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Parkinson's Disease (PD) is a slowly progressive, degenerative, neurologic disorder that destroys certain neurons and depletes the neurotransmitter dopamine. It usually strikes adults over the age of 60, but it may affect younger people, especially following acute encephalitis or carbon dioxide, metallic, or other poisoning. People with PD typically have motor symptoms of tremor, muscle rigidity, and bradykinesia (slowed or minimal movement). Other motor symptoms often associated with PD include poorly articulated speech, a shuffling gait and stooped posture, and loss of facial expression that creates the appearance of apathy and depression (masked face).
These patients suffer from nonmotor symptoms as well, which are frequently overlooked by physicians, according to a recent review of the disease by Andrew Siderowf, M.D., of the Parkinson's Disease and Movement Disorders Center, University of Pennsylvania, whose work is supported by the Agency for Healthcare Research and Quality (K08 HS00004). In many cases, neuropsychiatric disturbances are a highly disabling aspect of the disease. Dementia troubles from 20 to 30 percent of patients, and depression afflicts 30 to 60 percent of PD patients at some point. Sensory symptoms such as numbness, aching, tingling, and muscle soreness are reported by up to 40 percent of PD patients. Other nonmotor symptoms range from sleep disturbances to sexual dysfunction and urinary incontinence.
Increasing age is the strongest risk factor for PD, with only 5 per 100,000 people under age 40 affected compared with 700 per 100,000 of those over age 70, with a modestly increased risk for men. Surprisingly, being a smoker and heavy coffee drinker seems to reduce the risk of developing PD. There is sufficient rationale for studies into the role of caffeine, and the adenosine neurotransmitter system (the site of action of caffeine) in the pathogenesis of PD. Although currently available evidence suggests that most cases of PD do not have a major genetic component, studies of families with defined genetic defects have produced insights with relevance for sporadic as well as familial PD.
See "Parkinson's Disease: Clinical features, epidemiology, and genetics," by Dr. Siderowf, in the August 2001 Neurologic Clinics 19(3), pp. 565-578.
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