Understanding Memory Loss & Cognitive Impairment
Memory loss and changes in cognitive functioning are frightening for patients and their families. In a very real sense, we are very much the collection of our memories. How we see ourselves, how we relate to others, how we navigate through our daily lives involves memory. Receiving a general diagnosis of dementia, or being told that you or a loved one has a specific disorder like Alzheimer's disease, is typically bewildering and overwhelming. The material found in this section is written for patients and their families. It is intended to help clarify and explain dementia and its causes. While there are no cures for dementia, accurate information can help patients and their families cope with these problems, and effectively plan so that independence and life quality can be maintained for as long as possible.
At the outset, it is important to distinguish between forgetfulness, which is a common and normal occurrence, and dementia, which is not a normal part of aging. Forgetfulness can be thought of as a simple "miss" in concentration or attention. We all become forgetful from time to time. Forgetting where you placed the car keys, not remembering to pick up a grocery item, and forgetting to send an email are typically benign events. As we age, we become more forgetful.
This is a normal process. In almost all circumstances, benign forgetfulness can be prevented or remedied by improving our focus and concentration, or by being less distracted. However in the case of dementia, memory errors are not easily corrected. For persons with dementia, the actual ability to make new memories is impaired.
One way to help determine if apparent problems in memory are the result of simple forgetfulness or are instead an indicator of a serious memory disorder is through cognitive screening. Cognitive tests like the BCAT® can be quickly administered by your healthcare practitioner. They can indicate whether more thorough evaluation is necessary. Cognitive screening has many advantages, but is also associated with complex issues.
Below you will find short and basic descriptions of memory syndromes and disorders. They are presented to provide you with information to better cope with very challenging and often life-altering illnesses.
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What Do I Do Now?
Perhaps you have been told that you have Alzheimer's disease (AD), or that your mother has dementia. The question, "what do I do now?" - is one raised by millions of people after being given a dementia diagnosis. From our experience in working with patients and their families, we've learned that the following information can help one navigate the frightening world of dementia.
- Manage expectations. There are many misconceptions about dementia in general and Alzheimer's disease in particular. Some common examples are: Alzheimer's disease is a normal part of aging. Early diagnosis and treatment can reverse the disease. All dementia is caused by Alzheimer's disease. Misconceptions often lead to unrealistic and faulty expectations. Knowledge of the facts and a realistic perspective contribute to positive coping. Misconceptions and pessimism lead to conflict and blaming.
- Get the facts. The diagnosis of dementia should be made by a healthcare professional qualified to make this determination, and through at least two corroborating sources. Examples include a valid screening tool, like the BCAT; neuropsychological testing; PET scan or other neuro-imaging; a neurological exam; a geropsychiatric evaluation. You should ask the healthcare provider specifically what type of dementia has been diagnosed, what is the level of severity, and what cognitive skills remain intact. Review with your healthcare provider possible treatments and other professional resources in the community.
- Build the team. Dementia disorders are complex, requiring a team of supportive individuals. Dementia can adversely impact health, residential status, finances, legal issues, and social relationships. A team of supportive people who represent these areas is crucial. Suggested "team" members that represent a core of support include: a primary care physician to be a point person and oversee general medical health; at least one family/friend to provide ongoing social support; a psychologist, psychiatrist, or other professional to monitor and possibly treat cognitive changes and other potential psychiatric symptoms (e.g., depression, anxiety, illusions, delusions); an identified caregiver. Other supports may include legal and financial advisers, and a geriatric care manager.
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What is Mild Cognitive Impairment (MCI)?
Healthcare practitioners think about cognitive functioning in terms of a continuum. In normal cognitive functioning, forgetfulness is increasingly common as we age, and by itself, does not signify dementia. There is a syndrome, however, in which persons experience a cognitive deficit that goes beyond normal cognitive functioning but does not meet criteria for dementia. The typical deficit is in memory, but generally other cognitive features, such as language, judgment, and reasoning are intact. This syndrome is called Mild Cognitive Impairment (MCI).
Generally speaking, people with MCI are able to perform everyday tasks of living and can live independently. However, many experts believe that MCI is a pre-dementia stage. It does appear that the rate at which MCI patients eventually develop dementia is much higher than persons with no evidence of MCI. Therefore, careful monitoring of MCI progression is very important. Research shows that memory medications work more effectively in MCI than they do in actual dementia. There are practical considerations associated with MCI. For those who are living independently in the community, an assessment of IADLs is often important. IADL, or instrumental activities of daily living, is a term that refers to the more complex daily tasks. Examples are shopping, laundry, transportation, medication, telephone, housekeeping, and finances.
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What is Dementia?
Permanent and progressive loss in one's ability to make new memories and learn new information is the defining feature of dementia. Dementia is a general term that refers to a cluster of mental symptoms. Dementia is not a specific disease. There are many possible causes of dementia, but the most common cause of dementia is Alzheimer's disease. Alzheimer's disease accounts for 50 to 70 percent of dementia cases. Dementia always involves mental or cognitive decline. Indications of dementia are:
- Decline in mental functioning (from a higher baseline)
- Declines are serious enough to interfere with daily life
- Affects two or more of the following abilities, and always affects memory:
- Recall and learn new information
- Language – understanding and expressing in verbal or written form
- Visuospatial – recognizing and interpreting symbols of the visual world
- Executive functions – the "CEO" of the brain: reasoning, planning, organizing, problem-solving, judgment
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What is Alzheimer's Disease (AD)?
AD is a progressive brain disorder that gradually destroys one's ability to make new memories, learn new material, reason, make judgments, problem-solve, communicate with others, and complete activities of daily living. Person with AD become increasingly confused, misplace things, get lost in familiar places, and demonstrate changes in personality and behavior.
Some Facts about AD
- Persons with AD typically die within nine years of showing symptoms.
- The duration of the disease can vary from two to twenty years.
- There is no recognized single cause of AD.
- Age is the greatest risk factor for AD, with most persons beginning to show symptoms after age 65.
- The likelihood of developing AD approximately doubles every five to six years after age 65 until around age 85. Nearly 50% of adults age 85 and older have AD.
- In AD brain cells are destroyed by proteins the brain naturally makes. These proteins are called beta-amyloid and tau and they create plaques and tangles in the brain.
- Beta-amyloid appears to be a central feature in the development of AD.
- Plaques in AD appear to be identical to those found in Down's Syndrome.
- Problems with beta-amyloid appear to be linked to chromosome 21.
Specific Information about Beta-amyloid
- Beta-amyloid is a naturally occurring protein fragment in the brain.
- Beta-amyloid is the key component in brain plaques.
- Beta-amyloid interferes with the brain's cell-to-cell communication system, which impedes cognitive functions such as memory, communication, reason, judgment, and other functions.
- Under normal circumstances the brain eliminates much of this protein fragment, however, in AD, the clearance of beta-amyloid malfunctions.
Stages of AD
There are a number of staging models for describing the progression of AD. One relatively simple framework is a three-stage model:
- Stage 1: Mild impairment. Typically the first three years of the disease. Common indications include some word- or name-finding difficulties (worse than baseline), challenged by learning or remembering new information, mild performance issues in work and social situations, misplaced objects, declines in planning and organizing.
- Stage 2: Moderate impairment. Typically years four through six of the disease. Common indications include poor ability to make new memories, reduced memory of personal history, language problems, deficits in executive functions, decreased ability to perform complex tasks, visuospatial deficits, and depressive symptoms. Usually assistance with bathing, dressing, and eating are not needed.
- Stage 3: Severe impairment. Late years of the disease. Require assistance in dressing, hygiene, eating; increased episodes of incontinence, tend to wander and become lost; frequently fail to recognize what were familiar people and objects; delusional thinking; increased anxiety or apathy; severe deficits in memory and executive functions; and severe loss in verbal fluency. Require supervision at home, assisted-living, or skilled nursing facility care.
Diagnosis and Treatment of AD
- Simple forgetfulness is a part of normal aging and does not indicate AD.
- True memory deficits and associated mental problems may indicate AD.
- A skilled psychologist, neuropsychologist, psychiatrist, other mental health provider or physician can diagnose AD.
- There is not a single test for AD. However, PET scans with PIB show levels of beta-amyloid present in the brain.
- Psychologists and neuropsychologists can administer a battery of neuro-cognitive tests that can identify AD with over 90% accuracy.
- Other conditions, such as depression, thyroid conditions, medications, alcohol dependency, nutritional imbalances, and other dementing diseases must be "ruled out" in order to make an accurate diagnosis of AD.
- There is no recognized cure for AD.
- Treatment goals are to slow down the progression of the disease and improve associated symptoms such as depression, anxiety, delusional thinking, and behavioral problems.
- The FDA has approved several drugs for AD. Cholinesterase inhibitors remain core medications. These target the neuro-chemical, acetylcholine. They do not directly affect beta-amyloid.
- Counseling persons with AD, educating and supporting caregivers, and selecting or designing pro-dementia environments are important interventions.
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There are numerous diseases other than AD that can cause dementia. Some of these are summarized below.
- Vascular Dementia (VaD). Possibly the second most common cause of dementia, VaD is associated with strokes. VaD accounts for 10 to 30 percent of all dementia cases. There are likely several sub-groupings of the disease, depending on the specific underlying vascular disease. Generally speaking, strokes, or cerebrovascular accidents, cause blockages in the blood flow to parts of the brain. Such disruptions in blood flow can result in the death of brain cells. In addition to blockages, blood flow can be disrupted by a blood vessel hemorrhage in the brain. VaD can be caused by either a major stroke, or by a series of small strokes. Typically, mental declines occur in "steps" where there is a fairly sudden change in function. The onset of this type of dementia is usually abrupt. Also, persons with VaD may retain certain mental functions while losing others. There are risk factors for VaD; they include history of heart attacks or cardiovascular diseases, high blood pressure, high cholesterol, and diabetes. The specific cognitive features of VaD depend on the location of cerebrovascular accidents, however, impaired memory is the most common cognitive feature.
- Mixed Dementia with AD and VaD. Persons with this dementia have AD and VaD at the same time. There is some research suggesting a link between the two dementing processes. A number of autopsy studies have shown that up to 50% of people with AD also have vascular disease.
- Frontotemporal Dementia (FTD). FTD is a rare dementia, causing two to five percent of all dementia cases. It affects the front (frontal lobe) and sides (temporal lobes) of the brain and the corresponding functions associated with these brain areas. This dementia tends to occur earlier than AD, typically emerging in the fifth and sixth decade of life. Common indications of FTD are changes in personality, poor social tact (e.g. rude comments), impulsivity, feelings disconnected from the context (e.g. indifference about a major loss), decreased verbal output, and strong urges, especially to eat or hoard. Also common are repetitive behaviors, concrete reasoning, and deficits in executive functions (planning, organizing, judgment, abstraction). Memory performance, while impaired, is typically better than seen in AD.
- Dementia with Lewy Bodies (DLB). In this disease the protein, alpha-synuclein, builds up inside brain cells. These deposits are called "Lewy bodies." Two-thirds of DLB patients are male. Survival rates are judged to be from four to ten years. Experts believe that 14 to 20 percent of dementia is of this type. Specific symptoms of DLB include movement symptoms similar to other Parkinsonian disorders (stiffness, shuffled walking, falls, lack of facial expression, balance problems), severe memory deficits, excessive daytime drowsiness, visual hallucinations (40 to 70 percent of the time), and "acting out" dreams while asleep.
- Parkinson's Disease (PDD). PDD likely also involves Lewy bodies. At least 30% of persons with PD will develop PD dementia after the age of 65, and nearly 50% of PD patients have some cognitive deficits. One way to differentiate PDD from DLB is onset of cognitive decline. Generally, if the physical symptoms (motor) of PD are present at least two years before the cognitive ones emerge, then the eventual dementia is diagnosed as PDD. If, however, the cognitive symptoms occur before the physical ones or within the first two years, the eventual dementia is thought to be caused by DLB. The cognitive profile for PDD involves slowed mental speed, problems in of attention, poor speech output, poor retrieval memory (but better recognition memory), problems in executive functions (planning, organizing, judgment, abstraction), apathy and depression, visuospatial deficits, and disturbed gait (walking).
- Normal Pressure Hydrocephalus (NPH). In this rare disease, fluid surrounding the brain and spinal cord does not drain normally. Instead, fluids build-up putting "pressure" on brain tissue. The condition can be acute or chronic. The term "normal pressure" refers to the fact that the spinal fluid pressure as measured by a spinal tap often falls within the normal range. The three classic indications of NPH, often referred to as the NPH clinical triad, are difficulty walking, loss of bladder control, and decline in mental functioning. Mental processing is typically slowed. Other cognitive features often include apathy, problems with executive functions (planning, organizing, judgment, abstraction), attention, and verbal output. Persons with NPH often respond to questions with a delay, but tend to provide accurate answers. The medical procedure of placing a shunt often helps with walking and bladder control; however, it is less successful in reversing cognitive declines.
- Huntington's Disease (HD). This is a fatal brain disease caused by a single genetic defect. Life expectancy of persons with HD is 13 to 16 years after development of symptoms. HD affects 3 to 10 per 100,000 people, and mostly begins around age 30. Offspring from a parent with HD have a 50% chance of developing the disease. Physical symptoms include jerky, repetitive movements combined with slower, writhing movements. Transient facial grimacing, opening and closing of the mouth, head nodding, and finger flexing are involuntary and common. Depression is a frequent feature. Cognitive features of HD involve slowed psychomotor speed; decreased attention; lack of spontaneity; decreased verbal output; poor speech articulation; poor spontaneous memory, but fairly intact memory recognition; deficits in executive functions (planning, organizing, judgment, abstraction).
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