A delirium is characterized by a disturbance of consciousness and a change in cognition that develop over a short period of time (American Psychiatric Association, 1994). The changes in cognition can include difficulties with attention, memory, orientation, and language. Delirium can also affect perception, the sleep-wake cycle, personality, and mood. Although the onset of delirium usually is rapid, its course can vary a great deal over the course of a day, with cognitive symptoms in older adults generally more severe than in younger or middle-aged adults (Leentjens et al., 2008).
Delirium can be caused by any of a number of medical conditions (such as stroke, cardiovascular disease, metabolic condition), medication
374 CHAPTER 10 side effects, substance intoxication or withdrawal, exposure to toxins, or any combination of factors (Leentjens et al., 2008; Zarit & Zarit, 2006). Because they take more medications on average than other age groups, older adults are particularly susceptible to delirium. In the general community, the rate of delirium in people over age 55 is low (between 0.4% and 1.1%), but among people who are ill the rate is much higher, with as many as 50% of postoperative patients experiencing delirium (Qualls, 1999).
Assessment and treatment of delirium focus on the physiological causes. In general, the most important aspect of diagnosis is differentiating delirium from depression and dementia. The key features of each are shown in Table 10.4. The severity of delirium is related to the level of underlying physiological problem. In many cases, delirium is accompanied by severe misinterpretations of the environment and confusion, which is best alleviated by having one reliable family member or friend provide reassurance to the patient (Leentjens et al., 2008).
If the cause of the delirium can be identified and addressed, most cases of delirium can be cured. In some cases, however, delirium can be fatal or result in permanent brain damage (Leentjens et al., 2008).
Probably no other condition associated with aging is more feared than the family of disorders known as dementia. In dementia one can literally lose one’s mind, being reduced from a complex, thinking, feeling human being to a confused, vegetative victim unable even to recognize one’s spouse and children. Dementias serious enough to impair independent functioning affect over 5 million Americans, with the incidence increasing with age, rising from extremely low rates in the 50s to about half of the people aged 85 and older (National Institute on Aging, 2007a). Estimates are that unless a cure or prevention is found, the number of people with dementia will increase by 50% by 2030 to nearly 8 million and could triple by 2050 to over 16 million (Alzheimer’s Association, 2008a).
Comparison of Characteristics of Depression, Delirium, and Dementia
Source: Foreman, M. D., Fletcher, K., Mion, L. C., et al. (1996). Assessing cognitive function. Geriatric Nursing, 17, 228. Reprinted with permission from Elsevier.
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Although there is a real basis for fearing dementia, most older adults are not demented. For many people, the fear of dementia is the most serious problem, leading them to consider every lapse of memory a symptom. It is hard to know how many older adults have unstated fears about no longer being able to remember things in the same ways they did when they were younger. But as noted in Chapter 6, memory abilities show some normative changes with age. Consequently, what many people believe are signs that they are becoming demented are actually quite normal.
The Family of Dementias. Dementia is not a specific disease but rather a family of diseases that are characterized by cognitive and behavioral deficits involving some form of permanent damage to the brain. About a dozen forms of dementia have been identified. Dementia involves severe cognitive and behavioral decline and is not caused by a rapid onset of a toxic substance or by infection (American Psychiatric Association, 2000). If delirium is present, dementia cannot be diagnosed.
We focus on several types of dementias that are irreversible and degenerative. The most common and widely known of these is Alzheimer’s disease, but others are important as well: vascular dementia, Parkinson’s disease, Huntington’s disease, alcoholic dementia, and AIDS dementia complex.
Alzheimer’s Disease. Alzheimer’s disease is the most common form of progressive, degenerative, and fatal dementia, accounting for perhaps as many as 70% of all cases of dementia (Alzheimer’s Association, 2008a). New knowledge about Alzheimer’s disease is discovered all the time, so it is important to monitor the research literature. However, because it is such a terrible disease, news of potential breakthroughs too often do not pan out.
Alzheimer’s disease has several characteristics that we will consider, both in terms of specific changes in the brain and behavioral symptoms.
Neurological Changes in Alzheimer’s Disease The
changes in the brain that characterize Alzheimer’s disease are microscopic. Although great progress
has been made in diagnosing the disease, it is still the case that definitive diagnosis of the disease can be done only at autopsy (Feldman et al., 2008). These progressive changes eventually cause so much brain destruction that the person dies. The microscopic changes that define Alzheimer’s disease are rapid cell death, neurofibrillary tangles, and neuritic plaques. Several changes in neurotransmitter levels also are observed. Rapid cell death occurs most in the hippocampus (a structure in the brain most closely involved in memory), the cortex (the outer layer of the brain in which our higher-level cognitive abilities reside), and the basal forebrain (the lower portion of the front of the brain). This cell death occurs at a rate much greater than normal.
Neurofibrillary tangles (see Chapter 3) are accumulations of pairs of filaments in the neuron that become wrapped around each other; when examined under a microscope, these paired filaments look like intertwined spirals. Neurofibrillary tangles occur in several areas of the brain, and the number of tangles is directly related to the severity of symptoms, specifically the severity of memory impairment (Guillozet et al., 2003).
Neuritic or amyloid plaques (see Chapter3) are spherical structures consisting of a core of beta – amyloid, a protein, surrounded by degenerated fragments of dying or dead neurons. The plaques are found in various parts of the brain, with the amount of beta-amyloid moderately related to the severity of the disease (Guillozet et al., 2003). Degeneration of neurons in some areas of the brain results in the formation of vacuoles, or spaces that become filled with fluid and granular material. Considerable recent research has focused on beta-amyloid as a major factor in Alzheimer’s disease, both in terms of the cause and possible avenues for treatment. For example, there is some evidence that abnormal l evels of copper, zinc, and iron may cause beta – amyloid deposits (Finefrock, Bush, & Doraiswamy,
Although the structural changes occurring in the brains of people with Alzheimer’s disease are substantial, we must use caution in assuming that they represent qualitative differences from normal aging. They may not. As we saw in Chapter 3, all
the changes seen in Alzheimer’s disease, including the structural and neurotransmitter changes, are also found in normal older adults. To be sure, the changes in Alzheimer’s disease are much greater. But the important point is that Alzheimer’s disease may be merely an exaggeration of normal aging and not something qualitatively different from it.
Recent research has also implicated certain neurochemicals as other possible causes of Alzheimer’s disease. For example, increased levels of plasma homocysteine have been associated with the level of cognitive impairment observed in Alzheimer’s disease (Blasko et al., 2008; Bleich et al., 2003). Screening for these increased levels may improve diagnostic accuracy, and these levels are directly addressed by medication with memantine (discussed later).
Symptoms and Diagnosis The major symptoms of Alzheimer’s disease are gradual changes in cognitive functioning: declines in memory beginning with loss of recent memory and progressing to loss of remote memory, learning, attention, and judgment; disorientation in time and space; difficulties in word finding and communication; declines in
personal hygiene and self-care skills; inappropriate social behavior; and changes in personality (American Psychiatric Association, 2000).
These symptoms tend to be vague in the beginning, and they mimic other psychological problems such as depression or stress reactions. For example, an executive may not be managing as well as she once did and may be missing deadlines more often. Slowly, the symptoms get worse. This executive, who once could easily handle millions of dollars, can no longer add two small numbers. A homemaker cannot set the table. A person who was previously outgoing is now quiet and withdrawn; a gentle person is now hostile and aggressive. Emotional problems become increasingly apparent, including depression, paranoia, and agitation. Wandering becomes a serious problem, especially because the person may have no idea where he or she is or how to get home, thus posing a genuine safety concern.
As the disease progresses, the patient becomes incontinent and more and more dependent on others for care, eventually becoming completely incapable of even such simple tasks as dressing and eating. In general, the symptoms associated with Alzheimer’s disease are worse in the evening than
in the morning, a phenomenon that caregivers call sundowning.
The rate of deterioration in Alzheimer’s disease varies widely from one patient to the next, although progression usually is faster when onset occurs earlier in life (Wilson et al., 2000). However, we can identify a series of stages that the patient goes through (Reisberg et al., 1982). Many diseases cause problems similar to those observed in the early stages of Alzheimer’s disease. In fact, fewer than 10% of those who show mild cognitive impairment go on to develop more serious cognitive impairment within several years of the clinical evaluation (Reisberg et al., 1985).
Although a definitive diagnosis of Alzheimer’s disease depends on an autopsy, the number and severity of neurological and behavioral changes allow clinicians to make increasingly accurate early diagnoses (Feldman et al., 2008). For an earlier diagnosis to be accurate, however, it must be comprehensive and broad. Figure 10.3 provides an overview of the process that should be used to differentiate Alzheimer’s disease from other conditions. Note that a great deal of the diagnostic effort goes into ruling out other possible causes for the observed cognitive deficits: All possible treatable causes for the symptoms must be eliminated before a diagnosis of Alzheimer’s disease can be made. Unfortunately, many clinicians do not conduct such thorough diagnoses; general practice physicians miss nearly half the cases of dementia (Boise et al., 1999).
As noted in Figure 10.3, the clinical diagnosis of Alzheimer’s disease consists of carefully noting the history of the symptoms, documenting the cognitive impairments, conducting a general physical exam and neurological exam, performing laboratory tests to rule out other diseases, obtaining a psychiatric evaluation, performing neuropsychological tests, and assessing functional abilities. To rule out physical illness, it is critical to conduct a thorough medical examination prior to any psychological or other follow-up tests. Recent evidence suggests that the measurement of p-tau proteins may provide a good biological marker of Alzheimer’s disease (Hampel, Goernitz, & Buerger, 2003). More important, measures of p-tau proteins can differentiate between
Alzheimer’s disease, other forms of dementia, and depression. In addition, brain-imaging techniques, such as magnetic resonance imaging (MRI) and spiral computed tomography (spiral CT) scans, are often used to rule out other diseases.
As research findings provide ways to improve the accuracy of diagnosis of Alzheimer’s disease, home testing kits are becoming available. The Early Alert Alzheimer’s Home Screening Test (AHST), costing roughly $20, is one example (Higuera et al., 2008; Kier & Molinari, 2003). The AHST is based on the Smell Identification Test (SIT), which in turn is based on some research evidence that individuals with Alzheimer’s disease have trouble identifying certain smells. Unfortunately, so do individuals with several other disorders, such as vascular dementia, human immunodeficiency virus (HIV) infection, and multiple sclerosis, making it very difficult to conclude that olfactory dysfunction is uniquely related to Alzheimer’s disease. Moreover, the general public, untrained in Alzheimer’s disease diagnosis, may not understand the difference between a screening test (the AHST) and a diagnostic test. In short, although the concept of a home test for Alzheimer’s disease may have merit, a much more accurate test is necessary, coupled with better education in its use.
Searching for a Cause We do not know for certain what causes Alzheimer’s disease. There are many hypotheses, as described in Table 10.5. At present, the main focus of research is on a genetic link (McQueen & Blacker, 2008; Wilmot et al., 2008). The strong possibility that at least some forms of Alzheimer’s disease are inherited is a major concern of patients’ families. The research evidence to date indicates that genetic factors may be a powerful determinant of Alzheimer’s disease, and possible markers on chromosomes have been found (McQueen & Blacker, 2008; Wilmot et al., 2008). Genetic research has identified links to both early onset and late onset of Alzheimer’s disease. Other research has investigated other possible causes, such as beta-amyloid, as noted earlier.
Several sites on various chromosomes have been tentatively identified as being involved in the
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*It is required in patients with focal signs, rapid progression, and headache. tThis category contains rare dementias (e. g., frontotemporal degenerations, Jakob-Creutzfeldt disease, Parkinson’s disease, and other movement disorders that present with dementias) that should be considered when unusual clinical features are present or a rapidly progressive course is noted.
Figure 10.3 Differential diagnosis and Alzheimer’s disease algorithm.
Source: Alzheimer’s Association online document. http://www. alz. org/medical/rtalgrthm. htm Developed and endorsed by the TriAD Advisory Board. Copyright 1996 Pfizer Inc. and Esai Inc. with special thanks to J. L. Cummings. Algorithm reprinted from TriAD, Three for the Management of Alzheimer’s Disease, with permission.
Hypotheses of the Cause of Alzheimer’s Disease
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