Kaycee M. Sink MD
Kristine Yaffe MD
ESSENTIALS OF DIAGNOSIS
The prevalence of dementia approximately doubles every 5 years after age 60. Among community-dwelling elders older than 85, the prevalence is estimated to be 25–45%. Prevalence is even higher in nursing homes (>50%). Approximately 60–70% of dementia cases are due to Alzheimer's disease (AD); vascular dementia (VaD) and Lewy body dementia (DLB) are the other more common forms. In addition, a significant percentage of patients have mixed disease (AD and VaD or AD and DLB).
Cognitive function in the elderly ranges from cognitive changes seen in normal aging to mild cognitive impairment (MCI) to dementia. Compared with younger adults, older adults perform more slowly on timed tasks and have slower reaction times. Mild memory impairment may often present with subjective problems such as difficulty recalling names or where an object was placed. In the case of normal aging, however, the person often remembers the information later and has intact learning, and any deficits in memory function are subtle, stable over time, and do not cause functional impairment.
MCI is a cognitive impairment that is not within normal limits for that patient's age and education but is not severe enough to qualify as dementia. MCI is characterized by subjective memory complaint, preferably corroborated by someone else; evidence of objective memory impairment in the context of normal abilities on most other cognitive domains (language, executive function); and intact functional status. MCI is certainly associated with an increased risk of AD and may actually represent a form of very early AD. Among patients with MCI, 10–15% per year convert to AD compared with 1–2% of age-matched controls. Although most patients with MCI will progress to AD with time, it is probably a clinically heterogeneous group, with some patients progressing to other types of dementias and others remaining cognitively stable. Donepezil and vitamin E are currently being studied in the treatment of MCI to determine whether they can prevent or delay the onset of AD.
The most severe type of cognitive impairment is dementia. This diagnosis requires deficits in multiple domains of cognitive functioning (memory plus at least 1 other) that represent a significant change from baseline and that are severe enough to cause impairment in daily functioning (Table 11-1).
Dementia often goes undiagnosed or undocumented in primary care settings, especially early in the course of the disease. Cognitive impairment and dementia should be detected as early as possible in older patients so that secondary causes of cognitive impairment can be identified. Drug therapy for AD may improve a patient's quality of life, extend the period of relatively good function, and delay nursing home placement, thereby reducing health care costs. In addition, early diagnosis allows patients and caregivers to plan future needs.
Age, family history, female gender, and head trauma are known risk factors for AD. The risk factors for VaD are similar to those for stroke (hypertension [HTN], hyperlipidemia, diabetes mellitus, smoking, age, male gender). Prevention of VaD should be aimed at preventing and treating its modifiable risk factors. In fact, modification of these same risk factors may also be beneficial in the prevention of AD. In addition, increased education, physical activity, nonsteroidal anti-inflammatory
drugs (NSAIDs), estrogen, statins, antioxidants (such as vitamin E), and moderate levels of alcohol intake may be associated with a decrease in the risk of AD. At this point, however, insufficient evidence exists to recommend such therapies for older patients specifically to prevent dementia.
Table 11-1. DSM-IV diagnostic criteria for Alzheimer's Disease.
Forette F et al: Systolic hypertension in Europe investigators. The prevention of dementia with antihypertensive treatment: New evidence from the Systolic Hypertension in Europe (Syst-Eur) study. Arch Intern Med 2002;162:2046 [PMID: 12374512]
The patient history is the most important part of the evaluation of a patient with possible cognitive impairment or dementia. Although it may be unreliable, eliciting the history first from the patient can be very informative and useful. Allowing patients to give their version of the history enables assessment of recent and remote memory. The social history is particularly reliable for assessing memory and is generally nonthreatening to a patient who may feel uncomfortable having to respond to so many questions. Asking patients about their childhood, where they grew up, whether they have children and how many, any military experience, and so on helps to assess their remote memory. Questions about their medical and surgical history as well as current medications may help to assess both recent and remote memory. For example, if a patient has denied any medical or surgical history, the discovery of a large abdominal surgical scar on examination is very informative.
Because the history from a patient with cognitive impairment can be incomplete and incorrect, it is crucial to also obtain history from a family member, caregiver, or other source. The history should focus on how long the symptoms have been present, whether they began gradually or abruptly, and the rate and nature (stepwise vs. continual decline) of their progression. Specific areas on which to focus include the patient's ability to learn new things (eg, use of a microwave or a remote control), language problems (eg, word-finding difficulties or absence of content), trouble with complex tasks (eg, balancing the checkbook, preparing a meal), spatial ability (eg, getting lost in familiar places), and personality changes, behavioral problems, or psychiatric symptoms (eg, delusions, hallucinations, paranoia). Obtaining a good functional assessment will help to determine the severity of impairment and the need for caregiver support or, in patients without caregivers, the need for more supervised placement. This should include an assessment of the activities of daily living (ADLs) and instrumental ADLs (IADLs; eg, cooking, cleaning, shopping, managing finances, using the telephone, and driving or arranging transportation). In addition, the clinician should assess the patient's family and social situation because information obtained may be instrumental in developing a treatment plan.
It is important to obtain a detailed medication history and history of comorbid conditions, including symptoms of depression and alcohol and other substance use. Although potentially reversible causes of dementia account for <5% of cases, a large part of the workup is directed toward identifying and
treating these causes. Table 11-2 gives a summary of the key elements of the history and physical examination.
Roman GC: Vascular dementia revisited: Diagnosis, pathogenesis, treatment, and prevention. Med Clin North Am 2002;86: 477. [PMID: 12168556]
Early signs and symptoms of dementia are often missed by both physicians and families, especially in AD, in which social graces are often retained until moderate stages of the disease. Subtle hints of early dementia or mild cognitive impairment may include frequent repetition of the same questions or stories, reduced activities or interests, reduced participation in former hobbies, increased accidents, and missed appointments. Poorly controlled chronic conditions may suggest lack of adherence to medication prescriptions because of memory problems, especially if these conditions were previously well controlled. Self-neglect, difficulty handling money, and getting lost are more obvious signs.
Table 11-2. Key elements of the history and physical examination.
The current diagnostic criteria of several dementia categories need refinement and more research. With the exception of the criteria for AD (based on Diagnostic and Statistical Manual of Mental Disorders and NINCDS-ADRDA), the criteria for other dementia subtypes have not been rigorously validated in autopsy studies.
Behavioral changes are common in AD, as in all dementia subtypes, and no neuropsychiatric symptom or behavioral disturbance is pathognomonic. Early changes may be manifested by apathy and irritability (≤70% of patients) and depression (30–50% of patients). Agitation becomes more common as the disease progresses and may be especially notable regarding issues of grooming and dressing. Psychotic symptoms, such as delusions, hallucinations, and paranoia, are common, affecting up to 50% of patients in moderate to advanced stages.
supportive of the diagnosis, as are focal neurological findings on examination. However, because a considerable percentage of patients have mixed disease (VaD and AD), the course may appear to be more gradual. Mild, progressive, non-VaD may suddenly be unmasked by the occurrence of a stroke. In addition, patients with subcortical vascular disease may have a more progressive, rather than stepwise, course.
Memory impairments in VaD are often less severe than in AD. Patients with VaD have impaired recall but tend to have better recognition and benefit from cueing in contrast to AD patients. On formal neuropsychiatric testing, “patchy” deficits may be found, often with difficulty on speeded tasks and tests of executive function. As in AD, behavioral and psychological symptoms are common. Depression may be more severe in patients with VaD.
Like AD, DLB is insidious in onset and progressive, although it classically has a fluctuating quality on a day-to-day basis. The fluctuation is seen in the level of alertness, cognitive functioning, and functional status. Early in the course, memory and language deficits are less prominent than in AD. In contrast, visuospatial abilities, problem solving, and processing speed are more significantly impaired than in AD at the same stage. This may be exemplified by a markedly abnormal clock drawing in the setting of a relatively good overall MMSE score.
Visual hallucinations occur in 30–60% of DLB patients compared with 5–15% of AD patients. They are classically very vivid and often are of animals, people, or mystical things. Unlike true psychosis, most patients with DLB can distinguish hallucinations from reality and, early on, tend not to be disturbed by them. Caution is advised in the use of antipsychotic medications because patients with DLB are exquisitely sensitive to neuroleptics, and a dramatic worsening of extrapyramidal symptoms may occur. Neuroleptics should not be given as a diagnostic test because deaths have been reported among those with DLB.
FTD is often misdiagnosed as either a psychiatric disorder or AD because most patients meet the criteria for a diagnosis of AD. However, some symptoms are highly specific for FTD (97–100%; eg, hyperorality, early changes in personality and behavior, early loss of social awareness [disinhibition], compulsive or repetitive behaviors, progressive reduction in speech [early], and sparing of visuospatial abilities) and have been shown to reliably distinguish it from AD. The hyperorality may be manifested by marked changes in food preference (often toward junk food and carbohydrates) or simply excessive eating. One study showed a weight gain >5 kg for almost 67% of patients with FTD. Another interesting phenomenon is that some patients with FTD develop new artistic talents without having had any prior interest.
Cognitive testing in patients with FTD may reveal normal MMSE scores early in the disease. More formal neuropsychiatric testing reveals deficits in frontal systems tasks such as verbal fluency, abstraction, and executive functioning, and these deficits are seen earlier than in a typical patient with AD. In contrast to patients with AD, FTD patients tend to show preserved visuospatial abilities and relatively preserved memory, especially recognition memory.
to alcohol exists (separate from thiamine deficiency and head trauma), partly because there have been no large-scale studies.
The physical examination of a patient with cognitive impairment or dementia focuses on identifying clues to the cause of the dementia, comorbid conditions, conditions that may exacerbate the cognitive impairment (eg, sensory impairment or alcoholism), and signs of abuse or neglect. The neurological examination should be directed at identifying evidence of prior strokes, such as focal signs, and of parkinsonism, such as rigidity, bradykinesia, or tremor, keeping in mind that late in the course of dementia increased tone and brisk reflexes are nonspecific. Gait and balance are an important part of the examination and should be assessed routinely. A careful cardiovascular evaluation, including measurement of blood pressure and examination for carotid disease and peripheral vascular disease, may help in supporting the diagnosis of VaD. Some patients without dementia who have significant hearing or visual impairments may demonstrate behavior that suggests dementia and have a low score on mental status testing. Therefore, it is important to identify and correct, if possible, sensory impairments before making a diagnosis of dementia.
The effectiveness of screening asymptomatic patients for dementia is controversial. However, for patients with a high risk of dementia (eg, patients age 80 years and older) or for those who report memory impairment, screening with a standardized and validated tool is recommended.
The cognitive assessment of a patient with cognitive impairment or dementia should be paired with the physical examination. Patients are less likely to be threatened or offended by questions about cognitive abilities if the questions are framed as part of the physical
examination. In addition to administering a standardized assessment tool such as the MMSE, providers should also assess domains of cognitive functioning that are not well represented in the MMSE, such as judgment and insight. The diagnosis of dementia requires that, in addition to a memory deficit, there be impairment in another dimension of cognitive function such as language, motor memory (apraxia), or poor executive functioning. Language can be assessed by simply listening for a lack of content in the patient's dialogue or the use of vague terms to replace nouns, such as “thing” or “it.” Asking the patient to name common things in the room may be helpful if the language seems normal. To assess the presence of apraxia, the patient can be asked to show, for example, how he would brush his teeth, blow out a match, or salute. Giving the patient a common object such as a key and asking him or her to identify it with eyes closed can test for agnosia. Evidence of impaired executive functioning is often discovered in the history and can be assessed during the examination as well. For example, if the patient is not able to describe a complex function that he or she may normally do (or used to do) in fine detail, there may be a problem with executive functioning.
Borson S et al: The Mini-Cog: A cognitive “vital signs” measure for dementia screening the multilingual elderly. Int J Geriatr Psychiatry 2000;15:1021. [PMID: 11113982]
Petersen R et al: Current concepts in mild cognitive impairment. Arch Neurol 2001;58:1985. [PMID: 11735772]
Petersen R et al: Practice parameter: Early detection of dementia: Mild cognitive impairment (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1133. [PMID: 11342677]
In the evaluation of a patient with cognitive impairment or newly diagnosed dementia, laboratory studies are generally used to rule out potentially treatable causes of dementia (Table 11-3). Vitamin B12 deficiency and hypothyroidism are common in the elderly and can affect cognitive functioning. Treatment of these conditions is warranted, although few cases of dementia are actually caused by (or improved with treatment of) vitamin B12 deficiency or hypothyroidism. Most clinicians will also perform complete blood count, electrolytes, creatinine, glucose, calcium, and liver function tests. One should screen for latent syphilis and HIV if there is a high index of suspicion of these conditions.
Table 11-3. Potentially “reversible”/treatable causes of cognitive impairment.
Routine computed tomography (CT) or magnetic resonance imaging (MRI) scanning in the evaluation of patients with dementia remains controversial. Consensus guidelines have recommended that imaging be used only in patients with a relatively recent or rapid onset of symptoms, young age at presentation, or focal neurological signs or symptoms to rule out treatable causes of dementias such as subdural hematoma, normal pressure hydrocephalus, or tumor. However, a practice parameter of the American Academy of Neurology recommends neuroimaging with either a noncontrast CT or MRI in the routine evaluation of patients presenting with dementia. In addition to looking for structural lesions, imaging may be helpful in the diagnosis of the particular type of non-AD dementia. Neuroimaging is likely to be of low yield in patients with a typical clinical appearance of AD and symptoms that have been present for more than 1–2 years. Advantages and disadvantages of neuroimaging can be discussed with patients and families.
CT or MRI findings in AD are often nonspecific and nondiagnostic but include diffuse cerebral atrophy and ventriculomegaly disproportional to age-related norms. On MRI the hippocampus and medial temporal lobes are sometimes disproportionately affected. Imaging studies for VaD are also nonspecific. This is because many elderly patients will have some degree of small vessel ischemic disease on CT or MRI. In fact, by age 85, nearly 100% of patients will have white matter hyperintensities on imaging studies. Therefore, simply seeing evidence of vascular disease does not warrant diagnosis of VaD. If, however, there is extensive disease, multiple infarcts, or infarcts in key anatomical locations (eg, thalamus) in a patient with a history or neuropsychological findings consistent with VaD, it is probable that the imaging findings are clinically relevant. In FTD, there is classically asymmetric volume loss of the frontal or temporal lobes in comparison to the overall atrophy seen in AD.
Positron emission tomography (PET) scans measure glucose metabolism in specific areas of the brain and are currently being studied in the diagnosis of AD, especially early diagnosis. Sensitivity and specificity of the scan in diagnosing AD are reported to be 93% and 63%, respectively. Although promising, the role of PET scans in the clinical diagnosis of AD is still undetermined.
There is currently no role for single photon emission CT in either the initial or differential diagnosis of dementia because it has not shown superiority to clinical criteria.
Garde E et al: Relation between age-related decline in intelligence and cerebral white-matter hyperintensities in healthy octogenarians: A longitudinal study. Lancet 2000;356:628. [PMID: 10968435]
Gifford DR et al: Systematic review of clinical prediction rules for neuroimaging in the evaluation of dementia. Arch Intern Med 2000;160:2855. [PMID: 11025796]
Knopman DS et al: Practice parameter: Diagnosis of dementia (an evidence-based review). Report of the quality standards subcommittee of the American Academy of Neurology. Neurology 2001;56:1143. [PMID: 11342678]
In contrast to early-onset AD, late-onset AD (age >60–65 years) is associated with genes that increase the risk of AD but not in an autosomal dominant fashion. Physicians may be asked by patients or family members for the Alzheimer's blood test, most likely referring to apolipoprotein E (APOE) genotyping. The association between APOE and risk of AD is well established. The presence of one ε4 allele increases the risk of AD by about 2–3 times, whereas the ε2 allele may be protective. It is important to keep in mind that APOE-ε4 is only a genetic risk factor for AD; therefore, the absence of an ε4 allele does not rule out the diagnosis nor does the presence of homozygous ε4/ε4 rule it in. In fact, most patients with AD do not carry the ε4 allele. There is broad consensus that APOE testing be reserved for research purposes only.
Pinsky L et al: Why should primary care physicians know about the genetics of dementia? West J Med 2001;175:412. [PMID: 11733436]
The differential diagnosis of dementia includes the potentially treatable causes of dementia listed in Table 11-3, among them metabolic abnormalities, structural brain lesions, medications, alcoholism, and depression. The differential diagnosis also includes delirium, uncorrected
sensory deficits, amnestic disorders, and other psychiatric conditions.
Depression commonly coexists with dementia (up to 30–50% of patients), but it may also be the only cause for cognitive deficits and, therefore, must be ruled out or treated before a diagnosis of dementia can be made. A patient's memory complaints that are disproportional to objective deficits should alert a provider to the possibility of depression. This is in contrast to dementia, in which patients tend to minimize their deficits. It is important to keep in mind that older patients who develop reversible cognitive impairments while depressed are at high risk for dementia over the next few years.
Delirium is a common cause of confusion in the elderly, particularly in those who are hospitalized, and may be incorrectly labeled as dementia. In contrast to dementia, delirium is characterized by abrupt onset of altered cognition and consciousness, decreased attention, perceptual disturbances (commonly visual hallucinations), and impressive fluctuations in symptoms. Table 11-4 contrasts delirium, depression, and dementia. If delirium is suspected, underlying causes should be sought and treated. Dementia is one of the key risk factors for delirium. If cognitive deficits persist after the resolution of delirium, further workup for dementia should be pursued.
Table 11-4. Differentiating dementia from delirium and depression: Typical patterns.
Medications are commonly associated with confusion in the elderly. Many classes of drugs have been implicated, including opiates, benzodiazepines, neuroleptics, anticholinergic drugs (many unsuspected medications have significant anticholinergic properties), H2 blockers, and corticosteroids. Clinicians should ask patients or caregivers to bring in all medications, including over-the-counter medicines, for review. Drug–drug interactions and appropriateness of doses should be assessed. In addition, any nonessential medications should be discontinued. Reassessment of the patient may reveal marked improvement in cognition and function. Similarly, correction of sensory deficits (visual or hearing impairments) in patients who have been misidentified as having dementia can be equally rewarding.
Patients with cognitive impairment, disorganization, frequent accidents, or failure at home or work should be screened for alcohol abuse. Years of heavy alcohol use may contribute to permanent cognitive impairment, possibly through direct toxic effects on the brain or thiamine deficiency or from complications of alcohol abuse such as head trauma related to falls or violence. However, alcohol abuse may also be responsible for more acute declines in a patient's level of function; improvement in cognition and function may be seen on cessation of drinking.
Chronic psychiatric conditions such as schizophrenia or bipolar affective disorder may also be included in the differential diagnosis of dementia, especially when behavioral changes and psychiatric symptoms such as delusions and hallucinations predominate. In addition, elderly patients with chronic schizophrenia are more likely to develop dementia than unaffected adults. The pattern of cognitive deficits seen in geriatric schizophrenia patients is distinct from AD, and autopsy series
confirm that AD does not account for the cognitive impairments.
Delirium, as well as being considered in the differential diagnosis of dementia, is also a major complication of dementia. Risk factors for delirium include cognitive impairment, severe medical illness, elevated blood urea nitrogen–creatinine ratio, and visual impairment, among others. When demented patients are hospitalized, it is critical to be aware of their high risk for delirium and take measures to avoid precipitating factors, such as the use of physical restraints and bladder catheters, malnutrition, and use of multiple new medications.
Behavioral and psychological symptoms of dementia (BPSD) are very common, affecting up to 80% of patients with dementia. These symptoms, which are associated with worse prognosis, earlier nursing home referral, greater costs, and increased caregiver burden, include the following:
Although agitation and psychosis are common in dementia, especially as the disease progresses, any new behavioral symptoms should be evaluated before being attributed solely to the dementia. Precipitating causes of new agitation may include delirium, untreated pain, fecal impaction, urinary retention, new medications, sensory impairment, and environmental causes (eg, new environment, excessive stimulation).
The delusions seen in patients with AD are usually not as complex or bizarre as those of schizophrenia. Table 11-5 lists some common delusions of dementia. In addition, hallucinations, if present, tend to be visual compared with the auditory hallucinations common in schizophrenia. More than 50% of patients with AD will have psychosis at some point, often requiring drug therapy. However, in many patients the psychosis is self-limited. Thus, it is important to attempt periodically to withdraw any drug therapies being used to manage agitation or psychosis. In fact, federal regulations require an attempt to withdraw (or decrease the dose of) such medications every 6 mo in patients residing in nursing homes.
Table 11-5. Common delusions in patients with dementia.
Informal caregivers provide the majority of care to patients with dementia at considerable financial and personal costs. The risk of caregiver stress rises with the patient's advancing severity of dementia, increased dependence in ADLs, and the presence of problem behaviors. Clinicians should assess caregivers for stress because stress is associated with poor outcomes for both patients and caregivers, including increased risk of placement in a nursing home, increased risk of patient neglect or abuse, and increased risk of depression among caregivers (reported to affect 30–50%). Stress can be alleviated with therapeutic interventions.
In the management of patients with cognitive impairment or dementia, the goals are to preserve function and autonomy for as long as possible and to maintain quality of life for both the patient and the caregivers.
therefore, dosing regimen) and specificity for receptors (rivastigmine and galantamine also inhibit butyrylcholinesterase, but the clinical significance is still unknown). Gastrointestinal side effects, including nausea, vomiting, and diarrhea, are a class effect and are the most common reason for discontinuation. These side effects can usually be ameliorated by slow titration of the drug over 8–12 weeks. Reversible hepatotoxicity is common with tacrine, and this drug is generally not recommended for initial therapy. Table 11-6 lists the recommended initial doses and target doses for each of the AChEIs.
Assessing effectiveness of therapy with AChEIs in individual patients has not been formally standardized for clinical practice. Effect sizes are modest in clinical trials, with only 40–50% of patients showing evidence of improvement on measures of cognitive functioning, ADL scores, or subjective clinician ratings. Most experts recommend using the MMSE as well as subjective clinical impressions of the physician and caregivers to monitor effect because some of the improvements are not easily measured in clinical practice. Because MMSE scores typically decline about 3 points per year in patients with AD, monitoring MMSE scores every 6–12 mo can help providers assess effectiveness. A stable or improved MMSE score over 6–12 mo suggests the drug is effective. Although switching AChEIs because of lack of efficacy or intolerable side effects may be beneficial for some patients, there is no evidence to support doing so.
The appropriate length of treatment with AChEIs is still unknown, but some experts recommend that therapy be continued indefinitely if improvement or stabilization is noted. Clinicians and caregivers may notice a decline in function if AChEIs are discontinued.
Table 11-6. Cholinesterase inhibitors.
No drug therapies have been specifically approved for the treatment of VaD. The principles of treatment of VaD rely on the treatment of stroke risk factors such as smoking and hyperlipidemia. Treatment of HTN is somewhat controversial. Although controlling HTN may help reduce the incidence of dementia, some observational data suggest that, once dementia is present, permissive mild HTN (up to systolic blood pressures in the 150s) may be better for cognitive function than lower blood pressures. Data published on the use of galantamine in VaD and mixed dementia suggest a possible benefit on cognition and function, but confirmatory studies are needed.
Erkinjuntti T et al: Efficacy of galantamine in probable vascular dementia and Alzheimer's disease combined with cerebrovascular disease: A randomized trial. Lancet 2002;359:1283. [PMID: 11965273]
Feldman H et al: A 24-week, randomized, double-blind study of donepezil in moderate to severe Alzheimer's disease. Neurology 2001;57:613. [PMID: 11524468]
Rapp SR et al: Effect of estrogen plus progestin on global cognitive function in postmenopausal women: the Women's Health Initiative Memory Study: a randomized controlled trial. JAMA 2003;289:2663. [PMID: 12771113]
Reisberg B et al: Memantine in moderate-to-severe Alzheimer's disease. N Engl J Med 2003;348:1333. [PMID: 12672860]
Winblad B et al: A 1-year, randomized, placebo-controlled study of donepezil in patients with mild to moderate AD. Neurology 2001;57:489. [PMID: 11502918]
A few strategies that may be helpful in reducing agitation in patients with dementia include music, reminiscence therapy, exposure to pets, outdoor walks, and bright light exposure. One of the unifying themes in many of these strategies is that the therapy works best if it is tailored to the patient. For example, with music therapy, playing music that is consistent with patients' prior preferences seems to be superior to playing a standard tape for everyone. One study confirmed an intuitive assumption that providing intensive education and training on understanding and treating BPSD for nursing assistants or care providers also significantly decreases agitation among patients with dementia in nursing home settings.
Less evidence-based, but more practical tips for both caregivers and medical providers of patients with dementia-related difficult behaviors are presented in Table 11-7.
Although the incidence of EPS is lower with atypical antipsychotics, they may still occur. Other long-term side effects of atypical antipsychotics include weight gain, diabetes mellitus, and hyperprolactinemia. Although the atypical antipsychotics are clearly associated with fewer side effects, typical antipsychotics such as haloperidol may be preferable when cost is an important factor or if intravenous administration is required such as in an intensive care unit setting.
Mood stabilizers such as carbamazepine and valproic acid have shown benefit in small trials. However, because of side effects, drug–drug interactions, and necessary blood test monitoring, these agents are not recommended as first-line treatments. If attempts at nonpharmacological approaches and use of more common drug classes have failed, referral to a geriatrician or geropsychiatrist should be considered. Benzodiazepines are not recommended for the chronic management of BPSD. They have not been found to be more efficacious than other classes of drugs. In addition, adverse effects associated with benzodiazepine use, such as increased risk of falls, sedation, withdrawal, and occasionally paradoxical excitation, make them a particularly poor choice.
Carlson DL et al: Management of dementia-related behavioral disturbances: A nonpharmacologic approach. Mayo Clin Proc 1995;70:1108. [PMID: 7475342]
Doody RS et al: Practice parameter: Management of dementia (an evidence-based review). Report of the quality standards subcommittee of the American Academy of Neurology. Neurology 2001;56:1154. [PMID: 11342679]
Table 11-7. Dementia related difficult behaviors: Practical tips for caregivers and medical providers.
Establishing advance directives and having the patient appoint a durable power of attorney (DPOA) for health care should be a part of the management plan of patients with dementia. It is particularly important to have this discussion as early as possible so that patients can participate in decisions to direct their end-of-life care. Even patients with moderate dementia are able to consistently state preferences and choices, including the appointment of a DPOA. In addition to preferences regarding resuscitation, specific interventions such as the use of artificial hydration and nutrition should be addressed and included. Patients may also want to appoint a DPOA for finances. Consultation with an elder law attorney or estate planner may be helpful.
pathways through the house, reducing clutter, and disabling stoves if there is a concern for potential kitchen fires. If there is any indication that a patient may not be safe in the home or there is evidence of self-neglect or concern about elder abuse by others, the provider should contact Adult Protective Services, which has a variety of resources and can quickly develop a plan for ensuring patient safety.
Table 11-8. Pharmacotherapy for BPSD.
Dubinsky RM et al: Practice parameter: Risk of driving and Alzheimer's disease (an evidence-based review). Neurology 2000;54(12):2205. [PMID: 10881240]
Feinberg LF, Whitlatch CJ: Are persons with cognitive impairment able to state consistent choices? Gerontologist 2001;41:374. [PMID: 11405435]
The prognosis of dementia is variable depending on the cause and presence of comorbid conditions. Estimates of survival from time of onset or diagnosis of AD have been broad. Median life expectancy is 3–15 years. Patients with earlier ages of onset tend to have longer survival, and patients with VaD may have slightly shorter survival. Death is commonly due to terminal pneumonia in the degenerative dementias and to cardiovascular events in VaD.
As many as 90% of patients with dementia are eventually institutionalized. The median time to nursing home placement is 3–6 years from diagnosis. Dementia severity, dependence in ADLs, difficult behaviors, and caregiver age and burden are significant risk factors for placement. Interventions that include caregiver support and education in managing difficult behaviors may extend time to nursing home placement.
Yaffe K et al: Patient and caregiver characteristics and nursing home placement in patients with dementia. JAMA 2002;287: 2090. [PMID: 11966383]
RELEVANT WORLD WIDE WEB SITES
Alzheimer's Association: http://www.alz.org (Extensive informational materials addressing issues for patients and caregivers.)
Family Caregiver Alliance: http://www.caregiver.org (Provides information, support, and guidance for family and professional caregivers. Includes topic specific newsletters, information on care facilities and legal issues, and online discussion lists.)
Alzheimer's Disease Education and Referral Center (of the National Institutes of Health and National Institute on Aging): http://www.nia.nih.gov