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Parkinson's Disease






Parkinson's Disease


Parkinson's disease (PD) is a degenerative central nervous system (CNS) disorder characterized by uncontrolled body movements, rigidity, tremor, and gait difficulties. The American Parkinson Disease Association estimates that one million Americans are affected by the disease. The risk for developing PD increases with age, and onset usually occurs at around 50 years of age or older, although the disease is not unknown in people in their 30s and 40s. Parkinson's disease affects men and women equally. There are two types of Parkinson's disease: idiopathic PD and secondary PD. Idiopathic PD, also known as primary PD, has no known recognizable cause; secondary PD may result from trauma, tumor, or cerebrovascular disease, or may be drug induced. Patients with both types of PD are classified into stages (early, moderate, or advanced) based on the progression of disease. There is no known cure for the disease; rather, the treatment goal for patients with either form of PD is to control the symptoms and provide quality of life.

Parkinson's disease is actually a group of related CNS disorders caused by the destruction of the substantia nigra (pigmented brain cells), which produce dopamine (a neurotransmitter). The deficiency of dopamine results in the loss of muscle tone and voluntary muscle control seen in PD. Recent studies indicate that dopamine deficiencies in other areas of the brain and abnormalities of other neurotransmitters, such as norepinephrine and serotonin, may also contribute to the disease.

Signs and Symptoms

Although onset of PD can be rapid, it is generally insidious, with symptoms gradually progressing over a number of years until they interfere with daily activities. The four major symptoms of Parkinson's disease are

  • Rigidity (stiffness when neck or extremities are moved).
  • Resting tremor (involuntary movement of contracting muscles, especially when at rest).
  • Bradykinesis (slowness in initiating movement).
  • Poor posture and loss of balance.
Secondary symptoms of PD include

  • Depression.
  • Senility.
  • Postural deformity.
  • Speech difficulties.
  • Emotional changes (patients become fearful or insecure).
  • Memory loss and slowness of thought.
  • Difficulty swallowing or chewing.
  • Urinary dysfunction or constipation.
  • Skin problems.
  • Sleep disorders.

As PD progresses, patients develop a characteristic gait called festination, with which patients take small, hurried steps on tiptoe. Accidental falls occur frequently as a result of festination. As the disease progresses, it becomes more difficult for Parkinson's patients to manage daily activities, and full-time caregivers are often necessary.

Diagnosis of Parkinson's Disease

It is often difficult to diagnose the early stages of Parkinson's disease because the patient's symptoms may be vague. Often, diagnosis will be made only after the patient's tremors become readily apparent and one or more of the other classic symptoms appears. There is no specific test for the presence of the disease; rather, diagnosis is made on a thorough neurological examination. CT scans and MRIs may be ordered to rule out other diseases. There are multiple forms of PD, but the symptoms associated with all forms of the disease are similar. It is important to diagnose the specific form and the progression of PD because the treatment program will vary accordingly.

Conventional Treatment of PD

The treatment of PD patients is based on the type and stage of the disease, and is designed to alleviate symptoms. Some commonly used medications include anticholinergics (e.g., benztropine, biperiden, and orphenadine), dopamine receptor agonists (e.g., amantidine, bromocriptine, and pergolide), and monoamine oxidase (MAO) inhibitors, such as selegiline (deprenyl). Although deprenyl has been shown to be effective in the treatment of PD, recent research suggests that the effectiveness of this medication decreases over time. L-dopa, Sinemet, and Sinemet CR remain the most powerful medications for the treatment of PD, and are most often prescribed only during the advanced stage of the disease because their effectiveness decreases with time.

L-dopa can cross from the bloodstream to the brain and be converted to dopamine in the brain by the active form of vitamin B6. Dopamine itself cannot enter the brain from the bloodstream. Sinemet is L-dopa in combination with the peripheral dopa-decarboxylase inhibitor Carbidopa. Without the Carbidopa, dopa decarboxylase enzymes in the intestine would convert L-dopa to dopamine, which cannot enter the brain. Ropinirole, a synthetic, nonergot dopamine agonist receptor, has been shown to improve motor function and delay disability in PD patients. Ropinirole may be used prior to treatment with L-dopa.

Patients on long-term dopamine therapy may experience the on-off syndrome associated with the medication. During the on phase, dopamine levels in the brain are high and symptoms are controlled; during the off phase, dopamine levels in the brain decrease and the patient's symptoms return. These changes may be sudden and dramatic as dopamine levels fluctuate. The syndrome is particularly frustrating to PD patients, because there are no warning signs prior to the onset of either phase of the syndrome.

Because PD patients may experience sleep disorders and depression, sedatives and antidepressant agents may be prescribed. These medications should be used with caution in elderly patients, because of the increased risk for unsteadiness, confusion, and delirium.



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Stop Aging Now!: The Ultimate Plan for Staying Young & Reversing the Aging Process

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Alternative Treatments for Parkinson's

For every decade we live past age 40, we lose an average of about 10% of our dopamine-producing brain cells. Once 80% of these brain cells have died, Parkinson's disease is often diagnosed. Studies have shown that if healthy people take antioxidants throughout most of their lives, their risk of acquiring Parkinson's disease is reduced considerably. When Parkinson's patients are given vitamin E by itself, however, there is no slowdown in disease progression. Since Parkinson's patients have already sustained massive damage to crucial brain cells, aggressive multiple therapies are required to have a chance of significantly slowing the natural progression of the disease.

The Life Extension Foundation's protocol for Parkinson's disease is based on studies showing that low doses of several drugs work better than high doses of a single drug. The many components that compose this protocol are suggested because of evidence of their safety and benefits in treating the multiple underlying neurological disorders linked to the disease.

  • Bromocriptine. Take the lowest effective dose to begin with, usually 1.25 mg a day. May be withheld until later in the disease phase.
  • Sinemet CR (controlled release) (L-dopa plus a dopa decarboxylase inhibitor). Take lowest effective dose to begin with. Some doctors withhold Sinemet until later in the progression of the disease in order to give the Parkinson's patient more time to benefit from Sinemet before its effects wear off.
  • Amantadine (anticholinergic). Take lowest effective dose to begin with, usually 300 mg a day.
  • Deprenyl (MAO B inhibitor). Take lowest effective dose to begin with, between 1.25 and 5 mg a day. Deprenyl dosing has been significantly reduced based on studies showing that high doses of Deprenyl may be detrimental to Parkinson's patients.
  • Hydergine. Take 10 to 20 mg a day.
  • Acetyl-L-carnitine. Take 1000 mg twice a day.
  • Phosphatidylserine. Take 200 mg twice a day.
  • NADH. Take 5 to 10 mg twice a day.
  • DHEA. Take 100 mg 3 times a day, and/or pregnenolone at 50 mg 3 times a day.
  • Pregnenolone is a DHEA precursor.
    CAUTION: Refer to the DHEA-Pregnenolone Precautions in the DHEA Replacement Therapy protocol before taking DHEA or pregnenolone.
  • Coenzyme Q10. Take 100 mg 3 times a day.
  • Life Extension Mix. Take 3 tablets, 3 times a day.
    WARNING: May have to avoid if taking Sinemet because the vitamin B6 in Life Extension Mix may prevent L-dopa from reaching the brain. Take other antioxidants that do not contain vitamin B6 in place of Life Extension Mix.
  • Melatonin. Take 3 to 10 mg every night at bedtime.
  • Life Extension Booster. Take 1 capsule twice a day.
  • Human growth hormone. Take 2 IU daily, by injection.

Clinical research suggests that PD patients may derive some benefit from antioxidants and amino acids such as tyrosine. Antioxidants that may have some value in the treatment of PD include alpha-tocopherol (vitamin E) and Coenzyme Q10 (CoQ10). The results of two studies suggest that alpha-tocopherol may have prophylactic value in the prevention of PD.

The beneficial effects of L-dopa decrease with time; many studies have shown that vitamin B6 (pyridoxine) aggravates the loss of clinical effect of L-dopa by increasing decarboxylation. Patients taking L-dopa should not take more than 100 mg of pyridoxine a day, and should perhaps take much less. Clinical studies have suggested that L-tryptophan may help to ameliorate the motor complications sometimes seen in PD patients on long-term L-dopa therapy. L-tryptophan may also be helpful in the treatment of depression associated with this disease by increasing serotonin levels in the brain. A recent study of 23 patients with PD suggested that L-tyrosine may help to enhance dopamine synthesis.

Coenzyme Q10, a naturally occurring substance, may help to curb the oxidative stress common in Parkinsonism. Other therapies that may provide some protection from the loss of cognitive function in certain PD patients include the amino acid carnitine, Hydergine (a European medication), and phosphatidylserine (a phospholipid). Additional therapies that may be beneficial in treating the symptoms of PD include DHEA and NADH (hormones), and melatonin.


 

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