Learn About Parkinson's Disease
What is Parkinson's Disease?
Key Symptoms
What Causes Parkinson's Disease?
Conventional Treatments
Medications
Tests and Procedures
Treatment and Prevention
How Supplements Can Help
Self-Care Remedies
Alternative Therapies
When to Call a Doctor
Evidence Based Rating Scale
References
What is Parkinson's Disease?
Named for the English physician, James Parkinson, who first identified a condition he called "shaking palsy" in 1817, Parkinson's disease (PD) is a progressive nervous-system disorder. In the course of this illness, degenerative changes occur in an area of the brain called the substantia nigra, where the neurotransmitter dopamine is produced. Specifically, the nerve cells that manufacture dopamine, called nigral cells, start to die off. With insufficient dopamine to relay messages between nerve and muscle cells, it becomes progressively more difficult for the body to move in a smooth and normal way.
Parkinson's is one of the most common neurological diseases in the United States, affecting more than half a million people. More than 50,000 new cases are diagnosed annually, the majority in people around age 60. The diagnosis is typically made at the point at which a loss of substantial numbers of nigral cells (usually about two-thirds of the total) produces specific symptoms. The disease progresses slowly over the next decades.
Because symptoms come on so gradually and can remain mild for many years, PD is often wrongly assumed to be part of the aging process. While it is associated with older age groups, it by no means happens to everyone. In addition, because the disorder often progresses so slowly, many older people have such mild PD that they may never need medication or become disabled. Slightly more men than women are affected by the disease.
In the absence of definitive tests, a PD diagnosis is based on the presence of certain classic symptoms: increasingly noticeable tremor of the limbs; rigidity; loss of coordination; and a slow, shuffling gait. (Note: the most common kind of tremor, called essential tremor, is not related to Parkinson's disease.) While most people with PD develop only physical symptoms, about a third also experience mental deterioration. Depression also accompanies the disease in about two-thirds of patients. Spotting signs and symptoms at an early stage can make a big difference because, with proper treatment, most people with PD can go on to enjoy many productive and active years.
Key Symptoms
- Increased stiffness or rigidity in the muscles, affecting the quality of body movement.
- Shaking of the hands (called pill-roll tremor) and limbs, especially at rest or during tense moments. The tremor may be worse on one side of the body. It tends to lessen or stop with motion or sleep.
- Slowness of movement known as bradykinesia.
- Poor balance and loss of muscle coordination. Walking problems such as hesitant gait, shuffling steps, and difficulty negotiating turns.
- Trouble turning in bed, standing up from a chair, or otherwise changing position.
- Loss of facial expressiveness, infrequent blinking, and drooling.
- Difficulty swallowing.
- Characteristic pattern of deterioration in handwriting.
- A quavering voice, with loss of expression and volume.
- Bowel and bladder problems, such as constipation and incontinence.
- Anxiety, depression, and in some severe cases, memory loss, confusion, and other mental disorders.
What Causes Parkinson's Disease?
Why the dopamine-producing brain cells begin to deteriorate and die remains unknown, although some genetic and environmental factors appear to play a role. Ongoing research is focusing on several areas, including:
Genes. People who have a first-degree relative (a parent, sibling, or child) with PD are three times more likely to develop the disease. If two first-degree relatives have PD, the risk jumps as much as 10-fold.
Environment. Evidence is mounting that long-term exposure to certain chemicals, especially herbicides and pesticides involved in agriculture, is associated with PD. No link between specific chemicals and the disease has been conclusively established for humans; however the pesticide rotenone is used to create experimental PD for study of the disease in rats. Long-term ingestion of the food additive monosodium glutamate (MSG) is also thought to be a possible contributing factor because of the known role of glutamate in brain injury. Exposure to toxins such as carbon monoxide or other poisons is also considered to be a possible link.
Infection or injury. A virus such as encephalitis that infects the brain may be related to PD. Some cases also appear to be associated with a tumor or with a brain injury, which is widely believed to have played a role in the high profile case of boxer Mohammed Ali, for instance.
Free radicals. Some research suggests that PD may be yet another degenerative condition caused by unstable oxygen molecules called free radicals. With oxidative damage, free radicals destroy cells the way that rust oxidizes metal. One theory suggests that normal, age-related loss of anti-oxidative mechanisms in the body is accelerated in people who have PD.
Drugs. Certain medications that interfere with dopamine, such as antipsychotics and antiemetics (anti-nausea drugs), may cause parkinsonism, a cluster of symptoms that mimic those of PD. These symptoms can be reversed if the dose is lowered or the medication is changed.
While theories abound and research continues at a rapid pace, most cases of PD still cannot be linked to a definitive cause. Despite these underlying mysteries, however, there are effective treatments for people with Parkinson's disease.
Conventional Treatments
At present, Parkinson's disease is considered neither preventable nor curable. Conventional treatments aim to suppress symptoms and slow the progression of disease. In the earliest stages, there is no one-size-fits-all approach to treatment; an accurate diagnosis is key to determining the appropriate strategy for each individual.
Over the long term, certain medications can make a dramatic difference, enabling people to move and function quite normally. And in some advanced cases of PD, brain surgery can remarkably improve extreme symptoms, such as severe tremor or uncontrollable movements caused by long-term medication. Some lifestyle and dietary changes are also recommended.
Medications
After a thorough evaluation, a doctor may recommend a trial run of medication. Drugs can aid first in confirming the diagnosis, which can be challenging even for experienced neurologists. If a trial of medication produces no change, symptoms probably do not stem from Parkinson's disease. Likewise, if they are relieved, PD is most likely the cause.
Some doctors try to postpone daily medication for as long as possible because years of use of the basic drug combination (levodopa with carbidopa) can result in loss of effectiveness or the appearance of more serious side effects. Although numerous side effects are possible with drugs used for PD, they can often be managed by combining medications and adjusting dosages. For example, in the case of levodopa, the mainstay medication for PD, spasmodic movements called dyskinesia may eventually appear. Other drugs are often used to postpone the use of levodopa or to reduce its dosage.
Since no two patients react the same way, working closely with a doctor is recommended to find the regimen that works best for each individual. (For more information on the specific properties and side effects of PD medications, see WHMD drug database.)
Some primary medications are:
Levodopa (L-dopa). Although PD symptoms result from decreased levels of dopamine, the substance cannot be supplemented directly because it does not cross the blood-brain barrier. The drug L-dopa is converted into dopamine by nerve cells and can reverse many symptoms of PD for long periods. L-dopa is typically prescribed in combination with a related drug called carbidopa (Sinemet, Parcopa, Atamet, Stalevo, Madopar, Prolopa), which enhances L-dopa's action in the brain and reduces side effects in the peripheral nervous system.
Selegiline. Although not all sources agree, selegiline (L-deprenyl, Eldepryl, Emsam, Zelapar) is believed to slow the progression of PD. In early PD, use of L-dopa may be delayed. In later stages, it is often used with L-dopa to enhance its effectiveness and allow for use of lower doses.
Dopamine agonists. Often used for young adults or others in early stages, these drugs mimic the effects of dopamine by attaching to dopamine receptors in the brain. They are primarily given as an adjunct to L-dopa therapy.
COMT (catechol-O-methyltransferase) inhibitors. This newer class of drugs can prolong the effectiveness of L-dopa by blocking an enzyme that breaks down dopamine in the liver and other organs. Some believe that COMT inhibitors cause fewer side effects than other medications for Parkinson's disease.
Amantadine. In later stages of PD, amantadine can reduce the severe side effects that are sometimes result from taking L-dopa for a long time. Amantadine is sometimes used alone or, in the early stages of the disease, along with L-dopa.
SSRI antidepressants. It is not clear whether depression is a result of PD itself or an emotional response to it; it may be both. SSRIs (selective serotonin reuptake inhibitors) such as fluoxetine may be prescribed to combat depression and anxiety.
Tests and Procedures
There are no laboratory tests for Parkinson's disease. A comprehensive neurological examination will include an evaluation of coordination, dexterity, and ease in walking. The doctor will also ask about any symptoms the patient has been experiencing and look for subtle signs such as decreased facial expression, difficulty speaking or swallowing, or a very mild tremor. The doctor will consider personal medical history and any family history of Parkinson's disease. Tests involved are not designed to prove the presence of Parkinson's, but rather to rule out other neurological disorders that might be causing symptoms.
In advanced cases of PD, when symptoms or side effects have become extremely severe or when drugs are no longer effective, surgical treatment might be considered. Current interest involves transplanting part of the adrenal gland into the brain, a strategy that may especially benefit people under age 50.
Other procedures that may also be helpful include:
Thalamotomy and pallidotomy. Here, very small areas of the brain (the thalamus or the globus pallidus in the basal ganglia) are destroyed to control tremor or dyskinesia, the involuntary movements that can develop as a result of the disease or as a drug side effect.
Deep brain stimulation (DBS). The newest form of surgical therapy, DBS delivers high-frequency radio waves through electrodes implanted in different areas of the brain to control tremor or slowness of movement. Unlike thalamotomy or pallidotomy, which can only be done on one side of the brain due to health risks, DBS can be done on both sides of the brain and its effects are reversible.
Cell transplant. An experimental procedure in which fetal brain cells (human or pig) are implanted in the brain is currently being investigated. Early results suggest that this procedure holds promise for some younger people with Parkinson's disease. Because of the ethical controversy over the use of fetal cells in medical research and treatment, however, many researchers believe that embryonic stem cells or genetically engineered cells may provide a better answer. Researchers are also investigating the benefit of transplanting cells from the patient's own adrenal gland.
Treatment and Prevention
Although advances in drug, surgical, and gene therapies continue to unfold, medication is the only proven current treatment for Parkinson's disease. Several complementary therapies, particularly those that help with movement and balance, are also valuable in helping people to cope with the challenges of the condition. Physical and speech therapy, too, can help patients with Parkinson's disease adjust to new limitations. (For information on physical therapy, see the WholeHealthMD Reference Library.)
Many nutritionally oriented physicians contend that dietary supplements benefit people with Parkinson's disease and might even play a role in preventing it. The case for antioxidants in particular is growing stronger given the increasing evidence that damage to the brain in PD might be the result of the oxidative processes.
Although there is no proven way to prevent PD, it is probably prudent to avoid exposure to inhaled chemicals and monosodium glutamate (MSG). Some experts believe that even one episode of concentrated exposure to a chemical toxin could trigger Parkinson's disease in a person who is already susceptible to it for other reasons. Avoid unnecessary exposure to herbicides, pesticides, and other potent toxins. Those with a family history of PD should consider working with a nutritionally oriented practitioner on a lifelong plan to maximize resistance to toxic chemicals.
How Supplements Can Help
If oxidative damage from free radicals does prove to be a cause of Parkinson's disease, then antioxidant supplements may be of significant value in prevention. Other supplements that are known to benefit neurological function and support brain health may also benefit those who have been diagnosed. Supplements for Parkinson's disease can be taken singly or in combination.
Just a reminder: Those with a serious medical condition should check with a doctor before taking over-the-counter drugs or supplements.
Amino acids, known as the building blocks of proteins, may help to boost dopamine levels by nourishing the cells that produce it. Amino acids like tyrosine, methionine, and acetyl-L-carnitine are at the forefront of research in this area.
L-dopa is produced from the amino acid L-Tyrosine, which is also the precursor to dopamine production in the brain. Both Parkinson's disease itself and the drug L-dopa are associated with depleting the body's tyrosine levels. However, a 2011 case study found that when L-dopa is administered in proper balance with the amino acids tyrosine, cysteine, glutathione, SAMe (manufactured from methionine), and 5-HTP (a derivative of the amino acid tryptophan), side effects that can occur with L-dopa become controllable or do not occur at all. (1) More research is needed.
Some evidence suggests that taking creatine may help to slow progression of PD in patients with early stage disease who do not need to take medications to control symptoms. In a 2006 study of 200 patients diagnosed with PD within the previous five years, taking 10 gm of creatine daily significantly decreased the rate of disease progression compared to placebo. (2) In another study, patients whose disease was more advanced were able to have smaller increases in their dosages of conventional medications. (3) Creatine also has been shown to increase the benefits of resistance training in patients with PD, who generally experience decreases in muscle mass and strength. (4)
Studies have shown that patients with PD are often deficient in glutathione, a compound of three amino acids--cysteine, glutamic acid, and glycine--and an important part of the body's antioxidant defense system. (5-11) Adequate glutathione levels may help to protect the brain from free-radical damage and may also increase the body's sensitivity to dopamine. A 2006 review of antioxidant use in Parkinson's disease found only one study involving glutathione. With fewer than 30 subjects, it did show a small but statistically significant improvement in symptoms of Parkinson's disease. (12) However, a 2009 study had conflicting results. In the study, 20 patients with PD received either 1,400 mg of intravenous glutathione or placebo three times a week for twelve weeks. There were no statistically significant differences between groups in the Unified Parkinson's Disease Rating Scale (UPDRS). (13) Larger studies are needed to establish appropriate doses and timing of glutathione therapy.
Limited research indicates that DLPA (D, L-phenylalanine), which contains two forms of the amino acid phenylalanine, may help to improve rigidity, walking, speech, and depression associated with Parkinson's disease. (14) More research is needed.
Coenzyme Q10 (CoQ10) is an important component in energy generation in the body's cells. Some studies have shown that taking high doses (up to 2,400 mg) of CoQ10 daily slows functional decline in people with early Parkinson's disease who do not require medicine to treat symptoms. The effect seems to be dose dependent. (15, 16) However, patients with mid-stage Parkinson's disease did not experience the same benefit. In a 2007 study, symptoms in mid-stage patients taking 100 mg of a specific coenzyme Q10 supplement (Nanoquinon, MSE Pharmazeutika) three times daily did not significantly improve compared to placebo. (17) A 2011 Cochrane Database Review of four randomized, double-blind, placebo-controlled trials evaluating CoQ10 in 452 patients with early and mid-stage Parkinson's disease found that doses of 1,200 mg a day were well tolerated and led to improvements in measures of activities of daily living based on the UPDRS and the Schwab and England Activities of Daily Living Scale. However, sample sizes used in the trials reviewed were small, and results were unclear for the effect of CoQ10 on the total and other sub-scales of the UPDRS score. More research is needed. (18)
Ginkgo biloba, the herb best known for its purported effects on memory enhancement, acts as an antioxidant by scavenging free radicals. It is also thought to boost blood circulation to the brain, which, if true, may help dopamine get to where it's most needed. Animal studies have shown that ginkgo biloba significantly reduces uptake, or reabsorption, of dopamine and norepinephrine, which increases the active levels. (19-23) The effect was not seen after a single 100 mg/kg dose of ginkgo biloba, but was found after 14 days of treatment. (20) One study found that the neuroprotective effects of ginkgo biloba may help to protect cells from toxic effects of L-dopa, making the combination of the herb and the drug more effective than taking L-dopa alone. (22) Research is needed to confirm or refute efficacy in humans.
NADH (reduced nicotinamide adenine dinucleotide) is a coenzyme that may help to improve neurotransmitter function. Numerous studies demonstrate its role in mitochondria, the energy producing components in cells of the body—especially the brain—suggesting that supplementation may increase dopamine production. It is also an antioxidant. However, clinical trials in humans are limited and none are recent. In a 1996 trial of 15 patients, intravenous treatment with NADH in addition to L-dopa for seven days led to significant improvements in UPDRS scores. Perhaps more significantly, NADH seemed to stimulate the biosynthesis of L-dopa in the brain, thus increasing efficacy of the conventional drug in treating PD. (24) In a 1993 open-label trial of 885 patients with PD receiving NADH either intravenously or orally, both forms of the coenzyme led to significant improvement in disability. However, the effect of NADH was related to duration of disease and age of the patient. In the study, younger patients and patients with a shorter duration of disease had a better chance of marked improvement in disease symptoms than older patients and patients with longer duration of disease. (25) Conflicting studies have shown no benefits in PD patients after short-term treatment with NADH. (26) More studies are needed to determine efficacy.
Vitamin B6 may enhance the effectiveness of medications that combine L-dopa and carbidopa. (27) Although a 2006 review of studies found inconclusive results regarding the effects of vitamin B6on neurocognitive disorders like Parkinson's disease and Alzheimer's disease, there is some favorable evidence. (28) That same year, results were published from the Rotterdam Study, a prospective, population-based cohort study evaluating dietary intake of various B vitamins and the risk of PD. The results showed that a higher intake of vitamin B6was associated with a significantly decreased risk of PD. (29) A 2010 case-study of 249 patients with PD found similar results: low dietary intake of vitamin B6was associated with an increased risk of PD. (30) However, B6 supplementation is contraindicated in patients taking L-dopa alone because it increases the metabolism of the drug in peripheral sites outside the brain resulting in worsening side effects. (31) More research is needed.
Vitamin C and vitamin E have a protective effect on cells in general, including key dopamine-producing brain cells. These antioxidants may be especially useful in early stages of PD, before conventional drugs become necessary. A preliminary study suggests that high levels of vitamin E in the diet may reduce the risk of developing PD in the first place. (42) But conflicting evidence indicates that taking 2000 IU of vitamin E daily as a supplement does not seem to have any benefit for patients who have PD. (43-45) More research is needed.
Omega 3 fatty acids play crucial roles in the maintenance of normal neurological function. Levels are often deficient in people with Parkinson's disease. Animal studies have demonstrated neuroprotective effects with supplementation; however human studies are needed. (60)
Self-Care Remedies
Some experts speculate that Parkinson's is a disease of modern living, precipitated in part by exposure to environmental pollutants, nutrient-poor diets, and lack of exercise. Regardless of whether or not this is true, it seems clear that lifestyle changes may well help to slow the course of PD and help patients to better cope with the disease.
Stay as physically fit and active as possible. It's very important to keep muscles toned and flexible. Try to walk every day and stretch regularly. Exercise programs such as Yoga or Tai Chi may be particularly beneficial, as they address balance issues as well.
Keep mentally fit by taking up new interests and challenges. No matter what frustrating changes Parkinson's may inflict on the body, in most cases the mind will remain as sharp as patients help it to be.
Reduce protein in the diet. Several studies have found evidence that a diet relatively high in carbohydrates and low in protein will help the body make the best use of the L-dopa/carbidopa drug treatment. This is because certain dietary proteins can interfere with the stomach's absorption of L-dopa and the body's ability to get it to the brain cells that need it.
If symptom control with L-dopa is erratic, consider reducing protein in the diet to the recommended daily allowance (RDA), which is 0.8 grams per kilogram (or 0.36 grams per pound) of body weight. Most Americans eat far more protein than this on a daily basis. Some sources suggest eating protein only at the evening meal, and maintaining a 7-to-1 daily ratio of carbohydrates to protein. Ask a doctor or a nutritionist for more information about the protein-levodopa interaction.
Seek counseling for emotional support or to combat depression. Depression is v