Parkinson’s Disease

Parkinson’s disease is a slowly progressive degenerative  neurologic disorder affecting the brain center that are responsible for control and regulation of movement. The degenerative or idiopathic form of Parkinson’s disease is the most common; there is also a secondary form with a known or suspected cause. The cause of the disease is mostly unknown. The disease usually first appears in the fifth decade of life and is the fourth most common neurodegenerative disease.

PATHOPHYSIOLOGY

Stores of the neuotransmitter dopamine are lost in the substantia nigra ans the corpus striatum because of a degenerative process. The loss pf dopamine stores in this area of the brain results in excitatory neurotransmitter than inhibitory neurotransmitters, leading to an imbalance that affects voluntary movement . Other neurotransmitter pathways (responsible for cell metabolism, growth, nutrition, and so forth) may be involved as well. Cellular degeneration causes impairment of the extrapyramidal tracts that control semiautomatic functions and coordinated movements. Regional cerebral blood flow  is reduced, and there is a high prevalence of dementia. Biochemical and pathologic data suggest  that patients with Parkinson’s disease and dementia may have coexistent Alzheimer’s disease.

CLINICAL MANIFESTATIONS

The three cardinal signs of Parkinson’s disease are tremor, rigidity, and bradykinesia (abnormally slow movements).

  • Impatient movement: bradykinesia includes difficulty in initiating, maintaining, and performing motor activities, muscle stiffness or rigidity
  • Resting tremors: a slow unilateral turning of the forearm and hand and pill-rolling motion of the thumb against the fingers; tremors at rest and increasing with concentration and anxiety
  • Muscle weakness
  • Hypokinesia (abnormally diminished movement), gait disturbances, flexed posture, and postural instability (loss of postural reflexes, and the freezing phenomenon)

OTHER CHARACTERISTICS

Patients tend to develop micrographia (shrinking, slow hand-writing) as dexterity declines. Additional characteristics include:

  • Dysphonia (soft, slurred, low-pitched, and less audible speech)
  • Masklike facial expression
  • Loss of postural reflexes: patients stand with head bent forward and walks with propulsive gait ( shuffling gait); difficulty pivoting and loss of balance, resulting in risk for falls.
  • Depression and psychiatric manifestaitons (personality changes, psychosis, dementia, and confusion)
  • Sleep disorders, uncontrolled sweating, orthostatic hypotension, gastric and urinary retention, and constipation

ASSESSMENT AND DIAGNOSTIC METHODS

  • Patient’s history and presence of two of the three cardinal manifestations: tremor, muscle rigidity, and bradykinesia
  • Positron emission tomography (PET) scanning
  • Neurologic examination and response to pharmacologic management

MEDICAL MANAGEMENT

Goal of treatment is to control symptoms and maintain functional independence; no approach prevents disease progression.

Pharmacologic Therapy

  • Levodopa therapy ( converts to dopamine): most effective agent to relieve symptoms; usually given in combination with carbidopa (Sinemet), which prevents levodopa breakdown.
  • Budipine is a non-dopaminergic, antiparkinson medication that significantly reduce akinesia, rigidity, and tremor.
  • Antihistamine drugs to allay tremors.
  • Dopamine agonists (eg. pergolide [Permax], bromocriptine mesylate [Parlodel], ropinirole, and pramipexole are used to postpone the initiation of carbidopa and levodopa therapy.
  • Anticholinergic therapy to control the tremor and rigidity.
  • Amantadine hydrochloride  (Symmetrel), an antiviral agent, to reduce rigidity, tremor and bradykinesia.
  • Monoamine oxidase inhibitors (MAOI’s) to inhibit dopamine breakdown
  • Anntidepressant drugs
  • Trials of catechol-O-methyltransferase (COMT) inhibitors.

Surgical Management

  • Surgery to destory a part of the thalamus (stereotactic thalamotomy and pallidotomy) to interrupt nerve pathways and alleviate tremor or rigidity.
  • Transplantation of neural cells from fetal tissue of human or animal source to reestablish normal dopamine release.
  • Deep brain stimulation with pacemaker-like brain implants shows promise but is waiting for FDA approval.

 

 

Reference:

Handbook for Brunner &Suddarth’s Textbook of Medical-Surgical Nursing 11th edition by Joyce Young Johnson

Lippincott Williams & Wilkins pp. 594-596

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