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Parkinson's Disease

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Treatments for Parkinson's Disease

Conventional Western Treatment

At present, there is no cure for Parkinson's disease. But a variety of medications and therapies provide dramatic relief from the symptoms. There are two types of Parkinson's disease treatments, pharmacologic and surgical. Drugs remain, by far, the most common choice, but surgery, particularly pallidotomy and thalamotomy, has become increasingly popular in the past several years. Novel experimental procedures are being studied.

Usually, drug therapy will be tried first. Surgical interventions are performed only if the person does not respond to medications or the doctor feels that the quality of life can be improved substantially by non-drug interventions, such as when the symptoms get worse despite trying all available medicines.

Today, levodopa therapy remains the gold standard of symptomatic treatment for Parkinson's disease. However, long-term therapy with levodopa is less than satisfactory as disability continues to progress and most patients develop levodopa-associated motor fluctuations and dyskinesia within a few years of treatment. Many patients ultimately develop disability due to difficulty with balance and cognition. For this reason, much research in Parkinson's disease today focuses on how to forestall disability and maintain or improve function over the long-term. New combination druga and surgical procedures available.

There is considerable differences of opinion concerning whether the patient should be started immediately on drugs or wait till the disease has progressed. As noted, levodopa loses effectiveness and develops long term complications after 4-5 years. So, the doctors do not want to lose the window of opportunity. (Some prefer starting early on levodopa therapy at a lower dose and increasing the dosage as needed. Some doctors keep levodopa at very low levels by using other medicines in combination. Still others delay levodopa therapy as much as possible by using alternative drugs.) Newer drugs are available that provide earlier protection before levodopa therapy. The consensus is that a patient should see a doctor at the first opportunity if he/she suspects Parkinson's disease as early interventions are very beneficial.

The basic categories of therapies used to treat Parkinson's disease

Parkinson's Disease Treatments can be divided into three categories:

a) symptomatic

b) neuroprotective, and

c) restorative.

Symptomatic therapies: These therapies improve signs and symptoms without affecting the underlying disease state. Degeneration of the substantia nigra in Parkinson's disease causes a dopamine deficiency in the striatum.

Levodopa increases dopamine concentration in the striatum, especially when its peripheral metabolism is inhibited by a peripheral decarboxylase inhibitor (PDI). Levodopa/PDI therapy is currently the gold standard of symptomatic therapy for Parkinson's disease.

COMT (Catechol-O-methyltransferase) inhibitors enhances levodopa treatment as they inhibit levodopa's peripheral metabolism, thereby enhancing its bioavailability. They are a new class of medications that slow the peripheral metabolism of levodopa and thereby make more of the drug available for transport across the blood-brain barrier over a longer period.   Examples are: Toicapone and Entacapone.

Selegiline increases dopamine activity in the brain by inhibiting its metabolism.

Dopamine agonists provide symptomatic benefit by directly stimulating post-synaptic striatal dopamine receptors. Examples are: Bromocriptine, Pergolide, Ropinirole, Pramipexole and Cabergoline. . Dopamine agonists are effective as monotherapy early in the course of Parkinson's disease and as an adjunct to levodopa in more advanced stages. Currently there is great interest in determining whether the use of a dopamine agonist early in the course of the disease, with the addition of levodopa later when necessary, can yield a better long-term outcome than levodopa alone.

Other medications used in the treatment of Parkinson's disease include amantadine, which augments dopamine release and anticholinergics such as trihexyphenidyl and benztropine, which block striatal cholinergic function.

Neuroprotective therapies: These therapies slow neuronal degeneration, thereby delaying disease progression. An example is selegiline, a monoamine oxidase-B (MAO-B) inhibitor. Selegiline inhibits the oxidative metabolism of levodopa and may reduce oxidative stress and free radical formation.

Restorative therapies: These therapies aim to replace lost neurons. One approach to replacing lost neurons is the transplantation of embryonic tissue. Transplanted embryonic tissue may survive, restore neuronal connections, increase dopamine concentration and improve function. Genetically engineered cells, animal dopaminergic cells, and cells from other parts of the human body are being developed for transplantation and may also have restorative effects.

Surgical Methods

There are a number of innovative surgical treatments for Parkinson's Disease.

Thalamotomy was widely used in the treatment of Parkinson's disease about 30 years ago. The procedure, however, quickly fell out of favor after levodopa therapy was introduced.  In the past few years, however, interest has been renewed in surgical interventions for Parkinson's disease because existing techniques have been refined and shown to benefit many patients who are not responding adequately to drug therapy. Thalamotomy and thalamic stimulation are effective for ameliorating medically refractory tremor. Pallidotomy and pallidal stimulation alleviate dyskinesias. Stimulation of the subthalamic nucleus holds great promise for smoothing motor fluctuations, lessening dyskinesias, and improving signs of Parkinson's disease. Two of the better-known experimental procedures are the transplantation of neural tissue into the brain, which has produced some promising results, and deep brain stimulation.


Thalamotomy, a surgical procedure that destroys a specific group of cells in the thalamus, the brain's communications center, is aimed at the 5 to 10 percent of Parkinson's patients with disabling tremor in the hand or arm. It reduces or eliminates tremor in as many as 90 percent of patients.

During thalamotomy a stereotactic lesion is created in the thalamus. Thalamotomy is performed only when the patients do not respond to drug therapy. The candidates for the procedure are typically younger than 70 and must be free from dementia.

The most common complications of thalamotomy are ataxia, hemiparesis, and hemihypesthesia. Other possibilities include confusion and postural instability. Bilateral thalamotomy worsens dysarthria and dysphagia in up to one half of patients.


In pallidotomy, a surgeon makes a tiny hole in the skull and uses a tiny electric probe to destroy a small portion of the globus pallidus, which experts believe is overactive in Parkinson's patients. Before operating, the surgeon maps the patient's brain with imaging techniques such as magnetic resonance to determine precisely where the probe should go. The patient is kept awake, but under sedation, so the surgeon can note responses to stimuli. Though both sides of the brain have a globus pallidus, pallidotomies typically are performed on one side at a time. After the patient has recuperated, a second procedure is done if needed.

Pallidotomy has been found effective in improving rigidity, bradykinesia, and dyskinesia. It is less useful for correcting gait disturbance, tremor, and falling. The patients who tend to benefit most from the pallidotomy procedure are younger than 70 and suffering from disabling dyskinesia despite a generally good response to levodopa. The procedure is not typically performed in patients with dementia.

Complications of pallidotomy are rare but may include hemiparesis, stroke, or vision defects. Bilateral pallidotomy has been linked with dysphagia, impaired speech, or significant cognitive decline. Because of these severe complications, unilateral pallidotomy is the preferred procedure.

Deep Brain Stimulation

In this procedure, an implantable stimulator is placed in the globus pallidus or thalamus. The stimulator emits an electric current, which is supplied by an external pacer similar to those used for cardiac patients. The long-term efficacy of Deep Brain Stimulation has yet to be determined, but preliminary studies suggest it helps relieve or improve tremor in the majority of patients with Parkinson's disease who receive it. Deep Brain Stimulation also appears effective for reducing dyskinesia but tends to have little or no effect on rigidity and bradykinesia.

Neural Tissue Transplantation

This procedure involves transplanting neural cells that produce dopamine into the corpus striatum. It was first attempted about 10 years ago but was fell out of favor. Recently, researchers have been studying neurotransplantation using fetal nigral cells, which has been found to improve symptoms in a few patients.

Future Outlook

A number of potential Parkinson's treatments in research stage show much promise. They include:

Neurotrophic proteins -- These appear to protect nerve cells from the premature death that prompts Parkinson's. One hurdle is
getting the proteins past the blood-brain barrier.

Neuroprotective agents -- Researchers are examining naturally occurring enzymes that appear to deactivate "free radicals,"
chemicals some scientists think may be linked to the damage done to nerve cells in Parkinson's and other neurological disorders.

Neural tissue transplants -- Researchers are studying ways to implant neural tissues from fetal pigs into the brain to restore the
degenerate area. In a clinical trial conducted, three patients out of 12 implanted with the pig tissues showed significant reduction in symptoms.

Genetic engineering -- Scientists are modifying the genetic code of individual cells to create dopamine-producing cells from other
cells, such as those from the skin.

Treatment of Parkinson's Disease - Holistic Medicine Perspective

Parkinson's disease results from the brain's inability to produce adequate levels of dopamine, a neurotransmitter whose production is increased when high-protein foods are consumed. Some researchers have speculated that a lifetime of high-protein, high-fat foods have resulted in the overproduction of dopamine. Production of dopamine becomes weaker with time, until the neurons are unable to produce adequate quantities of the neurotransmitter.

Recent research has shown that people with Parkinson's disease respond better to treatment when placed on a high-carbohydrate, low-protein diet. Such a diet is composed chiefly of whole grains, fresh vegetables, beans, and fruit, along with occasional low-fat animal foods, such as fish. Such a diet provides an abundance of vitamins, minerals, trace elements, essential fatty acids, and protein.

Eat a diet that maximizes oxygen and glucose to the brain, one that is extremely low in fat and rich in complex carbohydrates, vitamins, and minerals. Brain function declines when oxygen levels fall due to a high-fat diet. The same is true when glucose levels fall. Blood sugar is increased on a diet rich in complex carbohydrates (found in whole grains, vegetables, and fruit), which are the basis for optimal blood sugar levels. Brain levels of both oxygen and blood sugar are also enhanced when a person gets regular exercise, even a daily walk. Other excellent exercises include yoga and gentle stretching.

The first line of treatment for Parkinson's disease is definitely should be based on Western Medicine. The natural alternatives should be used for synergistic improvements. Holistic Medicine has great potential when used in this way.


Although great advances have been made in treatment of symptoms, the causes and methods of prevention and cure of Parkinson's disease remain essentially unknown.However, research is steadily progressing, and should produce answers to these most critical questions.

There are many practical problems faced by people with Parkinson's disease as well as their family. They can get valuable information and support from the many Parkinson's disease support groups that exisit worldwide.

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