Deep brain stimulation for Parkinson's disease
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Treatment Overview
Deep brain stimulation uses electrical impulses to stimulate a target area in the brain. The stimulation affects movement by altering the activity in that area of the brain. The procedure does not destroy any brain tissue, and stimulation can be stopped at any time by turning off the device that supplies the electrical impulses.
Surgery is required to implant the equipment that produces the electrical stimulation. You are awake during the procedure (your scalp is numbed and you won't feel any pain) because you must work with the surgeon in placing the electrodes where they will have the most benefit. A small hole is drilled in your skull, and tiny wire electrodes are placed in your brain. A small battery-powered device (generator) similar to a pacemaker is implanted in your chest and connected to the electrodes in your brain by a wire. The procedure usually takes 3 to 4 hours, although it may take as long as 8 hours in some cases.
When the device is turned on, it sends 100 to 180 electrical pulses per minute to stimulate the specific area of the brain. You can turn the device on and off by holding a magnet against the skin over the device. Newer models can be turned on and off with a small remote control unit. The device can be programmed so that it delivers the correct level of stimulation to provide the greatest relief of symptoms.
What To Expect After Treatment
You will remain in the hospital for several days after the procedure while your doctor checks the effect of deep brain stimulation.
Why It Is Done
Deep brain stimulation may be used to relieve symptoms of Parkinson's disease, especially tremor, when they cannot be controlled with medicine. It is considered the surgical treatment of choice for Parkinson's disease because it is more effective, safer, and less destructive to brain tissue than other surgical methods.
Deep brain stimulation of the thalamus is done to treat disabling tremor caused by Parkinson's disease, as well as essential tremor.
Procedures that stimulate the subthalamic nucleus and the globus pallidus are done to help control a wider range of symptoms (in addition to tremor) and are used more often than stimulation of the thalamus.
How Well It Works
Deep brain stimulation of the thalamus is effective in reducing tremor. It does not affect slow movement (bradykinesia), stiffness (rigidity), or other symptoms.1
Deep brain stimulation of the subthalamic nucleus or the globus pallidus may:1
- Reduce tremor and, to a lesser extent, other symptoms of Parkinson's disease. Deep brain stimulation tends to have the greatest effect on tremor, but slow movement and stiffness can also be reduced and gait can be improved.
- Reduce the on-off motor fluctuations associated with long-term use of levodopa. During the course of a day, you may have “on” periods when the levodopa controls Parkinson's symptoms and “off” periods when the medicine stops working. Deep brain stimulation can reduce the length and severity of “off” periods.
- Reduce the abnormal movements (dyskinesias) that are side effects of levodopa therapy.
The practical effects of deep brain stimulation depend in part on which area of the brain receives the stimulation. Stimulation of the subthalamic nucleus reduces symptoms of Parkinson's disease, which allows people to reduce the amount of levodopa they are taking. Taking a lower dose helps reduce the abnormal movements (dyskinesias) that result from long-term levodopa therapy.
In contrast, stimulation of the globus pallidus reduces the dyskinesias associated with levodopa therapy, which allows people to increase the amount of levodopa they are taking without increasing side effects. In this case, the increased dosage of levodopa and the brain stimulation together help reduce tremor and other symptoms caused by Parkinson's disease.
Risks
Deep brain stimulation is less risky than other surgical procedures used to treat Parkinson's disease. Risks may include:
- Bleeding in the brain during the surgery, resulting in a stroke.
- Numbness, tingling, twitching, or other abnormal sensations when the device is turned on. (These usually do not last long and can be eliminated by adjusting the programming of the deep brain stimulation device.)
- Infection or skin irritation caused by the device in the chest (stimulator) or electrodes.
- A break in the wire leading from the electrode to the stimulator. Repairing the problem requires another surgery but not usually in the brain itself.
- Need for a new battery for the device. A battery typically will last about 5 years; surgery is needed to replace it. This is a relatively minor procedure and does not require surgery on the brain itself.
- Failure or malfunction of the stimulator or the electrodes.
What To Think About
A neurologist with special training in Parkinson's disease is most often the best kind of doctor to make a decision about deep brain stimulation. If you might benefit from the operation, your neurologist can refer you to a brain surgeon with experience doing the surgery.
Deep brain stimulation may be considered as an addition to levodopa therapy, not a replacement for it. It does not cure Parkinson's disease and does not eliminate the need for medicine. The surgery can help maintain and extend the benefits of levodopa therapy, but should not be considered for people with Parkinson's disease who also respond poorly to levodopa therapy.
One of the possible advantages of deep brain stimulation over "lesional" surgery for Parkinson's disease (such as pallidotomy) is that it can be reversed. Although the effects of lesional surgery, which involves creating a lesion or intentionally destroying a small portion of the brain, are permanent, the electrodes used in deep brain stimulation can be turned off or removed if they cause problems.
Complete the special treatment information form (PDF) (What is a PDF document?) to help you understand this treatment.
References
Citations
Samii A, et al. (2004). Parkinson's disease. Lancet, 363(9423): 1783–1793.
Credits
| Author | Monica Rhodes |
| Editor | Alison Allen |
| Editor | Kathleen M. Ariss, MS |
| Associate Editor | Denele Ivins |
| Associate Editor | Pat Truman, MATC |
| Primary Medical Reviewer | E. Gregory Thompson, MD - Internal Medicine |
| Specialist Medical Reviewer | Colin Chalk, MD, CM, FRCPC - Neurology |
| Last Updated | December 13, 2006 |
| Last updated: | December 13, 2006 |
|---|---|
| Author: | Monica Rhodes |
| Reviewed By: | E. Gregory Thompson, MD - Internal Medicine, Colin Chalk, MD, CM, FRCPC - Neurology |
| Editors: | Kathleen M. Ariss, MS, Pat Truman, MATC |
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