Overview of Parkinson's Disease

Parkinson's disease is a chronic, progressive neurodegenerative movement disorder. Tremors, rigidity, slow movement (bradykinesia), poor balance, and difficulty walking (called parkinsonian gait) are characteristic primary symptoms of Parkinson's disease. Parkinson's results from the degeneration of nuclei in a number of dopamine-producing nerve cells in the brainstem. Dopamine is a neurotransmitter that stimulates motor neurons, which are nerve cells that control the muscles. When dopamine production is depleted, the motor system nerves are unable to control movement and coordination. Parkinson's disease patients have lost 80% or more of their dopamine-producing cells by the time symptoms appear. In searching for a cause for Parkinson's disease, most of the attention has focused on areas of the brain called the substantia nigra and the locus coeruleus. Stages of Parkinsons Disease Stage 1: Initial Stage Unilateral limb involvement Minimal weakness Nand and arm trembling Stage 2: Mild stage Ilateral limb involvement Masklike facies Slow, shuffling gait Stage 3: moderate Disease Increased gait disturbances Stage 4: Severe Disability akinesia rigidity Stage 5: Complete Dependence

Incidence and Prevalence of Parkinson's

According to the Parkinson's Disease Foundation, Parkinson's disease affects about 1 million people in the United States and more than 4 million people worldwide. The disorder occurs in all races, but Parkinson's is somewhat more prevalent among Caucasians. Men develop the disease slightly more often than women. Symptoms of Parkinson's disease can appear at any age, but the average age of onset is 60. Parkinson's is rare in people younger than 30 years of age, and risk for the disease increases with age. It

is estimated that 510% of patients who have Parkinson's experience symptoms before the age of 40. Parkinson's disease is common in the elderly and affects one person in 20 over the age of 80.

Risk Factors for Parkinson's Disease

A genetic predisposition for Parkinson's disease is possible. In a small number of cases of Parkinson's disease worldwide, there is a strong inheritance pattern for the disorder. In these cases, the onset of the disease and its gradual development depend on a trigger, such as trauma, other illness, or exposure to an environmental toxin.

Parkinson's Disease Causes

The cause of Parkinson's disease is unknown. Many researchers believe that a combination of several factors is involved in the development of Parkinson's. These factors include free radicals, accelerated aging, environmental toxins, and genetic predisposition. It may be that free radicalsunstable and potentially damaging molecules that lack an electronare involved in the degeneration of dopamine-producing cells. Free radicals add an electron by reacting with nearby molecules in a process called oxidation. This process can damage nerve cells. Chemicals called antioxidants normally protect cells from oxidative stress and damage. If antioxidative action fails to protect dopamine-producing nerve cells, these cells may be damaged, resulting in Parkinson's disease. Dysfunctional antioxidative mechanisms are associated with older age, which suggests that the acceleration of age-related changes in dopamine production also may be a factor in Parkinson's. Exposure to an environmental toxin, such as a pesticide, that inhibits dopamine production and produces free radicals and oxidation damage may be involved in Parkinson's disease development. In some cases, the use of certain drugs can produce parkinsonian symptoms (called drug-induced parkinsonism). These drugs include chlorpromazine and haloperidol, which are prescribed for psychiatric patients, and metoclopramide, which often is used to treat stomach disorders. Changing the medication or adjusting the dosage of the drug moderates or eliminates Parkinson's symptoms in many cases. Roughly one-fifth of Parkinson's disease patients have at least one relative with parkinsonian symptoms, suggesting that a genetic factor may be involved in the disorder. Several genes that cause symptoms in younger patients have been identified. However, most cases are not thought to be caused by genetic factors alone.

Signs and Symptoms of Parkinson's

People with idiopathic Parkinson's disease may develop several symptoms over time; however, most patients do not develop all of the symptoms associated with the condition. In most cases, primary symptoms include slow movements (bradykinesia), tremor, rigidity, and parkinsonian gait. Symptoms of Parkinson's usually begin on one side of the body. Symptoms of Parkinson's can vary from day to day or even moment to moment. There often is no clear reason for this fluctuation of symptoms; however, it may be attributable to disease process or to antiparkinson medications. Primary Symptoms of Parkinson's Bradykinesia is slowness in voluntary movement. It produces difficulty initiating movement, as well as difficulty completing movement once it is in progress. The delayed transmission of signals from the brain to the skeletal muscles, due to diminished dopamine, produces bradykinesia. Bradykinesia and rigidity that affects the facial muscles can result in an expressionless, "masklike" appearance. Tremors in the hands, fingers, forearm, or foot tend to occur when the limb is at rest, but not when the patient is performing tasks. Tremor may occur in the mouth and chin as well. Rigidity, or stiff muscles, may produce muscle pain and facial masking. Rigidity tends to increase during movement. Poor balance is due to the impairment or loss of the reflexes that adjust posture in order to maintain balance. Falls are common in people with Parkinson's disease. Parkinsonian gait is the distinctive unsteady walk associated with Parkinson's disease. There is a tendency to lean unnaturally backward or forward, and to develop a stooped, head-down, shoulders-drooped stance. Arm swing is diminished or absent and people with Parkinson's tend to take small shuffling steps (called festination). Patient's with Parkinson's may have trouble starting to walk, may appear to be falling forward as they walk, may freeze in mid-stride, and may have difficulty making a turn. Secondary Symptoms of Parkinson's The progressive loss of voluntary and involuntary muscle control produces a number of secondary symptoms associated with Parkinson's. Most patients do not experience all of them, and symptoms vary in intensity from person to person.

Some secondary symptoms of Parkinson's disease include the following: Constipation Depression Difficulty swallowing (dysphagia)saliva and food may collect in the mouth or back of the throat may cause choking, coughing, or drooling Excessive salivation (hypersalivation) Excessive sweating (hyperhidrosis) Loss of intellectual capacity (dementia)late in the disease Psychosocial: anxiety, depression, isolation Scaling, dry skin on the face and scalp (seborrhea) Slow response to questions (bradyphrenia) Small, cramped handwriting (micrographia) Soft, whispery voice (hypophonia)

Pathophysiology

Nursing Diagnosis
Impaired Physical Mobility r/t neuromuscular impairment Risk for falls r/t decreased lower extremity strength and orthosthatic hypotention Risk for self-care deficit r/t neuromucular impairement Risk for impaired verbal communication r/t physiologic conditions Chronic confusion r/t denemtia Risk for imbalanced nutrition: Less than ody requirements r/t inability to ingest food due to biologic factors

Nursing Intervention
Nursing attention should focus on the physical and psychological deficit. Observe the patient's mood, cognition; organization and general well being Observe for features of depression esp. any suicidal ideas can be treated with tricyclic anti-depressants but selective sera tonin re-uptake inhibitors (SSRI) like Fluoxetine, etc. are preferred. If the patient is unresponsive or intolerant to pharmacotherapy, Electro convulsive therapy is indicated. Suicidal precautions to be followed, if the patient exhibits any suicidal ideas. In dementia, environmental modification is followed. Avoid frequent change in the environment to minimise confusion if the memory deficit is very severe, name boards and signboards by the side of the rooms and things will be very helpful. Sedatives are used if sleep related problems are noticed, when sleep hygiene is unsuccessfully. Patients should not be forced into situations in which they feel ashamed of their appearance. Encourage the patient to participate in moderate exercises, free-moving sports like swimming Sensory, rhythmic and other cues are used to keep the bradykinetic patients moving. Instruct the patients to speak slowly and clearly, and to pause and take a keep breath at appropriate levels. Advise the patient to organize thoughts before speaking and encourage the client to use facial expression and gestures if possible to assist with communication. If possible alternative methods like communication board, mechanical voice synthesizer, computer or electronic typewriter is advised.

 Patients are taught how to initiate raising from a chair by placing their hands on the arms of the chair. Patient's responses in the early stage of the disease process often are anxiety, depression or panic. Responses to protracted disease may be denial, hostility, withdrawal and dependency or in the other hand adjustment and acceptance. Relaxation therapy - The relaxation responses may be effective in decreasing a patient's anxiety and may evoke to diminish or eliminate problem behaviours related to tension based responses. Supportive individual psychotherapy to both patients and caregivers minimises distress. Caregivers inaccurately perceive the feelings of the patients. The discrepancy between caregiver's perception of patients suffering and patient's self reports, results in diagnosis of psychogenic suffering which in turn lead to stereotyping of patient's behavior. Caregivers are educated to avoid misinterpretation and misconception about the symptoms and expression of the patient and to respond, appropriately to the symptoms and problems. Family education and support are vital components as all members benefit from knowledge about course and prognosis, as well as needing assistance when assuming new roles in their relationship with the patients.

Diagnosis of Parkinson's Disease

Parkinson's disease diagnosis is based on signs and symptoms and ruling out other disorders that produce similar symptoms. A patient must have two or more of the primary symptoms of Parkinson's, one of which is a resting tremor or bradykinesia. In many cases, a diagnosis of Parkinson's is made after observing that symptoms have developed and become established over a period of time. After performing a thorough neurological exam and medical history, the neurologist may order computerized tomography (CT scan) or magnetic resonance imaging (MRI scan) to meet the other criterion for a diagnosis of Parkinson's disease: ruling out other disorders (e.g., brain tumor, stroke, focal lesions) that produce parkinsonian symptoms. Laboratory analysis (e.g., blood tests) may also be performed to detect particular blood abnormalities that may be associated with other disorders. Even experienced neurologists often find it difficult to diagnose the early stages of Parkinson's disease accurately. No blood or laboratory tests are available to aid in diagnosis, and the physician must rely on his or her observation of the patient. In many cases, this must be done over a period of time, as tremor or other classic symptoms become consistently present. Accurate diagnosis is

crucial, because other forms of parkinsonism often have similar features, but require different treatments. Parkinson's Symptoms Disease & Other Disorders with Similar

The term "parkinsonism" is used to describe the clinical features that are seen in true Parkinson's Disease, but occur because of some other disease cause (etiology). These other causes of rigidity, bradykinesia, and in some cases of tremor, include the following: Side effects of medications (e.g., antipsychotic medications, anti-nausea medications) Multiple strokes located in the basal ganglia and appropriate brain regions Progressive supranuclear palsy (disorder with Parkinsonian features, plus dementia and abnormal movements of the eyes) Shy-Drager Syndrome (disorder with Parkinsonian features plus severe orthostatic hypotension [low blood pressure when standing upright]) Wilson's Disease (genetic disorder with some Parkinsonian features, liver dysfunction, and tremors)

Medical Treatment for Parkinson's Disease

There is no cure for Parkinson's disease. Treatment centers on the administration of medication to relieve symptoms. The Food and Drug Administration (FDA) also has approved a surgically-implanted device that lessens tremors. In some severe cases, a surgical procedure may offer the greatest benefit.

Medications to Treat Parkinson's

Medication selection and dosage is tailored to each individual patient. In deciding on a treatment, the physician considers factors such as severity of symptoms, age, and presence of other medical conditions. No two patients respond identically to a particular drug or dosage level, so this process involves experimentation, persistence, and patience. As Parkinson's disease progresses, drug dosages may have to be modified and medication regimens changed. Sometimes a combination of drugs is given. Levodopa and carbidopa combined (Sinemet) is the mainstay of Parkinson's therapy. Levodopa is rapidly converted into dopamine by the enzyme dopa decarboxylase (DDC), which is present in the

central and peripheral nervous systems. Much of levodopa is metabolized before it reaches the brain. Carbidopa blocks the metabolism of levodopa in the liver, decreasing nausea and increasing the amount of levodopa that reaches the brain. Levodopa is most effective in treating bradykinesia and rigidity, less effective in reducing tremor, and often ineffective in relieving problems with balance. Side effects include nausea, especially early in treatment, low blood pressure (hypotension), and abnormal movements (dyskinesias). Slow dosage adjustment and taking medication with food can reduce these effects and using the lowest effective dose may prevent or delay the appearance of motor dysfunction. Levodopa can become ineffective over time. Depression, confusion, and visual hallucinations also may occur with these medications, especially in the elderly. Dopamine Agonists to Treat Parkinson's Dopamine agonists mimic dopamine's function in the brain. They are used primarily as adjuncts to levodopa/carbidopa therapy. In some cases, these drugs are used as monotherapy, but they are generally less effective in controlling symptoms. Side effects are similar to those produced by levodopa and include nausea, sleepiness, dizziness, and headache. Dopamine agonists include the following: Bromocriptine (Parlodel) Pramipexole (Mirapex) Ropinirole (Requip) Amantadine (Symmetryl) is an antiviral drug with dopamine agonist properties. It increases the release of dopamine and is often used to treat early-stage Parkinson's disease, either alone, with an anticholinergic drug, or with levodopa. Generally, it loses its effectiveness within 3 to 4 months. Side effects of amantadine include mottling of the skin, edema, confusion, blurred vision, insomnia, and anxiety. MAO-B Inhibitors to Treat Parkinson's Dopamine is oxidized by monoamine oxidase B (MAO-B). Rasagiline (Azilect) and selegiline (Carbex) inhibit MAO-B, increasing the amount of available dopamine in the brain. MAO-B inhibitors boost the effects of levodopa.

Side effects may include nausea, dizziness, abdominal pain, confusion, hallucinations, and dry mouth. MAO-B inhibitors are contraindicated for patients taking tricyclic antidepressants (e.g., Pamelor) , SSRIs (e.g., Prozac), or meperidine (Demerol) and other opiates. Patients who are taking MAO-B inhibitors must follow their physician's recommendations regarding a number of dietary precautions. Anticholinergics to Treat Parkinson's Anticholinergics reduce the relative overactivity of the neurotransmitter acetylcholine to balance the diminished dopamine activity. This class of drugs is most effective in the control of tremor, and they are used as adjuncts to levodopa. These drugs include the following: Benztropine mesylate (Cogentine) Biperiden (Akineton) Diphenhydramine (Benadryl) Trihyxyphenidyl (Artane)

Side effects associated with anticholinergic drugs include dry mouth, blurred vision, constipation, and urinary retention. In higher doses, these medications may impair memory. COMT (catechol-O-methyl transferase) Inhibitors to Treat Parkinson's These medications augment levodopa therapy by inhibiting the COMT enzyme, which breaks down dopamine after it is released in the brain. These drugs are only effective when used with levodopa. COMT inhibitors include entacapone (Comtan) and tolcapone (Tasmar). Side effects of these medications include vivid dreams, visual hallucinations, nausea, sleep disturbances, daytime drowsiness, headache, and dyskinesias. Carbidopa, levodopa, and entacapone are combined in Stalevo, which is available in flexible dosing and indicated for patients who experience a reduced effectiveness of their PD medication. Common side effects of Stalevo include dyskinesias and nausea, which may be controlled by altering the dosing schedule. Other side effects include the following: Abdominal pain Constipation Diarrhea

Discolored urine Dizziness Fatigue Hallucinations Hyperkinesias

The Exelon Patch (rivastigimine transdermal system) has been approved by the FDA to treat mild-to-moderate dementia associated with Parkinson's disease. This patch is applied to the skin (usually on the back, chest, or upper arm) and delivers medication continuously for 24 hours. Side effects include nausea, vomiting, diarrhea, and loss of appetite. Higher dosages of the medication increase the risk for these side effects. Other drugs that work in a similar manor include donepezil (Aricept) and galantamine (Razadyne).

Surgery to Treat Symptoms of Parkinson's Disease

Surgery may be used to control symptoms of Parkinson's disease and improve the quality of life when medication ceases to be effective or when medication side effects, such as jerking and dyskinesias, become intolerable.Not every Parkinson's patient is a good candidate for surgery. For example, if a patient never responded to, or responded poorly to levodopa/carbidopa, surgery may not be effective. Only about 10% of Parkinson's patients are estimated to be suitable candidates for surgery. Every surgical procedure carries inherent risks. Parkinson's patients who are suitable for surgery may forgo the procedure if they feel these risks outweigh the potential benefits. In some cases, Parkinson's symptoms do not improve or worsen following the operation. There are three surgical procedures for treating Parkinson's disease: ablative surgery, stimulation surgery or deep brain stimulation (DBS), and transplantation or restorative surgery. Ablative Surgery to Treat Parkinson's This procedure locates, targets, and then destroys (ablates) a clearly-defined area of the brain affected by Parkinson's disease. The goal of this surgery is to destroy tissue that produces abnormal chemical or electrical impulses that result in tremors and dyskinesias. In ablative surgery, a heated probe or electrode is inserted into the targeted area. During the procedure, it may be difficult to determine how much tissue to destroy and the amount of heat to use. It is

safer to treat a small area and risk the tremor returning or not being eliminated, than to treat a larger region and risk serious complications, such as paralysis or stroke. Types of ablative surgery include pallidotomy or thalamotomy. Pallidotomyablation in the part of the brain called the globus pallidusinvolves putting a hole (i.e., otomy) in the globe-shaped structure located deep inside the brain. This procedure is performed to eliminate uncontrolled dyskinesias. Thalamotomyablation of brain tissue in the thalamus involves creating an otomy in the structure located below the globus pallidus. The procedure is performed to eliminate tremors. A related procedure, called cryothalamotomy, uses a supercooled probe that is inserted into the thalamus to freeze and destroy areas that produce tremors. The patient remains awake during these procedures to determinine if the tremor or dyskinesia has been eliminated. A local anesthetic is used to dull the outer part of the brain and skull. The brain is insensitive to pain, so it can be manipulated and probed without causing pain. Deep Brain Stimulation (DBS) to Treat Parkinson's Deep brain stimulation targets the subthalamic nucleus, which is located below the thalamus. In DBS, the targeted region is inactivated, not destroyed, by an implanted electrode. The electrode is connected via a wire running beneath the skin to a stimulator and battery pack in the patient's chest. This procedure is reversiblejust turn off the currentand allows for precise calibrated symptom control. DBS does carry some risks. The electrode can become infected, the simulator may have to be periodically programmed, the battery must be replaced every 5 years, and the wires may break and need replacing. Battery replacement involves minor surgery. Transplantation or Restorative Surgery to Treat Parkinson's Transplantation or Restorative Surgery to Treat Parkinson's These procedures are still considered experimental for Parkinson's disease. In transplantation, or restorative, surgery dopamineproducing cells are implanted into the striatum. The cells used for transplantation may come from one of several sources: the patient's body, human embryos, or pig embryos. Using cells from the patient's body has been unsuccessful because of an insufficient supply of dopamine cells and the inability of the implanted cells to survive. To use fetal cells, between three and eight embryos are needed per procedure, and even under the most

favorable conditions, 90% of transplanted cells do not survive. This procedure is only moderately effective in some patients and usually in those younger than age 60. Preliminary studies have shown that pig embryo cells do survive transplantation and have an effect on symptoms. Stem cells, which are primitive cells that can grow into nerve cells, are able to survive and reproduce. Once they grow as nerve cells, they can be transformed into dopamine-producing cells. Stem cells are obtained from discarded blood in a newborn's umbilical cord, from the bone marrow of an adult, or from an aborted embryo. Complementary Treatments for Parkinson's A number of modalities and nutritional supplements can help relieve symptoms and improve quality of life for patients who have Parkinson's disease. It is necessary for patients to inform their physician of any over-the-counter medications, herbs, or other supplements that they use on a regular basis, because these substances can interact with medication and drug dosages may need to be adjusted. Physical therapy can help strengthen and tone underused muscles and give rigid muscles a better range of motion. The goals of physical therapy are to help build body strength, improve balance, overcome gait problems, and improve speaking and swallowing. Simple physical activity such as walking, gardening, and swimming can improve a patient's sense of well-being. Multiple studies have shown that regular exercise improves the level of function and quality of life for patients, as long as they continue to exercise. Yoga can improve flexibility and reduce the tendency of patients with Parkinson's disease to assume a stooped posture. The slow flowing movements of Tai Chi help maintain flexibility, balance, and relaxation. The Struthers Parkinson's Center in Minneapolis, which teaches a modified form of Tai Chi, consistently reports benefits achieved by patients in all stages of Parkinson's. Gentle, soothing massage techniques may provide relief from muscle rigidity and may have some neuromuscular benefit as well. Support groups provide a caring supportive environment in which patients and their loved ones can ask questions about Parkinson's, expressing their frustrations, and obtain advice about coping with and treating symptoms from people who share the same problem.

Parkinson's appears to progress more slowly in those who remain involved in activities that they enjoyed before the onset of symptoms and in those who engage in new interests.

Living with Parkinson's Disease This section is a place to share stories about Living with Parkinson's Disease. Below are entries of those who have already shared their stories. We hope that you find their experiences helpful to your own situation.

Symptoms My Husband Has

by: PJR on Mon, Feb 25 2008 My husband was diagnosed with Parkinsons in 1996. Initially, he had left hand tremor, a slower gait and changes in facial expression. As time went on, he was relatively healthy untill 2006. His medication was (and still is) Sinemet and Requip four times daily. He became incontinent,has nasal drainage, asphagia (which requires pureed food and heavy liquids..ice tea, cranberry juice and hydralyte thickened like honey. He developed daytime sleeping, probably due to the medication. His voice has become hoarse. Unfortunately, a knee replacement did not work and this has interfered with walking. At first with a cane, then a walker, then a wheelchair and now is in a nursing home as I am unable to lift him. He was extremely intelligent and well liked and it is so hard to see him when he is hallucinating. He seems to go into a different time zone, his voice changes and his personality is quite different from the gentle soul he was. These occurrences coincide with him hearing a loud noise and a flash of light. He then is confused and very tired. After several hours of rest, he is relatively normal. These times are of great anxiety to him. Since entering the nursing home he has had Aspirated Pneumonia and several bouts of urinary infections. It is notable that upon hospitalization for the last urinary infection it was found that he did not respond to cipro or several other drugs that are usually given. However there is a new drug, administered by IV called, Atazam (SP?) and that saved him as he had gone into sepsis. I am told that Parkinsons does not in itself cause death. Rather, it is from infection such as urinary, that eventually does not respond to antibiotics. In other words, what once helped him, may not be of usage again as his constitution may not be strong enough to resist the infection. I know how devastating this has been to me, and can only imagine what is ahead. I beg of the drug companies to use the donations made, and the stories told, to hasten there finding a cure for this terribly sad disease. It was interesting to see the outcry of Micheal J. Fox,s fans, but that seems to be a forgotten issue. I assure

you that the caretakers who are faced with the daily heartache of Parkinsons have not forgotten. In reading research, the likely causes of the disease are genetics and free radicals. If the estimated 5% of the population will be faced with diagnosis of Parkinsons, it is imperative that more medical intelligence be in force.