Study finds widespread sympathetic nerve damage in Parkinson's disease

For years, researchers have known that the symptoms of Parkinson's disease (PD) result from damage to a specific region of the brain. A new study shows that the disease also causes widespread damage to the sympathetic nervous system, which controls blood pressure, pulse rate, perspiration, and many other automatic responses to stress. The findings help explain the blood pressure regulation problems commonly found in PD and may lead to new treatments for the disease.

Physicians have long known that patients with PD often have incontinence and other symptoms of autonomic nervous system function, and previous studies have found evidence of sympathetic nerve damage in PD patients' hearts. The sympathetic nervous system is one component of the autonomic nervous system. However, this study is the first to show that the disease affects sympathetic nerve endings in the thyroid gland and the kidney, says David S. Goldstein, M.D., Ph.D., of the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, who led the study. It also shows that this damage is unrelated to treatment with the most commonly used Parkinson's drug, levodopa. The study appears in the April 23, 2002, issue of Neurology.*

Many people with PD develop a problem called orthostatic hypotension (OH), in which blood pressure falls suddenly when a person stands up. This condition can lead to dizziness, lightheadedness, and fainting. OH increases the risk of falls and other types of accidents, which can be disabling or even life-threatening. Patients with PD frequently have other symptoms of sympathetic nervous system failure, including intolerance to heat or cold and sexual dysfunction. However, the underlying cause of these problems has been unclear.

In the study, the researchers examined 18 patients with PD and OH, 23 patients with PD only, and 16 normal volunteers. The participants were given positron emission tomography (PET) scans of the heart, kidney,

Contact: Paul Girolami or Natalie Frazin
NIH/National Institute of Neurological Disorders and Stroke

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