Addressing Alzheimer’s: A pragmatic approach

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Applied Evidence

Addressing Alzheimer’s: A pragmatic approach

J Fam Pract. 2015 January;64(1):10-18

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References

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5. Centers for Medicare & Medicaid Services. The guide to Medicare preventive services. 4th ed. 2011. Available at: http://www.curemd.com/fqhc/The%20Guide%20to%20Medicare%20Preventative%20Services%20for%20Physicans,%20Providers%20and%20Suppliers.pdf. Accessed December 2, 2014.

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8. Cordell CB, Borson S, Boustani M, et al; Medicare Detection of Cognitive Impairment Workgroup. Alzheimer’s Association recommendations for operationalizing the detection of cognitive impairment during the Medicare Annual Wellness Visit in a primary care setting. Alzheimers Dement. 2013;9:141-150.

9. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:263-269.

10. The American Geriatrics Society. A guide to dementia diagnosis and treatment. The American Geriatrics Society Web site. Available at: http://dementia.americangeriatrics.org/documents/AGS_PC_Dementia_Sheet_2010v2.pdf. Accessed December
2, 2014.

11. Jack CR, Knopman DS, Jagust WJ, et al. Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol. 2013;12:207-216.

12. Johnson KA, Minoshima S, Bohnen NI, et al; Alzheimer’s Association; Society of Nuclear Medicine and Molecular Imaging; Amyloid Imaging Taskforce. Appropriate use criteria for amyloid PET: a report of the Amyloid Imaging Task Force, the Society of Nuclear Medicine and Molecular Imaging, and the Alzheimer’s Association. Alzheimers Dement. 2013;9:e1-e16.

13. Centers for Medicare and Medicaid Services. National coverage determination (NCD) for FDG PET for dementia and neurodegenerative diseases (220.6.13). Centers for Medicare and Medicaid Services Web site. Available at: http://www.cms.gov/medicare-coverage-database/details/ncd-details.aspx?NCDId=288&ncdver=3&bc=BAABAAAAAAAA&. Accessed December 2, 2014.

14. Albert MS, DeKosky ST, Ruckson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:270-179.

15. Mitchell AJ, Shiri-Feshki M. Rate of progression of mild cognitive impairment to dementia—meta-analysis of 41 robust inception studies. Acta Psychiatr Scand. 2009;119:252-265.

16. Farias ST, Mungas D, Reed BR, et al. Progression of mild cognitive impairment to dementia in clinic- vs community-based cohorts. Arch Neurol. 2009;66:1151-1157.

17. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013;29:847-871.

18. Ngo-Metzger Q, August KJ, Srinivasan M, et al. End-of-life care: guidelines for patient-centered communication. Am Fam Physician. 2008;77:167-174.

19. Sayegh P, Knight BG. Cross-cultural differences in dementia: the Sociocultural Health Belief Model. Int Psychogeriatr. 2013;25:517-530.

20. McDaniel SH, Campbell TL, Hepworth J, et al. Family-Oriented Primary Care. 2nd ed. New York, NY: Springer; 2005.

21. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013:29;847-871.

22. Russ TC, Morling JR. Cholinesterase inhibitors for mild cognitive impairment. Cochrane Database Syst Rev. 2012;9:CD009132.

23. Sadowsky CH, Galvin JE. Guidelines for the management of cognitive and behavioral problems in dementia. J Am Board Fam Med. 2012;25:350-366.

24. Birks J. Cholinesterase inhibitors for Alzheimer’s disease. Cochrane Database Syst Rev. 2006;(1):CD005593.

25. Fillit HM, Doody RS, Binaso K, et al. Recommendations for best practices in the treatment of Alzheimer’s disease in managed care. Am J Geriatr Pharmacother. 2006;4(suppl A):S9-S24;quiz S25-S28.

26. Schneider LS, Tariot PN, Dagerman KS, et al; CATIE-AD Study Group. Effectiveness of atypical antipsychotic drugs in patients with Alzheimer’s disease. N Engl J Med. 2006;355:1525-1538.

27. US Food and Drug Administration. Public health advisory: Deaths with antipsychotics in elderly patients with behavioral disturbances. US Food and Drug Administration Web site. Available at: http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm053171.htm. Published April 11, 2005. Updated August 16, 2013. Accessed December 2, 2014.

28. The American Geriatrics Society 2012 Beers Criteria Update Expert Panel. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2012;60:616-631.

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30. Huckans M, Hutson L, Twamley E, et al. Efficacy of cognitive rehabilitation therapies for mild cognitive impairment (MCI) in older adults: working toward a theoretical model and evidence-based interventions. Neuropsychol Rev. 2013;23:63-80.

31. Woods B, Aguirre E, Spector AE, et al. Cognitive stimulation to improve cognitive functioning in people with dementia. Cochrane Database Syst Rev. 2012;2:CD005562.

32. McLaren AN, Lamantia MA, Callahan CM. Systematic review of non-pharmacologic interventions to delay functional decline in community-dwelling patients with dementia. Aging Ment Health. 2013;17:655-666.

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For patients who already have mild-to-moderate dementia, cognitive stimulation seems to help in the short term.³¹ There is also some evidence that exercise and occupational therapy may slow functional decline,³² but the effects are small to modest and their actual clinical significance (eg, the ability to delay institutionalization) is unclear. There is promising but preliminary evidence that cognitive rehabilitation (helping patients devise strategies to complete daily activities) may improve functioning in everyday life.³³

While behavioral symptoms are often due to the dementia itself, it is important to identify and treat medical and environmental causes that may be contributing, such as infection, pain, and loud or unsafe environments.Interventions such as massage therapy, aromatherapy, exercise, and music therapy may be effective in the short term for agitated behavior. As noted before, nonpharmacologic treatments are generally preferred for behavioral problems and should be considered prior to drug therapy. Approaches that identify and modify both the antecedents and consequences of problem behaviors and increase pleasant events have empirical support for the management of behavioral symptoms.³⁴ Interventions including massage therapy, aromatherapy, exercise, and music therapy may also be effective in the short term for agitated behavior.³⁵

Caregivers should be encouraged to receive training in these strategies through organizations like AA. Caregiver education and support can reduce caregivers’ distress and increase their self-efficacy and coping skills.³⁶

End-of-life care must be addressed

Perhaps the most important aspect of end-of-life care in AD is assuring that families (or health care proxies) understand that AD is a fatal illness, with most patients dying within 4 to 8 years of diagnosis.¹ Evidence indicates that patients whose proxies have a clear recognition of this are less likely to experience “burdensome” interventions such as parenteral therapy, emergency department visits, hospital admissions, and tube feedings in their last 3 months of life.³⁷

Overall, decisions regarding discontinuing medical treatments in advanced AD should be made by balancing the likelihood of benefit with the potential for adverse effects.³⁸The progressive and ultimately fatal nature of Alzheimer's disease makes planning for the future a priority. For example, the American Geriatrics Society recently recommended against feeding tubes because they often result in discomfort due to agitation, use of restraints, and worsening pressure ulcers.³⁹

Unfortunately, only a minority of families receives straightforward information on the course and prognosis of AD, including the fact that patients eventually stop eating and that the natural cause of death is often an acute infection. Studies also show that patients with dementia are at risk for inadequate treatment of pain.⁴⁰ Assuring adequate pain control is an essential component of end-of-life care.

Hospice. End-of-life care can often be improved with hospice care. This service is underused by patients with dementia, even though hospice care is available at no cost through Medicare. Hospice eligibility criteria for patients with AD are shown in
TABLE 3.^41,42

Finally, a word about prevention

Numerous risk factors have been associated with an increased risk of AD (TABLE 4)^2,3. Some, like age and genetics, are nonmodifiable, while others—particularly cardiovascular risk factors—can be modified.¹ There are also factors associated with decreased risk, most notably, physical exercise and participating in cognitively stimulating activities.³ Identification of these factors has led to the hope that addressing them can prevent AD.

But association does not equal causation. In 2010, a report from the National Institutes of Health concluded that, although there are modifiable factors associated with AD, there is insufficient evidence that addressing any of them will actually prevent AD.⁴³ In fact, there is good evidence that some of these factors (eg, statin therapy) are not effective in reducing the incidence of dementia, and that others (eg, vitamin E and estrogen therapy) are potentially harmful.⁴⁴

The absence of empirically supported preventive interventions does not mean, however, that we should disregard these risks and protective factors. Encouraging social engagement, for example, may improve both emotional health and quality of life. Addressing cardiovascular risk factors can reduce the rate of coronary and cerebrovascular disease, potentially including vascular dementia, even if it does not reduce the rate of AD.

Studies are evaluating the use of monoclonal antibodies with anti-amyloid properties for preventing AD in individuals who have APOE ε4 genotypes or high amyloid loads on neuroimaging.⁴⁵ It will be several years before results are available, however, and the outcome of these studies is uncertain as the use of anti-amyloid agents for treating established dementia has not been effective.^46,47

CORRESPONDENCE
Marisa Menchola, PhD, Department of Psychiatry, University of Arizona College of Medicine, 1501 N. Campbell Ave., 7OPC. Tucson, AZ 85724; marisam@psychiatry.arizona.edu