Dementia In theClinic · 2016. 7. 21. · In theClinic In the Clinic Dementia Prevention page ITC2...

Inthe

ClinicIn the Clinic

DementiaPrevention page ITC2

Screening page ITC3

Diagnosis page ITC4

Treatment page ITC7

Tool Kit page ITC14

Patient Information page ITC15

CME Questions page ITC16

Physician WriterPeter V. Rabins, MD, MPHDavid M. Blass, MD

Section EditorsDeborah Cotton, MD, MPHJaya K. Rao, MD, MHSDarren Taichman, MD, PhDSankey Williams, MD

The content of In the Clinic is drawn from the clinical information and educationresources of the American College of Physicians (ACP), including ACP SmartMedicine and MKSAP (Medical Knowledge and Self-Assessment Program). Annalsof Internal Medicine editors develop In the Clinic from these primary sources incollaboration with the ACP’s Medical Education and Publishing divisions and withthe assistance of science writers and physician writers. Editorial consultants fromACP Smart Medicine and MKSAP provide expert review of the content. Readerswho are interested in these primary resources for more detail can consult https://mksap16.acponline.org/, and other resources referenced in each issue of In theClinic.

CME Objective: To review current evidence for prevention, screening, diagnosis,and treatment of dementia.

The information contained herein should never be used as a substitute for clinicaljudgment.

© 2014 American College of Physicians

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What medical interventions orhealth behaviors can help patientsprevent dementia or cognitivedecline?Although the different types of dementia have several risk factors,data supporting the effectiveness of specific preventive measures toaddress them are limited.

A 2011 meta-analysis identified 7 potential-ly modifiable risk factors for AD and calcu-lated a population attributable risk (PAR)and CI for each in the United States: physicalinactivity (PAR = 21% [95% CI, 5.8–36.6]), depression (PAR = 14.7% [CI, 9.6–20.3]),smoking (PAR = 10.8% [CI, 3.0–19.8]), midlifehypertension (PAR = 8.0% [CI, 2.2–15.1]),midlife obesity (PAR = 7.3% [CI, 4.3–10.8]) ,cognitive inactivity or low educational

© 2014 American College of Physicians ITC2 In the Clinic Annals of Internal Medicine 5 August 2014

1. Brookmeyer R, Gray S,Kawas C. Projectionsof Alzheimer’s dis-ease in the UnitedStates and the publichealth impact of de-laying disease onset.Am J Public Health.1998;88:1337-42.[PMID: 9736873]

2. Mitchell SL, Teno JM,Miller SC, Mor V. A na-tional study of the lo-cation of death forolder persons withdementia. J Am Geri-atr Soc. 2005;53:299-305.[PMID: 15673356]

3. Hurd MD, Martorell P,Delavande A, MullenKJ, Langa KM. Mone-tary costs of demen-tia in the UnitedStates. N Engl J Med.2013;368:1326-34.[PMID: 23550670]doi:10.1056/NEJM-sa1204629

4. Barnes DE, Yaffe K.The projected effectof risk factor reduc-tion on Alzheimer’sdisease prevalence.Lancet Neurol.2011;10:819-28.[PMID: 21775213]doi:10.1016/S1474-4422(11)70072-2

Prevention

Dementia is defined as a decline in 2 or more cognitive capacities, caus-ing impairment in function but not alertness or attention. The declinein cognition distinguishes it from lifelong intellectual disability (previ-

ously called “mental retardation”) and single learning disorders, both of whichare present from birth and symptomatic in childhood. That 2 or more cogni-tive capacities must be impaired distinguishes dementia from amnestic mildcognitive impairment (MCI), the amnestic syndrome (previously called theKorsakoff syndrome), and single focal brain lesions. Requiring impairment infunctional activity also distinguishes it from MCI, although this interpretationis controversial. The requirement for intact attention and alertness distinguish-es it from delirium. The Diagnostic and Statistical Manual of Mental Disorders,version 5, has recently proposed replacing the word “dementia” with the phrase“neurocognitive disorder” to destigmatize the syndrome. However, opponentspoint out that the term “neurocognitive disorder” lacks specificity because it in-cludes other categories of cognitive impairment, such as intellectual disability,learning disabilities, and delirium.

Dementia is a syndrome rather than a specific illness; the most commontypes are Alzheimer disease (AD), vascular dementia, Lewy body dementia,and frontotemporal dementia. One or 2% of these patients presenting withdementia has a potentially reversible disorder, such as normal pressure hydro-cephalus, medication-induced cognitive impairment, hypothyroidism, or ma-jor depression.

Although it can begin at any age after childhood, dementia is predominantlya syndrome of later life, with the prevalence in persons older than 65 yearsestimated to be 9%–13%. The annual incidence rate is 0.25% at age 65 anddoubles every 5 years, reaching approximately 15% at age 95 (1).

Caring for patients with dementia is a heavy emotional and financial burdenfor families and society as a whole. Patients can be cared for initially in thehome, but institutionalization is ultimately required for many patients—67%die in nursing homes (2). Depending on the methods used to value informalcare, the yearly per-person cost attributable to dementia ranged between $41 689 and $56 290 in 2010 (3).

Although most forms of dementia currently have no cure, research findingsand accumulated clinical experience support a set of practices that maximizesthe function and well-being of patients with dementia and their families. Thisapproach incorporates a broad range of practices, including comprehensive di-agnostic assessment, optimization of treatment for general medical conditions,attention to patient comfort and quality of life, pharmacotherapy, control ofpsychiatric symptoms, and education and support of the patient’s family.


© 2014 American College of PhysiciansITC3In the ClinicAnnals of Internal Medicine5 August 2014

5. Daviglus ML, Plass-man BL, Pirzada A,Bell CC, Bowen PE,Burke JR, et al. Riskfactors and preven-tive interventions forAlzheimer disease:state of the science.Arch Neurol.2011;68:1185-90.[PMID: 21555601]doi:10.1001/archneu-rol.2011.100

6. Larson EB, Kukull WA,Buchner D, Reifler BV.Adverse drug reac-tions associated withglobal cognitive im-pairment in elderlypersons. Ann InternMed. 1987;107:169-73. [PMID: 2886086]

7. Zandi PP, Carlson MC,Plassman BL, Welsh-Bohmer KA, Mayer LS,Steffens DC, et al;Cache County Mem-ory Study Investiga-tors. Hormone re-placement therapyand incidence ofAlzheimer disease inolder women: theCache County Study.JAMA. 2002;288:2123-9. [PMID: 12413371]

8. Shumaker SA, LegaultC, Rapp SR, Thal L,Wallace RB, OckeneJK, et al; WHIMS In-vestigators. Estrogenplus progestin andthe incidence of de-mentia and mild cog-nitive impairment inpostmenopausalwomen: the Women’sHealth InitiativeMemory Study: a ran-domized controlledtrial. JAMA.2003;289:2651-62.[PMID: 12771112]

9. DeKosky ST,Williamson JD, Fitz-patrick AL, KronmalRA, Ives DG, SaxtonJA, et al; Ginkgo Eval-uation of Memory(GEM) Study Investi-gators. Ginkgo bilobafor prevention of de-mentia: a random-ized controlled trial.JAMA. 2008;300:2253-62. [PMID: 19017911]doi:10.1001/jama.2008.683

10. U.S. Preventive Serv-ices Task Force.Screening for cogni-tive impairment inolder adults.Rockville, MD:Agency for Health-care Research andQuality; 2014. Ac-cessed at www.us-preventiveservices-taskforce.org/uspstf14/dementia/demen-tiasumm.htm on 5May 2014.

sedative-hypnotics. Several studieshave shown that elderly patientstaking benzodiazepines or othersedative-hypnotics perform morepoorly on cognitive tests than thosenot taking these medications (6).

Significant epidemiologic evidencelinks mid-life estrogen use to alower incidence of dementia later inlife (7). However, in prospectiveprevention trials, including thelarge Women’s Health InitiativeMemory Study (WHIMS), use ofestrogen plus progestin for preven-tion of dementia was associatedwith an increased incidence of de-mentia and other medical compli-cations (8).

The WHIMS was a placebo-controlled, ran-domized, controlled trial of estrogen plusprogestin (n = 2229) versus placebo (n =2303) for prevention of dementia inwomen aged 65 years and older. Use of es-trogen for a mean of 4 years was associat-ed with a relative risk of 2.05 (CI, 1.21–3.48)for dementia during the study period.

Ginkgo biloba did not prevent de-mentia in one prospective trial (9).

attainment (PAR = 7.3% [CI, 4.4–10.3]), anddiabetes mellitus (PAR = 3.3% [CI, 1.5–5.4]) (4).

However, the National Institutes ofHealth sponsored a panel reportpublished in the same year conclud-ing that “Currently, insufficient evidence exists to draw firm conclu-sions on the association of any mod-ifiable factors with the risk of AD”(5). Because avoiding or ameliorat-ing the risk factors for dementia pro-vides other health benefits, it seemsprudent to advise patients to addressthese risk factors for the potentialbenefit of lowering the risk for AD.Patients should also be advised tominimize risk for head trauma byusing seat belts in automobiles andhelmets for contact sports and ridinga bicycle or motorcycle.

What medications can be used inpatients presenting with signs ofdementia?Clinicians should regularly reviewthe medications of elderly patientsand minimize use of those that cancause cognitive impairment, partic-ularly benzodiazepines, anticholin-ergics, barbiturates, and other

ScreeningAs a result, the clinician shouldconsider dementia in the differen-tial diagnosis of adult patients ofany age with symptoms of memorydifficulty interfering with dailyfunction, unexplained functionaldecline, deterioration in hygiene,questionable adherence to medica-tion regimens, or new-onset psy-chiatric symptoms.

What methods should cliniciansuse when looking for dementia?When elderly patients are beingevaluated for dementia, cliniciansshould use a standardized screen-ing instrument together with abrief history from the patient anda knowledgeable informant. Thescreening instrument should beeasy to use, highly sensitive, widely available, and supported by

Should clinicians screen fordementia?Universal screening for dementia isnot recommended (10), but the dis-order is prevalent and often goesundetected in the primary care setting (11).

In a study reviewing the primary carerecords of 297 patients, dementia in 65%of patients meeting the criteria was notnoted on the patient’s chart, including20% of those with advanced dementia(11). In a retrospective review of 1489 pa-tients referred to a memory disorders pro-gram, those referred from a dementiascreening program had a mean Mini-Mental Status Examination (MMSE) scoreof 20.8 ± 5.7 compared with those re-ferred from their physicians (18.8 ± 6.6),from families (16.8 ± 6.6), or from othersources (15.3 ± 7.1) (11).



11. Valcour VG, MasakiKH, Curb JD,Blanchette PL. Thedetection of demen-tia in the primarycare setting. Arch In-tern Med.2000;160:2964-8.[PMID: 11041904]

12. Folstein MF, FolsteinSE, McHugh PR.“Mini-Mental State”.A practical methodfor grading the cog-nitive state of pa-tients for the clini-cian. J Psychiatr Res.1975;12:189-98.[PMID: 1202204]

13. Borson S, Scanlan J,Brush M, Vitaliano P,Dokmak A. The Mini-Cog: a cognitive ‘vi-tal signs’ measure fordementia screeningin multi-lingual eld-erly. Int J Geriatr Psy-chiatry.2000;15:1021-7.[PMID: 11113982]

14. Saint Louis Universi-ty School of Medi-cine. Saint Louis Uni-versity Mental StatusExamination. St.Louis: Saint LouisUniversity School ofMedicine. Accessedat http://aging.slu.edu/index.php?page=saint-louis-university-mental-status-slums-examon 7 May 2014.

similar to the MMSE (16), andthe MoCA has the best sensitivitybut lower specificity (17). An alternative instrument is the In-formant Questionnaire on Cogni-tive Decline in the Elderly (IQCODE), which can be filled outby a family member or other in-formant who knows the patientwell (18).

population data relevant to the pa-tient in question. The MMSE (12)has been widely used but is nowcopyrighted. Alternatives includethe Mini-Cog (13), the St. LouisUniversity Mental Status Exam(SLUMS) (14), and the MontrealCognitive Assessment (MoCA)(15). The Mini-Cog has the bene-fit of brevity, the SLUMS is most

Diagnosisare dominated by difficulties withshort-term memory, subtle lan-guage and visuospatial perceptualproblems, and changes in executivefunction. Significant reductions inefficiency and organizational abili-ties that the patient may or maynot recognize could also occur.Symptoms begin insidiously andare slowly progressive. The overalllevel of alertness remains unim-paired. Patients or families may notlabel these difficulties as memoryproblems but may instead reportconversations when the patient hasno recollection of previous discus-sions, increased forgetfulness thatcauses the patient to lose objects orbecome confused while shopping,or simply increased disorganizationand decreased efficiency. Symptomsare often first noticed or reportedat the time of a life change, such asthe death of a spouse, a move into anew residence, or being in an unfa-miliar place on vacation. Table 1describes the diagnostic criteria ofthe National Institute of Neurolog-ical and Communicative Diseasesand Stroke–Alzheimer’s Disease

What elements of the history areespecially important in evaluatingpatients with suspected dementia?Clinicians should use the patient’shistory to characterize the cognitivedeficits, generate a differential di-agnosis, and determine the cause ofthe dementia. This goal is best ac-complished by identifying medical,neurologic, and psychiatric signsand symptoms that may be clues tothe cause of the cognitive problemsand establishing their order of ap-pearance, severity, and associatedfeatures. In the case of cognitivedifficulties, it is most important totry to obtain collateral informationfrom a knowledgeable informant,because cognitive dysfunction canimpair the patient’s ability to reportaccurately. It is often easier to col-lect this information without thepatient present.

In taking the history, the physicianmust be knowledgeable about thedifferential diagnosis and naturalhistory of the most common typesof dementia (Appendix Table, avail-able at www.annals.org). For exam-ple, in classic AD, early symptoms

Prevention and Screening... Use of benzodiazepines, anticholinergics, barbiturates,and other sedative-hypnotics must be minimized in elderly patients. Screening fordementia in the elderly population is not recommended, but in selected patients abrief history from the patient and a knowledgeable informant together with a stan-dardized instrument, such as the MMSE, the Mini-Cog, the SLUMS, or the MoCA, canbe used to decide whether a more extensive evaluation is necessary.

CLINICAL BOTTOM LINE



and Related Disorders AssociationWork Group (19, 20).

Clinicians evaluating a patientwith a change in cognition oroverall function must considerdelirium. Delirium is characterizedby cognitive impairment and animpaired level of alertness/attention/consciousness. In contrast to de-mentia, the onset of delirium isusually abrupt, and fluctuationsover minutes or hours are promi-nent. Although some patients maybe agitated and manifest psychoticsymptoms, others are slow anddrowsy and appear mildly de-pressed or withdrawn. Prompt diagnosis of delirium is critical because it usually reflects an un-derlying systemic condition, suchas infection, metabolic derange-ment, medication effect, or cancer.Use of an instrument, such as the

Confusion Assessment Method,increases identification of deliriumin high-risk settings, such as theintensive care unit (21). It is im-portant to remember that manyelderly patients report minor cog-nitive problems, such as mild for-getfulness, difficulty rememberingnames, and reduced concentration.These problems are typically spo-radic, do not worsen significantlyover time, are easily compensatedfor, do not affect function, and areoften judged to be worse by thepatient than by others. In contrast,early dementia insidiously be-comes a pattern; worsens overtime; is difficult to offset; eventu-ally interferes with routine activi-ties, such as bill paying and mealpreparation; and is often judged tobe worse by others than by the patient. Patients with memoryproblems should be screened for

15. Nasreddine Z. Mon-treal Cognitive As-sessment. GreenfieldPark, Québec, Cana-da: Center for Diag-nosis & Research onAlzheimer’s Disease;2014. Accessed atwww.mocatest.orgon 7 May 2014.

16. Tariq SH, Tumosa N,Chibnall JT, Perry MH3rd, Morley JE. Com-parison of the SaintLouis UniversityMental Status Exami-nation and the Mini-Mental State Exami-nation for detectingdementia and mildneurocognitive dis-order—a pilot study.Am J Geriatr Psychia-try. 2006;14:900-10.[PMID: 17068312]

17. Roalf DR, Moberg PJ,Xie SX, Wolk DA,Moelter ST, ArnoldSE. Comparative ac-curacies of twocommon screeninginstruments for clas-sification ofAlzheimer’s disease,mild cognitive im-pairment, andhealthy aging.Alzheimers Dement.2013;9:529-37.[PMID: 23260866]doi:10.1016/j.jalz.2012.10.001

18. Jorm AF. The Inform-ant Questionnaireon Cognitive De-cline in the Elderly(IQCODE): a review.Int Psychogeriatr.2004;16:275-93.[PMID: 15559753]

19. McKhann G, Drach-man D, Folstein M,Katzman R, Price D,Stadlan EM. Clinicaldiagnosis ofAlzheimer’s disease:report of theNINCDS-ADRDAWork Group underthe auspices of De-partment of Healthand Human ServicesTask Force onAlzheimer’s Disease.Neurology.1984;34:939-44.[PMID: 6610841]

20. McKhann GM, Knop-man DS, ChertkowH, Hyman BT, JackCR Jr, Kawas CH, etal. The diagnosis ofdementia due toAlzheimer’s disease:recommendationsfrom the National In-stitute on Aging-Alzheimer’s Associa-tion workgroups ondiagnostic guide-lines for Alzheimer’sdisease. AlzheimersDement. 2011;7:263-9. [PMID: 21514250]doi:10.1016/j.jalz.2011.03.005

Table 1. Diagnostic Criteria for Different Kinds of Alzheimer Disease*Probable Alzheimer disease is defined by:

Dementia established by clinical examination and documented by an instrument, such as the MoCA, SLUMS or Mini-Mental Status Examination

Deficits in 2 or more areas of cognition, one of which is usually memoryProgressive declineNo disturbance of consciousnessOnset between age 40–90 yearsAbsence of other disorders that could account for the deficitsPossible Alzheimer disease is defined by:

Dementia established by clinical examination and documented by an instrument, such as the Mini-Mental Status Examination

Absence of other conditions that would cause dementiaVariations in the clinical course from the typical course of Alzheimer disease; when another condition is present that

could cause dementia but is not felt to be the primary cause; or when there is a single, severe, progressive cognitive deficit without an identifiable cause

Definite Alzheimer disease is defined by:

The presence of clinical criteria for probable Alzheimer disease combined with biopsy- or autopsy-confirmed histopathology.The diagnosis of probable Alzheimer disease is supported by the presence of:

Specific cognitive deficits, such as executive dysfunction, aphasia, agnosia, and apraxiaImpaired activities of daily livingPositive family historySupportive laboratory tests, such as normal lumbar puncture, normal electroencephalography, and cerebral atrophy on

neuroimagingThe diagnosis of Alzheimer disease is unlikely when:

The onset is acuteFocal neurologic findings are presentSeizure or gait disturbance is present early in the disease course

*Adapted from reference 25.


21. Ely EW, Inouye SK,Bernard GR, GordonS, Francis J, May L, etal. Delirium in me-chanically ventilatedpatients: validity andreliability of the Con-fusion AssessmentMethod for the In-tensive Care Unit(CAM-ICU). JAMA.2001;286:2703-10.[PMID: 11730446]

22. Knopman DS,DeKosky ST, Cum-mings JL, Chui H,Corey-Bloom J,Relkin N, et al. Prac-tice parameter: diag-nosis of dementia(an evidence-basedreview). Report ofthe Quality Stan-dards Subcommitteeof the AmericanAcademy of Neurol-ogy. Neurology.2001;56:1143-53.[PMID: 11342678]

23. Massoud F, Devi G,Moroney JT, Stern Y,Lawton A, Bell K, etal. The role of rou-tine laboratory stud-ies and neuroimag-ing in the diagnosisof dementia: a clini-copathologicalstudy. J Am GeriatrSoc. 2000;48:1204-10. [PMID: 11037005]


dementia, but a complete evaluationshould be reserved for those withmeasurable impairment in memoryor other aspects of cognition.

How should clinicians evaluate the physical, mental, and cogni-tive status of patients withsuspected dementia?During the physical examination,the clinician should look for condi-tions that can cause or worsen cog-nitive symptoms (Appendix Table,www.annals.org), with an emphasison vascular and neurologic disease.The examination should include amental status evaluation that beginswith an assessment of the patient’slevel of alertness, general appear-ance, and cooperation, which canprovide clues to delirium, depres-sion, or nutritional deficiencies.Speech should be evaluated for itscontent (grammatical or semanticerrors) and form (rate, fluency, andvolume); the patient’s mood and af-fect should be assessed for depres-sion, anxiety or mania, and the riskfor suicide; and thought content andperception should be examined fordelusions or hallucinations and ob-sessions or compulsions.

The cognitive examination shouldinclude a standard instrument,such as the SLUMS, which takes 5 minutes to administer, or theMOCA, which can take 10 min-utes. Both tests have strengths andlimitations. The MOCA empha-sizes executive function and ismore sensitive; the SLUMS evalu-ates orientation, immediate recall,concentration, naming, languagefunction, praxis, and visual–spatialperception. Naming and praxis canbe further tested by asking the pa-tient to name a series of commonand uncommon objects and by ask-ing them to demonstrate tasks,such as brushing hair or teeth orslicing bread. Abstract reasoningand judgment should be tested byasking for solutions to real-lifeproblems, such as what to do if onesmells smoke in the house, or by

having the patient interpret pro-verbs or similes. Asking the patientto draw a clock and put the handsat 10 minutes past 11 is a quicktest of visual-spatial perception,praxis, and planning ability. Also,the patient should be evaluated forcorticosensory deficits, such asneglect or left–right confusion.

What laboratory tests are helpfulin the evaluation of any patientwith cognitive dysfunction?According to guidelines from theAmerican Academy of Neurology,patients who are evaluated for cog-nitive problems should have a labo-ratory evaluation for common medical disorders, with selected additional studies depending on thespecific clinical situation (see theBox: Laboratory Studies for Pa-tients Being Evaluated for Cogni-tive Problems).

When should clinicians orderimaging studies and other, morespecialized laboratory studies?Patients with cognitive difficultiesless than 3 years in duration shouldhave a neuroimaging study of thehead using computed tomographyor magnetic resonance imaging toexclude cerebrovascular disease,hemorrhage, tumor, abscess,Creutzfeldt-Jakob disease, and hy-drocephalus. The yield is higher inpatients with early age of onset; rapid progression; focal neurologicdeficits; risk factors for cerebrovas-cular disease; recent falls; centralnervous system (CNS) infection;unexplained fluctuation of con-sciousness; or symptoms atypical ofAD, such as early and marked per-sonality change. Routine use of glu-cose or amyloid positron emissiontomography scanning is not recom-mended, although these tests maybe useful in certain cases, such asdifferentiating frontotemporal de-mentia from AD and in assessingfor early-onset dementia (24, 25).

Genetic studies are not indicatedin the evaluation of dementia

Laboratory Studies for PatientsBeing Evaluated for CognitiveProblems*Comprehensive metabolic profileComplete blood countThyroid-stimulating hormone levelVitamin B

12level

In addition, patients may need toundergo additional tests,including the following:• Rapid plasma reagin (fluores-

cent treponemal antibody canbe checked in cases where con-cern for neurosyphilis is higher)

• HIV test• Toxicology screen• Erythrocyte sedimentation rate• Heavy metal screen• Thiamine level• Paraneoplastic panel• Chest radiograph or computed

tomography of the chest• Urinalysis

*Adapted from references 22 and 23.



syndrome, CNS cancer, or im-munosuppression is possible. Neu-ropsychological testing providesthe most comprehensive assess-ment of cognitive function and isparticularly useful if the diagnosisof dementia is uncertain (27) or aprecise characterization of the pa-tient’s cognitive impairment isnecessary.

What other disorders shouldclinicians consider in theassessment of cognitivedysfunction?During assessment of patientswith cognitive disturbances, theyshould be evaluated for not onlythe most common disorders thatcause dementia but also medica-tions, depression, and MCI. Pa-tients with MCI (28) have cogni-tive decline without impairedfunction and should be followedclosely, because 7% to 15% “con-vert” each year and meet the crite-ria for dementia; after 5 years,nearly 50% of patients with MCImeet dementia criteria (28).

unless there is a specific concernabout Huntington disease. Cur-rent evidence does not supportroutine testing for the ApoE4allele (26). Testing for the autoso-mal dominant gene mutationsfound in patients with familialAD or fronto-temporal dementiashould be considered only if mul-tiple family members are affected,the clinical picture and workupsupport one of these disorders,and the patient is younger than 60 years at onset. Genetic coun-seling is recommended before ge-netic testing (26).

Other tests should be reserved forspecific situations. Electroen-cephalography may be useful ifthere is a question of delirium,seizures, encephalitis, orCreutzfeldt–Jakob disease. Lumbarpuncture may be indicated in pa-tients younger than 55 years andin those with rapidly progressivedementia; a positive rapid plasmareagin; and if acute or chronicCNS infection, the paraneoplastic

patients may be unable to identifysymptoms, such as constipation,dysuria, tooth pain, or diminishedvisual or auditory acuity, and theclinician should proactively lookfor these problems.

It is important to attend to generalmedical and preventive care asconscientiously as in patientswithout dementia. A stroke orheart attack due to uncontrolled

What should clinicians advisepatients and caregivers aboutgeneral health and hygiene?In the early stages of dementia,patients may have difficulty com-prehending the details of theirmedical care, organizing care, andkeeping track of appointments andmedications. The clinician shouldbe alert to these limitations andprepare a care plan that compen-sates for them. Later in the illness,

Diagnosis... Patients who report cognitive and functional decline should be evalu-ated through a detailed history of medical, neurologic, and psychiatric symptomsfrom the patient and a knowledgeable informant. They should also be given athorough physical and mental status evaluation and a cognitive examination.Whether to obtain basic laboratory studies and additional studies, including structural neuroimaging, is dictated by the clinical presentation.


Treatment

24. Foster NL, Heide-brink JL, Clark CM,Jagust WJ, Arnold SE,Barbas NR, et al.FDG-PET improvesaccuracy in distin-guishing frontotem-poral dementia andAlzheimer’s disease.Brain.2007;130:2616-35.[PMID: 17704526]

25. Johnson KA, Mi-noshima S, BohnenNI, Donohoe KJ, Fos-ter NL, Herscovitch P,et al; Amyloid Imag-ing Task Force of theAlzheimer’s Associa-tion and Society forNuclear Medicineand Molecular Imag-ing. Update on ap-propriate use criteriafor amyloid PET im-aging: dementia ex-perts, mild cognitiveimpairment, and ed-ucation. Amyloid Im-aging Task Force ofthe Alzheimer’s As-sociation and Socie-ty for Nuclear Medi-cine and MolecularImaging. AlzheimersDement.2013;9:e106-9.[PMID: 23809369]doi:10.1016/j.jalz.2013.06.001

26. Loy CT, Schofield PR,Turner AM, Kwok JB.Genetics of demen-tia. Lancet.2014;383:828-40.[PMID: 23927914]doi:10.1016/S0140-6736(13)60630-3

27. Schmand B, RienstraA, Tamminga H,Richard E, van GoolWA, Caan MW, et al.Responsiveness ofmagnetic resonanceimaging and neu-ropsychological as-sessment in memoryclinic patients. JAlzheimers Dis.2014;40:409-18.[PMID: 24473187]doi:10.3233/JAD-131484

28. Gauthier S, ReisbergB, Zaudig M, Pe-tersen RC, Ritchie K,Broich K, et al; Inter-national Psychogeri-atric Association Ex-pert Conference onmild cognitive im-pairment. Mild cog-nitive impairment.Lancet.2006;367:1262-70.[PMID: 16631882]



29. Iverson DJ, GronsethGS, Reger MA,Classen S, DubinskyRM, Rizzo M; QualityStandards Subcomit-tee of the AmericanAcademy of Neurol-ogy. Practice param-eter update: evalua-tion andmanagement ofdriving risk in de-mentia: report of theQuality StandardsSubcommittee ofthe American Acad-emy of Neurology.Neurology.2010;74:1316-24.[PMID: 20385882]doi:10.1212/WNL.0b013e3181da3b0f

30. Hunt LA, Murphy CF,Carr D, Duchek JM,Buckles V, Morris JC.Reliability of theWashington Univer-sity Road Test. A per-formance-based as-sessment for driverswith dementia ofthe Alzheimer type.Arch Neurol.1997;54:707-12.[PMID: 9193205]

31. Redelmeier DA,Yarnell CJ, Thiruchel-vam D, Tibshirani RJ.Physicians’ warningsfor unfit drivers andthe risk of traumafrom road crashes. NEngl J Med.2012;367:1228-36.[PMID: 23013074]

32. Lyketsos CG, Stein-berg M, Tschanz JT,Norton MC, SteffensDC, Breitner JC.Mental and behav-ioral disturbances indementia: findingsfrom the CacheCounty Study onMemory in Aging.Am J Psychiatry.2000;157:708-14.[PMID: 10784462]

patient continues to drive, the his-tory should be updated regularlyto determine whether the capacity to drive has deteriorated. Statelaws differ in regard to reporting patients with a diagnosis of de-mentia to local MVAs, and theclinician should be familiar withthe applicable regulations. TheAmerican Academy of NeurologyEvidence-Based Practice Parame-ter outlines an approach to assess-ing driving in patients with dementia (29).

In a prospective, case–control study usingthe Washington University Road Test,which has an off-road and on-road com-ponent, only 3% of controls failed the test,19% of patients with very mild AD failed,and 41% with mild AD failed (P< 0.001).Previous driving experience did not protectagainst failure (30).

A physician-directed recommen-dation can have beneficial and adverse outcomes. For example, aCanadian study of what happenedwhen physicians recommendedthat patients discontinue drivingfor a variety of disorders reporteda 45% reduction in road crashes(4.76 vs. 2.73) (P<0.001), a decrease in return visits to thephysician, and an increase in visitsto emergency departments for depression (31).

Clinicians should assess othersafety issues with the patient andfamily on an ongoing basis. Pa-tients with progressive dementiaeventually are unable to administermedications; cook; or use powertools, lawnmowers, or firearms.Home-safety assessments by hometherapists can determine which activities are still safe and whichneed to be limited or supervised.An activity can often be modifiedto allow ongoing participation in asafe fashion, such as cooking orgardening together with a familymember or friend. Wanderingfrom home is fairly common, pres-ents significant safety concerns,and must be assessed regularly.

hypertension is likely to impair apatient’s function and quality oflife as much as the dementia itself,at least in the early and middlestages of the disease. Thus, caringfor patients with dementia in-cludes careful attention to basicgeneral health practices, includinggood control of hypertension, dia-betes, and cholesterol; antiplatelettherapy where appropriate; andvaccinations. For patients withmore advanced dementia, it be-comes increasingly important topay attention to nutrition, skincare (particularly of the perineum),toileting schedules, and dentalcare.

What should clinicians adviseabout safety issues, such asdriving, cooking, and otheractivities that may requiresupervision?Patients with progressive dementiaultimately lose the ability to drive,but predicting when an individualpatient should stop driving is diffi-cult, particularly if the restrictionsignificantly burdens the patient orfamily members. Nonetheless, ad-dressing the issue is imperative, asnumerous studies have shown thatdriving ability becomes impairedin early stages of the disease.

The patient should be asked aboutrecent motor vehicle accidents,near misses, and changes in driv-ing ability. These inquiries shouldbe made in a setting that facilitatesan open exchange of informationand may necessitate meeting withan informant without the patientpresent. Patients with early de-mentia whose driving ability hasalready deteriorated should be instructed to stop driving immedi-ately. Those with early dementiawho have no history of drivingproblems should undergo a drivingevaluation through the local motorvehicle administration (MVA) oran occupational therapy programat a local hospital. If no impair-ment in driving is evident and the



pressure to perform, in pain, orlonely. Common examples in the in-stitutional setting include agitationwhen personal care is being provid-ed, during shift changes, and in thepresence of specific staff members.When patterns are recognized, tar-geted interventions can be devel-oped, implemented, and refined.Approaching behavioral distur-bances this way can often precludethe use of psychotropic medications.

Nonpharmacologic interventions were ef-fective in reducing behavioral and psycho-logical symptoms (overall effect size, 0.34 [CI, 0.20–0.48]; P=0.01) and improving care-giver reactions to these behaviors (overall effect size, 0.15 [CI, 0.040.26]; P=0.006) (33).

When should clinicians prescribeacetylcholinesterase inhibitors andmemantine to slow cognitivedecline?Acetylcholinesterase inhibitors, suchas donepezil, galantamine, or rivas-tigmine, can be prescribed to delaycognitive decline in patients withmild, moderate, or advanced AD.These drugs are better tolerated ifthey are slowly titrated to reach thetarget dose. Memantine is approvedfor use in moderate-to-advancedAD and can be used in conjunctionwith acetylcholinesterase inhibitors.

What should clinicians advise aboutnonpharmacologic approaches tosleep problems, behavioralproblems, and psychiatricmanifestations of dementia?Psychiatric symptoms, such as de-pression, anxiety, sleep problems, agitation, hallucinations, and delu-sions, are common and often requireintervention (32). Various nonphar-macologic approaches are effectiveand should be tried first unless thesymptoms are causing immediatedanger or marked distress (33).These approaches emphasize thenotion that many emotional and behavioral disturbances can be “de-coded” or understood in terms of in-ternal or environmental factors thatmake them more or less likely tooccur. This decoding process shouldbe done using systematic approach-es, such as 4-D or DICE (34, 35)(Table 2). Decoding involves de-scribing the behavior in detail andnoting its characteristics, includingthe time of day, location, antecedentfactors, people present and absent,proximity to eating or other key ac-tivities, and the consequences of thebehavior. Common examples of en-vironmentally driven behavioral dis-turbances include agitation whenthe patient is hungry, tired, under

Table 2. Approach for Assessing and Treating Behavioral and Psychiatric Disturbances*Define/Describe Decode (What Causes Devise a Treatment Plan Determine Whether the

the Problem) Treatment Has Worked

What occurs and Cognitive impairment, under what psychiatric symptoms, circumstances? medical condition,

environment?Persistent yelling What is being said Forgetfulness, fear— Treat psychiatric or medical Monitor frequency of yelling

and when is it said? perhaps from psychotic conditions, alter environment following the interventionsWhat consequences symptoms, pain, shift or patient placement within result from the changes, noise/other it, alter environment or yelling (to the bothersome stimuli, patient placement within it, patient and others)? presence/absence of redirect, reassure, medicate

particular individualsDepressed mood Describe patient’s Frustration with forget- Provide reassurance or distraction, Monitor/document patient’s

mood. What time of fulness, delirium, major treat depression—medications/ mood after intervention;day is it exhibited? depression, medications, electroconvulsive therapy, treat monitor/document sideIn what environment? general medical conditions, general medical conditions, effects; identify barriers toAround which people? environment (recent move, adjust medications, improve implementation of theAre there clear pre- departure of a caregiver, patient activity regimen, treatment plancipitating events? some trigger in the milieu) adjust milieu

*Adapted from reference 35.

33. Brodaty H, Arasarat-nam C. Meta-analy-sis of nonpharmaco-logical interventionsfor neuropsychiatricsymptoms of de-mentia. Am J Psychi-atry. 2012;169:946-53. [PMID: 22952073]doi:10.1176/appi.ajp.2012.11101529

34. Rabins PV, LyketsosCG, Steele CD. Practi-cal Dementia Care.2nd ed. New York:Oxford Univ Pr; 2006.

35. Kales HC, Gitlin LN,Lyketsos CG; DetroitExpert Panel on As-sessment and Man-agement of Neu-ropsychiatricSymptoms of De-mentia. Manage-ment of neuropsy-chiatric symptoms ofdementia in clinicalsettings: recommen-dations from a mul-tidisciplinary expertpanel. J Am GeriatrSoc. 2014;62:762-9.[PMID: 24635665]doi:10.1111/jgs.12730

36. Howard R, McShaneR, Lindesay J, RitchieC, Baldwin A, BarberR, et al. Donepeziland memantine formoderate-to-severeAlzheimer’s disease.N Engl J Med.2012;366:893-903.[PMID: 22397651]doi:10.1056/NEJ-Moa1106668


37. Emre M, Aarsland D,Albanese A, ByrneEJ, Deuschl G, DeDeyn PP, et al. Ri-vastigmine for de-mentia associatedwith Parkinson’s dis-ease. N Engl J Med.2004;351:2509-18.[PMID: 15590953]

38. McKeith I, Del Ser T,Spano P, Emre M,Wesnes K, Anand R,et al. Efficacy of ri-vastigmine in de-mentia with Lewybodies: a ran-domised, double-blind, placebo-con-trolled internationalstudy. Lancet.2000;356:2031-6.[PMID: 11145488]

39. Beversdorf DQ,Warner JL, Davis RA,Sharma UK, NagarajaHN, Scharre DW.Donepezil in thetreatment of de-mentia with Lewybodies [Letter]. Am JGeriatr Psychiatry.2004;12:542-4.[PMID: 15353396]

40. Sano M, Ernesto C,Thomas RG, KlauberMR, Schafer K,Grundman M, et al.A controlled trial ofselegiline, alpha-to-copherol, or both astreatment forAlzheimer’s disease.The Alzheimer’s Dis-ease CooperativeStudy. N Engl J Med.1997;336:1216-22.[PMID: 9110909]

41. Dysken MW, Sano M,Asthana S, VertreesJE, Pallaki M,Llorente M, et al. Ef-fect of vitamin E andmemantine on func-tional decline inAlzheimer disease:the TEAM-AD VA co-operative random-ized trial. JAMA.2014;311:33-44.[PMID: 24381967]doi:10.1001/jama.2013.282834

42. Schneider LS,DeKosky ST, FarlowMR, Tariot PN, HoerrR, Kieser M. A ran-domized, double-blind, placebo-con-trolled trial of twodoses of Ginkgobiloba extract in de-mentia of theAlzheimer’s type.Curr Alzheimer Res.2005;2:541-51.[PMID: 16375657]


When the benefit is unclear, thedrug may be stopped but should berestarted if acute cognitive deteriora-tion occurs. Patients and familiesmay need help in developing realisticexpectations for these agents. Sideeffects of cholinesterase inhibitorsinclude nausea, diarrhea, bradyar-rhythmia, syncope, weight loss, andataxia.

One study followed 295 community-livingpatients who had been receiving donepezilfor at least 3 months (36) and assessedoutcomes at the end of 1 year. The primaryoutcome included standard measures ofcognitive ability as determined by theStandardized MMSE and the ability to per-form activities of daily living as measuredby the Bristol Activities of Daily Living Scale(BADLS). Patients assigned to continuedonepezil, compared with those assignedto discontinue the drug, had a score on theStandardized MMSE that was higher (indi-cating better cognitive ability) by 1.9 points(1.4 points is the minimum clinically im-portant difference) (CI, 1.3–2.5) and a scoreon the BADLS that was lower (indicatingless impairment) by 3.0 points (3.5 points isthe minimum clinically important differ-ence) (CI, 1.8–4.3). Patients assigned to re-ceive memantine instead of placebo had ascore on the Standardizes MMSE that was1.2 points higher (CI, 0.6–1.8; P<0.001) anda score on the BADLS that was 1.5 pointslower (CI, 0.3–2.8; P<0.02). The differencesbetween donepezil and memantine werenot statistically significant, and addingmemantine to donepezil was not betterthan either drug alone.

Which other pharmacologicagents are helpful in treatingspecific types of dementia, and inwhat situations should cliniciansconsider prescribing these agents?The acetylcholinesterase inhibitorrivastigmine has been shown to beeffective in improving cognitive per-formance in patients with mild-to-moderate Parkinson disease in dosessimilar to those used in AD, and itis believed that this benefit occurswith the other acetylcholinesteraseinhibitors (37). Several trials havealso shown the benefits of acetyl-cholinesterase inhibitor treatmentfor cognition in dementia withLewy bodies (38, 39). However, use

of these drugs in patients with vas-cular dementia is not recommended.Vitamin E has been shown to havemodest benefit on function but notcognition in 2 well-designed trials ofpatients with dementia, and con-cerns about increased mortality werenot substantiated (40, 41).

Which pharmacologic agents areineffective in treating specifictypes of dementia and should beavoided?The herbal supplement ginkgobiloba does not slow progression ofdementia (42). Also, nonsteroidalanti-inflammatory drugs, estrogen,and ergoid mesylates should not beprescribed for cognitive decline.Data on whether the widely usedfood supplements coconut oil andAxona can be recommended are inadequate.

When should clinicians prescribeantidepressants in patients withdementia?Nearly one third of patients withdementia develop an episode ofmajor depression after the onset ofdementia (43), but evidence for theefficacy of antidepressant medica-tions is mixed (44). One explana-tion is that some symptoms of major depression, such as weightloss and disturbed sleep, may beproduced by dementia alone andcomplicate the diagnosis. Clinicianstherefore need to have a high indexof suspicion for major depression.

When should clinicians prescribeantipsychotic agents to treatbehavioral disturbances or psycho-tic symptoms, and what are theirside effects?Absent a significant risk for harm,psychotic symptoms, such as halluci-nations, delusions, and agitated be-havior, should first be treated non-pharmacologically (33) because alldrugs in this class carry a risk for el-evated mortality (1.6–2.0 in the sub-sequent 12–52 weeks) (45-48).Pharmacotherapy is indicated ifsymptoms are causing significant



antipsychotic medications is associat-ed with the metabolic syndrome,weight gain, hyperlipidemia, and dia-betes mellitus. Recent evidence sup-ports the effectiveness and relativesafety of nonpharmacologic interven-tions for neuropsychiatric and behavioral symptoms (33), which re-inforces the recommendations to usedrugs sparingly for these symptoms.However, head-to-head trials ofpharmacologic and nonpharmacolog-ic interventions have not been done.

Which drugs should clinicians useto treat sleep problems?Clinicians should try nonpharma-cologic methods before using med-ications in patients with dementiawho have insomnia because of thepotential risks associated with sedative-hypnotics in this popula-tion. Careful attention should bepaid to sleep environment, caffeineconsumption, daytime sleeping, af-ternoon and evening medications, and other elements of basic sleep hy-giene. Meta-analyses do not supportthe efficacy of any pharmacologic

distress for the patient or creating adangerous situation. The second-generation antipsychotic agents areusually recommended instead offirst-generation agents because of alower risk for tardive dyskinesia.Overall, the efficacy of these agentsis modest (46). Although more evi-dence supports the use of risperi-done and olanzapine, similar drugsalso are used. These drugs should beprescribed at the lowest possibledose and for the shortest possibletime. Ongoing use should be moni-tored regularly, and attempts shouldbe made to decrease the dose anddiscontinue the drug within 3months of starting. They should notbe routinely used only for sleep dueto toxicity (Table 3). The U.S. Foodand Drug Administration requiresblack-box warnings for second-generation antipsychotics because of increased rates of death and cere-brovascular events. The reasons forthese bad outcomes are unclear, butfalls, infections, and cardiovascularand cerebrovascular events may con-tribute. In addition, treatment with

Table 3. Cognitive Agents for Alzheimer Disease*Agent Mechanism of Dosage Benefits Side Effects Notes

Action

Donepezil Acetylcholin- Begin 5 mg/d; if Delayed symptom Nausea, vomiting, The higher end of the dosing esterase tolerated, increase progression in mild, diarrhea, anorexia, range may be harder for inhibition to target dose of moderate, and advanced syncope patients to tolerate; dose higher

10 mg/d after 1 month Alzheimer disease than 10mg not recommendedGalantamine Acetylcholin- Start 4 mg twice daily; Delayed symptom Nausea, vomiting, Routine liver function testing

esterase target dose total 24 mg/d; progression in mild, diarrhea, anorexia, is unnecessary; the higher end inhibition increase by 4 mg twice moderate, and advanced syncope of the dosing range may be

daily every 1 month until Alzheimer disease; harder for patients to tolerate; in target range improvement in caregiver begin extended-release (once

rated quality of life was daily) galantamine at 8 mg/d; observed increase by 8 mg/d every

1 month to the target dose of 24 mg/d; higher dose not recommended

Rivastigmine Acetylcholin- Start 1.5 mg twice daily; Delayed symptom Nausea, vomiting, Higher end of the dose range esterase target range is 6–12 mg/d; progression in mild, diarrhea, anorexia, may be less tolerable tolerate; inhibition increase by 1.5 mg twice moderate, and advanced syncope also available as a transdermal

daily every 1 month until Alzheimer disease patchin target range

Memantine NMDA- Begin 5 mg/d, increase by Less functional decline, Dizziness, confusion, Generic available; branded receptor 5 mg/d every 1 month until improved cognition, and headache, constipation drug only available in sustained-antagonism target of 10 mg twice daily reduced demands on care- release form; available in tablets

givers in moderate-to- or solution; avoid concomitant advanced Alzheimer disease use with amantadine

*NMDA = N-methyl-d-aspartic acid.

43. Zubenko GS,Zubenko WN,McPherson S, SpoorE, Marin DB, FarlowMR, et al. A collabo-rative study of theemergence and clin-ical features of themajor depressivesyndrome ofAlzheimer’s disease.Am J Psychiatry.2003;160:857-66.[PMID: 12727688]

44. Brodaty H. Antide-pressant treatmentin Alzheimer’s dis-ease. Lancet.2011;378:375-6.[PMID: 21764117]doi:10.1016/S0140-6736(11)61031-3

45. Schneider LS, Dager-man KS, Insel P. Riskof death with atypi-cal antipsychoticdrug treatment fordementia: meta-analysis of random-ized placebo-con-trolled trials. JAMA.2005;294:1934-43.[PMID: 16234500]

46. Schneider LS, Dager-man K, Insel PS. Effi-cacy and adverse ef-fects of atypicalantipsychotics fordementia: meta-analysis of random-ized, placebo-con-trolled trials. Am JGeriatr Psychiatry.2006;14:191-210.[PMID: 16505124]



preserved capacities would benefitthe patient.

Treatment of dementia requires abroad clinical approach that ideallyincludes preventive medicine, psy-choeducation, behavioral therapy,safety evaluation, and pharmaco-therapy. The clinician should expectto interact with a broad range ofprofessionals, including occupation-al therapists, social workers, physi-cal therapists, and speech and language pathologists, to provideoptimal care.

When should clinicians recom-mend hospitalization?During the assessment of cognitiveimpairment, hospitalization shouldbe considered for patients who can-not be evaluated safely or compre-hensively as outpatients because ofdangerous behavior, unsafe livingconditions, compromised nutrition,neglected medical conditions, orlack of cooperation. In addition tosafety issues, hospitalization can fa-cilitate thorough history-taking,neuroimaging, other diagnosticstudies, neuropsychological evalua-tion, safety evaluation by occupa-tional therapists, and future careplanning.

Psychiatric hospitalization is some-times required because of the severi-ty of psychiatric symptoms. For ex-ample, hospitalization should beconsidered for depressed patientswho exhibit suicidality, decreasedfood and fluid intake, delusions, de-pression, immobility, inability to at-tend to medical conditions, or needfor electroconvulsive therapy. Pa-tients with behavioral disturbanceswho are dangerous to themselves orwho cannot be treated safely or suc-cessfully as an outpatient because ofwandering, violence, calling out, hy-perphagia, or a severely disorderedsleep–wake cycle, should also behospitalized. Patients with psychotichallucinations and delusions may re-quire hospitalization if they do notrespond to outpatient treatment,

intervention. If necessary, 25–50mg of trazodone can be used withcautious monitoring (49).

What other steps should clinicianstake to maximize quality of life?Clinicians should proactively ad-dress issues that have the potentialto significantly affect quality oflife. Examples include the workingorder of sensory aids, such asglasses and hearing aids; dentalcare; noise, lighting, and tempera-ture; sufficient social and cognitivestimuli; cleanliness; pain levels;and constipation.

Advance directives have the poten-tial to benefit all patients. Since fullincapacitation is inevitable forevery person with progressive de-mentia who lives long enough toexperience the full course of thedisease, early advance directivesmaximize the likelihood that theperson’s wishes for end-of-life carewill be carried out.

When should clinicians consult aneurologist, psychiatrist, or otherprofessional?Clinicians should consider consult-ing a geriatric psychiatrist, neurolo-gist, geriatrician, or dementia specialist in patients with atypicalfeatures of dementia, such as earlyonset, early noncognitive neurolog-ic symptoms, rapid progression,early personality changes, or unusu-al symptom patterns. Consulting ageriatric psychiatrist or dementiaspecialist should also be consideredfor evaluation or management ofdifficult-to-treat neuropsychiatricsymptoms, such as depression, psy-chosis, or behavioral disturbances.These symptoms can create dan-gerous situations for the patientand others and reduce quality oflife. Consulting a specialist shouldalso be considered if patients re-quire physical retraint. Referral to aneuropsychologist may be necessaryif it is unclear whether dementia is present and when in-depth documentation of impaired and

47. Wang PS,Schneeweiss S,Avorn J, Fischer MA,Mogun H, SolomonDH, et al. Risk ofdeath in elderlyusers of convention-al vs. atypical an-tipsychotic medica-tions. N Engl J Med.2005;353:2335-41.[PMID: 16319382]

48. Gill SS, Bronskill SE,Normand SL, Ander-son GM, Sykora K,Lam K, et al. Antipsy-chotic drug use andmortality in olderadults with demen-tia. Ann Intern Med.2007;146:775-86.[PMID: 17548409]

49. Camargos EF, Louza-da LL, Quintas JL,Naves JO, LouzadaFM, Nóbrega OT. Tra-zodone improvessleep parameters inAlzheimer diseasepatients: a random-ized, double-blind,and placebo-con-trolled study. Am JGeriatr Psychiatry.2014.[PMID: 24495406]doi:10.1016/j.jagp.2013.12.174

50. Yaffe K, Fox P, New-comer R, Sands L,Lindquist K, Dane K,et al. Patient andcaregiver character-istics and nursinghome placement inpatients with de-mentia. JAMA.2002;287:2090-7.[PMID: 11966383]

51. Chan DC, Kasper JD,Black BS, Rabins PV.Presence of behav-ioral and psychologi-cal symptoms pre-dicts nursing homeplacement in com-munity-dwellingelders with cognitiveimpairment in uni-variate but not mul-tivariate analysis. JGerontol A Biol SciMed Sci.2003;58:548-54.[PMID: 12807927]



require the addition of multiple med-ications, are in distress or having behavioral disturbances, or present arisk to others. Involuntary commit-ment may be required in any ofthese situations.

How can clinicians help familiesdecide to move a patient withdementia into a long-term carefacility?As dementia progresses, moving toan environment that can adequatelyaddress the progressive needs of the patient with dementia is oftennecessary, either to an assisted-livingfacility or to a nursing home (50).Some patients may need to movebecause of inadequate support athome. Generally, a move into a nurs-ing home is prompted by develop-ment of physical and cognitive limitations that cannot be managedat home, such as the need for full as-sistance with transferring, ambula-tion, toileting, or feeding. Other patients have to move because of un-manageable psychiatric symptoms orhigh caregiver burden (51).

Families with ample financial re-sources may be able to provide manyservices at home that usually are pro-vided in a facility. Periods of respitecare may help families delay place-ment. Families should be supportedand guided through the difficult andpainful decision-making process.Families may be advised to proac-tively investigate facilities in their re-gion so a good decision can be madequickly—for example, because of asudden change in functional abilityafter a medical illness or accident.

What caregiver needs should beaddressed by the clinician?Caregiving for a patient with de-mentia is extremely taxing, both

physically and emotionally, and in-quiring about caregiver well-beingis a critical component of dementiacare. Common caregiver symptomsinclude guilt, anger, grief, fatigue,loneliness, demoralization, and de-pression. The patient’s symptomsand the demands on the caregiverchange over time, so the well-beingof the caregiver must be assessed atevery visit.

Most caregivers benefit from a rangeof interventions (33) that focus oneducation about dementia, skillstraining, and the caregiver’s own well-being. Many pamphlets, books, andeducational Web sites are available.Patient and caregiver safety must beevaluated at each follow-up visit, andcaregivers need to be informed aboutlocal respite programs and supportedin long-term planning.

Caregivers should also be informedof the potential benefits of psychoed-ucational and other support groups,which are available in most areas.Several large, well-conducted trialshave shown that groups with a focuson problem-solving, communication,management of behavioral distur-bances, and emotional support wereeffective in delaying nursing homeplacement for up to 1 year, diminish-ing caregiver and patient depression,and reducing patient agitation andanxiety (52-54).

What are the options for end-of-life care?Hospice criteria for persons with de-mentia are specific to dementia.Therapy for pain, neuropsychiatricsymptoms, and supportive medicalcare are paramount. Consider dis-continuation of medications thathave no short-term benefit, such ascholesterol-lowering agents (55, 56).

52. Teri L, Logsdon RG,Uomoto J, McCurrySM. Behavioral treat-ment of depressionin dementia pa-tients: a controlledclinical trial. J Geron-tol B Psychol Sci SocSci. 1997;52:P159-66.[PMID: 9224439]

53. Haupt M, Karger A,Jänner M. Improve-ment of agitationand anxiety in de-mented patients af-ter psychoeducativegroup interventionwith their caregivers.Int J Geriatr Psychia-try. 2000;15:1125-9.[PMID: 11180469]

54. Mittelman MS, HaleyWE, Clay OJ, RothDL. Improving care-giver well-being de-lays nursing homeplacement of pa-tients withAlzheimer disease.Neurology.2006;67:1592-9.[PMID: 17101889]

55. Bekelman DB, BlackBS, Shore AD, KasperJD, Rabins PV. Hos-pice care in a cohortof elders with de-mentia and mildcognitive impair-ment. J Pain Symp-tom Manage.2005;30:208-14.[PMID: 16183004]

56. Rabins PV, Hicks KL,Black BS. Medical de-cisions made by sur-rogates for personswith advanced de-mentia within weeksor months of death.AJOB Prim Res.2011;2:61-65.[PMID: 24818042]


Inthe

C linicTool Kit

In the Clinic ACP Smart Medicine Modulehttp://smartmedicine.acponline.org/content.aspx?gbosID=164Access the American College of Physicians Smart Medicine module

on dementia.

Patient Informationhttp://psychiatryonline.org/pdfaccess.ashx?ResourceID=243205&PDF

Source=6American Psychiatric Association practice guideline for the treatment

of patients with Alzheimer disease and other types of dementia.www.alz.orgwww.alz.org/care/overview.aspInformation from the Alzheimer’s Associationwww.caregiver.orgHelp for caregivers from the National Caregiver Alliance.www.nia.nih.gov/Alzheimers/Alzheimer’s Disease Education and Referral Center (ADEAR)

(1-800-438-4380)

Clinical Guidelineswww.guideline.gov/summary/summary.aspx?doc_id=36902014 guideline from the U.S. Preventive Services Task Force guideline

on screening for cognitive decline in older adults.https://www.aan.com/Guidelines/Home/ByTopic?topicId=15American Academy of Neurology guidelines on diagnosing

Creutzfeldt-Jakob disease, assessing driving risk in patients withdementia, early detection of dementia and mild cognitiveimpairment, and diagnosis of dementia.

5 August 2014Annals of Internal MedicineIn the ClinicITC14© 2014 American College of Physicians

Dementia

Treatment... A broad approach that addresses comfort and quality of life, cognitiveenhancement, stabilization of psychiatric symptoms, and caregiver well-being needsto be adopted. Patients with AD can be treated with acetylcholinesterase inhibitors,and memantine can be added for patients with moderate-to-severe AD. It is impor-tant to identify and treat psychiatric symptoms, such as depression, psychosis, anxi-ety, and behavioral disturbances with both behavioral and pharmacologic treatmentto minimize risk factors for cerebrovascular disease and to treat any other condi-tions that could reduce cognition. Attending to safety issues, regular monitoring ofthe caregiver’s well-being, and suggesting referral to support groups and other psy-choeducational activities are also important.



In the ClinicAnnals of Internal Medicine

Pati

ent

Info

rmat

ion

WHAT YOU SHOULDKNOW ABOUT DEMENTIA

What is dementia?Dementia is a group of symptoms related to impaired

memory and thinking skills. People with dementiabegin to forget things and can have problems witheveryday tasks. There are different types ofdementia. Dementia symptoms usually start slowlyand get worse over time.

What are the symptoms?• Forgetting things more and more often• Trouble with familiar activities, like making a meal

or a phone call• Having trouble finding the right words• Poor judgment, such as leaving the house with no

coat in the winter• Misplacing things or putting things in unusual

places, such as keys in the refrigerator• Personality changes, such as becoming very con-

fused, suspicious, fearful, or dependent• Unable to follow instructions, such as taking

medications• Unexplained weight loss• New onset of depression or anxiety

How is it diagnosed?There is no one specific test for dementia. If a doctor

thinks a patient may have dementia, they willreview symptoms and ask about medical history.Some other tests a doctor may perform are:

• Memory test—to check memory and concentration• Neurologic examination—to check for problems that

may indicate a brain disorder. A doctor will testthings like speech, reflexes, and coordination.

• Brain scans—like MRI or CT scans.• Laboratory blood tests—which can rule out problems

that may cause symptoms similar to dementia.

How is it treated?There are treatments that may help to manage

different symptoms of dementia. These may helppeople with dementia think better and slow downthe worsening of symptoms. Behavior changes canbe treated in ways that promote comfort for thepatient. For example, creating a calm environmentand making sure people with dementia have enoughrest can help to manage behavior symptoms.Medicines also may help these and other symptoms.Talk with a doctor for the best treatment options.

For More Information

www.acponline.org/patients_families/products/health_tips/dem_en.pdfAmerican College of Physicians

www.alz.org/what-is-dementia.aspAlzheimer’s Association

https://caregiver.org/node/92Family Caregiver Alliance

www.nlm.nih.gov/medlineplus/dementia.htmlMedline Plus


CME Questions

5 August 2014Annals of Internal MedicineIn the ClinicITC16© 2014 American College of Physicians

Questions are largely from the ACP’s Medical Knowledge Self-Assessment Program (MKSAP, accessed at http://www.acponline.org/products_services/mksap/15/?pr31). Go to www.annals.org/intheclinic/

to complete the quiz and earn up to 1.5 CME credits, or to purchase the complete MKSAP program.

1. A 79-year-old man is evaluated for a 1-year history of forgetfulness and notbeing able to remember names. He is aretired attorney. He reports no problemswith performing activities of daily living,planning his day, or managing hisfinances. He is frustrated but notdepressed and is still able to enjoy life.He has hypertension and hyperlipidemiacontrolled with hydrochlorothiazide andsimvastatin.

On physical examination, he is afebrile,blood pressure is 140/82 mm Hg, andpulse rate is 78/min. Mini-Mental StateExamination score is 25. His lungs areclear. The heart is without murmur.Neurologic, motor, and sensoryexaminations are normal.

Which of the following is the most likelydiagnosis?

A. Alzheimer diseaseB. Mild cognitive impairmentC. PseudodementiaD. Vascular dementia

2. A 77-year-old woman is evaluated in theemergency department for a 1-weekhistory of progressive agitation andconfusion. She has no history of fever orfalling episodes. The patient lives in anursing home, has advanced dementia,and is dependent on others for allactivities of daily living. She can indicatewhen she needs to void and generally isnot incontinent. She can ambulate with acane but must be accompanied because ofa tendency to wander. Although sheenjoys being around others and can makesimple conversation with family membersand nursing home personnel, she does notrecognize anyone by name or rememberwhat was said. She has a history of osteo-arthritis, hypertension, atrial fibrillation,anxiety, and depression. There have beenno recent additions or changes to hermedications, which are hydro-chlorothiazide, warfarin, amitriptyline,alprazolam, and oxybutynin.

Physical examination is noncontributory.Results of a complete blood count,comprehensive metabolic profile, andurinalysis are normal. A chest radiographreveals no evidence of infection or heartfailure.

Which of the following is mostappropriate as an initial step inmanagement?

A. Add donepezilB. Add risperidoneC. Discontinue anticholinergic and

sedative medicationsD. Obtain an electroencephalogram

3. A 66-year-old man is evaluated for a 2-month history of odd behavior. He is aretired high school principal and has a 5-year history of Parkinson disease.According to his wife, his lifelong interestin repairing household items has latelyescalated out of control. Increasingly, the patient starts new tasks he nevercompletes; stays up all night taking apartappliances and furniture but never fixes orreassembles them, and leaves parts strewnthroughout the house. The patient insiststhat he is making necessary repairs and willsoon put everything back together. HisParkinson symptoms remain well controlledwith ropinirole and levodopa-carbidopa. Hismotor function is generally good, and he isable to function independently.

On physical examination, temperature is36.7°C (98.1°F), blood pressure is 126/80mm Hg sitting and standing, pulse rate is72/min, and respiration rate is 16/min;BMI is 27.

Which of the following is the most likelycause of this patient’s symptoms?

A. Dementia with Lewy bodiesB. Dopamine agonist medicationC. Frontotemporal dementiaD. Progression of Parkinson disease

4. A 73-year-old woman is evaluated forshort-term memory loss. She has troubleremembering names, where she placedcertain items such as her keys, andoccasionally what she did earlier in theday. She avoids some social situationsand has lower self-esteem because ofmemory problems and decreased socialcontact, but notes no depression, lowenergy, or sleep disturbance. She stillenjoys playing cards with her husband.She does not need help with eating,dressing, or bathing. Her hypertension iswell controlled with hydrochlorothiazide.She has no history of stroke. She isconcerned about her condition and wantsto know if anything can be done about it.

On physical examination, temperature is37.2°C (98.9°F), blood pressure is 135/84mm Hg, and pulse rate is 72/min. She isconversant with a normal range of affect.Neurologic examination is without focaldeficit. The remainder of the physicalexamination is normal. Mini-MentalState Examination score is 26.

Which of the following is the mostappropriate management of this patient?

A. Anticholinesterase inhibitorB. Cognitive rehabilitationC. Positron-emission tomography scanD. Reassurance that progression to

dementia is unlikely

Disclosures: Drs. Rabins and Blass, ACPContributing Authors, have disclosedthe following conflict of interest:Payment for manuscript preparation:American College of Physicians.Disclosures can also be viewed atwww.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M14-1345.


Dementia In theClinic · 2016. 7. 21. · In theClinic In the Clinic Dementia Prevention page ITC2...

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