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 characteristicprimary symptomsof Parkinson's disease.

Parkinson's results from the degeneration of nuclei in a number ofdopamine-producing nerve cellsin 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 thesubstantia nigraand thelocus coeruleus.

Stages of Parkinson’s 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 5–10% 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

Agenetic predispositionfor 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 acombination of several factorsis involved in the development of Parkinson's. These factors include free radicals, accelerated aging, environmental toxins, and genetic predisposition.

It may be thatfree radicals—unstable and potentially damaging molecules that lack an electron—are 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 calledantioxidantsnormally 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 ofage-related changesin dopamine production also may be a factor in Parkinson's.

Exposure to anenvironmental 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 ofcertain drugscan produce parkinsonian symptoms (calleddrug-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 agenetic factormay 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

Bradykinesiais 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, "mask-like" appearance.

Tremorsin 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 balanceis 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 gaitis 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 thoroughneurological examandmedical history, the neurologist may ordercomputerized tomography(CT scan) ormagnetic 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 Disease & Other Disorders with Similar Symptoms

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 strokeslocated 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 ofmedicationto relieve symptoms.The Food and Drug Administration (FDA) also has approved a surgically-implanted device that lessens tremors. In some severe cases, asurgical proceduremay 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.

Levodopaand 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 effectsinclude 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 effectsare 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 effectsof 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 effectsmay 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 effectsassociated 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 effectsof 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.

Commonside effectsof 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 effectsinclude 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.