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Autonomic neuropathy

Autonomic neuropathy is a group of symptoms that occur when there is damage to nerves that regulate blood pressure, heart rate, bowel and bladder emptying, digestion, and other body functions.

Causes

Autonomic neuropathy is a form of peripheral neuropathy. It is a group of symptoms, not a specific disease. There are many causes.

Autonomic neuropathy involves damage to the nerves that run through a part of the peripheral nervous system. The peripheral nervous system includes the nerves used for communication to and from the brain and spinal cord (central nervous system) and all other parts of the body, including the internal organs, muscles, skin, and blood vessels.

Damage to the autonomic nerves affects the function of areas connected to the problem nerve. For example, damage to the nerves of the gastrointestinal tract makes it harder to move food during digestion (decreased gastric motility).

Autonomic neuropathy affects the nerves that regulate vital functions, including the heart muscle and smooth muscles.

Damage to the nerves supplying blood vessels causes problems with blood pressure and body temperature.

Autonomic neuropathy is associated with the following:

Symptoms

Symptoms vary depending on the nerve(s) affected. They usually develop gradually over years.

Symptoms may include:

Digestive tract

Heart

Urinary tract

Other symptoms

Exams and Tests

A medical history and general physical exam are critical. A brain and nervous system (neurological) examination may show evidence of injury to other nerves. However, it is very difficult to directly test for autonomic nerve damage.

Signs of autonomic neuropathy include:

Occasionally, other symptoms may indicate a problem in the function of the autonomic nervous system, including:

Special measurements of sweating and heart rate are called "autonomic testing" and can assist in diagnosis and treatment.

Other tests include:

Other tests for autonomic neuropathy are based on the suspected cause of the disorder, as suggested by the history, symptoms, and the way symptoms developed.

Treatment

Treatment is supportive and may need to be long-term. Several treatments may be attempted before a successful one is found.

Various strategies may be used to reduce symptoms in the feet, legs, and arms. These include:

Treatments for reduced gastric motility include:

Diarrhea, constipation, bladder problems, and other symptoms are treated as appropriate. These symptoms may respond poorly to treatment. Drugs that block bladder contractions may be used to help with urinary control problems.

Phosphodiesterase type 5 (PDE-5) drugs, such as sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) are safe and effective for treating impotence in patients with diabetes.

Outlook (Prognosis)

The outcome varies. If the cause can be found and treated, there is a chance that the nerves may repair or regenerate. The symptoms may improve with treatment, or they may continue or get worse, even with treatment.

Most symptoms of autonomic neuropathy are uncomfortable, but they are rarely life-threatening.

Possible Complications

When to Contact a Medical Professional

Call for an appointment with your health care provider if you have symptoms of autonomic neuropathy. Early symptoms might include:

Early diagnosis and treatment increases the likelihood of controlling symptoms.

Prevention

Preventing or controlling disorders associated with autonomic neuropathy may reduce the risk. For example, diabetics should closely control blood sugar levels. Alcoholics should stop drinking.

Alternative Names

Neuropathy - autonomic

References

Hunt D. American Diabetes Association (ADA). Standards of medical care in diabetes--2008. Diabetes Care. 2008;31:S12-S54.

Vardi M, Nina A. Phosphodiesterase inhibitors for erectile dysfunction in patients with diabetes mellitus. Cochrane Database Syst Rev. 2007;24(1):CD002187.

Benarroch E, Freeman R, Kaufman H. Autonomic nervous system. In: Goetz CG, eds. Textbook of Clinical Neurology. 3rd ed. Philadelphia, Pa: Saunders Elsevier; 207: chap 21.

Update Date: 9/25/2008

Updated by: Daniel B. Hoch, MD, PhD, Assistant Professor of Neurology, Harvard Medical School, Department of Neurology, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.


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