. He did not form a nor-
mal parental attachment. He never anticipated being picked up
by his mother, and when he
was hugged, he did not hug back. Leo Kanner’s descriptions
emphasized this aspect of autism
(Kanner, 1943). In fact, the term autism comes from the Greek
word for “self.” Kanner believed
that autistic children are alone within themselves, unable to
relate to others. Eddie’s failure
to respond to his name or to other sounds gave his parents the
impression that he was deaf.
When they realized that he could hear, they interpreted his
“deafness” as indifference. This
impression was reinforced by his avoidance of eye contact—he
looked through people rather
than at them—and his insensitivity to pain.
About 50% of people with autism spectrum disorder never
develop intelligible speech or are
silent (Sachdeva & Dutta, 2012). The remainder learn to
produce words, but they have dif-
ficulty using them to communicate (Neff & Teska, 2016).
Instead, their speech is like Eddie’s,
mere parroting of what they have heard others say (a symptom

called echolalia). Although the
DSM–5 emphasizes the communication disorder, most people
with autism spectrum disorder
also have a cognitive deficit (McLuckey & Therivel, 2016).
Ingenious experiments have shown that people with autism
spectrum disorder are unable to
see the world from another person’s point of view (Sachdeva &
Dutta, 2012). This is referred
to as theory of mind (Golan & Baron-Cohen, 2006; Slaughter,
2017). Although people with
intellectual disabilities may have similar difficulties (Sachdeva
& Dutta, 2012), people with
autism spectrum disorder do poorly on “mind-reading” tasks,
even when they have good lan-
guage skills and high IQs. For people with autism spectrum
disorder who do not have intel-
lectual and language impairment, their difficulty is not with
perception but with inferring
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317
Table 11.1 DSM–5 diagnostic criteria for autism spectrum
disorder
A. Persistent deficits in social communication and social
interaction across multiple contexts, as manifested

by the following, currently or by history (examples are
illustrative):
1. Deficits in social-emotional reciprocity, ranging, for
example, from abnormal social approach and
failure or 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
abnormalities 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
difficulties in sharing imaginative play
or in making friends; to absence of interest in peers.
Specify current severity based on social communication
impairments and restricted, repetitive patterns of
behavior.
B. Restricted, repetitive patterns of behavior, interests, or
activities, as manifested by at least two of the
following, currently or by history (examples are illustrative):
1. Stereotyped or repetitive motor movements, use of objects, or
speech (e.g., simple motor stereotypes,
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 transitions, rigid thinking patterns,
greeting rituals, need to take same route or eat same food every
day).
3. Highly restricted, fixed interests that are abnormal in
intensity or focus (e.g., strong attachment to or
preoccupation with unusual objects, excessively circumscribed
or perseverative interests).
4. Hyper- or hyporeactivity to sensory input or unusual interest
in sensory aspects of the environment
(e.g., apparent indifference to pain/temperature, adverse
response to specific sounds or textures,
excessive smelling or touching of objects, visual fascination
with lights or movement).
Specify current severity based on social communication
impairments and restricted, repetitive patterns of
behavior.
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 strategies 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
disability (intellectual developmental
disorder) or global developmental 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.
Specify if:
With or without accompanying intellectual impairment
With or without accompanying language impairment
Associated with a known medical or genetic condition or
environmental factor
Associated with another neurodevelopmental, mental, or
behavioral disorder
With catatonia
Source: Reprinted with permission from the Diagnostic and
Statistical Manual of Mental Disorders, Fifth Edition,
(Copyright
©2013). American Psychiatric Association. All Rights
Reserved.
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318
mental states (Autism Society of America, 2006; Baron-Cohen,
Jolliffe, Mortimore, & Robert-
son, 1997; Sachdeva & Dutta, 2012).
Kanner believed that the avoidance of change was an important
sign of autism. Kanner’s
autistic children insisted on keeping objects in their accustomed
place and in maintaining
routines. Any change might result in a catastrophic reaction (an
intense temper tantrum).
Stereotyped body movements (such as rocking, whirling, and
hand waving) are also common
in autism.
Epidemiology and Course
Kanner considered autism to be a rare disorder; however, the
latest available figures reveal
that it occurs in 1 out of 110 children (CDC, 2009). More recent
data indicate that about 1%
of the population has an autism spectrum disorder (APA, 2013).
Put into numbers, autism
spectrum disorder now affects 1 in 68 children and 1 in 42 boys
(Autism Speaks, 2017).
Etiology
Although everything from smothering mothers to perceptual
defects to viruses to childhood
vaccinations has been implicated by one theorist or another as a
potential cause of autism
spectrum disorder, there is still no generally agreed-on
etiological theory (Sachdeva & Dutta,

2012). There are some notable trends, however. For a long time,
theories that implicated
parental behavior were dominant. Child psychoanalysts blamed
autism partly on “refrigera-
tor” parents who behave in a cold, detached manner toward their
children (Kanner, 1943,
1954) or described autism as a defense against a destructive
maternal environment (Bettel-
heim, 1967). Some behaviorists also held similar views. For
example, Ferster (1961) claimed
that the home environment of children with autism spectrum
disorder failed to reinforce
proper social behavior.
However, because there is no evidence that the parents of
children with autism spectrum
disorder differ from other parents in personality or child-rearing
practices (Koegel, Schreib-
man, O’Neill, & Burke, 1983), blame-the-parent theories have
largely disappeared. There is no
reason for parents, whose lives have already been made more
trying by having a child with an
autism spectrum disorder, to also feel guilty for having caused
their child’s problems.
Parental behavior may not cause autism spectrum disorder, but
something must. The sex
ratio (many more boys than girls), the remarkable similarity of
one child to another, and
physical signs all suggest that biology is a good place to look
for etiological explanations. In
several studies from the 1980s and 1990s that used a strict
definition of autism, a 69% to
95% concordance was demonstrated in monozygotic twins,
whereas the chance in dizygotic
twins was only 0% to 24% (Verhoeven, Egger, & Feenstra,

2011). The contribution of the
hereditary components is estimated to be about 90% (El-
Fishawy & State, 2010). The male-
female ratio is approximately 5:1 (Baio, 2014). Cognitive and
language disorders also appear
with greater than average frequency among the relatives of
people with an autism spectrum
disorder (Constantino, Zhang, Frazier, Abbacchi, & Law, 2010).
It is likely that no single gene
causes autism; it takes many genes acting together. At one time
or another, practically every
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319
chromosome has been implicated in the genesis of autism
spectrum disorder (El-Fishawy &
State, 2010), yet we still are unsure which genes are actually
responsible (McLuckey, 2016).
There have been reports of monozygotic twins in which only
one had autism spectrum disor-
der (Wong et al., 2014). Given their identical inheritance, some
other factor(s) must interact
with genetics to produce the disorder (McLuckey, 2016). One
possibility is that autism spec-
trum disorder is the result of an unlucky conjunction—a genetic
predisposition to develop

cognitive and language disorders combined with exposure to an
environmental trigger. Pos-
sible candidates for this trigger include toxins, viruses, birth
trauma, and a variety of illnesses
(Modabbernia, Velthorst, & Reichenberg, 2017). As yet,
definitive triggers have not been iden-
tified; most have proved to be dead ends. Attempts to link an
increased prevalence of autism
to rates of vaccination have also been unsuccessful. As reported
in a 2013 study from The
Journal of Pediatrics, “The notion that the measles, mumps,
rubella (MMR) vaccine, or any
other vaccine or vaccine constituent, may cause autism is a
hypothesis with little supporting
evidence” (DeStefano, Price, & Weintraub, 2013, p. 836).
In the past, researchers have enlisted every conceivable blood
test, hormonal assay, neuro-
psychological test, and imaging technique to shed light on the
pathology underlying autism
spectrum disorder (Dawson, Meltzoff, Osterling, & Rinaldi,
1998; Hashimoto et al., 1998; Lin-
coln, Courchesne, Allen, Hanson, & Ene, 1998; Piven &
O’Leary, 1997); however, it is gener-
ally agreed upon that neurobiological causes are the
main etiological factors in autism spectrum disorder
(Sachdeva & Dutta, 2012). Although these research-
ers have produced intriguing findings—including
an association between the mild form of autism
spectrum disorder (formerly called Asperger’s) and
Tourette’s disorder (Neff & Teska, 2016)—there is
still no agreement on the neurological defects that
cause the symptoms and signs of autism spectrum
disorder. All we can conclude at present is that peo-
ple with autism spectrum disorder probably have a

congenital vulnerability that combines with a trig-
ger, resulting in an inability to form normal human
attachments and, in people with more severe forms
of autism, a language disability as well.
Treatment
Children with autism spectrum disorder have been
subjected to just about every known psychological
and medical treatment. For decades, psychoana-
lytically oriented psychotherapists labored to bring
insight into autism spectrum disorder. However,
whereas there are some psychodynamic views of
the disorder (Duckham & Yann, 2016), most psy-
chologists agree that behavior modification, par-
ent education and training, and communication
Dorling Kindersley/Thinkstock
Researchers have attempted several
methods to teach spoken language
to children with autism spectrum
disorder, including conditioning trials
that proved to be ineffective. Although
autistic children may be somewhat
limited by their abilities, the use
of sign language has been a more
effective way to teach communication
skills.
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320

training are the most helpful treatment methods (Teicher et al.,
2008). None of these treat-
ments can cure autism spectrum disorder, although effective
early interventions may help to
improve the quality of life of sufferers and their families
(Sachdeva & Dutta, 2012). In addi-
tion, antipsychotic medications such as risperidone (Risperdal)
can be used to control the
behavioral outbursts that often accompany autism spectrum
disorder (Ellerbeck, Smith, &
Courtemanche, 2014; Procyshyn et al., 2017; Virani et al.,
2009).
A continuing problem for clinicians, and for the families of
people with autism spectrum
disorder, is the false hope given by well-meaning amateurs and
outright charlatans (see the
accompanying Highlight). Consider, for example, the Cheneys’
experience with an approach
called facilitated communication (also called supportive
typing), which they describe in Part
6 of the support group case study (see the appendix).
The Cheneys’ experience is not unusual. Facilitated
communication is based on the notion
that there is a person trapped inside the individual with autism
spectrum disorder. These
trapped people have lots to say, and it takes a facilitator to
allow them to say it.
Despite a total lack of empirical support, facilitated
communication was widely applied, not
only to individuals with communication disorders, but also to

help people recover suppos-
edly lost memories of child abuse. However, research has
confirmed that it is not the person
being facilitated whose thoughts are being communicated but
the facilitator’s (Schlosser et
al., 2014).
Highlight: A Different Look at Autism Spectrum Disorder
Treatments and Etiologies
Of all of the disorders and disabilities discussed in this book,
none seem to have produced
as many false etiological explanations and treatments as autism
spectrum disorder. We have
discussed the scientific fact that vaccines do not cause autism
spectrum disorder, yet that
has not stopped discredited researcher Andrew Wakefield from
continuing to espouse this
view, even though it was based on his fraudulent research.
Many others continue to embrace
this view as well in spite of the overwhelming evidence to the
contrary. Autism spectrum
disorder has also been linked to refrigerator mothers, discussed
earlier, another fraudulent
claim that puts unnecessary blame on the mother. Facilitated
communication, discussed in
the text, has been proven to have no scientific efficacy (APA,
1994; Mostert, 2001). These are
just a few examples.
Do you believe that these false etiologies and treatments are
limited to autism spectrum
disorder and if so, why might that be? What is it about autism
spectrum disorder that makes
it so ripe for inaccurate, unsupported, or fraudulent etiologies
and treatments? One theory

is that parents of special needs children will latch onto any
explanation, no matter how
improbable or fantastic, that might bring comfort and a sense of
closure. Autism spectrum
disorder is particularly heartbreaking as parents see their child
gradually manifest the
disorder.
Although fraudulent theories and treatments will no doubt
continue to surface, parents of
special needs children have to understand that their child’s
condition is not their fault, nor
the fault of childhood vaccines, and that for some disorders,
treatment modalities are often
not successful.
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321
Behavior Training Techniques
People with autism spectrum disorder, and their families, can be
helped to lead higher qual-
ity lives. They may be taught useful communication and
survival skills, and those who care
for them may benefit from learning useful coping skills. Using a
combination of behavior
modification, behaviorally based special education, and speech
therapy, children can be toilet

trained (Wenger, 2017), taught to play games (Odluyurt, 2013),
and helped to acquire aca-
demic skills (Koegel, Singh, & Koegel, 2010). This should not
imply that behavioral treatment
can work miracles (Sachdeva & Dutta, 2012). Sometimes, the
techniques fail.
If, as the research suggests, the problems faced by people with
autism spectrum disorder in
forming attachments, engaging in social relations, and
conducting normal conversations are
partly because they lack a “theory of mind,” perhaps they would
benefit from being explicitly
taught how to empathize with the feelings and thoughts of
others, as well as how to prop-
erly perceive and interpret social cues (Golan & Baron-Cohen,
2006; Slaughter, 2017). The
research in this area is still too new to interpret accurately.
Drug Therapy
In addition to behavioral treatments, at one time or another just
about every drug, vitamin,
and herb has been administered to children with autism
spectrum disorder (Höfer, Hoffmann,
& Bachmann, 2017). However, there are currently no drugs,
vitamins, or herbal treatments
that cure autism spectrum disorder, although some of these
items may alleviate symptoms
(such as sleeplessness). See the accompanying Highlight.
Behavioral treatments, sometimes combined with drugs, have
made it possible for some chil-
dren with autism spectrum disorder to learn much-needed skills
and have led to significant
improvements in their social behavior. However, progress
comes at great cost to their fami-

lies. Having a child with an autism spectrum disorder affects
every aspect of life and often
leads to the parents not focusing on their own emotional needs
and other issues. Therapy and
support groups for these parents are available and often helpful
(Neff & Teska, 2016).
Highlight: Atypical Antipsychotic Medications and Autism
Spectrum Disorder
Did you know that atypical antipsychotic agents, sometimes
called second-generation
antipsychotic medications, are used widely for the treatment of
irritable and aggressive
behaviors in children with autism spectrum disorder (Elvins &
Green, 2010). In October
2006, the FDA approved the use of risperidone (Risperdal) in
children and adolescents aged
5–16 years who have symptoms of irritability associated with
autism (Yan, 2007). Currently
no agents are approved by the American Academy of Pediatrics
for prescription in children
younger than five years of age because of a lack of scientific
evidence of efficacy and safety
(Sharma & Shaw, 2012). Side effects tend to be rare; however,
an exception is rapid weight
gain, which is common and can create significant health
problems. Sharma and Shaw
(2012) conclude that for most children with autism and irritable
and aggressive behavior,
risperidone is an effective psychopharmacological treatment.
(continued)
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322
Chapter Summary
Chapter Summary
Understanding Developmental Psychopathology
• Because differences in temperament are noticeable from the
first day of life, before
the environment can exert any effect, they are most likely
biologically based.
• Whether children develop a psychological disorder depends on
the fit between their
temperaments and their environments.
• Children who fail to achieve toilet training by the usual age
(or developmental level,
if they have an intellectual disability) are diagnosed as having
enuresis (poor control
of urination) or encopresis (poor control of defecation).
• Both disorders occur more often in boys than in girls and seem
to run in families.
• There also appear to be environmental influences; for
example, the disorders are
linked to child abuse.
• Behavior therapy is effective for enuresis and may also help
encopresis.

Conduct Disorder
• Conduct disorders are relatively common, share many of the
features of antisocial
personality disorder, and affect boys more often than girls.
• Childhood-onset disorders have worse outcomes than disorders
that begin later.
• Parental neglect and exposure to antisocial models are
particularly important etio-
logical factors in conduct disorders.
Attention-Deficit/Hyperactivity Disorder
• Children with attention-deficit/hyperactivity disorder (ADHD)
are impulsive and
distractible (mainly at school, but sometimes at home as well).
Many are also
hyperactive.
There are some important aspects to consider here. First and
foremost, a medication that
was initially approved to treat psychotic disorders in adults has
been approved to treat
behavioral issues (irritability) in children with autism spectrum
disorder. Therefore, it is
possible that a child with autism could be taking a potent
antipsychotic medication . . . at age
five! If you were the child’s parent, how would you feel about
this? In addition, risperidone
does not treat autism spectrum disorder, just the irritability that
sometimes goes with it.
Does it make sense for a very young child to take this drug?
That is, do the benefits outweigh
the risks? Finally, what does it say about the helping

professions that there seems to be a
medication to treat, or to help to treat, most psychiatric
conditions? Are these advances,
or are we moving backward, masking the underlying causes and
conditions with endless,
perhaps unnecessary medications? Think about this as you
conclude your reading of
this chapter.
Highlight: Atypical Antipsychotic Medications and Autism
Spectrum Disorder (continued)
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323
Chapter Summary
• ADHD is more common among boys than girls.
• Once a disorder only of children, ADHD is now being
identified in adults as well.
• Many environmental factors have been blamed for ADHD at
one time or another, but
its cause remains unclear.
• Although many different drugs have been used to treat ADHD,
stimulant drugs are
the most common treatment.
• Cognitive-behavioral treatments can help many people with
ADHD to focus their

attention and change their behavior.
Tourette’s Disorder
• Tourette’s disorder is characterized by sudden movements,
strange utterances
(swearing, barking), and multiple motor tics (sudden repetitive
but irregular
movements).
• The DSM–5 also identifies other tic disorders (chronic motor
or vocal tic disorder,
provisional tic disorder) that share some of the symptoms of
Tourette’s disorder.
• Tic disorders affect boys more often than girls.
• The discovery that small doses of haloperidol, a dopamine-
suppressing drug used
to treat schizophrenia, suppress Tourette’s symptoms in many
people has led to the
hypothesis that Tourette’s patients may have an excess of the
chemical dopamine.
• There is also evidence that Tourette’s disorder is inherited.
Separation Anxiety Disorder
• Developmentally inappropriate separation anxiety can lead to
a refusal to attend
school and may presage adult anxiety disorders.
• Separation anxiety may also be associated with social phobia,
avoidant personality
disorder, and nightmares.

Autism Spectrum Disorder
• Autism spectrum disorder is the most serious
psychopathological condition occur-
ring in childhood.
• Autism spectrum disorders are marked by poor interpersonal
relationships, dis-
torted thinking, defective perception, and inappropriate affect.
• In addition to poor attachments and communication problems,
children with autism
spectrum disorder also lack a “theory of mind.”
• Most people with these disorders have an intellectual
disability.
• These disorders have been blamed on everything from
smothering mothers to per-
ceptual defects to viruses.
Critical Thinking Questions
1. The text discusses the hypothesis that elimination disorders
are a result of child
abuse. Discuss how you would go about researching this
hypothesis.
2. Suppose that you are a research assistant and your research
indicates that conduct
disorder is in fact more prevalent in girls than in boys. This
finding goes against what
previous research has shown. Discuss some possible reasons for
your new finding.
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324
Chapter Summary
Key Terms
attention-deficit/hyperactivity disorder
(ADHD) Children with ADHD are impul-
sive and distractible (mainly at school, but
sometimes at home as well); many are also
hyperactive.
autism spectrum disorder A disorder
that typically is noticed from ages 12 to 24
months, but symptoms may be seen earlier
than 12 months if the symptoms are severe,
or after 24 months if the symptoms are sub-
tler. It is marked by poor social interactions,
impaired communication, and odd motor
behaviors.
conduct disorder A repetitive and persis-
tent pattern of behavior in which the basic
rights of others or major age-appropriate
societal norms or rules are violated.
elimination disorder A disorder marked
by poor bladder or bowel control; often
associated with child abuse.
encopresis Poor control of defecation.

enuresis Poor control of urination.
externalizing disorders Disorders that
involve behaviors that annoy or threaten
others; often referred to as “acting out.”
internalizing disorders Disorders such as
depression and anxiety, in which symptoms
are directed inward.
oppositional defiant disorder A disorder
marked by children who are frequently in
trouble at school, and who may use temper
tantrums to get their way.
separation anxiety disorder Developmen-
tally inappropriate and excessive anxiety
concerning separation from home or from
those to whom the individual is attached.
Tourette’s disorder A disorder character-
ized by strange utterances (swearing, bark-
ing) and multiple motor tics (sudden repeti-
tive but irregular movements).
3. The most common treatment modality for ADHD is stimulant
use. Discuss this treat-
ment and your views on giving medications to young children.
4. Facilitated communication was once a popular form of
treatment for autism spec-
trum disorder in the United States and in Canada. Some people
still believe in its
efficacy. Imagine that you are a clinician and have begun
working with a mother who

has a child with autism. She has read about facilitated
communication and regardless
of the research still believes in its efficacy. She is convinced
that it works and that her
daughter is “trapped inside, waiting to come out.” Discuss how
you would explain
to this mother that this method does not work and is not
supported by research. In
addition, discuss what emotions you might see from the mother
as you talk to her.
5. Suppose you were asked to sit on a panel with some experts
who believe that vac-
cines cause autism, and that people with Tourette’s are “faking”
the illness to gain
attention. These experts also believe that autism can also be
caused by having a
refrigerator mother. Discuss how, in a professional manner, you
would respond on
the panel to the experts’ claims.
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10 Neurocognitive Disorders
Wildpixel/iStock/Thinkstock
Chapter Objectives

After reading this chapter, you should be able to do the
following:
• Describe major neurocognitive disorder (dementia) and
explain how it differs from the other
neurocognitive disorders.
• Describe and explain the four steps to diagnosing dementia.
• Describe in detail the amnestic disorders.
• Explain how to treat and prevent the neurocognitive disorders.
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282
Major Neurocognitive Disorder and the Other Neurocognitive
Disorders Section 10.1
10.1 Major Neurocognitive Disorder and
the Other Neurocognitive Disorders
By robbing people of their memories, neurocognitive disorders
disconnect sufferers from
their own lives and from the lives of their loved ones. Sufferers
are caught in the present
moment, unable to relate to the past or to plan for the future.
The DSM–5 contains a number
of neurocognitive disorders, but we will specifically discuss
two: major neurocognitive dis-

order and delirium (American Psychiatric Association [APA],
2013). Each is characterized by
cognitive deficits that represent a significant change from the
person’s previous level of func-
tioning. Neurocognitive disorders, which are always the result
of neurological dysfunction,
are traceable to one of three possible causes: a general medical
condition, a substance (drug
or toxin) intoxication or withdrawal, or a combination of both.
Cognitive problems include
memory deficits, language disturbances, perceptual
disturbances, impairment in the capac-
ity to plan and organize, and failure to recognize or identify
objects. By far the most common
neurocognitive disorder is major neurocognitive disorder
(dementia). The DSM–5 category
of major neurocognitive disorder covers the DSM–IV–TR
diagnoses of dementia and amnestic
disorder. Although there are many neurocognitive disorders, we
will focus on dementia and
continue to use that term, as it remains accepted in the
psychiatric community.
Dementia (the technical name for what most people call
senility) refers to multiple cognitive
deficits including forgetfulness, disorientation, concrete
thinking, and perseveration (repeti-
tive speech or movements). It can occur at any age but is most
common among older people.
For most of history, dementia was considered to be rare,
probably because people did not live
long enough to develop it. As recently as the 1800s, the average
life expectancy was about 45
years. Today, most residents of the developed world can expect
to live well into their 70s and
beyond. As the number of older people increases, so does the

prevalence of dementia. Far
from being rare, dementia has become a major health problem.
As you will see in the case of Helen Lee, the diagnosis of
dementia is usually based on observ-
able signs and symptoms as well as psychological tests,
neuropsychological tests, and brain
imaging.
The Case of Helen Lee, Part 1
Psychological Assessment
Date: February 5, 2012
Client: Helen Lee; DOB: January 4, 1975
Tests Administered
Mini Mental Status Examination-2 (MMSE-2)
Wechsler Memory Scale-Fourth Edition (WMS-IV)
Wechsler Adult Intelligence Scale Fourth Edition (WAIS-IV)
Halstead-Reitan Neuropsychological Battery
Psychologist: Dr. Stuart Berg
(continued)
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283

Section 10.2 Dementia
10.2 Dementia
Diagnosing Dementia
There is no single or simple test that can be used to accurately
diagnose dementia. Typically
the general practitioner, with the help of a neurologist or
gerontologist, will obtain a complete
family and medical history of the individual, including a
psychiatric history and a history
of cognitive and behavioral changes; solicit a family member’s
input about the individual’s
cognitive and behavioral changes; and order blood tests and
brain imaging to rule out other
potential causes such as tumors or vitamin deficiencies
(Alzheimer’s Association, 2016).
The process for diagnosing dementia consists of three steps (see
also Weiner, 1996). First, the
clinician must confirm that the person suffers from multiple
cognitive deficits. These deficits
Reason for Referral: The client, Helen Lee, was referred for
psychological assessment. Helen
has been increasingly forgetful and seems to have lost some
cognitive skills. For example, she
could previously count to at least 20, whereas now she has
trouble counting at all. She had
to quit her job and now seems to be losing self-help skills that
she formerly had. When left
unsupervised, she often wanders off.
Behavioral Observations: Helen’s blouse half hung out of her
skirt, her hair was disheveled,
and she was unsteady on her feet. During the testing session,

her hand had a slight tremor,
and she struggled to find the right words to express herself. In
response to a general inquiry
(“How are you feeling?”), Helen said that she was “sad.” Her
parents, who accompanied her,
denied ever hearing her say she was sad before. During
assessment, Helen referred to me
several times as “father.”
Assessment: Helen was not able to answer correctly any of the
questions on the MMSE-
2. When questioned about the date, she was off by two years.
She was unable to write a
sentence, or to name “pencil” and “watch.” It also proved
impossible to administer the
intelligence test and most of the memory scale because Helen
was unable to concentrate long
enough to respond. She could not learn new associations, nor
could she perform the digit–
symbol subtest. She had trouble even copying symbols. Helen
had difficulty naming common
objects and, at one point, referred to a radio as an oven. She
could write only a few letters and
could not perform any planning task. In a separate task, when
given a clock face and asked to
fill in the numbers, she omitted most, and those she included
she put in the wrong place.
Diagnostic Considerations: The client seems to meet the DSM–5
diagnostic criteria for major
neurocognitive disorder due to Alzheimer’s disease. There are
no signs of hallucinations or
delusions nor of the confusion that is characteristic of delirium.
Her cognitive ability seems to
have deteriorated gradually from previous levels, to the extent
that her social adaptation is now

impaired. She has clumsy movements, misrecognizes common
objects, and is unable to learn
new material. She also seems to be depressed, a common
finding in people with Alzheimer’s.
Diagnosis
Major neurocognitive disorder due to Alzheimer’s disease,
probable Alzheimer’s disease.
See appendix for full case study.
The Case of Helen Lee, Part 1 (continued)
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284
generally include a memory impairment and one or more of the
following symptoms: apha-
sia (a deterioration of ability to comprehend or produce
language), agnosia (a failure to rec-
ognize familiar objects despite normal vision, touch, and
hearing), apraxia (an inability to
carry out desired motor actions despite normal muscle control—
for example, an inability to
dress oneself ), or a disturbance in executive functioning
(planning, organizing, sequenc-
ing, initiating, monitoring, and stopping complex behaviors).

Sometimes these symptoms can
appear quite strange: One patient with visual agnosia attempted
to grab his wife’s head to put
it on his own because he mistook her for his hat (Sacks, 1998).
Let’s briefly look at aphasia before continuing. In aphasia, the
ability to read or write is also
impaired. Aphasia is always due to brain injury, most often
from a stroke, particularly in older
individuals. Aphasia can be so severe as to make
communication with the individual almost
impossible, or it can be very mild. This means that it may affect
a single aspect of language
use, such as the ability to retrieve the names of objects, or the
ability to put words together
into sentences, or the ability to read. More commonly, however,
multiple aspects of communi-
cation are impaired at the same time.
Assessing cognitive deficits can be difficult in older people
because they often tire easily. In
most cases, their performance on cognitive tests is slower than
that of younger people (Birren
& Fisher, 1995; Robitaille et al., 2013). For instance, they will
be penalized on “timed” tests
but perform well on untimed ones (Robitaille et al., 2013). In
addition, reaction time inconsis-
tency increases as one ages (Nilsson, Thomas, O’Brien, &
Gallagher, 2014). Thus, depending
on which tests are used, older people can appear cognitively
impaired or normal.
Episodic memory is the type of long-term,
declarative memory in which we store mem-
ories of personal experiences that are tied
to particular times and places. For example,

if you discuss with a friend a car accident
you witnessed two nights ago, this is stored
in episodic memory. Typically, these kind of
memories are used in eyewitness testimony.
Semantic memory is a type of long-term
memory in which we store general world
knowledge like facts, ideas, words, problem
solving, and the like. An example would be
knowing who is the current U.S. president.
Episodic memory declines with advanc-
ing age, yet semantic memory increases
with age (Khan, Martin-Martinez, Navarro-
Lobato, & Muly, 2014).
A Three-Step Process
No matter which cognitive tests are used, it is crucial that
clinicians be culturally sensitive. For
example, in Western countries, people who do not know their
birth date are almost certainly
cognitively impaired. In cultures where birthdays are not
celebrated, however, not knowing
one’s birthday may be perfectly normal. According to the DSM–
5, cognitive deficits are signs
vadimguzhva/iStock/Thinkstock
Cognitive decline can be difficult to measure
in older people since reaction time slows and
becomes more inconsistent with age, so they
may do poorly on certain tests even though
they are cognitively healthy.
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285
of dementia only when they impair social and occupational
functioning. This criterion intro-
duces another cultural element into the diagnostic process.
Cultures that honor older people
(the Chinese, for example) may tolerate cognitive impairments
that our own society would
consider debilitating.
The second step in diagnosing dementia requires the clinician to
determine, on the basis
of a client’s family and medical history, whether the observed
cognitive deficits are lifelong
or acquired. By definition, dementia is acquired. People who
have always been cognitively
impaired, such as those with intellectual disabilities
(intellectual developmental disorder)
are excluded (unless, like Helen, they show signs of
deterioration). Determining whether cog-
nitive functioning has deteriorated is not always easy because
self-reports are often unreli-
able; however, many factors can lead to cognitive decreases in
an individual, including normal
aging and medical conditions (Jessen et al., 2014). Some
research has demonstrated only a
minor association between self-reports and objective abilities,
so this needs to be consid-
ered as well (Rickenbach, Almeida, Seeman, & Lachman, 2014).
Some older people complain
about their poor memories even though testing reveals few, if
any, memory deficits (Fyock &

Hampstead, 2015). Others never complain about their poor
memories even though they have
serious memory deficits. Determining whether cognitive skills
have deteriorated requires an
account from an accurate informant who has known the client
for some time.
The third step, once the clinician has determined that a person
has acquired multiple cogni-
tive deficits, is to rule out conditions that are superficially
similar to dementia. The two most
likely alternatives are delirium and major depressive disorder.
Brain imaging techniques are a
common way to diagnose neurocognitive disorders. For a more
detailed look at brain imaging
techniques, read the accompanying Highlight.
Highlight: Seeing Inside the Brain
Until relatively recently, the only way to examine an
individual’s nervous system was to wait
for the person to die and do an autopsy. Today, thanks to brain
imaging technology, scientists
can examine the structure and function of the living brain with
minimal disturbance to the
individual being studied. One of the most widely used imaging
techniques is computerized
tomography, better known as CT scanning. To perform a CT
scan, multiple X-ray beams are
revolved around the head. Transmitted radiation is computer
analyzed to produce a cross-
sectional image of the brain. Although CT scans do not produce
clear pictures of brain tissue,
they can show the outlines of certain structures, such as the
brain’s ventricles.

An imaging technique that is having an enormous impact on
research is magnetic resonance
imaging, or MRI. In MRI, powerful magnetic fields are used to
attract the protons found in
the nuclei of the body’s hydrogen atoms. The protons are forced
to change their alignment,
giving off radio transmissions that are translated into images of
the brain. The clarity of these
pictures depends on the strength of the magnetic fields. Strong
magnets can produce images
that are almost as clear as photographs of brains taken at
autopsy.
MRI provides a picture of brain structure. To answer questions
about brain function (for
example, which parts of the brain process different types of
cognitive stimuli) requires some
way of imaging brain function. Functional MRI (fMRI) was
developed for this purpose. It
enables us to see which parts of the brain are activated when
information is being processed.
(continued)
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286
The technique capitalizes on the increased blood flow produced

by brain metabolism. Blood
flows to activated parts of the brain. This produces magnetic
signals that can be read by MRI.
The result is an image of brain activity.
Positron emission tomography, or PET, scans can also reveal
brain function. The process
begins with the administration of a radioactive form of the
sugar glucose. Active brain cells
metabolize the glucose, releasing radiation that is detected by
the PET scanner. The result is
an image of the metabolic activity in different parts of the
brain. When people are required
to perform certain cognitive tasks and the resulting radiation
pattern is recorded, PET scans
allow researchers to identify the parts of the brain that are
associated with different forms of
mental activity. It is like “seeing” people think.
PET scans have serious drawbacks. Because they use
radioactive materials and require
considerable staff time, they are expensive; safety regulations
limit individuals to one scan
a year; and no woman of childbearing age may be tested. For
these reasons, researchers
have turned to electroencephalographic methods as a safer and
cheaper alternative.
Electroencephalographs (EEGs) are recordings of brain
electrical activity made from
the scalp (or directly from within the brain). By recording EEGs
after the presentation of a
stimulus (a flash of light or a tone), researchers can isolate the
brain’s electrical response to
the stimulus. This is known as an event-related potential, or
ERP. By recording ERPs from
various sites on the head simultaneously, researchers can

construct a topographic map
that represents the electrical activity in various parts of the
brain (Koenig, Stein, Grieder, &
Kottlow, 2014). Comparisons of the topographic maps produced
by people with different
cognitive disorders can identify differences in information
processing.
Topographic maps may also be constructed using a technique
called single photon emission
computerized tomography (SPECT). Like fMRI, SPECT scans
monitor blood flow while people
perform cognitive tasks. Because the active parts of the brain
use more blood, changes
in blood flow indicate which parts of the brain are active. By
recording blood flow from
different areas of the brain, researchers can produce a
topographic map of brain activity
during cognition. This technique provides similar information to
fMRI.
Phanie/SuperStock; Cultura Limited/SuperStock
Here we see two brains: a healthy one on the left, and one with
Alzheimer’s on the
right. The large dark spot in the brain on the right shows how
brain function declines
when Alzheimer’s sets in.
Highlight: Seeing Inside the Brain (continued)
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287
Ruling Out Delirium and Major Depressive Disorder
(Depression)
Delirium is a cognitive disorder marked by a “clouding” of
consciousness most often found
among older people (Trzepacz & Meagher, 2008). This is
accompanied by disorientation, a
disturbance in attention and awareness, memory deficits,
perceptual disturbances such as
hallucinations, and language deficits (Morandi et al., 2017).
Delirium develops rapidly (within
a few hours or days) and is common in hospitalized patients,
especially among senior citizens
(it affects up to 50% of hospitalized seniors; Inouye,
Westendorp, & Saczynksi, 2014). While
delirious, patients seem to be unaware of where they are or what
is going on around them.
They have difficulty focusing, sustaining, or shifting attention;
their memories may be poor;
they may lose track of the day or even the month; their language
may be rambling and inco-
herent; and they may have hallucinations and delusions. In
addition to showing cognitive
symptoms, delirious people are often anxious, fearful, and
irritable (Na & Manning, 2015).
People who become delirious during the night have been known
to pull off their bedclothes,
claiming that their sheets are crawling with bugs. Hospitalized
delirious patients have pulled
catheters out of their arms and disconnected respirators that
they need in order to breathe.
There are several etiology-specific subtypes: delirium due to

another medical condition, sub-
stance intoxication delirium, substance withdrawal delirium,
and delirium due to multiple
etiologies.
Delirium has numerous causes: brain tumors, blows to the head,
systemic diseases such
as AIDS, organ failure, infection, and intoxication with
prescription or illicit drugs (Heeder,
Azocar, & Tsai, 2015; Lawlor & Bush, 2014). Giving up a drug
or substance (substance with-
drawal) can also trigger an episode, especially among habitual
drug users. Delirium tremens,
for example, occurs when alcohol is withdrawn from habitual
drinkers. In addition to these
immediate causes, there are several psychological and social
factors that can facilitate the
development of delirium. These include severe stress, sleep
deprivation, sensory deprivation
(as in solitary confinement), and forced immobilization (as in
patients being treated for seri-
ous burns; Na & Manning, 2015).
The appropriate treatment for delirium depends on the cause. If
delirium is caused by another
medical condition, treatment focuses on curing the condition. If
delirium is the result of sub-
stance abuse or withdrawal, then it is treated by either gradually
withdrawing the substance
or substituting another, less harmful one. Delirium normally
disappears once its cause is
identified and eliminated (APA, 2013; Heriot et al., 2017).
Although the two disorders share some symptoms, delirium can
usually be differentiated
from dementia by its rapid onset, short duration, alternating

lucid intervals, the presence of
hallucinations and delusions, and its minimal long-term effect
on personality (see Table 10.1).
Keep in mind, however, that none of these differences is
absolute. For example, although they
are more common in delirium, hallucinations and delusions are
also found in 14% to 22%
of dementia cases in one study (Selbaek, Engedal, & Bergh,
2013). Another study found psy-
chotic symptoms present in about 50% of individuals with
dementia (Murray, Kumar, DeMi-
chele-Sweet, & Sweet, 2014). Moreover, it is possible to be
delirious and suffer from dementia,
so a definitive diagnosis may not be possible until the delirium
has cleared.
Ruling out depression as a cause of cognitive impairment is
more difficult than ruling out
delirium. Not only are the symptoms of depression and dementia
similar (Heriot et al., 2017),
but both conditions also tend to co-occur among older people
and those with Down syn-
drome (Tasse et al., 2016). Some depressed people behave like
people with dementia. They
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288

withdraw from their normal activities, lose interest in everyday
life, and have difficulty con-
centrating or sleeping. In addition, their speech is confused and
slow. People who show all
the signs of dementia but are really suffering from depression
are often labeled as having
pseudo-dementia. Note that pseudo-dementia is not a
diagnosable condition.
Table 10.1 Distinguishing delirium from dementia
Characteristic Delirium Dementia
Onset Rapid Gradual
Duration Short Long
Degree of cognitive impairment Varies, with some lucid
intervals Severe most of the time
Personality Intact Disorganized
Hallucinations Active Vague or none
Delusions Prominent, especially of
persecution
Vague or none
Affect Anxious and fearful Apathetic and unemotional
Despite their similarities, dementia and depression have some
important differences. Major
depressive episodes have at least a vague beginning and an end,
whereas dementia develops
too gradually to pinpoint a date. Depressed people are aware of

and complain about their cog-
nitive functioning, and most respond to antidepressant
medication. Neither of these is true of
people with dementia (at least not in its later stages). There may
also be subtle differences in
the clinical presentation of depression and dementia. For
instance, the symptoms of depres-
sion are usually worse in the morning, whereas dementia
symptoms become more obvious
late in the day when the person is tired, often called sundowner
syndrome or sundowning
(Antyna, Vogelzangs, Meesters, Schoevers, & Penninx, 2016;
Na & Manning, 2015). Using
these various signs, it is possible for clinicians to separate
pseudo-dementia from dementia.
Keep in mind, however, that it is common to be both depressed
and suffering from dementia
(Leyhe et al., 2017) and, interestingly, more common if the
individual suffers from diabetes
(Wayne, Perez, Kaplan, & Ritvo, 2015).
Major Neurocognitive Disorder Due to Alzheimer’s Disease
Dementia has long been considered to be an illness of old age.
But, at a scientific meeting
held in 1906, Alois Alzheimer (1864–1915) reported a case of
“senile” dementia in a woman
who was only 51. The woman had trouble recognizing common
objects, frequent memory
lapses, and difficulty speaking. Her personality also changed. In
contrast to her former serene
demeanor, she became impulsive and capricious. She also
developed hallucinations and
severe delusions of persecution. Most poignant of all was her
own description of her dis-
ease: “I have lost myself.” After the woman’s death at age 55,
Alzheimer performed an autopsy

and found three abnormalities in her brain. First, she had many
neurofibrillary tangles in
her hippocampus and cerebral cortex. Neurofibrils are narrow
fibers found within neurons.
Scientists believe that these fibers provide structural support for
neurons and also assist in
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289
transporting neurotransmitters and other chemicals within nerve
cells. In normal neurons,
the neurofibrils are organized in symmetrical columns, but in
Alzheimer’s patients they are
found to be tangled and disorganized. The second abnormality
that Alzheimer uncovered
during the autopsy was the presence of numerous plaques.
Modern protein sequencing has
shown that these plaques contain a protein fragment known as
beta-amyloid surrounded by
the debris of destroyed neurons. The third abnormality that
Alzheimer found was arterioscle-
rosis (a common arterial disease in which high cholesterol
causes plaque to form on the inner
surfaces of the arteries, obstructing blood flow).
None of Alzheimer’s observations were new. Neurofibrillary
tangles, senile plaques, and arte-

riosclerosis had all been reported before (see Berrios, 1994).
The main point of his 1906
paper was that dementia could occur in relatively young people.
It was Emil Kraepelin who
first referred to “Alzheimer’s disease,” suggesting that so-called
pre-senile dementia might
be different from the dementia of old age. Each year, more than
1,500 articles are published
on Alzheimer-type dementia. Ironically, this huge body of
research, which was stimulated
by Kraepelin, has not substantiated his distinction between pre-
senile and old-age dementia
(Atwood & Bowen, 2015). Except for the age at which they
begin, the conditions are essen-
tially identical. The only difference is that mental deterioration
tends to progress more quickly
among people who show the first signs in their 40s and 50s.
Today, it is common to refer to
both pre-senile and senile dementia as Alzheimer’s disease or
major neurocognitive disor-
der due to Alzheimer’s disease (hereafter called Alzheimer’s
disease).
The bulk of modern dementia research is motivated by a desire
to find the “cause” of Alzheim-
er’s disease. Early detection is the key to preventing, slowing,
and ideally stopping the disease.
Research, especially during the past decade, has made
significant progress in early detection
(Alzheimer’s Association, 2016). Researchers rarely question
the assumption that Alzheim-
er’s is a single disease. Yet Alzheimer’s has few, if any,
specific signs or symptoms (Koric et al.,
2016). For instance, neurofibrillary tangles and senile plaques
are also common in “healthy”
older people who have no symptoms of dementia; it is possible

that they are natural conse-
quences of aging. This could mean that Alzheimer’s is not a
specific disease but simply an
acceleration of the normal aging process (Fjell et al., 2016).
In the decades since Alois Alzheimer’s case report, numerous
anomalies have been found in
the brains of older people with dementia (Iadecola, 2016).
Unfortunately, none of these anom-
alies is specific to Alzheimer’s. For this reason, Alzheimer’s
has become a clinical diagnosis
that does not depend on any specific laboratory test or
pathology. It is diagnosed only when
other potential causes of dementia have been excluded (see
Table 10.2). For example, if the
symptoms of dementia come on suddenly and are accompanied
by signs of focal brain dam-
age (when an injury or damage occurs in a specific location, or
focus; blindness or numbness,
for example) in a person with a history of circulatory disease,
and if MRI or other laboratory
evidence confirms a vascular event, then the dementia is
diagnosed as vascular. Alzheimer’s
is diagnosed only when a person with an acquired cognitive
impairment does not meet the
diagnostic criteria for any other type of major or mild
neurocognitive disorder; it is a diagno-
sis made by exclusion. Nevertheless, the diagnosis of
Alzheimer’s seems to be accurate 70%
to 90% of the time (Cure, Abrams, Belger, Dell’agnello, &
Happich, 2014).
The DSM–5 has two specifiers: probable Alzheimer’s disease,
and possible Alzheimer’s dis-
ease (APA, 2013).

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Major or Mild Vascular Neurocognitive
Disorder (Vascular Dementia)
Major or mild vascular neurocognitive disorder (also known as
multi-infarct dementia,
and called vascular dementia throughout the remainder of the
chapter) is considered to
be the second most common cause of dementia after
Alzheimer’s disease (Iadecola, 2013).
Approximately 10% to 20% of all dementia cases involve
vascular dementia (Iadecola, 2013).
The lifetime risk of vascular dementia is about 0.2% in people
aged 65–70 (APA, 2013). The
risk increases to 16% from age 80 and up (APA, 2013). The risk
is higher for men (APA, 2013;
Iadecola, 2013). This higher risk can be explained by causal
factors, such as heart problems
and high blood pressure, which are more common in men than
women (Alzheimer’s Society,
2017). The cause of vascular dementia is an interruption in
blood supply to part of the brain, a
condition known as a stroke. Typically, a stroke is caused by a
blood clot in one of the brain’s
blood vessels. This “infarct” cuts off the supply of blood to the
surrounding neural tissue. In
some cases, the brain’s blood supply is gradually reduced by

arteriosclerosis, a generic name
for any condition that causes blood vessels to become narrowed.
In a few cases, blood vessels
may burst. Whatever the cause, the result is the same. Neural
tissue dies because of a lack of
oxygen and nutrients. Unless there are numerous infarcts,
widespread arteriosclerosis, or
damage to large blood vessels, vascular dementia usually affects
only a small part of the brain.
The affected part may be detected using modern imaging
techniques. When such tests are
unavailable or their results are difficult to interpret, it may still
be possible to localize brain
damage using clinical signs and neuropsychological tests (Khan,
Kalaria, Corbett, & Ballard,
2016). However, other research demonstrates that localizing
brain damage using these tech-
niques, in fact, may not be possible (Arevalo-Rodriguez et al.,
2015).
Table 10.2 Core differences between dementia and Alzheimer’s
disease
Dementia Alzheimer’s Disease
Disease? Dementia is a category, not a dis-
ease. It refers to symptoms that
negatively impact memory.
Alzheimer’s is a form of demen-
tia and also a disease.
Similarities Both can cause
• Decline in ability to think
• Memory impairment
• Communication impairment

Differences • Several diseases may cause
dementia: Alzheimer’s, Par-
kinson’s, nutritional problems
• Can be reversed in some
instances
• Symptoms can be diagnosed
without knowing underlying
disease
• Is a disease
• Cannot be reversed
• Exact cause of symptoms is
usually known
• Conclusive diagnosis may
rely on brain autopsy after
death (according to some
researchers)
get83787_10_c10_281-304.indd 290 2/16/18 4:52 PM
291
Substance/Medication-Induced Major or
Mild Neurocognitive Disorder

When there is evidence that the symptoms of dementia are
related to drugs or poisons, the
correct DSM–5 diagnosis is substance/medication-induced
major or mild neurocogni-
tive disorder. The dementia continues even after the substance
is withdrawn. The list of sub-
stances that can cause dementia is endless—drugs (both legal
and illicit), alcohol, inhalants,
lead, mercury, carbon monoxide, insecticides, and solvents. All
act by destroying brain tissue
or disrupting brain metabolism. Perhaps the most common cause
of substance/medication-
induced major or mild neurocognitive disorder is alcohol abuse.
An excessive intake of alco-
hol leads people to neglect their diets, which in turn produces
cognitive disorders.
Dementia Due to Medical Conditions
Major or Minor Neurocognitive Disorder Due to Parkinson’s
Disease
Parkinson’s disease was mentioned in Chapter 8 in connection
with the dopamine hypoth-
esis of schizophrenia. In Parkinson’s disease, some of the
brain’s dopamine-producing cells
in the substantia nigra spontaneously die (Hirsch, Hunot, &
Hartmann, 2005). The result is
an undersupply of dopamine, which disrupts activity in parts of
the brain that rely on dopa-
mine. One such area is the basal ganglia, which plays an
important role in controlling motor
behavior. As a result, people with Parkinson’s disease develop
tremors, rigid muscles, and
difficulty initiating or stopping movements. After a while, these
symptoms are accompanied
by a stooped posture, slow body movements, and a

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