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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).
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
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).
Description and Statistics
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
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
A. The criteria are met for major or mild neurocognitive
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.
D. The neurocognitive disorder is not attributable to
another medical condition and is not better explained
by another mental disorder.
From American Psychiatric Association. (2013). Diagnostic and statistical
manual of mental disorders (5th ed.). Washington, DC.
TABLE 15.11 Diagnostic Criteria for Major or
Mild Neurocognitive Disorder
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.
Description and Statistics
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
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
A. The criteria are met for major or mild neurocognitive disorder.
B. The neurocognitive impairments do not occur exclusively during the course of
a delirium and persist beyond the usual
duration of intoxication and acute withdrawal.
C. The involved substance or medication and duration and extent of use are 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.
From American Psychiatric Association. (2013). Diagnostic and statistical manual
of mental disorders (5th ed.). Washington, DC.
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
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
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
Photodisc/Getty Images
Simon Fraser/Royal Victoria Inrmary,
Newcastle upon Tyne/Science SourcePhotodisc/Getty ImagesChristian Martnez Kempin/E+
/Getty Images
Photodisc/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
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.
Major and Mild Neurocognitive Disorders
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
neurocognitive disorder
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.
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
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.
Major and Mild Neurocognitive Disorders
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
neurocognitive disorder
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