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hi all

i love 'first time' findings in research!

janet

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Study Finds Widespread Sympathetic Nerve Damage In Parkinson's Disease

Tuesday, April 23, 2002  - 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, 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 norepinephrine levels in
their blood than patients with PD alone, suggesting that they had a
widespread loss of sympathetic nerve endings.

For years, neurologists have believed that OH in PD was due to treatment
with the drug levodopa.

However, several of the patients in this study who had OH had never taken
levodopa, and blood levels of levodopa were the same in patients with and
without OH.

This shows that the development of OH is unrelated to treatment with
levodopa, although it is possible that the levodopa may cause the blood
vessel walls to dilate, making the OH worse, Dr. Goldstein says.

Since significant loss of sympathetic nerve endings in the heart was found
in all the patients with OH, the study suggests that OH in PD is due to the
loss of these nerve endings.

"One implication of this finding is that if we can understand what causes
the sympathetic nerve loss, we may be able to identify the cause of the
entire disease," says Dr. Goldstein.

Since norepinephrine and dopamine are part of the same family of chemicals,
called catecholamines, the findings suggest that whatever causes the loss
of dopamine-producing nerve fibers in the brain also causes the loss of
sympathetic nerve endings in other parts of the body.

The pattern of sympathetic nerve fiber loss in the heart suggests that
these fibers gradually die back over time, Dr. Goldstein notes.

However, more study is needed to determine what causes the fibers to die.

The NINDS is a component of the National Institutes of Health in Bethesda,
Maryland, and is the nation’s primary supporter of biomedical research on
the brain and nervous system.

Source: NIH/National Institute Of Neurological Disorders And Stroke
Copyright 1995-2002 ScienceDaily Magazine
Email: [log in to unmask]
http://www.sciencedaily.com/releases/2002/04/020423080758.htm

janet paterson: an akinetic rigid subtype, albeit perky, parky
pd: 55/41/37 cd: 55/44/43 tel: 613 256 8340 email: [log in to unmask]
smail: 375 Country Street, Almonte, Ontario, Canada, K0A 1A0
a new voice: http://www.geocities.com/janet313/

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