Cognitive Impairment Evaluation
Cognitive Impairment Evaluation
Cognitive Impairment Evaluation
KEYWORDS
Dementia Mild cognitive impairment Mental status examination
Alzheimer’s disease Neuropsychiatric symptoms
KEY POINTS
The goal of the diagnostic evaluation for cognitive impairment is to determine both the
severity of impairment and the likely cause or causes.
A knowledgeable informant is crucial for a reliable evaluation and, depending on the
cause, patient care.
The mental status examination should incorporate one or more validated instruments to
assess cognition.
An assessment of functional status informs both the diagnostic work-up and patient care.
Environmental, psychological, and behavioral interventions are first line for neuropsychi-
atric symptoms and can be beneficial for cognition and function in cognitively impaired
patients.
INTRODUCTION
Cognitive impairment is highly prevalent in the elderly and increases with advancing
age.1–3 Worldwide, dementia is estimated to affect 1.8% of people in their 60s,
5.1% of people in their 70s, 15.1% of people in their 80s, and 35.7% of people in their
90s.3 A study from the Centers for Disease Control and Prevention using the 2011
Behavioral Risk Factor Surveillance survey found that 12.7% of respondents aged
60 years and older self-reported memory loss and confusion that had worsened in
the preceding year.4 Clinicians providing primary care to the elderly are often tasked
with evaluating and managing cognitive concerns in their patient population.
a
Penn Memory Center, University of Pennsylvania, Philadelphia, PA, USA; b Ralston House,
Penn Memory Center, ATTN: Maria Crudele, 3615 Chestnut Street, Philadelphia, PA 19104-2612,
USA; c Division of Geriatrics, Penn Memory Center, University of Pennsylvania, Philadelphia,
PA, USA
* Corresponding author. Ralston House, Penn Memory Center, ATTN: Maria Crudele, 3615
Chestnut Street, Philadelphia, PA 19104-2612.
E-mail address: [email protected]
Twitter: @lauren_mccollum (L.M.); @jasonkarlawish (J.K.)
APPROACH
To diagnose and treat a patient presenting with a cognitive complaint, the clinician
uses a systematic approach that identifies the presence and severity of the impair-
ment, the cognitive domains involved, the likely underlying causes, and the most
appropriate interventions. Although some aspects of the work-up are completed for
all patients (eg, selected laboratory tests and imaging), the decision to pursue a
more detailed work-up is influenced by the goals of the evaluation. A brief discussion
with the patient and family about the goal of the visit provides the necessary informa-
tion to customize the approach.
The decision to refer a patient to a specialist can be considered at the close of the
initial assessment. Cases of early-onset, rapidly progressive, or otherwise atypical
cognitive impairment (eg, prominent language or social-behavioral symptoms with lit-
tle or no memory loss) should be referred to a specialist.5–7 Other factors that might
influence a decision to refer include provider experience, clinic resources, patient pref-
erence, and availability of specialty centers.2 One particularly compelling reason to
refer to an academic center is interest in participation in clinical research.2
EVALUATION
History of Present Illness
A concern for cognitive change (commonly called a chief complaint of memory loss)
triggers a work-up for cognitive impairment. This concern can be voiced by the patient
or a knowledgeable informant. In general, a knowledgeable informant provides the
most helpful historical information. The interview with the informant is best done pri-
vately, although this is not always practical or possible. Privacy allows the informant
to feel comfortable describing the full extent of the problem. However, there is no
need to hide this conversation from the patient. In our experience, patients are agree-
able to allowing the informant to speak privately with the clinician if they are told that
this is a routine part of the cognitive evaluation and they will have private time as well
with the clinician.
The informant interview should begin with an assessment of how long the informant
has known the patient and how frequently interaction with the patient occurs. An
open-ended question about the reason for concern often provides a great deal of in-
formation. Next, it is helpful to take a step back and learn about the patient’s cognitive
achievements and background, including education, occupation, and living situation.
The history covers all cognitive domains, including memory, attention, language, vi-
suospatial processing, executive function, and social comportment, and addresses
aspects of timing and tempo. Domains that are not covered when the informant an-
swers an open-ended question can be addressed with a few key targeted questions
(Box 1).
It is helpful to ask for examples that illustrate the patient’s symptoms. These contex-
tual details aid the physician in assessing the severity of the problem.
After establishing the pattern of cognitive impairment, the clinician should assess
the functional impact of the symptoms. The activities of daily living are the instrumental
activities of daily living (IADL), such as handling finances, cooking, managing medica-
tions, and using transportation, and the basic activities of daily living (BADL), which
include bathing, dressing, grooming, feeding, and toileting.8 An ecologically valid
and holistic way to assess function is to begin by asking what a typical day is like or
what the patient does to stay busy. The clinician should then ask questions to deter-
mine whether the patient’s day-to-day activities represent a change from the baseline
and, if so, are the result of cognitive problems. Questions should probe whether the
Cognitive Impairment Evaluation and Management 809
Box 1
Targeted questions to address cognitive domains
Memory
Does the patient forget appointments or have difficulty keeping track of the day or time?
Does the patient repeat questions or comments?
Does the patient forget recent events or conversations?
Attention
Does the patient have periods of decreased alertness?
Is the patient easily distracted?
Language
Does the patient have word-finding difficulties? Struggle to find common words?
Does the patient have trouble communicating thoughts or understanding what is being
said to them?
Visuospatial processing
Does the patient tend to get lost or turned around?
Does the patient ever fail to see something that is right in front of them?
Executive function
Can the patient successfully complete tasks that require multiple steps; for example,
planning a trip or throwing a dinner party?
Can the patient use appliances and devices as well as they used to?
Social comportment
Does the patient behave appropriately in social situations?
Has the patient become impulsive, careless, or unguarded?
Note: these questions refer to “the patient,” but a more personal term, such as “your wife” or
“your father,” is used in practice.
patient is less efficient at performing tasks (ie, takes them longer) or makes errors and
needs help.
Neuropsychiatric symptoms should be discussed, both because mood disorders,
especially depression, can be a primary (and treatable) cause of cognitive change
and because neurodegenerative diseases can cause various neuropsychiatric symp-
toms. For example, dementia with Lewy bodies (DLB) often results in anxiety, system-
atized delusions, and formed visual hallucinations.9
Sleep should be discussed, both because untreated sleep disorders (eg, obstruc-
tive sleep apnea [OSA]) may affect cognitive function in some older adults10 and
because neurodegenerative conditions are associated with sleep disturbance.11,12
The possibility of rapid eye movement sleep behavior disorder (RBD), which is
commonly seen in DLB, can be assessed for by asking whether the patient’s arms
and legs move during sleep, as if acting out dreams.13
A focused review of systems should inquire about gait dysfunction, falls, tremor, in-
continence, and dysphagia. The past medical history should elucidate vascular risk
factors and general medical, psychiatric, or neurologic diseases that could affect
cognition. The social history assesses for illicit drug use, problematic alcohol use,
and social stressors. The family history identifies genetic risk factors. In addition,
the medication reconciliation should flag drugs that contribute to cognitive decline,
particularly anticholinergic drugs.
The interview with the patient should include questions about cognitive symptoms
and a typical day. This history from the patient is a part of the cognitive examination
because it provides information about the patient’s insight. Patients should be asked
directly about their mood and hallucinations, because informants do not always know
810 McCollum & Karlawish
Examination
The mental status examination should include both a “bedside” examination and the
use of one or more validated instruments to assess cognition and, if applicable, mood
(Table 1). There are some scenarios in which the results of formal cognitive tests must
be interpreted with caution. For example, the psychometric test performance of per-
sons with limited education, particularly less than high school, and for whom English is
a second language may underestimate their cognitive abilities. In addition, certain
cognitive deficits, such as marked impairments in language or attention, can cause
performance on tests that is markedly poorer than expected.
The bedside mental status examination touches on the various cognitive domains.
From the start of the encounter with the patient, the clinician makes observations
regarding the patient’s cognition and behavior. While taking the history, the clinician
is also taking note of the patient’s affect, social comportment, speech, facial expres-
sions, and insight. The versions of the bedside mental status examination are limitless,
and clinicians often tailor the examination based on preference, patient factors, and
the evolving differential diagnosis. The various bedside tests available are best orga-
nized according to the cognitive domains they test (Box 2).
Next, the clinician should perform a focused neurologic examination designed to
detect findings that the chief complaint and history suggest might be present (Box 3).
A brief general medical examination with attention to the cardiac and pulmonary
systems assesses for signs of a non-neurologic problems that could affect cognition.
Referral for a formal neuropsychological evaluation should be considered when
there is significant psychiatric comorbidity or when there is a mismatch between the
history and the cognitive test results—for example, a patient whose cognitive test per-
formance is normal but in whom a decline from baseline is still suspected. More in-
depth testing may reveal deficits too subtle to show up on simpler office-based tests.
Neuropsychologists can also assist in refining the differential diagnosis by identifying
patterns of cognitive dysfunction.
811
812
McCollum & Karlawish
Table 1
(continued )
Instrument Description How It Is Administered Scoring Considerations
Mini-Cog Psychometric test of Examiner administers Score range 0–5; higher Takes 3–4 min
memory, executive to patient score c/w less cognitive 76%–100% sensitive and
function, language, impairment 54%–85.2% specific for dementia
and praxis using clock Low sensitivity for MCI
draw and 3-word May perform better in
recall test low-education populations
Mini Mental State Psychometric test of Examiner administers Score range: 0–30; 21–24, Takes 7–10 min
Examination memory, attention, to patient mild dementia; 13–20, 88.3% sensitive and 86.2%
orientation, language, moderate dementia; specific for dementia with
and praxis 3-point change a cut point of 23/24 or 24/25
considered clinically Limited sensitivity and
significant specificity for MCI
Has copyright restrictions
Montreal Cognitive Psychometric test of Examiner administers Score range 0–30; higher Takes 10 min
Assessment memory, executive to patient score c/w less cognitive 80%–100% sensitive and
function, language, impairment 50%–76% specific for MCI
and praxis; designed using cut point of 25/26
to detect MCI
NPI-Q Informant questionnaire Informant NPI-Q severity score range: Takes 5 min
on 12 behavioral self-administers 0–36. NPI-Q distress score: Must have reliable informant
symptoms (items are 0–60; higher scores c/w Assesses for behavioral
yes/no; yes answers get more severe behavioral symptoms associated with
1–3 severity rating) and symptoms and caregiver multiple dementia syndromes
caregiver distress (1–5) distress
Box 2
Selected components of a bedside mental status examination grouped by cognitive domain
Orientation
State name, month, date, year, day of the week, season, and current location
Attention
Spell “world” forward and backward
State months of the year in reverse order
Count backward from 100 by 7s
Memory
Repeat 3 words and remember them for 5 minutes
Describe what has been going on in the news lately
Language
Name 3 common items (eg, thumb, knuckles, collar, pointed to by the examiner)
Repeat a phrase (eg, “Traffic conditions are expected to be heavy today.”)
Provide a speech sample (eg, by describing a picture or current event)
Visuospatial processing
Draw a clock (also tests executive function)
Bisect a line
Executive function
Name as many words that begin with the letter F as you can think of in 1 minute
State the letters of the alphabet, alternating with sequential numbers (ie, “A1B2” and so
on)
Box 3
Focused neurologic examination for a patient with a cognitive complaint
Cranial nerves:
Assess for masked facies or reduced eye blink rate
Listen for dysarthria
Look for facial asymmetry, including flattening of the nasolabial fold
Determine whether eye movements and visual fields are full
Motor, sensory, and reflexes
Test briefly, assessing for focal weakness, fasciculations, or hyperreflexia concerning for
amyotrophic lateral sclerosis, which is sometimes comorbid with frontotemporal
dementia, or other asymmetry suggestive of a focal lesion (eg, stroke, tumor)
Tone
Assess for cogwheel rigidity at the elbows, wrists, and neck by asking the patients to relax
and allow you to move their bodies for them
Coordination and extrapyramidal function
Evaluate rapid alternating movements (eg, by having the patients alternate striking their
thighs with a closed fist and open palm)
Evaluate for emergence of a rest tremor by having the patients rest their hands in their laps
and count backward from 20 to zero with eyes closed
Gait and postural stability
Have patients stand without the use of their hands
Observe gait (noting arm swing, posture, stride length, and turn)
Assess tandem gait
Use pull test to assess for postural instability
814 McCollum & Karlawish
the patient is independent in BADL and requires some assistance with IADL. In
the moderate stage, the patient requires some assistance with BADL and re-
quires assistance with or is dependent in IADL. In the severe stage, the patient
requires assistance with or is dependent in BADL and is dependent in IADL.
The labels MCI and dementia both denote a concern that a disease, most likely a
brain disease, is causing the cognitive problems, and so should not be applied if
the deficits are explained by delirium or some other cause that is not a brain disease,
such as decompensated congestive heart failure.
Work-up
Patients with cognitive impairment should be screened for hypothyroidism and vitamin
B12 deficiency, because these entities can cause cognitive decline that may improve
with treatment.17–19 It is reasonable to obtain a complete blood count with differential
and comprehensive metabolic panel to screen for other general medical problems (eg,
anemia, kidney or liver failure, electrolyte derangements) that could affect cogni-
tion.17,20 Depending on clinical context, clinicians may consider ordering other labora-
tory tests, such as folate, vitamin D, heavy metal screen, erythrocyte sedimentation
rate, C-reactive protein, antinuclear antibodies, Lyme serologies, human immunode-
ficiency virus-1/2 immunoassay, and rapid plasma reagin.16,20,21 Patients in whom
OSA is suspected should undergo a sleep study or be referred to a sleep specialist.
All patients with cognitive impairment should undergo structural brain imaging.
Brain imaging is not indicated in patients with SCD because normal age-related
changes can overlap with the early atrophic changes seen in neurodegenerative dis-
ease.22 Thus, structural brain imaging, in the absence of objective cognitive impair-
ment, is often clinically uninterpretable, because mild atrophy could be age related,
and a normal result does not rule out the small possibility of occult disorder.
Although both computed tomography (CT) and magnetic resonance imaging (MRI)
are acceptable, the preferred brain imaging modality for cognitive impairment is MRI
without contrast, which has greater diagnostic yield and avoids ionizing radiation. CT
without contrast, which is generally less costly, is a suitable alternative when MRI is
contraindicated or otherwise unable to be obtained.16 Imaging enables the clinician
both to assess for unexpected structural findings that could be affecting cognition
(eg, a tumor, silent stroke, or subdural hematoma) and to identify features suggestive
of specific underlying neurologic diagnoses.23 Several of the diseases that cause de-
mentia have characteristic imaging findings (eg, hippocampal and posterior parietal
atrophy in Alzheimer disease [AD]) (Table 2).24 However, these findings can be subtle,
and the relationship between imaging findings and underlying disorder is best thought
of as probabilistic, with the most compelling cases being those in which the clinical
symptoms and the imaging findings align.
MRI is also helpful for identifying cerebrovascular disease, because many types of
vascular brain injuries have identifiable imaging correlates. White matter hyperinten-
sities, which are suggestive of chronic small vessel ischemic disease, are commonly
related to typical cardiovascular risk factors (eg, hypertension, smoking),25,26 but are
also commonly seen in AD.27,28 Similarly, cerebral microbleeds (CMBs) are commonly
seen in both vascular cognitive impairment and AD. Deep subcortical CMBs are usu-
ally hypertensive in origin, whereas lobar CMBs are more often associated with cere-
bral amyloid, and thus are suggestive of AD.29
Normal-pressure hydrocephalus (NPH) can be suggested, but not definitively diag-
nosed, by characteristic imaging findings, including ventriculomegaly and dispropor-
tionately enlarged subarachnoid space.30 There has been growing recognition that
Cognitive Impairment Evaluation and Management 815
Table 2
Common MRI findings in selected causes of progressive cognitive impairment
mixed dementia (ie, multiple disorders together causing the impairment) is common,
particularly in the elderly.31,32
If the diagnosis is still unclear, additional studies or a referral to a cognitive specialist
may be needed. A fluorodeoxyglucose-PET scan of the brain can distinguish between
frontotemporal dementia (FTD) and AD. Amyloid PET scans are approved for the
detection of amyloid by the Food and Drug Administration (FDA) in the United States,
but, as of this writing, are not covered by any insurance plans. Cerebral spinal fluid
from a lumbar puncture (LP) can be tested for biomarkers of specific diseases,
including AD (with amyloid-beta-42 and phosphorylated tau),33 sporadic
Creutzfeldt-Jakob disease (with real-time quaking-induced conversion),34,35 autoim-
mune and paraneoplastic encephalitides (with respective panels),36 and other inflam-
matory entities (with protein and white blood cell counts).37 A high-volume LP,
preceded and followed by cognitive and timed walking tests, can evaluate for NPH,
in the appropriate context of the clinical triad (gait disturbance, urinary incontinence,
and dementia) and suggestive neuroimaging.30
Providing a Diagnosis
Discussions about the diagnosis should include information about the level of impair-
ment (MCI or dementia) and the causes. If the patient has SCD, the clinician should
explain that cognitive testing was normal and provide prognostic information. Individ-
uals with SCD are at a modestly increased risk of progression to MCI and dementia
over subsequent years, compared with the general population.38–40 It is reasonable to
follow the patient over time with repeated cognitive assessments to assess for onset
of objective cognitive decline. Education about cognitive aging is warranted as well.
Clinicians giving a diagnosis of MCI discuss with patients and their families the
meaning of the diagnosis and its prognosis.2 People with MCI can progress to demen-
tia, remain in an MCI state, or revert to normal cognition, and studies have shown that
all 3 outcomes are common.2 Each year, 5% to 20% of patients with MCI progress to
dementia.20
816 McCollum & Karlawish
A diagnosis of dementia merits disclosure of the disease that is causing it, or, if that
cause is uncertain, an offer for referral to a specialist. Table 3 lists abbreviated diag-
nostic criteria of selected commonly diagnosed neurodegenerative diseases that
cause dementia. Some common dementia syndromes, such as NPH and vascular de-
mentia, do not have a single set of widely agreed-on diagnostic criteria.
If the patient has a neurodegenerative disease, it is important to stage the disease.
Diagnostic disclosure should explain that these conditions are gradually progressive,
and the goal of any intervention is to slow down or stabilize the functional decline and
other symptoms. Family members in particular need to understand this so they can
Table 3
Abbreviated diagnostic criteria for commonly diagnosed neurodegenerative dementias
help the patient live well with the disease and prepare for the future. Each cause of de-
mentia has its own prognosis, but clinicians should emphasize that there is variability
in rates of progression.
Pharmacotherapy
As of 2020, there are no approved therapies shown to modify neurodegenerative dis-
orders, although many are being studied in clinical trials. The available medications are
symptomatic treatments.
Acetylcholinesterase inhibitors
Acetylcholinesterase inhibitors, including donepezil, galantamine, and rivastigmine, are
labeled for use in AD dementia and may also be effective for vascular dementia and
DLB.41 Acetylcholinesterase inhibitors can worsen behaviors in FTD,42 and there is
insufficient evidence of efficacy in MCI.2 The goal of treatment with acetylcholinesterase
inhibitors is to improve or stabilize memory and attention by inhibiting the breakdown of
acetylcholine, a neurotransmitter released by cholinergic neurons in the basal forebrain,
an area known to be affected by AD.43 Common side effects include diarrhea, nausea,
leg cramps, abnormal dreams, and bradycardia. Patients with a history of bradycardia
or conduction abnormalities should not be prescribed acetylcholinesterase inhibitors.
Some patients who cannot tolerate oral donepezil because of gastrointestinal side ef-
fects are able to tolerate the rivastigmine patch.41 If the side effects persist and are both-
ersome, the clinician should consider discontinuing the medication because any mild
symptomatic benefit is likely to be overshadowed by side effects. Patients and families
should be advised that, because the benefits of acetylcholinesterase inhibitors tend to
be subtle, it is often not obvious that the medication is helping, even in patients who are
doing a little better than they otherwise would be.
Memantine
Memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist, is thought to work
by blocking the effects of excess glutamate and by upregulating NMDA receptor
expression.44 Memantine is indicated for use in moderate to severe AD,45 and there
is also evidence to support off-label use in mild to moderate vascular dementia.46
Memantine has been shown to confer modest improvements in thinking, everyday
functioning, behavior and mood.47 Although memantine is generally well tolerated,
the most common side effect is dizziness.47 As is the case with acetylcholinesterase
inhibitors, patients and families should be counseled that the benefits of memantine
tend to be subtle.
A common practice for patients with AD, vascular dementia, or mixed dementia is to
start an acetylcholinesterase inhibitor at the mild dementia stage and to add meman-
tine to the drug regimen when the patient progresses to a moderate stage of dementia.
giving a dementia diagnosis, clinicians should counsel patients and families to work to
create a safe, structured, social, and engaged day. All patients with SCD, MCI, and
dementia should be active physically, mentally, and socially. Activities that combine
physical, mental, and social activity in some way are especially valuable; for example,
joining a book club (which is mentally and socially stimulating) or taking a dance class
(which is stimulating in all 3 regards). Unfortunately, the Covid-19 pandemic has
rendered many common lifestyle measures unsafe for elderly individuals because of
infection risk in group settings. Caregivers should endeavor to facilitate stimulating ex-
periences that are also safe; for example, home exercise programs and video
conference–based social experiences.
Exercise
In people with dementia, exercise programs have been shown to improve or stabilize
functional status48 and cognition.49 The type and amount of exercise with the best ev-
idence basis in people with MCI or AD is 3 or 4 w45-minute moderate-intensity aer-
obic exercise workouts per week.49 Mind-body exercises (eg, yoga, tai chi) have
also been shown to improve cognition in MCI.50
Cognitive stimulation
Studies have shown some benefit to cognitively stimulating activities, including com-
puter activities, video games, and virtual reality programs for MCI51 and dementia.52,53
It is reasonable to refer patients to cognitive fitness/rehabilitation programs to the
extent that they are available and affordable. Clinicians should also encourage pursuit
of cognitively stimulating activities in day-to-day life. The choice of activity depends on
the abilities and interests of the patient. Mindfulness meditation may help patients with
MCI build cognitive reserve, become more socially engaged, and feel better about
their diagnoses.54 Speech therapy can be helpful for people with prominent language
disturbance.
Social engagement
Poor social engagement (ie, loneliness) is associated with an increased risk of demen-
tia,55,56 and community cultural engagement (eg, visiting museums, going to the the-
ater) may be a protective factor for dementia risk.57 Social engagement is most
stimulating when it involves people outside the patient’s innermost circle. Some care-
givers try to provide round-the-clock care and companionship, but it is in the best in-
terest of both patients and caregivers to intersperse interactions with other people,
which can take the form of visiting aides, an adult day program, or having an old friend
take the patient out for lunch once a week.
Nutrition
The Mediterranean diet has been associated with a lower risk of conversion from MCI
to dementia.58,59 Patients with dementia are at increased risk of malnutrition, and
nutritional status may have some bearing on functional status.60 For patients at risk
for malnutrition, caregivers should provide routine meals and snacks. (Often, even if
they say they are not hungry, they will eat once a meal is served to them.) Nutrition
supplements, such as shakes, can provide additional nutrition.61 Patients should
avoid moderate or heavy alcohol use.
Sleep
Behavioral interventions for sleep disturbance include counseling about sleep hy-
giene, light therapy, and referral for cognitive behavioral therapy for insomnia.62,63
Sleep disturbance can be exacerbated by excessive napping and insufficient daytime
Cognitive Impairment Evaluation and Management 819
activity. Crafting a more active day that involves leaving the house during daylight
hours can result in improved sleep.
CONSIDERATIONS
Safety is a major issue for patients with cognitive impairment. Clinicians should be pre-
pared to discuss driving with patients and families. Some patients with MCI and mild
dementia can drive safely, whereas others cannot. People with moderate or severe
dementia should not drive. Some states mandate that clinicians formally report unsafe
drivers. When in doubt, a driver evaluation, performed at a rehabilitation center by an
occupational therapist, can clarify whether the patient is safe behind the wheel.
Varying levels of supervision are needed for patients with cognitive disorders. Many
patients with MCI or mild dementia need little supervision except in error-prone do-
mains, particularly managing finances and medications. Patients with moderate to se-
vere dementia should have near-constant supervision. Potential hazards for
cognitively impaired patients should be addressed proactively; for example, removing
guns from the home and turning off the gas to the stove. Gait instability during the ex-
amination or report of falls warrants referral to physical therapy to aid in fall prevention.
Patients with dysphagia should see a speech pathologist.
Patients with cognitive impairment should be advised, together with their families, to
plan for the future, which could include discussions about advance directives, powers
of attorney, finances, and living arrangements.2
SUMMARY
diagnosis consists of 2 parts: a level of impairment (eg, MCI or dementia) and probable
cause (eg, AD, DLB, vascular dementia). Patients with unusual presentations or who
are interested in research should be referred to an academic memory or cognitive cen-
ter. Regardless of the underlying disorder, treatment is symptomatic, and nonpharma-
cologic interventions are preferred to pharmacologic ones for neuropsychiatric
symptoms. Safety is a “moving target” in patients with cognitive impairment and
should be a focus for clinicians.
DISCLOSURE
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