Parkinson disease

Robert Fekete MD (

Dr. Fekete of New York Medical College received consultation fees from Acadia, Acorda, Adamas, Amneal/Impax, Kyowa Kirin, Lundbeck, Neurocrine, and Teva.

Originally released April 12, 1993; last updated April 27, 2020; expires April 27, 2023


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 current 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, using current clinical management strategies patients can attain an improved quality of life with their disease.

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 currently 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 (Parkinson 1817; Obeso et al 2017). Parkinson discussed loss of function, but he misunderstood it as weakness (Obeso et al 2017). Not until 50 years later did Charcot describe the hallmarks of bradykinesia and rigidity (Charcot 1879; Obeso et al 2017). 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 (Brissaud 1895; Greenfield and Bosanquet 1953). 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 (Barbeau 1962; Cotzias et al 1967; Hornykiewicz 2001). 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) (Cotzias et al 1969). Surgical interventions have a more recent history in Parkinson disease treatment (Jankovic 2001) and are now valuable in managing these motor complications.

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