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Parkinson's Disease

Oct 03, 20249 min read

PD is a slowly progressing neurologic movement disorder that eventually leads to disability. It affects men more than women, usually appearing in the fifth decade of life. PD may be idiopathic or degenerative (primary), but can also take a secondary form with a known or suspected cause. Most cases have unknown etiologies, but are suggested to stem from a multifactorial combination of age, environment, and heredity.

Pathophysiology

  • Degeneration of dopamine storage cells in the substantia nigra in the basal ganglia region of the brain results in decreased levels of dopamine.
  • Dopamine acts as inhibitory neurotransmitters against acetylcholine (excitatory neurotransmitters) in the neuronal pathways that project from the substantia nigra to the corpus striatum, a vital area for complex body movements. Imbalance leads to excitation and affectation of voluntary movement.
  • Symptoms appear when 60% of pigmented neurons have been lost, with striatal dopamine levels decreased by 80%.
  • Cellular degeneration impairs the extrapyramidal tracts (used in semiautomatic functions and coordinated movements).

Clinical Manifestations

PD features a gradual onset, progressing slowly over a chronic, prolonged course. Its cardinal signs are ==tremors, rigidity, bradykinesia/akinesia, and postural instability==. Two major subtypes are determined from the types of manifestation: tremor dominant, where most of the other symptoms are absent, and non-tremor dominant, featuring akinesia, rigidity, and postural instability.

  1. Tremor: a slow, unilateral resting tremor is present in the majority of patients at the time of diagnosis.
  2. Rigidity: resistance to passive limb movement characterizes muscle rigidity. Passive movement may also result in jerky increments, referred to as lead-pipe or cog-wheel movements.
  3. Bradykinesia: overall slowing of active movement. Activities take longer to finish, and initiation of movement (rising from sitting position, turning in bed) is difficult.
    • Hypokinesia is also common and may appear after tremors; thought to be an extreme form of bradykinesia.
  4. Postural Instability with associated gait problems appear due to the loss of postural reflexes, resulting in a heightened risk for falls. Balance is lost forwards (propulsion) or backwards (retropulsion).
    • The patient stands with their head bent forward and uses a “propulsive gait”.
    • Forward flexion of the neck, hips, knees, and elbows shift the center of gravity, and the patients attempt to walk forward in order to regain balance. This is a “shuffling gait”.
  5. Autonomic symptoms that include excessive and uncontrolled sweating, drooling, paroxysmal flushing, orthostatic hypotension, gastric and urinary retention, constipation, and sexual dysfunction.
    • Dysphagia is a substantial problem, with more than 50% of patients reporting choking as well as vision and olfactory changes.
    • Neurogenic Orthostatic Hypotension is found in 30% to 50% of patients.
  6. Psychiatric symptoms include depression, anxiety, dementia, delirium, hallucinations (auditory, visual), and psychosis.
    • Depression and anxiety are common (not certain if as a biophysical manifestation or as a reaction to the disorder).
    • Stress, medications, and depression contribute to the cognitive changes of diminished executive functions, attention difficulties, decreased thinking, and word-finding challenges.
    • 80% of patients with a 20 year history of PD have Dementia; a general decline in higher brain functioning.
  7. Further loss of dexterity results in micrographia (small handwriting) and a masklike, expressionless face. Dysphonia may occur as a result of weakness and incoordination of the muscles responsible for speech. This also often results in dysphagia and drooling; risks for choking and aspiration.
  8. Complications are often as a result of disordered movement: respiratory and urinary infection, skin breakdown, and fall injuries. Treatment may also have adverse results of dyskinesia or orthostatic hypotension.

Diagnostic Examination

The disease is currently diagnosed through patient history and the presence of at least two of the four cardinal manifestations (tremors, bradykinesia, rigidity, postural changes). Laboratory testing and imaging studies do not help. PET and SPECT have been helpful in advancing treatment.

Management

  1. Medical: symptomatic and maintenance of functional independence. No current medical approaches can prevent disease progression. Care is individualized based on symptoms and other needs.
  2. Pharmacologic: the mainstay of treatment. Antiparkinsonian medications increase striated dopaminergic activity, counteracting the neurotransmitter imbalance. Benefits of treatment wane over time, being most pronounced in the first year or two of treatment.
    • Levodopa is the most effective agent. It is converted to dopamine in the basal ganglia, producing symptom relief.
    • Carbidopa is often added to Levodopa to prevent it from being metabolized before reaching the brain.
    • Responses to Levodopa in most patients become dyskinetic after 5 to 10 years: facial grimacing, rhythmic jerking movements of the hands, head bobbing, chewing and smacking movements, and involuntary movements of the trunk and extremities. An “on-off” syndrome, switching from effective treatment (on) to periods of near immobility (off) may occur as response to levodopa treatment.
    • Nausea, vomiting, anorexia, decrease in BP, dystonia, dyskinesia, and confusion are other adverse effects. To minimize adverse effects, delaying the use of levodopa treatment as long as possible is done in current practice, using other drugs for symptomatic control.
  3. Surgical approaches may be considered for disabling tremors, rigidity, or severe levodopa-induced dyskinesia. Surgical procedures often only occur 10 to 13 years after diagnosis. Stereotactic procedures for permanent brain tissue destruction (thalamotomy, pallidotomy) were previously used to relieve tremors and other symptoms. Ablative tissues are no longer used, and have been replaced by deep-brain stimulation (DBS).
    • Deep-Brain Stimulation: an electrode is surgically inserted into the brain in the globus pallidus or subthalamic nucleus (bilaterally). A small shock is used to test if electrode placement is correct. If successful, this acts to increase dopamine secretion or block anticholinergic secretion, improving tremor and rigidity.
      • Eligible only for patients who experience dyskinesia in response to levodopa, have a 5-year history of PD, or have disabling tremors.
    • Experimental Neural Transplantation is being studied in an attempt to replace degenerated striatal cells.

Nursing Process

Assessment

  1. ADL and functional level of the patient: observe for degree of disability and functional changes that occur throughout the day, such as responses to medication.
    • “Do you have leg or arm stiffness?”
    • “Have you experienced any irregular jerking of your arms or legs?”
    • “Have you ever been “frozen” or unable to move?”
    • “Does your mouth water excessively? Has anyone noticed you grimacing, making faces, or perform chewing movements?”
    • “What specific activities do you have difficulty doing?”
    • “Have you had any recent falls?”
  2. Observe for quality of speech, loss of facial expression, swallowing deficits, tremors, slowness of movement (bradykinesia), weakness, forward posture, rigidity, evidence of mental slowness, and confusion.
  3. Fall risk assessment

Diagnosis

  • Impaired mobility associated with muscle rigidity and postural impairment
  • Impaired self-feeding, impaired ability to dress, impaired ability to perform hygiene, impaired self-toileting associated with tremor and muscle rigidity
  • Constipation associated with medication and reduced activity
  • Impaired nutritional intake associated with tremor, slowness in eating, difficulty in chewing and swallowing
  • Impaired verbal communication associated with decreased speech volume, slowness of speech, inability to move facial muscles
  • Difficulty coping associated with depression and dysfunction due to disease progression
  • (Collaborative) Sleep disturbances
  • (Collaborative) Psychiatric disturbances

Planning, Goals, Intervention

  1. Improve Mobility: improve functional mobility and maintain independence in ADLs
    • Progressive daily exercise improves strength, coordination, dexterity; and reduces rigidity and prevents contractures. Joint mobility and ROM are important aspects of exercise. Postural exercises are also useful for preventing postural changes.
    • Warm baths and massage relaxes muscles and relieves muscle spasm and rigidity.
  2. Enhancing Self-Care Activities: encouraging, educating, and supporting the patient during ADLs promote self-care. Environmental modifications, adaptive or assistive devices e.g. an overhead trapeze for getting up out of bed, and consultation with an occupational therapist also help.
    • Improving Bowel Elimination: resulting from smooth muscle weakness, lack of exercise, inadequate fluid intake, medications, and decreased autonomic nervous system activity. A regular bowel routine and schedule, increasing fluid intake, and moderate fiber content in diets can help. Laxatives are not suggested. Elevated toilet seats can help due to difficulties in moving from a standing to a sitting position.
    • Improving Nutrition: xerostomia, difficulty in chewing, bradykinesia, and dysphagia impede adequate nutritional intake. Risks for choking and aspiration are present due to impaired swallowing and accumulation of saliva. Aspiration may not be felt. Aspiration pneumonia may occur. Weekly weight monitoring indicate whether caloric intake is adequate. An NGT or PEG tube may be used as the disease progresses. A dietitian consultation may be required.
    • Enhancing Swallowing: patients should be put in an upright position during mealtime to reduce aspiration risk resulting from swallowing difficulties and choking. A semisolid diet with thick liquids is easier to swallow than solids. Thin liquids should be avoided. It is encouraged for the patient to consciously and voluntarily perform the swallowing sequence. Consciously swallowing can also prevent saliva buildup.
    • Encouraging the Use of Assistive Devices: electric warming tray for prolonged eating time, special utensils, stabilized plates, and non-spill cups.
  3. Improving Communication: speech disorders are present in most cases. Low-pitched, monotonous, soft-speech of patients require them to put conscious effort and attention into speaking. Facing the listener, exaggerating pronunciation, and using short sentences all help. A few deep breaths before speaking maintains breath during speech. Consultation with a speech therapist may be helpful. A small electronic amplifier can be used for low speech volume.
  4. Supporting Coping Abilities: encourage the patient and point out that activities are maintained through active participation. Patients become withdrawn, embarrassed, apathetic, inadequate, bored, and lonely. A positive self-concept is important. Allow the patient to set achievable goals and perform independently as much as possible.
  5. (Collaborative) Sleep Disturbances: planning daytime activities reduce daytime sleeping, apathy, and disinterest. Caffeine intake and nocturia should also be checked as sources of sleep disturbance.
  6. (Collaborative) Depression: monitor regularly for signs and symptoms of depression.
  7. (Collaborative) Altered sensory perception: hallucinations, psychosis, paranoid delusions may occur in late stage PD. Management includes low-dose antipsychotic drugs and avoidance of dopamine depleting medications.

Evaluation

  1. Strives towards improved mobility
    • Participates in exercise program daily
    • Walks with wide base of support; exaggerates arm swinging when walking
    • Takes medications as prescribed.
  2. Progresses toward self-care
    • Allows time for self-care activities
    • Uses self-help devices
  3. Maintains bowel function
    • Consumes adequate fluid
    • Increases dietary intake of fiber
    • Reports regular pattern of bowel function
  4. Attains improved nutritional status
    • Swallows without aspiration
    • Takes time while eating
  5. Achieves a method of communication
    • Communicates needs
    • Practices speech exercises
  6. Copes with effects of PD
    • Sets realistic goals
    • Demonstrates persistence in meaningful activities
    • Verbalizes feelings to appropriate person

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