Dementia n Alzheimer's

8/8/2019 Dementia n Alzheimer's

1/21

1

Dementia and amnestic disorders.

Dementia.

1. DEFINITIONDementia is defined as a progressive impairment of cognitive

functions occurring in clear consciousness (that is, in the absence

of delirium). Dementia consists of a variety of symptoms that

suggest chronic and widespread dysfunction. Global impairment of

intellect is the essential feature, manifested as difficulty with

memory, attention, thinking, and comprehension. Other mental

functions may often be affected, including mood, personality, and

social behavior. Nevertheless, the diagnosis of dementia should not

be made without evidence of memory deficits and at least one other

cognitive deficit/Dementia must be distinguished from mental

retardation and other cognitive disorders, such as amnestic

disorder, that involve impairment of only one intellectual function,

memory. Although there are specific diagnostic criteria for various

dementias, such as Alzheimer's disease or vascular dementia, all

dementias have certain common elements, as defined by the

revised fourth edition of the Diagnostic and Statistical Manual of

Mental Disorders (DSM-IV): The symptoms result in significantimpairment in social or occupational functioning, and they represent

a, significant decline from a previous level of functioning.

Epidemiology

With the aging population, the prevalence of dementia is rising. The


2/21

prevalence of moderate to severe dementia in different population

groups is approximately 5 percent in the general population older

than 65 years of age, 20 to 40 percent in the general population

older than 85 years of age, 15 to 20 percent in outpatient general

medical practices, and 50 percent in chronic care facilities. By 2050,

current predictions suggest that there will be 14 million Americans

with AIzheimer's disease and, therefore, more than 18 million

people with dementia.

ETIOLOGY

The most common causes of dementia in individuals older than 65

ears of age are: AIzheimer's disease (which accounts for

approximately 60 percent), vascular dementia (15 percent), and

mixed vascular and AIzheimer's dementia (15 percent). Other

illnesses that account for approximately 10 percent include Lewy

body dementia; Pick's disease; frontotemporal dementias; normal

pressure hydrocephalus (NPH); alcoholic dementia; infectiousdementia, such as human immunodeficiency virus (HTV) or syphilis;

and Parkinson's disease. Some sources suggest that as much as 5

percent of dementias evaluated in clinical settings may be

attributable to reversible causes, such as metabolic abnormalities

(e.g., hypothyroidism, nutritional deficiencies (e.g., vitamin B12 or

folate deficiencies), or dementia syndrome due to depression.

Possible Etiologies of Dementia

Degenerative dementias:Alzheimer's disease

Frontotemporal dementias (e.g., Pick's disease)Parkinson's disease ;

Lewy body dementia .


3/21

Idiopathic cerebral ferrocalcinosis(Fahr's disease)Progressive supranuclear palsyMiscellaneousHuntington's diseaseWilson's disease

MetachromaticleukodystrophyNeuroacanthocytosis

PsychiatricPseudodementia of depressionCognitive decline in late-life schizophrenia

PhysiologicNormal pressure hydrocephalusMetabolicVitamin deficiencies (e.g., vitamin B12,folate)Endocrinopathies (e.g., hypothyroidism)Chronic metabolic disturbances (e.g., uremia)

TumorPrimary or metastatic (e.g., meningioma or metastatic breast or

Jungcancer)

TraumaticDementia pugilistica,posttrauniatic dementia

SubduralhematomaInfection

Prion diseases (e.g., Creutzfeldt-Jakob disease, bovinespongiform encephalitis, Gerstmann-Straussler syndrome)

Acquired immune deficiency syndrome

Syphilis

Cardiac, vascular, and anoxiaInfarction (single or multiple or strategic lacunar)

Binswanger's disease (subcorticalarterioscleroticencephalopathy)

Hemodynamic insufficiency (e.g., hypoperfusion or hypoxia)

Demyelinating diseases

Multiple sclerosisDrugs and toxins

Alcohol

Heavy metals

Irradiation

Pseudodementia due to medications(e.g.,anticholinergics)

Carbon monoxide


4/21

DIAGNOSIS

The diagnosis of dementia is made by careful history, clinical

examination, and selected diagnostic tests. The clinical history is

most valid if corroborated with a family member or other

knowledgeable informant, as patients with memory disorders are

often poor historians. A social history, including occupationalexposures to toxins or heavy metals, substance use, and HIV risk

factors, is important in the evaluation. The medical history should

include current medical conditions and their trpaffnents, history of

head trauma, cardiovascular illness, vascular risk factors, and

history of transient ischemic attacks or cerebrovascular accidents

(CVAs). A family history of dementia is particularly important in

early-onset Alzheimer's disease or other known genetically

transmitted diseases, such as Huntington's chorea. A physical and

neurological examination should be performed to look for activemedical problems, evidence of focal neurological signs, or

movement disorders.

Another important aspect to the evaluation of a patient for a

dementia is a complete mental status examination. In addition to

the usual components of a mental status examination (appearance,

mood,thought form and content, etc.), the clinician should evaluate

of level of alertness and should conduct a screening cognitive

assessment that addresses language (comprehension, fluency, etc.)

and cognition. To assess cognition, the clinician must evaluatememory (as observed on interview as well as tested, such as

remembering a list of words), orientation, reading, writing, speech

production, calculation, abstraction, executive functioning, and

constructional ability. Depending on the history, other areas may be

evaluated, such as fine sensory function (e.g., two-point

discrimination or graphesthesia) and visuospatial skills. There are a

variety of standardized assessments used to evaluate cognition.

The clinical history should include the onset of symptoms, the

quality of symptom progression (i.e., in a gradual and progressivemanner, stepwise), a review of the cognitive domains defined in the

DSM-IV (Table), and an assessment of how the cognitive changes

have affected various areas of functioning. An evaluation for other

psychiatric disorders is also crucial, as severe depression may

present as dementia. In addition, schizophrenia is associated with a

decrease in cognitive abilities, especially after 60 years of age.


5/21

Table

Screening Laboratory TestsAssessments RationaleLabs: complete blood count, serum electro- Rule out

correctable orlytes, renal and hepatic function, glu- contributory causesof

cose, albumin and protein, vitamin B 12 dementiaand folate, rapid plasma reagin (syphilis),

thyroid-stimulating hormone, urinalysisImaging: computed tomography without Rule out infarcts,mass

contrast or magnetic resonance imaging lesions, tumors,and

hydrocephalusNeurological examination Correlate imaging

find-ings with clinicalexamination

Neuropsychological testing Mini-Mental StateExamination

: screening test

of cognitivefunction

Formaldescription of cognitive

impairments

CLINICAL FEATURES

Although the core features are the same for all dementias, the

onset and course may vary. For example, a stroke followed by a

dementia is, by definition, rapid in onset. Alzheimer's disease is

usually insidious in onset.

The time from the onset of clinical features to presentation for

evaluation varies considerably and depends on the etiology of the

dementia, as well as personal and social factors, including


6/21

individual and cultural attitudes and beliefs about aging, premorbid

personality, and intelligence. Studies show that, although

physicians are aware of the prevalence and diagnostic criteria for

dementia, they .often do not screen for cognitive impairment.

Cognitive Impairment. The core symptoms of cognitive dysfunction

in dementia, as defined in the DSM-IV, are described in the

following sections.

Memory.Loss of short-term memory is often the first clinical

feature that comes to the notice of patients and their relatives.

Typically, memory impairment is manifested by difficulty in learning

new information. As dementia progresses, retrieval of highly

learned information (long-term memory) also becomes impaired.

Memory deficits may be reflected in repetitiveness, missing

appointments, misplacing objects, and burning meals.

Topographical memory is also commonly affected, and patients

may get lost. In mild-stage dementia, disorientation is usuallyconfined to unfamiliar places. As the disease progresses, this

impairment can occur in familiar environments as well.

Confabulation may also occur and may manifest itself as insertion

of false memories.

Language.Aphasia (impaired or absent comprehension or

production of speech, writing, or signs) may present as

impoverished speech and can eventually progress to mutism in the

severe stage. Nominal aphasia, the difficulty in naming objects, is

common in the mild stage. Typically, this presents as word-finding

difficulty, initially for low-frequency words (such as harmonica) but


7/21

later for higher-frequency words (such as telephone). Later, fluent

and nonfluent aphasias and jargon aphasia (meaningless phrases)

may occur. Receptive aphasia, the inability to understand, is also-

common and is severely disabling. An important clinical point to

note is that, even when language has disintegrated completely,

patients may understand nonverbal communication, such as

gestures and pictures.

Praxis.Apraxia is the loss or diminished ability to perform

coordinated motor tasks, assuming that there is no neurological or

other damage to the peripheral motor apparatus. It reflects

dominant parietal involvement in the dementia process. Apraxia is a

major cause of loss of independence in patients, as it is reflected in

the inability to cook, to dress, to wash, to go to the toilet, and to eat.

Occasionally, and unwittingly, relatives add to the patient's distress

by misinterpreting the inability to carry out these acts as laziness or

as a lowering of standards. This is an area in which the education ofrelatives is important.

Gnosis.Agnosia, derived from the Greek word gnosis, which means

knowledge, is the failure to accurately recognize sensory stimuli in

the absence of sensory (e.g., visual or olfactory) deficits. Visual

agnosia may be reflected in the functional misuse of everyday

objects (e.g., urinating in the sink). Prosopagnosia is the inability to

recognize faces, even of friends and relatives. Agnosias can occur in

all sensory modalities. Some demented patients may, for example,

be unable to recognize familiar smells.


8/21

Executive Functioning. Executive functioning is defined as the

ability to plan, to sequence, to abstract, and to carry through

complex tasks. Deficits in executive functioning are seen

particularly in disorders affecting the frontal lobes. Executive

functioning can be assessed by reviewing the patient's ability to

perform at work, to pay bills, and to plan activities.

Neuropsychological tests directly address executive functioning by

asking the person to have flexibility in how they approach an

organizational task (i.e., the ability to shift sets) or to copy complex

figures, drawing a clock. These latter tests are not specific to

executive functioning but can demonstrate how the patient

addresses a task that involves planning and organization.

Personality and Behavioral Changes. Notwithstanding the

devastating effects of the cognitive deficits described previously, it

is, not infrequently, the changes in personality and behavior that

families find most distressing. In assessing personality changes, theclinician must rely on close family members or friends, because the

patient often does not have insight into these symptoms. Relatives

may vary in their description of personality and behavioral change.

Some overemphasize unpleasant behaviors, whereas others deny

any changes at all. Individuals with dementia may lose drive and

initiative and become indecisive and introverted. The spectrum of

emotions displayed may be narrowed, with the loss of warmth and

humor. As the illness progresses, patients may sit all day in the

same place, apparently doing little. This constellation of symptoms,

often called negative symptoms, is usually characterized by

prominent apathy. It is important to differentiate these latter


9/21

symptoms from depression, which characteristically has prominent

sadness, tearfulness, neurovegetative changes, suicidal tendency,

and inappropriate guilt,among other characteristics. The negative

symptoms do not respond to antidepressant medication.

Abnormalities of mood are well described in; the early stages of

dementia. In addition, severe depression may mimic or exacerbate

dementia. Mania is,also occasionally seen.

In other patients, changes in behavior are reflected in agitation

or

disinhibition. Social skills may be lost, and there may be sexual

disinhibition, use of inappropriate language, or both. Agitation may

include irritability, angry outbursts, and threatening or aggressive

behavior, as well as pacing and purposeless behaviors (e.g., packing

and unpacking). Patients may wander, including leaving their homes

in the middle of the night.

ALZHEIMER'S disease.

Alzheimer's disease is the most common cause of dementiain

the elderly. Alzheimer first described the illness in 1907 whenhe

reported the case of a 51-year-old woman with memory loss, topo-

graphical disorientation, persecutory delusions, misidentifications,

and behavioral disturbances. At her death, he examined her brain

and documented the neuropathological hallmarks of amyloid

plaque and neurofibrillary tangles. A definitive diagnosis ofAlzheimer's disease can only be made at autopsy, using specific

histopathological criteria that have been laid out by the

Consortium to Establish a Registry for Alzheimer's Disease

(CERAD). Clinical diagnoses are made by evaluating the course

and history and by ruling out other causes of dementia, as


10/21

discussed previously. With an appropriate history and laboratory

workup, Alzheimer's disease has becomea diagnosis of inclusion,

and the clinical accuracy in specialized centers is more than 85

percent.

DSM-lV Diagnostic

Criteria for Dementia of the

Alzheimer's Type

A. The development of multiple cognitive

deficits manifested by both:

(1) Memory impairment (impaired ability to

learn new information or to recall previously

learned information)

(2) One (or more) of the following cognitive

disturbances:

(a) Aphasia (language disturbance)

(b) Apraxia (impaired ability to carry outmotor activities, despite intact motor function)

(c) Agnosia (failure to recognize or to identify

objects, despite intact sensory function)


11/21

(d) Disturbance in executive functioning (i.e.,

planning, organizing, sequencing, or

abstracting).

B. The cognitive deficits in Criteria A1 and A2 each cause

significant impairment in social or occupational functioning and

represent a significant decline from a previous level of functioning.

C. The course is characterized by gradual onset and continuing

cognitive decline.

D.The cognitive deficits in Criteria A1 and A2 are not due to any of

the following:

(1) Other central nervous system conditions that cause

progressive deficits in memory and cognition (e.g.,

cerebrovascular disease, Parkinson's disease, Huntington's disease,

subdural hematoma, normal-pressure hydrocephalus, and brain

tumor).

(2) Systemic conditions that are known to cause dementia (e.g.,

hypothyroidism, vitamin B, or folic acid deficiency, niacin

deficiency, hypercalcemia, neurosyphilis, or human

immunodeficiency virus infection)

(3) Substance-induced conditions.

E. The deficits do not occur exclusively during the course of a

delirium.

F. The disturbance is not better accounted for by another Axis I


12/21

disorder (e.g., major depressive disorder or schizophrenia).

Code based on presence or absence of a clinically significant

behavioral disturbance:

Without behavioral disturbance: if the cognitive disturbance is not

accompanied by any clinically significant behavioral disturbance.

With behavioral disturbance: if the cognitive disturbance is

accompanied by a clinically significant behavioral disturbance

(e.g., wandering or agitation).

Specify subtype: With early onset: if onset is at 65 years of age or

younger .With late onset: if onset is after 65 years of age.

Coding note: Also code Alzheimer's disease on Axis III. Indicate

other prominent clinical features related to the Atzheimer's

disease on Axis I (e.g., mood disorder due to Alzheimer's disease,with depressive features, and personality change to Alzheimer's

disease, aggressive type).

VASCULAR dementia.

Vascular dementia is the secondmost common cause of dementiaafter Alzheimer's disease. There are several important conceptual

changes that have occurred over the past decade with regard to

vascular dementia, and specific criteria have been developed to aid

in clinical and pathological diagnosis.


13/21

DSM-IV Diagnostic Criteria for Vascular Dementia.

A; The development of multiple cognitive deficits manifested by

both:

(1) Memory impairment (impaired ability to learn new informationor to recall previously learned information)

(2) One (or more) of the following cognitive disturbances:

(a) Aphasia (language disturbance)

(b)Apraxia(impaired ability to carry out motor activities, despite

intact motor function)

(c) Agnosia (failure to recognize or to identify objects, despite

intact sensory function)

(d) Disturbance in executive functioning (i.e., planning,

organizing, sequencing, or abstracting).

B. The cognitive deficits in Criteria A1 and A2 each cause

significant impairment in social or occupational functioning and

represent a significant decline from a previous level of functioning.

C. Focal neurological signs and symptoms (e.g., exaggeration of

deep tendon reflexes, extensor plantar response, pseudobulbar

palsy, gait abnormalities, and weakness of an extremity) or

laboratory evidence indicative of cerebrovascular disease (e.g.,

multiple infarctions involving cortex and underlying white matter)

that are judged to be etiologically related to the disturbance.

D. The deficits do not occur exclusively during the course of a

delirium.

Code based on predominant features:

With delirium: if delirium is superimposed on the dementia.

With delusions: if delusions are the predominant feature.


14/21

With depressed mood: if depressed mood (including presentations

that meet full symptom criteria for a major depressive episode) is

the predominant feature. A separate diagnosis of mood disorder due

to a general medical condition is not given.

Uncomplicated: if none of the previous conditions predominates in

the current clinical presentation.

Specify if: With behavioral disturbance/

Coding note: Also code cerebrovascular condition on Axis III.

Amnestic disorders

Perhaps no other psychiatric disorder has so captured the

imagination of the public as the amnestic disorder. The notion of

losing the ability to identify one's self, to recognize friends and

family or even one's own life has been incorporated into countless

novels, plays, and movies. The amnestic is a central literary device

that allows the author to then detail the search for self and the

ramifications and repercussions of such a search. Often, the


15/21

rediscovery of self depends on unearthing an unspeakable trauma,

the liberating force of a powerful kiss or other such manifestation of

love, or simply a second head injury that mysteriously corrects the

impact of the original.

Unfortunately, these fanciful dramatizations bear little

resemblance to the clinical picture ofamnestic disorders, 'neither in

their clinical presentations nor in the natural course or response to

treatment. Amnesia for person is rare if not unheard of. The picture

of a highly intelligent, fully functional, introspective and articulate

subject experiencing amnesia is also rare; more often, the amnestic

has associ ated impairments in personality and function. The

amnestic nonetheless experiences an existential predicament, the

loss of a personal history and one's place in that history. Every day,

if not every moment, is isolated and independent of its predecessor.

The only comfort for such an existential limbo is that the subject

often cannot retain awareness of his or her condition beyond

fleeting and evanescent insights. The amnestic disorders are a broad category that includes a

variety of diseases and conditions that present with an amnestic

syndrome. The syndrome is defined primarily by impairment in the

ability to create new memories. More details regarding the

syndrome and its signs, symptoms, course, and treatment are

presented in the following sections.

DIAGNOSIS AND CLINICAL FEATURES

Symptoms and Signs. Amnestic disorders of a nonhysterical nature

always involve anterograde amnesia, meaning impaired ability to

leam and to retain new information, and a lesser degree of


16/21

retrograde amnesia, meaning impaired ability to recall previously

learned information. The retrograde amnesia typically follows

Ribot's law, as it is most prominent for recently learned information,

with older memories being the best protected.

The following, then, are the core features ofall amnestic disorders:

- There are severe deficits in new learning (anterograde amnesia).

-Attention span (roughly the same as working memory, short-term

memory, immediate memory, and registration)is intact

-General intelligence is intact.

-Retrograde amnesia is present but temporally graded,with more

remote memories preserved.

-Procedural memory or the ability to leam new tasks as opposed

to new ideas, events, or words is intact.

Amnestic subjects can also learn with priming and conditioning in

laboratory circumstances. The practical usefulness of such

preserved learning skills appears limited however; without the

ability to consciously recall the new information, the learning

accomplished is not pragmatically useful.

Korsakoff's syndromewas the test amnestic syndrome described,

and it is a good clinical model for the amnestic sydrome. As noted

by Korsakoff, the memory deficit involves new learning but not older

established memories and knowledge. Korsakovian patients

typically demonstrate a change in personality as well, such that

they display a lack of initiative, diminished spontaneity, and a lack

of interest or concern. These changes appear frontal lobe-like,

similar to the personality change ascribed to patients with frontal

lobe lesions or degeneration. Indeed, Korsakov an patients often


17/21

demonstrate executive function deficits on neuropsychological tasks

involving attention, planning, set shifting, and inferential reasoning

consistent with frontal pattern injuries. For this reason, Korsakoff's

syndrome is not a pure memory disorder, although it certainly is a

good paradigm of the more common clinical presentations for the

amnestic syndrome.

Much of what is known about memory derives from the study of

patients with pure lesions of memory and discretely localized brain

damage. The patient H.M., studied over several decades by a series

of distinguished neuropsychologists, developed amnesia after

surgical extirpation of significant portions of the medial temporal

lobe bilaterally to alleviate intractable epilepsy.These well-defined

lesions allowed the delineation of differential aspects of memory

through descriptions of what memory capacities H. M. had lost and

which were retained. H. M., although providing an invaluable lesion

model for memory function, is not a typical example of a patient

with an amnestic disorder. The more common etiologies ofnutritional deficiency, cerebrovascular disease, tumor, and cerebral

infection tend to have more widespread cerebral involvement and,

therefore, at least subtle deficits in domains other than memory.

The DSM-IV offers subtypes of amnestic disorders: amnestic

disorder due to general medical condition, substance-induced

(specifying alcohol, sedative-hypnotic, anxiolytic, or unknown

substances) persisting amnestic disorder, and amnestic disorder not

otherwise specified. These subtypes do not differ in clinical signs

and symptoms but only in the putative etiology.

Associated Signs and Symptoms.

Confabulation refers to the fabrication of information


18/21

spontaneously or in response to questions. Confabulation can be

distinguished from conscious dissimulation or lying, as the patient

believes his or her utterances and has no intent to mislead.

Confabulations are not delusions per se either: They lack the

systematic and fixed quality of a delusion. Two types of

confabulation are noted: the more common momentary

confabulations and the more rare, fantastic confabulations.

Typically, confabulations arise in response to a question and have a

fill in the gap quality:

"Did you have your breakfast?" is met with the confabulatory

response of "I certainly did, let's see ... a good breakfast at that:

orange juice, eggs, bacon, and a blueberry muffin." The

confabulations may not be noted until the patient is asked open-

ended questions that challenge his or her recall of details. The

content is mundane and related to the question at hand. Fantastic

confabulations, on the other hand, are often offered spontaneously

and are striking for their dramatic content.The fill-in-the-gaps quality of the confabulation has led many to

associate confabulations with memory disorders. However,

confabulations may relate more to a failure of executive function

than memory dysfunction. This is clearly the case with fantastic

confabulations as presented in the previous case. The notion of

"little Indians" or Nazis populating the closets is striking more for its

patent absurdity than for how it solves the riddle of what the noises

are that are emanating from the closet. There is obviously a failure

of the frontal lobe executive function responsible for inhibiting

absurd interpretations and responses. This executive function has

the role of censoring the hypotheses that other regions of the brain


19/21

develop as explanations for sensory stimuli. Confabulation and

personality change are more common in diencephalic amnesia (e.g.,

Korsakoff's syndrome) than in pure hippocampal amnesia, perhaps

reflecting a concomitant involvement of frontal lobe structures or

connections.

Personality Change. The personality change seen in amnesticdisorders may involve apathy or irritability, or a combination of the

two. The following case illustrates the inactivity and constriction of

interests that can be seen, as well as the persistent irritability and

agitation that can accompany the amnesia.

Motor and Sensory Symptoms. Motor and sensory symptoms may

variably accompany an amnestic disorder, depending on the

etiology. Some amnestic syndromes, such as transient global

amnesia, are striking for the preservation of motor and sensory

function. In contrast, the vitamin deficiencies are often accompanied

by motor and sensory symptoms that persist beyond the initial

recovery from acute Wernicke'sencephalopathy.

Patients with amnestic disorders deriving from Wemicke-Korsakoff

syndrome may have gait abnormalities due to peripheral neurop

athies, muscle weakness, or gait instability related to the comorbid

cerebellar degeneration of chronic alcoholism. The latter may also

account for the frequently seen fine motor dyscoordination.

Although the more striking ocular abnormalities related to an acute

Wernicke's encephalopathy often resolve with vitamin

replenishment, patients might still manifest residual restriction in

gaze, as well as subtle lateral nystagmus. Anosmia can accompany

some amnestic disorders, such as that due to herpes simplex


20/21

encephalitis and certain strokes.

As described previously, the signs and symptoms of the amnestic

disorder are not restricted to the domain of memory. The foltowing

case exemplifies the more common real-life presentation of a

patient with amnestic disorder. Although the primary and most

obvious deficit is in memory, this patient also has obvious

impairments in comportment and judgment. The latter appear as an

exaggeration of premorbid traits. This case illustrates the

devastating impact of memory impairment on daily functioning and

the capacity to live independently.

Assessment. The assessment of a memory disorder begins even

before the patient is seen. Is it the patient calling with subjective

worries regarding his or her memory function or is it a friend or

relative calling with concerns that the patient seems unaware of?

How the patient arrives for evaluation is pertinent. Did he or she

travel alone and maneuver public transportation or was he or she

driven? Many patients with severe amnestic disorders areevaluated on inpatient medical or psychiatric services, where they

are held out

of concern for their ability to manage on their own. The typical office

or bedside examination can provide many clues. The Folstein MMSE

is the most widely used cognitive screen and is available in a

multitude of languages. Poor performance on the ten orientation

items provides a general estimate of overall cognitive function.

Although the overall score may not be reflective of severe

impairment, specific answers can be informative. For example,

responding "1968" to the year is far more suggestive of memory

impairment, perhaps a retrograde amnesia of decades, than missing


21/21

the-year by 1 or 2 years. Asking the patient to repeat three items

assesses registration or immediate recall. Patients with amnestic

disorders ought to be able to repeat these items accurately.

Documents

Dementia n Alzheimer's