Study finds widespread sympathetic nerve damage in Parkinson's disease

and several other organs using a chemical (fluorodopamine) that highlights sympathetic nerve endings. The researchers also measured levels of the sympathetic nerve signaling chemical norepinephrine in the blood coming from the heart and studied blood pressure responses to the Valsalva maneuver, a common test of sympathetic nervous system function in which patients blow into a tube against a resistance. The Valsalva maneuver causes a temporary decrease in the amount of blood pumped by the heart. People with a fully functioning sympathetic nervous system are able to compensate for the decrease in blood output by the heart because the brain responds by signaling the sympathetic nervous system to constrict the blood vessels. If the sympathetic nervous system is damaged, however, the blood vessels do not constrict and blood pressure progressively decreases.

The researchers found that all of the patients with PD and OH had abnormal blood pressure responses to the Valsalva maneuver and significant loss of sympathetic nerve endings in the left side of the heart. About 75 percent of the patients without OH also had lost sympathetic nerve endings in one or more areas of the heart, and six of the patients without OH had an abnormal Valsalva response. The abnormal blood pressure response to the Valsalva maneuver and loss of fluorodopamine-derived radioactivity in the heart were not seen in any age-matched normal volunteers. These findings suggest that most PD patients have at least some loss of sympathetic nerves, even if they do not develop OH, says Dr. Goldstein. In the patients who have OH, the loss of sympathetic nerves seems more widespread in the body.

The study also found that patients with PD had fewer sympathetic nerve endings in the thyroid and kidneys than the normal volunteers. PET scans of the PD patients showed normal numbers of nerve endings in the liver, spleen, and several other organs. However, patients with both PD and OH had lower n

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

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