ANSWERS: 9
  • I'm not sure of any "alternative treatments" but here's what i could find. ----------------------------------------- Treatment Parkinson's disease is a chronic disorder that requires broad-based management including patient and family education, support group services, general wellness maintenance, exercise, and nutrition. At present, there is no cure for PD, but medications or surgery can provide relief from the symptoms. Levodopa Stalevo for treatment of Parkinson's disease The most widely used form of treatment is L-dopa in various forms. L-dopa is transformed into dopamine in the dopaminergic neurons by L-aromatic amino acid decarboxylase (often known by its former name dopa-decarboxylase). However, only 1-5% of L-DOPA enters the dopaminergic neurons. The remaining L-DOPA is often metabolised to dopamine elsewhere, causing a wide variety of side effects. Due to feedback inhibition, L-dopa results in a reduction in the endogenous formation of L-dopa, and so eventually becomes counterproductive. Carbidopa and benserazide are dopa decarboxylase inhibitors. They help to prevent the metabolism of L-dopa before it reaches the dopaminergic neurons and are generally given as combination preparations of carbidopa/levodopa (co-careldopa) (e.g. Sinemet, Parcopa) and benserazide/levodopa (co-beneldopa) (e.g. Madopar). There are also controlled release versions of Sinemet and Madopar that spread out the effect of the L-dopa. Duodopa is a combination of levodopa and carbidopa, dispersed as a viscous gel. Using a patient-operated portable pump, the drug is continuously delivered via a tube directly into the upper small intestine, where it is rapidly absorbed. Tolcapone inhibits the COMT enzyme, thereby prolonging the effects of L-dopa, and so has been used to complement L-dopa. However, due to its possible side effects such as liver failure, it's limited in its availability. A similar drug, entacapone, has similar efficacy and has not been shown to cause significant alterations of liver function. A recent follow-up study by Cilia and colleagues looked at the clinical effects of long-term administration of entacapone, on motor performance and pharmacological compensation, in advanced PD patients with motor fluctuations: 47 patients with advanced PD and motor fluctuations were followed for six years from the first prescription of entacapone and showed a stabilization of motor conditions, reflecting entacapone can maintain adequate inhibition of COMT over time. Mucuna pruriens, is a natural source of therapeutic quantities of L-dopa. Dopamine agonists The dopamine-agonists bromocriptine, pergolide, pramipexole, ropinirole , cabergoline, apomorphine, and lisuride, are moderately effective. These have their own side effects including those listed above in addition to somnolence, hallucinations and /or insomnia. Several forms of dopamine agonism have been linked with a markedly increased risk of problem gambling. Dopamine agonists initially act by stimulating some of the dopamine receptors. However, they cause the dopamine receptors to become progressively less sensitive, thereby eventually increasing the symptoms. Dopamine agonists can be useful for patients experiencing on-off fluctuations and dyskinesias as a result of high doses of L-dopa. Apomorphine can be administered via subcutaneous injection using a small pump which is carried by the patient. A low dose is automatically administered throughout the day, reducing the fluctuations of motor symptoms by providing a steady dose of dopaminergic stimulation. After an initial "apomorphine challenge" in hospital to test its effectiveness and brief patient and caregiver, the primary caregiver (often a spouse or partner) takes over maintenance of the pump. The injection site must be changed daily and rotated around the body to avoid the formation of nodules. Apomorphine is also available in a more acute dose as an autoinjector pen for emergency doses such as after a fall or first thing in the morning. MAO-B inhibitors Selegiline and rasagiline reduce the symptoms by inhibiting monoamine oxidase-B (MAO-B), which inhibits the breakdown of dopamine secreted by the dopaminergic neurons. By-products of selegiline include amphetamine and methamphetamine, which can cause side effects such as insomnia. Use of L-dopa in conjunction with selegiline has increased mortality rates that have not been effectively explained. Another side effect of the combination can be stomatitis. One report raised concern about increased mortality when MAO-B inhibitors were combined with L-dopa; however subsequent studies have not confirmed this finding. Unlike other non selective monoamine oxidase inhibitors, tyramine-containing foods do not cause a hypertensive crisis. Surgical interventions Illustration showing an electrode placed deep seated in the brain Treating Parkinson's disease with surgery was once a common practice. But after the discovery of levodopa, surgery was restricted to only a few cases. Studies in the past few decades have led to great improvements in surgical techniques, and surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient. Deep brain stimulation is presently the most used surgical means of treatment, but other surgical therapies that have shown promise include surgical lesion of the subthalamic nucleus and of the internal segment of the globus pallidus, a procedure known as pallidotomy. Speech therapies The most widely practiced treatment for the speech disorders associated with Parkinson's disease is Lee Silverman Voice Treatment (LSVT). LSVT focuses on increasing vocal loudness. A study found that an electronic device providing frequency-shifted auditory feedback (FAF) improved the clarity of Parkinson's patients' speech. Physical exercise Regular physical exercise and/or therapy, including in forms such as yoga, tai chi, and dance can be beneficial to the patient for maintaining and improving mobility, flexibility, balance and a range of motion. Physicians and physical therapists often recommend basic excercises, such as bringing the toes up with every step, carrying a bag with weight to decrease the bend having on one side, and practicing chewing hard and move the food around the mouth. Methods undergoing evaluation Gene therapy Currently under investigation is gene therapy. This involves using a harmless virus to shuttle a gene into a part of the brain called the subthalamic nucleus (STN). The gene used leads to the production of an enzyme called glutamic acid decarboxylase (GAD), which catalyses the production of a neurotransmitter called GABA. GABA acts as a direct inhibitor on the overactive cells in the STN. GDNF infusion involves the infusion of GDNF (glial-derived neurotrophic factor) into the basal ganglia using surgically implanted catheters. Via a series of biochemical reactions, GDNF stimulates the formation of L-dopa. GDNF therapy is still in development. In the future, implantation of cells genetically engineered to produce dopamine or stem cells that transform into dopamine-producing cells may become available. Even these, however, will not constitute cures because they do not address the considerable loss of activity of the dopaminergic neurons. Neuroprotective treatments Neuroprotective treatments are at the forefront of PD research, but are still under clinical scrutiny. These agents could protect neurons from cell death induced by disease presence resulting in a slower pregression of disease. Agents currently under investigation as neuroprotective agents include apoptotic drugs (CEP 1347 and CTCT346), lazaroids, bioenergetics, antiglutamatergic agents and dopamine receptors. Clinically evaluated neuroprotective agents are the monoamine oxidase inhibitors selegiline and rasagiline, dopamine agonists, and the complex I mitochondrial fortifier coenzyme Q10. Neural transplantation The first prospective randomised double-blind sham-placebo controlled trial of dopaminergic transplants failed to show an improvement in quality of life although some significant clinical improvements were seen in patients below the age of 60 Nutrients Nutrients have been used in clinical studies and are widely used by people with Parkinson's disease in order to partially treat Parkinson's disease or slow down its deterioration. The L-dopa precursor L-tyrosine was shown to relieve an average of 70% of symptoms. Ferrous iron, the essential cofactor for L-dopa biosynthesis was shown to relieve between 10% and 60% of symptoms in 110 out of 110 patients. More limited efficacy has been obtained with the use of THFA, NADH, and pyridoxine—coenzymes and coenzyme precursors involved in dopamine biosynthesis.Vitamin C and vitamin E in large doses are commonly used by patients in order to theoretically lessen the cell damage that occurs in Parkinson's disease. This is because the enzymes superoxide dismutase and catalase require these vitamins in order to nullify the superoxide anion, a toxin commonly produced in damaged cells. However, in the randomized controlled trial, DATATOP of patients with early PD, no beneficial effect for vitamin E compared to placebo was seen[ Coenzyme Q10 has more recently been used for similar reasons. MitoQ is a newly developed synthetic substance that is similar in structure and function to coenzyme Q10. However, proof of benefit has not been demonstrated yet. Qigong There have been two studies looking at qigong in Parkinson's disease. In a trial in Bonn, an open-label randomised pilot study in 56 patients found an improvement in motor and non-motor symptoms amongst patients who had undergone one hour of structured Qigong exercise per week in two 8-week blocks. The authors speculate that visualizing the flow of "energy" might act as an internal cue and so help improve movement. The second study, however, found Qigong to be ineffective in treating Parkinson's disease. In that study, researchers used a randomized cross-over trial to compare aerobic training with Qigong in advanced Parkinson's disease. Two groups of PD patients were assessed, had 20 sessions of either aerobic exercise or qigong, were assessed again, then after a 2 month gap were switched over for another 20 sessions, and finally assessed again. The authors found an improvement in motor ability and cardiorespiratory function following aerobic exercise, but found no benefit following Qigong. The authors also point out that aerobic exercise had no benefit for patients' quality of life. Source: http://en.wikipedia.org/wiki/Parkinson%27s_disease
  • High-dose Coenzyme Q10 has been shown to improve bodily functions in Parkinsons patients. The google search engine listed numerous clinical studies in this area.
  • From the book, "The Juiceman's Power of Juicing," by Jay Kordich, page 203, comes this experience: "You probably have never considered ingesting wheatgrass, and to be honest, I never had either until I met a fellow by the name of LeClaire in St. Petersburg, Florida. This was back in the 1950's and Mr. LeClaire came to a juicing demonstration even though he shook so much from Parkinson's disease he could not hold a cup and sample any of the juices. Nevertheless he bought a juicer. The next year when I returned to Florida, Mr. LeClaire approached the front of the room and shook my hand without trembling. I was amazed. He explained that he had put himself on a regimen of carrot juice, wheatgrass juice, and leafy greens. Wheatgrass juice was the centerpiece of his diet and he consumed six ounces every day. Fascinated, I accepted his invitation to his rooming house to see how he grew wheatgrass in trays, using carrot and leafy green waste for compost and growing worms to aerate the soil in five-gallon, stainless steel milk cans. Since that day, I have believed as strongly as anyone in the power of wheatgrass." That was quite the experience. I do not have Parkinson's, but if I did, you can bet I would sure give that wheatgrass a try. (Incidentally, the author goes on to advice never to drink more than two ounces of wheatgrass juice at a time. It is best to start off slowly. Wheatgrass juice is very sweet and may make you nauseated.)
  • Coenzyme Q10 has no symptomatic benefit. It was tested for neuroprotection - slowing down the disease process - in a small study. It was suggestive so now a large multi-center study is underway. There is a plant - mucuna - which has a very high concentration of l-dopa, the main component of Sinemet (carbidopa/levodopa). You can buy seeds on the internet. The only problem is that you wont know how much l-dopa you are getting and wont get the carbidopa component which blocks the nausea assocated with l-dopa. I guess if Sinemet becomes unavailable it might be useful. The best alternative treatment for Parkinson's is regular exercise and avoidance of obesity. Treadmill walking seems to preserve the gait.
  • L-tyrosine may help with Parkinson's. Here is an article I wrote about l-tyrosine: Brighten Your Mood & Enhance Your Health With L-Tyrosine http://hubpages.com/.../...h-With-L-Tyrosine I hope it is helpful to you! :)
  • ask your doctor , he would know
  • I have video that shows a Parkinson's victim with extreme trembling in his hands take a few hits of weed and the trembling and all physical affects of the Parkinson's stopped entirely. It's too bad some people are still hung up in the Reefer Madness days of demonizing cannibis but some of the health benefits are really incredible and that list is growing..
  • Most are related to stimulating increased dopamine using cannabis and/or narcotics. But they are best done under medical supervision only.
  • Cell replacement therapy involves differentiating stem cells into dopamine signaling or dopaminergic neurons and transplanting them into patients' brains to replace dying neurons.However, the variability of differentiated cells - including other neuronal cell types or residual contamination of undifferentiated stem cells - may affect transplant outcomes.For example, in clinical trials in the 1990s, this pollution caused serious movement disorders in some patients, uncontrollable jerks that were worse than the movement problems caused by Parkinson's disease. To avoid unwanted cell type interference, researchers need a differentiation scheme that produces a more homogeneous group of dopaminergic neurons.Researchers led by Hossein Baharvand of the university of science and culture in Tehran, Iran, and education of Iran, the centre for culture and research and Ghasem Hosseini Salekdeh of Macquarie university in Australia set out to develop such an agreement. First, the team developed a special stem cell line containing a green fluorescent protein or GFP reporter gene for transcription factors involved in the development of dopaminergic neurons.Fluorescent reporter molecules are not expressed in undifferentiated cells from this line.When cells begin to produce transcription factors, the first step in dopaminergic neurons, they also begin to produce GFP proteins. The team then used a standard protocol to distinguish the cells and classify them by GFP expression.Then, they identified proteins that accumulate on the surface of a partially differentiated cell called a dopaminergic progenitor.By selecting a protein characteristic of dopaminergic progenitor cells called contactin 2, they isolated the progenitor cells and transplanted them into rats that mimicked Parkinson's disease.Rats that received allografts enriched with contactin 2 had better dopamine release, suggesting that the transplanted cells better matched the dying neurons they intended to replace.Classifying cells also reduced movement symptoms in Parkinson's disease compared with rats treated with unsorted cells. The team's use of isolation procedures could be an important step toward more successful cell replacement therapies.

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