Zvi D. Gellis, PhD. University of Pennsylvania
Kim McClive-Reed, PhD, University at Albany
Stanley G. McCracken, PhD, University of Chicago
1-2 hours, depending on class size and time spent on exercises.
Didactic lecture, exercises.
Chalkboard, flipchart, or dry erase board with markers.
LCD projector & laptop computer.
PowerPoint slides (see separate file).
Review of the literature (see separate file).
Cognitive impairment in older adults exists on a continuum beginning with normal age-associated memory decline (AAMD), also called age-associated memory impairment (AAMI) or cognitive impairment no dementia (CIND). The next stage, which is earliest diagnosable stage of dementia, is called mild cognitive impairment (MCI). Individuals with MCI experience mild impairment of memory, concentration, and occupational performance (Agronin, 2008; See Table 1. Global Deterioration Scale). Mini-mental State Exam (MMSE; Folstein, Folstein, & McHugh, 1975) scores of 24-27 (out of 30) are common in people with MCI. Dementia refers to a spectrum of brain disorders, all of which involve cognitive impairment but vary widely in terms of cause, course, and prognosis. The essential feature of dementia is the development of multiple cognitive deficits that include memory impairment and at least one of the following cognitive disturbances: aphasia (deterioration of language function), apraxia (impaired ability to execute motor activities despite intact motor abilities, sensory function, and comprehension of the required task), agnosia (failure to recognize or identify objects despite intact sensory function), or a disturbance in executive functioning (ability to think abstractly and to plan, initiate, sequence, monitor, and stop complex behavior). Memory impairment is required to make the diagnosis of a dementia and is a prominent early symptom (DSM-IV-TR, American Psychiatric Association [APA], 2000).
An estimated 24.3 million people had dementia in 2005, with 4.6 million new cases of dementia occurring annually. The number of people affected is expected to double every 20 years (Ferri et al., 2005). Alzheimer’s and other dementias ranked as the 4th leading cause of disease burden in adults age 60 and older worldwide, outranked only by heart disease, arthritis, and chronic obstructive pulmonary disease (World Health Organization, 2003).
A variety of instruments are used to screen for dementia. The most common of these is the Mini-Mental State Examination (MMSE, Folstein et al. 1975). The MMSE is a 30-point scale that assesses orientation, memory registration and recall, attention, calculation, language, and constructional ability. It typically takes 5-10 minutes to complete, is relatively simple to administer, and provides a relatively high degree of sensitivity and specificity for dementia. Among its disadvantages are that differences in administration and scoring can lead to inconsistent results. It also contains an education and language/cultural bias, and at 10 minutes, it is too long to be practical for use in primary care settings in which physicians have limited time to administer a screening test (Brodaty, Withall, Altendorf, & Sachdev, 2007). The Mini-Cog (Borson et al., 2000) can be administered in under 5 minutes, has similar psychometric properties to the MMSE, and has become popular in primary care settings. (See Table 2 for links to the MMSE and Mini-Cog).
BPSD have important implications for the prognosis of dementia in older adults. BPSD reduce patients’ quality of life, may accelerate cognitive and functional decline, and are associated with increased mortality (Amore, Tagariello, Laterza, & Savoia, 2007; Teng, Lu, & Cummings, 2007; Fitzpatrick, Kuller, Lopez, Kawas, & Jagust, 2005; Potter & Steffens, 2007). Furthermore, these symptoms significantly increase caregiver burden and stress, and are associated with increased rates of depression in caregivers (Black & Almeida, 2004). They have also been found to increase the risk for institutionalization (Coehlo, Hooker, & Bookman, 2007). Finally, management of BPSD has been estimated to account for approximately one-third of the total cost of dementia care (Beeri, Werner, Davidson, & Noy, 2002).
The reported prevalence of depression in older patients with dementia ranges from 30% to 96% (Amore et al., 2007; Kales, Chen, Blow, Welsh, & Mellow, 2005; Starkstein, Jorge, Mizrahi, & Robinson, 2005), and moderate to high rates of depression or its symptoms are consistently reported for persons with MCI (i.e., 36% by Palmer et al., 2007; 63.3% by Solfrizzi et al., 2007; 39% by Hwang, Masterman, Ortiz, Fairbanks, & Cummings, 2004). The width of the prevalence range for depression in dementia is due to several factors, including the following: differences in researchers’ focus on symptoms versus specifically defined depressive disorders; diverse study samples varying in causes of dementia, stage of illness, country of residence, and placement of older patient; and instrument variation used to assess depressive symptoms and disorders.
Detection and assessment of depression in older adults with dementia can be challenging. Many long-term care residents with dementia present with signs and symptoms that overlap with depression (for example, anhedonia, irritability, flat affect) (Gauthier, 2003; Riccio, Solinas, Astara, & Mantovani, 2007). Based on current evidence-based practice guidelines, screening for depression should occur at least every 6 months (Brown, Raue, & Halpert, 2007). The depression screening assessment consists of the (a) Mini Mental State Exam (MMSE) used frequently to screen for dementia, and either the (b) Cornell Scale for Depression in Dementia (CSDD; Alexopoulos, Abrams, Young, & Shamoian, 1988), or the (c) Short Geriatric Depression Scale (GDS-15 item; Sheik & Yesavage, 1986) depending on patient cognitive functioning. The guidelines suggest using the GDS for patients scoring 15 to 23 on the MMSE, or the CSDD if the patient scores below 15 on the MMSE. The CSDD collects interview information from both the patient and the informant. If patients score 6 or greater on the GDS, or 11 or greater on the CSDD, the primary health care provider should be notified for further evaluation and/or treatment for clinically significant depression (Brown et al., 2007). If the older adult with dementia does not screen positive for depressive symptoms, the guidelines suggest that the individual be reevaluated in 1 month if clinically warranted, otherwise, 6 months later. Interviewing caregivers and other reliable informants on behalf of the individual with moderate to severe dementia is also recommended (American Geriatrics Society & American Association of Geriatric Psychiatry, 2003). Attention needs to be paid to the biopsychosocial factors during assessment to obtain a clear picture of the patient.
Lopez and colleagues (2003) examined the relationship between major depression and other observed psychiatric symptoms across mild, moderate, and severe stages of cognitive impairment. They found that fewer observed symptoms were associated with diagnosed depression as the stage of dementia increased. For example, confirmed depression in those with mild dementia was associated with anhedonia, sleep disturbance, depressed mood, and hopelessness, whereas moderate dementia and depression were associated with these symptoms, minus the anhedonia, and severe dementia with depression was associated only with hopelessness.
Another explanation of the differences in findings on the prevalence rates of depression over the course of dementia may be disagreement on whether and how to distinguish apathy from depression. Researchers administered a structured interview (developed from caregiver ratings) to measure apathy and depression separately. They reported that 12% met distinct criteria for both apathy and depression, 7% met criteria for apathy only, and 31% met criteria for depression only (Starkstein, Ingram, Garau, & Mizrahi, 2005). Supporting their argument that the two constructs were different, apathy, but not depression, was significantly associated with more severe cognitive deficits. However, a later study found that apathy was related to a higher frequency of both minor and major depression, with apathy at baseline significantly predicting depression at follow-up evaluations, findings that support a relationship between the two constructs (Starkstein, Jorge, Mizrahi, & Robinson, 2006).
Depression may be a risk factor for progression from MCI to dementia. The occurrence of depression in persons with MCI or dementia has also been linked to increased general severity of cognitive deficits (Nakaaki et al., 2007). Co-morbid cognitive impairment and depression have also been associated with several other negative consequences, including an increased risk of death (Sutcliffe et al., 2007). Although suicide attempts have been observed in less than 1% of dementia patients, suicidal ideation, intent, passive death wishes, and feelings that life is not worth living have been reported in 1% to 42% of dementia patients, particularly in those suffering from depression (Thompson, Herrmann, Rapoport, & Lanctot, 2007; Tsai, Tsai, Yang, & Hwang, 2007).
A recent meta-analysis (Thompson et al., 2007) reviewed treatment of depression with tricyclic antidepressants (TCA; imipramine and clomipramine), and SSRIs (sertraline and fluoxetine) in patients with dementia. The findings indicated that patient treatment response and remission was superior to placebo in the combined sample from all studies, but cautioned that significant declines in cognitive scores occurred during the use of TCAs. Other reviews (Buhr & White, 2006; Sink, Holden, & Yaffee, 2005) provide further support for positive effects of treatment with various antidepressants (including sertraline, fluoxetine, citalopram, trazodone, and moclobemide) on depression in dementia, with citalopram and sertraline being the most commonly prescribed (Caballero, Hitchcock, Beversdorf, Scharre, & Nahata, 2006; Daiello, 2007; Starkstein & Mizrahi, 2006). Alexopoulos, Jeste, Chung, Carpenter, Ross, and Docherty (2005) constructed an expert consensus response after surveying 50 experts in dementia from North America on preferred, alternate, and unacceptable treatment choices for BPSD. The general consensus was that SSRIs were the preferred pharmacological treatment for depression in patients with dementia.
Different classes of antipsychotics have also been used to treat depression with varying degrees of success (Lee et al., 2004; Snowdon, Sato, & Roy-Byrne, 2003). However, older adults with dementia taking haloperidol and other “typical” antipsychotics have been found to be at significant risk of extrapyramidal symptoms (EPS), including parkinsonism and tardive dyskinesia (Sink et al., 2005). Atypical antipsychotics such as risperidone and olanzapine have been shown to have significant, though modest, effects, and fewer adverse effects than typical antipsychotics at lower doses (Herrmann & Lanctot, 2007; Sink et al., 2005). However, since both risperidone and olanzepine have been associated with an increased risk of stroke and associated mortality, subsequent safety warnings have led providers to be cautious and somewhat restrictive about their use in older patients with dementia. Yet, a recent meta-analysis (Katz et al., 2007) concluded that although cerebrovascular events and mortality observations across trials were more frequent in risperidone-treated groups, the frequency did not differ significantly from that in placebo groups.
Cholinesterase inhibitors, which increase levels of acetylcholine, have been used to target cognitive deficits and BPSD with some success, particularly in patients with mild to moderate dementia (Birks, 2006; Garcia-Alloza, 2005). A recent review of the literature on the effects of rivastigmine on BPSD reports that positive effects have been found for patients with a wide range of dementia, and that apathy and anxiety are among the behavioral domains demonstrating the most consistent positive response (Figiel & Sadowsky, 2008).
A recent review and meta-analysis of the research on memantine for the treatment of psychological symptoms (e.g., depression) of dementia showed small but significant improvements with limited adverse effects (Maidment et al., 2008).
At least one clinical trial of valproate resulted in significant improvement in melancholic and sorrowful behaviors (Sival, Haffmans, Jansen, Duursma, & Eikelenboom, 2002), but the results of other small trials are contradictory (Sink et al., 2005). Preliminary studies of another anticonvulsant, lamotrigine, in elderly patients with dementia noted improvement in symptoms of agitation and depression (Sajatovic, Ramsay, Nanry, & Thompson, 2007). Studies provide some support for the theory that Ginkgo biloba special extract EGb 761 enhances cognitive functioning and stabilizes mood in cognitively impaired elderly subjects (Woelk, Arnoldt, Kieser, & Hoerr, 2007). A review of the research (Birks & Grimely-Evans, 2007) concluded that the evidence that the extract has predictable and clinically significant benefit for older people with dementia or cognitive impairment is inconsistent and unconvincing. However, a recent trial of this extract involving patients with dementia found that compared to controls, those taking the extract experienced improvements in apathy and depression (Scripnikov, Khomenko, & Napryeyenko, 2007).
As well as avoiding potential effects of polypharmacy, drug interactions, or exacerbation of comorbid conditions, non-pharmacological treatments may improve the quality of life for the patient with dementia above and beyond the reduction of depression (Burgio & Fisher, 2000; Cohen-Mansfield, 2005; Woods, 2004).
Livingston and colleagues (2005) reported the results of 11 studies consisting of randomized and quasi-experimental designs on Reality Orientation. The largest controlled trial (N=57 subjects) demonstrated no differences between Reality Orientation and active hospital ward orientation (Hanley, McGuire, & Boyd, 1981). The smaller sample nonrandomized studies mostly showed benefits of Reality Orientation in decreasing depressive symptoms or delaying admission to an institution. The current research does not offer clear evidence of its benefits for older adults with dementia.
Two reviews that included information on Reminiscence Therapy reported potentially positive effects on depressed mood in patients with dementia, but caution that most trials were small or otherwise methodologically questionable and therefore the evidence is weak and inconclusive (Douglas, James, & Ballard, 2004; Livingston et al., 2005).
Neal and Briggs (2003) reviewed trials of Validation Therapy and reported that only one study (Toseland et al., 1997) showed a trend towards improvement of depression a year after completing therapy, but the finding was not statistically significant. Another recent study using Validation Therapy in a group format found similar results (Deponte & Missan, 2007). The empirical evidence for this therapy for depression in dementia is weak and unconvincing.
Cognitive and behavioral therapies
A recent systematic review examined 20 studies using behavioral management techniques for treating depressive (n= 3 studies) and neuropsychiatric symptoms (17 studies) in older adults with dementia (Livingston et al., 2005). Of the three evaluating depression outcomes, one large randomized controlled trial showed significant improvement in depressive symptoms at post-treatment and at 6-month follow-up in one large randomized controlled trial showed significant improvement in depressive symptoms immediately post-treatment and at 6-month follow-up examination in two treatment conditions: (1) one emphasizing patient pleasant events and one emphasizing caregiver problem solving, as compared to treatment as usual and waitlist control conditions (Teri, Logdson, Uomoto, & McCurry, 1997). The two smaller randomized trials also demonstrated significant reductions in behavioral symptoms compared to usual primary care (Benedict et al., 2000; Suhr, Anderson, & Tranel, 1999). However, no significant effects were found on depression (Benedict et al., 2000).
Hyer and colleagues (1990) compared the effectiveness of a 12-week group psychotherapy, in a cognitive behavioral format, to usual care in a small sample of 22 residents. At post-treatment, depression scores had decreased in the treatment group but not in the control group. Koder (1998) discussed two case reports in which cognitive behavioral therapy was offered using techniques such as relaxation, distraction, and cognitive restructuring. Teri, Curtis, Gallagher-Thompson, and Thompson (1994) reported positive findings from a clinical trial of CBT with people in the early stages of Alzheimer’s disease. Individual and group CBT has also been used by other researchers with some favorable results (Kipling, Bailey, & Charlesworth, 1999).
There are several limitations to the literature on non-pharmacological interventions. First, most research studies have focused on behavioral and not depressive symptom outcomes. Second, the diversity of sample elderly populations makes it difficult to compare across studies. Third, the majority of studies lack a description of intervention protocols or manuals making it difficult to understand, analyze, or replicate the treatment components. Finally, the inconsistency of follow-up protocols across studies provides further barriers to determining long-term effects of the intervention.
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