Hidden Damage: Parkinson’s harm to nerves in heart may explain dizziness and fainting

Standing up suddenly can precipitate an unsteady moment as the body struggles to ratchet up blood pressure in response to the posture change. In some people, particularly those with Parkinson’s disease, a stronger woozy feeling indicates a transient low-blood-pressure condition, called orthostatic hypotension, which can lead to falls.

While the muscle rigidity and tremors of Parkinson’s disease result from cell death in parts of the brain that produce the neurotransmitter dopamine, the cause of orthostatic hypotension is less clear. Recently, scientists have found evidence suggesting that nerve endings in the hearts of Parkinson’s patients can be damaged. A new study now directly links such cardiac-nerve dysfunction with orthostatic hypotension.

Earlier work had also pointed to a role for the nervous system in the problems that many Parkinson’s patients have with their bladder and digestive tract. The new study “really expands what we know” about damage to organs regulated by the autonomic nervous system, says Robert F. Pfeiffer, a neurologist at the University of Tennessee Health Science Center in Memphis. The autonomic nervous system guides functions–such as heart rate, blood pressure, and perspiration–for which there is no voluntary control.

To assess autonomic function in Parkinson’s patients, neurocardiologist Shengting Li of the National Institute of Neurological Disorders and Stroke in Bethesda, Md., and his colleagues examined 56 volunteers, including 40 with Parkinson’s disease. The average age was 62 years. Each participant was told to blow forcefully into a tube–a test designed to boost blood pressure. For all 17 Parkinson’s patients with orthostatic hypotension, the rise in blood pressure was abnormally low, a sign of an impaired autonomic system. Only 6 of 23 Parkinson’s patients without orthostatic hypotension had such a weak response. Among the healthy controls, blood pressure rose normally. The study appears in the April 23 Neurology.

In a separate test, the scientists injected dopamine tagged with a radioactive fluorine into each volunteer. A positron emission tomography (PET) scan revealed that all 17 Parkinson’s patients with orthostatic hypotension had significantly less dopamine in the muscular left ventricle of the heart than did the healthy controls. This indicates that nerve terminals in those patients were not functioning, Li says. Roughly half the Parkinson’s patients without orthostatic hypotension had significantly less nerve-terminal function than the controls did.

The scans also revealed diminished nerve activity in the kidneys and thyroid glands of the Parkinson’s patients as compared with the controls.

Norepinephrine, a cousin of dopamine, also acts as a neurotransmitter within the autonomic nervous system. Whereas the majority of Parkinson’s patients without orthostatic hypotension had blood concentrations of norepinephrine that shot up in a normal response to standing up from a lying-down position, none of the orthostatic-hypotension patients who were tested registered such an increase, Li and his colleagues report.

Previously, some scientists had theorized that the Parkinson’s drug levodopa causes orthostatic hypotension. However, the new study suggests that the drug isn’t responsible. Among the 17 patients with orthostatic hypotension, 4 had never taken levodopa and 3 had discontinued its use.