Neurocognitive Disorders

CHAPTER OUTLINE
Perspectives on Neurocognitive
Disorders
Delirium
Clinical Description and Statistics
Treatment
Prevention
Major and Mild Neurocognitive
Disorders
Clinical Description and Statistics
Neurocognitive Disorder Due to
Alzheimer’s Disease
Vascular Neurocognitive Disorder
Other Medical Conditions That Cause
Neurocognitive Disorder
Substance/Medication-Induced
Neurocognitive Disorder
Causes of Neurocognitive Disorder
Treatment
Prevention
Christian MartÃ-nez Kempin/E+/Getty Images

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 [ student learning outcomes*
Use scientific reasoning to interpret behavior:
Engage in innovative and integrative thinking and
problem solving:
Describe applications that employ discipline-based
problem solving:
* Portions of this chapter cover learning outcomes suggested by the American Psychological Association
(2012) in its guidelines for the undergraduate psychology major. Chapter coverage of these outcomes is
identified above by APA Goal and APA Suggested Learning Outcome (SLO).
R
esearch on the brain and its role in psychopathology has
increased at a rapid pace, and we have described many of the
latest advances throughout this book. All the disorders we
have reviewed are in some way influenced by the brain. You have
seen, for example, that relatively subtle changes in neurotransmit-
ter systems can significantly affect mood, cognition, and behavior.
Unfortunately, the brain is sometimes affected profoundly, and,
when this happens, drastic changes occur. In earlier editions of this
book, the tone of this chapter was quite dark given the lack of infor-
mation on these cognitive disorders that impair all aspects of mental
functioning. The typically poor prognosis of the people afflicted led
to pessimistic conclusions. A great deal of new research is leading
us to be more optimistic about the future, however. For example,
we used to think that once neurons died there was no hope of any
replacement, yet we now know brain cells can regenerate even in
the aging brain (Stellos et al., 2010). In this chapter, we examine this
exciting new work related to the brain disorders that affect cognitive
processes such as learning, memory, and consciousness.
Perspectives on Neurocognitive Disorders
Most neurocognitive disorders develop much later in life, whereas
intellectual disability and specific learning disorder are believed to
be present from birth (see Chapter 14). In this chapter, we review
two classes of cognitive disorders: delirium, an often temporary
condition displayed as confusion and disorientation; and mild or
major neurocognitive disorder, a progressive condition marked by
gradual deterioration of a range of cognitive abilities.
The label “neurocognitive disorders” in DSM-5 reflects a shift in
the way these disorders are viewed (American Psychiatric Associa-
tion, 2013). In early editions of the DSM, they were labeled “organic
mental disorders,” along with mood, anxiety, personality, hallucino-
sis (an abnormal mental state involving hallucinations), and delu-
sional disorders. The word organic indicated that brain damage
or dysfunction was believed to be involved. The “organic mental
55618_ch15_ptg01_hr_542-569.indd 543
]
Identify basic biological, psychological, and social
components of behavioral explanations (e.g., inferences,
observations, operational definitions and interpretations)
(APA SLO 1.1a) (see textbook pages 557–560)
Describe problems operationally to study them
empirically. (APA SLO 1.3a) (see textbook pages 543–557)
Correctly identify antecedents and consequences of
behavior and mental processes (APA SLO 5.3c) (see
textbook pages 560–564). Describe examples of relevant
and practical applications of psychological principles to
everyday life (APA SLO 5.3a) (see textbook pages 560–564)
disorders” category, however, covered so many disorders that the
distinction was meaningless. Consequently, the traditional organic
disorders—delirium, dementia, and amnestic disorders—were kept
together, and the others—organic mood, anxiety, personality, hallu-
cinosis, and delusional disorders—were categorized with disorders
that shared their symptoms (such as anxiety and mood disorders).
Once the term organic was dropped, attention moved to devel-
oping a better label for delirium, dementia, and the amnestic dis-
orders. The label “cognitive disorders” was used in DSM-IV to
signify that their predominant feature is the impairment of such
cognitive abilities as memory, attention, perception, and think-
ing. Although disorders such as schizophrenia, autism spectrum
disorder, and depression also involve cognitive problems, cogni-
tive issues are not believed to be primary characteristics (Ganguli
et al., 2011). Problems still existed with the “cognitive disorder”
label, however, because although the cognitive disorders usu-
ally first appear in older adults, intellectual disability and specific
learning disorder (which are apparent early) also have cognitive
impairment as a predominant characteristic. Finally, in DSM-5,
neurocognitive disorders is the new category name for the vari-
ous forms of dementia and amnestic disorders, with “major” or
“mild” subtypes; DSM-5 retains the “delirium” label (American
Psychiatric Association, 2013). This new categorization was cre-
ated because of the overlap of the different types of dementia (e.g.,
Alzheimer’s disease) and amnestic disorder found in people such
that one person may actually suffer from multiple types of neuro-
cognitive problems (Ganguli et al., 2011).
As with certain other disorders, it may be useful to clarify why
neurocognitive disorders are discussed in a textbook on abnormal
psychology. Because they so clearly have organic causes, you could
argue that they are purely medical concerns. You will see, however,
that the consequences of a neurocognitive disorder often include
profound changes in a person’s behavior and personality. Intense
anxiety, depression, or both are common, especially among people
with major neurocognitive disorder. In addition, paranoia is often
P e r spe c t i ve s on Ne uro c o g ni t i v e D i sorders 543
25/11/13 2:11 PM
 reported, as are extreme agitation and aggression. Families and
friends are also profoundly affected by such changes. Imagine your
emotional distress as a loved one is transformed into a different
person, often one who no longer remembers who you are or your
history together. The deterioration of cognitive ability, behavior,
and personality and the effects on others are major concerns for
mental health professionals.
Delirium
The disorder known as delirium is characterized by impaired
consciousness and cognition during the course of several hours or
days. Delirium is one of the earliest-recognized mental disorders:
Descriptions of people with these symptoms were written more
than 2,400 years ago (Solai, 2009). Consider the case of Mr. J.
MR.J Sudden Distress
M r. J., an older gentleman, was brought to the hospital
emergency room. He didn’t know his own name, and
at times he didn’t seem to recognize his daughter, who was
with him. Mr. J. appeared confused, disoriented, and a little
agitated. He had difficulty speaking clearly and could not
focus his attention to answer even the most basic questions.
Mr. J.’s daughter reported that he had begun acting this way
the night before, had been awake most of the time since
then, was frightened, and seemed even more confused today.
She told the nurse that this behavior was not normal for
him and she was worried that he was becoming “senile.” She
mentioned that his doctor had just changed his hyperten-
sion medication and wondered whether the new medication
could be causing her father’s distress. Mr. J. was ultimately
diagnosed as having substance-induced delirium (a reaction
to his new medication); once the medication was stopped, he
improved significantly over the course of the next 2 days.
The preceding scenario is played out daily in most major
metropolitan hospital emergency rooms.
Clinical Description and Statistics
People with delirium appear confused, disoriented, and out of
touch with their surroundings. They cannot focus and sustain their
attention on even the simplest tasks. There are marked impair-
ments in memory and language (Meagher & Trzapacz, 2012). Mr.
J. had trouble speaking; he was not only confused but also couldn’t
remember basic facts, such as his own name. As you saw, the
symptoms of delirium do not come on gradually but develop over
hours or a few days, and they can vary over the course of a day.
Delirium is estimated to be present in approximately 20% of
older adults who are admitted into acute care facilities such as
emergency rooms (Meagher & Trzapacz, 2012). It is most preva-
lent among older adults, people undergoing medical procedures,
cancer patients, and people with acquired immune deficiency syn-
drome (AIDS). Delirium subsides relatively quickly. Once thought
54 4 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s
55618_ch15_ptg01_hr_542-569.indd 544
to be only a temporary problem, more recent work indicates that
the effects of delirium may be more lasting (Cole, Ciampi, Belzile, &
Zhong, 2009). Some individuals continue to have problems on and
off; some even lapse into a coma and may die. Concern by medical
professionals is increasing—perhaps because of the increased num-
ber of adults living longer—leading some to recommend that delir-
ium be included as one of the “vital signs” (along with heartbeat,
breathing rate, temperature, and blood pressure) that physicians
routinely check when seeing older adults (Flaherty et al., 2007).
Many medical conditions that impair brain function have
been linked to delirium, including intoxication by drugs and poi-
sons; withdrawal from drugs such as alcohol and sedative, hypnot-
ic, and anxiolytic drugs; infections; head injury; and various other
types of brain trauma (Meagher & Trzapacz, 2012). DSM-5 recog-
nizes several causes of delirium among its subtypes. The diagnosis
received by Mr. J.—substance-induced delirium—as well as delir-
ium not otherwise specified all include disruptions in the person’s
ability to direct, focus, sustain, and shift attention. The rise in the
use of drugs such as Ecstasy (methylene-dioxymethamphetamine)
is of particular concern because of such drugs’ potential to pro-
duce delirium (Solai, 2009). The last two categories indicate the
often complex nature of delirium.
That delirium can be brought on by the improper use of
medication is a particular problem for older adults, because
they tend to use prescription medications more than any other
age group. The risk of problems among the elderly is increased
further because they tend to eliminate drugs from their systems
less efficiently than younger individuals. It is not surprising,
then, that adverse drug reactions resulting in hospitalization are
almost 6 times higher among elderly people than in other age
groups (Olivier et al., 2009). And it is believed that delirium is
responsible for many of the falls that cause debilitating hip frac-
tures in the elderly (Stenvall et al., 2006). Although there has
been some improvement in the use of medication among older
adults with physicians using more care with drug dosages and
the use of multiple drugs, improper use continues to produce
serious side effects, including symptoms of delirium (Olivier
et al., 2009). Because possible combinations of illnesses and
medications are so numerous, determining the cause of delir-
ium is extremely difficult (Solai, 2009).
Delirium may be experienced by children who have high
fevers or who are taking certain medications and is often mistaken
for noncompliance (Smeets et al., 2010). It often occurs during
the course of dementia; as many as 50% of people with dementia
suffer at least one episode of delirium (Kwok, Lee, Lam, & Woo,
2008). Because many of the primary medical conditions can be
treated, delirium is often reversed within a relatively short time.
Yet, in about a quarter of cases, delirium can be a sign of the end
of life (Wise, Hilty, & Cerda, 2001). Factors other than medical
conditions can trigger delirium. Age itself is an important fac-
tor; older adults are more susceptible to developing delirium as a
result of mild infections or medication changes (Fearing & Inouye,
2009). Sleep deprivation, immobility, and excessive stress can also
cause delirium (Solai, 2009).
Researchers studying the brain functioning of persons
with and without delirium are beginning to understand the
mechanisms underlying this disorder of attention. In one study,
25/11/13 2:11 PM
 nonmedical treatment is to
DSM
5
TABLE 15.1 Diagnostic Criteria for Delirium reassure the individual to help
him or her deal with the agi-
tation, anxiety, and hallucina-
A. A disturbance in attention (i.e., reduced ability to direct, tions of delirium. A person in
focus, sustain, and shift attention) and awareness the hospital may be comforted
(reduced orientation to the environment). by familiar personal belongings
B. The disturbance develops over a short period of time such as family photographs

(usually hours to a few days), represents a change from
baseline attention and awareness, and tends to fluctuate
in severity during the course of a day.
C. An additional disturbance in cognition (e.g., memory
deficit, disorientation, language, visuospatial ability, or
perception).
D. The disturbances in Criteria A and C are not better
explained by another preexisting, established, or
evolving neurocognitive disorder and do not occur in
the context of a severely reduced level of arousal,
such as coma.
E. There is evidence from the history, physical examina-
tion, or laboratory findings that the disturbance is a
direct physiological consequence of another medical
condition, substance intoxication or withdrawal (i.e., due
to a drug of abuse or to a medication), or exposure to a
toxin, or is due to multiple etiologies.
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
scientists assessed brain activity using fMRI scanning during
active episodes of delirium as well as after these episodes and
found both lasting disruption of connectivity (between the dor-
solateral prefrontal cortex with the posterior cingulate cortex)
as well as reversible disruptions (such as between the thalamus
with the reticular activating system) (S.-H. Choi et al., 2012).
Although such research is potentially important for efforts to
both prevent and treat delirium, there are potential ethical
concerns. For example, a person experiencing delirium is not
capable of providing informed consent for participating in such
research and therefore someone else (e.g., a spouse or relative)
must agree. In addition, fMRI testing can be anxiety-provoking
for many people and was possibly very frightening for some-
one already so disoriented (Gaudreau, 2012). We discuss these
issues in more detail in Chapter 16.
Treatment
Delirium brought on by withdrawal from alcohol or other drugs
is usually treated with haloperidol or other antipsychotic medica-
tions, which help calm the individual. Infections, brain injury, and
tumors are given the necessary and appropriate medical interven-
tion, which often then resolves the accompanying delirium. The
antipsychotic drugs haloperidol or olanzapine are also prescribed
for individuals in acute delirium when the cause is unknown
(Meagher & Trzapacz, 2012).
The recommended first line of treatment for a person
experiencing delirium is psychosocial intervention. The goal of
©Richard Hutchings/PhotoEdit
(Fearing & Inouye, 2009). Also,
a patient who is included in
all treatment decisions retains
a sense of control (Katz, 1993).
This type of psychosocial treat-
ment can help the person
manage during this disruptive Elderly patients with delirium
period until the medical causes in care facilities are often com-
are identified and addressed forted by having their personal
belongings nearby.
(Breitbart & Alici, 2012). Some
evidence suggests that this type of support can also delay institu-
tionalization for elderly patients (Rahkonen et al., 2001).
Prevention
Preventive efforts may be most successful in assisting people who
are susceptible to delirium. Proper medical care for illnesses and
therapeutic drug monitoring can play significant roles in prevent-
ing delirium (Breitbart & Alici, 2012). For example, the increased
number of older adults involved in managed care and patient
counseling on drug use appear to have led to more appropriate use
of prescription drugs among the elderly (U.S. General Accounting
Office, 1995).
Concept Check 15.1
Match the terms with the following descriptions of delirium:
(a) memory, (b) cause, (c) counseling, (d) confused, (e) elderly,
and (f) trauma.
1. Managed care and patient ____________ have been
successful in preventing delirium in older adults.
2. Treatment of delirium depends on the ____________ of
the episode and can include medications, psychosocial
intervention, or both.
3. Delirium severely affects people’s ____________, making
tasks such as recalling one’s own name difficult.
4. The ____________ population is at the greatest risk of
experiencing delirium resulting from improper use of
medications.
5. Various types of brain ____________, such as head
injury or infection, have been linked to delirium.
6. People who suffer from delirium appear to be
____________ or out of touch with their surroundings.

D e lirium 545

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 Major and Mild Neurocognitive Disorders
Few things are more frightening than the possibility of one day not
recognizing those you love, not being able to perform the most
basic of tasks and, worse yet, being acutely aware of this failure of
your mind. When family members show these signs, initially adult
children often deny any difficulty, coming up with excuses (“I forget
things, too”) for their parents’ failing abilities. Major neurocogni-
tive disorder (previously labeled dementia) is a gradual deteriora-
tion of brain functioning that affects memory, judgment, language,
and other advanced cognitive processes. Mild neurocognitive dis-
order is a new DSM-5 disorder that was created to focus attention
on the early stages of cognitive decline. Here the person has modest
DSM
5
TABLE 15.2 Diagnostic Criteria for Major
Neurocognitive Disorder
A. Evidence of significant cognitive decline from a previous
level of performance in one or more cognitive domains
(complex attention, executive function, learning and
memory, language, perceptual-motor, or social cognition)
based on:
1. Concern of the individual, a knowledgeable infor-
mant, or the clinician that there has been a significant
decline in cognitive function; and
2. A substantial impairment in cognitive performance,
preferably documented by standardized neuropsy-
chological testing or, in its absence, another quanti-
fied clinical assessment.
B. The cognitive deficits interfere with independence in
everyday activities (i.e., at a minimum, requiring assis-
tance with complex instrumental activities of daily living
such as paying bills or managing medications).
C. The cognitive deficits do not occur exclusively in the
context of a delirium.
D. The cognitive deficits are not better explained by an-
other mental disorder (e.g., major depressive disorder,
schizophrenia).
Specify whether due to:
Alzheimer’s disease
Frontotemporal lobar degeneration
Lewy body disease
Vascular disease
Traumatic brain injury
Substance/medication use
HIV infection
Prion disease
Parkinson’s disease
Huntington’s disease
Another medical condition
Multiple etiologies
Unspecified
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
54 6 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s
55618_ch15_ptg01_hr_542-569.indd 546
impairments in cognitive abilities but can, with some accommoda-
tions (for example, making extensive lists of things to do or creat-
ing elaborate schedules), continue to function independently.
Causes of neurocognitive disorders include several medi-
cal conditions and the abuse of drugs or alcohol that produce
negative changes in cognitive functioning. Some of these
conditions—for instance, infection or depression—can cause
neurocognitive impairment, although it is often reversible
through treatment of the primary condition. Some forms of the
disorder, such as Alzheimer’s disease, are at present irrevers-
ible. Although delirium and neurocognitive disorder can occur
DSM
5
TABLE 15.3 Diagnostic Criteria for Mild
Neurocognitive Disorder
A. Evidence of modest cognitive decline from a previous
level of performance in one or more cognitive domains
(complex attention, executive function, learning and
memory, language, perceptual motor, or social cognition)
based on:
1. Concern of the individual, a knowledgeable infor-
mant, or the clinician that there has been a mild
decline in cognitive function; and
2. A modest impairment in cognitive performance,
preferably documented by standardized neuropsy-
chological testing or, in its absence, another quanti-
fied clinical assessment.
B. The cognitive deficits do not interfere with capacity
for independence in everyday activities (i.e., complex
instrumental activities of daily living such as paying bills
or managing medications are preserved, but greater
effort, compensatory strategies, or accommodation may
be required).
C. The cognitive deficits do not occur exclusively in the
context of a delirium.
D. The cognitive deficits are not better explained by
another mental disorder (e.g., major depressive
disorder, schizophrenia).
Specify whether due to:
Alzheimer’s disease
Frontotemporal lobar degeneration
Lewy body disease
Vascular disease
Traumatic brain injury
Substance/medication use
HIV infection
Prion disease
Parkinson’s disease
Huntington’s disease
Another medical condition
Multiple etiologies
Unspecified
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
25/11/13 2:12 PM
 together, neurocognitive disorder has a gradual progression as to the brain such as stroke (which destroys blood vessels), the
opposed to delirium’s acute onset; people with neurocognitive infectious diseases of syphilis and HIV, severe head injury, the
disorder are not disoriented or confused in the early stages, introduction of certain toxic or poisonous substances, and dis-
unlike people with delirium. Like delirium, however, neurocog- eases such as Parkinson’s, Huntington’s, and, the most common
nitive disorder has many causes, including a variety of traumas cause of dementia, Alzheimer’s. Consider the personal account
Pat Summitt:
Grit and Determination
Simon Bruty/Sports Illustrated/Getty Images
chest and I said, “Hey, Tyler, I’ve been
waitin’ on you.” (pp. 6–7)
Her memory for important
experiences that occurred years ago
remains intact. However, recent expe-
riences and facts are more elusive.
She then goes on to describe some of
the things she no longer remembers.
A
Sometimes, when I first wake up,
t the age of 57, Pat Summitt was a
I don’t remember where I am. For a
highly successful basketball coach
moment I’m disoriented and uneasy,
and mother, but she was beginning to
and I have to lie there until it comes
experience lapses in her memory.
to me.
Friends started asking, “Are you Occasionally when I’m asked a
having trouble with your memory?” question, I begin to answer it but then
Finally I admitted, “Sometimes I draw I forget the subject—it slips away like
blanks.” I grew uncertain, and then a thread through my fingers.
a little frightened. I began staying in I struggle to remember directions.
bed until late in the morning, which There are moments when I’m driving
was unlike me. I’d always been a to someplace I should know, and I
bolter, the first person up and the have to ask, “Do I go left or right here?”
most energetic one, too, and I’d I tend not to remember what hotel
always gone to work earlier than room I’m in. I don’t remember what
anyone on my staff. But I began to times my appointments are. (p. 7)
dread going into the office. (p. 11)
Many people who begin to have these
Despite having cognitive difficulties, not cognitive difficulties retell these initial
all of her memories are lost to her in this experiences as incredibly frightening.
initial stage of the disease. She begins her However, Pat Summitt is known for her
memoir with the things she remembers. tough determination both on the basket-
ball court and now battling Alzheimer’s
I remember a tiny saloon in the
disease. Her reaction to her diagnosis and
Tennessee hills where the bartender
her doctor’s recommendations show an
squirted bourbon shots from a squeeze
incredible level of courage and strength.
bottle, straight into the customers’
mouths. I remember teaching a clinic In my case, symptoms began to
to other coaches and opening the floor appear when I was only 57. In fact,
for questions, and a guy raised his hand the doctors believe early-onset
and asked if I had any advice when it Alzheimer’s has a strong genetic
came to “coaching women.” I remem- predictor, and that it may have been
ber leveling him with a death ray stare progressing hidden in me for some
and then relaxing and curling up the years before I was diagnosed. I’d been
corner of my mouth and saying, “Don’t walking around with a slow-ticking,
worry about coaching ‘women.’ Just go slow-exploding bomb in my brain
home and coach ‘basketball.’” (p. 6) cells, and it only became apparent
I remember the night my son was when it began to seriously interfere
born. The doctor placed him on my with my work. (p. 9)
Major a n d Mi l d Ne u ro c o g ni ti ve D i sorder s
55618_ch15_ptg01_hr_542-569.indd 547
The doctor told me that given my
diagnosis, frankly, he felt I could no
longer work at all. I should step down
immediately, because in his opinion
the dementia would progress rapidly. I
needed to quit, and get myself out of
the public eye as quickly as possible,
or I would “embarrass” myself and
ruin my legacy. As he spoke, I felt my
fist clench. It was all I could do not to
lunge across the desk and drop him
with one punch. Who did he think he
was? Even if I had an irreversible brain
disease—even if I did—what right did
he have to tell me how to cope with
it? Quit? Quit? (pp. 17–18)
She goes on to write about her unusu-
ally practical and optimistic perspective
on having Alzheimer’s disease—a view
of this degenerative disease that should
serve as a role model for the millions of
people impacted by this disorder.
Above all, I know that Alzheimer’s
has brought me to a point that I was
going to arrive at someday anyway.
With or without this diagnosis, I was
going to experience diminishment.
We all do. It’s our fate. No, I can’t size
up a court of ten players anymore,
see the clock out of one eye and
the shifting schemes of opposing
players with the other, and order up
a countermove by hollering “Five!”
or “Motion!” But I can suggest that
people with mild to moderate stages
of dementia have far more abili-
ties than incapacities. I can suggest
that just because certain circuits of
memory or swiftness of synapses
may fail, thought and awareness and
consciousness do not. (p. 375)
Source: Summitt, P. H. (2013). Sum it up: A
thousand and ninety-eight victories, a couple
of irrelevant losses, and a life in perspective.
New York: Crown Archetype.
547
25/11/13 2:12 PM
 by Pat Summitt, the most successful NCAA basketball coach of
all time. She coached the Tennessee Lady Vols basketball team
from 1974 to 2012—winning a record setting 1,098 games—
until her symptoms of neurocognitive disorder due to Alzheim-
er’s disease prevented her from working with the team full-time.
She courageously writes of her experiences with this disorder
(Summitt, 2013).
After several evaluations, which included neurological evalu-
ations, magnetic resonance imaging (MRI) showing some dam-
age in several parts of her brain, and a spinal tap that showed
the presence of beta amyloid protein, Pat Summitt’s neurologist
concluded that she had early onset neurocognitive disorder due
to Alzheimer’s disease. People at the same stage of decline as she
will continue to deteriorate and eventually may die from compli-
cations of their disorder.
Clinical Description and Statistics
Depending on the individual and the cause, the gradual pro-
gression of neurocognitive disorder may have somewhat differ-
ent symptoms, although all aspects of cognitive functioning are
eventually affected. In the initial stages, memory impairment is
typically seen as an inability to register ongoing events. In other
words, a person can remember how to talk and may remember
events from many years ago but will have trouble remembering
what happened in the past hour. For example, Pat Summitt had
vivid recollections about her childhood but could not remember
which direction to drive in familiar places.
Pat Summitt couldn’t find her way home because visuo-
spatial skills are impaired among people with neurocognitive
disorder. Agnosia, the inability to recognize and name objects,
is one of the most familiar symptoms. Facial agnosia, the inabil-
ity to recognize even familiar faces, can be extremely distress-
ing to family members. A general deterioration of intellectual
function results from impairment in memory, planning, and
abstract reasoning.
Perhaps partly because people suffering from neurocogni-
tive disorder are aware that they are deteriorating mentally,
emotional changes often occur as well. Common side effects are
delusions (irrational beliefs), depression, agitation, aggression,
and apathy (Lovestone, 2012). It is difficult, however, to estab-
lish the cause-and-effect relationship. It is not known how much
behavioral change is caused by progressive brain deterioration
directly and how much is a result of the frustration and discour-
agement that inevitably accompany the loss of function and the
isolation of “losing” loved ones. Cognitive functioning contin-
ues to deteriorate until the person requires almost total support
to carry out day-to-day activities. Ultimately, death occurs as
the result of inactivity, combined with the onset of other illness-
es, such as pneumonia.
Globally, it is estimated that one new case of major neurocog-
nitive disorder is identified every 7 seconds (Ferri et al., 2005).
Major neurocognitive disorder can develop at almost any age,
although this disorder is more frequent in older adults. Estimates
in the United States suggest a prevalence of a little more than 5%
in people older than 65; this rate increases to 20%–40% in those
older than 85 (Richards & Sweet, 2009). The increasing number
of people with just one form of neurocognitive disorder—due to
54 8 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s
55618_ch15_ptg01_hr_542-569.indd 548
Alzheimer’s disease—is alarming. ● Figure 15.1 illustrates how
the prevalence of neurocognitive disorder due to Alzheimer’s
disease is projected to dramatically increase in older adults,
partly as a result of the increase of baby boomers who will
become senior citizens (Hebert, Weuve, Scherr, & Evans, 2013).
Among the eldest of adults, research on centenarians (people
100 years and older) indicates that up to 100% showed signs
of neurocognitive disorder (Imhof et al., 2007). Neurocogni-
tive disorder due to Alzheimer’s disease rarely occurs in people
under 45 years of age.
A dramatic rise in Alzheimer’s disease is predicted through the
year 2050 as larger numbers of people are expected to live beyond
85 years of age.
Estimates of the prevalence of the new DSM-5 diagnosis—
mild neurocognitive disorder—have been studied by the
Einstein Aging Study at Yeshiva University (Katz et al., 2012).
Researchers recruited 1,944 adults aged 70 or older and assessed
them for mild neurocognitive disorder as well as mild amnestic
neurocognitive disorder in this group. This latter disorder—
in its more severe state—was previously a separate DSM
disorder (amnestic disorder) but has been folded into the gen-
eral neurocognitive disorder group. Almost 10% of those over
70 had mild neurocognitive disorder and 11.6% met the cri-
teria for mild amnestic neurocognitive disorder. Race also
seemed to be a factor with black men and women at higher risk
for mild neurocognitive disorder than white men and women
(Katz et al., 2012).
Aged 65-74 years
Aged 75-84 years
Aged 85 years or older
Total
16
14
12
10
Millions
8
6
4
2
0
2010 2015 2020 2030 2040 2050
Year
● FIGURE 15.1 With the increasing numbers of persons living longer,
the rate of Alzheimer’s disease is predicted to escalate dramatically through
the year 2050. (From Hebert, L. E., Weuve, J., Scherr, P. A., & Evans, D. A.
(2013). Alzheimer disease in the United States (2010–2050) estimated using
the 2010 census. Neurology, 80(19), 1778–1783.)
25/11/13 2:12 PM
 A problem with confirming prevalence figures for neurocog-
nitive disorder is that survival rates alter the outcomes. Because
adults are generally living longer and are therefore more at risk
of developing neurocognitive disorder, it is not surprising that
the disorder is more prevalent. Incidence studies, which count
the number of new cases in a year, may thus be the most reliable
method for assessing the frequency of neurocognitive disorder,
especially among the elderly. Research shows that the rate for
new cases doubles with every 5 years of age after age 75. Many
studies find greater increases of neurocognitive disorder among
women (Carter, Resnick, Mallampalli, & Kalbarczyk, 2012).
Neurocognitive disorder due to Alzheimer’s disease may, as we
discuss later, be more prevalent among women. Together, results
suggest that neurocognitive disorder is relatively common
among older adults and the chances of developing it increase
rapidly after the age of 75.
In addition to the human costs of neurocognitive disorder, the
financial costs are staggering. Estimates of the costs of caring for
people with neurocognitive disorder due to Alzheimer’s disease
are often quoted to be about $100 billion per year in the United
States. One estimate indicates that the total worldwide societal
cost of major neurocognitive disorder is more than $315 billion
(Wimo, Winblad, & Jonsson, 2007). These numbers do not, how-
ever, factor in the costs to businesses for health care in the form of
insurance and for those who care for these individuals—estimated
to be more than $140 billion in the United States alone (Weiner et
al., 2010). Many times, family members care for an afflicted person
around the clock, which is an inestimable personal and financial
commitment (Lovestone, 2012).
DSM-5 identifies classes of neurocognitive disorder based on
etiology: (1) Alzheimer’s disease, (2) vascular injury, (3) fronto-
temporal degeneration, (4) traumatic brain injury, (5) Lewy body
disease, (6) Parkinson’s disease, (7) HIV infection, (8) substance
use, (9) Huntington’s disease, (10) prion disease, and (11) another
medical condition. We emphasize neurocognitive disorder due to
Alzheimer’s disease because of its prevalence (almost half of those
with neurocognitive disorder exhibit this type) and the relatively
large amount of research conducted on its etiology and treatment.
©Francisco Cruz/SuperStock
People with facial agnosia, a common symptom of neurocognitive
disorder, are unable to recognize faces, even of their closest friends
and relatives.
55618_ch15_ptg01_hr_542-569.indd 549
Neurocognitive Disorder Due to Alzheimer’s Disease
In 1907 the German psychiatrist Alois Alzheimer first described
the disorder that bears his name. He wrote of a 51-year-old woman
who had a “strange disease of the cerebral cortex” that manifested
as progressive memory impairment and other behavioral and
cognitive problems, including suspiciousness (Richards & Sweet,
2009). He called the disorder an “atypical form of senile demen-
tia”; thereafter, it was referred to as Alzheimer’s disease.
Description and Statistics
The DSM-5 diagnostic criteria for neurocognitive disorder due
to Alzheimer’s disease include multiple cognitive deficits that
develop gradually and steadily. Predominant are impairment of
memory, orientation, judgment, and reasoning. The inability to
integrate new information results in failure to learn new associa-
tions. Individuals with Alzheimer’s disease forget important events
and lose objects. Their interest in nonroutine activities narrows.
They tend to lose interest in others and, as a result, become more
socially isolated. As the disorder progresses, they can become agi-
tated, confused, depressed, anxious, or even combative. Many of
these difficulties become more pronounced late in the day—in a
phenomenon referred to as “sundowner syndrome”—perhaps as
a result of fatigue or a disturbance in the brain’s biological clock
(Lemay & Landreville, 2010).
People with neurocognitive disorder due to Alzheimer’s
disease also display one or more other cognitive disturbances,
including aphasia (difficulty with language), apraxia (impaired
motor functioning), agnosia (failure to recognize objects), or
difficulty with activities such as planning, organizing, sequencing,
or abstracting information. These cognitive impairments have a
serious negative impact on social and occupational functioning,
and they represent a significant decline from previous abilities.
Research using brain scans is being conducted on people with
mild neurocognitive disorder to see whether changes in brain
structure early in the development of Alzheimer’s disease can be
detected, which could lead to early diagnosis. In the past, a defini-
tive diagnosis of Alzheimer’s disease could be made only after an
autopsy determined that certain characteristic types of damage
were present in the brain. There is now growing evidence, how-
ever, that the use of sophisticated brain scans along with new
chemical tracers may soon be able to help clinicians identify the
presence of Alzheimer’s disease before the significant declines in
cognitive abilities (through a project called the Alzheimer’s Dis-
ease Neuroimaging Initiative [ADNI]) or death (Douaud et al.,
2013; Weiner et al., 2012b). In addition, research on the presence
of certain markers for Alzheimer’s (e.g., beta amyloid—the sub-
stance in the amyloid plaques found in the brains of persons with
this disease) in spinal fluid also appears to increase the accuracy
of a diagnosis (Vanderstichele et al., 2012). Currently, to make a
diagnosis without direct examination of the brain, a simplified
version of a mental status exam is used to assess language and
memory problems (see Table 15.1).
In an interesting, somewhat controversial study—referred
to as the “Nun Study”—the writings of a group of Catholic nuns
collected over several decades appeared to indicate early in life
which women were most likely to develop Alzheimer’s disease
later (Snowdon et al., 1996). Researchers observed that samples
Major a n d Mi l d Ne u ro c o g ni ti ve D i sorder s 549
25/11/13 2:12 PM
 TABLE 15.1 Testing for Neurocognitive Disorder due to Alzheimer’s Disease
Type* Maximum Score† Question

Orientation 5 Ask the patient, “What is the (year) (season) (date) (day) (month)?”
5 Ask the patient, “Where are we—(state) (country) (town) (hospital) (floor)?”

Registration 3 Name three objects, using 1 second to say each. Then ask the patient all
three after you have said them. (Give one point for each correct answer.)
Then repeat them until the patient learns all three. (Count and record the
number of trials.)

Attention and Calculation 5 Count backward from given number (like 100) by subtracting 7s. (Give one
point for each correct answer; stop after five answers.) Alternatively, spell
“world” backward.

Recall 3 Have the patient name the three objects learned previously. (Give one
point for each correct answer.)

Language 9 Have the patient name a pencil and a watch. (1 point)

Have the patient repeat the following: “No ifs, ands, or buts.” (1 point)
Have the patient follow a three-stage command: “Take a piece of paper in
your right hand, fold it in half, and put it on the floor.” (3 points)
Have the patient read and obey the following: “Close your eyes.” (1 point)
Have the patient write a sentence. (1 point)
Have the patient copy a design. (1 point)

Note: One part of the diagnosis of the neurocognitive disorder due to Alzheimer’s disease uses a relatively
simple test of the patient’s mental state and abilities, like this one, called the Mini Mental State Inpatient
Consultation Form. A low score on such a test does not necessarily indicate a medical diagnosis of the disorder.
*The examination also includes an assessment of the patient’s level of consciousness: alert, drowsy, stupor, or coma.
†
Total maximum score is 30.
Adapted from the Mini Mental State Inpatient Consultation Form (Folstein, Folstein, & McHugh, 1975).

from the nuns’ journals over the years differed in the number of
ideas each contained, which the scientists called “idea density.” In
other words, some sisters described events in their lives simply: “I
was born in Eau Claire, Wis, on May 24, 1913 and was baptized
in St. James Church.” Others were more elaborate in their prose:
“The happiest day of my life so far was my First Communion Day
which was in June nineteen hundred and twenty when I was but
eight years of age, and four years later in the same month I was
confirmed by Bishop D. D. McGavich” (Snowdon et al., 1996, pg.,
530). When findings of autopsies on 14 of the nuns were correlated
with idea density, the simple writing (low idea density) occurred
among all 5 nuns with Alzheimer’s disease (Snowdon et al., 1996).
This is an elegant research study, because the daily lives of the nuns
were similar, which ruled out many other possible causes. There
is some concern, however, about overgeneralizing from this one
study and we must be cautious about depending too much on
these observations, because only a small number of people were
examined. It is not yet clear that neurocognitive disorder due to
Alzheimer’s disease has such early signs, but research continues
in the hope of early detection so that early intervention can be
developed (Farias et al., 2012; Tyas et al., 2007).
Cognitive deterioration with Alzheimer’s disease is slow dur-
ing the early and later stages but more rapid during the middle
stages (Richards & Sweet, 2009). The average survival time is
estimated to be about 8 years, although many individuals live
dependently for more than 10 years. In some forms, the dis-
ease can occur relatively early, during the 40s or 50s (sometimes
referred to as early onset), but it usually appears during the 60s
or 70s. Approximately 50% of the cases of neurocognitive dis-
order are found to be the result of Alzheimer’s disease, which is
believed to afflict more than 5 million Americans and millions
more worldwide (Alzheimer’s Association, 2010).
Some early research on prevalence suggested that Alzheimer’s
disease may occur more often in people who are poorly educated
(Fratiglioni et al., 1991; Korczyn, Kahana, & Galper, 1991). Great-
er impairment among uneducated people might indicate a much
earlier onset, suggesting that Alzheimer’s disease causes intellec-
tual dysfunction that in turn hampers educational efforts. Or there
could be something about intellectual achievement that prevents
or delays the onset of symptoms of the disorder. Later research
seems to confirm the latter explanation. It appears that educational
level may predict a delay in the observation of symptoms (Pernec-
zky et al., 2009). Unfortunately, people who attain a higher level
of education also decline more rapidly once the symptoms start
to occur (Scarmeas, Albert, Manly, & Stern, 2006), suggesting that
education does not prevent Alzheimer’s disease but just provides
a buffer period of better functioning. Educational attainment may
somehow create a mental “reserve,” a learned set of skills that help
someone cope longer with the cognitive deterioration that marks
the beginning of neurocognitive deficits. Some people may adapt
more successfully than others and thus escape detection longer.
Brain deterioration may thus be comparable for both groups, but
better-educated individuals may be able to function successfully
on a day-to-day basis for a longer period. This tentative hypoth-
esis may prove useful in designing treatment strategies, especially
during the early stages of the disorder.

55 0 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s

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 A biological version of this theory—
the cognitive reserve hypothesis—
suggests that the more synapses a per-

© Tim Beddow/Science Source/Photo

© Tim Beddow/Science Source/Photo

son develops throughout life, the more
neuronal death must take place before
the signs of dementia are obvious
(Farias et al., 2012). Mental activity

Researchers, Inc.

Researchers, Inc.
that occurs with education presumably
builds up this reserve of synapses and
serves as an initial protective factor in
the development of the disorder. It is
likely that both skill development and The PET scan of a brain afflicted with Alzheimer’s disease (left) shows significant tissue deteriora-
the changes in the brain with educa- tion in comparison with a normal brain (right).
tion may contribute to how quickly the
disorder progresses. and important study—the Women’s Health Initiative Memory
Research suggests that Alzheimer’s disease may be more Study—looked at hormone use among women and its effect on
prevalent among women (Craig & Murphy, 2009), even when Alzheimer’s disease (Shumaker et al., 2004). In its initial findings,
women’s higher survival rate is factored into the statistics. In the study followed women over age 65 using a type of combined
other words, because women live longer than men on average, estrogen plus progestin known as Prempro and, contrary to the
they are more likely to experience Alzheimer’s and other diseases, belief that giving women estrogen would decrease their chance of
but longevity alone does not account for the higher prevalence developing neurocognitive disorder, they observed an increased
of the disorder among women. A tentative explanation involves risk for Alzheimer’s disease (Coker et al., 2010). More research
the hormone estrogen. Women lose estrogen as they grow older, is ongoing into the individual effects of these two types of
so perhaps estrogen is protective against the disease. A large hormones on dementia.

DSM
5
TABLE 15.4 Diagnostic Criteria for Major or Mild Neurocognitive Disorder due to Alzheimer’s Disease

A. The criteria are met for major or mild neurocognitive disorder.

B. There is insidious onset and gradual progression of impairment in one or more cognitive domains (for major neurocognitive
disorder, two domains must be impaired).
C. Criteria are met for either probable or possible Alzheimer’s disease as follows:
For major neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if either of the following is present; otherwise, possible Alzheimer’s disease should be
diagnosed.
1. Evidence of a causative Alzheimer’s disease genetic mutation from family history or genetic testing
2. All three of the following are present:
a. Clear evidence of decline in memory and learning and at least one other cognitive domain (based on detailed history or
serial neuropsychological testing).
b. Steadily progressive, gradual decline in cognition, without extended plateaus.
c. No evidence of mixed etiology (i.e., absence of other neurodegenerative or cerebrovascular disease, or another neuro-
logical, mental, or systemic disease or condition likely contributing to cognitive decline).
For mild neurocognitive disorder:
Probable Alzheimer’s disease is diagnosed if there is evidence of a causative Alzheimer’s disease genetic mutation from either
genetic testing or family history.
Possible Alzheimer’s disease is diagnosed if there is no evidence of a causative Alzheimer’s disease genetic mutation from either
genetic testing or family history, and all three of the following are present:
1. Clear evidence of decline in memory and learning.
2. Steadily progressive, gradual decline in cognition, without extended plateaus.
3. No evidence of mixed etiology (i.e., absence of other neurodegenerative or cerebrovascular disease, or another neurological
or systemic disease or condition likely contributing to cognitive decline).
D. The disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a
substance, or another mental, neurological, or systemic disorder.

From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC.

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 Finally, there appear to be questions about the prevalence of
Alzheimer’s disease according to racial identity. Early research
seemed to suggest that certain populations (such as those with
Japanese, Nigerian, certain Native American, and Amish back-
grounds) were less likely to be affected (for example, see Pericak-
Vance et al., 1996; Rosenberg et al., 1996). More recent work
indicates, however, that some of these differences may have been
the result of differences in who seeks assistance (which is seen as
unacceptable in some cultural groups), as well as differences in
education (which we saw may delay the onset of obvious symp-
toms) (Wilson et al., 2010). Alzheimer’s disease is found in roughly
the same numbers across all ethnic groups, with one study find-
ing a slightly lower rate among American Indians (Weiner, Hynan,
Beekly, Koepsell, & Kukull, 2007). As you will see, findings like
these help bring us closer to understanding the causes of this
devastating disease.
Vascular Neurocognitive Disorder
Each year, 500,000 people die from strokes (any diseases or trau-
mas to the brain that result in restriction or cessation of blood flow).
Although stroke is the third-leading cause of death in the United
States, many people survive, but one potential long-term consequence
can be severely debilitating. Vascular neurocognitive disorder is
a progressive brain disorder that is a common cause of neurocogni-
tive deficits. It is one of the more common causes of neurocognitive
disorder (Erkinjuntti, 2012).
Description and Statistics
The word vascular refers to blood vessels. When the blood ves-
sels in the brain are blocked or damaged and no longer carry oxy-
gen and other nutrients to certain areas of brain tissue, damage
results. Because multiple sites in the brain can be damaged, the
profile of degeneration—the particular skills that are impaired—
differs from person to person. DSM-5 lists as criteria for vascular
neurocognitive disorder cognitive disturbances such as declines
in speed of information processing and executive functioning
(e.g., complex decision-making) (Erkinjuntti, 2012). In contrast,
those with Alzheimer’s disease have memory problems as their
initial cognitive disturbance.
Compared with research on neurocognitive disorder due to
Alzheimer’s type, there are fewer studies on vascular neurocog-
nitive disorder, perhaps because of its lower incidence rates. The
prevalence of vascular neurocognitive disorder is approximate-
ly 1.5% in people 70 to 75 years of age and increases to 15% for
those over the age of 80 (Neugroschi, Kolevzon, Samuels, & Marin,
2005). The risk for men is slightly higher than among women, in
contrast with the higher risk among women for Alzheimer’s type
dementia, and this has been reported in many developed and
developing countries (Kalaria et al., 2008). The relatively high rate
of cardiovascular disease among men in general may account for
their increased risk of vascular neurocognitive disorder. The onset
of vascular dementia is typically more sudden than the onset for
the Alzheimer’s type, probably because the disorder is the result
of stroke, which inflicts brain damage immediately. The outcome,
however, is similar for people with both types: Ultimately, they will
require formal nursing care until they succumb to an infectious
disease such as pneumonia, to which they are susceptible because
of weakening of the immune system.
Other Medical Conditions That Cause
Neurocognitive Disorder
In addition to Alzheimer’s disease and vascular damage, a num-
ber of other neurological and biochemical processes can lead to
neurocognitive disorder. DSM-5 identifies eight specific causes
in addition to Alzheimer’s disease and vascular damage: fron-
totemporal degeneration, traumatic brain injury, Lewy body

DSM
5
TABLE 15.5 Diagnostic Criteria for Major or Mild Vascular Neurocognitive Disorder

A. The criteria are met for major or mild neurocognitive disorder.

B. The clinical features are consistent with a vascular etiology as suggested by either of the following:
1. Onset of the cognitive deficits is temporally related to one or more cerebrovascular events.
2. Evidence for decline is prominent in complex attention (including processing speed) and frontal-executive function.
C. There is evidence of the presence of cerebrovascular disease from history, physical examination, and/or neuroimaging con-
sidered sufficient to account for the neurocognitive deficits.
D. The symptoms are not better explained by another brain disease or systemic disorder. Probable vascular neurocognitive disor-
der is diagnosed if one of the following is present, otherwise, possible vascular neurocognitive disorder should be diagnosed:
1. Clinical criteria are supported by neuroimaging evidence of significant parenchymal injury attributed to cerebrovascular
disease (neuroimaging-supported).
2. The neurocognitive syndrome is temporally related to one or more documented cerebrovascular events.
3. Both clinical and genetic (e.g., cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
evidence of cerebrovascular disease is present.
Possible vascular neurocognitive disorder is diagnosed if the clinical criteria are met but neuroimaging is not available and the
temporal relationship of the neurocognitive syndrome with one or more cerebrovascular events is not established.

From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC.

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 disease, Parkinson’s disease, HIV infec- & Brun, 2012). Pick’s disease usually
tion, substance use, Huntington’s dis- occurs relatively early in life—during a
ease, and prion disease. Each of these person’s 40s or 50s—and is therefore con-
is discussed here. In addition, a final sidered an example of early onset neuro-

© Cengage Learning®
category—neurocognitive disorder due cognitive disorder.
to another medical condition—is pro- Severe trauma to the head causes
vided for other causes. Other medical the brain to sustain lasting injuries
conditions that can lead to neurocogni- (called traumatic brain injury or
tive disorder include normal pressure TBI) which can lead to neurocognitive
hydrocephalus (excessive water in the Neurocognitive Disorder disorder (Fleminger, 2012). Neurocog-
cranium, resulting from brain shrink- with Amnesia: Mike nitive disorder due to traumatic brain
age), hypothyroidism (an underactive “I still have a pretty major memory problem, injury includes symptoms that persist
thyroid gland), brain tumor, and vita- which has since brought about a divorce for at least a week following the trauma,
min B12 deficiency. There is increasing and which . . . I now have a new girlfriend, including executive dysfunction (e.g.,
recognition of neurocognitive disorder which helps very much. I even call her . . . my difficulty planning complex activities)
among athletes who receive repeated new brain or my new memory. . . . If I want and problems with learning and mem-
blows to the head. In the past this type to know something, besides on relying on ory. Those that are at greatest risk for
of neurocognitive disorder was referred this so-called memory notebook, which I jot TBI are teens and young adults, espe-
to as dementia pugilistica (which sug- notes down in constantly and have it every cially accompanied by alcohol abuse
gested that it was restricted to boxers day dated, so I know what’s coming up or or lower socio-economic class (Flem-
or pugilists) but it is currently referred what’s for that day.” inger, 2012). Traffic accidents, assaults,
to as chronic traumatic encephalopa- falls, and suicide attempts are common
thy (CTE). CTE is caused by repetitive Go to MindTap at
causes, as is being exposed to bomb
head trauma that can provoke distinc- www.cengagebrain.com blasts in combat.
tive neurodegeneration (Gavett, Stern, to watch this video. The second most common type
Cantu, Nowinski, & McKee, 2010). In of neurocognitive disorders (after
their effect on cognitive ability, all of Alzheimer’s disease) is neurocognitive
these disorders are comparable to the other forms of neurocog- disorder due to Lewy body disease (Aarsland, Ballard, Rongve,
nitive disorder we have discussed so far. Broadstock, & Svenningsson, 2012; McKeith et al., 2005). Lewy
bodies are microscopic deposits of a protein that damage brain
Descriptions and Statistics cells over time. The signs of this disorder come on gradually
Frontotemporal neurocognitive disorder is an overarching term and include impairment in alertness and attention, vivid visual
used to categorize a variety of brain disorders that damage the hallucinations, and motor impairment as seen in Parkinson’s
frontal or temporal regions of disease. In fact, there is some overlap between this disorder and
the brain—areas that affect per- neurocognitive disorder due to Parkinson’s disease (Mind-
sonality, language, and behav- ham & Hughes, 2012).
ior (Gustafson & Brun, 2012). Parkinson’s disease is a degenerative brain disorder
DSM-5 identifies two variants that affects about 1 in every 1,000 people worldwide (Marsh
of frontotemporal neurocogni- & Margolis, 2009). Movie and television star Michael J. Fox
tive disorder—through declines and former U.S. Attorney General Janet Reno both suffer from
in appropriate behavior (e.g., this progressive disorder. Motor problems are characteris-
socially inappropriate actions, tic among people with Parkinson’s disease, who tend to have
Jim McIsaac/Staff/Getty Images

apathy, making poor judg-
ments) or language (e.g., prob-
lems with speech, finding the
right word, naming objects).
One of the disorders in this
category of neurocognitive dis-
orders is Pick’s disease, a rare
neurological condition—occur-
Junior Seau was an NFL star foot-
ball player who committed suicide
ring in about 5% of those people
in 2012. The National Institutes with neurocognitive impair-
of Health—at the request of his ment—that produces symptoms
family—determined through an similar to that of Alzheimer’s
examination of his brain that he disease. The course of this dis-
had abnormalities consistent
with repetitive blows to the head
ease is believed to last from 5 to
which resulted in chronic trau- 10 years, and appears to have a
matic encephalopathy (CTE). genetic component (Gustafson
stooped posture, slow body movements (called bradykinesia),
tremors, and jerkiness in walking. The voice is also affected;
afflicted individuals speak in a soft monotone. The changes
in motor movements are the result of damage to dopamine
pathways. Because dopamine is involved in complex move-
ment, a reduction in this neurotransmitter makes affected indi-
viduals increasingly unable to control their muscle movements,
which leads to tremors and muscle weakness. In addition
to degeneration of these pathways, Lewy bodies are also
present in the brains of affected persons. The course of the
disease varies widely, with some individuals functioning well
with treatment. It is estimated that about 75% of people who
survive more than 10 years with Parkinson’s disease develop
neurocognitive disorder; conservative estimates place the rate
at 4 to 6 times that found in the general population (Aarsland
& Kurz, 2010).

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 DSM
5
TABLE 15.6 Diagnostic Criteria for Major or Mild Frontotemporal Neurocognitive Disorder

A. The criteria are met for major or mild neurocognitive disorder.

B. The disturbance has insidious onset and gradual progression.
C. Either (1) or (2):
1. Behavioral variant:
a. Three or more of the following behavioral symptoms:
i. Behavioral disinhibition.
ii. Apathy or inertia.
iii. Loss of sympathy or empathy.
iv. Perseverative, stereotyped, or compulsive/ritualistic behavior.
v. Hyperorality and dietary changes.
b. Prominent decline in social cognition and/or executive abilities.
2. Language variant:
a. Prominent decline in language ability, in the form of speech production, word finding, object naming, grammar, or word
comprehension.
D. Relative sparing of learning and memory and perceptual-motor function.
E. The disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a
substance, or another mental, neurological, or systemic disorder.
Probable frontotemporal neurocognitive disorder is diagnosed if either of the following is present; otherwise, possible fronto-
temporal neurocognitive disorder should be diagnosed:
1. Evidence of a causative frontotemporal neurocognitive disorder genetic mutation, from either family history or genetic
testing.
2. Evidence of disproportionate frontal and/or temporal lobe involvement from neuroimaging.
Possible frontotemporal neurocognitive disorder is diagnosed if there is no evidence of a genetic mutation, and neuroimaging
has not been performed.

From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC.

DSM
5
TABLE 15.7 Diagnostic Criteria for Major or Mild Neurocognitive Disorder due to Traumatic Brain Injury

A. The criteria are met for major or mild neurocognitive disorder.

B. There is evidence of a traumatic brain injury—that is, an impact to the head or other mechanisms of rapid movement or
displacement of the brain within the skull, with one or more of the following:
1. Loss of consciousness.
2. Posttraumatic amnesia.
3. Disorientation and confusion.
4. Neurological signs (e.g., neuroimaging demonstrating injury; a new onset of seizures; a marked worsening of a preexist-
ing seizure disorder; visual field cuts; anosmia; hemiparesis).
C. The neurocognitive disorder presents immediately after the occurrence of the traumatic brain injury or immediately after
recovery of consciousness and persists past the acute post-injury period.

From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC.

The human immunodeficiency virus type 1 (HIV-1), which accompany HIV; in other words, the HIV infection itself seems
causes AIDS, can also cause neurocognitive disorder (called to be responsible for the neurological impairment. The early
neurocognitive disorder due to HIV infection) (Maj, 2012). This symptoms of neurocognitive disorder resulting from HIV are
impairment seems to be independent of the other infections that cognitive slowness, impaired attention, and forgetfulness. Affected

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 DSM
5 5
TABLE 15.8 Diagnostic Criteria for Major or
Mild Neurocognitive Disorder
with Lewy Bodies
A. The criteria are met for major or mild neurocognitive
disorder.
B. The disorder has an insidious onset and gradual
progression.
C. The disorder meets a combination of core diagnostic
features and suggestive diagnostic features for either prob-
able or possible neurocognitive disorder with Lewy Bodies.
For probable major or mild neurocognitive disorder with
Lewy Bodies, the individual has two core features, or one
suggestive feature with one or more core features.
For possible major or mild neurocognitive disorder with
Lewy Bodies, the individual has only one core feature, or
one or more suggestive features.
1. Core diagnostic features:
a. Fluctuating cognition with pronounced variations
in attention and alertness.
b. Recurrent visual hallucinations that are well
formed and detailed.
c. Spontaneous features of parkinsonism, with onset
subsequent to the development of cognitive decline.
2. Suggestive diagnostic features:
a. Meets criteria for rapid eye movement sleep
behavior disorder.
b. Severe neuroleptic sensitivity.
D. The disturbance is not better explained by cerebrovas-
cular disease, another neurodegenerative disease, the
effects of a substance, or another mental, neurological,
or systemic disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
individuals also tend to be clumsy, to show repetitive movements
such as tremors and leg weakness, and to become apathetic and
socially withdrawn.
People with HIV seem particularly susceptible to impaired
thinking in the later stages of HIV infection, although significant
declines in cognitive abilities may occur earlier. Cognitive impair-
ments were highly common among those infected with AIDS,
but with the introduction of new medications (highly active anti-
retroviral therapies, or HAARTs) less than 10% of patients now
experience neurocognitive disorder (Maj, 2012). HIV-1 accounts
for a relatively small percentage of people with neurocognitive
disorder compared to Alzheimer’s disease and vascular causes,
but its presence can complicate an already-devastating set of
medical conditions.
Like neurocognitive disorder from Parkinson’s disease and
several other causes, neurocognitive disorder resulting from
HIV is sometimes referred to as subcortical dementia, because
it affects primarily the inner areas of the brain, below the outer
55618_ch15_ptg01_hr_542-569.indd 555
DSM
TABLE 15.9 Diagnostic Criteria for
Neurocognitive Disorder
due to Parkinson’s Disease
A. The criteria are met for major or mild neurocognitive
disorder.
B. The disturbance occurs in the setting of established
Parkinson’s disease.
C. There is insidious onset and gradual progression of
impairment.
D. The neurocognitive disorder is not attributable to
another medical condition and is not better explained
by another mental disorder.
Major or mild neurocognitive disorder probably due to
Parkinson’s disease should be diagnosed if 1 and 2 are both
met. Major or mild neurocognitive disorder possibly due to
Parkinson’s disease should be diagnosed if 1 or 2 is met:
1. There is no evidence of mixed etiology (i.e., absence
of other neurodegenerative or cerebrovascular
disease or another neurological, mental, or systemic
disease or condition likely contributing to cognitive
decline).
2. The Parkinson’s disease clearly precedes the onset of
neurocognitive disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
layer called the cortex (Bourgeois, Seaman, & Servis, 2003).
The distinction between cortical (including neurocognitive dis-
order due to Alzheimer’s disease) and subcortical dementia is
important because of the different expressions of neurocogni-
tive disorder in these two categories (see Table 15.2). Aphasia,
which involves impaired language skills, occurs among people
DSM
5
TABLE 15.10 Diagnostic Criteria for Major or
Mild Neurocognitive Disorder
due to HIV Infection
A. The criteria are met for major or mild neurocognitive
disorder.
B. There is documented infection with human immunodefi-
ciency virus (HIV).
C. The Neurocognitive Disorder is not better explained by
non-HIV conditions, including secondary brain diseases
such as progressive multifocal leukoencephalopathy or
cryptococcal meningitis.
D. The neurocognitive disorder is not attributable to
another medical condition and is not better explained
by a mental disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
Major a n d Mi l d Ne u ro c o g ni ti ve D i sorder s 555
25/11/13 2:12 PM

Simon Fraser/Royal Victoria Infirmary, Newcastle upon Tyne/Science Source
The AIDS virus may cause neurocognitive disorder in the later stages.
with neurocognitive disorder due to Alzheimer’s disease but not
among people with subcortical dementia. In contrast, people with
subcortical dementia are more likely to experience severe depres-
sion and anxiety than those with neurocognitive disorder due to
Alzheimer’s disease. In general, motor skills including speed and
coordination are impaired early on among those with subcortical
dementia. The differing patterns of impairment can be attributed
to the different areas of the brain affected by the disorders causing
the neurocognitive disorder.
Huntington’s disease is a genetic disorder that initially affects
motor movements, typically in the form of chorea, involuntary
limb movements (Marsh & Margolis, 2009). People with Hunting-
ton’s disease can live for 20 years after the first signs of the dis-
ease appear, although skilled nursing care is often required during
the last stages. Just as with Parkinson’s disease, only a portion of
people with Huntington’s disease go on to display neurocognitive
disorder—somewhere between 20% and 80%—although some
researchers believe that all patients with Huntington’s disease
would eventually display neurocognitive impairments if they lived
long enough (Marsh & Margolis, 2009). Neurocognitive disorder
due to Huntington’s disease also follows the subcortical pattern.
TABLE 15.2 Characteristics of Neurocognitive Disorders
Characteristic Dementia of the Alzheimer’s Type
Language Aphasia (difficulties with articulating speech)
Memory Both recall and recognition are impaired
Visuospatial skills Impaired
Mood Less severe depression and anxiety
Motor speed Normal
Coordination Normal until late in the progression
Source: Adapted, with permission of Oxford University Press, from Cummings, J. L. (Ed.) (1990). Subcortical dementia. New York, NY: Oxford University Press,
© 1990 Jeffrey L. Cummings.
55 6 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s
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DSM
5
TABLE 15.11 Diagnostic Criteria for Major or
Mild Neurocognitive Disorder
due to Huntington’s Disease
A. The criteria are met for major or mild neurocognitive
disorder.
B. There is insidious onset and gradual progression.
C. There is clinically established Huntington’s disease, or
risk for Huntington’s disease based on family history or
genetic testing.
D. The neurocognitive disorder is not attributable to
another medical condition and is not better explained
by another mental disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
The search for the gene responsible for Huntington’s disease
reads like a detective story. For some time, researchers have known
that the disease is inherited as an autosomal dominant disorder,
meaning that approximately 50% of the offspring of an adult with
Huntington’s disease will develop the disease. Since 1979, behav-
ioral scientist Nancy Wexler and a team of researchers have been
studying the largest known extended family in the world afflicted
by Huntington’s disease, in small villages in Venezuela. The
villagers have cooperated with the research, partly because Wexler
herself lost her mother, three uncles, and her maternal grandfa-
ther to Huntington’s disease, and she, too, may develop the dis-
order (Wexler, 2012). Using genetic linkage analysis techniques
(see Chapter 4), these researchers first mapped the deficit to an
area on chromosome 4 (Gusella et al., 1983) and then identified
the elusive gene (Huntington’s Disease Collaborative Research
Group, 1993). Finding that one gene that causes a disease is
unusual; research on other inherited mental disorders typically
points to multiple gene (polygenic) influences.
Neurocognitive disorder due to prion disease is a rare pro-
gressive neurodegenerative disorder caused by “prions”—proteins
that can reproduce themselves and cause damage to brain cells
Subcortical Dementias
No aphasia
Impaired recall; normal or less impaired recognition
Impaired
More severe depression and anxiety
Slowed
Impaired
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 DSM Description and Statistics

5
TABLE 15.12 Diagnostic Criteria for
Neurocognitive Disorder due
to Prion Disease
A. The criteria are met for major or mild neurocognitive
disorder.
B. There is insidious onset, and rapid progression of
impairment is common.
C. There are motor features of prion disease, such as
myoclonus or ataxia, or biomarker evidence.
D. The neurocognitive disorder is not attributable to
another medical condition and is not better explained
by another mental disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
leading to neurocognitive decline (Collinge, 2012). Unlike other
infectious agents such as bacteria or viruses, prions are thought by
some to have no DNA or RNA that can be destroyed by chemicals
or radiation. As a result, there is no known treatment for prion
disease and the course of this disorder is always fatal. On the posi-
tive side, prions are not contagious in humans and have only been
contracted through cannibalism (causing kuru) or accidental
inoculations (e.g., through blood transfusions from an infected
person) (Collinge, 2012). One type of prion disease, Creutzfeldt-
Jakob disease, is believed to affect only one in every million indi-
viduals (Heath et al., 2010). An alarming development in the study
of Creutzfeldt-Jakob disease is the finding of 10 cases of a new
variant that may be linked to bovine spongiform encephalopathy,
more commonly referred to as “mad cow disease” (Neugroschi et
al., 2005). This discovery led to a ban on exporting beef from the
United Kingdom for a number of years because the disease might
be transmitted from infected
cattle to humans. We do not
yet have definitive information
about the link between mad
cow disease and the new form
of Creutzfeldt-Jakob disease
(Wiggins, 2009).
Substance/
Medication-Induced
Neurocognitive
Slaven Vlasic/Stringer/Getty Images
As many as 7% of individuals dependent on alcohol meet the cri-
teria for neurocognitive disorder (Neugroschi et al., 2005). The
long-term abuse of a number of drugs can lead to symptoms of
neurocognitive disorder, including alcohol, inhalants such as glue
or gasoline (which some people inhale for the euphoric feeling
they produce), and sedative, hypnotic, and anxiolytic drugs (see
Chapter 11). These drugs pose a threat because they create depen-
dence, making it difficult for a user to stop ingesting them. The
resulting brain damage can be permanent and can cause the same
symptoms as seen in neurocognitive disorder due to Alzheimer’s
type. The DSM-5 criteria for substance/medication-induced
neurocognitive disorder are essentially the same as many of the
other forms of neurocognitive disorder; they include memory
impairment and at least one of the following cognitive distur-
bances: aphasia (language disturbance), apraxia (inability to carry
out motor activities despite intact motor function), agnosia (fail-
ure to recognize or identify objects despite intact sensory func-
tion), or a disturbance in executive functioning (such as planning,
organizing, sequencing, and abstracting).
Causes of Neurocognitive Disorder
As our technology for studying the brain advances, so does our
understanding of the many and varied causes of neurocognitive
disorder. A complete description of what is known about the
origins of this type of brain impairment is beyond the scope of this
book, but we highlight some insights available for more common
forms of this disorder.
Biological Influences
Cognitive abilities can be adversely compromised in many ways.
As you have seen, neurocognitive disorder can be caused by a
number of processes: Alzheimer’s disease, Huntington’s disease,
Parkinson’s disease, head trauma, substance abuse, and others. The
most common cause of neurocognitive disorder, Alzheimer’s dis-
ease, is also the most mysterious. Because of its prevalence and our
relative ignorance about the factors responsible for it, Alzheimer’s
disease has held the attention of many researchers, who are trying
to find the cause and ultimately a treatment or cure for this
devastating condition.
Findings from Alzheimer’s research seem to appear almost
daily. We should be cautious when interpreting the output of this
fast-paced and competitive field; too often, as you have seen in
other areas, findings are heralded prematurely as conclusive and
important. Remember that “discoveries” of a single gene for bipo-

lar disorder, schizophrenia, and alcoholism were later shown to

Michael J. Fox provides his time
and celebrity status to efforts
to cure Parkinson’s disease, a
degenerative disease that is
severely affecting his life.
Disorder
Prolonged drug use, especially
combined with poor diet, can
damage the brain and, in some
circumstances, can lead to
neurocognitive disorder. This
impairment unfortunately lasts
beyond the period involved
in intoxication or withdrawal
from these substances.
be based on overly simplistic accounts. Similarly, findings from
Alzheimer’s research are sometimes too quickly sanctioned as
accepted truths before they have been replicated, an essential
validation process.
One lesson in scientific caution comes from research that
demonstrates a negative correlation between cigarette smoking
and Alzheimer’s disease (Brenner et al., 1993). In other words,
the study found that smokers are less likely than nonsmokers
to develop Alzheimer’s disease. Does this mean smoking has
a protective effect, shielding a person against the development

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 DSM
5
TABLE 15.13 Diagnostic Criteria for Substance/Medication-Induced Major or Mild Neurocognitive Disorder

A. The criteria are met for major or mild neurocognitive disorder.

B. The neurocognitive impairments do not occur exclusively during the course of a delirium and persist beyond the usual
duration of intoxication and acute withdrawal.
C. The involved substance or medication and duration and extent of use are capable of producing the neurocognitive impairment.
D. The temporal course of the neurocognitive deficits is consistent with the timing of substance or medication use and abstinence
(e.g., the deficits remain stable or improve after a period of abstinence).
E. The neurocognitive disorder is not attributable to another medical condition and is not better explained by another mental
disorder.

From American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC.

of this disease? On close examination, the finding may instead
be the result of the differential survival rates of those who smoke
and those who do not. In general, nonsmokers tend to live longer
and are thereby more likely to develop Alzheimer’s disease, which
appears later in life. Some even believe the relative inability of
cells to repair themselves, a factor that may be more pronounced
among people with Alzheimer’s disease, may interact with ciga-
rette smoking to shorten the lives of smokers who are at risk for
Alzheimer’s disease (Riggs, 1993). Put another way, smoking may
exacerbate the degenerative process of Alzheimer’s disease, caus-
ing people with the disease who also smoke to die earlier than
nonsmokers who have Alzheimer’s disease (Ashare, Karlawish,
Wileyto, Pinto, & Lerman, 2012). These types of studies and the
conclusions drawn from them should make us sensitive to the
complicated nature of the disorders.
What do we know about Alzheimer’s disease, the most common
cause of neurocognitive disorder? After the death of the patient he
described as having a “strange disease of the cerebral cortex,” Alois
Alzheimer performed an autopsy. He found that the brain contained
large numbers of tangled, strandlike filaments within the brain cells
(referred to as neurofibrillary tangles). This type of damage occurs in
everyone with Alzheimer’s disease. A second type of degeneration
results from gummy protein deposits—called amyloid plaques (also
referred to as neuritic or senile plaques)—that accumulate between the
neurons in the brains of people with this disorder. Amyloid plaques
are also found in older adults who do not have symptoms of neuro-
cognitive disorder, but they have far fewer of them than do individu-
als with Alzheimer’s disease (Richards & Sweet, 2009). Both forms of
damage—neurofibrillary tangles and amyloid plaques—accumulate
over the years and are believed to produce the characteristic cognitive
disorders we have been describing (Weiner et al., 2012a).
These two types of degeneration affect extremely small areas and
can be detected only by a microscopic examination of the brain. As
mentioned earlier, scientists are close, however, to developing the
neuroimaging technology and measures to assess amyloid proteins in
spinal fluid that may soon detect the early development of these types
of brain cell damage without having to rely on an autopsy (Weiner et
al., 2012a). In addition to having neurofibrillary tangles and amyloid
plaques, over time the brains of many people with Alzheimer’s disease
atrophy (shrink) to a greater extent than would be expected through
normal aging (Lovestone, 2012). Because brain shrinkage has many
causes, however, only by observing the tangles and plaques can a
diagnosis of Alzheimer’s disease be properly made.
Rapid advances are being made toward uncovering the genetic
bases of Alzheimer’s disease (e.g., Seshadri et al., 2010). As with most
other behavioral disorders we have examined, multiple genes seem
to be involved in the development of Alzheimer’s disease. Table 15.3
illustrates what we know so far. Genes on chromosomes 21, 19, 14,
12, and 1 have all been linked to certain forms of Alzheimer’s disease
(Neugroschi et al., 2005). The link to chromosome 21 was discovered
first, and it resulted from the unfortunate observation that individu-
als with Down syndrome, who have three copies of chromosome 21
instead of the usual two, developed the disease at an unusually high
rate (Report of the Advisory Panel on Alzheimer’s Disease, 1995).
More recent work has located relevant genes on other chromosomes.
These discoveries indicate that there is more than one genetic cause
of Alzheimer’s disease. Some forms, including the one associated
with chromosome 14, have an early onset. Pat Summitt was diag-
nosed with an early-onset form. In contrast, Alzheimer’s disease
associated with chromosome 19 seems to be a late-onset form of the
disease that has an effect only after the age of about 60.
Some genes that are now identified are deterministic, mean-
ing that if you have one of these genes you have a nearly 100%
chance of developing Alzheimer’s disease (Bettens, Sleegers, & Van
Broeckhoven, 2010). Deterministic genes such as the precursor
gene for small proteins called amyloid beta peptides (also referred
to as beta-amyloid or A(!) and the Presenilin 1 and Presenilin 2
genes will inevitably lead to Alzheimer’s disease, but, fortunately,
these genes are also rare in the general population. For treatment
purposes, this means that even if researchers can find a way to
prevent these genes from leading to Alzheimer’s disease, it will
only help a relatively small number of people. On the other hand,
some genes—including the apolipoprotein E4 (apo E4) gene—are
known as susceptibility genes. These genes only slightly increase
the risk of developing Alzheimer’s disease, but in contrast to the
deterministic genes, these are more common in the general popu-
lation (Lovestone, 2012). If future research can find ways to inter-
fere with the apo E4 gene, many people will be helped.
Although closing in on the genetic origins of Alzheimer’s disease
has not brought immediate treatment implications, researchers are

55 8 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s

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 TABLE 15.3 chromosome 19 pair) increases the risk for Alzheimer’s disease:
Genetic Factors in Alzheimer’s Disease
As many as 90% of people with two genes developed Alzheimer’s
Age of Onset disease (Reiman et al., 2007). In addition, having two apo E4
Gene Chromosome (years)
genes seemed to decrease the mean age of onset from 84 years to
APP 21 43 to 59 68 years. These results suggest that apo E4 may be responsible for
late-onset Alzheimer’s disease and that a gene on chromosome 19
Presenilin 1 14 33 to 60 is responsible. What is still not completely understood is how apo
Presenilin 2 1 50 to 90 E4 causes amyloid proteins to build up in the neurons of people
who ultimately exhibit Alzheimer’s disease and whether this pro-
apo E4 19 60 cess is responsible for the disease.
Researchers are just beginning to try to examine potential
AAP " amyloid precursor protein; apo E4 " apolipoprotein E4. gene–environment interactions in Alzheimer’s disease. Several
Source: Lovestone, S. (2012). Dementia: Alzheimer’s disease. In M. G.
Gelder, N. C. Andreasen, J. J. Lopez Jr. & J. R. Geddes (Eds.), New Oxford
studies suggest a few areas of promise. One study found that hav-
textbook of psychiatry (2nd. ed., Vol. 1, pp. 333–343). New York: Oxford ing the apo E4 genotype was more likely to produce cognitive
University Press. decline in those persons living in stressful environments—suggest-
ing a gene (apo E4)—environment (stress) interaction (Boardman,
Barnes, Wilson, Evans, & de Leon, 2012). Another study found
nearer to understanding how the disease develops, which may result that among African Americans, having low levels of cholesterol
in medical interventions. Genetic research has advanced our knowl- seemed to reduce risk of Alzheimer’s disease—but only among
edge of how the amyloid plaques develop in the brains of people with those who did not carry the apo E4 gene (Evans et al., 2000). Finally,
Alzheimer’s disease and may hold a clue to its origins. In the core of researchers found that physical exercise reduced the likelihood of
the plaques is a solid waxy substance made up of a peptide called developing the disease but, like the previous study, only among
amyloid beta or A!. Just as cholesterol buildup on the walls of blood those without the apo E4 gene (Podewils et al., 2005). This type of
vessels chokes the blood supply, deposits of A! are believed by some research holds the potential for better understanding the complex
researchers to cause the cell death associated with Alzheimer’s disease nature of Alzheimer’s disease and may lead to important preven-
(Lovestone, 2012). An important question, then, is Why does this pro- tion strategies (such as lowering cholesterol levels and exercising
tein accumulate in the brain cells of some people but not of others? regularly) (Pedersen, 2010).
Two mechanisms that may account for amyloid protein build- For all disorders described in this book, we have identified
up are being studied. The first involves amyloid precursor protein the role of biological, psychological, or both types of stressors as
(APP), a large protein that is eventually broken down into the partially responsible for the onset of the disorder. Does neuro-
amyloid protein found in the amyloid plaques. Important work cognitive disorder due to Alzheimer’s disease—which appears to
resulted in identifying the gene responsible for producing APP, be a strictly biological event—follow the same pattern? One of
on chromosome 21 (Lovestone, 2012). This finding may help the leading candidates for an external contributor to this disorder
integrate two observations about Alzheimer’s disease: (1) APP is head trauma. As we have seen, it appears that repeated blows
produces the amyloid protein found in the amyloid plaques, and to the head can bring on neurocognitive disorder (chronic trau-
(2) Down syndrome, associated with an extra 21st chromosome, matic encephalopathy or CTE). Fighters who carry the apo E4
results in a higher incidence of the disease (see Chapter 14). The gene may be at greater risk for developing neurocognitive disor-
gene responsible for producing APP and, ultimately, amyloid pro- der attributed to head trauma (Jordan et al., 1997). In addition to
tein, may be responsible for the relatively infrequent early-onset
form of the disease, and its location could explain why people
with Down syndrome—who have an extra 21st chromosome and
therefore an extra APP gene—are more likely than the general
population to develop Alzheimer’s disease.
A second, more indirect way that amyloid protein may build
up in brain cells is through apolipoprotein E (apo E), which nor-
mally helps transport cholesterols, including amyloid protein,
through the bloodstream. There are at least three forms of this
Acey Harper/Time Life Pictures/Getty Images

transporter protein: apo E2, apo E3, and apo E4. Individuals who
have late-onset Alzheimer’s disease, the most common form, are
likely to carry the gene associated with apo E4, located on chro-
mosome 19. Researchers have found that the majority of people
with Alzheimer’s disease who also have a family history of the
disease will have at least one gene for apo E4 (Lovestone, 2012).
In contrast, approximately 64% of individuals with Alzheimer’s
disease who have no family history of the disease have at least one
gene for apo E4, and only 31% of nonaffected individuals have the Nancy Wexler headed the team of scientists who found the gene for
gene. Having two genes for apo E4 (one on each member of the Huntington’s disease.

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 boxers, news accounts suggest links to the trauma experienced
by NFL players and the development of CTE in these former
athletes (Schwarz, 2007). Head trauma may be one of the stress-
ors that initiate the onset of neurocognitive disorder of varying
types. Other such stressors include having diabetes, high blood
pressure, or herpes simplex virus-1 (Richards & Sweet, 2009). As
with each of the disorders discussed, psychological and biologi-
cal stressors may interact with physiological processes to produce
Alzheimer’s disease.
We opened the section with a word of caution, which it is
appropriate at this point to repeat. Some of the findings just
reviewed are considered controversial, and many questions
remain to be answered about neurocognitive disorder and one of
its most common causes, Alzheimer’s disease.
Psychological and Social Influences
Research has mostly focused on the biological conditions that pro-
duce neurocognitive disorder. Although few would claim that psy-
chosocial influences directly cause the type of brain deterioration
seen in people with neurocognitive disorder, they may help deter-
mine onset and course. For example, a person’s lifestyle may involve
contact with factors that can cause neurocognitive disorder. You
saw, for instance, that substance abuse can lead to neurocognitive
disorder and, as we discussed previously (see Chapter 11), whether
a person abuses drugs is determined by a combination of biologi-
cal and psychosocial factors. In the case of vascular neurocognitive
disorder, a person’s biological vulnerability to vascular disease will
influence the chances of strokes that can lead to this form of disor-
der. Lifestyle issues such as diet, exercise, and stress influence car-
diovascular disease and therefore help determine who experiences
vascular neurocognitive disorder (see Chapter 9).
Cultural factors may also affect this process. For example,
hypertension and strokes are prevalent among African Americans
and certain Asian Americans (King, Mainous III, & Geesey, 2007),
which may explain why vascular neurocognitive disorder is more
often observed in members of these groups. In an extreme exam-
ple, exposure to prion disease can lead to neurocognitive disorder
described previously as kuru. Prions can be passed on through
a ritual form of cannibalism practiced in Papua New Guinea as
a part of mourning (Collinge et al., 2006). Neurocognitive disor-
der caused by head trauma and malnutrition are relatively preva-
lent in preindustrial rural societies (Del Parigi, Panza, Capurso,
& Solfrizzi, 2006). Not getting enough of vitamins B9 and B12 in
particular seems to lead to neurocognitive disorder, although the
process is as yet unknown (Michelakos et al., 2013). These find-
ings suggest that occupational safety (such as protecting workers
from head injuries) and economic conditions influencing diet also
affect the prevalence of certain forms of neurocognitive disorders.
It is apparent that psychosocial factors help influence who does
and who does not develop certain forms of neurocognitive dis-
order. Brain deterioration is a biological process but, as you have
seen throughout this text, even biological processes are influenced
by psychosocial factors.
Psychosocial factors themselves influence the course of neu-
rocognitive disorder. Recall that educational attainment may
affect the onset of dementia (Richards & Sweet, 2009). Having
56 0 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s
55618_ch15_ptg01_hr_542-569.indd 560
certain skills may help some people cope better than others with
the early stages of neurocognitive disorder. The early stages of
confusion and memory loss may be better tolerated in cultures
with lowered expectations of older adults. In certain cultures,
including the Chinese, younger people are expected to take the
demands of work and care from older adults after a certain age,
and symptoms of dementia are viewed as a sign of normal aging
(Gallagher-Thompson et al., 2006; Hinton, Guo, Hillygus, &
Levkoff, 2000). Neurocognitive disorder may go undetected for
years in these societies.
Much remains to be learned about the cause and course of
most types of neurocognitive disorder. As you saw with Alzheim-
er’s disease and Huntington’s disease, certain genetic factors make
some individuals vulnerable to progressive cognitive deteriora-
tion. In addition, brain trauma, some diseases, and exposure to
certain drugs, such as alcohol, inhalants, and sedative, hypnotic,
and anxiolytic drugs, can cause the characteristic decline in cog-
nitive abilities. We also noted that psychosocial factors can help
determine who is subject to these causes and how they cope with
the condition. Looking at neurocognitive disorder from this inte-
grative perspective should help you view treatment approaches in
a more optimistic light. It may be possible to protect people from
conditions that lead to neurocognitive disorder and to support
them in dealing with the devastating consequences of having it.
We next review attempts to help from both biological and psycho-
social perspectives.
Treatment
For many of the disorders discussed in other chapters, treatment
prospects are fairly good. Clinicians can combine various strate-
gies to reduce suffering significantly. Even when treatment does
not bring expected improvements, mental health professionals
have usually been able to stop problems from progressing. This is
not the case in the treatment of neurocognitive disorder.
One factor preventing major advances in the treatment of neu-
rocognitive disorder is the nature of the damage caused by this dis-
order. The brain contains billions of neurons, many more than are
used. Damage to some can be compensated for by others because
of plasticity. There is a limit to where and how many neurons
can be destroyed, however, before vital functioning is disrupted.
Researchers are closing in on how to use the brain’s natural process
of regeneration to potentially reverse the damage caused in neuro-
cognitive disorder (Khachaturian, 2007). Currently, however, with
extensive brain damage, no known treatment can restore lost abili-
ties. The goals of treatment therefore become (1) trying to prevent
certain conditions, such as substance abuse or strokes, that may
bring on neurocognitive disorder; (2) trying to delay the onset of
symptoms to provide better quality of life; and (3) attempting to
help these individuals and their caregivers cope with the advanc-
ing deterioration. Most efforts in treating neurocognitive disorder
have focused on the second and third goals, with biological treat-
ments aimed at stopping the cerebral deterioration and psychoso-
cial treatments directed at helping patients and caregivers cope.
A troubling statistic further clouds the tragic circumstances
of neurocognitive disorder: More than 23% of caregivers of
people with neurocognitive disorder—usually relatives—have the
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 symptoms characteristic of one or more because of the potential for liver damage

© Cengage Learning®
anxiety disorders and 10% are clinically (Rabins, 2006). These drugs prevent the
depressed (Katona & Livingston, 2009). breakdown of the neurotransmitter ace-
Compared with the public, these caregiv- tylcholine (which is deficient in people
ers use more psychotropic medications with Alzheimer’s disease), thus making
(designed to reduce symptoms of vari- more acetylcholine available to the brain.
ous psychological disorders) and report Research suggests that, when using these
stress symptoms at 3 times the normal Computer Simulations drugs, people’s cognitive abilities improve
rate. Caring for people with neurocogni- and Neurocognitive to the point where they were 6 months
tive disorder, especially in its later stages, Disorder earlier (Lyketos, 2009). But the gain is not
is clearly a trying experience. In fact, “Our cognitive activity arises from the neural permanent. Even people who respond
there is some evidence to suggest that the networks in the brain. Whenever you lose an positively do not stabilize but continue to
stress associated with caring for a person individual neuron, you’re not losing an idea, experience the cognitive decline associat-
with neurocognitive disorder may place you’re just losing a tiny bit of the resolution, ed with Alzheimer’s disease. In addition,
the caregiver at greatly increased risk or the crispness, of that idea.” if they stop taking the drug—as almost
for developing neurocognitive disorder three-quarters of the patients do because
themselves (Norton et al., 2010). As a of negative side effects such as liver dam-
Go to MindTap at
result, clinicians are becoming increas- age and nausea—they lose even that
www.cengagebrain.com
ingly sensitive to the needs of these care- to watch this video. 6-month gain (Lyketos, 2009). Newer
givers, and research is now exploring drugs are now being investigated for the
interventions to assist them in caring for treatment of Alzheimer’s disease. These
people with neurocognitive disorder (Lee, Czaja, & Schulz, 2010). include drugs that target the beta amyloid (plaques) in the brain,
and it is hoped that these advances will finally provide a positive
prognosis for this devastating disease (Lukiw, 2012).
Biological Treatments Several other medical approaches are being explored to slow
Neurocognitive disorder resulting from known infectious dis- the course of Alzheimer’s disease, but initial excitement generated
eases, nutritional deficiencies, and depression can be treated if by these approaches has waned with the findings from research-
it is caught early. Unfortunately, however, no known treatment ers. For example, most of you have heard of using Ginkgo biloba
exists for the types of neurocognitive disorder that account for the (maidenhair) to improve memory. Initial research suggested that
vast majority of cases. Neurocognitive disorder caused by stroke, this herbal remedy may produce modest improvements in the
Parkinson’s disease, or Huntington’s disease is not currently treat- memory of people with Alzheimer’s disease, but other studies have
able, because there is no effective treatment for the primary disor- not replicated this benefit (DeKosky et al., 2008). Similarly, the
der. However, exciting research in several related areas has brought effects of vitamin E have been evaluated. One large study found
us closer to helping individuals with these forms of neurocognitive that among individuals with moderately severe impairment, high
disorder. A substance that may help preserve and perhaps restore doses of the vitamin (2,000 international units per day) delayed
neurons—glial cell–derived neurotrophic factor—may someday progression compared with a placebo (Sano et al., 1997), but it
be used to help reduce or reverse the progression of degenera- did not prevent the development of the disease. Further research,
tive brain diseases (Zuccato & Cattaneo, 2009). Researchers are in fact, indicates that taking high doses of vitamin E may actu-
also looking into the possible benefits of transplanting stem cells ally increase mortality and therefore this intervention is no longer
(fetal brain tissue) into the brains of people with such diseases. recommended (Richards & Sweet, 2009). Modest slowing of the
Initial results from these studies are still preliminary but appear progression of the disease also may be obtained by introducing
promising (Arenas, 2010). Neurocognitive disorder brought on by exercise to patients (Rockwood & Middleton, 2007; Teri et al.,
strokes may now be more preventable by new drugs that help pre- 2003). To date, however, no medical interventions are available
vent much of the damage inflicted by the blood clots characteristic that directly treat and therefore stop the progression of the condi-
of stroke (Erkinjuntti, 2012). Most current attention is on a treat- tions that cause the cerebral damage in Alzheimer’s disease.
ment for dementia of the Alzheimer’s type, because it affects so Medical interventions for neurocognitive disorder also include
many people. Here, too, however, success has been modest at best. the use of drugs to help with some associated symptoms. A variety
Much work has been directed at developing drugs that will of antidepressants—such as serotonin-specific reuptake inhibi-
enhance the cognitive abilities of people with neurocognitive tors—are commonly recommended to alleviate the depression
disorder due to Alzheimer’s type. Many seem to be effective ini- and anxiety that too often accompany the cognitive decline. Anti-
tially, but long-term improvements have not been observed in psychotic medication is sometimes used for those who become
placebo-controlled studies (Richards & Sweet, 2009). Several unusually agitated (Richards & Sweet, 2009).
drugs (called cholinesterase inhibitors) have had a modest impact Other researchers are targeting vaccines that would poten-
on cognitive abilities in some patients and include donepezil tially treat and prevent—rather than just delay—the symptoms
(Aricept), rivastigmine (Exelon), and galantamine (Reminyl) of Alzheimer’s disease. Much of the research is attempting to get
(Trinh, Hoblyn, Mohanty, & Yaffe, 2003). Tacrine hydrochloride the immune system to attack the process that overproduces the
(Cognex), another in this family of drugs, is rarely used today small proteins (A!) that lead to cell death. Prior efforts had to

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 be abandoned because of the severe negative side effects of activity and improve the quality of life in those patients when
the vaccine, which included serious brain inflammation. More compared with controls (J. Choi & Twamley, 2013).
recent research with humans and animals indicates that there What impact do the medical and nonmedical treatments
may be several vaccines that could be effective in preventing the have on those with Alzheimer’s disease? ● Figure 15.2 illustrates
damage caused by A! formation and therefore represent the first how these interventions may delay the worst of the symptoms—
glimmer of hope for patients and their families (Subramanian, essentially compressing the time when the person is most impaired
Bandopadhyay, Mishra, Mathew, & John, 2010). (Becker, Mestre, Ziolko, & Lopez, 2007). The red line illustrates the
This type of research currently begins with transgenic mice— typical course of the disease, which results in 3 to 5 years of severe
mice in which the DNA has been altered. In the case of testing an impairment before death. However, with the interventions we high-
Alzheimer’s vaccine, the mice DNA is engineered to produce the lighted (illustrated by the purple line), people are able to live more
same small proteins thought to be responsible for the neurocog- fully for a longer period, despite the still-inevitable impairment and
nitive disorder. Mice are good subjects because they age rapidly, death. Families find this extra time with their loved ones to be invalu-
with a 22-month-old mouse equivalent to a 65-year-old human able, and hopefully with more advancements we will see progress on
(Morgan, 2007). This allows researchers to study how the brain improving mortality rates of this progressive disease.
reacts to the potential vaccine if it has already started the progres- Individuals with advanced neurocognitive disorder are not able
sion of Alzheimer’s. If the results are promising in these transgenic to feed, bathe, or dress themselves. They cannot communicate with
mice, only then do researchers try small studies with humans. or recognize even familiar family members. They may wander away
Researchers are optimistic that there may finally be intervention from home and become lost. Because they are no longer aware of
approaches that would reverse the current trend of increasing social stigma, they may engage in public displays of sexual behavior,
numbers of people with neurocognitive disorder. Next we describe such as masturbation. They may be frequently agitated or even physi-
psychosocial approaches that are used with medication to address cally violent. To help both the person with dementia and the caregiver,
the variety of problems that accompany memory difficulties. researchers have explored interventions for dealing with these conse-
quences of the disorder (Lovestone, 2012). For example, some research
Psychosocial Treatments indicates that a combination of exercise for patients and instruction
for caregivers on how to handle behavior problems can improve the
Psychosocial treatments are now receiving a great deal of atten-
overall health and the depression in people with Alzheimer’s disease
tion for their ability to delay the onset of severe cognitive decline.
(Logsdon, McCurry, Pike, & Teri, 2009; Teri et al., 2003).
These efforts focus on enhancing the lives of people with neuro-
Of great concern is the tendency of people with neurocogni-
cognitive disorder, as well as those of their families.
tive disorder to wander. Sometimes they wind up in places or situ-
People with neurocognitive disorder can be taught skills to
ations that may be dangerous (for example, stairwells or the street).
compensate for their lost abilities. Some researchers have evaluated
Sometimes the person may be tied to a chair or bed, or sedated, to
formal adaptations to help people in the early stages of neurocogni-
prevent roaming. Unfortunately, physical and medical restraint has
tive disorder. Michelle Bourgeois (2007) created “memory wallets”
its own risks, including additional medical complications; it also
to help people with Alzheimer’s disease carry on conversations. On
adds greatly to the loss of control and independence that already
white index cards inserted into a plastic wallet are printed declara-
tive statements such as, “My husband John and I
have 3 children,” or “I was born on January 6, 1921, Typical course of neurocognitive disorder due to Alzheimer's disease
in Pittsburgh.” In one of her studies, Bourgeois Modified course of neurocognitive disorder when patient is treated with medical
(1992) found that adults with neurocognitive disor- and nonmedical interventions
der due to Alzheimer’s disease could, with minimal Improved function
training, use this memory aid to improve their con-
+
versations with others. With advances in technology
such as tablet computers that can be programmed
to “speak” for the person, adaptations such as these
help people communicate with others, help them
remain aware of their surroundings, and can reduce
the frustration that comes with the awareness of
Severe impairment
their own decline (Fried-Oken et al., 2012).
Cognitive stimulation—encouraging people
with neurocognitive disorder to practice learn-
ing and memory skills—seems to be an effective Less time with
severe impairment ≤1 year
method for delaying the onset of the more severe 3 to 5 years
cognitive effects of this disorder (Knowles, 2010). − Death
Years of clinical disease
These activities include word games, tests of mem-
ory of famous and familiar faces, and practice with
● FIGURE 15.2 Improving the course of Alzheimer’s disease with medical and non-
numbers (for example, how much change back medical interventions. (From Becker, J. T., Mestre, L. T., Ziolko, S., & Lopez, O. L. [2007].
you would receive from a purchase). These types Gene– environment interactions with cognition in late life and compression of morbidity.
of skill-building exercises can maintain cognitive American Journal of Psychiatry, 164, 849–852.)

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 aggressive behavior in persons with neurocognitive disorder
(Baker & LeBlanc, 2011). In addition, caregivers are often given
©Dakim [m]Power Cognitive Fitness Systems: Kara Kenna photographer

assertiveness training to help them deal with hostile behaviors

(see Table 15.4). Some caregivers may either passively accept all
criticism inflicted by the person with neurocognitive disorder,
which increases stress, or become angry and aggressive in return.
This last response is of particular concern because of the poten-
tial for elder abuse. Withholding food or medication or inflicting
physical abuse is most common among caregivers of elderly peo-
ple who have cognitive deficits (Post, Page, Conner, & Prokhorov,
2010). It is important to teach caregivers how to handle stressful
circumstances so that they do not escalate into abusive situations.
.www.dakim.com

Not a great deal of objective evidence supports the usefulness

A resident of an assistive living facility practices cognitive stimulation
using one of several computer-based systems (the Dakim [m]Power
Brain Fitness System).
plague the person with neurocognitive disorder. Psychological treat-
ment as an alternative to restraint sometimes involves providing
cues for people to help them safely navigate around their home or
other areas. New innovations in surveillance technology—creating a
“smart home” that can monitor the location of the patient and warn
caregivers—may provide more piece of mind for those who care
for these patients. At the same time, ethical concerns are being
raised about the use of this technology because of its ability to invade
privacy (Bharucha et al., 2009; Mahoney et al., 2007).
Someone with neurocognitive disorder can become agitated
and sometimes verbally and physically aggressive. This behav-
ior is understandably stressful for people trying to provide care.
In these situations, medical intervention is often used, although
many times with only modest results (Testad, Ballard, Brønnick,
& Aarsland, 2010). Some research suggests that teaching com-
munication skills in a manner similar to programs for persons
with autism spectrum disorder (Durand, 2012) may help reduce
of assertiveness training for reducing caregiver stress, and more
research is needed to guide future efforts.
In general, families of people with mild to moderate neurocog-
nitive disorder can benefit from supportive counseling to help them
cope with the frustration, depression, guilt, and loss that take a
heavy emotional toll. Clinicians must first recognize, however, that
the ability to adapt to stressors differs among people. One study, for
example, found cultural differences in the coping styles of caregiv-
ers. In one area of rural Alabama, white caregivers used acceptance
and humor as coping strategies, and black caregivers used religion
and denial (Kosberg, Kaufman, Burgio, Leeper, & Sun, 2007).
Another large-scale study of 555 principal caregivers over a 3-year
period identified a number of steps that can be taken to support
caregivers through this difficult time (Aneshensel, Pearlin, Mullan,
Zarit, & Whitlatch, 1995). Despite numerous studies aimed at sup-
porting caregivers, however, the results to date remain weak and
additional work is needed to determine how best to support these
individuals (Schoenmakers, Buntinx, & DeLepeleire, 2010).
Early on, caregivers need basic information on the causes and
treatment of neurocognitive disorder, financial and legal issues,
and locating help for the patient and the family. As the disorder
progresses, and the affected person requires increasing amounts
of assistance, caregivers will need help managing behavioral dif-
ficulties (wandering away or violent outbursts) and developing

TABLE 15.4 Sample Assertive Responses

Patient Behavior Assertive Response

Calmly but firmly say:

The patient refuses to eat, bathe, or “We agreed to do this at this time so that we will be able to (give specific activity
change clothes. or reward).”

The patient wants to go home. “I know you miss some of the places we used to be. This is our home now, and
together we are safe and happy here.”

The patient demands immediate “It’s not possible to have everything we want. As soon as I’ve finished (describe
gratification. specific task or action), we can discuss other things we want to do.”

The patient accuses the caregiver of tak- “We both enjoy our own things. I’ll help you look for (specific item missing) so that
ing the patient’s possessions. you can enjoy it just as soon as I have finished (describe specific task or action).”

The patient is angry, rebellious, or both. “I like to be treated fairly just as you do. Let’s discuss what’s bothering you so that
we can go back to our usual good relationship.”

Source: Adapted, with permission, from Edwards, A. J. (1994). When memory fails: Helping the Alzheimer’s and dementia patient. New York, NY: Plenum Press,
p. 174, © 1994 Plenum Press.

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 effective ways to communicate with the patient. Clinicians also
assist the family with decisions about hospitalizations and, finally, Concept Check 15.2
help them adjust during bereavement (Peeters, Van Beek,
Meerveld, Spreeuwenberg, & Francke, 2010). Identify the following symptoms of dementia from the
Overall, the outlook for slowing (but not stopping) the cogni- descriptions: (a) facial agnosia, (b) agnosia, and (c) aphasia.
tive decline characteristic of neurocognitive disorder is optimistic.
1. Timmy’s elderly grandmother does not recognize her
The best available medications provide some recovery of function,
own home any more. ____________
but they do not stop the progressive deterioration. Psychological
interventions may help people cope more effectively with the loss 2. She can no longer form complete, coherent sentences.
of cognitive abilities, especially in the earlier stages of this disor- ____________
der. In addition, emphasis is placed on helping caregivers—the
3. She no longer recognizes Timmy when he visits, even
other victims of neurocognitive disorder—as the person they care
though he is her only grandchild. ____________
for continues to decline.

Prevention
Without treatment, we need to rely even more heavily on preven-
tion strategies for neurocognitive disorder. You can imagine that
it is difficult to study prevention efforts for neurocognitive disor-
der because of the need to follow individuals for long periods to
see whether the efforts are effective. One major study conducted
in Sweden—where socialized medicine provides complete medical
histories of all residents—looked at many of the risk factors (those
factors that increase the chance of having neurocognitive disorder)
and protective factors (those that decrease the risk) under study
today (Fratiglioni, Winblad, & von Strauss, 2007). They looked at
the medical records of 1,810 participants who were older than 75 at
the time and followed them for about 13 years. Through interviews
and medical histories, they came to three major conclusions: con-
trol your blood pressure, do not smoke, and lead an active physical
and social life! These recommendations came out as the major fac-
tors that individuals can change—because you cannot change your
genetics, for example—that will decrease the chances of developing
neurocognitive disorder (Rizzuto, Orsini, Qiu, Wang, & Fratiglioni,
2012). Additional prevention research is ongoing, and there may be
other potentially fruitful research areas that can lead to the success-
ful prevention of this devastating disorder.
Concept Check 15.3
Identify the cognitive disorders described.
1. Julian is a recovering alcoholic. When asked about his
wild adventures as a young man, his stories usually end
quickly because he can’t remember the whole tale. He
even has to write down things he has to do in a notebook;
otherwise, he’s likely to forget. ____________
2. Mr. Brown has suffered from a number of strokes but can
still care for himself. His ability to remember important
things, however, has been declining steadily for the past
few years. ____________
3. A decline in cognitive functioning that is gradual and
continuous and has been associated with neurofibrillary
tangles and amyloid plaques. ____________

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 DSM Controversies: Is Normal Aging a Mental Disorder?
Researchers and clinicians
have, for some time, recognized that
many older adults begin to show cogni cogni-
tive decline in areas such as memory that
is more pronounced than expected for
their age and begins to affect their daily
functioning (Petersen et al., 1999). This
interest in the distinction between the
normal forgetting that occurs as we age
and the onset of neurocognitive disorder
is motivated by a desire to both under
under-
stand the progression of the cognitive
changes that accompany neurocognitive
disorder and to attempt early intervention.
In response to this concern, DSM-5 introintro-
disorder—mild
duced a new psychiatric disorder—
neurocognitive disorder—to categorize
the condition and bring it to the attention
of clinicians (Ganguli et al., 2011).
This proposed distinction
is consistent with some of the
breakthroughs in diagnoses involving
improved brain scanning and
identification of biomarkers that we
covered earlier in this chapter (Weiner et
al., 2012a). Researchers are becoming
more sophisticated in their ability to
identify beginning signs of neurocognitive
disorder, which not only allows for early
diagnosis but also can highlight for
clinicians the need to track cognitive
abilities over time. However, this new
disorder raised concerns among some in
the field (Rabins & Lyketsos, 2011).
First, the distinction between
“major” and “mild” neurocognitive
disorder is a difficult one to make.
DSM-5 attempts to quantify the declines
by tying the diagnosis to cognitive
test performance in the range of 1 1#2
standard deviations below what would
be expected for a person of that age
(American Psychiatric Association,
2013). Below-average performance
does not necessarily mean, however,
that the person has declining cognitive
function. That can be assessed only if
performance was measured through
cognitive assessment before the decline
occurred. But, it has been argued, routine
cognitive testing is not typically done on
adults until after some concern is raised,
making conclusions about changes in
functioning problematic (Frances, 2010).
A second concern is one that is
relevant for a number of other disorders
as well. The addition of new disorders
(such as mild neurocognitive disorder as
well as others such as premenstrual mood
dysphoric disorder) and the broadening
of the definitions of others have some
concerned that eventually most people
will meet the criteria for one or more
psychiatric disorders. In the case of
mild neurocognitive disorder, will we be
labeling people—and perhaps prescribing
drugs—to those who exhibit normal
forgetting related to age? As a whole,
the consequences of these changes
across DSM-5 are not trivial (Frances,
2010). Pharmaceutical companies are
incentivized to find more customers for
psychiatric drugs and therefore expanding
the number of people with a diagnosis
could increase business. The legal system
could be impacted with a greater number
of people using “mental illness” as a
mitigating factor in their defense. These
issues are far from being resolved and it
is important to note that DSM-5 is a work
in progress that will hopefully evolve with
our expanding scientific understanding
of the nature and causes of all of the
maladies impacting us.

Summary

Delirium ● Alzheimer’s disease is the leading cause of neurocognitive disorder,

● Delirium is a temporary state of confusion and disorientation
that can be caused by brain trauma, intoxication by drugs or poi-
sons, surgery, and a variety of other stressful conditions, especially
among older adults.
Major and Mild Neurocognitive Disorders
● Neurocognitive disorder is a progressive and degenerative con-
dition marked by gradual deterioration of a range of cognitive
abilities including memory, language, and planning, organizing,
sequencing, and abstracting information.
● Mild neurocognitive disorder is a condition in which there are
early signs of cognitive decline such that it begins to interfere with
activities of daily living.
affecting approximately 4 million people in the United States; there
is currently no known cause or cure.
● To date, there is no effective treatment for the irreversible neuro-
cognitive disorder caused by Alzheimer’s disease, Lewy bodies,
vascular disease, Parkinson’s disease, Huntington’s disease, and
various less common conditions that produce progressive cognitive
impairment. Treatment often focuses on helping patients cope with
the continuing loss of cognitive skills and helping caregivers deal
with the stress of caring for affected individuals.

Summary 565

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 Key Terms Answers to Concept Checks
delirium, 544 neurocognitive disorder due 15.1 15.3
major neurocognitive disorder to Lewy body disease, 553 1. c; 2. b; 3. a; 4. e; 5. f; 6. d 1. substance-induced neuro-
(dementia), 546 neurocognitive disorder due cognitive disorder; 2. vascular
mild neurocognitive disorder, to Parkinson’s disease, 553
15.2 neurocognitive disorder;
546 Parkinson’s disease, 553 3. neurocognitive disorder
agnosia, 548 human immunodeficiency 1. b; 2. c; 3. a
due to Alzheimer’s disease
facial agnosia, 548 virus type 1 (HIV-1), 554
Alzheimer’s disease, 549 neurocognitive disorder due
neurocognitive disorder due to HIV infection, 554
to Alzheimer’s type, 549 aphasia, 555
vascular neurocognitive Huntington’s disease, 556
disorder, 552 Neurocognitive disorder due to
head trauma, 553 Huntington’s disease, 556
frontotemporal neurocognitive Neurological disorder due to
disorder, 553 prion disease, 556
Pick’s disease, 553 Creutzfeldt-Jakob disease, 557
traumatic brain injury (TBI), substance/medication-
553 induced neurocognitive
neurocognitive disorder disorder, 557
due to traumatic brain deterministic, 558
injury, 553 susceptibility, 558

56 6 C ha p t e r 1 5 Neu ro c o gni ti ve D isorde r s

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 © Cengage Learning®
Media Resources C O N T I N U U M video project
Myriam Alzheimer’s Disorder
MindTap
MindTap for Barlow and Durand’s Abnormal Psychology: An Integra- “I’m going to forget their names. I’m going to
tive Approach is a highly personalized, fully online learning platform forget who they are. Alzheimer’s is eating away at my brain.”
of authoritative content, assignments, and services offering you a tai-
lored presentation of course curriculum created by your instructor. Access the Continuum Video Project in MindTap at
MindTap guides you through the course curriculum via an innovative www.cengagebrain.com
learning path where you will complete reading assignments, annotate
your readings, complete homework, and engage with quizzes and as-
sessments. MindTap includes Abnormal Psychology Videos and the
Continuum Video Project.
Go to cengagebrain.com to access MindTap.

Summary 567

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 Exploring
Exploring
Neurocognitive
Neurocognitive
Disorders
Disorders
◗ When ◗ the
Whenbrain
theisbrain
damaged,
is damaged,
the effects
the effects
are irreversible,
are irreversible,
accumulating
accumulating
until learning,
until learning,
memory,memory,
or consciousness
or consciousness
are obviously
are obviously
impaired.
impaired.
◗ Neurocognitive
◗ Neurocognitive
disorders
disorders
developdevelop
much later
much than
laterintellectual
than intellectual
disability
disability
and otherandlearning
other learning
disorders,
disorders,
which are
which are
believed
believed
to be present
to be present
at birth.at birth.

TYPESTYPES OF NEUROCOGNITIVE
OF NEUROCOGNITIVE DISORDERS
DISORDERS

Description
Description Causes
Causes
(subtypes)
(subtypes)
Treatment
Treatment

Delirium
Delirium ■ Impaired
■ Impaired
consciousness
consciousness■ Delirium ■ Delirium
due to adue to a ■ Pharmacological
■ Pharmacological
and cognition
and cognition
for several
for several general medical
general medical – benzodiazepines
– benzodiazepines
hours orhours
days or days conditioncondition – antipsychotics
– antipsychotics
– confusion,
– confusion,
disorientation,
disorientation,
■ Substance-induced
■ Substance-induced■ Psychosocial
■ Psychosocial
inability to
inability
focus to focus delirium delirium – reassurance
– reassurance
■ Most prevalent
■ Most prevalent
among among ■ Delirium ■ Delirium
due to due to – presence
– presence
of personal
of personal
older adults,
olderpeople
adults,with
people with multiple multiple
etiologiesetiologies objects objects
AIDS, and AIDS,
patients
and patients
on on ■ Delirium ■ Delirium
not otherwise
not otherwise– inclusion
– inclusion
in treatment
in treatment
medicationmedication specifiedspecified decisionsdecisions

©Photodisc/Getty Images

©Photodisc/Getty Images
©Photodisc/Getty Images

©Photodisc/Getty Images

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 Major
Majorand
and
Mild
Mild
Neurocognitive
Neurocognitive
Disorders
Disorders
◗ Gradual
◗ Gradual
deterioration
deterioration
of brainof functioning
brain functioning
that affects
that affects
judgment,
judgment,
memory,memory,
language,
language,
and other
and advanced
other advanced
cognitive
cognitive
processes
processes
◗ Caused
◗ Caused
by medical
by medical
condition
condition
or drugorabuse
drug abuse
◗ Some
◗ Some
forms forms
are irreversible;
are irreversible;
some some
are resolved
are resolved
by treatment
by treatment
of primary
of primary
condition.
condition.

Description
Description Causes
Causes Treatment
Treatment

Neurocognitive
Neurocognitive ■ Increasing
■ Increasing
memorymemory ■ Progressive
■ Progressive
brain brain ■ No cure
■ No socure
far, but
so far, but
Disorder
Disorder
due todue to impairment
impairment
and other and other damage, damage,
evident evident
in in hope lies
hopein genetic
lies in genetic
Alzheimer’s
Alzheimer’s multiplemultiple
behavioral
behavioral
and and neurofibrillary
neurofibrillary
tangles tangles
and and researchresearch
and amyloidand amyloid
cognitive
cognitive
deficits,deficits,
affectingaffecting neuritic neuritic
plaque,plaque,
confirmed confirmed protein.protein.
Disease
Disease
language,
language,
motor function-
motor function- by autopsy
by autopsy
but assessed
but assessed■ Management
■ Management may may
ing, ability
ing,toability
recognize
to recognize by simplified
by simplified
mental mental include include
lists, maps,
lists, and
maps, and
people people
or things,
or and/or
things, and/or status exam
status exam notes tonotes
help tomaintain
help maintain
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©Christian Martínez Kempin/E+/Getty Images

©Christian Martínez Kempin/E+/Getty Images

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neurocognitive
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©Photodisc/Getty Images

©Photodisc/Getty Images

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on prevention.
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Disorder

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also include
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■ Treatment
■ Treatment
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©Photodisc/Getty Images

©Photodisc/Getty Images

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©Simon Fraser/Royal Victoria Infirmary,

©Simon Fraser/Royal Victoria Infirmary,

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Newcastle upon Tyne/Science Source

Newcastle upon Tyne/Science Source

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■ Treatment
■ Treatment
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condition
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is sometimes
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Conditions
Conditions

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