Parkinson Disease (PD)

Pathophysiology

Progressive neurodegenerative disease

Can be primary , secondary or idiopathic

Separated into 5 stages according to symptoms and degree of disability

Debilitating disease affecting motor ability and is characterized by four cardinal symptoms: tremor, rigidity, bradykinesia or akinesia, and postural instability.

Widespread degeneration of the substantia nigra leads to decreased dopamine in the brain. Decreased dopamine causes loss of ability to refine voluntary movement.

Large numbers of excitatory ACH-secreting neurons remain active, creating an imbalance between excitatory and inhibitory neuronal activity.This prevents the person from controlling or initiating voluntary movement.

PD reduces the sympathetic nervous sytem influence on the heart and blood vessels.

PD

Stage 1

Initial stage:

• Unilateral limb involvement
• Minimal weakness
• Hand and arm trembling

PD

Stage 2

Mild stage:

• Bilateral limb involvement
• Masklike facies
• Slow, shuffling gait

PD

Stage 3

Moderate Disease:

• Postural instability
• Increased gait disturbances

PD

Stage 4

Severe disability:

• Akinesia
• Rigidity

PD

Stage 5

PD

Posture Manifestations

• Stooped posture
• Flexed trunk
• Fingers abducted and flexed at the metacarpophalangeal joint
• Wrist slightly dorsiflexed

PD

Gait Manifestations

• Slow and shuffling
• Short, hesitant steps
• Propulsive gait
• Difficulty stopping quickly

PD

Motor Manifestations

• Bradykinesia
• Muscular rigidity
• Akinesia
• Tremors
• "Pill-rolling" movement
• Masklike facies
• Difficulty chewing and swallowing
• Uncontrolled drooling
• Fatigue
• Difficulty getting into and out of bed
• Reduced arm swinging on one side of the body when walking
• Micrographia

PD

Speech Manifestations

• Soft, low-pitched voice
• Dysarthria
• Echolalia
• Hypophonia

PD

Autonomic Dysfunction Manifestations

• Orthostatic hypotension
• Excessive perspiration
• Oily skin
• Seborrhea
• Flushing
• Changes in skin texture
• Blepharospasm

PD

Psychosocial Manifestations

• Emotionally labile
• Depressed
• Paranoid
• Easily upset
• Rapid mood swings
• Cognitive impairments
• Delayed reaction time
• Sleep disturbances

PD

Complications

• Dementia-developed later as disease progresses
•  Cognitive problems and thinking difficulties- occur in the later stages of Parkinson's disease
• Sleep problems and sleep disorders-(waking up frequently throughout the night, waking up early or suddenly falling asleep during the day, or rapid eye movement sleep behavior disorder — acting out your dreams)
• Bladder problems-may cause inability to control urine or having difficulty urinating
• Constipation- primarily due to a slower digestive tract
• Sexual dysfunction- decrease in sexual desire or performance

• Vision Problems-impaired color perception and contrast sensitivity. These problems progress and can impair motor functioning.

PD

Outcomes

• The Patient can participate in training programs, joint contractures did not occur, increased muscle strength and the client indicates an act to increase the mobility
• The patient can indicate a change of life for the needs of taking care of themselves, clients are able to do self-care activities in accordance with the level of ability, and identify personal / community that can help.
• The patient will maximize the ability to communicate.
  
  
  
  

PD

Interventions

• Assess existing mobility and the observation of increased damage-to determine baseline information.
• Administer medications promptly on schedule to maintain continuous therapeutic drug levels.
• Monitor for side effects of medications.
• Conduct training program increases muscle strength.
• Encourage warm bath and massage the muscle- to relax muscles.
• Help clients to perform ROM exercises, self-care as tolerated- increases muscle strenght and decreases complications of disease
• Collaboration physiotherapists/physical therapy/ occupational therapy to keep the patient as mobile and as independent as possible.
• Allow the patient time to perform ADLs and mobility skills-allows patient to feel in control and decreases stress
• Schedule appointments and activities late in the morning to prevent rushing the patient, or schedule them at the time of teh patient's optimal level of functioning.
• Refer to speech therapy.
• Teach clients to use facial exercises and breathing methods to correct the words, volume, and intonation-eases ability to speak
• Deep breath before speaking to increase the volume and number of words in sentences of each breath.
• Allow the patient extra time to respond to questions.
• Provide high-protein, high-calorie foods or supplements to maintain weight.
• Recognize that Parkinson disease affects the patient's body image. Focus on patient's strengths.

PD

Drug Therapy

Dopamine Agonists

Catechol O-methyltransferases (COMTs)

Monamine oxidate type B inhibitors

MAOIs

PD

Labs/Diagnostics

Diagnosis of PD is made of the basis of clinical findings after other neurologic diseases are eliminated

No specific diagnostic tests

Cerebrospinal fluid (CSF) may show a decrease in dopamine levels although the results of the studies are usually normal.

MRI

Single-photonemission computed tomography (SPECT)-allows the measurement of the amount of dopamine releasing neurons.

Positron emission test (PET)-provide 3D images of the brain which allows one to analyze the unique brain of each patient.

http://www.parkinsons.org/parkinsons-diagnosis.html

Ignatavicius, D., & Workman, L. (2010). Medical-surgical nursing patient-centered collaborative care. (6 ed., Vol. 2, pp. 965-969). St. Louis: Missouri.

Dopamine Agonists

• Mimic dopamine by stimulating dopamine receptors in the brain.
• Most effective during the first 3-5 years of use.
• Fewer incidents of dyskinesias and "wearing off" phenomenon

Adverse effects: orthostatic hypotension, hallucinations, sleepiness, and drowsiness

PD

Teaching

• Teach patients on dopamine agonists to avoid operating heavy machinery or driving if they experience adverse effects.
• Teach the patient and family taking levodopa-carbidopa to give the drug before meals to increase absorption and transport across the blood-brain barrier.
• Teach patients taking MAOIs about the need to avoid foods, beverages, and drugs that contain tyramine, including aged, smoked, or cured foods and sausage. Also avoid red wine and beer to prevent severe headache and life-threatening hypertension. Continue restrictions for 14 days after drug is discontinued.
• Teach patients about drug tolerance and drug toxicity
• Teach patients about drug holidays
• Proper exercise and ambulation
• Self-management
• Injury prevention
• Nutrition
• Psychosocial support
• Enhancing communication
• Teach patient and family to monitor sleeping pattern and discuss fall risk and risk for injury
• Teach patient to avoid concentrating on their feet when walking to prevent falls
• Remind UAP and teach the family to be careful when serving or feeding the patient
• Weekly weight

Action: Increases dopamine levels

Side effects include: nausea, vomiting, hallucinations, paranoia, compulsive behaviour, drowsiness, long-term use results in dyskinesias

Catechol o-methyltransferases inhibitor

Action: Block COMTs enzymes that inactivate dopamine, thus prolonging the action of levodopa.

Benifits of combinations is that the disease is treated in several ways.

Adverse effects include:

• Accumulation of Levodopa in cells which can cause dyskinesias
• Psychosis
• Diarrhea
• Abdominal pain
• Dryness of the mouth
• Urine discoloration
• Orthostatic hypotension

MAO-B inhibitor

Action: Slow the main type B of monamine oxidase in the brain, increasing dopamine concentrations and helping reduce the clinical manifestations of PD.

Side effects include:

• Insomnia
• Hallucinations
• Orthostatic hypotension

Dopamine receptor antagoinist

Used when other drugs are no longer effective

Action: Stimulates dopamine receptors in the brain promoting the release of dopamine

Side effects: Cold sensitivity in fingers and toes; constipation; diarrhea; dizziness; drowsiness; dry mouth; fatigue; headache; indigestion; light-headedness; loss of appetite; nausea; stomach cramps; stuffy nose; vomiting.

Antiviral

Action: Potentiates the action of dopamine in the CNS.

• Prevents penetration of influenza A virus into host cell.

• Relief of Parkinson's symptoms.

• Prevention and decreased symptoms of influenza A viral infection.

Side effects: Ataxia, dizziness, insomnia, anxiety, confusion, depression, drowsiness, psychosis, seizures, urges, nausea, vomiting, anorexia, constipation, blurred vision, dry mouth, dyspnea, hypotension, HF, edema, urinary retention, mottling, livedo reticularis, melanoma, rashes,leukopenia, neutropenia.
Has antiParksinson benefits

May be given early in disease to reduce symptoms

May be prescribed with Sinemet to reduce dyskinesias

Anticholinergic drug

Used for severe motor symptoms such as tremors and rigidity

Avoid use in older adults

May cause acute confusion, urinary retention, constipation, dry mouth, and blurred vision.

Used to control symptoms of PD

Target area within pallidum identified by CT or MRI.

The stereotactic head frame is place on the patient.

IV sedation is given and a burr hole is made into the cranium.

An electrode is inserted into the target area.

The target area receives a mild electrical stimulation, and the patient's reaction is assessed for reduction of tremor and rigidity.

When the probe is in the ideal location, a permanent lesion is mad to destroy the tissue.

Patient is monitored in postanesthesia for 1 hour and returns to inpatient unit.

Used when drug therapy is no longer effective

A thin electrode is implanted in the thalamus or subthalamus and then connected to a "pace maker" that delivers electrical current to interfere with "tremor" cells. The electrodes are connected to an implantable pulse generator that is placed underneath the skin the the chest

The patient uses a magnet placed over the IPG to adjust the settings and to check the battery status

Experimental and highly controversial procedure

Fetal substantia nigra tissue, either human or pig, is transplanted into the caudate nucleus of the brain.

Improves motor symptoms without dykinesias