10 Neurocognitive DisordersWildpixeliStockThinkstock.docx

10 Neurocognitive Disorders
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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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290
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)
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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
characteristic speech pattern in which
the person speaks only in a soft monotone. Although dementia
is not a necessary accompani-
ment of Parkinson’s disease, it occurs twice as often with
Parkinson’s victims, typically being
a subcortical dementia (subcortical refers to the region of the
brain below the cortex; Safa-
rpour & Willis, 2016). The symptoms of subcortical dementia
consist mainly of psychomotor
slowness and a memory defect (Whitehouse, Friedland, &
Strauss, 1992). In common with
most other types of dementia, depression frequently
accompanies Parkinson’s disease and
has been observed in as many as 35% to 40% of Parkinson’s
patients, though the rates can
vary from 4% to about 70% (Menon et al., 2015).
Parkinson’s disease is rarely diagnosed before age 50, but there
are some famous exceptions,
such as actor Michael J. Fox, who began experiencing
symptoms in his 30s. Incidence in the
population over 50 years of age has been rising from 30 to 440
per 100,000 persons (de Lau
et al., 2004). More recent analyses show that Parkinson’s
affects about 315 per 100,000 peo-
ple per year in North America (Goodarzi et al., 2016). The

lifetime risk is less than 0.1%, and
it affects about 50% more men than women (Lee & Gilbert,
2016; Savica, Grossardt, Bower,
Ahlskog, & Rocca, 2016). Parkinson’s disease is more common
in northern states than in the
South, although the significance of this geographic difference is
unknown (Willis, Evanoff,
Lian, Criswell, & Racette, 2010). Exposure to industrialized
toxins, as well as exposure to pes-
ticides and herbicides, may contribute, though undoubtedly a
variety of factors are involved
(Willis et al., 2010). Although some cases of Parkinson’s are
preceded by infections or blows
to the head (as in the boxer Muhammad Ali), most cases are of
unknown origin. Parkinson’s
disease may be treated with L-dopa (levodopa), a drug that
enhances the production of dopa-
mine. Although L-dopa may provide temporary relief from some
troubling symptoms of Par-
kinson’s disease, it can also produce symptoms like those of
schizophrenia. If Parkinson’s
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292
patients develop psychoses, they cannot be treated with most
antipsychotic medications
because these drugs worsen the motor symptoms (Desmarais,

Massoud, Filion, Nguyen, &
Bajsarowicz, 2016).
Major or Mild Neurocognitive Disorder Due to Huntington’s
Disease
Huntington’s disease is a form of chorea (a Greek word meaning
“dance” but which refers
today to brain syndromes that include irregular, jerky
movements). Huntington’s results from
the progressive degeneration of the basal ganglia, a part of the
brain involved in controlling
movements and other functions (Gargouri et al., 2016). The first
signs are a mild memory
impairment, an inability to concentrate, and depression. Next
come personality changes: Suf-
ferers become irritable and erratic. As the disease progresses,
cognitive impairments become
more noticeable (Warby, Graham, & Hayden, 2014). Sufferers
may have paranoid delusions,
especially the belief that they are being persecuted. Some act on
these beliefs by resorting to
violence. Initially, Huntington’s disease may be mistaken for
schizophrenia, but as the condi-
tion progresses, the syndrome becomes unmistakable (there is
no chorea in schizophrenia).
Death occurs 10 to 20 years after the first symptoms appear.
Current estimates place the number of cases at 2.7 per 100,000
people worldwide. The preva-
lence is much higher in North America, Europe, and Australia
(5.7 cases per 100,000) than in
Asia (0.40 cases per 100,000) (APA, 2013). Symptoms almost
always appear by the age of 40.
The condition seems to affect mainly people of European
extraction; there are no reported
cases among native Australian Aborigines or the Eskimos of

North America, although the
shorter life expectancies in these populations may mean that
people are dying before the dis-
ease becomes manifest (Rawlins et al., 2016). Huntington’s
disease is caused by a single dom-
inant gene, specifically on chromosome 4 (Gargouri et al.,
2016). (See Figure 10.1.) Although
the disease may be passed on by a child’s mother or father,
early-onset Huntington’s disease is
associated with inheritance from the father. This is one of very
few cases in which the paren-
tal origin of a gene seems to affect the gene’s expression
(Warby et al., 2014). There is no cure
for Huntington’s, but carriers can be tested and may decide to
forgo having children.
Creutzfeldt-Jakob Disease
In the early part of the 20th century, two clinicians, Creutzfeldt
and Jakob, independently
reported cases of dementia associated with symptoms similar to
those of tardive dyskinesia.
They described people who walked with a stiff gait, had trouble
maintaining their balance,
and had difficulty controlling their voluntary movements. These
people also had a dimin-
ished ability to plan ahead and organize their behavior, two
signs of frontal lobe damage. As
Creutzfeldt-Jakob disease progresses, these movement
symptoms are followed by mem-
ory defects, hallucinations, and delusions. Patients usually die
within two years of diagnosis.
Autopsies find nerve cells that look like “sponges,” making the
disease one of the spongiform
encephalopathies, a category that includes “mad cow” disease
(National Institute of Neuro-
logical Disorders and Stroke, 2017).

Creutzfeldt-Jakob disease has been estimated to affect 1.2 in
one million people, with no gen-
der differences (Geschwind, 2015). Because it is so uncommon,
the disease would have been
a mere curiosity if it had not been for Daniel Carleton
Gajdusek’s studies of kuru in 1997.
Kuru is a spongiform disease found among the Fore tribe of
Papua New Guinea. Its symptoms
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293
Figure 10.1: Types of intellectual disabilities and neurological
disorders
caused by chromosomal abnormalities
Source: From S. Schwartz, Abnormal Psychology: A Discovery
Approach. Mountain View, CA: Mayfield Publishing Company,
2000, Figure
11.2, p. 473.
Degenerative neurological
disease that produces
involuntary, contorted
movements and dementia.
Huntington’s disease

Degenerative neurological
disease that causes
tremors, muscular stiffness,
and difficulty with balance.
Parkinson’s disease
Short stature, mental retardation,
incomplete sexual development,
poor muscle tone, and an
involuntary urge to eat constantly.
Prader-Willi syndrome
Distinctive facial features,
muscular abnormalities, mental
retardation, and absence of
speech but unprovoked,
excessive laughter.
Angelman syndrome
Progressive disorder of lipid
metabolism that destroys the
central nervous system.
Tay-Sachs disease
Mild-to-severe mental retardation,
prominent ears and jaw, and in males,
large testicles; more frequent and
more severe in males than in females.
Fragile X syndrome

Learning disorders, long legs, and
incomplete sexual development
caused by a second X chromosome
in males.
Klinefelter syndrome
Learning disorders, short stature, and
incomplete sexual development
caused by the absence of one X
chromosome in females
Turner syndrome
Elfin appearance; heart
problems; difficulty with
spatial task, reading,
and writing; unusual
competence in language,
music, and interpersonal
relations.
Williams syndrome
Skin lesions, benign
tumors, epileptic seizures,
and mild-to-severe mental
retardation.
Tuberous sclerosis
Progressive disorder
of lipid metabolism that
destroys the central
nervous system.

Niemann-Pick disease
A third chromosome 21
causes distinctive physical
characteristics, such as an
epicanthic fold over the
eye and a depressed nasal
bridge, and slight-to severe
mental retardation.
Down syndrome
Kittenlike cry during
infancy, distinctive facial
characteristics, and
mental retardation.
Cri du chat syndrome
Dementia caused by brain lesions and
neurofibrillary tangles; mutations in genes on
chromosomes 1, 14, 19, and 21 play a role.
Alzheimer’s disease
Progressive disorder of amino acid metabolism
that can produce mental retardation, seizures,
and hyperactivity if not treated early.
Phenylketonuria
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Y X
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Y X
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294
include dementia. Gajdusek won the Nobel Prize for showing
that kuru is a very slow-growing
virus that is transmitted through ritual cannibalism. The disease
is transmitted when mem-
bers of the Fore tribe eat the dead bodies of other tribe
members, but symptoms do not appear
for many years. In developed countries, Creutzfeldt-Jakob
disease is not spread through can-
nibalism, but it may be transmitted by eating affected animals
(Geschwind, 2015). Most cases
of Creutzfeldt-Jakob disease are sporadic (they do not run in
families); but cases that begin
early in life may be the result of a family history of brain
disease. Less than 1% of cases are
acquired (Geschwind, 2015).
Head Injuries, Tumors, and Other Brain Diseases
If they are severe enough, head injuries, tumors, and brain
diseases can produce the symp-
toms of dementia. The behavioral effects of head injuries are
determined by the location and
extent of brain damage. The precise cognitive and behavioral
effects of brain injury depend
on the victim’s premorbid personality, his or her coping skills,
and the extent of his or her
social supports. Brain injury can also cause the seizures

associated with epilepsy, known
more commonly today as seizure disorder (Nemes, Choi,
Zamarbide, & Manzini, 2016). In
veterans, 57% of seizures can be linked to traumatic brain
injury (Lucke-Wold, 2015). Nearly
40% to 50% of patients with severe traumatic brain injury
develop seizure disorder. In addi-
tion, brain injuries account for 10% to 20% of seizure disorder
(Pitkanen & Immonen, 2014).
Brain tumors (depending on their size and location) and
endocrine disorders may also pro-
duce cognitive impairments and personality changes resembling
those found in dementia
(Feldman, Shrestha, & Hennessey, 2013; Madhusoodanan, Ting,
Farah, & Ugur, 2015). Infec-
tious diseases, such as syphilis, encephalitis (inflam-
mation of the brain), and meningitis (inflammation
of the membrane that surrounds the brain and spi-
nal cord), may also produce symptoms of dementia.
Fortunately, all of these conditions are treatable or
preventable. Brain tumors are treated with surgery,
drugs, or radiation; endocrine disorders can be
ameliorated by drugs and diet; and infectious dis-
eases can be prevented by immunization and safer-
sex programs.
Prevalence, Incidence, and
Course of Dementia
Major neurocognitive disorder due to Alzheimer’s
disease is the most common form of dementia,
accounting for 60% to 90% of cases, depending on
diagnostic criteria used and on the setting, among
other factors (APA, 2013). An estimated 5.4 million
Americans of all ages have major neurocognitive
disorder due to Alzheimer’s disease (Alzheimer’s

Association, 2016), and we can expect this num-
ber to increase as the U.S. population ages and lives
Visions of America/SuperStock
Former president Ronald Reagan was
diagnosed with Alzheimer’s disease in
1994, five years after leaving office.
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295
At present, there are more women with dementia than men, but
this may simply reflect the
longer life expectancy of females. (The longer a woman lives,
the greater the chance that she
will develop dementia.) Dementia has a high prevalence and
incidence among lower socio-
economic groups, but the reasons for this finding remain
somewhat unclear (Alzheimer’s
Association, 2016). Some factors to consider include poor
health care, inadequate diet, and,
in some cases, substance abuse. Chronic conditions such as high
blood pressure and vascular
disease are poorly managed among those in lower
socioeconomic groups (Alzheimer’s Asso-
ciation, 2016). With better medical care and public health
awareness, social class differences
would probably disappear.

Cross-cultural estimates of prevalence and incidence are not
always reliable because, as
already mentioned, cultures have different attitudes toward and
expectations of elderly peo-
ple (Cipriani & Borin, 2015; Sayegh & Knight, 2013). Cultural
practices may distort estimates
of the prevalence and incidence of dementia.
longer. The prevalence of dementia rises with age from about
1% to 2% at age 65 to as high
as 30% by age 85 (APA, 2013). The lifetime risk of developing
major neurocognitive disorder
due to Alzheimer’s disease, specifically by the time the
individual reaches 65, is about 9%
for men and 17% for women (Alzheimer’s Association, 2016).
By the year 2050, more than
13.8 million people in the United States are expected to suffer
from the disorder (Alzheimer’s
Association, 2016). The estimate may go as high as 16 million.
Care for these individuals will
cost billions of dollars (see the accompanying Highlight).
Highlight: The Costs of Alzheimer’s Disease
When people think of the cost of Alzheimer’s disease, they
usually focus on the economic
aspects. To be sure, Alzheimer’s, which is expected to affect
more than 44 million individuals
in 2017, has been estimated to cost $605 billion globally (in
2016, the most recent year
for which an estimate is available; Alzheimer’s Association,
2016). To put the increase
in perspective, Sifferlin (2013) estimates that, if a cure is not
found, the number of cases
of neurocognitive disorder (including Alzheimer’s) is estimated

at 135 million people
worldwide. This represents more than one third of the U.S.
population as of this writing.
These figures will increase annually while a cure or effective
preventive measures continue
to be sought.
What are the emotional and physical costs to the caregivers?
Fortunately, more emphasis has
been placed on caregivers recently, and with good reason:
According to Alzheimers.net,
more than 40% of family caregivers report that the emotional
stress of their role is high or
very high. Emotional stress is difficult to quantify accurately,
but the next fact is a lot more
alarming: In 2014, Alzheimer’s and dementia caregivers had
$9.7 billion in additional health
care costs of their own. We’re including mental health care
here. Many caregivers experience
depression, anxiety, and other issues. AARP has discussed this
issue as well, and many
agencies have called for more attention to be given to
caregivers. Psychologists and other
clinicians should be alert that these issues will no doubt
increase as the population continues
to age. As psychologists as well as educators, we need to
continue to educate the public about
the costs to caregivers and to let politicians know how serious
these issues are now, and will
be in the future.
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296
Dementia caused by operable tumors, drugs, and treatable
infections may be reversed, but
such cases represent the minority. Most people with dementia,
especially those with Alzheim-
er’s, deteriorate progressively until they die (Alzheimer’s
Association, 2016). In late-onset
Alzheimer’s, the average period between diagnosis and death is
about 5.6 years (Wattmo,
Londos, & Minthon, 2014). In early-onset cases (about one
fourth of the total), the period
between diagnosis and death is longer, about 6.5 years (Wattmo
et al., 2014). Both early- and
late-onset cases usually begin with a mild memory disturbance
that is often dismissed as
mere forgetfulness. As time passes, the memory disturbance
becomes more obvious (Butters,
Delis, & Lucas, 1995). Not only does the person forget facts
and events, but new learning also
becomes increasingly difficult. Initially, old memories are
preserved, but eventually those,
too, are lost. Personality changes, sometimes dramatic, come
next. People with dementia
become childish, irritable, and depressed. This is followed by
increasing confusion, disorien-
tation, aphasia, agnosia, and apraxia. In the late stages of
dementia, people may lose control
over body functions. Death usually follows soon after. (See Part
2 of Helen Lee’s case in the
appendix.)

Risk and Protective Factors for, and Etiology of, Dementia
The list of potential etiologies for dementia is exceedingly long.
It includes not only the spe-
cific causes of dementia that have already been discussed (for
example, tumors, blows to the
head, the Creutzfeldt-Jakob virus) but also a disparate
collection of risk factors that have been
linked to Alzheimer’s: autoimmune disorders, deficient levels
of neurotransmitters, viruses—
the list of potential causes of Alzheimer’s goes on and on.
However, few of these possible
causes have withstood close scrutiny.
So-called protective factors that supposedly prevent the
development of Alzheimer’s are
equally suspect. For example, some researchers have suggested
that cigarette smoking has
a protective effect because smokers, it seems, have lower rates
of Alzheimer’s than do non-
smokers, though the evidence is inconsistent (Momtaz, Ibrahim,
Hamid, & Chai, 2015). Per-
haps the relationship is the result of smokers not living long
enough to develop Alzheimer’s.
Education has also been identified as a potential protective
factor. Educated people are
alleged to have a lower risk of Alzheimer’s because they
maintain an active intellectual life
(Alzheimer’s Association, 2016). Educated people tend to be
wealthier, have access to bet-
ter health care, eat better diets, smoke less, and take better care
of themselves than do those
who are less well educated. Any of these factors could be
responsible for the lower incidence
of Alzheimer’s among the better educated. Education also
appears to be related to a delay in

observing Alzheimer’s symptoms. Once their symptoms begin,
those who have more edu-
cation tend to decline much faster (Contador, Fernández-Calvo,
Ramos, & Olazarán, 2016).
Regardless of the educational level, evidence suggests that
participating in stimulating cogni-
tive activities, such as doing crossword puzzles, solving Sudoku
and logic problems, among
other things, may delay the onset of dementia (Contador et al.,
2016).
Observed correlations can lead to important discoveries. For
example, the relationship
between Alzheimer’s and Down syndrome has been known for
some time. Researchers fol-
lowing up this correlation have found a gene on chromosome 21
that predisposes people to
develop Alzheimer’s (genes on chromosomes 1 and 14 are also
linked to the disease); the
same chromosome is overexpressed in Down syndrome
(Alzheimer’s Association, 2016).
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297
Section 10.3 Amnestic Disorders
A question that has preoccupied investigators is whether
Alzheimer’s can be inherited. This
question remains largely unanswered because of the difficulties

involved in researching a
condition that usually does not become apparent until old age.
Ordinarily, researchers would
identify a person with Alzheimer’s and then study that person’s
relatives to see whether they
also have the disease. However, what happens if a relative is
run over by a bus while still
in his or her 20s? Because he died with all his faculties intact,
researchers may conclude
that Alzheimer’s does not run in families. It is possible,
however, that the relative would have
developed Alzheimer’s if he or she had lived long enough. To
determine whether Alzheim-
er’s runs in families, researchers must follow relatives for many
years in longitudinal stud-
ies. When they do, they find that anywhere from 30% to 48% of
relatives of a person with
Alzheimer’s disease have a first-degree relative (mother, father,
sibling) who is affected, com-
pared with 13% to 19% of a control group (Cuyverse &
Sleegers, 2016). The familial type
seems to be characterized by an earlier age of onset and rapid
deterioration (Corder et al.,
1993), but more recent research contradicts this finding
(Cuyverse & Sleegers, 2016). Several
researchers have suggested that the gene responsible for the
familial type of Alzheimer’s is
apoE4, the one that controls the production of beta-amyloid, the
major component of senile
plaques (Gatz, 2007). More recent findings suggest that as many
as 20 genes as well as focal
points in the brain may be responsible for Alzheimer’s disease
(Cuyverse & Sleegers, 2016).
What this demonstrates is that research is progressing, albeit at
a rate that is slower than the
increase of Alzheimer’s incidence itself.

Another possible interpretation of the genetic data is that it is
not Alzheimer’s that is inherited
but the tendency to live a long life. The increased incidence of
Alzheimer’s in some families
may not be evidence of an inherited disease but may simply be a
consequence of living longer.
The best way to differentiate these two possibilities is to
compare the relatives of Alzheimer’s
patients with control subjects of the same age whose family
members do not have Alzheim-
er’s. If there is a specific genetic factor predisposing people to
develop Alzheimer’s, the rela-
tives of Alzheimer’s patients should have a higher probability
of developing Alzheimer’s than
control subjects of the same age who do not have relatives with
Alzheimer’s.
10.3 Amnestic Disorders
Although one of the important signs of dementia is a memory
disorder, there are people with
memory disorders who do not have dementia. These people fall
into a category that the DSM–
IV–TR called amnestic disorders. (In the DSM-5 amnestic
disorders have been subsumed
under the category major neurocognitive disorder due to another
medical condition. Due to
their importance, we are discussing them in this section and will
continue to call them amnes-
tic disorders.) People with amnestic disorders are able to
perform simple memory tasks.
They can usually attend to their immediate situation, retrieve
old memories, and repeat a list
of four or five digits. However, their cognitive impairment
becomes obvious when they are
required to hold on to an experience or to learn something new.

For example, when asked to
memorize the names of one or two objects, people with
amnestic disorders forget them in a
few minutes. This is why they feel as if they are continually
meeting “new” people and being
put into “new” situations.
Traumatic brain injury, stroke, exposure to highly toxic
substances, and brain disease tend to
produce amnestic disorders quickly, whereas drugs, chronic
substance abuse (especially of
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298
Section 10.4 Treatment and Prevention of Neurocognitive
Disorders
alcohol, sedative medications, and tranquilizers), and nutritional
deficiencies produce mem-
ory disorders that develop gradually. Permanent brain injury,
especially to the middle tempo-
ral lobes, usually produces an irreversible memory impairment.
An amnestic disorder, especially one caused by head trauma or
substance intoxication, may
begin with an episode of delirium. Because memory disorders
are also common in dementia,
care must be taken to rule out delirium and dementia before
making the diagnosis of amnes-

tic disorder. Amnestic disorders must also be distinguished from
the dissociative amnesias.
This distinction is not difficult to make. Unlike dissociative
disorders, amnestic disorders
always result from a general medical condition or a substance.
Another hallmark of amnestic
disorders is an inability to learn new material, whereas
dissociative disorders are typically
characterized by the forgetting of traumatic events.
One of the best-known amnestic disorders is Korsakoff ’s
syndrome, which is the result of pro-
longed alcohol abuse. The syndrome results from two causes:
(a) the poisoning of nerve cells
by alcohol and (b) a vitamin B (thiamine) deficiency caused by
the poor diet characteristic
of many heavy drinkers (Gerridzen et al., 2016). The disorder is
often accompanied by other
signs of alcohol poisoning, such as inflammation of the nerves
in the fingers and toes. Korsa-
koff ’s syndrome usually begins with an acute episode of
delirium. When the delirium clears,
the person is left with a severe memory deficit that affects
mainly new memories. Typically,
people with Korsakoff ’s syndrome can relate accurately the
events of their childhood but are
unable to say what happened an hour earlier. Despite their
apparent inability to form new
memories, people with Korsakoff ’s syndrome are not totally
incapable of learning. They may
be unable to verbalize facts and events, yet they may still be
able to learn unconsciously. For
example, people with Korsakoff ’s can draw a map, and estimate
the time it would take to
reach a destination by a particular route. Thus it appears that in
spite of the amnesia they

can still acquire spatial information (Oudman et al., 2016). It
seems as if explicit (verbalized)
learning is impaired, whereas implicit (unconscious) learning
can still take place (Gerridzen
et al., 2016). This learning can sometimes be enhanced by
drugs, particularly SSRIs (Martin
et al., 1995), but for most people with Korsakoff ’s, the memory
impairment is irreversible (de
la Monte & Kril, 2015).
10.4 Treatment and Prevention of
Neurocognitive Disorders
Some types of dementia (and even some amnestic disorders) are
reversible with treatment
(Burke & Bohac, 2001). Specifically, reversible causes of
dementia include some infections,
anemia, illicit substance use, emotional and psychological
issues, and some brain lesions
or tumors (Tripathi & Vibha, 2009). However, no single
treatment works for all cases (Neu-
groschl, Kolevzon, Samuels, & Marin, 2005). Treatment must
be tailored to the specific case.
Substance/medication-induced major or mild neurocognitive
disorder may be successfully
treated by removing the offending substance. Thyroxine (a
hormone produced by the thy-
roid gland) will usually reverse dementia (or at least prevent
further deterioration) in peo-
ple whose cognitive deficits are caused by hypothyroidism (low
levels of thyroxine). The
symptoms of Parkinson’s disease may be controlled, at least
temporarily, by L-dopa and,
perhaps more permanently, by transplants of dopamine-
producing brain tissue. Surgery

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299
Disorders
can sometimes reverse dementia caused by brain tumors, and
cognitive decline may also be
delayed by ensuring that older people have regular exercise and
good nutrition.
The symptoms of dementia and amnestic disorders may also be
minimized by treating asso-
ciated conditions. For example, antidepressant medications and
cognitive-behavioral modi-
fication may help to relieve the cognitive impairments caused
by the depression that often
accompanies dementia (Neugroschl et al., 2005). However, more
recent research has discov-
ered that although SSRIs and SNRIs (discussed in Chapter 6)
reduce major depressive disor-
der symptoms in those who also have dementia, the same
amount of decrease was seen in
a placebo control group. Therefore, it seems that, at least based
on this current study, anti-
depressants are not responsible for the depressive symptom
decrease, and therefore there
is little to suggest that antidepressants lead to cognitive
improvement (Farina, Morrell, &
Banerjee, 2017). In a similar manner, hallucinations and

delusions can be treated with anti-
psychotic medications, and the cognitive disturbances caused by
circulatory disease may be
relieved by vasodilator drugs that increase blood flow. Major or
mild vascular neurocognitive
disorder can also be reduced by eliminating aggravating factors,
such as hypertension, high
cholesterol, diabetes, and obesity (Khan et al., 2016).
Unfortunately, the majority of people with dementia fall into
category of major or mild neu-
rocognitive disorder due to Alzheimer’s disease. For them,
medical treatments are primitive,
at best. For example, the first drug approved to treat
Alzheimer’s was tacrine (Cognex), which
prevents the breakdown of acetylcholine, a neurotransmitter
known to be deficient in some
people with Alzheimer’s. The result was a modest improvement
in cognitive functioning
(Hasan & Mooney, 1994). Cognex was approved by the FDA in
1993. Soon afterward, it was
discovered to have little clinical efficacy in treating dementia
and was withdrawn shortly after
it received approval (Romero, Cacabelos, Oset-Gasque, Samadi,
& Marco-Contelles, 2013).
Donepezil (Aricept), which inhibits the breakdown of
acetylcholine but is less likely to cause
liver damage, is now in more common use. Aricept is not a cure
for Alzheimer’s nor a preven-
tive measure; it simply slows down the progression of the
disease, specifically preventing
acetylcholine breakdown in these patients (Julien, 2008). A
more recently approved medica-
tion, memantine (Namenda XR [extended release]) received
FDA approval in 2010. Namenda
works by blocking glutamate receptors and seems to have some

effect in slowing the cogni-
tive decline in patients with moderate to severe Alzheimer’s
disease, and in some instances
temporarily reducing symptoms. There is little evidence that it
is efficacious in slowing the
cognitive decline in patients with mild Alzheimer’s disease.
Because there is no specific medical cure for Alzheimer’s or
other forms of undifferentiated
dementia, treatment usually involves more than just drugs. It
also includes a variety of envi-
ronmental and psychological interventions. The aims of
treatment are to preserve the per-
son’s sense of independence and self-esteem, to keep up social
contacts, and to provide as
much enjoyment and meaning as is possible in clients’ lives and
in the lives of those who care
for them (Dobkin, Allen, & Menza, 2006).
If they cannot live at home, people with dementia and amnestic
disorders, and 75% of those
with Alzheimer’s, will almost always be sent to nursing homes
(Alzheimer’s Association, 2016;
Gatz, 2007). At age 80, 75% of surviving Alzheimer’s patients
are expected to be in a nurs-
ing home. Additionally, by the ages of 74 and 76, about 29%
and 48% of Alzheimer’s victims,
respectively, are expected to be in a nursing home (Alzheimer’s
Association, 2016). Although
they vary in standards, nursing homes are not ideal places for
people with dementia. They
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300
Disorders
focus mainly on the custodial aspects of care and often lack the
personnel qualified to deal
with the psychological features of dementia. Consequently,
people who live in nursing homes
often lose their sense of autonomy and self-worth. Without
significant intellectual challenge
and independence, their cognitive decline accelerates.
If possible, it is preferable to keep people with dementia and
amnestic disorders at home.
Often this requires certain modifications to both the home
environment and daily routines
(Clarkson et al., 2016). These modifications are designed to
foster the person’s sense of inde-
pendence and control. For example, hand rails permit a person
with apraxia to get around
the house and to use the bathroom without assistance. Colored
arrows drawn on floors help
people with dementia navigate around their homes without
getting lost, and memory aids
such as strategically placed reminders can help people to
function more or less independently
even while suffering from cognitive impairments (van Hoof,
Kort, van Waarde, & Blom, 2010).
Community services, such as meal preparation and visiting
nurses, are also helpful in allow-
ing people who would otherwise need institutional care to live
at home. (See the accompany-

ing Highlight.)
Because dementia often involves significant
disinhibition, sufferers have to be taught
to regulate their own behavior. Specifically,
they are trained to self-consciously scruti-
nize their behaviors and to silently remind
themselves about how they should behave
(Kohlenberg & Tsai, 1991). The idea is to
replace unconscious inhibitory mechanisms
with conscious ones.
It is much better to prevent neurocognitive
disorders than to treat them. Treating high
blood pressure reduces the probability of a
stroke, and low-fat diets and certain drugs
can prevent arteriosclerosis—two impor-
tant causes of vascular dementia. Early
diagnosis of diabetes mellitus and hypo-
thyroid conditions will reduce the chances that these conditions
will lead to neurocognitive
disorders. Programs designed to combat alcohol and drug abuse
and immunizations against
the causes of encephalitis and meningitis are also important
ways of preventing cognitive
disorders from developing.
lisafx/iStock/Thinkstock
Because a lack of intellectual stimulation and
independence accelerates cognitive decline,
it is important to help people maintain their
sense of autonomy.
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301
Chapter Summary
Chapter Summary
Dementia (Major Neurocognitive Disorder)
• The prevalence of dementia, in which cognitive functioning
falls from previous lev-
els, is increasing as the population ages.
• Dementia can be caused by a drug, an accident, or a medical
condition. It can have
specific symptoms (as in Huntington’s disease) or vague
uncertain ones.
• People with dementia always have a memory impairment.
They may also have a lan-
guage disorder, motor disabilities, disturbances in their ability
to plan, and various
agnosias (failures to recognize or identify objects despite intact
sensory function).
• Diagnosing dementia involves three steps: confirming the
presence of multiple cog-
nitive deficits, determining whether the deficits are lifelong or
acquired, and ruling
out conditions that are superficially similar to dementia (for
example, delirium and
depression).

Highlight: Issues Affecting Senior Citizens, and Some
Suggestions
In the United States, discrimination toward senior citizens (here
defined as those over the
age of 65) is common. Seniors often have problems getting
around their neighborhoods,
and they may have difficulty navigating stairs, getting to
doctor’s appointments, and
remembering to take their medications, to name just a few
issues. In addition, many seniors
suffer from unipolar depression. Perhaps many of their friends
have passed away and
they are widowed, a somewhat common occurrence. Many may
be totally alone, with their
children and grandchildren living far away or perhaps not
visiting due to the fear of seeing a
loved one with a cognitive disorder.
What can we do to work with senior citizens to make their later
years less stressful, more
fulfilling, and happier? It is crucial for seniors to continue to be
intellectually and cognitively
stimulated to keep their brains active and fresh. Some assisted
living centers and nursing
homes use video game systems, such as Nintendo’s Wii and the
new Switch, to engage
seniors in cognitive exercises, problem solving, as well as
physical exercise. (The Wii is
excellent in that it involves hand-eye coordination as well as
physical movement.) Awareness
of mental health issues and instituting proper treatment before
seniors become significantly
debilitated is also crucial.
Pet therapy, using trained dogs to calm agitated seniors and to

provide contact comfort,
is a somewhat new technique that is becoming more popular.
Research has demonstrated
that children who have autism spectrum disorder benefit from
spending time with guinea
pigs; the children tend to display more interactive social
behavior and become less anxious
(O’Haire, McKenzie, Beck, & Slaughter, 2015). Guinea pigs are
easy to care for, relatively
inexpensive, and irresistibly cute. Why not use them with
seniors, as a form of pet therapy?
Petting animals can be very calming, and seniors have a lot of
love to give. If this is not
realistic, a newer form of interactive pet, PARO, is a
possibility. PARO, an interactive robotic
Harp seal, was developed by AIST, a leading Japanese
industrial automation company. PARO
may reduce stress in seniors and in their caregivers, as well as
improve seniors’ socialization
with their caregivers. Although little if anything will replace
human-to-human contact and
interaction, if animal therapy is not available, perhaps PARO is
the next step in senior care.
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302
Chapter Summary
• Depression, which shares many symptoms with dementia,

usually has a more rapid
onset and a more fluctuating course.
• Delirium is a rapidly progressing disorder of consciousness.
Sufferers are forgetful,
confused, incoherent, and unaware of where they are or what is
going on around
them. Many are also anxious, fearful, and irritable.
• Any illness, injury, or substance that affects the brain has the
potential to cause
delirium. If delirium is due to a general medical condition,
treatment focuses on
curing the condition. If delirium is caused by a substance, it is
treated by gradually
withdrawing the substance.
• Alzheimer’s is the most common form of dementia, accounting
for more than half of
all cases.
• Alzheimer’s begins with a mild memory disturbance, which
gradually becomes more
obvious. Personality changes come next, followed by confusion,
disorientation, apha-
sia, agnosia, and apraxia.
• In the late stages, the person may lose control over bodily
functions.
• Alzheimer’s seems to run in families and is closely related to
Down syndrome.
• Major or mild vascular neurocognitive disorder is caused by a
sudden loss of blood
supply to parts of the brain, resulting in the destruction of
surrounding tissue. It

affects men more often than women, probably because of men’s
higher level of car-
diovascular disease.
• Substance/medication-induced major or mild neurocognitive
disorder is caused by a
substance and continues even after the substance is withdrawn.
Amnestic Disorders
• People with amnestic disorders have difficulty learning new
information and, in
some cases, may be unable to recall previously learned
information or events.
Distant events are often remembered better than recent ones,
and recall is usually
affected more than recognition.
• Traumatic brain injury, stroke, or exposure to toxic substances
can all produce an
acute amnestic disorder.
• Drugs, chronic substance abuse, and nutritional deficiencies
usually produce a more
gradually developing disorder.
• Although people with amnestic disorders have difficulty with
explicit verbal learn-
ing, they may still learn implicitly.
Treatment and Prevention of Neurocognitive Disorders
• Some types of dementia are reversible with treatment. Most
people with dementia
have Alzheimer’s, a condition for which drug treatments are
crude at best.

• Social-psychological treatment aimed at maintaining
independence and self-esteem
may be helpful.
• Antihypertensive treatment, careful control of diabetes
mellitus, immunizations
against certain viruses, remaining intellectually active, and
moderate use of alcohol
can help to prevent or delay the onset of dementia.
• People with dementia may benefit from psychological
interventions.
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303
Chapter Summary
Key Terms
agnosia A failure to recognize familiar
objects despite having normal sensory
abilities.
amnestic disorders Loss of past memories
or an inability to learn new information.
aphasia A language disorder in which
impairment or loss of language skills occurs;
usually associated with damage to the left

cerebral hemisphere.
apraxia An inability to carry out desired
motor actions despite normal muscle
control.
chorea Brain syndromes that include
irregular, jerky movements.
Creutzfeldt-Jakob disease A type of
dementia associated with symptoms similar
to those of tardive dyskinesia; symptoms
include walking with a stiff gait, trouble
maintaining balance, and difficulty control-
ling voluntary movements.
delirium A cognitive disorder marked by
rapid onset and fluctuating daily course,
plus a change in cognition including memory
deficit, disorientation, and reduced ability to
focus, sustain, or shift attention.
dementia Multiple cognitive deficits,
including memory deficits, disorientation,
concrete thinking, and perseveration (repet-
itive speech or movements).
disinhibition An inability to inhibit
impulses.
Critical Thinking Questions
1. This chapter notes the similarities between dementia and
depression. Discuss your
views on how these two disorders are similar or dissimilar. How
would you explain

to a family member the connection between the two disorders?
2. Major or mild neurocognitive disorder due to Alzheimer’s is
a rapidly increasing
health problem in the United States. Like many other disorders,
it was identified
years ago, yet it has no cure and there are no definitive ways to
prevent its onset. If
you were asked to research Alzheimer’s, what aspects would
you choose to investi-
gate and why?
3. Parkinson’s is another insidious disease that has no cure at
this time. Too little dopa-
mine is known to be a causal factor. If you were a researcher,
what else would you
investigate as possible causal factors, and why?
4. Alzheimer’s may run in families, which can be said about
many of the disorders in
this book. Give your opinion on how all of this knowledge
would impact preventive
measures for Alzheimer’s.
5. The chapter mentioned a number of treatment interventions
for dementia. Choose
two of those that were mentioned and discuss why you think
they would be the most
effective treatment methods.
6. The last Highlight in the chapter briefly discussed pet
therapy as a treatment adjunct
for patients with neurocognitive disorder. Discuss your views
on this, especially
focusing on your views about using robotic pets like PARO with
these individuals.

Will robots replace humans in treatment modalities?
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304
Chapter Summary
electroencephalograph (EEG) Recordings
of brain electrical activity made from the
scalp (or directly from within the brain).
episodic memory The type of long-term,
declarative memory in which we store
memories of personal experiences that are
tied to particular times and places.
executive functioning Those functions
of the brain that involve the ability to plan,
organize, sequence, initiate, monitor, and
stop complex behaviors.
hypothyroidism Low levels of thyroxine.
major neurocognitive disorder due to
Alzheimer’s disease A form of senile and
pre-senile dementia; symptoms include
trouble recognizing people and common
objects, frequent memory lapses, and diffi-
culty speaking. Personality changes can also
occur.

major or mild vascular neurocognitive
disorder (vascular dementia) A type of
dementia caused by a sudden loss of blood
supply to parts of the brain, resulting in the
destruction of surrounding tissue.
neurocognitive disorders A class of
disorders characterized by memory impair-
ment and any of a number of other cognitive
impairments including language distur-
bances, perceptual disturbances, impair-
ment in the capacity to plan and organize,
and failure to recognize or identify objects.
neurofibrillary tangles Neurofibrils are
narrow fibers found within neurons; in
Alzheimer’s patients, they are tangled and
disorganized.
Parkinson’s disease A type of dementia
caused by a dopamine deficiency; symptoms
include tremors, rigid muscles, and difficulty
initiating or stopping movements.
pseudo-dementia A diagnosis applied to
people who show all the signs of dementia
but are really suffering from depression.
semantic memory A type of long-term
memory in which we store general world
knowledge like facts, ideas, words, problem
solving, and the like.
stroke A condition caused by a blood clot
in one of the brain’s blood vessels that cuts

off the supply of blood to the surrounding
neural tissue.
subcortical dementia Some Parkinson’s
patients develop this condition; symptoms
consist mainly of psychomotor slowness and
a memory defect.
substance/medication-induced major
or mild neurocognitive disorder A type
of dementia caused by a substance (often
alcohol); the dementia continues even after
the substance is withdrawn.
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11 NeurodevelopmentalDisorders
Bowdenimages/iStock/Thinkstock
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.

get83787_11_c11_305-324.indd 310 2/16/18 4:49 PM
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).

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