Ma. Nerizza D.

Navarro Alzheimer's Disease

Page 1

10/27/2012 Diagnostic Tests Definitive diagnosis can be made only through autopsy. Clinical evaluation Any of the above manifestations after depression, delirium, and other dementia disorders (e.g., head injury, brain tumor, alcoholism, drug toxicity, arteriosclerosis) have been ruled out; family history

--A chronic, progressive, neurologic disorder characterized by degeneration of the neurons in the cerebral cortex and subcortical structures, resulting in irreversible impairment of intellect and memory. Causes and Incidence The cause is unknown, although theories involving genetic links, neurotransmitter deficiencies, viruses, aluminum poisoning, autoimmune disease, and viruses have been advanced. Alzheimer's disease is the fourth leading cause of death among the elderly in the United States. Approximately 3% of individuals over 65 years of age show signs of the disease; the proportion climbs to 20% in those over 80 years of age. The incidence is higher in women. Disease Process Selective neuronal cells, primarily those involved in the transmission and reception of acetylcholine, degenerate in the cerebral cortex and basal forebrain, resulting in cerebral atrophy of the frontal and temporal lobes, with wide sulci and dilated ventricles. Senile plaques and neurofibrillary tangles are present. The basic pathophysiologic processes accompanying the brain damage are unknown.

Mental status examination Decreased orientation, impaired memory, impaired insight/ judgment, loss of abstraction/ calculation abilities, altered mood Computed tomography/magnetic resonance imaging Brain atrophy; symmetric, bilateral, ventricular enlargement Electroencephalogram Slowed brain wave activity, reduced voltage Treatments Surgery None Drugs Medications for treating specific symptoms or behavioral manifestations (i.e., antidepressants, stimulants, antipsychotics, sedatives); experimental drugs include cholinergic, dopamine, and serotonin precursors; neuropeptides; and transcerebral dilators General Structured, supportive, familiar environment; orientation and cueing program for daily tasks; safety program; family support and counseling; respite care; institutionalization when home care is no longer possible

Symptoms Early Short-term memory loss, impaired insight/judgment, momentary disorientation, emotional lability, anxiety, depression, decline in ability to perform activities of daily living (ADLS) Midcourse Apraxia, ataxia, alexia, astereognosis, auditory agnosia, agraphia, prolonged disorientation, progressive memory loss (longand shortterm), aphasia, lack of comprehension, decline in care abilities, insomnia, loss of appetite, repetitive behavior, socially unacceptable behavior, hallucinations, delusions, paranoia Late Total dependence in ADLs, bowel and bladder incontinence, loss of speech, loss of individuation, myoclonic jerking, seizure activity, loss of consciousness Potential Complications The end stage of Alzheimer's disease invites complications commonly associated with comatose conditions (e.g., skin breakdown, joint contractures, fractures, emaciation, aspiration pneumonia, infections).

Ma. Nerizza D. Navarro Bell's Palsy

Page 2

10/27/2012 Diagnostic Tests Diagnosis is based on clinical examination and history of onset. Treatments Surgery Hypoglossal: facial nerve anastomosis to restore partial facial function if none has returned by 6-12 months Drugs Methylcellulose drops for affected eye; analgesics as required for pain General Patching of affected eye; stimulation of faradic nerve and physical therapy to prevent facial contracture

--Unilateral facial paralysis with sudden loss of the ability to use the muscles that control expression on one side of the face. Causes and Incidence The cause is unknown but is thought to be related to a virus or immune disorder. Most individuals are 20 to 60 years of age, and men and women are affected equally. Disease Process Cranial nerve VII (facial nerve) is compressed at the temporal bone pathway by edema produced by an unknown cause. As a result, the muscles controlling expression on one side of the face are paralyzed. Symptoms Facial weakness, numbness and heaviness, pain behind the ear, followed by inability to work facial muscles on one side. The extent of the symptoms depends on the severity of compression; symptoms can include inability to wrinkle the forehead, upward rolling of the eyeball, inability to close the eyelid, and unilateral lack of smile or frown expression. Taste, lacrimation, and salivation may also be affected. Potential Complications Facial contractures, corneal ulceration, and synkinesia are possible complications. Paralysis may be transient or permanent. Any return of function usually occurs in 1 to 6 months.

Ma. Nerizza D. Navarro Parkinson's Disease

Page 3

10/27/2012 Symptoms Early Infrequent blinking; lack of facial expression; deliberateness of speech; impaired postural reflexes, particularly in the arm; resting pill-rolling tremor of one hand that is absent during sleep Midcourse Progressive rigidity, slowness and poverty of movement, difficulty initiating movement; muscle aches and fatigue; masklike, openmouthed facial expression; stooped posture; gait begins slow and shuffling and quickens to a run with a forward lean; hypophonic speech with stuttering dysarthria; drooling; dysphagia; forgetfulness; resting tremors of lips, jaw, tongue, and limbs; depression Late Severe postural instability; urinary retention; orthostatic hypotension; paranoia with visual hallucinations; delirium; dementia Potential Complications Injury from falls is a common threat. Other complications include aspiration pneumonia, drug reactions, and disuse syndrome. Diagnostic Tests The diagnosis is based primarily on the pattern of clinical manifestations and must be distinguished from individuals with essential tremor in which the tremor is action related and without facial or gait involvement. Treatments Surgery Stereotactic thalamotomy to alleviate tremors and rigidity in drug-resistant individuals Drugs Antiparkinsonian agents such as levodopa, Sinemet, Artane, Cogentin, Parsidol, and Parlodel to reduce tremor and rigidity; antihistamines and anticholinergics to extend the effects of levodopa; antidepressants for depression; anticholinergics with neuroleptics to prevent parkinsonism General Long-term physical therapy to maintain muscle tone, function, and range of motion, gait training, and transfer training; occupational therapy to maintain activities of daily living and teach safety skills; speech therapy to evaluate and improve swallowing abilities, reduce dysarthria, and strengthen facial muscles; warm baths and massage to relax muscles; consistent exercise program; assistive devices (canes, walkers, wheelchairs, electric lift chairs, grab bars, raised toilet seats, bath seats, eating and hygiene devices); counseling for depression and long-term adaptation; measures to prevent skin breakdown, urinary tract infections, falls, and corneal abrasions; deep breathing to maintain vital capacity; balanced, low-protein diet; bowel and bladder programs; treatment of underlying cause in secondary parkinsonism

--A slowly progressive, degenerative neurologic disorder characterized by slow, impoverished movement; muscle rigidity; resting tremor; and postural instability. Causes and Incidence Primary parkinsonism is idiopathic, whereas secondary forms of the disease can be caused by drugs (neuroleptics, reserpine, metoclopramide, tetrabenazine, N-MPTP [a byproduct of heroin synthesis]); toxins (carbon monoxide, carbon disulfide, manganese); structural lesions of the midbrain or basal ganglia; vascular lesions of the striatum from repeated head trauma; and in rare cases encephalitis. Parkinsonism is the fourth most common neurodegenerative disease of the elderly. It affects about 1% of those over 65 in the United States, and an estimated 40,000 cases are diagnosed each year. Men and women are equally affected; the mean age of onset is 57 years, and peak onset is in the seventh decade. Disease Process Some agent or event triggers a degeneration and loss of pigmented neurons in the substantia nigra, locus ceruleus, and other brainstem dopaminergic cell groups. The loss of these neurons leads to a depletion in neurotransmitter dopamine and interferes with the motor production of the basal ganglia. Interneuronal inclusion bodies (Lewy bodies) are left in surviving pigmented neurons and serve as biologic markers of the disease. Clinical manifestations emerge only after 75% to 80% of the dopamine innervation has been destroyed.

Ma. Nerizza D. Navarro Guillain-Barre Syndrome

Page 4

10/27/2012 Potential Complications About 5% of affected individuals die of respiratory failure. Another 10% have permanent residual neurologic deficits. About 90% of survivors make a full recovery, but the recovery time may be as long as 3 years. Diagnostic Tests The diagnosis is based on the clinical presentation and cerebrospinal fluid samples, which show an increase in protein without an increase in lymphocyte count. Electromyography produces abnormal nerve conductionresults. Treatments Surgery Tracheostomy to provide ventilation in the event of respiratory failure Drugs Immunoglobulin given IV to counteract neurologic defect; narcotic analgesics for pain; prophylactic antiinfectives Corticosteroids are contraindicated because they worsen the ultimate outcome General Plasma exchange to speed recovery of neurologic deficit; respiratory monitoring and mechanical ventilation for respiratory paralysis; cardiac monitoring for sinus tachycardia, bradyarrhythmia; communication systems if ventilator is used or with facial paralysis; passive range-of-motion exercises; turning to prevent contracture and skin breakdown; rehabilitation to aid neurologic recovery; counseling and support of individual and family for long-term adaptation

--A rapidly progressive, acute inflammatory demyelinating polyneuropathy characterized by muscle weakness and paralysis of the extremities and possible respiratory paralysis with abnormal sensation and loss of reflexes. Causes and Incidence The cause is unknown, but Guillain-Barre syndrome (GBS) is hypothesized to be an autoimmune disorder involving sensitization of peripheral nerve myelin. It is thought to be connected to a previous nonspecific infection and has been associated with inoculation for the swine flu. The incidence of GBS in the United States is 1.7 per 100,000 individuals, and the disorder occurs across age and gender lines. Disease Process Mononuclear cells infiltrate the peripheral nervous system and set up an inflammatory response in the blood vessels of the cranial and spinal nerves. Demyelination of the peripheral nerves results, causing muscle weakness that begins in the lower extremities and ascends through the body in a symmetric fashion. Respiratory paralysis and facial weakness occur in 30% to 40% of cases. In some cases axonal destruction can cause atrophy in distal muscles and permanent neurologic impairment. Symptoms The first sign is symmetric muscle weakness in the distal extremities accompanied by paresthesia. This weakness spreads upward to the arms and trunk and then to the face. This ascension usually peaks about 2 weeks after onset. Deep tendon reflexes are absent. Difficulty chewing, swallowing, and speaking may occur, and respiratory paralysis may develop. Bladder atony, postural hypotension, tachycardia, and heart block may be seen. Deep, aching muscle pain is also common.