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Alzheimer's disease (AD) affects the mental abilities including memory, language, and cognition. Progressively it leads to dementia and death. AD usually arises in late middle age or the elderly but there is a rare familial subtype that occurs earlier. Because AD is so well-known, other causes of dementia or memory loss may be overlooked. Other possible diagnoses include normal aging (if very mild symptoms), emotional problems, fatigue, depression, and certain medical conditions such as thyroid disease, brain tumors, multi-infarct disease, or Huntington's disease. In its early stages, a correct diagnosis of AD can also be overlooked itself and misdiagnosed as other conditions such as depression, dementia, simple forgetfulness, or senility.
Signs and Symptoms:
• Early symptoms
Loss of concentration
Progressing symptoms Memory loss Language deterioration Impaired visual skills Impaired spatial skills Disorientation Confusion Poor
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Forgetting how to do everyday tasks Thinking difficulty judgment Difficulty speaking
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Indifferent attitude Apathy Anxiety Depression Aggression
Cognition disintegration Personality disintegration Suspicion Hostility Inability to function
Loss of speech Difficulty swallowing Drooling Incontinence Wandering
Normal motor function (AD affects the brain but not the body)
Urine tests Blood tests Neuropsychological tests Memory tests Cognitive tests Brain Scans: Brain CT scan Brain MRI scan Brain PET scan
Types of Alzheimer’s Disease:
Familial Alzheimer's disease - an early-onset inherited genetic form. CURABLE TYPE: Sporadic Alzheimer's disease RARE TYPE: Right parietal lobe syndrome related Alzheimer's disease
Spastic paraparesis related alzheimer's disease Two types of AD exist: familial AD (FAD), which is found in families where AD follows a certain inheritance pattern; and sporadic (seemingly random) AD, where no obvious inheritance pattern is seen. Because of differences in age at onset, AD is further described as either early-onset (younger than 65 years old) or late-onset (65 years and older). Early-onset AD is rare and generally affects people aged 30 to 60. Early-onset AD progresses faster than the more common, late-onset forms of AD.
Cerebral hypoxia After recovery from hypoxia (brought on by such conditions as carbon monoxide poisoning or acute respiratory failure), the patient may experience total amnesia for the event, along with sensory disturbances, such as numbness and tingling. Head trauma Depending on the trauma’s severity, amnesia may last for minutes, hours, or longer. Usually, the patient experiences brief retrograde and longer anterograde amnesia as well as persistent amnesia about the traumatic event. Severe head trauma can cause permanent amnesia or difficulty retaining recent memories. Related findings may include altered respirations and LOC; headache; dizziness; confusion; visual disturbances, such as blurred or double vision; and motor and sensory disturbances, such as hemiparesis and paresthesia, on the side of the body opposite the injury. Herpes simplex encephalitis Recovery from herpes simplex encephalitis commonly leaves the patient with severe and possibly permanent amnesia. Associated findings include signs and symptoms of meningeal irritation, such as headache, fever, and altered LOC, along with seizures and various motor and sensory disturbances (such as paresis, numbness, and tingling). Hysteria Hysterical amnesia, a complete and long-lasting memory loss, begins and ends abruptly and is typically accompanied by confusion. Seizures In temporal lobe seizures, amnesia occurs suddenly and lasts for several seconds to minutes. The patient may recall an aura or nothing at all. An irritable focus on the left side of the brain primarily causes amnesia for verbal memories, whereas an irritable focus on the right side of the brain causes graphic and nonverbal amnesia. Associated signs and symptoms may include decreased LOC during the seizure, confusion, abnormal mouth movements, and visual, olfactory, and auditory hallucinations. Wernicke-Korsakoff syndrome Retrograde and anterograde amnesia can become permanent without treatment in this syndrome. Accompanying signs and symptoms include apathy, an inability to concentrate or to put events into sequence, and confabulation to fill memory gaps. The syndrome may also cause diplopia, decreased LOC, head-ache, ataxia, and symptoms of peripheral neuropathy, such as numbness and tingling. Drugs
Anterograde amnesia can be precipitated by general anesthetics, especially fentanyl, halothane, and isoflurane; barbiturates, most commonly pentobarbital and thiopental; and certain benzodiazepines, especially triazolam. Electroconvulsive Therapy The sudden onset of retrograde or anterograde amnesia occurs with electroconvulsive therapy. Typically, the amnesia lasts for several minutes to several hours, but severe, prolonged amnesia occurs with treatments given frequently over a prolonged period. Temporal lobe surgery Usually performed on only one lobe, this surgery causes brief, slight amnesia. However, removal of both lobes results in permanent amnesia.
The major risk factors for AD are age and family history. Other possible risk factors include a serious head injury and lower levels of education. Scientists are also studying additional factors to see if they may cause the disease. Some of these factors include: Genetic (Inherited) Factors: Scientists believe that genetic factors may be involved in more than half of the cases of AD. For example, a protein called apolipoprotein E (ApoE) may be important. Everyone has ApoE, which helps carry cholesterol in the blood. However, the function of ApoE in the brain is less understood. The ApoE gene has three forms. One form seems to protect a person from AD, and another form seems to make a person more likely to develop the disease. Scientists still need to learn a lot more about ApoE and its role in AD. Environmental Factors: Scientists have found aluminum, zinc, and other metals in the brain tissue of people with AD. They are studying these metals to see if they cause AD or if they build up in the brain as a result of the disease. Viruses: Some scientists think that a virus may cause AD. They are studying viruses that might cause the changes seen in the brain tissue of people with AD.
AD probably is not caused by any one factor. It is more likely to be several factors that act differently in each person. For example, genetic factors alone may not be enough to cause the disease. Other risk factors may combine with a person’s genetic makeup to increase her or his chance of developing the disease
Mental stimulation Tacrine (THA, Cognex) Aricept (donepezil) - reversible acetylcholinesterase inhibitors Exelon (rivastigmine) - reversible acetylcholinesterase inhibitors Supportive care Nursing homes
AMNESIA TREATMENT Immediate attention to airway, breathing, and circulation
Prompt treatment of suspected infections and trauma:
CNS infections: Antibiotic and/or antiviral therapy
Cases with Head trauma: Surgical intervention may be necessary to evacuate space-occupying traumatic lesions; concussions are treated symptomatically, patients should refrain from contact sports until symptoms resolve control elevated intracranial pressure with head elevation moderate hyperventilation mannitol administration and/or surgical drainage
DELIRIUM TREATMENT Delirium is usually reversible with correction of the underlying cause Discontinue possible contributing medications Treat infection if present Correct metabolic or electrolyte abnormalities Pharmacologic therapy Antipsychotics (e.g., haloperidol) for hallucinations, delusions, or illusions Benzodiazepines (e.g., lorazepam) for anxiety, agitation, insomnia, or alcohol withdrawal Environmental supports (e.g., calendars, direction signs) to help with orientation Psychosocial support Physical restraints paradoxically increase patient agitation; thus, other alternatives (e.g., safe environment, door alarms) should be used initially
DEMENTIA TREATMENT Treat reversible causes (e.g., hypothyroidism, vitamin deficiency, cerebral vasculitis, neurosyphilis, HIV) Manage nonreversible etiologies, including genetic risks, health care planning, and help groups (e.g., Alzheimer's Association)
APRAXIA During your assessment, be alert for signs and symptoms of increased intracranial pressure, such as headache and vomiting. If you detect any, elevate the head of the bed 30 degrees and monitor the patient closely for altered pupil size and reactivity, bradycardia, widened pulse pressure, and irregular respirations. Have emergency resuscitation equipment nearby, and be prepared to give mannitol I.V. to decrease cerebral edema. If the patient is experiencing seizures, stay with him and have another nurse notify the physician immediately. Avoid restraining the patient. Help him to a lying position, loosen tight clothing, and place a pillow or other soft object beneath his head. If the patient’s teeth are clenched, don’t force anything into his mouth. If his mouth is open, protect the tongue by placing a soft object, such as a washcloth, between his teeth. Turn the patient’s head to provide an open airway. Prepare the patient for diagnostic studies, which may include computed tomography and radionuclide brain scans. Because weakness, sensory deficits, confusion, and seizures may accompany apraxia, take measures to ensure the patient’s safety. For example, assist him with gait apraxia in walking. AMNESIA Prepare the patient for diagnostic tests, such as computed tomography scan, magnetic resonance imaging, EEG, or cerebral angiography. Provide reality orientation for the patient with retrograde amnesia, and encourage his family to help by supplying familiar photos, objects, and music. If the patient has severe amnesia, consider basic needs, such as safety, elimination, and nutrition. If necessary, arrange for placement in an extended-care facility. CONFUSION Never leave a confused patient unattended, to prevent injury to himself and others. Take measures to ensure patient safety. Keep the patient calm and quiet, and plan uninterrupted rest periods. Correct the underlying cause of the patient's confusion.
APRAXIA Explain the disorder to the patient. Encourage him to participate in his normal activities as tolerated.
Help him overcome frustration arising from the inability to perform routine tasks by breaking each task down into separate steps, demonstrating these steps, and having the patient repeat the actions you demonstrated as taught by the physical and occupational therapists. Allow him sufficient time to perform each step. Avoid giving complex directions. Encourage family members to assist in the patient’s rehabilitation. AMNESIA Adjust your patient-teaching techniques for the patient with anterograde amnesia because he can't acquire new information. Include his family in teaching sessions. In addition, write down all instructions—particularly medication dosages and schedules—so the patient won't have to rely on his memory. CONFUSION To help the patient stay oriented, keep a large calendar and a clock visible, and make a list of his activities with specific dates and times. Always reintroduce yourself to the patient each time you enter his room. If possible, explain to the patient and his family the cause of his confusion.
Poor. Progressive deterioration from 5-20 years. Prognosis for Alzheimer's Disease: AD is a progressive disease. The course of the disease varies from person to
person. Some people have the disease only for the last 5 years of life, while others may have it for as many as 20 years. The most common cause of death in AD patients is infection.
Deaths from Alzheimer's Disease: 53,852 deaths in USA 2001 (CDC); 44,536 annual deaths (NVSR Sep 2001) Cause of death rank: 8th leading cause of death in 1999 and 2000 (CDC) Estimated mortality rate: (from prevalence and deaths statistics) Deaths: 53,852 (USA annual deaths calculated from this data: 53,852 deaths in USA 2001 (CDC); 44,536 annual deaths (NVSR Sep 2001) Incidence: 4,000,000 (USA prevalence calculated from this data: more than 4 million Americans (CDC); estimated 4 million people in the U.S (NHWIC) 1.3% (ratio of deaths to prevalence).
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