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NEUROCOGNITIVE DISORDERS (NCD)
NCD is a syndrome that exhibits multiple cognitive deficits that
compromise normalsocial or occupational function. There are numerous
etiologies such as Alzheimer’s disease (AD), dementia with Lewy
bodies (DLB), and vascular disease, which require a comprehensive
evaluation to define a potential diagnosis.
NCD DUE TO ALZHEIMER’S DISEASE
AD is a chronic, progressive, neurodegenerative disorder that results
other neurochemical changes in the brain.
AD has multiple risk factors such as age, family history, Down
syndrome, head trauma, hypertension, and mild cognitive impairment,
yet the exact etiology is still unknown.
Treatment for AD currently is symptomatic management, not disease
altering, and focuses on neurotransmission (e.g., cholinergic system).
Cholinesterase inhibitors may be used as monotherapy or in combination
with an N-methyl-D-aspartate antagonist for patients in the moderate to
Monitoring for treatment efficacy should focus on cognition, function,
and possibly behaviors, whereas treatment toxicity should look for
common adverse effects such as gastrointestinal complaints with
Has similar neuropathology noted with α-synuclein aggregates found in
Lewy bodies and neuritis (α-synucleinopathies), which typically present
with parkinsonian findings as well as associated symptoms such as falls
Cholinesterase inhibitors have demonstrated symptomatic benefit in
patients with Lewy body dementias, yet monitoring for worsening of
motor symptoms such as tremor is needed.
Vascular dementia is a broad classification of cognitive disorders caused
by vascular disease, and notable multiple risk factors include advancing
age, diabetes mellitus, small vessel cerebrovascular disease,
hypertension, heart disease, hyperlipidemia, cigarette smoking, and
Treatment for vascular dementia strives to control the underlying
modifiable risk factors owing to limited efficacy and controversial
evidence with cholinesterase inhibitors.
BEHAVIORAL DISTURBANCES IN DEMENTIA
When evaluating a dementia patient with behavior disturbances, the first
step is to ensure that the problem is not caused by an unrecognized
medical problem or adverse effect of a medication.
Nonpharmacologic strategies are effective for managing many behavior
disturbances and should be attempted before using medications to
Delusions and hallucinations are common behaviors in dementia patients,
yet the use of antipsychotics for these symptoms is not approved by the
US Food and Drug Administration and has been associated with the
increased risk of stroke and mortality in this patient population.
Wandering is a safety concern that often does not respond to
pharmacologic intervention; instead, other strategies such as
environmental modifications are used.
Antidepressants such as selective serotonin reuptake inhibitors have
shown promise in addressing depressive symptoms, as well as
Caregiver support is essential to maintaining a dementia patient safely in
his or her home as long as possible.
Neurocognitive disorders span a wide range of conditions that exhibit a global
decline in cognition. Among the disorders included are delirium, dementia, and
several other disorders with various etiologies (e.g., head trauma, HIV, Huntington
1 Among older adults, the dementias are the most commonly encountered
diseases and are the focus of this chapter.
With the continuing growth in the elderly population, the incidence and prevalence of
neurocognitive disorders continues to rise.
1,2 Alzheimer’s disease (AD) is the most
common cause, and accounts for more than half of all diagnosed cases.
dementia (VaD), dementia with Lewy bodies (DLB), and Parkinson’s disease with
dementia (PDD) are the next most common dementias, with frontotemporal dementia,
pseudodementia, and other forms occurring less often.
leading cause of death for people age 65 years and older and the sixth leading cause
of death for all people in the United States.
It is estimated that 5.3 million Americans have AD, including approximately 11% of
people age 65 years and older and 32% of people age 85 years and older. Of these,
more than 3.2 million are women. Prevalence is greater among both African
Americans and Hispanics compared with whites.
3 The annual incidence of AD in the
United States rises from 53 per 1,000 among people age 65 to 74 years to 170 per
1,000 for those age 75 to 84 years, and to 231 per 1,000 for those at least 85 years of
9 Worldwide prevalence has been estimated to be as high as 24.3 million, with
8.4 million new cases annually.
2,10 Projections into the mid-century include a
worldwide prevalence of more than 81 million, with cases in undeveloped countries
occurring at about three times the rate as in developed countries.
States, AD accounts for nearly 70% of cases; VaD accounts for 17.4%, with the
remaining 12.6% attributable to DLB, frontotemporal dementia, and other forms.
Life expectancy after a diagnosis of AD is reduced by as much as 69% for those
diagnosed before age 70 years and by 39% for those diagnosed after age 90 years.
The cost of dementia is staggering. Annual costs for Medicare recipients with
dementia average $21,585, compared with $8,191 for those without dementia. For
Medicaid recipients with dementia, the annual costs are $11,021, compared with
$574 for those without dementia. The annual direct costs, in 2014 dollars, of treating
a dementia patient are $47,752 annually, compared with $15,115 for an older adult
without dementia. This translates to an estimated annual direct cost for dementia care
of $226 billion for the year 2015.
Dementia is a neurocognitive disorder that exhibits impaired short- and long-term
memory as its most prominent feature. Multiple cognitive deficits that compromise
normal social or occupational function must be present before dementia can be
1 Commonly, forgetfulness is the primary complaint of
patients or the first symptom noted by the family.
12 Family members or others may
note several symptoms that should prompt a medical evaluation (Table 108-2).
Memory loss often accompanies several diseases or disorders in elderly individuals.
Therefore, a medical history, physical examination, and medication history are
essential in excluding systemic illness or medication toxicity as causes of the memory
13–16 Laboratory and other tests to assist in differentiating
dementia from other disorders are listed (Table 108-4). In patients with AD, test
results will generally be normal; evidence of cerebrovascular disease is present in
Brain imaging, such as a computed tomography (CT) scan or magnetic resonance
imaging (MRI), can be useful in establishing the presence of a dementia, but neither
is diagnostic. A CT scan is useful when a space-occupying lesion, such as a tumor, is
suspected as a possible cause. An MRI scan is capable of identifying small infarcts,
such as those found in some forms of VaD, and atrophy of subcortical structures such
Mental Status (SLUMS) exam are appropriate for initial screening of people with
suspected cognitive impairment.
17–19 The Folstein Mini-Mental State Exam (MMSE)
also can be used; however, it is less sensitive than others
for dementia and now is proprietary.
20 These tests rapidly assess multiple
domains, typically including orientation, registration, attention and calculation,
recall, and language. Patients with dementia exhibit deficits in multiple areas. Those
who score below the normal range on the MMSE or other screens, or who exhibit
symptoms characteristic of dementia receive further testing. A somewhat more
detailed screen, the Cognitive Abilities Screening Instrument (CASI), provides
quantitative assessment on attention, concentration, orientation, short-term memory,
long-term memory, language abilities, visual construction, list-generating fluency,
21 All screening tests are subject to limitations. Therefore,
additional psychometric testing is often ordered to further establish the presence and
Dementias may be classified as cortical or subcortical, according to the areas of
the brain preferentially affected by the disorder. AD, a typical cortical dementia,
disrupts the cerebral cortex. Patients with cortical dementias display impaired
language rather than impaired speech, a learning deficit (amnesia), reduced higher
cortical functions (e.g., inability to perform calculations, poor judgment), and an
unconcerned or disinhibited affect. Subcortical dementias such as PDD primarily
affect the basal ganglia, thalamus, and brainstem. Deficits include abnormal motor
function, disrupted speech patterns rather than language difficulties, forgetfulness
(impaired recall), slowed cognitive function, and an apathetic or depressed affect.
Differentiating Neurocognitive Disorders
Mild (formerly Mild Cognitive Impairment) Major (formerly Dementia)
Modest cognitive decline from previous (baseline)
performance in at least one cognitive domain, including:
The deficits do not impair the capacity to be
independent in everyday activities
The cognitive symptoms do not occur exclusively
The cognitive deficits are not better explained by
depression, schizophrenia or other mental disorders
Significant cognitive decline from previous (baseline)
performance in at least one cognitive domain, including:
The deficits impair the capacity to be independent in
The cognitive symptoms do not occur exclusively
The cognitive deficits are not better explained by
depression, schizophrenia or other mental disorders
NCD due to Alzheimer’s Disease
Criteria for either mild or major NCD are met
Insidious onset and gradual progression of impairment
Mild: impairment in one cognitive domain
Major: impairment in at least two cognitive domains
Probable Alzheimer’s disease (either of the following must be present)
Alzheimer’s disease genetic mutation based on family history or genetic testing
All of the following are present:
Decline in memory and learning plus one other cognitive domain
Steady and gradual cognitive decline
No evidence of another condition that is likely to cause cognitive decline
Lack of an Alzheimer’s disease genetic mutation
All of the following are present:
Decline in memory and learning
Steady and gradual cognitive decline
No evidence of another condition that is likely to cause cognitive decline
cognitive decline or neurodegeneration
Criteria for either mild or major NCD are met
Clinical presentation is consistent with a vascular cause (either of the following is present)
Onset of cognitive impairment follows a cerebrovascular event or multiple events
Prominent decline in complex attention and executive function
Probable vascular NCD (at least one of the following is present)
Neuroimaging supports cerebrovascular disease as the cause of the clinical presentation
The neurocognitive deficit follows at least one cerebrovascular event
Presence of both clinical and genetic evidence of cerebrovascular disease
A systemic disorder or other brain disease do not adequately explain the symptoms
Criteria for either mild or major NCD are met
The onset is insidious, with gradual progression
A combination of the following core and suggestive diagnostic features are present
Fluctuating cognition accompanied by variable attentiveness and alertness
Recurrent, well-formed and detailed visual hallucinations
Onset of Parkinsonian features that are exhibited after the onset of cognitive decline
Criteria for rapid eye movement (REM) sleep behavior disorder are met
Severe sensitivity to neuroleptic agents
Probable NCD with Lewy Bodies (either of the following is present)
One or more core features and one suggestive feature
Possible NCD with Lewy Bodies (either of the following is present)
One or more suggestive features
cognitive decline or neurodegeneration
1,36,75,77,81,83 and Jack CR Jr, Albert MS, Knopman DS, et al. Introduction to the
DeKosky ST, Dickson D, et al: The diagnosis of mild cognitive impairment due to Alzheimer’s disease:
NINDS-AIREN International Workshop. Neurology 43(2):250–260, 1993
Difficulty learning or retaining
Repeats questions; difficulty remembering recent conversations, events, etc.;
Impaired reasoning Difficulty solving everyday problems; inappropriate social behavior
Impaired spatial orientation and
Gets lost in familiar places; difficulty with driving
Language deficits Problems finding appropriate words (e.g., difficulty with naming common
Behavior changes Changes in personality; suspiciousness
Service, Agency for Health Care Policy and Research. AHCPR Publication No. 97-0702. November 1996.
Disorders Systemic Illness Medications
Adjustment disorder (e.g., inability to
Amnestic syndrome (e.g., isolated
Nonsteroidal anti-inflammatory
Sedative hypnotics and anxiolytics
Complete blood count with sedimentation rate Anemic anoxia, infection, neoplasms
Serum electrolytes Hypernatremia, hyponatremia; renal function
Blood urea nitrogen, creatinine Renal function
Bilirubin Hepatic dysfunction (e.g., portalsystemic
encephalopathy, hepatocerebral degeneration)
Thyroid function Hypothyroidism, hyperthyroidism
, folate, vitamin D Deficiency states (vitamin B12
vitamin D deficiency), anemias
Stool occult blood Blood loss, anemia
Urinalysis Infection, proteinuria
Chest roentgenogram Neoplasms, infection, airway disease (anoxia)
Electrocardiogram Cardiac disease (stagnant anoxia)
Brain scan Cerebral tumors, cerebrovascular disease
Mentalstatus testing General cognitive screen
Depression testing Depression, pseudodementia
A definitive cause for AD has yet to be determined. Several risk factors, however,
have been identified. Advancing age is the primary risk factor for AD; other risks
include family history, head trauma, metabolic syndrome, diabetes, hypertension and
3,23-27 Genetics plays a significant role in the development of
Alzheimer’s disease. The high familial occurrence of AD has been linked to
autosomal-dominant traits on chromosomes 21, 14, and 1.
amyloid precursor protein (APP), a normal protein, is located on chromosome 21. A
defect on chromosome 14 has been identified as the locus for the presenilin-1 gene,
which codes for an inherited form of AD. The presenilin-2 gene, located on
chromosome 1, also codes for an inherited form. Despite a strong genetic link in
some pedigrees, the great majority of AD cases are sporadic.
sporadic form appears to be linked to a susceptibility gene, apolipoprotein E, which
29 APP, a normal protein found throughout the body, maps on
chromosome 21 and plays a pivotal role in AD neuropathology. Because of
overproduction or transcription errors, an abnormal subunit (i.e., β-amyloid) is
29 Mutations on chromosomes 14 (presenilin-1 gene) and 1 (presenilin-2
gene) and the presence of apolipoprotein E4 allele code for alterations in the
processing of APP. The abnormal cleavage of APP produces a 42–amino acid form
of β-amyloid (Aβ) that demonstrates a higher toxicity than other amyloid forms.
Apolipoprotein E (ApoE), a protein that is involved in cholesterol and
phospholipid metabolism, plays a role in the development of sporadic, late-onset
AD. The ApoE gene possesses three alleles: E2, E3, and E4. The E3 allele is most
common, the E2 allele appears to be protective against AD, and the E4 allele
29 The presence of ApoE-4, the protein coded for by the E4
allele, appears to increase the deposition of Aβ and promote its change to a more
29 The presence of one or two copies of ApoE4 increases
the risk of developing AD twofold or fivefold, respectively.
amyloid protein found in other regions of the body, appears to contribute to neuronal
death through a combination of apoptosis, a direct toxic effect, and an increased risk
for damage owing to oxidative and metabolic stresses.
atrophy accompanies normal aging. Atrophic changes induced by AD are found
primarily in the temporal, parietal, and frontal areas of the brain; the occipital region,
primary motor cortex, and somatosensory areas are generally unaffected (Fig. 108-
Neuronal changes in the cerebral cortex associated with AD include
neurofibrillary tangles, neuritic plaques, amyloid angiopathy, and granulovacuolar
degeneration. These changes lead to loss of neurons and synapses (Fig. 108-2).
Neurofibrillary tangles (NFTs) are found primarily in the pyramidal regions of the
neocortex, hippocampus, and amygdala, but they are also noted in areas of the
brainstem and locus coeruleus.
5,31 NFTs are composed of paired helical filaments,
combinations of fibrils with a characteristic width and contour, containing a tau
protein with an abnormal pattern of phosphate deposition. They are highly
immunoreactive and are most likely to form in large pyramidal neurons.
generalized atrophy, with greater atrophy present near the temporal areas.
cortex in Alzheimer-type dementia.
Neuritic plaques are spherical bodies of tissue composed of granular deposits and
remnants of neuronal processes.
5 The typical neuritic plaques of AD are spherical
structures that exhibit a three-tiered structure: a central amyloid core, a middle region
of swollen axons and dendrites, and an outer zone containing degenerating neuritic
28 Plaques contain APP, which can be cleaved by a defective metabolic
In addition to Aβ, plaques also contain protein, ApoE, and
acute-phase inflammatory proteins such as α1
The deposition of amyloid in neuritic plaques correlates with the severity of AD, and
the density of cortical plaques is associated with decreased choline acetyltransferase
and the severity of cognitive impairment.
5 Aβ has been identified in plaques
associated with Down syndrome and in both familial and sporadic forms of dementia
29 The pathological process of AD development may begin as
early as 20 to 30 years before any disease symptoms appear.
Granulovacuolar degeneration is the other major histologic finding in AD. It
consists of clusters of intracytoplasmic vacuoles that contain tiny granules. The
vacuoles appear to be specifically located in the pyramidal neurons of the
5,16,28 The loss of cortical neurons that originate in the nucleus basalis
and project into the cerebral cortex is the most significant histopathological
31 Cell loss, granulovacuolar degeneration, and neurons with
NFTs are concentrated in this area.
Accompanying these changes are decreased concentrations of several
neurotransmitters and enzymes. Choline acetyltransferase levels are reduced 60% to
90% in the cortical and hippocampal regions.
acetylcholinesterase (AChE) are also decreased, whereas muscarinic receptors in the
cortex and hippocampus remain at normal levels or are moderately decreased.
Nicotinic receptor proteins are also reduced in patients with Alzheimer-type
dementia when compared with age-matched controls. Decreased choline
acetyltransferase activity has been correlated with plaque density and disease
severity. Cortical synapse loss, especially in the midfrontal region, is associated
Changes affecting AChE have significant implications for the management of AD
symptoms. Many isoforms of AChE have been identified; they possess identical
amino acid sequences, but display different posttranslational modifications,
predominate at diverse anatomical and microanatomical locations, and function in
different ways. The predominant form of AChE in the cortical and hippocampal
regions of humans is G4, a tetrameric form that is membrane bound. The monomeric
form, G1, is found in a much lower concentration. There is a selective loss of the G4
form in patients with AD, allowing the G1 form to assume greater importance.
Although cholinergic activity is most significantly affected by Alzheimer-type
dementia, other neurochemical systems are also altered. Norepinephrine, serotonin,
and γ-aminobutyric acid receptors are affected.
Clinical Presentation and Diagnosis
QUESTION 1: T.D. is a 72 year old man who is accompanied by his wife for a memory assessment. During
fell off the ladder and broke his leg, the wife admits he is not quite the same.
from the AD, which worries him.
rates of 56 beats/minute and 62 beats/minute, respectively.
What additional evaluation steps should be considered for T.D.?
Before any conclusions can be reached, potentially reversible causes for T.D.’s
impaired cognition must be evaluated. Although he displays several trigger symptoms
associated with dementia (Table 108-2), including difficulty with managing finances
(change especially noted in light that he was an accountant) and word finding issues
coupled with memory impairment impacting day to day function.
Several systemic diseases and other disorders can cause cognitive impairment, as
shown in Table 108-3. T.D. should undergo a battery of laboratory tests to rule out
anemia, cardiac and renal disease, thyroid abnormalities, and tumors. In addition, he
should receive thorough neuropsychological testing, including depression screening
and more in-depth assessment of his cognitive function. The testing should be
conducted by clinicians who are skilled in cognitive assessment, as educational and
cultural factors can influence an individual’s performance on these tests.
CASE 108-1, QUESTION 2: T.D. is referred by his physician for additional testing. Laboratory tests
performed include renal and liver chemistries, thyroid function tests, vitamin B12
and folate levels, syphilis and
just worried about his future.
What is the most probable diagnosis for T.D.?
T.D.’s score of 22/30 on the Folstein MMSE is consistent with mild cognitive
impairment or early dementia as evidenced by errors in orientation, calculation,
20 Secondary medical causes of cognitive impairment can be
eliminated by T.D.’s generally normal physical examination and laboratory test
results. MRI or CT scanning may be useful in many cases to help eliminate brain
34 A positron emission tomography (PET) scan or a single
photon emission computed tomography (SPECT) scan may be useful to help locate
specific areas of pathology and assist with a differential diagnosis, but are not
35 Secondary psychiatric causes for T.D.’s decline can also be discounted.
Although he is sad and anxious, the absence of alterations in appetite or sleep
patterns, absence of suicidal thoughts, and the results of psychologic testing indicate
T.D. is not depressed. He is fully conscious, alert, and oriented to place and person.
He exhibits no psychotic behavior and no evidence of delirium.
T.D.’s slowly progressive decline and its impact on his social and occupational
function (forgetting appointments, failing to pay bills), normal physical examination
and laboratory findings, and family history meet the Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition (DSM-V) criteria for dementia (Table
108-1). His history and course to date satisfy the criteria for AD and do not indicate
a likely alternative explanation for his condition. Thus, T.D. can be classified as
CASE 108-1, QUESTION 3: T.D. ’s children are very concerned about the family history for dementia.
Although there is a strong genetic association with AD, such instances account for
29 There is no apparent family history of Down syndrome.
Mutations in the presenilin-1 and presenilin-2 genes are associated with only a small
29 Although several potential biomarkers have been identified,
they have not been sufficiently validated to be considered reliable predictors for the
CASE 108-1, QUESTION 4: What is the likely prognosis for T.D.?
AD follows a predictable course that may progress over the course of 10 years or
2,10 Two common rating scales for dementia are the Global Deterioration Scale
and the Clinical Dementia Rating Scale. According to the Global Deterioration Scale
(Table 108-5), T.D.’s impaired social functioning, anxiety, and objective cognitive
decline as well as his continued ability to concentrate and perform some complex
skills, combined with his preserved affect and social interaction, are consistent with
the features of stage three dementia of the Alzheimer type. This stage of AD is
generally associated with a period of mild cognitive decline.
Clinical Dementia Rating Scale also places T.D. in the category of mild dementia.
Clinical diagnoses of AD using clinically appropriate criteria and assessment
methods for probable AD have a sensitivity of up to 90% when compared with
Because of technologic advances, it is possible to diagnose dementia earlier and
to keep patients alive into the final stages of the disease.
in T.D. will allow his condition to be followed closely. To ensure the most favorable
outcome, T.D. should receive a thorough assessment beyond his dementia. This
should include evaluation of his daily function (i.e., ability for self-care), comorbid
medical conditions, medications, living arrangements, safety, and potential for abuse
and neglect. Attention also should be given to T.D.’s caregivers and support
41,42 He should be reassessed every 6 months to both document disease
progression and ensure that he is receiving the most appropriate care. At some point,
care at home may become unrealistic. At that time, T.D. should be moved into a
sheltered environment (e.g., residential-care facility or nursing home) before
suffering an injury caused by his poor judgment (e.g., failing to dress properly for the
weather, falling). In the later stages, interventions ranging from tube feedings to life
support may prolong life, yet prove to be controversial.
AD is commonly associated with the development of infections such as pneumonia,
urinary tract infections, or decubitus ulcers.
Stages of Dementia of the Alzheimer Type
Stage of Cognitive Decline Features
No cognitive decline Normal cognitive state
Very mild cognitive decline Forgetfulness, subjective complaints only; no objective decline
Moderate cognitive decline Concentration, complex skills decline; flat affect and withdrawal
Early dementia; difficulty in interactions; unable to recall or recognize people
Severe cognitive decline Requires assistance with bathing, toileting; behavioralsymptoms present
(agitation, delusions, aggressive behavior)
Am J Psychiatry. 1982;139:1136.
Maintaining independence as long as possible is an important goal in treating a
patient with dementia. Keeping patients in familiar surroundings allows them to
function without the added burden of having to attempt to adapt to a strange
environment. Concurrent diseases and many medications can reduce function and
increase cognitive impairment in patients with dementia.
CASE 108-1, QUESTION 5: What is an appropriate initial treatment strategy for T.D.?
T.D.’s family needs to be educated about what to expect as his dementia
progresses. They should be referred to the Alzheimer’s Association (www.alz.org)
and to the Family Caregiver Alliance (www.caregiver.org). Both organizations
provide a wealth of information and community resources, including caregiver
support groups. They also should be encouraged to enroll in the MedicAlert +
Alzheimer’s Association Safe Return program, which provides 24-hour nationwide
emergency response for people with dementia who wander or suffer a medical
emergency. T.D.’s family should include him in any advance planning, seek legal
advice regarding advance directives and durable power of attorney for health care
and finance, and conduct estate planning to avoid having to perform these tasks when
T.D. is no longer competent to participate.
Currently, there are two classes of medications that are used in the treatment of
Alzheimer’s disease, cholinesterase inhibitors (ChEIs) and N-methyl-D-aspartate
44 They are pharmacologically distinct and can be
prescribed concurrently in patients in the moderate to severe stages of the illness.
ChEIs act on inhibiting acetylcholinesterase, an enzyme directly involved in the
destruction of acetylcholine leading to increasing its concentration in the nucleus
basalis of Meynert in the brain and hence ameliorating the cognitive and functional
aspects of AD. Cholinesterase inhibitors have been shown to improve cognition and
function, and delay symptom progression in people with dementia, however benefits
are limited Cholinergic-related effects, particularly in the gastrointestinal (GI) tract,
are the most common adverse effects cause by all of the agents.
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