Parkinson’s Disease

For as many as one million people living with Parkinson's Disease, everyday activities like walking or standing can become painful, sometimes even impossible. While medications may alleviate some symptoms of the disease, such as tremor, slowness of movement and muscle stiffness, many long-term sufferers are turning to surgery to help regain control of their lives.

 What is Parkinson's Disease?

Parkinson's disease is both chronic meaning that it persists over a long period of time, and progressive meaning that symptoms grow worse over time. Parkinson's disease is a disorder of the nervous system that occurs most commonly in the middle-aged and elderly (although approximately 10 percent of sufferers are under age 40). It can strike down active, vital people at the peak of their lives, as evidenced by the revelation one year ago by actor Michael J. Fox of ABC-TV’s "Spin City," that he suffers from Parkinson’s. Other well-known sufferers include Attorney General Janet Reno, former Heavyweight Boxing Champ Muhammad Ali, and Pope John Paul.

Parkinson's occurs when certain brain cells, or neurons, in an area of the brain known as the substantia nigra die or become impaired. These neurons produce an important chemical known as dopamine a chemical messenger responsible for transmitting signals between the substantia nigra and the next "messenger center" of the brain, the corpus striatum.

Normally, dopamine operates in a delicate balance with other neurotransmitters to help coordinate the millions of nerve and muscle cells involved in movement. Without enough dopamine, this balance is disrupted, resulting in tremor (characterized by trembling in the hands, arms, legs and jaw); rigidity, exemplified by stiffness of the limbs; slowness of movement; and impaired balance and coordination hallmark symptoms of Parkinson's. Studies have shown that Parkinson's patients have a loss of 80 percent or more of dopamine-producing cells in the substantia nigra. The cause of this cell death or impairment is unknown, but research in this area is alive and growing.

Common Symptoms

How is it Diagnosed?

The cause of Parkinson's remains unknown. However, theories involving oxidative damage, environmental toxins, genetic factors, and accelerated aging have been put forth as potential causes for the disease.

Presently, the diagnosis of Parkinson's is primarily based on the common symptoms outlined above. However, non-invasive diagnostic imaging, such as positron emission tomography (PET) can support the physician's diagnosis. Conventional criteria for diagnosis include: 1) the presence of two of the three primary symptoms (tremor, muscle rigidity and slowness and changes in the rhythm of voluntary movement); 2) the absence of other neurological signs on examination, such as overactivity of reflexes, inability to coordinate voluntary muscular movements, or sensory loss; 3) the absence of a history of other possible causes of Parkinsonism, such as the use of tranquilizer drugs, head trauma or stroke; and 4) responsiveness to Parkinson's medications, such as Levodopa.

Medical Therapies

Most Parkinson's patients are treated with medications to relieve the symptoms of the disease. These drugs work by stimulating the remaining cells in the substantia nigra to produce more dopamine (Levodopa drugs), or by inhibiting some of the acetylcholine that is produced (anticholinergic drugs), therefore restoring the balance between the chemicals in the brain. Anti-parkinson medications are usually quite effective, and may include:

Levodopa: This drug is often regarded as the gold standard of Parkinson's therapy. Levodopa works by crossing the blood-brain barrier, the elaborate meshwork of fine blood vessels and cells that filter blood reaching the brain, where it is converted to dopamine. Levodopa is effective in treating 90 percent of Parkinson's patients, in particular those that present with a loss of spontaneous movement and muscle rigidity. The drug, however, does not stop or slow the progression of the disease. Common side effects of Levodopa include: nausea, vomiting, low-blood pressure, and jerky movements. In addition, progressive use of Levodopa may result in the fluctuation of symptom control, shifting from full-symptom control ("on-time") to periods of reduced voluntary movement ("off-time"). Altering the dosage or frequency of Levodopa may reduce fluctuations in motor control. In addition, patients may develop "dyskinesias" or excessive involuntary movement when they take their medicine.

Bromocriptine, Pergolide, Pramipexole and Ropinirole: These drugs mimic the role of chemical messengers in the brain, causing the neurons to react as they would to dopamine. They can be given alone or with Levodopa, and may be used in the early stages of the disease or started later to lengthen the duration of response to Levodopa in patients experiencing "wearing off" or "on-off" effects. They are generally less effective than Levodopa in controlling muscle rigidity and gradual loss of spontaneous movements. Side effects may include paranoia, hallucinations, confusion, jerky movements, nausea, and vomiting.

COMT Inhibitors: This new group of medications are used to treat fluctuations in response to Levodopa. COMT is an enzyme that metabolizes Levodopa in the bloodstream. By blocking COMT, more Levodopa can penetrate the brain and, in doing so, increase the half-life of Levodopa.

Selegiline: This drug slows down the activity of the enzyme monoamine oxidase B (MAO-B), the enzyme that metabolizes dopamine in the brain, delaying the breakdown of naturally occurring dopamine and of dopamine formed from Levodopa. When given with Levodopa, Selegiline enhances and prolongs the response to the drug, thus reducing "wearing-off fluctuations." Side effects from this drug may include nausea, low blood pressure, or an inability to sleep.

Trihexyphenidyl and Benztropine: These anticholinergic drugs work by blocking acetylcholine, a chemical in the brain whose effects become more pronounced when dopamine levels drop. These medications are most useful in the treatment of tremor and muscle rigidity, as well as reducing drug-induced Parkinsonism. They are generally not recommended for extended use in elderly patients because of complications, including dry mouth, constipation, hallucinations, memory loss, blurred vision, and confusion. Amantadine. Amantadine is an antiviral drug that also helps reduce symptoms of Parkinson's disease (unrelated to its antiviral activities) and is often used in the early stages of the disease or with an anticholinergic drug or Levodopa. It is effective in treating the jerky motions associated with Parkinson's, and side effects may include a skin rash, confusion, blurred vision, and anticholinergic-type effects

When Surgery is the Answer

Generally, surgery is not the first option when treating Parkinson's patients. However, if a patient is in the later stages of the disease and symptoms are poorly controlled with medical treatment, a neurosurgical consultation is recommended. Based upon the type and severity of symptoms the patient presents, the deterioration of a patient's quality of life and overall health of the patient, surgery may be recommended.

Neurosurgeons relieve the involuntary movements of conditions like Parkinson's by operating on the deep brain structures involved in motion control - namely the thalamus, globus pallidus and subthalamic nucleus. To target these clusters, neurosurgeons use a technique called stereotactic surgery. This type of surgery requires the neurosurgeon to fix a metal frame to the skull under local anesthesia. Using diagnostic imaging, the surgeon will precisely locate the desired area in the brain and drill a small hole, about the size of a nickel. The surgeon may then create small lesions using high frequency radio waves within these structures, or may implant a deep brain stimulating electrode, thereby relieving the symptoms associated with Parkinson's.

Pallidotomy: In pallidotomy, the neurosurgeon targets a structure of the brain known as the globus pallidus - a region, about the size of a Tic Tac, involved in the control of movement. Normally, the effects of dopamine help to regulate this area of the brain. However, in Parkinson's patients, loss of dopamine leads to overactivity. Lesioning the global pallidus helps restore the balance that normal movement requires.  

Pallidotomy is performed by inserting a wire probe into the globus pallidus. Once in place, the probe uses radio waves to heat the surrounding tissue, thereby destroying the desired tissue. The goal of pallidotomy is to eliminate drug-induced dyskinesia, tremor, muscle rigidity and gradual loss of spontaneous movement, along with other motor manifestations of Parkinson's Disease. Pallidotomy is most effective in patients under the age of 65.  

Thalamotomy: In thalamotomy, a radiofrequency energy current is used to destroy a small, but specific, portion of the thalamus. The goal of thalamotomy is to permanently stop tremor by placing a small lesion in a specific nucleus of the thalamus. This is an effective treatment for tremor only. It does not treat any other symptoms of Parkinson’s Disease. It is especially useful for patients without pre-existing walking or speech problems.  

Deep Brain Stimulation: With deep brain stimulation (DBS), small electrodes are implanted in the brain and connected to a pacemaker-like device implanted under the skin of the patient's chest, just below the collarbone. The pulse-generating device sends continuous, high frequency electrical stimulation to the brain via the implanted electrodes when implanted into the thalamus. This form of stimulation helps "rebalance" the control messages in the brain, thereby suppressing tremor. Patients may turn the pulse generator on or off by passing a hand-held magnet over the device. DBS of the subthalamic nucleus or globus pallidus is effective in treating all of the primary motor features of Parkinson's, and sometimes allows for significant decreases in medication doses.

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