Problem 8 - Neurocognitive

Research on the brain and its role in psychopathology has increased at a rapid pa
ce, 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 neurotransmitter systems ca
n significantly affict mood, cognition, and behavior.
Unfortunately, the brain is sometimes afflicted 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 information on t
hese cognitive disorders that impair all aspects of mental
functioning. Th 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 affct cognitive
processes such as learning, memory, and consciousness.
Perspectives on Neurocognitive Disorders
Most neurocognitive disorders develop much later in life, whereas
intellectual disability and specifi learning disorder are believed to
be present from birth (see Chapter 14). In this chapter, we review
two classes of cognitive disorders: delirium, an oftn 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.
Th label neurocognitive disorders in DSM-5 reflcts a shif in
the way these disorders are viewed (American Psychiatric Association, 2013). In
early editions of the DSM, they were labeled organic
mental disorders, along with mood, anxiety, personality, hallucinosis (an abnorma
l mental state involving hallucinations), and delusional disorders. Th word orga
nic indicated that brain damage
or dysfunction was believed to be involved. Th organic mental
disorders category, however, covered so many disorders that the
distinction was meaningless. Consequently, the traditional organic
disordersdelirium, dementia, and amnestic disorderswere kept
together, and the othersorganic mood, anxiety, personality, hallucinosis, and del
usional disorderswere categorized with disorders
that shared their symptoms (such as anxiety and mood disorders).
Once the term organic was dropped, attention moved to developing a better label
for delirium, dementia, and the amnestic disorders. Th label cognitive disorders w
as used in DSM-IV to
signify that their predominant feature is the impairment of such
cognitive abilities as memory, attention, perception, and thinking. Although dis
orders such as schizophrenia, autism spectrum
disorder, and depression also involve cognitive problems, cognitive issues are n
ot believed to be primary characteristics (Ganguli
et al., 2011). Problems still existed with the cognitive disorder
label, however, because although the cognitive disorders usually fist appear in
older adults, intellectual disability and specifi
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 various forms of demen
tia and amnestic disorders, with major or
mild subtypes; DSM-5 retains the delirium label (American
Psychiatric Association, 2013). Ths new categorization was created because of th
e overlap of the diffrent types of dementia (e.g.,
Alzheimers disease) and amnestic disorder found in people such
that one person may actually suffr from multiple types of neurocognitive problem
s (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 oftn include
profound changes in a persons behavior and personality. Intense
anxiety, depression, or both are common, especially among people
with major neurocognitive disorder. In addition, paranoia is often reported, as
are extreme agitation and aggression. Families and
friends are also profoundly affcted by such changes. Imagine your
emotional distress as a loved one is transformed into a diffrent
person, oftn one who no longer remembers who you are or your
history together. Th deterioration of cognitive ability, behavior,
and personality and the effcts on others are major concerns for
mental health professionals.
Delirium
Th 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.
to be only a temporary problem, more recent work indicates that
the effcts 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 increasingperhaps because of the increased number of adults livi
ng longerleading some to recommend that delirium be included as one of the vital s
igns (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 poisons; withdrawal
from drugs such as alcohol and sedative, hypnotic, and anxiolytic drugs; infect
ions; head injury; and various other
types of brain trauma (Meagher & Trzapacz, 2012). DSM-5 recognizes several cause
s of delirium among its subtypes. Th diagnosis
received by Mr. J.substance-induced deliriumas well as delirium not otherwise spec
ifid all include disruptions in the persons
ability to direct, focus, sustain, and shif attention. Th rise in the
use of drugs such as Ecstasy (methylene-dioxymethamphetamine)
is of particular concern because of such drugs potential to produce delirium (Sol
ai, 2009). Th last two categories indicate the
oftn complex nature of delirium.
Tht 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. Th risk of problems among the elderly is increased
further because they tend to eliminate drugs from their systems
less effiently 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 fractures in the e
lderly (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 effcts, including symptoms of delirium (Olivier
et al., 2009). Because possible combinations of illnesses and
medications are so numerous, determining the cause of delirium is extremely diff
ilt (Solai, 2009).

Delirium may be experienced by children who have high
fevers or who are taking certain medications and is oftn mistaken
for noncompliance (Smeets et al., 2010). It oftn occurs during
the course of dementia; as many as 50% of people with dementia
suffr at least one episode of delirium (Kwok, Lee, Lam, & Woo,
2008). Because many of the primary medical conditions can be
treated, delirium is oftn 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 factor; 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,
MR.J Sudden Distress
Mr. J., an older gentleman, was brought to the hospitalemergency room. He didnt k
now his own name, and
at times he didnt seem to recognize his daughter, who was
with him. Mr. J. appeared confused, disoriented, and a little
agitated. He had diffilty 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 hypertension medication and wonde
red whether the new medication
could be causing her fathers distress. Mr. J. was ultimately
diagnosed as having substance-induced delirium (a reaction
to his new medication); once the medication was stopped, he
improved signifiantly over the course of the next 2 days.
Th 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. Thy cannot focus and sustain their
attention on even the simplest tasks. Thre are marked impairments in memory and
language (Meagher & Trzapacz, 2012). Mr.
J. had trouble speaking; he was not only confused but also couldnt
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 prevalent among older adu
lts, people undergoing medical procedures,
cancer patients, and people with acquired immune defiiency syndrome (AIDS). Deli
rium subsides relatively quickly. Once thought
scientists assessed brain activity using fMRI scanning during
active episodes of delirium as well as aftr these episodes and
found both lasting disruption of connectivity (between the dorsolateral prefront
al 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 effrts 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 someone already so disorie
nted (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 medications, which he
lp calm the individual. Infections, brain injury, and
tumors are given the necessary and appropriate medical intervention, which oftn
then resolves the accompanying delirium. Th
antipsychotic drugs haloperidol or olanzapine are also prescribed
for individuals in acute delirium when the cause is unknown
(Meagher & Trzapacz, 2012).
Th recommended fist line of treatment for a person
experiencing delirium is psychosocial intervention. Th goal of
nonmedical treatment is to
reassure the individual to help
him or her deal with the agitation, anxiety, and hallucinations of delirium. A p
erson in
the hospital may be comforted
by familiar personal belongings
such as family photographs
(Fearing & Inouye, 2009). Also,
a patient who is included in
all treatment decisions retains
a sense of control (Katz, 1993).
Ths type of psychosocial treatment can help the person
manage during this disruptive
period until the medical causes
are identifid and addressed
(Breitbart & Alici, 2012). Some
evidence suggests that this type of support can also delay institutionalization
for elderly patients (Rahkonen et al., 2001).
Prevention
Preventive effrts may be most successful in assisting people who
are susceptible to delirium. Proper medical care for illnesses and
therapeutic drug monitoring can play signifiant roles in preventing delirium (Br
eitbart & 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
Offi, 1995).
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 oftn deny any diffilty, coming up with excuses (I forget
things, too) for their parents failing abilities. Major neurocognitive disorder (p
reviously labeled dementia) is a gradual deterioration of brain functioning that
affcts memory, judgment, language,
and other advanced cognitive processes. Mild neurocognitive disorder is a new DS
M-5 disorder that was created to focus attention
on the early stages of cognitive decline. Here the person has modest
impairments in cognitive abilities but can, with some accommodations (for exampl
e, making extensive lists of things to do or creating elaborate schedules), cont

inue to function independently.
Causes of neurocognitive disorders include several medical conditions and the ab
use of drugs or alcohol that produce
negative changes in cognitive functioning. Some of these
conditionsfor instance, infection or depressioncan cause
neurocognitive impairment, although it is oftn reversible
through treatment of the primary condition. Some forms of the
disorder, such as Alzheimers disease, are at present irreversible. Although delir
ium and neurocognitive disorder can occur
together, neurocognitive disorder has a gradual progression as
opposed to deliriums acute onset; people with neurocognitive
disorder are not disoriented or confused in the early stages,
unlike people with delirium. Like delirium, however, neurocognitive disorder has
many causes, including a variety of traumas
to the brain such as stroke (which destroys blood vessels), the
infectious diseases of syphilis and HIV, severe head injury, the
introduction of certain toxic or poisonous substances, and diseases such as Park
insons, Huntingtons, and, the most common
cause of dementia, Alzheimers. Consider the personal account
Simon Bruty/Sports Illustrated/GettyImages
by Pat Summitt, the most successful NCAA basketball coach of
all time. She coached the Tennessee Lady Vols basketball team
from 1974 to 2012winning a record setting 1,098 games
until her symptoms of neurocognitive disorder due to Alzheimers disease prevented
her from working with the team full-time.
She courageously writes of her experiences with this disorder
(Summitt, 2013).
Aftr several evaluations, which included neurological evaluations, magnetic reso
nance imaging (MRI) showing some damage in several parts of her brain, and a spi
nal tap that showed
the presence of beta amyloid protein, Pat Summitts neurologist
concluded that she had early onset neurocognitive disorder due
to Alzheimers disease. People at the same stage of decline as she
will continue to deteriorate and eventually may die from complications of their
disorder.
Clinical Description and Statistics
Depending on the individual and the cause, the gradual progression of neurocogni
tive disorder may have somewhat diffrent symptoms, although all aspects of cogni
tive functioning are
eventually affcted. 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 couldnt fid her way home because visuospatial skills are impaired amo
ng people with neurocognitive
disorder. Agnosia, the inability to recognize and name objects,
is one of the most familiar symptoms. Facial agnosia, the inability to recognize
even familiar faces, can be extremely distressing to family members. A general
deterioration of intellectual
function results from impairment in memory, planning, and
abstract reasoning.
Perhaps partly because people suffring from neurocognitive disorder are aware th
at they are deteriorating mentally,
emotional changes oftn occur as well. Common side effcts are
delusions (irrational beliefs), depression, agitation, aggression,
and apathy (Lovestone, 2012). It is diffilt, however, to establish the cause-and

-effct 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 discouragement that ine
vitably accompany the loss of function and the
isolation of losing loved ones. Cognitive functioning continues to deteriorate unt
il 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 illnesses, such as pn
eumonia.
Globally, it is estimated that one new case of major neurocognitive disorder is
identifid 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). Th increasing number
of people with just one form of neurocognitive disorderdue to
Alzheimers diseaseis alarming. Figure 15.1 illustrates how
the prevalence of neurocognitive disorder due to Alzheimers
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). Neurocognitive disorder due to
Alzheimers disease rarely occurs in people
under 45 years of age.
A dramatic rise in Alzheimers 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 disorderhave 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 statewas previously a separate DSM
disorder (amnestic disorder) but has been folded into the general neurocognitive
disorder group. Almost 10% of those over
70 had mild neurocognitive disorder and 11.6% met the criteria 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).
A problem with confiming prevalence fiures for neurocognitive disorder is that s
urvival 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 aftr age 75. Many
studies fid greater increases of neurocognitive disorder among
women (Carter, Resnick, Mallampalli, & Kalbarczyk, 2012).
Neurocognitive disorder due to Alzheimers 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 aftr the age of 75.

In addition to the human costs of neurocognitive disorder, the
fiancial costs are staggering. Estimates of the costs of caring for
people with neurocognitive disorder due to Alzheimers disease
are oftn 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). Thse numbers do not, however, factor in the co
sts to businesses for health care in the form of
insurance and for those who care for these individualsestimated
to be more than $140 billion in the United States alone (Weiner et
al., 2010). Many times, family members care for an afflted person
around the clock, which is an inestimable personal and fiancial
commitment (Lovestone, 2012).
DSM-5 identifis classes of neurocognitive disorder based on
etiology: (1) Alzheimers disease, (2) vascular injury, (3) frontotemporal degener
ation, (4) traumatic brain injury, (5) Lewy body
disease, (6) Parkinsons disease, (7) HIV infection, (8) substance
use, (9) Huntingtons disease, (10) prion disease, and (11) another
medical condition. We emphasize neurocognitive disorder due to
Alzheimers 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.
Neurocognitive Disorder Due to Alzheimers Disease
In 1907 the German psychiatrist Alois Alzheimer fist 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 dementia; thereaftr, it w
as referred to as Alzheimers disease.
Description and Statistics
Th DSM-5 diagnostic criteria for neurocognitive disorder due
to Alzheimers disease include multiple cognitive defiits that
develop gradually and steadily. Predominant are impairment of
memory, orientation, judgment, and reasoning. Th inability to
integrate new information results in failure to learn new associations. Individu
als with Alzheimers disease forget important events
and lose objects. Thir interest in nonroutine activities narrows.
Thy tend to lose interest in others and, as a result, become more
socially isolated. As the disorder progresses, they can become agitated, confuse
d, depressed, anxious, or even combative. Many of
these diffilties become more pronounced late in the dayin a
phenomenon referred to as sundowner syndromeperhaps as
a result of fatigue or a disturbance in the brains biological clock
(Lemay & Landreville, 2010).
People with neurocognitive disorder due to Alzheimers
disease also display one or more other cognitive disturbances,
including aphasia (diffilty with language), apraxia (impaired
motor functioning), agnosia (failure to recognize objects), or
diffilty with activities such as planning, organizing, sequencing,
or abstracting information. Thse cognitive impairments have a
serious negative impact on social and occupational functioning,
and they represent a signifiant 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 Alzheimers disease can be
detected, which could lead to early diagnosis. In the past, a defiitive diagnosi
s of Alzheimers disease could be made only aftr an
autopsy determined that certain characteristic types of damage
were present in the brain. Thre is now growing evidence, however, that the use o
f sophisticated brain scans along with new
chemical tracers may soon be able to help clinicians identify the
presence of Alzheimers disease before the signifiant declines in
cognitive abilities (through a project called the Alzheimers Disease Neuroimaging
Initiative [ADNI]) or death (Douaud et al.,
2013; Weiner et al., 2012b). In addition, research on the presence
of certain markers for Alzheimers (e.g., beta amyloidthe substance in the amyloid
plaques found in the brains of persons with
this disease) in spinal flid 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 simplifid
version of a mental status exam is used to assess language and
memory problems (see Table 15.1).
In an interesting, somewhat controversial studyreferred
to as the Nun Studythe writings of a group of Catholic nuns
collected over several decades appeared to indicate early in life
which women were most likely to develop Alzheimers disease
later (Snowdon et al., 1996). Researchers observed that samples
People with facial agnosia, a common symptom of neurocognitive
disorder, are unable to recognize faces, even of their closest friends
and relatives.
from the nuns journals over the years diffred 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:
Th 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
confimed by Bishop D. D. McGavich (Snowdon et al., 1996, pg.,
530). When fidings of autopsies on 14 of the nuns were correlated
with idea density, the simple writing (low idea density) occurred
among all 5 nuns with Alzheimers disease (Snowdon et al., 1996).
Ths is an elegant research study, because the daily lives of the nuns
were similar, which ruled out many other possible causes. Thre
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
Alzheimers 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 Alzheimers disease is slow during the early and late
r stages but more rapid during the middle
stages (Richards & Sweet, 2009). Th average survival time is
estimated to be about 8 years, although many individuals live
dependently for more than 10 years. In some forms, the disease can occur relativ
ely 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 disorder are found to b
e the result of Alzheimers disease, which is
believed to afflt more than 5 million Americans and millions
more worldwide (Alzheimers Association, 2010).
Some early research on prevalence suggested that Alzheimers
disease may occur more oftn in people who are poorly educated
(Fratiglioni et al., 1991; Korczyn, Kahana, & Galper, 1991). Greater impairment
among uneducated people might indicate a much
earlier onset, suggesting that Alzheimers disease causes intellectual dysfunction
that in turn hampers educational effrts. Or there

could be something about intellectual achievement that prevents
or delays the onset of symptoms of the disorder. Later research
seems to confim the latter explanation. It appears that educational
level may predict a delay in the observation of symptoms (Perneczky 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 Alzheimers disease but just provides
a buffr 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 defiits. 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. Ths tentative hypothesis may prove us
eful in designing treatment strategies, especially
during the early stages of the disorder.
Type* Maximum Score Question
Orientation 5
5
Ask the patient, What is the (year) (season) (date) (day) (month)?
Ask the patient, Where are we(state) (country) (town) (hospital) (flor)?
Registration 3 Name three objects, using 1 second to say each. Then ask the pati
ent 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 subtr
acting 7s. (Give one
point for each correct answer; stop after fie 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 flor. (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 Alzheimers
disease uses a relatively
simple test of the patients 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 me
dical diagnosis of the disorder.
*The examination also includes an assessment of the patients level of consciousne
ss: alert, drowsy, stupor, or coma.
Total maximum score is 30.
A biological version of this theory
the cognitive reserve hypothesis
suggests that the more synapses a person develops throughout life, the more
neuronal death must take place before
the signs of dementia are obvious
(Farias et al., 2012). Mental activity
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 changes in the brain with education may contribute to how quickly the
disorder progresses.
Research suggests that Alzheimers disease may be more
prevalent among women (Craig & Murphy, 2009), even when
womens higher survival rate is factored into the statistics. In
other words, because women live longer than men on average,
they are more likely to experience Alzheimers and other diseases,
but longevity alone does not account for the higher prevalence
of the disorder among women. A tentative explanation involves
the hormone estrogen. Women lose estrogen as they grow older,
so perhaps estrogen is protective against the disease. A large
and important studythe Womens Health Initiative Memory
Studylooked at hormone use among women and its effct on
Alzheimers disease (Shumaker et al., 2004). In its initial fidings,
the study followed women over age 65 using a type of combined
estrogen plus progestin known as Prempro and, contrary to the
belief that giving women estrogen would decrease their chance of
developing neurocognitive disorder, they observed an increased
risk for Alzheimers disease (Coker et al., 2010). More research
is ongoing into the individual effcts of these two types of
hormones on dementia.
The PET scan of a brain afflcted with Alzheimers disease (left) shows signifiant
tissue deterioration in comparison with a normal brain (right).
Tim Beddow/Science Source/Photo
Researchers, Inc.
Tim Beddow/Science Source/Photo
Researchers, Inc.
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 Alzheimers disease as follow
s:
For major neurocognitive disorder:
Probable Alzheimers disease is diagnosed if either of the following is present; o
therwise, possible Alzheimers disease should be
diagnosed.
1. Evidence of a causative Alzheimers disease genetic mutation from family histor
y 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 cogn
itive domain (based on detailed history or
serial neuropsychological testing).
b. Steadily progressive, gradual decline in cognition, without extended plateau
s.
c. No evidence of mixed etiology (i.e., absence of other neurodegenerative or c
erebrovascular disease, or another neurological, mental, or systemic disease or
condition likely contributing to cognitive decline).
For mild neurocognitive disorder:
Probable Alzheimers disease is diagnosed if there is evidence of a causative Alzh
eimers disease genetic mutation from either
genetic testing or family history.
Possible Alzheimers disease is diagnosed if there is no evidence of a causative A
lzheimers 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 plateau
s.
3. No evidence of mixed etiology (i.e., absence of other neurodegenerative or c
erebrovascular 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 n
eurodegenerative 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.
DSM TABLE 15.4 Diagnostic Criteria for Major or Mild Neurocognitive Disorder du
e to Alzheimers Disease
5
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552 C h a p t e r 1 5 Ne u ro c o g n i t i v e D i s o r d e r s
Finally, there appear to be questions about the prevalence of
Alzheimers disease according to racial identity. Early research
seemed to suggest that certain populations (such as those with
Japanese, Nigerian, certain Native American, and Amish backgrounds) were less li
kely to be affcted (for example, see PericakVance et al., 1996; Rosenberg et al.
, 1996). More recent work
indicates, however, that some of these diffrences may have been
the result of diffrences in who seeks assistance (which is seen as
unacceptable in some cultural groups), as well as diffrences in
education (which we saw may delay the onset of obvious symptoms) (Wilson et al.,
2010). Alzheimers disease is found in roughly
the same numbers across all ethnic groups, with one study fiding a slightly lowe
r rate among American Indians (Weiner, Hynan,
Beekly, Koepsell, & Kukull, 2007). As you will see, fidings 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 traumas to the brain
that result in restriction or cessation of blood flw).
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 neurocognitive defiits. I
t is one of the more common causes of neurocognitive
disorder (Erkinjuntti, 2012).
Th word vascular refers to blood vessels. When the blood vessels in the brain ar
e blocked or damaged and no longer carry oxygen and other nutrients to certain a
reas of brain tissue, damage
results. Because multiple sites in the brain can be damaged, the
profie of degenerationthe particular skills that are impaired
diffrs 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 Alzheimers disease have memory problems as their
initial cognitive disturbance.
Compared with research on neurocognitive disorder due to
Alzheimers type, there are fewer studies on vascular neurocognitive disorder, per
haps because of its lower incidence rates. Th
prevalence of vascular neurocognitive disorder is approximately 1.5% in people 7

0 to 75 years of age and increases to 15% for
those over the age of 80 (Neugroschi, Kolevzon, Samuels, & Marin,
2005). Th risk for men is slightly higher than among women, in
contrast with the higher risk among women for Alzheimers type
dementia, and this has been reported in many developed and
developing countries (Kalaria et al., 2008). Th relatively high rate
of cardiovascular disease among men in general may account for
their increased risk of vascular neurocognitive disorder. Th onset
of vascular dementia is typically more sudden than the onset for
the Alzheimers type, probably because the disorder is the result
of stroke, which inflcts brain damage immediately. Th 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 Alzheimers disease and vascular damage, a number of other neurolog
ical and biochemical processes can lead to
neurocognitive disorder. DSM-5 identifis eight specifi causes
in addition to Alzheimers disease and vascular damage: frontotemporal degeneratio
n, traumatic brain injury, Lewy body
B. The clinical features are consistent with a vascular etiology as suggested by
either of the following:
1. Onset of the cognitive defiits is temporally related to one or more cerebrova
scular 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, p
hysical examination, and/or neuroimaging considered suffiient to account for the
neurocognitive defiits.
D. The symptoms are not better explained by another brain disease or systemic di
sorder. Probable vascular neurocognitive disorder is diagnosed if one of the fol
lowing is present, otherwise, possible vascular neurocognitive disorder should b
e diagnosed:
1. Clinical criteria are supported by neuroimaging evidence of signifiant parenc
hymal 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 wit
h 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 cerebrovas
cular events is not established.
DSM TABLE 15.5 Diagnostic Criteria for Major or Mild Vascular Neurocognitive Di
sorder
5
disease, Parkinsons disease, HIV infection, substance use, Huntingtons disease, an
d prion disease. Each of these
is discussed here. In addition, a fial
categoryneurocognitive disorder due
to another medical conditionis provided for other causes. Other medical
conditions that can lead to neurocognitive disorder include normal pressure

hydrocephalus (excessive water in the
cranium, resulting from brain shrinkage), hypothyroidism (an underactive
thyroid gland), brain tumor, and vitamin B12 defiiency. Thre is increasing
recognition of neurocognitive disorder
among athletes who receive repeated
blows to the head. In the past this type
of neurocognitive disorder was referred
to as dementia pugilistica (which suggested that it was restricted to boxers
or pugilists) but it is currently referred
to as chronic traumatic encephalopathy (CTE). CTE is caused by repetitive
head trauma that can provoke distinctive neurodegeneration (Gavett, Stern,
Cantu, Nowinski, & McKee, 2010). In
their effct on cognitive ability, all of
these disorders are comparable to the other forms of neurocognitive disorder we
have discussed so far.
Descriptions and Statistics
Frontotemporal neurocognitive disorder is an overarching term
used to categorize a variety of brain disorders that damage the
frontal or temporal regions of
the brainareas that affct personality, language, and behavior (Gustafson & Brun,
2012).
DSM-5 identifis two variants
of frontotemporal neurocognitive disorderthrough declines
in appropriate behavior (e.g.,
socially inappropriate actions,
apathy, making poor judgments) or language (e.g., problems with speech, fiding t
he
right word, naming objects).
One of the disorders in this
category of neurocognitive disorders is Picks disease, a rare
neurological conditionoccurring in about 5% of those people
with neurocognitive impairmentthat produces symptoms
similar to that of Alzheimers
disease. Th course of this disease is believed to last from 5 to
10 years, and appears to have a
genetic component (Gustafson
& Brun, 2012). Picks disease usually
occurs relatively early in lifeduring a
persons 40s or 50sand is therefore considered an example of early onset neurocogni
tive disorder.
Severe trauma to the head causes
the brain to sustain lasting injuries
(called traumatic brain injury or
TBI) which can lead to neurocognitive
disorder (Fleminger, 2012). Neurocognitive disorder due to traumatic brain
injury includes symptoms that persist
for at least a week following the trauma,
including executive dysfunction (e.g.,
diffilty planning complex activities)
and problems with learning and memory. Thse that are at greatest risk for
TBI are teens and young adults, especially accompanied by alcohol abuse
or lower socio-economic class (Fleminger, 2012). Traff accidents, assaults,
falls, and suicide attempts are common
causes, as is being exposed to bomb
blasts in combat.
Th second most common type
of neurocognitive disorders (aftr
Alzheimers disease) is neurocognitive
disorder due to Lewy body disease (Aarsland, Ballard, Rongve,
Broadstock, & Svenningsson, 2012; McKeith et al., 2005). Lewy

bodies are microscopic deposits of a protein that damage brain
cells over time. Th signs of this disorder come on gradually
and include impairment in alertness and attention, vivid visual
hallucinations, and motor impairment as seen in Parkinsons
disease. In fact, there is some overlap between this disorder and
neurocognitive disorder due to Parkinsons disease (Mindham & Hughes, 2012).
Parkinsons disease is a degenerative brain disorder
that affects about 1 in every 1,000 people worldwide (Marsh
& Margolis, 2009). Movie and television star Michael J. Fox
and former U.S. Attorney General Janet Reno both suffer from
this progressive disorder. Motor problems are characteristic among people with P
arkinsons disease, who tend to have
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 movement, a reduction in this
neurotransmitter makes affected individuals 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 Parkinsons disease develop
neurocognitive disorder; conservative estimates place the rate
at 4 to 6 times that found in the general population (Aarsland
& Kurz, 2010).
Junior Seau was an NFL star football player who committed suicide
in 2012. The National Institutes
of Healthat the request of his
familydetermined through an
examination of his brain that he
had abnormalities consistent
with repetitive blows to the head
which resulted in chronic traumatic encephalopathy (CTE).
Jim McIsaac/Staff/Getty Images
with Amnesia: Mike
I still have a pretty major memory problem,
which has since brought about a divorce
and which . . . I now have a new girlfriend,
which helps very much. I even call her . . . my
new brain or my new memory. . . . If I want
to know something, besides on relying on
this so-called memory notebook, which I jot
notes down in constantly and have it every
day dated, so I know whats coming up or
whats for that day.
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
fiding, 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 fo
llowing is present; otherwise, possible frontotemporal neurocognitive disorder s
hould be diagnosed:
1. Evidence of a causative frontotemporal neurocognitive disorder genetic mutati
on, from either family history or genetic
testing.
2. Evidence of disproportionate frontal and/or temporal lobe involvement from n
euroimaging.
Possible frontotemporal neurocognitive disorder is diagnosed if there is no evid
ence of a genetic mutation, and neuroimaging
has not been performed.
DSM TABLE 15.6 Diagnostic Criteria for Major or Mild Frontotemporal Neurocognit
ive Disorder
5
B. There is evidence of a traumatic brain injurythat 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 preexisting seizure disorder; visual fild 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.
DSM TABLE 15.7 Diagnostic Criteria for Major or Mild Neurocognitive Disorder du
e to Traumatic Brain Injury
5
Th human immunodefiiency virus type 1 (HIV-1), which
causes AIDS, can also cause neurocognitive disorder (called
neurocognitive disorder due to HIV infection) (Maj, 2012). Ths
impairment seems to be independent of the other infections that
accompany HIV; in other words, the HIV infection itself seems
to be responsible for the neurological impairment. Th early
symptoms of neurocognitive disorder resulting from HIV are
cognitive slowness, impaired attention, and forgetfulness. Affcted
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 signifiant
declines in cognitive abilities may occur earlier. Cognitive impairments were hi
ghly common among those infected with AIDS,

but with the introduction of new medications (highly active antiretroviral thera
pies, 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 Alzheimers disease and vascular causes,
but its presence can complicate an already-devastating set of
medical conditions.
Like neurocognitive disorder from Parkinsons disease and
several other causes, neurocognitive disorder resulting from
HIV is sometimes referred to as subcortical dementia, because
it affcts primarily the inner areas of the brain, below the outer
layer called the cortex (Bourgeois, Seaman, & Servis, 2003).
Th distinction between cortical (including neurocognitive disorder due to Alzhei
mers disease) and subcortical dementia is
important because of the diffrent expressions of neurocognitive disorder in thes
e two categories (see Table 15.2). Aphasia,
which involves impaired language skills, occurs among people
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 probable or possible neur
ocognitive 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 cerebrovascular disease, another n
eurodegenerative 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.
TABLE 15.8 Diagnostic Criteria for Major or
Mild Neurocognitive Disorder
with Lewy Bodies
DSM
5
disorder.
B. The disturbance occurs in the setting of established
Parkinsons 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
Parkinsons disease should be diagnosed if 1 and 2 are both
met. Major or mild neurocognitive disorder possibly due to
Parkinsons 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 Parkinsons disease clearly precedes the onset of
neurocognitive disorder.
TABLE 15.9 Diagnostic Criteria for
due to Parkinsons Disease
DSM
5
disorder.
B. There is documented infection with human immunodefciency 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.
by a mental disorder.
due to HIV Infection
DSM
5
with neurocognitive disorder due to Alzheimers disease but not
among people with subcortical dementia. In contrast, people with
subcortical dementia are more likely to experience severe depression and anxiety
than those with neurocognitive disorder due to
Alzheimers disease. In general, motor skills including speed and
coordination are impaired early on among those with subcortical
dementia. Th diffring patterns of impairment can be attributed
to the diffrent areas of the brain affcted by the disorders causing
the neurocognitive disorder.
Huntingtons disease is a genetic disorder that initially affcts
motor movements, typically in the form of chorea, involuntary
limb movements (Marsh & Margolis, 2009). People with Huntingtons disease can live
for 20 years aftr the fist signs of the disease appear, although skilled nursin
g care is oftn required during
the last stages. Just as with Parkinsons disease, only a portion of
people with Huntingtons disease go on to display neurocognitive
disordersomewhere between 20% and 80%although some
researchers believe that all patients with Huntingtons disease
would eventually display neurocognitive impairments if they lived
long enough (Marsh & Margolis, 2009). Neurocognitive disorder
due to Huntingtons disease also follows the subcortical pattern.
Th search for the gene responsible for Huntingtons 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 offpring of an adult with
Huntingtons disease will develop the disease. Since 1979, behavioral scientist Na
ncy Wexler and a team of researchers have been
studying the largest known extended family in the world afflted
by Huntingtons disease, in small villages in Venezuela. Th
villagers have cooperated with the research, partly because Wexler
herself lost her mother, three uncles, and her maternal grandfather to Huntingto
ns disease, and she, too, may develop the disorder (Wexler, 2012). Using genetic
linkage analysis techniques
(see Chapter 4), these researchers fist mapped the defiit to an
area on chromosome 4 (Gusella et al., 1983) and then identifid
the elusive gene (Huntingtons 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) inflences.
Neurocognitive disorder due to prion disease is a rare progressive neurodegenera
tive disorder caused by prionsproteins
that can reproduce themselves and cause damage to brain cells
The AIDS virus may cause neurocognitive disorder in the later stages.
Simon Fraser/Royal Victoria Infimary, Newcastle upon Tyne/Science Source
Characteristic Dementia of the alzheimers Type Subcortical Dementias
Language Aphasia (diffiulties with articulating speech) No aphasia
Memory Both recall and recognition are impaired Impaired recall; normal or less
impaired recognition
Visuospatial skills Impaired Impaired
Mood Less severe depression and anxiety More severe depression and anxiety
Motor speed Normal Slowed
Coordination Normal until late in the progression Impaired
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.
Table 15.2 Characteristics of Neurocognitive Disorders
disorder.
B. There is insidious onset and gradual progression.
C. There is clinically established Huntingtons disease, or
risk for Huntingtons disease based on family history or
genetic testing.
due to Huntingtons Disease
DSM
5
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 positive side, p
rions 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, CreutzfeldtJakob disease, i
s believed to affct only one in every million individuals (Heath et al., 2010).
An alarming development in the study
of Creutzfeldt-Jakob disease is the fiding 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). Ths 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 defiitive information
about the link between mad
cow disease and the new form
of Creutzfeldt-Jakob disease
(Wiggins, 2009).
Substance/
Medication-Induced
Neurocognitive
Disorder
Prolonged drug use, especially
combined with poor diet, can
damage the brain and, in some
circumstances, can lead to
neurocognitive disorder. Ths
impairment unfortunately lasts
beyond the period involved
in intoxication or withdrawal
from these substances.
As many as 7% of individuals dependent on alcohol meet the criteria for neurocog
nitive disorder (Neugroschi et al., 2005). Th
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). Thse drugs pose a threat because they create dependence, making it
diffilt for a user to stop ingesting them. Th
resulting brain damage can be permanent and can cause the same
symptoms as seen in neurocognitive disorder due to Alzheimers
type. Th 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 disturbances: aphasia (la
nguage disturbance), apraxia (inability to carry
out motor activities despite intact motor function), agnosia (failure to recogni
ze or identify objects despite intact sensory function), or a disturbance in exe
cutive 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 Inflences
Cognitive abilities can be adversely compromised in many ways.
As you have seen, neurocognitive disorder can be caused by a
number of processes: Alzheimers disease, Huntingtons disease,
Parkinsons disease, head trauma, substance abuse, and others. Th
most common cause of neurocognitive disorder, Alzheimers disease, is also the mos
t mysterious. Because of its prevalence and our

relative ignorance about the factors responsible for it, Alzheimers
disease has held the attention of many researchers, who are trying
to fid the cause and ultimately a treatment or cure for this
devastating condition.
Findings from Alzheimers research seem to appear almost
daily. We should be cautious when interpreting the output of this
fast-paced and competitive fild; too oftn, as you have seen in
other areas, fidings are heralded prematurely as conclusive and
important. Remember that discoveries of a single gene for bipolar disorder, schizo
phrenia, and alcoholism were later shown to
be based on overly simplistic accounts. Similarly, fidings from
Alzheimers research are sometimes too quickly sanctioned as
accepted truths before they have been replicated, an essential
validation process.
One lesson in scientifi caution comes from research that
demonstrates a negative correlation between cigarette smoking
and Alzheimers disease (Brenner et al., 1993). In other words,
the study found that smokers are less likely than nonsmokers
to develop Alzheimers disease. Does this mean smoking has
a protective effct, shielding a person against the development
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.
TABLE 15.12 Diagnostic Criteria for
Neurocognitive Disorder due
to Prion Disease
DSM
5
Michael J. Fox provides his time
and celebrity status to efforts
to cure Parkinsons disease, a
degenerative disease that is
severely affecting his life.
Slaven Vlasic/Stringer/Getty Images
of this disease? On close examination, the fiding may instead
be the result of the diffrential 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 Alzheimers 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 Alzheimers disease, may interact with cigarette smoking to shor
ten the lives of smokers who are at risk for
Alzheimers disease (Riggs, 1993). Put another way, smoking may
exacerbate the degenerative process of Alzheimers disease, causing people with th
e disease who also smoke to die earlier than
nonsmokers who have Alzheimers disease (Ashare, Karlawish,
Wileyto, Pinto, & Lerman, 2012). Thse 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 Alzheimers disease, the most common
cause of neurocognitive disorder? Aftr 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 fiaments within the brain cells
(referred to as neurofirillary tangles). Ths type of damage occurs in
everyone with Alzheimers disease. A second type of degeneration
results from gummy protein depositscalled 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 neurocognitive disord
er, but they have far fewer of them than do individuals with Alzheimers disease (
Richards & Sweet, 2009). Both forms of
damageneurofirillary tangles and amyloid plaquesaccumulate
over the years and are believed to produce the characteristic cognitive
disorders we have been describing (Weiner et al., 2012a).
Thse two types of degeneration affct 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 flid 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 neurofirillary tangles and amyloid
plaques, over time the brains of many people with Alzheimers 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 Alzheimers disease be properly made.
Rapid advances are being made toward uncovering the genetic
bases of Alzheimers 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 Alzheimers 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 Alzheimers disease
(Neugroschi et al., 2005). Th link to chromosome 21 was discovered
fist, and it resulted from the unfortunate observation that individuals with Dow
n 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 Alzheimers Disease, 1995).
More recent work has located relevant genes on other chromosomes.
Thse discoveries indicate that there is more than one genetic cause
of Alzheimers disease. Some forms, including the one associated
with chromosome 14, have an early onset. Pat Summitt was diagnosed with an early
-onset form. In contrast, Alzheimers disease
associated with chromosome 19 seems to be a late-onset form of the
disease that has an effct only aftr the age of about 60.
Some genes that are now identifid are deterministic, meaning that if you have on
e of these genes you have a nearly 100%
chance of developing Alzheimers 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(b) and the Presenilin 1 and Presenilin 2
genes will inevitably lead to Alzheimers disease, but, fortunately,
these genes are also rare in the general population. For treatment
purposes, this means that even if researchers can fid a way to
prevent these genes from leading to Alzheimers disease, it will
only help a relatively small number of people. On the other hand,
some genesincluding the apolipoprotein E4 (apo E4) geneare
known as susceptibility genes. Thse genes only slightly increase
the risk of developing Alzheimers disease, but in contrast to the
deterministic genes, these are more common in the general population (Lovestone,
2012). If future research can fid ways to interfere with the apo E4 gene, many
people will be helped.
Although closing in on the genetic origins of Alzheimers disease
has not brought immediate treatment implications, researchers are
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 capa
ble of producing the neurocognitive impairment.
D. The temporal course of the neurocognitive defiits is consistent with the timi
ng of substance or medication use and abstinence
(e.g., the defiits 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.
DSM TABLE 15.13 Diagnostic Criteria for Substance/Medication-Induced Major or Mi
ld Neurocognitive Disorder
nearer to understanding how the disease develops, which may result
in medical interventions. Genetic research has advanced our knowledge of how the
amyloid plaques develop in the brains of people with
Alzheimers disease and may hold a clue to its origins. In the core of
the plaques is a solid waxy substance made up of a peptide called
amyloid beta or Ab. Just as cholesterol buildup on the walls of blood
vessels chokes the blood supply, deposits of Ab are believed by some
researchers to cause the cell death associated with Alzheimers disease
(Lovestone, 2012). An important question, then, is Why does this protein accumul
ate in the brain cells of some people but not of others?
Two mechanisms that may account for amyloid protein buildup are being studied. T
h fist involves amyloid precursor protein
(APP), a large protein that is eventually broken down into the
amyloid protein found in the amyloid plaques. Important work
resulted in identifying the gene responsible for producing APP,
on chromosome 21 (Lovestone, 2012). Ths fiding may help
integrate two observations about Alzheimers disease: (1) APP
produces the amyloid protein found in the amyloid plaques, and
(2) Down syndrome, associated with an extra 21st chromosome,
results in a higher incidence of the disease (see Chapter 14). Th
gene responsible for producing APP and, ultimately, amyloid protein, may be resp
onsible for the relatively infrequent early-onset
form of the disease, and its location could explain why people
with Down syndromewho have an extra 21st chromosome and
therefore an extra APP geneare more likely than the general
population to develop Alzheimers disease.
A second, more indirect way that amyloid protein may build
up in brain cells is through apolipoprotein E (apo E), which normally helps tran
sport cholesterols, including amyloid protein,
through the bloodstream. Thre are at least three forms of this
transporter protein: apo E2, apo E3, and apo E4. Individuals who
have late-onset Alzheimers disease, the most common form, are
likely to carry the gene associated with apo E4, located on chromosome 19. Resea
rchers have found that the majority of people
with Alzheimers 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 Alzheimers
disease who have no family history of the disease have at least one
gene for apo E4, and only 31% of nonaffcted individuals have the
gene. Having two genes for apo E4 (one on each member of the
chromosome 19 pair) increases the risk for Alzheimers disease:
As many as 90% of people with two genes developed Alzheimers
disease (Reiman et al., 2007). In addition, having two apo E4
genes seemed to decrease the mean age of onset from 84 years to
68 years. Thse results suggest that apo E4 may be responsible for
late-onset Alzheimers disease and that a gene on chromosome 19
is responsible. What is still not completely understood is how apo
E4 causes amyloid proteins to build up in the neurons of people
who ultimately exhibit Alzheimers disease and whether this process is responsible
for the disease.
Researchers are just beginning to try to examine potential
geneenvironment interactions in Alzheimers disease. Several
studies suggest a few areas of promise. One study found that having the apo E4 g
enotype was more likely to produce cognitive
decline in those persons living in stressful environmentssuggesting a gene (apo E
4)environment (stress) interaction (Boardman,
Barnes, Wilson, Evans, & de Leon, 2012). Another study found
that among African Americans, having low levels of cholesterol
seemed to reduce risk of Alzheimers diseasebut only among
those who did not carry the apo E4 gene (Evans et al., 2000). Finally,
researchers found that physical exercise reduced the likelihood of
developing the disease but, like the previous study, only among
those without the apo E4 gene (Podewils et al., 2005). Ths type of
research holds the potential for better understanding the complex
nature of Alzheimers disease and may lead to important prevention strategies (suc
h as lowering cholesterol levels and exercising
regularly) (Pedersen, 2010).
For all disorders described in this book, we have identifid
the role of biological, psychological, or both types of stressors as
partially responsible for the onset of the disorder. Does neurocognitive disorde
r due to Alzheimers diseasewhich appears to
be a strictly biological eventfollow the same pattern? One of
the leading candidates for an external contributor to this disorder
is head trauma. As we have seen, it appears that repeated blows
to the head can bring on neurocognitive disorder (chronic traumatic encephalopat
hy or CTE). Fighters who carry the apo E4
gene may be at greater risk for developing neurocognitive disorder attributed to
head trauma (Jordan et al., 1997). In addition to
Gene Chromosome
age of Onset
(years)
APP 21 43 to 59
Presenilin 1 14 33 to 60
Presenilin 2 1 50 to 90
apo E4 19 60
AAP 5 amyloid precursor protein; apo E4 5 apolipoprotein E4.
Source: Lovestone, S. (2012). Dementia: Alzheimers disease. In M. G.
Gelder, N. C. Andreasen, J. J. Lopez Jr. & J. R. Geddes (Eds.), New Oxford
textbook of psychiatry (2nd. ed., Vol. 1, pp. 333343). New York: Oxford
University Press.
Table 15.3 Genetic Factors in Alzheimers Disease
Nancy Wexler headed the team of scientists who found the gene for
Huntingtons disease.
Acey Harper/Time Life Pictures/Getty Images
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 stressors 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 biological stressors may
interact with physiological processes to produce
Alzheimers disease.
We opened the section with a word of caution, which it is
appropriate at this point to repeat. Some of the fidings just
reviewed are considered controversial, and many questions
remain to be answered about neurocognitive disorder and one of
its most common causes, Alzheimers disease.
Psychological and Social Inflences
Research has mostly focused on the biological conditions that produce neurocogni
tive disorder. Although few would claim that psychosocial inflences directly cau
se the type of brain deterioration
seen in people with neurocognitive disorder, they may help determine onset and c
ourse. For example, a persons 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 biological and psychosoc
ial factors. In the case of vascular neurocognitive
disorder, a persons biological vulnerability to vascular disease will
inflence the chances of strokes that can lead to this form of disorder. Lifestyl
e issues such as diet, exercise, and stress inflence cardiovascular disease and
therefore help determine who experiences
vascular neurocognitive disorder (see Chapter 9).
Cultural factors may also affct 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
oftn observed in members of these groups. In an extreme example, exposure to pri
on 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 disorder caused by he
ad trauma and malnutrition are relatively prevalent in preindustrial rural socie
ties (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). Thse fidings suggest that o
ccupational safety (such as protecting workers
from head injuries) and economic conditions inflencing diet also
affct the prevalence of certain forms of neurocognitive disorders.
It is apparent that psychosocial factors help inflence who does
and who does not develop certain forms of neurocognitive disorder. Brain deterio
ration is a biological process but, as you have
seen throughout this text, even biological processes are inflenced
by psychosocial factors.
Psychosocial factors themselves inflence the course of neurocognitive disorder.
Recall that educational attainment may
affct the onset of dementia (Richards & Sweet, 2009). Having
certain skills may help some people cope better than others with
the early stages of neurocognitive disorder. Th 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 aftr a certain age,
and symptoms of dementia are viewed as a sign of normal aging
(Gallagher-Thmpson 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 Alzheimers disease and Hun
tingtons disease, certain genetic factors make
some individuals vulnerable to progressive cognitive deterioration. 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 cognitive abilitie
s. 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 integrative perspect
ive 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 psychosocial perspectiv
es.
Treatment
For many of the disorders discussed in other chapters, treatment
prospects are fairly good. Clinicians can combine various strategies to reduce s
uffring signifiantly. Even when treatment does
not bring expected improvements, mental health professionals
have usually been able to stop problems from progressing. Ths is
not the case in the treatment of neurocognitive disorder.
One factor preventing major advances in the treatment of neurocognitive disorder
is the nature of the damage caused by this disorder. Th brain contains billions
of neurons, many more than are
used. Damage to some can be compensated for by others because
of plasticity. Thre 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 brains natural process
of regeneration to potentially reverse the damage caused in neurocognitive disor
der (Khachaturian, 2007). Currently, however, with
extensive brain damage, no known treatment can restore lost abilities. Th 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 advancing deterioratio
n. Most effrts in treating neurocognitive disorder
have focused on the second and third goals, with biological treatments aimed at
stopping the cerebral deterioration and psychosocial treatments directed at help
ing patients and caregivers cope.
A troubling statistic further clouds the tragic circumstances
of neurocognitive disorder: More than 23% of caregivers of
people with neurocognitive disorderusually relativeshave the
symptoms characteristic of one or more
anxiety disorders and 10% are clinically
depressed (Katona & Livingston, 2009).
Compared with the public, these caregivers use more psychotropic medications
(designed to reduce symptoms of various psychological disorders) and report
stress symptoms at 3 times the normal
rate. Caring for people with neurocognitive disorder, especially in its later st
ages,
is clearly a trying experience. In fact,
there is some evidence to suggest that the
stress associated with caring for a person
with neurocognitive disorder may place
the caregiver at greatly increased risk

for developing neurocognitive disorder
themselves (Norton et al., 2010). As a
result, clinicians are becoming increasingly sensitive to the needs of these car
egivers, and research is now exploring
interventions to assist them in caring for
people with neurocognitive disorder (Lee, Czaja, & Schulz, 2010).
Biological Treatments
Neurocognitive disorder resulting from known infectious diseases, nutritional de
fiiencies, and depression can be treated if
it is caught early. Unfortunately, however, no known treatment
exists for the types of neurocognitive disorder that account for the
vast majority of cases. Neurocognitive disorder caused by stroke,
Parkinsons disease, or Huntingtons disease is not currently treatable, because the
re is no effctive treatment for the primary disorder. However, exciting research
in several related areas has brought
us closer to helping individuals with these forms of neurocognitive
disorder. A substance that may help preserve and perhaps restore
neuronsglial cellderived neurotrophic factormay someday
be used to help reduce or reverse the progression of degenerative brain diseases
(Zuccato & Cattaneo, 2009). Researchers are
also looking into the possible benefis of transplanting stem cells
(fetal brain tissue) into the brains of people with such diseases.
Initial results from these studies are still preliminary but appear
promising (Arenas, 2010). Neurocognitive disorder brought on by
strokes may now be more preventable by new drugs that help prevent much of the d
amage inflcted by the blood clots characteristic
of stroke (Erkinjuntti, 2012). Most current attention is on a treatment for deme
ntia of the Alzheimers type, because it affcts so
many people. Here, too, however, success has been modest at best.
Much work has been directed at developing drugs that will
enhance the cognitive abilities of people with neurocognitive
disorder due to Alzheimers type. Many seem to be effctive initially, but long-ter
m improvements have not been observed in
placebo-controlled studies (Richards & Sweet, 2009). Several
drugs (called cholinesterase inhibitors) have had a modest impact
on cognitive abilities in some patients and include donepezil
(Aricept), rivastigmine (Exelon), and galantamine (Reminyl)
(Trinh, Hoblyn, Mohanty, & Yaff, 2003). Tacrine hydrochloride
(Cognex), another in this family of drugs, is rarely used today
because of the potential for liver damage
(Rabins, 2006). Thse drugs prevent the
breakdown of the neurotransmitter acetylcholine (which is defiient in people
with Alzheimers disease), thus making
more acetylcholine available to the brain.
Research suggests that, when using these
drugs, peoples cognitive abilities improve
to the point where they were 6 months
earlier (Lyketos, 2009). But the gain is not
permanent. Even people who respond
positively do not stabilize but continue to
experience the cognitive decline associated with Alzheimers disease. In addition,
if they stop taking the drugas almost
three-quarters of the patients do because
of negative side effcts such as liver damage and nauseathey lose even that
6-month gain (Lyketos, 2009). Newer
drugs are now being investigated for the
treatment of Alzheimers disease. Thse
include drugs that target the beta amyloid (plaques) in the brain,
and it is hoped that these advances will fially provide a positive
prognosis for this devastating disease (Lukiw, 2012).

Several other medical approaches are being explored to slow
the course of Alzheimers disease, but initial excitement generated
by these approaches has waned with the fidings from researchers. For example, mo
st of you have heard of using Ginkgo biloba
(maidenhair) to improve memory. Initial research suggested that
this herbal remedy may produce modest improvements in the
memory of people with Alzheimers disease, but other studies have
not replicated this benefi (DeKosky et al., 2008). Similarly, the
effcts of vitamin E have been evaluated. One large study found
that among individuals with moderately severe impairment, high
doses of the vitamin (2,000 international units per day) delayed
progression compared with a placebo (Sano et al., 1997), but it
did not prevent the development of the disease. Further research,
in fact, indicates that taking high doses of vitamin E may actually increase mor
tality and therefore this intervention is no longer
recommended (Richards & Sweet, 2009). Modest slowing of the
progression of the disease also may be obtained by introducing
exercise to patients (Rockwood & Middleton, 2007; Teri et al.,
2003). To date, however, no medical interventions are available
that directly treat and therefore stop the progression of the conditions that ca
use the cerebral damage in Alzheimers disease.
Medical interventions for neurocognitive disorder also include
the use of drugs to help with some associated symptoms. A variety
of antidepressantssuch as serotonin-specifi reuptake inhibitorsare commonly recomm
ended to alleviate the depression
and anxiety that too oftn accompany the cognitive decline. Antipsychotic medicat
ion is sometimes used for those who become
unusually agitated (Richards & Sweet, 2009).
Other researchers are targeting vaccines that would potentially treat and preven
trather than just delaythe symptoms
of Alzheimers disease. Much of the research is attempting to get
the immune system to attack the process that overproduces the
small proteins (Ab) that lead to cell death. Prior effrts had to
Computer Simulations
and Neurocognitive
Disorder
Our cognitive activity arises from the neural
networks in the brain. Whenever you lose an
individual neuron, youre not losing an idea,
youre just losing a tiny bit of the resolution,
or the crispness, of that idea.
be abandoned because of the severe negative side effcts of
the vaccine, which included serious brain inflmmation. More
recent research with humans and animals indicates that there
may be several vaccines that could be effctive in preventing the
damage caused by Ab formation and therefore represent the fist
glimmer of hope for patients and their families (Subramanian,
Bandopadhyay, Mishra, Mathew, & John, 2010).
Ths type of research currently begins with transgenic mice
mice in which the DNA has been altered. In the case of testing an
Alzheimers vaccine, the mice DNA is engineered to produce the
same small proteins thought to be responsible for the neurocognitive disorder. M
ice are good subjects because they age rapidly,
with a 22-month-old mouse equivalent to a 65-year-old human
(Morgan, 2007). Ths allows researchers to study how the brain
reacts to the potential vaccine if it has already started the progression of Alz
heimers. If the results are promising in these transgenic
mice, only then do researchers try small studies with humans.
Researchers are optimistic that there may fially be intervention

approaches that would reverse the current trend of increasing
numbers of people with neurocognitive disorder. Next we describe
psychosocial approaches that are used with medication to address
the variety of problems that accompany memory diffilties.
Psychosocial Treatments
Psychosocial treatments are now receiving a great deal of attention for their ab
ility to delay the onset of severe cognitive decline.
Thse effrts focus on enhancing the lives of people with neurocognitive disorder,
as well as those of their families.
People with neurocognitive disorder can be taught skills to
compensate for their lost abilities. Some researchers have evaluated
formal adaptations to help people in the early stages of neurocognitive disorder
. Michelle Bourgeois (2007) created memory wallets
to help people with Alzheimers disease carry on conversations. On
white index cards inserted into a plastic wallet are printed declarative stateme
nts such as, My husband John and I
have 3 children, or I was born on January 6, 1921,
in Pittsburgh. In one of her studies, Bourgeois
(1992) found that adults with neurocognitive disorder due to Alzheimers disease c
ould, with minimal
training, use this memory aid to improve their conversations with others. With a
dvances 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
their own decline (Fried-Oken et al., 2012).
Cognitive stimulationencouraging people
with neurocognitive disorder to practice learning and memory skillsseems to be an
effctive
method for delaying the onset of the more severe
cognitive effcts of this disorder (Knowles, 2010).
Thse activities include word games, tests of memory of famous and familiar faces
, and practice with
numbers (for example, how much change back
you would receive from a purchase). Thse types
of skill-building exercises can maintain cognitive
activity and improve the quality of life in those patients when
compared with controls (J. Choi & Twamley, 2013).
What impact do the medical and nonmedical treatments
have on those with Alzheimers disease? Figure 15.2 illustrates
how these interventions may delay the worst of the symptoms
essentially compressing the time when the person is most impaired
(Becker, Mestre, Ziolko, & Lopez, 2007). Th red line illustrates the
typical course of the disease, which results in 3 to 5 years of severe
impairment before death. However, with the interventions we highlighted (illustr
ated by the purple line), people are able to live more
fully for a longer period, despite the still-inevitable impairment and
death. Families fid this extra time with their loved ones to be invaluable, and
hopefully with more advancements we will see progress on
improving mortality rates of this progressive disease.
Individuals with advanced neurocognitive disorder are not able
to feed, bathe, or dress themselves. Thy cannot communicate with
or recognize even familiar family members. Thy may wander away
from home and become lost. Because they are no longer aware of
social stigma, they may engage in public displays of sexual behavior,
such as masturbation. Thy may be frequently agitated or even physically violent.
To help both the person with dementia and the caregiver,
researchers have explored interventions for dealing with these consequences of t

he disorder (Lovestone, 2012). For example, some research
indicates that a combination of exercise for patients and instruction
for caregivers on how to handle behavior problems can improve the
overall health and the depression in people with Alzheimers disease
(Logsdon, McCurry, Pike, & Teri, 2009; Teri et al., 2003).
Of great concern is the tendency of people with neurocognitive disorder to wande
r. Sometimes they wind up in places or situations that may be dangerous (for exa
mple, stairwells or the street).
Sometimes the person may be tied to a chair or bed, or sedated, to
prevent roaming. Unfortunately, physical and medical restraint has
its own risks, including additional medical complications; it also
adds greatly to the loss of control and independence that already
Typical course of neurocognitive disorder due to Alzheimer s disease
Modified course of neurocognitive disorder when patient is treated with medical
and nonmedical interventions
Improved function
+
Severe impairment
Less time with
severe impairment 1 year
3 to 5 years
Years of clinical disease
Death
FIGURE 15.2 Improving the course of Alzheimers disease with medical and nonmedical
interventions. (From Becker, J. T., Mestre, L. T., Ziolko, S., & Lopez, O. L. [
2007].
Gene environment interactions with cognition in late life and compression of morb
idity.
American Journal of Psychiatry, 164, 849852.)
plague the person with neurocognitive disorder. Psychological treatment as an al
ternative to restraint sometimes involves providing
cues for people to help them safely navigate around their home or
other areas. New innovations in surveillance technologycreating a
smart home that can monitor the location of the patient and warn
caregiversmay 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. Ths behavior is understandably
stressful for people trying to provide care.
In these situations, medical intervention is oftn used, although
many times with only modest results (Testad, Ballard, Brnnick,
& Aarsland, 2010). Some research suggests that teaching communication skills in
a manner similar to programs for persons
with autism spectrum disorder (Durand, 2012) may help reduce
aggressive behavior in persons with neurocognitive disorder
(Baker & LeBlanc, 2011). In addition, caregivers are oftn given
assertiveness training to help them deal with hostile behaviors
(see Table 15.4). Some caregivers may either passively accept all
criticism inflcted by the person with neurocognitive disorder,
which increases stress, or become angry and aggressive in return.
Ths last response is of particular concern because of the potential for elder ab
use. Withholding food or medication or inflcting
physical abuse is most common among caregivers of elderly people who have cognit
ive defiits (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.
Not a great deal of objective evidence supports the usefulness

of assertiveness training for reducing caregiver stress, and more
research is needed to guide future effrts.
In general, families of people with mild to moderate neurocognitive disorder can
benefi from supportive counseling to help them
cope with the frustration, depression, guilt, and loss that take a
heavy emotional toll. Clinicians must fist recognize, however, that
the ability to adapt to stressors diffrs among people. One study, for
example, found cultural diffrences in the coping styles of caregivers. In one ar
ea 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 identifid a number of steps that can be taken to support
caregivers through this diffilt time (Aneshensel, Pearlin, Mullan,
Zarit, & Whitlatch, 1995). Despite numerous studies aimed at supporting caregive
rs, 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, fiancial and legal issues,
and locating help for the patient and the family. As the disorder
progresses, and the affcted person requires increasing amounts
of assistance, caregivers will need help managing behavioral diffiulties (wander
ing away or violent outbursts) and developing
A resident of an assistive living facility practices cognitive stimulation
using one of several computer-based systems (the Dakim [m]Power
Brain Fitness System).
Dakim [m]Power Cognitive Fitness Systems: Kara Kenna photographer
.www.dakim.com
Patient behavior assertive Response
Calmly but fimly say:
The patient refuses to eat, bathe, or
change clothes.
We agreed to do this at this time so that we will be able to (give specifi activi
ty
or reward).
The patient wants to go home. I know you miss some of the places we used to be. T
his is our home now, and
together we are safe and happy here.
The patient demands immediate
gratifiation.
Its not possible to have everything we want. As soon as Ive fiished (describe
specifi task or action), we can discuss other things we want to do.
The patient accuses the caregiver of taking the patients possessions.
We both enjoy our own things. Ill help you look for (specifi item missing) so that
you can enjoy it just as soon as I have fiished (describe specifi task or action
).
The patient is angry, rebellious, or both. I like to be treated fairly just as yo
u do. Lets discuss whats 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 Alzheimers and dementia patient. New York, NY: Plenum Press,
p. 174, 1994 Plenum Press.
Table 15.4 Sample Assertive Responses
effctive ways to communicate with the patient. Clinicians also
assist the family with decisions about hospitalizations and, fially,
help them adjust during bereavement (Peeters, Van Beek,
Meerveld, Spreeuwenberg, & Francke, 2010).
Overall, the outlook for slowing (but not stopping) the cognitive decline charac
teristic of neurocognitive disorder is optimistic.
Th best available medications provide some recovery of function,
but they do not stop the progressive deterioration. Psychological
interventions may help people cope more effctively with the loss
of cognitive abilities, especially in the earlier stages of this disorder. In ad
dition, emphasis is placed on helping caregiversthe
other victims of neurocognitive disorderas the person they care
for continues to decline.
Prevention
Without treatment, we need to rely even more heavily on prevention strategies fo
r neurocognitive disorder. You can imagine that
it is diffilt to study prevention effrts for neurocognitive disorder because of
the need to follow individuals for long periods to
see whether the effrts are effctive. One major study conducted
in Swedenwhere socialized medicine provides complete medical
histories of all residentslooked 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). Thy looked at
the medical records of 1,810 participants who were older than 75 at
the time and followed them for about 13 years. Though interviews
and medical histories, they came to three major conclusions: control your blood
pressure, do not smoke, and lead an active physical
and social life! Thse recommendations came out as the major factors that individ
uals can changebecause you cannot change your
genetics, for examplethat 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 successful preven
tion of this devastating disorder.
Identify the following symptoms of dementia from the
descriptions: (a) facial agnosia, (b) agnosia, and (c) aphasia.
1. Timmys elderly grandmother does not recognize her
own home any more. ____________
2. She can no longer form complete, coherent sentences.
____________
3. She no longer recognizes Timmy when he visits, even
though he is her only grandchild. ____________
Concept Check 15.2
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 cant remember the whole tale. He
even has to write down things he has to do in a notebook;
otherwise, hes likely to forget. ____________
2. Mr. Brown has suffred 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 neurofirillary
tangles and amyloid plaques. ____________
Concept Check 15.3
S u m m a ry 565
Researchers and clinicians
have, for some time, recognized that
many older adults begin to show cognitive 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 understand the progression of the cognitive
changes that accompany neurocognitive
disorder and to attempt early intervention.
In response to this concern, DSM-5 introduced a new psychiatric disordermild
neurocognitive disorderto 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
identifiation 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 fild (Rabins & Lyketsos, 2011).
First, the distinction between
major and mild neurocognitive
disorder is a diffiult one to make.
DSM-5 attempts to quantify the declines
by tying the diagnosis to cognitive
test performance in the range of 1 22
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 defiitions 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 peopleand perhaps prescribing
drugsto 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 fid 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 scientifi understanding
of the nature and causes of all of the
maladies impacting us.
DSM Controversies: Is Normal Aging a Mental Disorder?
is motivated by a desire to both under
stand the progression of the cognitive
In response to this concern,
many older adults begin to show 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
is motivated by a desire to both understand the progression of the cognitive
In response to this concern, DSM-5 intro
duced a new psychiatric disorder
neurocognitive disorderto categorize
the condition and bring it to the attention
of clinicians (Ganguli et al., 2011).
disorder is a diffiult one to make.
DSM-5
by tying the diagnosis to cognitive
test performance in the range of 1
standard deviations below what would
Delirium
Delirium is a temporary state of confusion and disorientation
that can be caused by brain trauma, intoxication by drugs or poisons, surgery, a
nd a variety of other stressful conditions, especially
among older adults.
Neurocognitive disorder is a progressive and degenerative condition marked by gr
adual 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.

Alzheimers disease is the leading cause of neurocognitive disorder,
affcting approximately 4 million people in the United States; there
is currently no known cause or cure.
To date, there is no effctive treatment for the irreversible neurocognitive diso
rder caused by Alzheimers disease, Lewy bodies,
vascular disease, Parkinsons disease, Huntingtons disease, and
various less common conditions that produce progressive cognitive
impairment. Treatment oftn focuses on helping patients cope with
the continuing loss of cognitive skills and helping caregivers deal
with the stress of caring for affcted individuals.
Summary
Key Terms
delirium, 544
major neurocognitive disorder
(dementia), 546
mild neurocognitive disorder,
546
agnosia, 548
facial agnosia, 548
Alzheimers disease, 549
neurocognitive disorder due
to Alzheimers type, 549
vascular neurocognitive
disorder, 552
head trauma, 553
frontotemporal neurocognitive
disorder, 553
Picks disease, 553
traumatic brain injury (TBI),
553
neurocognitive disorder
due to traumatic brain
injury, 553
to Lewy body disease, 553
to Parkinsons disease, 553
Parkinsons disease, 553
human immunodefiiency
virus type 1 (HIV-1), 554
to HIV infection, 554
aphasia, 555
Huntingtons disease, 556
Neurocognitive disorder due to
Huntingtons disease, 556
Neurological disorder due to
prion disease, 556
Creutzfeldt-Jakob disease, 557
substance/medicationinduced neurocognitive
disorder, 557
deterministic, 558
susceptibility, 558
15.1
1. c; 2. b; 3. a; 4. e; 5. f; 6. d
15.2
1. b; 2. c; 3. a
15.3
1. substance-induced neurocognitive disorder; 2. vascular

neurocognitive disorder;
3. neurocognitive disorder
due to Alzheimers disease
answers to Concept Checks
CONTINUUM video project
Myriam Alzheimers Disorder
Im going to forget their names. Im going to
forget who they are. Alzheimers is eating away at my brain.
Access the Continuum Video Project in MindTap at
www.cengagebrain.com
Media Resources
MindTap
MindTap for Barlow and Durands Abnormal Psychology: An Integrative Approach is a
highly personalized, fully online learning platform
of authoritative content, assignments, and services offring you a tailored prese
ntation of course curriculum created by your instructor.
MindTap guides you through the course curriculum via an innovative
learning path where you will complete reading assignments, annotate
your readings, complete homework, and engage with quizzes and assessments. MindT
ap includes Abnormal Psychology Videos and the
Continuum Video Project.
Exploring Neurocognitive Disorders
When the brain is damaged, the effects are irreversible, accumulating until lear
ning, memory, or consciousness
are obviously impaired.
Neurocognitive disorders develop much later than intellectual disability and oth
er learning disorders, which are
believed to be present at birth.
Gradual deterioration of brain functioning that affects judgment, memory, langua
ge, and other advanced
cognitive processes
Caused by medical condition or drug abuse
Some forms are irreversible; some are resolved by treatment of primary condition
.
TYPES OF NEUROCOGNITIVE DISORDERS
Description Causes Treatment
Neurocognitive
Disorder due to
Alzheimers
Disease
Delirium Increasing memory
impairment and other
multiple behavioral and
cognitive de
cits, affecting
language, motor functioning, ability to recognize
people or things, and/or
planning
Most prevalent
Subject of most research
No cure so far, but
hope lies in genetic
research and amyloid
protein.
Management may
include lists, maps, and

notes to help maintain
orientation.
New medications that
prevent acetylcholine
breakdown and vitamin
therapy delay but do
not stop progression of
decline.
Progressive brain
damage, evident in
neuro
brillary tangles and
neuritic plaque, con
rmed
by autopsy but assessed
by simpli
ed mental
status exam
Involves multiple genes
Substanceinduced
Neurocognitive
Disorder
Caused by brain damage due to prolonged drug use, especially in combination with
poor diet, as in alcohol dependency; other substances may include inhalants, and
the sedative, hypnotic, and anxiolytic drugs
Treatment focuses on prevention.
Permanent deterioration due to blocked or damaged blood vessels in the brain (st
roke)
Symptoms include declines in speed of information processing and executive funct
ioning (e.g., complex decision making) and may also include problems with walkin
g and
weakness of limbs.
Treatment focuses on coping.
Similar in effect to other cognitive disorders, but caused by:
head trauma
Lewy bodies, HIV, Parkinsons, Huntingtons, Picks, or Creutzfeldt-Jakob disease
hydrocephalus, hypothyroidism, brain tumor, and vitamin B12 de
ciency
Treatment of primary condition is sometimes possible.
Vascular
Neurocognitive
Disorder
Neurocognitive Disorders
Due to Other
Medical
Conditions
Photodisc/Getty Images
Simon Fraser/Royal Victoria Inrmary,
Newcastle upon Tyne/Science SourcePhotodisc/Getty ImagesChristian Martnez Kempin/E+
/Getty Images
Description Causes (subtypes) Treatment
Impaired consciousness
and cognition for several
hours or days
confusion, disorientation,
inability to focus
Most prevalent among
older adults, people with

AIDS, and patients on
medication
Pharmacological
benzodiazepines
antipsychotics
Psychosocial
reassurance
presence of personal
objects
inclusion in treatment
decisions
Delirium due to a
general medical
condition
Substance-induced
delirium
Delirium due to
multiple etiologies
Delirium not otherwise
speci
ed
cognitive processes
.
Neurocognitive
Disorder due to
Alzheimers
Disease
cognitive de
cits, affecting
planning
Most prevalent
No cure so far, but
protein.
Management may
orientation.
decline.
Progressive brain
damage, evident in
neuro
rmed
by simpli
ed mental
status exam
Substanceinduced
Neurocognitive
Disorder
roke)
g and
weakness of limbs.
head trauma
ciency
Vascular
Neurocognitive
Disorder
Due to Other
Medical
Conditions
/Getty Images
hours or days
inability to focus
medication
Pharmacological
benzodiazepines
antipsychotics
Psychosocial
reassurance
objects
decisions
Delirium due to a
general medical
condition
Substance-induced
delirium
Delirium due to
multiple etiologies
speci
ed
cognitive processes
.
Neurocognitive
Disorder due to
Alzheimers
Disease
cognitive de
cits, affecting
planning
Most prevalent
No cure so far, but
protein.
Management may
orientation.

decline.
Progressive brain
damage, evident in
neuro
rmed
by simpli
ed mental
status exam
Substanceinduced
Neurocognitive
Disorder
roke)
g and
weakness of limbs.
head trauma
ciency
Vascular
Neurocognitive
Disorder
Due to Other
Medical
Conditions
/Getty Images
hours or days
inability to focus
medication
Pharmacological
benzodiazepines
antipsychotics
Psychosocial
reassurance
objects
decisions
Delirium due to a
general medical
condition
Substance-induced
delirium
Delirium due to
multiple etiologies
speci
ed
cognitive processes
.
Neurocognitive
Disorder due to
Alzheimers
Disease
cognitive de
cits, affecting
planning
Most prevalent
No cure so far, but
protein.
Management may
orientation.

decline.
Progressive brain
damage, evident in
neuro
rmed
by simpli
ed mental
status exam
Substanceinduced
Neurocognitive
Disorder
roke)
g and
weakness of limbs.
head trauma
ciency
Vascular
Neurocognitive
Disorder
Due to Other
Medical
Conditions
Newcastle upon Tyne/Scie

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Research on the brain and its role in psychopathology has increased at a rapid pa

As with certain other disorders, it may be useful to clarify why

ilt (Solai, 2009).

Although such research is potentially important for effrts to

e, making extensive lists of things to do or creating elaborate schedules), cont

and apathy (Lovestone, 2012). It is diffilt, however, to establish the cause-and

rapidly aftr the age of 75.

that in turn hampers educational effrts. Or there

serves as an initial protective factor in

prevalence of vascular neurocognitive disorder is approximately 1.5% in people 7

conditions that can lead to neurocognitive disorder include normal pressure

Broadstock, & Svenningsson, 2012; McKeith et al., 2005). Lewy

iv. Perseverative, stereotyped, or compulsive/ritualistic behavior.

ghly common among those infected with AIDS,

another medical condition and is not better explained

t mysterious. Because of its prevalence and our

cause of neurocognitive disorder? Aftr the death of the patient he

the onset of neurocognitive disorder of varying

Levkoff 2000). Neurocognitive disorder may go undetected for

the caregiver at greatly increased risk

prognosis for this devastating disease (Lukiw, 2012).

Researchers are optimistic that there may fially be intervention

researchers have explored interventions for dealing with these consequences of t

Not a great deal of objective evidence supports the usefulness

their age and begins to affect their daily

forgetting related to age? As a whole,

activities of daily living.

1. substance-induced neurocognitive disorder; 2. vascular

include lists, maps, and

older adults, people with

New medications that

breakdown and vitamin

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