Dementia
Content
I. Introduction: Dementia is a brain disorder that seriously affects a person’s ability to carry out daily activities. The most common form of dementia among older people is Alzheimer’s disease (AD), which initially involves the parts of the brain that control thought, memory, and language. Although scientists are learning more every day, right now they still do not know what causes AD, and there is no cure. Scientists think that as many as 4.5 million Americans suffer from AD. The disease usually begins after age 60, and risk goes up with age. While younger people also may get AD, it is much less common. About 5 percent of men and women ages 65 to 74 have AD, and nearly half of those age 85 and older may have the disease. It is important to note, however, that AD is not a normal part of aging. AD is named after Dr. Alois Alzheimer, a German doctor. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. He found abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary tangles). Today, these plaques and tangles in the brain are considered signs of AD. Scientists also have found other brain changes in people with AD. Nerve cells die in areas of the brain that are vital to memory and other mental abilities, and connections between nerve cells are disrupted. There also are lower levels of some of the chemicals in the brain that carry messages back and forth between nerve cells. AD may impair thinking and memory by disrupting these messages. II. Definition: Alzheimer’s disease is characterized by progressive cognitive decline and memory loss. Individuals who suffer from Alzheimer’s Disease will have difficulties with activities of daily living and need full time assistance in the later stages of the disease. It accounts for 50-60% of all dementia cases in the elderly. Alzheimer’s is a unique condition that is not the result of common aging and natural senility. The brain tissue in Alzheimer’s patients has a specific pattern of degeneration marked by senile plaques and neurofibullary tangles. There is also a loss of neurons in the cerebral cortex, hippocampus, and subcortical structures, such as the locus caeruleus and nucleus raphe dorsalis. An increase in beta-amyloid proteins is thought to contribute to the disease as well. This increase is pararlleled with a marked decrease in brain neurotransmitters, with acetylcholine being affected the greatest. The distinct cause of Alzheimer’s disease is not completely known. There is a familiar pattern in 15-20% of the cases. For the other 80-85% of cases there are several causal relationships. A genetic etiology is suspected in some individuals, due to findings of an increase in certain proteins in the brain that are coded for on specific chromosomes (1, 14, 19, and21). The most significant findings are with the protein apolipoprotein E. Certain forms of the protein (e4-type) are linked with greater incidence, while one form (e2type) is associated with a more protective effect. Environmental factors are also suspected to play a role in the development of Alzheimer’s disease with specific attention to heavy metal toxicity, oxidative damage, and abnormal hormone metabolism. What Causes AD? Scientists do not yet fully understand what causes AD. There probably is not one single cause, but several factors that affect each person differently. Age is the most important known risk factor for AD. The number of people with the disease doubles every 5 years beyond age 65. Family history is another risk factor. Scientists believe that genetics may play a role in many AD cases. For example, early-onset familial AD, a rare form of AD that usually occurs between the ages of 30 and 60, is inherited. The more common form of AD is known as late-onset. It occurs later in life, and no obvious inheritance pattern is seen in most families. However, several risk factor genes may interact with each other and with non-genetic factors to cause the disease. The only risk factor gene identified so far for late-onset AD is a gene that makes one form of a protein called apolipoprotein E (ApoE). Everyone has ApoE, which helps carry cholesterol in the blood. Only about 15 percent of people have the form that increases the risk of AD. It is likely that other genes also may increase the risk of AD or protect against AD, but they remain to be
discovered. Scientists still need to learn a lot more about what causes AD. In addition to genetics and ApoE, they are studying education, diet, and environment to learn what role they might play in the development of this disease. Scientists are finding increasing evidence that some of the risk factors for heart disease and stroke, such as high blood pressure, high cholesterol, and low levels of the vitamin folate, may also increase the risk of AD. Evidence for physical, mental, and social activities as protective factors against AD is also increasing. Primary Dementia Primary dementias are degenerative disorders that are progressive, irreversible, and not due to any other condition. Specific disorders are dementia of the Alzheimer’s type (DAT) and vascular dementia (formerly multi-infarct dementia). Dementia of Alzheimer’s type demonstrates progression of symptoms from the initial stage, which is characterized by mild cognitive deficits in the area of short-term memory and accomplishment of goal-directed activity, to the final stage in which profound impairment occurs in the areas of cognition and self-care abilities. Research is ongoing. Dementia of Alzheimer’s type believed to have multiple causative factors. 1. Genetic Factors: Familial Alzheimer’s disease is associated with abnormal genes on chromosomes 1, 14, and 21. In particular, with genes located on these chromosomes (1 and 14) that encode for amyloid precursor protein which leads to mutation of the amyloid beta-peptide in plaques. A specific cholesterol-bearing protein, apolipoprotein E4 (Apoe4), is found on chromosome 19 twice as often as people with DAT as in general population. 2. Biochemical and brain structure factors: The neurotransmitter acetylcholine has been implicated in terms of relative deficit and/or receptor abnormalities as related to Alzheimer’s disease. Autopsy findings reveal presence of brain changes, that is, the presence of amyloid plaquesand neurofibrillary. Additional areas of investigation includes: slow viral infection, autoimmune processes, and head trauma. Secondary Dementia Occur as a result of another pathologic process. 1. Infection-related dementias Acquired immunodeficiency syndrome Chronic meningitis Creutzfeldt-Jakob disease Progressive multifocal leukoencephalopathy Postencephalitic dementia syndrome Syphilis Subacute sclerosing panencephalitis Tuberculosis 2. Subcortical degenerative disorders Huntington’s disease Parkinson’s disease Wilson’s disease Thalamic dementia 3. Hydrocephalus 4. Vascular dementias 5. Traumatic conditions, such as post traumatic encephalopathy and subdural hematoma. 6. Neoplastic dementias Glioma
Meningioma Meningeal carcinomatosis Metastatic deposits
7. Inflammatory conditions, such as sarcoidosis, systemic lupus erythematous, and temporal arteritis. 8. Toxic conditions, such as alcohol-related syndrome and iatrogenic dementias 9. Metabolic disorders Anemia’s Deficiency states Cardiac or pulmonary failure Hepatic encephalopathy Porphyria Uremia Introduction: Dementia is an acquired syndrome that causes progressive loss of intellectual abilities, such as memory, as well as aphasia, apraxia, and loss of executive function. Dementing disorders are characterized by gradual onset plus continuing cognitive decline that is not due to other brain disease. Screening tests can identify persons who should be referred for a complete diagnostic workup. Early diagnosis of dementia is the goal of a diagnostic workup, which is done to exclude potentially reversible causes and initiate therapy as early as possible. Short term memory impairment is usually the first symptom of dementia. Clinical diagnosis of dementia requires (1) loss of an intellectual ability with impairment severe enough to interfere with social or occupational functioning and (2) ruling out delirium. Delirium must be ruled out because cognitive impairment caused by delirium may be reversible. Mild cognitive impairment is another risk factor for dementia. Persons with mild cognitive impairment have complaints and objective evidence of memory problems, but do not have deficits in activities of daily living or in other cognitive functions and do not meet the diagnostic criteria for dementia. Mild cognitive impairment refers to a transitional state between normal aging and dementia; it is associated with an increased risk of death, greater decline in cognitive abilities, and incident, with annual conversion rate of 8.3% to Alzheimer disease. Elder persons with mild cognitive impairment who are depressed are at greater risk of converting to Alzheimer disease. Dementia may be caused by more than one mechanism, even in the same individual. An autopsy examination is necessary to confirm the diagnosis. Anatomy and Physiology of the human brain Pathophysiology of Dementia Clinical Manifestations: Dementia DSM –IV DIAGNOSIS Dementia of the Alzheimer’s type Vascular dementia Dementia due to a general medical condition Dementia due to multiple etiologies DEFINING CHARACTERISTICS Slow, insidious onset Impaired long and short term memory Deterioration of cognitive abilities – judgement, abstract thinking Often irreversible if untreated Personality changes No or slow EEG changes Diagnostic Evaluation:
Various diagnostic tests may be done to determine the cause. A comprehensive neuropsychiatric evaluation must be completed to make an accurate diagnosis. 1. Basic laboratory examination, including CBC with differential, chemistry panel (including blood urea nitrogen, creatinine, and ammonia), arterial blood gas values, chest x-ray, toxicology screen (comprehensive), thyroid function tests, and serologic tests for syphilis. 2. Additional test may include CT scan, MRI, additional blood chemistries (heavy metals, thiamine, folate, antinuclear antibody, and urinary porphobilinogen), lumbar puncture, PET/ single photon emission computed tomography scans. 3. Complete mental status examination.
4.
Comprehensive physical examination.
Treatment: 1. Treatment is generally community focused; the goal of treatment is to maintain the quality of life as long as possible despite the progressive nature of the disease. Effective treatment is based on: Diagnosis of primary illness and concurrent psychiatric disorders. Assessment of auditory and visual impairment Measurement of the degree, nature, and progression of cognitive deficits. Assessment of functional capacity and ability for self care Family and social system assessment. 2. Environmental strategies in order to assist in maintaining the safety and functional abilities of the patient as long as possible. Pharmacologic Treatment 1. Pharmacologic therapy used for the person with DAT is directed toward the use of anticholinesterase drugs to slow the progression of the disorder by increasing the relative amount of acetylcholine. Available drugs include donepezil (Aricept), galantamine (Reminyl), rivastigmine (Exelon) and tacrine (Cognex). An NMDA-receptor antagonist memantine (Namenda) may be provided in an attempt to improve recognition. Other drugs may be used for behavioral control and symptom reduction. Agitation management: neuroleptic drugs Psychosis: neuroleptic drugs Depression: antidepressants, ECT Complications: 1. Without accurate diagnosis and treatment, secondary dementias may become permanent. 2. Falls with serious orthopedic or cerebral injuries. 3. Self-inflicted injuries 4. Aggression or violence to self, others, or property. 5. Wandering events, in which the person can get lost and potentially suffer exposure, hypothermia, injury, and even death. 6. Serious depression is demonstrated in caregivers who receive inadequate support. 7. Caregiver stress and burden may result in patient neglect or abuse. Nursing Interventions: Improving communication 1. Speak slowly and use short, simple words and phrases. 2. Consistently identify yourself, and address the person by name at each meeting. 3. Focus on one piece of information at a time. Review what has been discussed with patient. 4. If patient has vision or hearing disturbances, have him wear prescription eye glasses and/orhearing device. 5. Keep environment well lit. 6. Use clocks, calendars, and familiar personal effects in the patient’s view.
7. If patient becomes aggressive, shift the topic for a safer, more familiar one. Promoting Independence in Self-care 1. Assess and monitor patient’s ability to perform activities of daily living. 2. Encourage decision making regarding activities of daily living as much as possible. 3. Monitor food and fluid intake. 4. Weigh patient weekly. 5. Provide food that patient can eat while moving. 6. Sit with the patient during meals and assist by cueing. Ensuring Safety 1. Discuss restriction of driving when recommended. 2. Assess patient’s home for safety; remove throw rugs, label rooms, and keep the house well lit. 3. Assess community for safety. 4. Alert neighbors about the patient’s wandering behavior. 5. Alert police and have current picture taken 6. Install safety bars in the bathroom. 7. Encourage physical activity during day time Preventing Violence and Aggression 1. Respond calmly and do not raise your voice. 2. Remove objects that might be used to harm self or others. 3. Identify stressors that increase agitation. 4. Distract patient when an upsetting situation develops.
discovered. Scientists still need to learn a lot more about what causes AD. In addition to genetics and ApoE, they are studying education, diet, and environment to learn what role they might play in the development of this disease. Scientists are finding increasing evidence that some of the risk factors for heart disease and stroke, such as high blood pressure, high cholesterol, and low levels of the vitamin folate, may also increase the risk of AD. Evidence for physical, mental, and social activities as protective factors against AD is also increasing. Primary Dementia Primary dementias are degenerative disorders that are progressive, irreversible, and not due to any other condition. Specific disorders are dementia of the Alzheimer’s type (DAT) and vascular dementia (formerly multi-infarct dementia). Dementia of Alzheimer’s type demonstrates progression of symptoms from the initial stage, which is characterized by mild cognitive deficits in the area of short-term memory and accomplishment of goal-directed activity, to the final stage in which profound impairment occurs in the areas of cognition and self-care abilities. Research is ongoing. Dementia of Alzheimer’s type believed to have multiple causative factors. 1. Genetic Factors: Familial Alzheimer’s disease is associated with abnormal genes on chromosomes 1, 14, and 21. In particular, with genes located on these chromosomes (1 and 14) that encode for amyloid precursor protein which leads to mutation of the amyloid beta-peptide in plaques. A specific cholesterol-bearing protein, apolipoprotein E4 (Apoe4), is found on chromosome 19 twice as often as people with DAT as in general population. 2. Biochemical and brain structure factors: The neurotransmitter acetylcholine has been implicated in terms of relative deficit and/or receptor abnormalities as related to Alzheimer’s disease. Autopsy findings reveal presence of brain changes, that is, the presence of amyloid plaquesand neurofibrillary. Additional areas of investigation includes: slow viral infection, autoimmune processes, and head trauma. Secondary Dementia Occur as a result of another pathologic process. 1. Infection-related dementias Acquired immunodeficiency syndrome Chronic meningitis Creutzfeldt-Jakob disease Progressive multifocal leukoencephalopathy Postencephalitic dementia syndrome Syphilis Subacute sclerosing panencephalitis Tuberculosis 2. Subcortical degenerative disorders Huntington’s disease Parkinson’s disease Wilson’s disease Thalamic dementia 3. Hydrocephalus 4. Vascular dementias 5. Traumatic conditions, such as post traumatic encephalopathy and subdural hematoma. 6. Neoplastic dementias Glioma
Meningioma Meningeal carcinomatosis Metastatic deposits
7. Inflammatory conditions, such as sarcoidosis, systemic lupus erythematous, and temporal arteritis. 8. Toxic conditions, such as alcohol-related syndrome and iatrogenic dementias 9. Metabolic disorders Anemia’s Deficiency states Cardiac or pulmonary failure Hepatic encephalopathy Porphyria Uremia Introduction: Dementia is an acquired syndrome that causes progressive loss of intellectual abilities, such as memory, as well as aphasia, apraxia, and loss of executive function. Dementing disorders are characterized by gradual onset plus continuing cognitive decline that is not due to other brain disease. Screening tests can identify persons who should be referred for a complete diagnostic workup. Early diagnosis of dementia is the goal of a diagnostic workup, which is done to exclude potentially reversible causes and initiate therapy as early as possible. Short term memory impairment is usually the first symptom of dementia. Clinical diagnosis of dementia requires (1) loss of an intellectual ability with impairment severe enough to interfere with social or occupational functioning and (2) ruling out delirium. Delirium must be ruled out because cognitive impairment caused by delirium may be reversible. Mild cognitive impairment is another risk factor for dementia. Persons with mild cognitive impairment have complaints and objective evidence of memory problems, but do not have deficits in activities of daily living or in other cognitive functions and do not meet the diagnostic criteria for dementia. Mild cognitive impairment refers to a transitional state between normal aging and dementia; it is associated with an increased risk of death, greater decline in cognitive abilities, and incident, with annual conversion rate of 8.3% to Alzheimer disease. Elder persons with mild cognitive impairment who are depressed are at greater risk of converting to Alzheimer disease. Dementia may be caused by more than one mechanism, even in the same individual. An autopsy examination is necessary to confirm the diagnosis. Anatomy and Physiology of the human brain Pathophysiology of Dementia Clinical Manifestations: Dementia DSM –IV DIAGNOSIS Dementia of the Alzheimer’s type Vascular dementia Dementia due to a general medical condition Dementia due to multiple etiologies DEFINING CHARACTERISTICS Slow, insidious onset Impaired long and short term memory Deterioration of cognitive abilities – judgement, abstract thinking Often irreversible if untreated Personality changes No or slow EEG changes Diagnostic Evaluation:
Various diagnostic tests may be done to determine the cause. A comprehensive neuropsychiatric evaluation must be completed to make an accurate diagnosis. 1. Basic laboratory examination, including CBC with differential, chemistry panel (including blood urea nitrogen, creatinine, and ammonia), arterial blood gas values, chest x-ray, toxicology screen (comprehensive), thyroid function tests, and serologic tests for syphilis. 2. Additional test may include CT scan, MRI, additional blood chemistries (heavy metals, thiamine, folate, antinuclear antibody, and urinary porphobilinogen), lumbar puncture, PET/ single photon emission computed tomography scans. 3. Complete mental status examination.
4.
Comprehensive physical examination.
Treatment: 1. Treatment is generally community focused; the goal of treatment is to maintain the quality of life as long as possible despite the progressive nature of the disease. Effective treatment is based on: Diagnosis of primary illness and concurrent psychiatric disorders. Assessment of auditory and visual impairment Measurement of the degree, nature, and progression of cognitive deficits. Assessment of functional capacity and ability for self care Family and social system assessment. 2. Environmental strategies in order to assist in maintaining the safety and functional abilities of the patient as long as possible. Pharmacologic Treatment 1. Pharmacologic therapy used for the person with DAT is directed toward the use of anticholinesterase drugs to slow the progression of the disorder by increasing the relative amount of acetylcholine. Available drugs include donepezil (Aricept), galantamine (Reminyl), rivastigmine (Exelon) and tacrine (Cognex). An NMDA-receptor antagonist memantine (Namenda) may be provided in an attempt to improve recognition. Other drugs may be used for behavioral control and symptom reduction. Agitation management: neuroleptic drugs Psychosis: neuroleptic drugs Depression: antidepressants, ECT Complications: 1. Without accurate diagnosis and treatment, secondary dementias may become permanent. 2. Falls with serious orthopedic or cerebral injuries. 3. Self-inflicted injuries 4. Aggression or violence to self, others, or property. 5. Wandering events, in which the person can get lost and potentially suffer exposure, hypothermia, injury, and even death. 6. Serious depression is demonstrated in caregivers who receive inadequate support. 7. Caregiver stress and burden may result in patient neglect or abuse. Nursing Interventions: Improving communication 1. Speak slowly and use short, simple words and phrases. 2. Consistently identify yourself, and address the person by name at each meeting. 3. Focus on one piece of information at a time. Review what has been discussed with patient. 4. If patient has vision or hearing disturbances, have him wear prescription eye glasses and/orhearing device. 5. Keep environment well lit. 6. Use clocks, calendars, and familiar personal effects in the patient’s view.
7. If patient becomes aggressive, shift the topic for a safer, more familiar one. Promoting Independence in Self-care 1. Assess and monitor patient’s ability to perform activities of daily living. 2. Encourage decision making regarding activities of daily living as much as possible. 3. Monitor food and fluid intake. 4. Weigh patient weekly. 5. Provide food that patient can eat while moving. 6. Sit with the patient during meals and assist by cueing. Ensuring Safety 1. Discuss restriction of driving when recommended. 2. Assess patient’s home for safety; remove throw rugs, label rooms, and keep the house well lit. 3. Assess community for safety. 4. Alert neighbors about the patient’s wandering behavior. 5. Alert police and have current picture taken 6. Install safety bars in the bathroom. 7. Encourage physical activity during day time Preventing Violence and Aggression 1. Respond calmly and do not raise your voice. 2. Remove objects that might be used to harm self or others. 3. Identify stressors that increase agitation. 4. Distract patient when an upsetting situation develops.
