Sample Dementia

7/28/2019 Sample Dementia

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BASIC INFORMATION

DEFINITION

Dementia means loss of mental func-tions. It is a syndrome of acquired andpersistent cognitive deficits that includesmemory impairment in association withimpairments in abstract thinking, judg-

ment, or other disturbances of highercortical function (e.g., aphasia, apraxia,agnosia, executive functioning) or per-sonality change. The disturbances aresevere enough to interfere significantlywith work, usual social activities, or rela-tionships with others. Dementia is not di-agnosed if the symptoms occur exclu-sively in the context of delirium. It mustbe an acquired loss of function, andhence is distinguished from develop-mental disorders such as mental retarda-tion. Dementia can have many etiolo-gies, as will be noted. (Adapted fromDSM-III-R and DSM-IV.)

ICD-9CM CODES

290.0 Senile dementia, uncomplicatedDSM-IV: Dementia of theAlzheimers type, late onset

290.1 Presenile dementiaDSM-IV: Dementia of theAlzheimers type, early onset,uncomplicated

290.4 Arteriosclerotic dementiaDSM-IV: Vascular dementia

294.1 Dementia in conditions classifiedelsewhere (code first underlyingphysical condition, e.g., listed asfollows)DSM-IV: Dementia due to:

331.0 Alzheimers disease331.82 Dementia with Lewybodies331.19 Frontotemporal dementia310.1 Mild memory disturbances,not amounting to dementia,associated with senile braindisease

294.9 Unspecified organic brainsyndrome (chronic)DSM-IV: Cognitive Disorder NOS

SYNONYMS

Senile dementiaPresenile dementia

Senile psychosis

EPIDEMIOLOGY &

DEMOGRAPHICS

INCIDENCE:Annual dementia incidencerate approximately doubles every 5 yearsafter age 65; approximately 7 to 9 per1000 at age 65-69 and 85 to 118 per 1000at age 85 and older.PREVALENCE: Approximately 8% to10% of U.S. population (4 million to 6million) above age 65 have dementia;prevalence approximately doubles every5 years after age 65; prevalence is ap-

Genetics and family history: Risk of AD is about four times greater

in patients with a first-degree relativewith AD.

ApoE 4 allele on chromosome 19 in-creases risk of AD and shifts age of on-set 3 to 7 years earlier than in thosewith sporadic onset who do not havean 4 allele; risk is further increased inpresence of first-degree relative withAD.

Approximately 2% of AD cases areearly-onset familial AD related to mu-tations in either chromosome 14 (pre-senilin 1), 1 (presenilin 2), or 21 (amy-loid precursor protein).

Almost all patients with Down syn-drome will develop AD pathology af-ter age 40.

Key cognitive features: Memory impairment is cardinal fea-

ture; impairment in language, visuo-constructional ability, executive func-tioning, and other cognitive domains

follows. Motor and sensory function generally

intact until late stages.Neurologic features: Normal exam early. Later stages can be associated with ex-

trapyramidal or parkinsonian features. Impairment in gait, speech, urinary

and fecal continence, and reemer-gence of primitive reflexes may occurin final stages.

Key neuroimaging features: Useful for ruling out alternate (e.g.,

neoplasm, hydrocephalus) or con-comitant (e.g., vascular lesions) causes

of dementia. MRI may reveal diffuse cortical atro-phy with ex vacuo ventricular enlarge-ment particularly in temporal horns oflateral ventricle due to hippocampalvolume loss; severity of imaging find-ings generally increases with severityof dementia.

Temporoparietal hypometabolism onSPECT or PET.

Neuroimaging is not diagnostic.Course: Insidious onset with gradual progres-

sion; memory is usually first symptom. Average survival is about 8 years de-

pending on age at diagnosis and con-comitant medical conditions; survivalmay be up to 20 years.

VASCULAR DEMENTIA (VAD)

Prevalence: VaD is the second or thirdmost common cause of dementia, ac-counting for about 10% to 30% of all de-mentia cases; prevalence increases withage; more common in men.

Core features: Focal neurologic signs/symptoms. Neuroimaging evidence of cerebrovas-

cular disease.

proximately 2% at age 65 and 34% to68% at age 85 and older.PREDOMINANT ETIOLOGY:Alzheimersdisease (AD) is by far the most commoncause of dementia. Approximately 55% to70% of all dementias have a significantcontribution from Alzheimers pathologyand approximately 35% of all dementiasmay be attributable to pure AD. Vasculardementia and dementia with Lewy bodiesare thought to be the next most commonetiologies. Prevalence rates of dementiaetiologies vary across ethnic groups.PREDOMINANT SEX:Varies by demen-tia diagnosis; AD is more common in fe-males; vascular dementia and dementiawith Lewy bodies is more common inmales; frontotemporal dementia appearsto occur equally in males and females.PREDOMINANT AGE: Incidence andprevalence increase over age 65 and arehighest at age 85 and older; average ageof onset is younger in frontotemporal de-mentia and some relatively rare, familial

subtypes of AD (see as follows).PEAK INCIDENCE AND PREVALENCE:

Age 85 and older.GENETICS: First-degree relatives may beat increased risk for certain types of de-mentia (e.g., AD, frontotemporal demen-tia); apolipoprotein 4 allele is a geneticrisk factor for AD but is not diagnostic.Genetic disorders causing dementia in-clude Huntingtons disease, CADASIL(cerebral autosomal dominant arteriopa-thy with subcortical infarcts andleukoencephalopathy), and early-onsetfamilial AD. Some forms of frontotempo-ral dementia have genetic linkages.

PHYSICAL FINDINGS & CLINICAL

PRESENTATION

See Fig. 1-13.Physical findings and clinical presenta-tion differ across dementia etiologies.

ETIOLOGY

ALZHEIMERS DISEASE

Prevalence: AD is the most commoncause of dementia; contributes to de-mentia in approximately 55% to 70% ofall cases; pure AD accounts for approxi-mately 35% of all cases.

Core features: Gradually progressive memory impair-

ment with insidious onset. Impairment in executive function, spa-

tial abilities, and language follow later. Behavioral dysregulation may also oc-

cur later.Pathology: Extraneuronal plaques (protein:

amyloid-42). Intraneuronal neurofibrillary tangles

(protein: hyperphosphorylated form oftau).

Definitive diagnosis requires clinico-pathologic correlation.

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Dementia

Impairment in executive functioning,speed of mental processing, with rela-

tively mild memory deficits in mostcases (particularly true for VaD due tomicrovascular disease).

Apathy may be prominent.Pathology: VaD can result from large-vessel or small-vessel disease or a com-bination of the two. Most VaD cases arecaused by small-vessel disease. Mendezand Cummings (2003) identify threemain pathologic mechanisms of VaD: Large-vessel (macrovascular) VaD typ-

ically arises from multiple bilateralthromboembolic infarctions; involve-ment of cortical regions.

Small-vessel (microvascular) VaD typi-

cally arises from arterioscleroticchanges in subcortical arteries causinginjury to periventricular and deepwhite matter and to subcortical greynuclei (e.g., caudate, putamen, andthalamus). The injuries include com-plete infarction (i.e., lacunar infarc-tion) and incomplete infarction thatappear as diffuse white matter lesionson neuroimaging (i.e., hyperintenseon T2 MRI sequences; hypodense onCT). In some cases, a single strategicsmall-vessel infarction in a critical cir-cuit (e.g., left thalamus) may causemultiple cognitive deficits of sufficient

Neurologic features: Focal neurologic signs or symptoms

(e.g., exaggerated deep tendon re-flexes, extensor plantar response,spastic limb weakness) that vary withlocation and size of lesions.

Key neuroimaging features: Evidence of cortical or subcortical in-

farction. Diffuse areas of high signal on T2-

weighted MRI (low signal on CT), par-ticularly in periventricular and deepwhite matter regions.

Clinical or radiologic evidence of cere-brovascular disease required for diag-nosis.

Absence of cortical or hippocampal at-

rophy adds confidence to differentialdiagnosis of VaD vs. AD.Course: Difficult to predict. May have abrupt onset with stepwise

course. Onset and course may be more grad-

ual, especially when due to subcorticalsmall-vessel disease.

Onset and progression may be gradualwith punctuated declines associatedwith discrete cerebrovascular events.

High mortality rate and lower life ex-pectancy than AD; 50% survival ratefrom symptom onset is about 6.7

severity to warrant a diagnosis of de-mentia. Diffuse white matter lesions

may also cause dementia, if suffi-ciently extensive (i.e., involves 25%of white matter).

Episodes of hypoperfusion hypoxia.Genetics and family history: Increased risk with family history of

stroke. Genetic causes are relatively rare;

CADASIL is one cause of dementiadue to microvascular disease; it is au-tosomal dominant and linked to muta-tion in the notch3 gene on chromo-some 19.

Key cognitive features: When due to multiple cortical infarcts,

the pattern of cognitive impairmentmay vary depending on location of in-farcts (e.g., language deficits from lefthemisphere lesion, spatial deficitsfrom right hemisphere lesion).

Subcortical ischemic vascular diseaseis characterized by deficits in psy-chomotor processing speed, mentalflexibility, executive function, andmemory retrieval.

Single subcortical strategic infarct (i.e.,anterior thalamus) may be sufficient tocause widespread cognitive dysfunc-tion and dementia.

Apathy may be prominent.

At least mild deficits inmemory and other

cognitive domains, clearimpact on ADLs

Neuropsychologicalassessment for diagnosis,

etiology, baseline forfuture comparison

Mild deficits,ADLs generally

intactNeuropsychology

Psychiatric

Other explanations

Normal agingAge-associated

cognitive decline

Specificdiagnosis/probable

etiology

Cognitive complaint/symptom

Possible dementiaPossible MCI

EquivocalWithin normal limits

Clinical hxPhysical and neuro examMSA and behavior assmt

Labs and imagingReversible causes

Objectivecognitive/behavioral

dysfunction

FIGURE 1-13 Evaluation of dementia. ADLs, Activities of daily living



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years; heart disease or stroke is com-mon cause of death.

DEMENTIA WITH LEWY BODIES (DLB)

Prevalence: Second or third most com-mon cause of dementia; accounts for ap-proximately 14% to 20% of all dementiacases. Almost two thirds are male. Majority do not have pure DLB but

also have concomitant AD pathology.Core features: Parkinsonism Cognitive fluctuations Visual hallucinations (occur in 40% to

70% of cases) Usually vivid, well-formed of hu-

mans or animals Dementia plus two core features are

needed for diagnosis ofprobableDLB;one core feature is needed forpossibleDLB.

Other supportive features: Repeated falls Syncope; transient loss of conscious-

ness Delusions Rapid eye movement (REM) sleep

behavior disorder Neuroleptic sensitivity

Pathology: Lewy body inclusions (pro-tein: mainly -synuclein, but ubiquitinand tau are also present) in diffuse brainregions including cortical neurons.

Genetics and family history: No genes identified in sporadic DLB

cases. A rare autosomal dominant form exists

related to mutations in -synucleingene on chromosome 4.

Key cognitive features: Marked attentional fluctuations. Frontal-executive dysfunction. Prominent visuospatial impairment. Deficits occur in memory, confronta-

tional naming, and praxis; may not beas severe as in AD.

Neurologic features: Extrapyramidal signs present in 25% to

50% at diagnosis and most develop itover disease course.

Up to 25% of autopsy-confirmed casesmay not have report of extrapyramidalsymptoms.

Axial bias to symptoms; i.e., greaterpostural instability, gait impairment,and facial impassivity and relativelyless tremor than in Parkinsons disease.

Key neuroimaging features: Less pronounced hippocampal/medial

temporal lobe atrophy compared withAD.

Quantitative volumetric measurementsmay show atrophy of putamen.

Neuroimaging not diagnostic.Course: Initial symptoms could be parkinson-

ism followed by cognitive impairmentor the opposite: cognitive symptomsfollowed by parkinsonism.

ration of the environment with di-etary preference alterations, hyper-metamorphosis (exploration of envi-ronmental stimuli as soon asnoticed), sensory agnosia, alteredsexual behavior.

Reduction of verbal output. Pattern of memory deficits suggests re-

trieval impairment rather than storageimpairment characteristic of AD.

Neurologic features: Neurologic features may be absent

early with exception of primitive(frontal release) reflexes (grasp,snout, suck).

Parkinsonism may be present; mayprecede dementia and may resembleprogressive supranuclear gaze palsy;fasciculations may occur.

Urinary or fecal incontinence may oc-cur later.

Key imaging features: MRI might not be sensitive to early

changes; the majority of patients will

eventually show anterior-posteriorasymmetry of cortical atrophy, beinggreater in frontal and anterior tempo-ral lobe regions than in posterior brainregions.

SPECT reveals frontotemporal hy-pometabolism

Neuroimaging not diagnostic by itself.Course: Initial and most prominent symptoms

are usually changes in personality, so-cial awareness, and behavior, espe-cially disinhibition or apathy.

Mean age of onset is 57 years with arange of 51 to 63 years.

Duration is typically 8 to 11 years; maybe shorter in MND variant.MISCELLANEOUS CAUSES OF DEMEN-

TIA

Toxic-metabolic etiologies (4%, includingalcohol, recreational drugs, medications);infectious (3%); other movement disor-ders (6%, e.g., Parkinsons disease, pro-gressive supranuclear palsy, Hunting-tons disease, corticobasal degeneration);normal pressure hydrocephalus (2.5%);other psychiatric (4%); and miscella-neous (1%, e.g., dementia due to AIDS,head trauma)POTENTIALLY REVERSIBLE CAUSES

OF DEMENTIA

Medication toxicity/drug interactions; hy-drocephalus; brain tumor; infection; elec-trolyte imbalance; malnutrition; meta-bolic (i.e., B12 deficiency, hepaticencephalopathy); and endocrine disor-ders (i.e., hypothyroidism)COGNITIVE CHANGES IN NORMAL

AGING

General slowing of mentation andphysical responses; declines occur incomplex and divided attention, abilityto recall names, executive and visu-ospatial functions; reduced efficiencyin learning and spontaneous recall of

Shorter survival times than AD; about7.7 3.0 years from onset of cognitivesymptoms.

FRONTOTEMPORAL DEMENTIA

(FTD)

Prevalence: Accounts for approximately 2% to 5%

of all dementia cases. Accounts for 20% of neurodegenera-

tive dementias in people under 65years old.

Average age of onset is 57 years witha typical range of 51 to 63.

Core features: Personality changes are most promi-

nent symptom and typically precedecognitive changes: Decline in social comportment Impaired regulation of personal

conduct May become disinhibited but are

more likely to display apathy Lack of attention to personal hy-

giene can be supportive of diagno-

sisPathology: FTD is the main syndrome of fron-

totemporal lobar degeneration(FTLD)a spectrum of dementing dis-orders involving degeneration of thefrontal and anterior temporal lobes.

Mendez and Cummings (2003) de-scribe three main pathologic variantsof FTD: Lacking distinctive histology (FTLD-

ldh): neuronal loss, astrogliosis withspongiosis in frontotemporal cortex

Pick bodies (FTLD-Pick): severefrontal atrophy (knife-like gyri);

enlarged neurons called Pick cellsand neuronal Pick body inclusions(tau-positive, ubiquitin-positive);FTLD-Pick is diagnosed when Pickbodies are present irrespective ofpresence of Pick cells

Motor neuron disease (MND): in-volvement of anterior horn cellswith or without ubiquitin inclusions

Genetics and family history: 38% to 50% of cases have positive his-

tory of similar dementia in first-degreefamily member.

Several mutations in tau gene havebeen found in familial FTD.

Some cases associated with mutationson chromosome 17; linkage to chro-mosome 3 in some families; presenilin1 may be involved in some pheno-types.

Key cognitive and behavioral fea-tures: Early blunting of emotional respon-

siveness; loss of basic emotions. Executive cognitive impairment promi-

nent. Compulsive behaviors are common:

Klver-Bucy syndrome may occur:emotional blunting, reduction orloss of fear responding, oral explo-

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Dementia

new information but memory storageis maintained.

Terms used to describe cognitivechanges in aging: normal aging, age-associated cognitive decline, age-asso-ciated memory impairment.

MILD COGNITIVE IMPAIRMENT (MCI)

MCI is a syndrome (not an etiology)defined by subjective and objectiveimpairment in memory or other cogni-tive domains that represents a declineand is greater than expected for age,but is of insufficient severity to signifi-cantly affect activities of daily living orto warrant a diagnosis of dementia.

The term mild cognitive impairment isoften used to describe this period, butthe term is not universally accepted andalternatives have been proposed (e.g.,cognitive impairment no dementia).

Diagnostic criteria for MCI were devel-oped based on those at high risk forAD. Criteria include subjective mem-ory complaint, objective memory im-

pairment for age/education on formaltesting; generally intact global cogni-tive functioning; generally persevereddaily functioning; and no dementia. These criteria are now thought to

describe amnestic MCIa groupwith an approximately 12% annualrate of conversion to AD (vs. 1% to2% for normal elderly).

Current MCI conceptualization in-cludes other subtypes that might goon to develop different types of de-mentia.

DIAGNOSIS

Two-step process:1. Is dementia present? and if so2. What is the most likely etiology?

No definitive test or algorithm for de-termining the presence or absence ofdementia exists; differentiating normalaging from MCI and MCI from mild de-mentia is difficult.

DIFFERENTIAL DIAGNOSIS

Determining etiology requires carefulassessment of cognitive and behav-ioral symptoms, neurologic features,and the onset and temporal course of

illness along with laboratory and neu-roimaging assessments. Determining etiology requires differ-

entiating non-AD dementia from AD.DEMENTIA VS. AMNESIA

Amnesia is isolated and profoundmemory impairment; dementia in-volves multiple cognitive domains.

DEMENTIA VS. APHASIA

Difficult because many cognitive testsrequire a strong language component.

Nonverbal testing may reveal intactnon-language-based cognitive func-tions.

Frontal release signs ApraxiasMENTAL STATUS ASSESSMENT (MSA)

Evaluate arousal, orientation, atten-tion/mental control, memory, lan-guage, conceptual or semantic knowl-edge, praxis (ability to perform skilledmovements, e.g., ask the patient topretend to light a cigarette), mentalcalculations, visuoconstructional abili-ties, executive functions, and behavior.

Mini Mental State Exam (MMSE): themost commonly administered formalmental status test; takes 5 to 10 min-utes (see Appendix 2); can be supple-mented with assessment of executivefunctions and abstract reasoning. Executive function

1. Alternating figures: copy andcontinue producing alternatingfigures (e.g., O O). Lookfor loss of sequence or persever-ations.

2. Alternating movements: place

both hands on a table, one in afist, one palm down; then alter-nate repeatedly. Demonstratebriefly and then have the patientcontinue independently. Lookfor loss of sequence.

Abstract conceptualization: similari-ties (e.g., How are an apple and abanana alike? include more thanone similarity pair e.g., boat-car,watch-ruler, desk-bookcase). Lookfor concrete responses; differencesinstead of similarities. Responsescan be influenced by educationaland intellectual background.

Mini-Cog exam consists of a 3-itemmemory test and clock drawing; it takes2 to 3 minutes to administer. It may beas accurate as the MMSE in a primarycare setting.

Behavior: appearance; mood and af-fect; level of insight; thought contentand process; psychosis; anxiety disor-ders; sleep and appetite.

LABORATORY TESTS

Blood Thyroid panel or thyroid stimulating

hormone Complete blood count, vitamin B12,

folate Electrolytes, BUN, creatinine Liver function tests Glucose Syphilis or AIDS if high clinical sus-

picion Other tests directed by differential

diagnosis Urinalysis Lumbar puncture: optional; if suspicion

of cancer, infectious process, atypicalpresentation (e.g., rapid progression)

EEG: if history of seizures, rapid de-cline, suspicion of Creutzfeldt-Jacobdisease

Patients with aphasia are more likelythan dementia patients to recognizeand respond to what is happeningaround them; and to remember peo-ple, places, and routines.

DEMENTIA VS. DEPRESSION

Depression with cognitive impairmentis common in the elderly and may bea risk factor for dementia. Moreover,depression occurs in 12% to 20% ofpatients with dementia.

Cognitive deficits: attention, psy-chomotor processing speed, executivefunctioning, and memory retrieval;may reflect reduced concentration,loss of interest, and motivation.

Neuropsychologic testing may behelpful. Depressed patients are likelyto benefit from cueing and recognitionformats during memory testing,whereas AD patients do not.

Follow-up assessment after a period oftreatment may be needed to rule outdementia.

DEMENTIA VS. DELIRIUM Delirium generally has a more rapid

onset than dementia. Marked attentional disturbances/

fluctuations are more common indelirium.

Delirium can be superimposed on apreexisting dementia or mild cognitiveimpairment.

NORMAL AGING VS. MCI

The key judgments are whether thecomplaints and severity of cognitiveimpairment represent a decline thatexceeds normal aging; the extent towhich the impairments disrupt normal

functioning; and whether they are bet-ter explained by psychiatric disorder,substance abuse, medication effects,situational stressors, or other nonneu-rodegenerative etiologies.

Neuropsychologic testing may be veryhelpful.

MCI VS. MILD DEMENTIA

The key judgments are the scope andseverity and stability of cognitive orbehavioral impairment and the degreeto which they affect daily functioning.

Neuropsychologic testing may be veryhelpful.

WORKUP

CLINICAL HISTORY Key symptoms; onset and progression;

impact on activities of daily living. Obtain information from a reliable in-

formant. Obtain a medication history and iden-

tify those that can disrupt cognition. Screen for depression. Family history of dementia. Review of systems.PHYSICAL AND NEUROLOGIC EXAM

General health Focal neurologic signs



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Neuroimaging: CT or MRI of the headis appropriate to rule out hydro-cephalus, mass lesions, and subduralhematomas and to assess for extent ofcortical and subcortical atrophy, andcerebrovascular lesion load; SPECT orPET for cerebral metabolism may behelpful, especially for FTD

TREATMENT

NONPHARMACOLOGIC

THERAPY

Ensure patient safety: e.g., driving,wandering, cooking, ironing, tool use,medication management, nutrition, hy-giene and grooming, financial man-agement.

Establish routines, avoid chaotic oroverstimulating environments.

Family education. Caregiver support/respite: support

groups, daycare, sharing caregivingwith other family members.

Cerebrovascular risk factor control in-cludes adequate treatment of hyper-tension, hypercholesterolemia, anddiabetes.

PHARMACOLOGIC THERAPY

Cognitive impairment: Acetylcholinesterase inhibitors (i.e.,

donepezil, galantamine, rivastig-mine) approved for AD; they slowthe course of cognitive decline, notdisease modifying. May also be use-ful for vascular dementia.

Memantine (NMDA receptor antago-nist) for moderate to severe AD.

For dementias other than AD, thereare few pharmacologic options.

Agitation and psychosis: Atypical antipsychotics including

risperidone and olanzapine arewidely used but not FDA approved.

Reduce/control risk factors for cogni-tive impairment: cerebrovascular risk;medications that may contribute to cog-nitive impairment; alcohol; depression.

PREVENTION

Reduction of cardiovascular risk factorsincluding treatment of hypertension,hypercholesterolemia, and diabetes.

Promoting cognitive exercises andmental activity can help ward off pro-gression.

Maintaining a healthy social life.

PATIENT/FAMILY EDUCATION

Alzheimers Association local supportgroups can offer useful education forfamilies and caregivers.

SUGGESTED READINGS

Knopman DS et al: Practice parameter: diag-nosis of dementia (an evidence-based re-

view). Report of the quality standards sub-committee of the American Academy of

Neurology, Neurology56:1143-1153, 2001.McKeith I et al: Dementia with Lewy bodies,

Lancet Neurol3:19-28, 2004.Mendez MF, Cummings JL: Dementia: A Clin-

ical Approach, ed 3, Philadelphia, 2003,Butterworth Heinemann.

Petersen RC: Mild cognitive impairment as adiagnostic entity, J Intern Med256:183-194,2004.

Roman GC: Vascular dementia revisited: diag-nosis, pathogenesis, treatment, and preven-tion, Med Clin North Am86:477-499, 2002.

Rosenstein LD: Differential diagnosis of themajor progressive dementias and depres-sion in middle and late adulthood: a sum-mary of the literature of the early 1990s,Neuropsychol Rev8:109-167, 1998.

Strub RL, Black FW: The Mental Status Exam-ination in Neurology, ed 4, Philadelphia,2000, FA Davis.

AUTHORS: STEPHEN CORREIA, PH.D., andLYNN MCNICOLL, M.D.

Use lowest dose needed and try towean off as soon as possible. Po-tential increased risk of cerebrovas-cular accidents. Avoid use of an-tipsychotics in patients with diffuseLewy body dementia.

Benzodiazepines can occasionallybe useful usually as second linetherapy.

Depression: selective serotonin reup-take inhibitors can be effective for thetreatment of coexisting depressionamong those with dementia.

DISPOSITION

Deterioration over time is a commonfeature of most dementias.

Goals of currently available treatmentsare to slow course and maximize func-tioning.

Transition to assisted living facilitiesmay be helpful as dementia worsens;nursing home placement may follow.

REFERRAL Neuropsychologic assessment can

help determine presence/absence ofdementia and the pattern of cognitiveimpairment may help identify etiology.

Geriatric psychiatry if depression orother psychiatric disturbance is promi-nent.

Neurology referral is necessary to as-sess general neurologic status, espe-cially if motor, sensory, or gait distur-bance is present.

PEARLS &

CONSIDERATIONS

Search for and treat potentiallyreversible causes of dementia.

Treat psychiatric disturbances (e.g.,depression, agitation, psychosis, butbe careful with antipsychotics in DLB).

Dementia8

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