Skip to Main Content

Source: Chen JJ, Nelson MV, Swope DM. Parkinson’s Disease. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. Accessed June 9, 2012.

  • Parkinsonism
  • Paralysis agitans
  • Shaking palsy

  • Progressive, chronic disorder of central nervous system (CNS) characterized by impaired muscular coordination and tremor.

  • Unknown; likely result of interactions between aging, genetic constitution, and environmental factors.

  • Loss of neurons and presence of Lewy bodies in substantia nigra pars compacta.
  • Degree of nigrostriatal dopamine loss correlates directly with severity of motor symptoms.
  • Reduced activation of dopamine-1 and dopamine-2 receptors results in greater inhibition of thalamus.
  • Loss of presynaptic nigrostriatal dopamine neurons inhibits thalamic activity and reduces activation of motor cortex.

  • Affects up to 1 million individuals in United States.
  • Annual incidence ranges from 10 to 120 per 100,000 persons depending on age.
  • Affects 1% of people older than age 65 and 2.5% of those older than age 80.
  • Usual age at diagnosis is 55–65 years.
  • Male-to-female ratio is 2:1.

  • Increasing age
  • Male sex
  • Heredity (close relative with disease)
  • Toxin exposure (e.g., herbicides, pesticides)

Signs and Symptoms

  • General features
    • Resting tremor
    • Muscular rigidity
    • Bradykinesia (usually asymmetric)
    • Postural instability in advanced disease
  • Motor symptoms
    • Decreased manual dexterity
    • Difficulty arising from seated position
    • Diminished arm swing during ambulation
    • Dysarthria
    • Dysphagia
    • Festinating gait
    • Flexed posture
    • “Freezing” at initiation of movement
    • Hypomimia
    • Hypophonia
    • Micrographia
  • Autonomic and sensory symptoms
    • Bladder and anal sphincter disturbances
    • Constipation
    • Diaphoresis
    • Fatigue
    • Olfactory disturbance
    • Orthostatic blood pressure changes
    • Pain
    • Paresthesias
    • Paroxysmal vascular flushing
    • Seborrhea
    • Sexual dysfunction
    • Sialorrhea
  • Mental status changes
    • Anxiety
    • Apathy
    • Bradyphrenia
    • Confusion
    • Dementia
    • Depression
    • Sleep disorders

Means of Confirmation and Diagnosis

  • At least two of the following clinical findings:
    • Limb muscle rigidity
    • Resting tremor (at 3–6 Hz and abolished by movement)
    • Bradykinesia
  • Obtain medication history to exclude drug-induced parkinsonism, for example:
    • Antipsychotics
    • Phenothiazine antiemetics
    • Metoclopramide

Laboratory Tests

  • None available to diagnose Parkinson’s disease.


  • Neuroimaging may be useful for excluding other diagnoses.

Differential Diagnosis

  • Essential tremor
  • Corticobasal ganglionic degeneration
  • Multiple system atrophy
  • Progressive supranuclear palsy
  • Creutzfeldt-Jakob disease

  • Minimize symptoms, disability, and side effects.
  • Maintain quality of life.
  • Ensure appropriate exercise and proper nutrition.
  • Educate patients and caregivers about disease, treatments, and prognosis.

  • Figure 1: Algorithm for management of early and late disease.
  • Monoamine oxidase-B (MAO-B) inhibitor (e.g., rasagiline) as monotherapy typically first treatment.
  • Either rasagiline or dopamine agonist can be used first in physiologically young patients.
  • Levodopa (e.g., carbidopa/levodopa) is preferred initial therapy for patients older, cognitively impaired, or who have moderately severe functional impairment.
  • Consider adding catechol-O-methyltransferase (COMT) inhibitor to extend levodopa duration of activity when motor fluctuations develop. Alternatively, consider adding MAO-B inhibitor or dopamine agonist.
  • Amantadine may be added to manage levodopa-induced peak-dose dyskinesias.

Figure 1.

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.