term Alzheimer’s disease be used when discussing pathology or the continuum of the disease (Alzheimer’s Association, 2018a). The intent is to allow researchers to have a common language for the preclinical stages of the disease; whereas in the clinical realm, this could be considered an issue of semantics only, thus, this course utilizes “AD” to indicate both Alzheimer’s disease and Alzheimer’s dementia. Ultimately, the destruction and death of neurons in AD leads to the macropathology of brain atrophy. Significant shrinkage of the hippocampus and surrounding cortex occurs as the disease progresses, and with the atrophy of the cortex, the ventricles appear larger. Although there is some variability in the clinical course of AD, symptoms appear to develop through the same general stages. The time from diagnosis to death varies and can be as short as 3 years or as long as 20 years, with average survival after diagnosis being 4 to 8 years (Alzheimer’s Association, 2018a).
20 years. This preclinical phase is important to researchers as an opportunity to determine therapeutic interventions that may stay the clinical course of the disease. Researchers continue to try to correlate the neuropathological cascade of events with the clinical appearance of AD. This antecedent stage may be identifiable by biological markers (biomarkers) that portend the progression of the pathological process into the initial clinical stages of the disease. Biomarkers are identified through CSF and/or imaging studies (i.e., MRI, positron-emitting tomography [PET] scan) and currently, the National Institute on Aging (NIA) and the Alzheimer’s Association (AA) are refining the definition of “Alzheimer’s Disease” to refer to the presence of biomarkers as opposed to the presence of dementia in an effort to support a common language for Alzheimer’s research efforts (Jack et al., 2018). Whereas “Alzheimer’s disease” previously suggested the presence of dementia, the current language suggestion from NIA/AA is that the term “Alzheimer’s dementia” be used in place of Alzheimer’s disease when dementia is present and that the
Figure 2: Alzheimer’s Pathology at the Level of the Neuron
a. Beta-amyloid plaques block neuron-to-neuron transmission.
b. Neurofibrillary tangles impair the neuron’s microtubule transport system.
Note . Figure (a) from Alzheimer’s Association (2014). Alzheimer’s disease and dementia. Retrieved from http://www.alz.org. Jannis Productions. Rebekah Fredenburg, computer animation; Stacy Jannis, ullustration/art direction. Reprinted with permission. Figure (b) by William Rosenblum. STAGES OF ALZHEIMER’S DISEASE
The brain changes that occur in AD are associated with distinct symptoms and behavior changes that progress throughout the course of the disease. Behavior is the result of complex brain processes. In AD, the disturbance of many of these processes is the basis for distressing or inappropriate behaviors. For example, an individual with AD may angrily refuse to take a bath or get dressed because he or she does not understand or forgets what the caregiver has asked. The anger is a mask for confusion and anxiety. Another individual with AD may constantly follow his or her spouse and display heightened anxiety when the person is out of sight. To an individual who cannot remember the past or anticipate the future, the world can be strange and frightening. Sticking close to a trusted and familiar caregiver may be the only thing that makes sense and provides security. Taking off clothes may seem reasonable to a person with AD who feels hot and does not understand or remember that undressing in public is not acceptable. Clinical staging can include three or seven stages of disease. The seven-stage model is based on the work of Barry Reisberg (Reisberg, Ferris, & Franssen, 1985) and is a useful framework for education on the progression of the disease and categorizing function for rehabilitation studies. The seven stages are: 1. No impairment (normal function). 2. Very mild cognitive impairment (may be normal changes of aging, e.g., subjective difficulty in word finding, forgetfulness). 3. Mild cognitive decline (may be incipient AD, e.g., difficulty in a challenging work environment).
4. Moderate cognitive decline (mild or early-stage AD, e.g., difficulty in complex tasks such as balancing a checkbook, planning a party). 5. Moderately severe cognitive decline (moderate or midstage AD, e.g., requires assistance choosing appropriate clothing). 6. Severe cognitive decline (moderately severe or late midstage AD, e.g., requires assistance with acts of dressing, bathing, toileting). 7. Very severe cognitive decline (severe or end-stage AD, e.g., loss of ability to communicate, ambulate, interact). A widely used, more simplified model identifies three major stages of disease: mild, moderate, and severe. The first noticeable signs of memory loss and decreased cognitive abilities mark the mild stage. The growing number of plaques and tangles first damage areas of the brain that control memory and, to a lesser extent, language and reasoning. Obvious physical problems are not clinically apparent at this stage, although subclinical gait and balance deficits are likely present. This leads to a situation in mild AD in which a person seems to be healthy but is actually having increasing trouble making sense of the world. The realization that something is wrong often comes gradually because the early signs may be confused with normal aging. Accepting these signs and deciding to go for diagnostic tests can be difficult for patients and families to face. The clinical diagnosis of AD is usually made during this mild stage. The signs and symptoms of mild AD can include: ● Memory loss.
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