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  • Updated 03.23.2023
  • Released 04.12.1993
  • Expires For CME 03.23.2026

Parkinson disease



Parkinson disease can be challenging to diagnose and treat. In this article, the author provides an introduction to its clinical features, etiology, pathophysiology, epidemiology, and differential diagnosis. The author reviews treatment strategies in managing motor and nonmotor symptoms of Parkinson disease, including advances in pharmacologic and surgical treatments. Although Parkinson disease is a chronic progressive neurodegenerative disease, patients can attain an improved quality of life with their disease using clinical management strategies.

Key points

• Parkinson disease is a neurodegenerative disorder characterized by motor signs of bradykinesia, rest tremor, rigidity, and balance, which also affects cognition, mood, sleep, and autonomic function.

• Parkinson disease is diagnosed clinically, although SPECT imaging may be used to aid in diagnosis, and emerging biomarkers provide promise for earlier diagnosis and monitoring disease progression.

• Multiple genes have been identified that cause Parkinson disease or modify risk, and there is increasing evidence for environmental and dietary factors that modify risk.

• Parkinson disease is progressive, and moreover in most patients, long-term treatment with levodopa is complicated by the gradual emergence of dyskinesias and motor fluctuations.

• Treatment with medications and surgery remains symptomatic but improves quality-of-life and lifespan.

• Protective and restorative therapies are under development, but none are proven.

• Nonmotor symptoms include psychosis and neurogenic orthostatic hypotension.

Historical note and terminology

James Parkinson, a London physician, first described Parkinson disease in 1817 and recognized features of tremor and gait difficulties (189; 173). Parkinson discussed loss of function, but he misunderstood it as weakness (173). Not until 50 years later did Charcot describe the hallmarks of bradykinesia and rigidity (44; 173). Brissaud drew attention to midbrain lesions, but Greenfield and Bosanquet performed the most complete delineation of the selective cell loss, depigmentation, and degeneration of the substantia nigra (30; 91). In the 1960s, the discovery that dopamine was depleted in Parkinson disease, and that levodopa as the precursor to this neurotransmitter could improve symptoms, was described in landmark studies (13; 52; 113). Soon after, however, it was observed that chronic levodopa treatment produced choreoathetoid movement (dyskinesia) in some patients and that intermittent episodes of parkinsonism recurred during the day (the on-off syndrome) (51). Surgical interventions have a more recent history in Parkinson disease treatment (118) and are now valuable in managing these motor complications.

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