Parkinson's Disease

Introduction

What should I know about Parkinson's Disease?

Parkinson’s disease is a serious brain condition that results from nerve damage in certain regions of the brain that regulate the body’s voluntary muscles. Also referred to as "PD," Parkinson’s disease is a movement disorder that causes muscle rigidity, shaking, and slow difficult walking. (1) , (2) PD usually strikes in mid to late adult life, although 30 percent of people with the disease experience symptoms before age 50. (3) Another 40 percent develop the disease between ages 50 and 60. PD is a slowly progressive and incurable disease.

Like all cells in the nervous system, brain neurons function in response to electrical impulses that travel with lightning speed from cell to cell. These impulses need assistance in order to jump from one neuron to the next. They get this help in the form of neurotransmitters, chemicals in the body that carry messages across the gaps between adjacent neurons. Without neurotransmitters, brain neurons would be isolated and alone, wholly unable to communicate with each other and with the rest of the body.

The hallmark feature of PD is a loss of neurons governed by a neurotransmitter called "dopamine." (4) These cells are found in areas of the brain that allow us to control voluntary muscles. When we want to move, walk, write with a pen, throw a ball, swing a golf club, drive a car, or do just about anything, the brain sends a message to the muscles that perform the given task. The muscles contract properly and movement occurs. As dopamine-containing neurons die off in PD, signals from the brain that coordinate movement and muscle function are transmitted too slowly. (5) When the signals are received, the body is unable to respond normally.

The first sign of PD is often a slight tremor in one hand. This tremor is most visible when the individual with PD is standing or sitting still. The shaking is generally not noticeable when the hands are moving or doing something. However, tremor is absent in a small percentage of people with PD. (6) Other classic symptoms include slow movements, "shuffling" while walking, muscle stiffness, stooped posture, and a blank facial expression. (7) , (8) Before these symptoms begin, a person with oncoming PD may experience vague, aching pain in the limbs, neck, or back and decreased spinal flexibility. Other early and subtle symptoms include impaired handwriting ability and low speaking volume. (9) As the disease progresses, cognitive function often suffers, and some patients develop dementia. In the later stages, people with PD often become depressed, which is certainly not difficult to understand.

Although much is known about the brain degeneration that occurs in Parkinson’s disease, why this happens remains a mystery. (10) Viral infections and exposure to certain substances have been implicated, but in most cases PD is an "idiopathic" disease, one with no known cause.

Statistic

European Parkinson’s Disease Association, 2004.

  • Parkinson’s disease affects 6.3 million people worldwide.

Mayo Clinic, 1999.

    30-40% of all people with Parkinson’s Disease will develop dementia.

The National Parkinson Foundation, 1999.

    It is estimated that up to 1.5 million Americans are affected, more persons than those suffering from Multiple Sclerosis and Muscular Dystrophy combined. Parkinson's disease affects one of every 100 persons over the age of 60. Approximately 25%, of PD patients do not have tremors.

CDC NCHS Data on Parkinson’s Disease, 2000.

  • In 2000, 15,600 deaths were attributed to PD, a rate of 5.5% per 100,000 people in the total population.
  • In 1999 and 2000, there was an average of 238,400 hospital discharges per year relating to PD.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

The primary symptoms of Parkinson’s disease include the following:

  • Muscle rigidity and stiffness: This is sometimes accompanied by pain in the arms and shoulders.
  • Tremors: May be worse on one side of the body. Up to 25% of patients experience very slight tremor or none at all. (11) Besides affecting the limbs, it sometimes involves the head, neck, face, and jaw.
  • Slowness of movement.
  • Poor balance: This often occurs with abrupt movement or sudden change in body position. (12) Some patients experience repeated falls due to poor balance.
  • Difficulty in walking: This commonly includes a decreased or non-existent arm swing; short, shuffling steps; trouble negotiating turns; and sudden freezing spells (inability to take the next step). (13)
It is important to note that most patients do not experience all of these symptoms  

Treatment Options

Conventional

Medications commonly prescribed for PD include:

    Anticholinergic agents Levodopa/carbidopa Benserazide Bromocriptine Pergolide Amantadine Monoamine Oxidase b inhibitors such as deprenyl Catechol-O-Methyltransferase inhibitors

Nutritional Suplementation


Nicotinamide Adenine Dinucleotide (NADH)

Some patients in the earlier stages of Parkinson’s disease have gained improvements from taking NADH supplements. NADH is a co-enzyme that occurs naturally in the body. NADH helps power the energy-producing machinery inside cells that generates the energy needed for metabolic functions and DNA repair. NADH also increases dopamine synthesis and thus may help the body compensate for the loss of dopamine-producing brain neurons that occurs in PD.

In one study, 885 patients with Parkinson’s disease took NADH, either orally or intravenously. About 80% showed measurable improvements. The oral and intravenous forms were more or less equally effective. After statisticians had analyzed the data, it was apparent that NADH was most beneficial in younger patients still in the early stages of PD. (14) While this study looks promising, it was an "open" trial, meaning it was not designed to eliminate a placebo effect that might have at least partially accounted for the results.

Another study, this one being a placebo-controlled trial, failed to show any clear benefit from NADH. While NADH may yet prove helpful for relieving PD symptoms, some researchers feel the evidence is too preliminary to justify recommending it. (15)


Coenzyme Q10 (CO-Q10)

CoQ10 is another co-enzyme that, like NADH, supports the production of energy in cells. CoQ10 works within the mitochondria, which are the power stations inside cells. Studies have found low CoQ10 levels in the mitochondria of people with PD, and reduced activity of a key energy-producing mechanism in the mitochondria. (16) , (17) Many other hints that CoQ10 may be helpful in PD have come from animal experiments. In one study, CoQ10 counteracted the effects of a toxin that damages the dopamine-producing neurons. (18)

In a human study, 80 patients with early PD were placed in one of four groups; Co-Q10 300 milligrams per day (mg/d), Co-Q10 600 mg/d, Co-Q10 1,200 mg/d or in a placebo group. The researchers concluded that those receiving Co-Q10 developed less disability than those taking placebo. (19)


Vitamin B3, Vitamin B6

An animal study suggests that benserazide and carbidopa, two drugs commonly used to treat PD, might deplete the body’s supply of niacin. Though no one taking these drugs has developed pellagra, a disease that results from severe niacin deficiency, some degree of niacin deficiency could in theory follow their use. (20) The authors of this study have found signs of B6 deficiency in blood tests of people taking carbidopa along with another drug called a "decarboxylase inhibitor." (21) To further complicate matters, B6 supplements may increase the potency of a drug called "Sinemet," which is a combination of carbidopa and L-dopa. (22) , (23) If you are taking any of these medications, you may want to check with your health care provider to see if you need a B vitamin supplement.

Herbal Suplementation


Ginkgo

The venerable ginkgo tree is the world’s oldest living tree species. Fossil records place ginkgo on the earth more than 200 million years ago. Ginkgo is famous for its longevity; a famous 1,000 year-old ginkgo tree thrives today in a Japanese monastery. Fittingly enough for such a hardy tree, the ginkgo leaf is one of today’s most promising herbs for increasing longevity and reversing the effects of aging on the brain.

In China, the medicinal use of ginkgo leaf as a brain tonic dates back 4,000 years. Ginkgo biloba extract is the most frequently prescribed herbal medicine in Europe, and it ranks high on the list of America’s most popular herbal supplements. Ginkgo is also one of the world’s most extensively researched herbs, with more than 100 clinical studies to its credit. The most dramatic benefits are reported in improving circulation in the elderly. (24) , (25) This research shows ginkgo is a focused and effective brain tonic that improves memory and mental function. Ginkgo biloba extract may be helpful for people with Parkinson’s disease whose cognitive abilities are starting to decline, although this possibility has not been tested yet in scientific studies.


Grape Seed Extract

Grape seeds are one of nature’s richest sources of substances called "PCO's." Belonging to the "flavonoid" family, PCO's neutralize unstable molecules called "free radicals" that are generated by the body’s metabolic processes. If not held in check, free radicals can damage DNA and other cell structures. Substances that disable free radicals are called "antioxidants," and PCO's are some of the more robust antioxidants known. (26) , (27) , (28) PCO's help protect blood vessels and support healthy circulation. While grape seed extract has not been studied as a treatment for PD, keeping blood vessels in the undamaged areas of the brain healthier can only be helpful.

References

  1. Devising RC. Parkinson's Disease: A Guide For Patient and Family. New York: Raven Press; 1978;14:149.
  2. View Abstract: Olanow CW, et al. Etiology and pathogenesis of Parkinson's disease. Annu Rev Neurosci. 1999;22:123-44.
  3. View Abstract: Scott B, et al. Gender differences in Parkinson's disease symptom profile. Acta Neurol Scand. Jul2000;102(1):37-43.
  4. View Abstract: Porritt MJ, et al. New dopaminergic neurons in Parkinson's disease striatum. Lancet. Jul2000;356(9223):44-5.
  5. View Abstract: Giovannoni G, et al. Bradykinesia akinesia inco-ordination test (BRAIN TEST): an objective computerised assessment of upper limb motor function. J Neurol Neurosurg Psychiatry. Nov1999;67(5):624-9.
  6. View Abstract: Jankovic J. Essential tremor: clinical characteristics. Neurology. 2000;54(11 Suppl 4):S21-5.
  7. View Abstract: Louis ED, et al. Progression of parkinsonian signs in Parkinson disease. Arch Neurol. Mar1999;56(3):334-7.
  8. View Abstract: Singer C. Urinary dysfunction in Parkinson's disease. Clin Neurosci. 1998;5(2):78-86.
  9. View Abstract: Grossman M, et al. Cognitive resource limitations during sentence comprehension in Parkinson's disease. Brain Lang. Jun2000;73(1):1-16.
  10. View Abstract: Schrag A, et al. Cross sectional prevalence survey of idiopathic Parkinson's disease and parkinsonism in London. BMJ. Jul2000;321(7252):21-22.
  11. View Abstract: Marjama-Lyons J, et al. Tremor-predominant Parkinson's disease. Approaches to treatment. Drugs Aging. Apr2000;16(4):273-8.
  12. View Abstract: Grill S. Postural instability in Parkinson's disease. Md Med J. Jul1999;48(4):179-81.
  13. View Abstract: Swinnen SP, et al. Motor learning and Parkinson's disease: refinement of within-limb and between-limb coordination as a result of practice. Behav Brain Res. Jun2000;111(1-2):45-59.
  14. View Abstract: Birkmayer JG, et al. Nicotinamide adenine dinucleotide (NADH)--a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application. Acta Neurol Scand Suppl. 1993;146:32-5.
  15. View Abstract: Swerdlow RH. Is NADH effective in the treatment of Parkinson's disease? Drugs Aging. Oct1998;13(4):263-8.
  16. View Abstract: Muller T, Buttner T, Gholipour AF, Kuhn W. Coenzyme Q10 supplementation provides mild symptomatic benefit in patients with Parkinson's disease. Neurosci Lett. May2003;341(3) 201-4.
  17. View Abstract: Winkler-Stuck K, Wiedemann FR, Wallesch CW, Kunz WS. Effect of coenzyme Q10 on the mitochondrial function of skin fibroblasts from Parkinson patients. J Neurol Sci. May2004;220(1-2):41-8.
  18. View Abstract: Shults CW, et al. A possible role of coenzyme Q10 in the etiology and treatment of Parkinson's disease. Biofactors. 1999;9(2-4):267-72.
  19. View Abstract: Shults CW, Oakes D, Kieburtz K, Beal MF, Haas R, Plumb S, et al. Effects of coenzyme q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol. Oct2002;59(10):1541-50.
  20. View Abstract: Bender DA, et al. Niacin depletion in Parkinsonian patients treated with L-dopa, benserazide and carbidopa. Clin Sci. Jan1979;56(1):89-93.
  21. View Abstract: Bender DA, et al. Niacin depletion in Parkinsonian patients treated with L-dopa, benserazide and carbidopa. Clin Sci. Jan1979;56(1):89-93.
  22. Namba S, Omoto T, Kishikawa H. Effects of simultaneous administration of pyridoxine in the combined administration of L-dopa and peripheral decarboxylase inhibitors. Experimental and clinical studies. No To Shinkei. Aug1976;28(8):815-22.
  23. View Abstract: Hanzal F. Treatment of Parkinson's syndrome with L-dopa and L-carbidopa. MMW Munch Med Wochenschr. May1976;118(20):653-6.
  24. View Abstract: Kleijnen J, et al. Ginkgo biloba for Cerebral Insufficiency. Br J Clin Pharm. 1992;34:352-58.
  25. Kleijnen J, et al. Ginkgo biloba. Lancet. 1992;340(8828):1136-39.
  26. View Abstract: Fitzpatrick DF, et al. Endothelium-dependent Vasorelaxing Activity of Wine and Other Grape Products. Am J Physiol. 1993;265(2 Pt 2):H774-H778.
  27. Uchida S, et al. Active Oxygen Free Radicals Are Scavenged by Condensed Tannins. Prog Clin Biol Res. 1988;280:135-38.
  28. View Abstract: Hatano T, et al. Effects of Interaction of Tannins with Co-existing Substances. VII. Inhibitory Effects of Tannins and Related Polyphenols on Xanthine Oxidase. Chem Pharm Bull. Tokyo. 1990;38(5):1224-29.