Friday, November 2, 2007

Parkinson's progression with times? Open Forum

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teokimhoeJoined: 03 Mar 2007Posts: 23Location: Malaysia
Posted: Sat Oct 13, 2007 8:29 pm Post subject: parkinson's progression with times

Do you agree that Parkinson's progression with time?

Despites there are new medications i.e one, second and third lines for Parkinson's treatment there are still no way to stop it's progression with time. Is it a shame for the medical world? Yes ,Parkinson's progression with times is individual and some come earlier or later. Nobody could tell you even doctors themselve could not .

The Parkinson's progression aggravates any part of body movement and emotional mood.

Exercise is not the treatment and the medication too. Both are helpful to relieve your muscles stiffness and emotional disorders i.e motor and non motor symdome. Do you agree?

TEOKIMHOE

to help the PD patients aware the diseases and encourage to set up support groups to educate the patients and their immediate families
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 11:45 am Post subject:

Yes, I agree with you Teokimhoe. It is a shame. There is, lately though, some promising treatment and new diagnostic aids on the horizon. I believe Altropane SPECT will allow physicians to more accurately diagnose Parkinson's much quicker and at a fraction of the cost compared to PET. I believe some of the new non-dopamine type drugs that are now gaining excitement among scientists will all but cure Parkinson's in the next 20 years. Asridipine (spelling?) alone has had really great results for some during it's testing (still in progress). Exercise and "mind activity" certainly help.
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Joe or BobJoined: 12 Aug 2007Posts: 38
Posted: Sun Oct 14, 2007 12:19 pm Post subject:

The primary fault in Parkinson's Disease is the insufficient formation of dopamine. That is why L-dopa initially relieves it. Parkinson's Disease gets progressively worse because the drugs used to treat it cause it to get worse. No substance lowers somebody's capacity to produce their own L-dopa as L-dopa does. So although L-dopa helps at first, in the long term it is a cause of Parkinson's Disease. Although dopamine agonists stimulate the dopamine receptors at first, they eventually cause the dopamine receptors to become progressively less sensitive. They make the problem worse. Unless any method increases dopamine formation it has no chance of relieving Parkinson's Disease. So none of the methods in development that don't increase dopamine have any chance of ridding it. Isradipine certainly won't be of any use. Isradipine has never benefited or been tested in Parkinson's Disease. Israpidine doesn't even in theory raise dopamine levels. It claims that it rejuvenates the cells involved in forming dopamine. However, they are being very misleading by claiming this. Israpidine alters only one aspect of the biochemistry of those cells. It doesn't rejuvenate their activity, which should be the primary aim of any treatment. Parkinson's Disease : http://viartis.net/parkinsons.disease
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 12:58 pm Post subject:

Joe or Bob, I will research Isradipine more. If you have anything more current than the information below, please provide to me. I would certainly appreciate it. Does your Viartis site discuss this in detail? I know Northwestern has a grant to complete studies. You may find some reference in the forum "Patients Like Me". One individual in this forum is taking it with great success. Additionally, one individual in our local support group has been taking for two months in trial participation and reports good results. I do not want to spew false statements though. Anything you have is appreciated. Please read below: Isradipine shown to slow down Parkinson's disease Medical Studies/Trials Published: Thursday, 14-Jun-2007 Printer Friendly Email to a Friend Northwestern University researchers have discovered a drug that slows and may even halt the progression of Parkinson's disease. The drug rejuvenates aging dopamine cells, whose death in the brain causes the symptoms of this devastating and widespread disease. D. James Surmeier, the Nathan Smith Davis Professor and chair of physiology at Northwestern University's Feinberg School of Medicine, and his team of researchers have found that isradipine, a drug widely used for hypertension and stroke, restores stressed-out dopamine neurons to their vigorous younger selves. The study is described in a feature article in the international journal Nature, which will be published on-line June 10. Dopamine is a critical chemical messenger in the brain that affects a person's ability to direct his movements. In Parkinson's disease, the neurons that release dopamine die, causing movement to become more and more difficult. Ultimately, a person loses the ability to walk, talk or pick up a glass of water. The illness is the second most common neurodegenenerative disease in the country, affecting about 1 million people. The incidence of Parkinson's disease increases with age, soaring after age 60. "Our hope is that this drug will protect dopamine neurons, so that if you began taking it early enough, you won't get Parkinson's disease, even if you were at risk. " said Surmeier, who heads the Morris K. Udall Center of Excellence for Parkinson's Disease Research at Northwestern. "It would be like taking a baby aspirin everyday to protect your heart." Isradipine may also significantly benefit people who already have Parkinson's disease. In animal models of the disease, Surmeier's team found the drug protected dopamine neurons from toxins that would normally kill them by restoring the neurons to a younger state in which they are less vulnerable. The principal therapy for Parkinson's disease patients currently is L-DOPA, which is converted in the brain to dopamine. Although L-DOPA relieves many symptoms of the disease in its early stages, the drug becomes less effective over time. As the disease progresses, higher doses of L-DOPA are required to help patients, leading to unwanted side-effects that include involuntary movements. The hope is that by slowing the death of dopamine neurons, isradipine could significantly extend the time in which L-DOPA works effectively. "If we could double or triple the therapeutic window for L-DOPA, it would be a huge advance," Surmeier said. The work by Surmeier's group is particularly exciting because nothing is known to prevent or slow the progression of Parkinson's disease. "There has not been a major advance in the pharmacological management of Parkinson's disease for 30 years," Surmeier said. Surmeier, who has researched Parkinson's disease for 20 years, had long been frustrated because it wasn't known how or why dopamine cells die in the disease. "It didn't seem like we were making much progress in spite of intense study on several fronts," he said. Because he's a physiologist, Surmeier decided to investigate whether the electrical activity of dopamine neurons might provide a clue to their vulnerability. All neurons in the brain use electrical signals to do their job, much like digital computers. First, Surmeier observed that dopamine neurons are non-stop workers called pacemakers. They generate regular electrical signals seven days a week, 24 hours a day, just like pacemaker cells in the heart. This was already known. But then he probed more deeply and discovered something very strange about these dopamine neurons. Most pacemaking neurons use sodium ions (like those found in table salt) to produce electrical signals. But Surmeier found that adult dopamine neurons use calcium instead. Sodium is a mild mannered ion that does its job without causing a whit of trouble to the cell. Calcium ions, however, are wild and rambunctious. Remember when Marlon Brando rode into town with his motorcycle gang in "The Wild One" Those guys were like calcium ions. "The reliance upon calcium was a red flag to us," Surmeier said. Calcium ions need to be chaperoned by the cell almost as soon as they enter to keep them from causing trouble, he noted. The cell has to sequester them or keep pumping them out. This takes a lot of energy. "It's a little like having a room full of two year olds you have to watch like a hawk so they don't get into trouble," Surmeier said. "That's really going to stress you." With three boys under age eleven, he can relate to the stressed dopamine neuron. Surmeier theorized that the non-stop stress on the dopamine neurons explains why they are more vulnerable to toxins and die at a more rapid rate as we age. But these findings still didn't offer him a new therapy. Then, serendipity struck when he was working on a different problem. He discovered that young dopamine neurons and adult ones have an entirely different way of operating. When the neurons are young, Surmeier found they actually use sodium ions to do their work. But as the neurons age, they become more and more dependent on the troublesome calcium and stop using sodium. This calcium dependence and the stress it causes the neurons --is what makes them more vulnerable to death. What would happen, Surmeier wondered, if he simply blocked the calcium's route into the adult neuron cells" Would the neurons revert to their youthful behavior and start using sodium again" "The cells had put away their old childhood tools in the closet. The question was if we stopped them from behaving like adults would they go into the closet and get them out again", Surmeier asked. "Sure enough, they did." When he gave the mice isradipine, it blocked the calcium from entering the dopamine neuron. At first, the dopamine neurons became silent. But within a few hours, they had reverted to their childhood ways, once again using sodium to get their work done. "This lowers the cells stress level and makes them much more resistant to any other insult that's going to come along down the road. They start acting like they're youngsters again," Surmeier said. The next step will be launching a clinical study. "This animal study suggests that calcium channel blockers, drugs currently used to reduce blood pressure, might someday be used to slow the steady progression of Parkinson's disease," said Walter J. Koroshetz, M.D., deputy director of the NINDS. http://www.northwestern.edu/
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Joe or BobJoined: 12 Aug 2007Posts: 38
Posted: Sun Oct 14, 2007 1:37 pm Post subject:

Somebody asked about this quite some time ago on the Viartis site. I have basically repeated the response that was made at the time. The article you have added provides everything of significance concerning Israpidine. Even if Israpidine was fully developed it couldn't get rid of Parkinson's Disease. Right now, there are a lot of non-dopamine methods being developed. Israpidine is one of them. Biochemically, the approaches these drugs use are so removed from the primary problem in Parkinson's Disease, that they have no chance of being of any long term use. The biochemistry involved is usually so complicated that most people, including even biochemists, don't understand it well enough to realise that that it will never lead to anything. In the meantime, the researchers and pharmaceutical companies are able to hype these drugs, raising more funding in the process. We always seem to hear from them "This could lead to....." but of course it never does.
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 4:13 pm Post subject:

Thanks for your take on this. I am a little skeptical too. Will do more study on this.
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johnball20Joined: 09 Mar 2007Posts: 96Location: Whittier, California
Posted: Sun Oct 14, 2007 7:14 pm Post subject: Isradipine and other treatments

Viartis and Cowboy, I am surprised at the assertion that Isradipine won't do anything to help slow or stop Parkinson's disease progression, You say "they have no chance of being of any long-term use." That assumes that we already know exactly why we have PD. i don't believe we as patients, or the doctors who treat us, or the scientists who are studying the underlying disease process are all that certain that there is one cause or one process at work. I believe that the underlying disease pocess affects far more than just the dopamine-producing cells or the dopamine receptors or even the dopamine transport system. It seems to me that it is a cellular decay that begins in the brain stem and moves selectively through the brain geography and will eventually reach the outer cortical layers if given sufficient time. It may result from cellular stress such as prolonged periods of anxiety, or emotional stress; from toxic stress, such as paraquat, rotennone or other biological contaminants; from misfolded proteins, from faulty genetic coding as in alpha-synuclein, or perhaps a combination of these toxic insults...At any rate there are so many varied symptoms and so many different reactions to the medications that I don't think we should rule out any potential strategy. Perhaps calcium-based processes could be replaced with sodium-based and re-invigorate the neurons. This will take time to figure out. Let's not shut off potential avenues of new thought just because it doesn't agree with our particular belief about the nature of the disease. John_________________We are working to raisea wareness and find a cure.
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Joe or BobJoined: 12 Aug 2007Posts: 38
Posted: Sun Oct 14, 2007 7:53 pm Post subject:

There's no great mystery about Parkinson's Disease. It is primarily due to a lack of dopamine. That is why L-dopa (which forms dopamine) can relieve the symptoms so readily. When they speak of calcium-based processes changing to sodium-based in order to reinvigorate the neurons they are talking biochemical nonsense. Even in theory, let alone practice, that would have no direct effect on dopamine formation. The amount of dopamine that is formed is not dependent on whether the process is calcium based or sodium based. Both processes exist anyway. People don't change from one to the other as they have claimed. Unfortunately, it is now almost the norm that drugs and methods are being hyped that fail to have a scientific basis.
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cowboyJoined: 03 Oct 2007Posts: 68
Posted: Sun Oct 14, 2007 8:42 pm Post subject:

JohnBall20, thanks for your take on this. My primary skepticism comes from the blood pressure lowering aspects of Isradipine and whether or not this can be neutralized and provide the same benefit to those without blood pressure problems. Northwestern has a great reputation for having a first class Neurology Sciences Team so I am taking this seriously with some degree of hope. That, and the fact that I know it is already being prescribed for certain individuals. Admittedly, I tread lightly because of my ignorance in brain chemistry and the fact I am neither physician or neuro-scientist. I am an Engineer by trade.
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teokimhoeJoined: 03 Mar 2007Posts: 23Location: Malaysia
Posted: Thu Oct 18, 2007 3:08 am Post subject: parkinson's progression survival with times

Dear Mr Teo For an incurable illness such as PD, it is certainly hoped that there should be at least a way to slow down the progression of illness, i.e. the rate of brain cell loss. Unfortunately, so far, no medication has been unequivocably proven to be able to slow down the progression of PD. The good news is that dopamine agonists (Pramipexole, Ropinirole) have been shown to have potential neuroprotective effect - the ability to slow down the rate of brain cell loss. Experimental studies have shown that dopamine agonists can protect nerve cells from the damage caused by poison. The ability of dopamine agonists to protect the brain cells (if it is true) can help Parkinson's patients to have additional several years of relatively good quality of life, and without motor complications (the involuntary movement). Despite this, I still think that there is a potential neuroprotective property of dopamine agonists. I still prefer to use dopamine agonists as the first-line medications for my PD patients. I am happy that Pramipexole and Ropinirole have recently arrived in Malaysia, and I am already prescribing them to my patients. Dr Chew Nee Kong, Kuala Lumpur, Malaysia._________________to help the PD patients aware the diseases and encourage to set up support groups to educate the patients and their immediate families
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Thursday, November 1, 2007

Ask the expert

Ask the Expert

Q) How do I find a neurologist specializing in the diagnosis and treatment of Parkinson's disease?

A) The Parkinson's Disease Foundation maintains a referral list of qualified and experienced movement disorders specialists (the sub-category of neurology under which Parkinson's falls) that covers most areas in the United States and many major cities abroad. Please contact our office on (800) 457-6676 and our staff will be happy to check our lists for a specialist close to you. One caveat: Medicare and most other insurance plans do not accept the Parkinson's Disease Foundation as an official referral. To be evaluated by a movement disorders specialist approved and covered under the health plan, the patient may need a physician's referral first. This can typically be easily obtained from the patient's current neurologist or primary care physician.

Q) Is Parkinson's disease inherited?
A) For the vast majority of individuals, Parkinson's disease is not thought to be an inherited disease. Even when a second person within a family is diagnosed with Parkinson's disease, this is thought to be more of a coincidence than an emerging genetic pattern. This is because Parkinson's is a fairly common disorder among the older population.
For younger-onset patients (typically, less than 50 years old at the time when symptoms start), ongoing research is suggesting a possible, minor inheritance factor, but this is still a theory under scientific evaluation.
And finally, there is what is considered to be a very rare form of Parkinson's that is inherited. It has been found to affect only a very small percentage of Parkinson's disease patients worldwide (probably less than one percent of all patients). In these families there are multiple patients diagnosed in multiple, consecutive generations. Even for this form of Parkinson's disease, the inheritance patterns are still being worked out.
While research continues on all possible genetic aspects of Parkinson's disease, there is currently no way to predict one's risk of developing Parkinson's disease based on having other family members affected by this disease.
Q) Is Co-EnzymeQ-10 of benefit to Parkinson's disease patients?
A) Recent studies are suggesting that Co-enzyme Q-10 may help to slow the progression of Parkinson's disease. However, these findings were reached in a preliminary study of a very small number of patients over a short period of time. The findings have however, provided the justification to expand the studies (by increasing the number of patients involved and studying the effects over a much longer period of time) to prove or disprove the theory and to determine safety both short- and long-term.
At this time, PDF advisers, as well as the primary author of the most recent study on CoQ10, are not recommending that their PD patients take Co-Q-10 in the dosages suggested in this preliminary study. They are instead recommending their patients wait until further, more detailed studies are completed.
Q) How fast does Parkinson's disease progress?
A) For the vast majority of individuals, Parkinson's disease is a very slow-progressive disorder, measured in decades rather than in months or in just a few years. As the disorder does progress over the years, new symptoms may appear or older ones may become more noticeable. For this reason, regular evaluations by a movement disorders specialist are needed to maintain sufficient symptomatic control via adjustments to the medication regimen.
When a more rapid progression rate is observed, there are generally outside factors contributing to this increase that need to be identified and properly managed. These factors might include:
A need to adjust the timing and dosages of the prescribed antiparkinson medications
A new health issue that, by itself or through its treatments, is interfering with the disease or the PD drugs' benefits or
The diagnosis of Parkinson's disease was in error and a different diagnosis may need to be considered
Q) What causes Parkinson's disease to appear?
A) At this time, we do not yet know the cause(s) of classic (idiopathic) Parkinson's disease. Many different theories have been and continue to be under investigation in an effort to pinpoint the factor/factors that need to be involved for this disease to develop. Investigative areas include environmental exposures (to naturally-occurring or man-made toxins), past illnesses/disorders, trauma and even the inheritance of a slight genetic predisposition to develop this disorder (and combinations of any or all these possible factors).
Non-classic forms of parkinsonism can, for example, include drug-induced forms (caused by any number of pharmacologic agents that can produce, as side effects, symptoms similar to those seen as part of Parkinson's); vascular forms (caused, for example, by a stroke in specific brain structures), and atypical forms (such as multiple system atrophy, corticobasal degeneration and progressive supranuclear palsy). Most of these forms are very rare and can typically be differentiated from classic Parkinson's disease by different brain scans, blood tests and/or a thorough review of the patient's history.
Q) Are there any known vitamins or supplemental compounds that can be beneficial in limiting the severity of Parkinson's disease symptoms or that can slow or stop the progression of the disease?
A) At this time, there is no scientific evidence to prove any type of benefit to a patient with Parkinson's disease from vitamins and/or supplements.
The only vitamin that has undergone rigorous investigation with regard to Parkinson's disease is Vitamin E, which was originally thought to be neuroprotective because of its antioxidant properties. Five years of study, following almost 5000 patients, failed to show that Vitamin E has any neuroprotective properties in Parkinson's disease. The only suggested benefit may be in reducing constipation, which can be a common problem associated with Parkinson's disease. Vitamin E is a naturally oily substance that assists constipation by greasing the bowels.
Q) What is Parkinson's disease?
A) Parkinson's disease is a chronic, progressive, neurologic disorder. An important part of its mechanism is the loss of the neurotransmitter dopamine in a group of brain structures that control movements. Its major manifestations are variable but can include hand tremor, slowness of movements, limb stiffness, and difficulties with gait and balance.

Surgical treatment

Surgical Treatments
Surgical Treatment for Parkinson's
Surgery for Parkinson's disease has come a long way since it was first developed more than 50 years ago. The newest version of this surgery, deep brain stimulation (DBS), was developed in the 1990s and is now a standard treatment. Although it is certainly the most important therapeutic advance since the development of levodopa, it is not for every person with Parkinson's. It is most effective - sometimes, dramatically so - for individuals who experience disabling tremors, wearing-off spells and medication-induced dyskinesias.
During deep brain stimulation surgery, electrodes are inserted into the targeted brain region using MRI and neurophysiological mapping to ensure that they are implanted in the right place. A device called an impulse generator or IPG (similar to a pacemaker) is implanted under the collarbone to provide an electrical impulse to a part of the brain involved in motor function. Patients have a controller, which allows them to check the battery and to turn the device on or off. An IPG battery lasts for about three to five years and is relatively easy to replace under local anesthesia.
It is very important that a person with Parkinson's who is thinking of surgery be well informed about the procedures and realistic in his or her expectations. For more information on DBS, request your print copy of the booklet Deep Brain Stimulation for Parkinson's Disease, written by PDF Scientific Editor Dr. Blair Ford.

Medications for Parkinson's


Parkinson’s Medications – An Overview
People with Parkinson’s disease often take a variety of medications in different doses in order to manage the symptoms of the disease. These factors, combined with the frequency with which one must take their medicines, can result in confusion. People with Parkinson’s and their caregivers should become familiar with their medications in order to use them most effectively and avoid possible interactions. Understanding a medication regime and sticking to it will provide the greatest benefit from the drug and avoid unpleasant “off” periods due to missed doses or confusion.
This section of our website contains information about medications for Parkinson’s disease. Included is a table of Parkinson’s drugs, a section on over-the-counter medications, tips for administering drugs and hints to help you save money.
Please note that the side-effects listed in the tables that accompany each class of medication are the most commonly experienced. Not all patients will experience such side-effects. For many people who do experience side-effects, they can often be effectively limited or eliminated with careful adjustments to dosage or the timing of the individual doses. If any side-effects are experienced, speak to the treating physician immediately. For a complete description of each drug and its possible side-effects, please request a “package insert” from your pharmacist for each drug being used. It is recommended that all prescriptions be filled at the same pharmacy to avoid interactions between medications. Interactions can be dangerous and even life-threatening, so make sure the pharmacist knows of all medications and supplements being taken – including over-the-counter medications and supplements.
Although there are general guidelines that doctors use to choose a treatment regimen, each patient must be individually evaluated to determine which drug or combination of drugs is best for them. For some, a “first choice” drug might be one of the levodopa preparations, and for others, an initial prescription may be given for one of the agonists, an MAO inhibitor or an anticholinergic. The choice of drug treatment depends on many variables including symptom presentation, other concurrent health issues (and the medications being used to treat them) and a person’s age. And while the suggested starting dosages (as indicated by the package insert) are listed here, remember that they too can vary greatly depending on a person’s needs and metabolism.
Carbidopa/Levodopa (Sinemet®) Levodopa is a substance that is converted into dopamine by an enzyme in the brain. It is then released by brain cells and activates dopamine receptors allowing for normal function of the movement control centers of the brain. Forty years after its discovery, levodopa remains the most effective medication for Parkinson’s disease. In fact, 70 to 80 percent of treated Parkinson’s patients are on levodopa therapy. Levodopa is the “gold standard” by which all treatments for Parkinson’s are measured.
Levodopa combined with carbidopa (or Sinemet®) represented a significant improvement in the treatment of Parkinson's disease. The addition of carbidopa prevents levodopa from being converted into dopamine in the bloodstream, allowing more of it to get to the brain. Therefore, a smaller dose of levodopa is needed to treat symptoms. In addition, the nausea and vomiting often associated with levodopa treatment is greatly reduced by the presence of carbidopa. Unfortunately, with increased dosing and prolonged use of levodopa, patients experience other side-effects including dyskinesias (spontaneous, involuntary movements) and "on-off" periods when the medication will suddenly and unpredictably start or stop working.
Check with a doctor before taking any of the following to avoid possible interactions: antacids, anti-seizure drugs, anti-hypertensives, anti-depressants and high protein food.
Stalevo® (carbidopa, levodopa and entacapone) is a combination tablet for patients who experience end-of-dose "wearing-off." The tablet combines carbidopa/levodopa with entacapone. While carbidopa reduces the side effects of levodopa, entacapone extends the time levodopa is active in the brain (up to 10 percent longer). The same drugs that interact with carbidopa/levodopa and entacapone interact with Stalevo®.
Medication
Available Doses
Initial Dosing
Side Effects
Indications
Interactions
Carbidopa/
Levodopa
(Sinemet®)
10/100 mg
25/100 mg
50/200 mg
25/100 mg 2-3X/day
Low blood pressure, nausea, confusion, dyskinesia, dry mouth, dizziness
First course of treatment; converts to dopamine to manage major symptoms
Antacids, anti-seizure drugs, anti-hypertensives, anti-depressants, high protein food
Carbidopa/
Levodopa
controlled release
(Sinemet CR®)
10/100 mg
25/100 mg
50/200 mg
50/200 mg 2X/day
Low blood pressure, nausea, confusion, dyskinesia, dry mouth, dizziness
First course of treatment; converts to dopamine to manage major symptoms and may prolong effectiveness
Antacids, anti-seizure drugs, anti-hypertensives, anti-depressants, high protein food
Carbidopa/
Levodopa/
Entacapone
(Stalevo®)
12.5/50/200 mg
25/100/200 mg
37.5/150/200 mg
12.5/50/200 mg
Dyskinesia, nausea, diarrhea, hyperkinesia, abdominal pain, dizziness, harmless discoloration of urine, saliva and/or sweat
Secondary course of treatment; combines entacapone with levodopa/carbidopa to block COMT enzyme and prolong levodopa’s effectiveness
Same as levodopa/carbidopa, MAO inhibitors, Comtan, Sinemet, high doses (10 mg or more) of selegiline
Carbidopa/
Levodopa
Orally disintegrating tablet
(Parcopa®)
10/100 mg
25/100 mg
25/250 mg
25/100 mg 2-3X/day
Low blood pressure, nausea, confusion, dyskinesia, dry mouth, dizziness
First course of treatment; converts to dopamine to manage major symptoms; also for patients with swallowing difficulties
Antacids, anti-seizure drugs, anti-hypertensives, anti-depressants, high protein food
Dopamine agonists are drugs that stimulate the parts of the human brain that receive dopamine. In effect, the brain "thinks" it is receiving dopamine, so these drugs help satisfy the brain's need for dopamine. Dopamine agonists can be taken alone or in combination with medications containing levodopa. Agonists available in the United States include bromocriptine (Parlodel®), pramipexole (Mirapex®) and ropinirole (Requip®). In March 2007, the dopamine agonist pergolide (Permax) was pulled from the market by the US Food and Drug Administration in response to reports of heart valve damage.
Consult a doctor before taking any of the following to avoid possible interactions: alcohol, anti-psychotics, medications that lower blood pressure, Navane® (thiothixene), Taractan® (chlorprothixene), Haldol® (haloperidol), Reglan® (metoclopramide), phenothiazines, thiozanthenes, cimetidine, phenothiazines, butyrophenones, Cipro® and benzodiazepines.
Medication
Available Doses
Initial Dosing
Side Effects
Indications
Interactions
APOKYN™ injection (apomorphine hydrochloride)
.02 mL –
.06 mL
.02 mL during “off” periods
Nausea, vomiting, low blood pressure, sleepiness, dyskinesias, hallucinations, chest pain
Adjunct levodopa therapy to treat “off” periods
5HT3 agonists (for example, Zofran®, Kytril®) antihypertensives (for example Norvasc® and Zestril®)
Bromocriptine
(Parlodel®)
2.5 mg
5 mg
2.5 mg 3X/day

Low blood pressure, nausea, edema, confusion, dry mouth, depression, headaches
First course of treatment alone or with levodopa;
mimics dopamine to manage major symptoms
Alcohol, anti-psychotics, blood pressure lowering medications
Rotigotine Transdermal System (Neupro®)
2mg/24hrs4 mg/24hrs6 mg/24hrs
One 2 mg patch a day
Nausea, application site reactions, somnolence, dizziness, headache, vomiting, sleep attacks, insomnia.
First course of treatment alone or with levodopa in early-stage idiopathic Parkinson’s disease; mimics dopamine to manage major symptoms
May cause allergic-type reactions including anaphylactic symptoms especially in people sensitive to sulfites, including those with asthma.
Pramipexole
(Mirapex®)
.125 mg
.25 mg
.5 mg
1 mg
1.5 mg
.125 mg 3X/day
Arthritis, chest pain, nausea, low blood pressure, sleep disturbances, sedation
First course of treatment alone or with levodopa;
mimics dopamine to manage major symptoms
Sedatives and tranquilizers; metocipramide, thiozanthenes, cimetidine, phenothiazines, butyrophenones

Ropinirole
(Requip®)
.25 mg
.5 mg
1 mg
2 mg
3 mg
4 mg
5mg

.25 mg 2X/day
Abdominal pain, sleep disturbances, nausea, low blood pressure, sedation
First course of treatment alone or with levodopa;
mimics dopamine to manage major symptoms
Alcohol, anti-depressants, Cipro®, anti-psychotics, benzodiazipines
Anticholinergics (trihexyphenidyl, benztropine mesylate, procyclidine, etc.) do not act directly on the dopaminergic system. Instead they decrease the activity of another neurotransmitter that controls movement, called acetylcholine, to balance out the production of dopamine and acetylcholine. In general, mild PD that consists of tremor at rest can often be treated initially with anticholinergic agents. Adverse effects of these drugs include blurred vision, dry mouth and urinary retention. Anticholinergics may be contraindicated in older patients because they can cause confusion and hallucination.
Check with a doctor before using anticholinergics with anti-histamines, Haldol®, Thorazine®, Symmetrel®, Clozaril® and alcohol.
Medication
Available Doses
Initial Dosing
Side Effects
Indications
Interactions
Benzotropine mesylate
(Cogentin®)
.5 mg
.5 mg 2X/day
Confusion, hallucinations, nausea, blurred vision, dry mouth, urinary retention, nervousness; not used long-term due to side effects
Secondary medication; tremor; attempts to restore balance by inhibiting other enzymes and nerve cells that may attack dopamine
Anti-histamines, Propulside®, Haldol®, Thorazine®, Symmetrel®, Clozaril®, alcohol
Trihexyphenidyl HCL
(Artane®)
1 mg
2 mg
1-2 mg 2X/day
Confusion, hallucinations, nausea, blurred vision, dry mouth, urinary retention, nervousness; not used long-term due to side effects
Secondary medication; tremor; attempts to restore balance by inhibiting other enzymes and nerve cells that may attack dopamine
Anti-histamines
MAO-B inhibitors such as selegiline or deprenyl (Eldepryl®) are used to block an enzyme in the brain that breaks down levodopa. They have been shown to delay the need for Sinemet® when prescribed in the earliest stage of Parkinson’s, and have also been approved for use in later stages of the disease to boost the effects of Sinemet®. Eldepryl® may interact with anti-depressants, narcotic pain killers and decongestants. Check with a doctor before taking any new medications.
Medication
Available Doses
Initial Dosing
Side Effects
Indications
Interactions
Selegiline
(Eldepryl®, Carbex®)
5 mg
5 mg 2X/day
(max dose)
Agitation, insomnia, hallucinations
Tertiary medication; controls brain’s metabolism of dopamine
Anti-depressants, narcotic painkillers, decongestants
Selegiline HCIOrally disintegrating tablet(Zelapar®)
1.25mg
1.25mg 1X daily
Dizziness, nausea, pain, headache, insomnia, rhinitis, dyskinesias, back pain, stomatitis, dyspepsia
Adjunct to levodopa in patients with significant "off" periods
Anti-depressants, narcotic painkillers, decongestants
Rasagiline (Azilect®)
0.5mg1mg
0.5mg 1X daily
Increased dyskinesias, postural hypotension, headaches, joint pain, indigestion
Signs and symptoms of PD as initial monotherapy and adjunct to levodopa
High tyramine content foods (for example, draft beer, red wine, aged cheeses, soy sauce and other products), narcotic painkillers, anti-depressants, decongestants

COMT inhibitors such as entacapone (Comtan®) represent a different class of Parkinson's medications and they must be taken with levodopa. COMT inhibitors prolong symptom relief by blocking the action of an enzyme which breaks down levodopa, allowing a larger amount of levodopa to reach the brain, which raises the dopamine level. This helps provide a more stable, constant supply of levodopa.
Medication
Available Doses
Initial Dosing
Side Effects
Indications
Interactions
Entacapone
(Comtan®)
200 mg
200 mg with levodopa; max 8 per day
Abdominal pain, back pain, constipation, nausea, diarrhea, blood in urine
Secondary medication; delays wearing off by prolonging effectiveness of levodopa
MAO inhibitors
Tolcapone
(Tasmar®)
100 mg
200 mg
100 mg 3X/day
Abdominal pain, back pain, constipation, nausea, diarrhea, blood in urine, liver failure
Tertiary medication for motor fluctuations; limited in use to those who have exhausted other treatment options
MAO inhibitors
Other medications
Medication
Available Doses
Initial Dosing
Side Effects
Indications
Interactions
Amantadine
(Symmetrel®)
100 mg
100 mg 2-3 X/day
Dizziness, weakness, dry mouth, constipation, skin blotches
Secondary medication for tremor and muscle rigidity
Cogentin® (benztropine), Disipal® (orphenadrine), Sinemet® (levodopa), Artane® (trihexyphenidyl), amphetamines, alcohol
Rivastigmine tartrate
(Exelon®)
1.5mg3mg4.5mg6mg Patch 10 (9.5 mg/24 hrs) Patch 20 (17.4 mg/24 hrs)
1.5mg 2X per day
Nausea, vomiting, loss of appetite, weight loss
Dementia associated with PD
No known drug-drug interactions

Over-the-Counter Medications
Although there is little conclusive scientific information on natural supplements, researchers are examining several substances to evaluate their effectiveness on slowing Parkinson's disease progression and managing its symptoms. Nutritional supplements are not regulated with the same approval method for prescription drugs, and people with Parkinson's should discuss any medications (prescription or over-the-counter) with a doctor before taking them to avoid potentially dangerous interactions.
Since there is evidence relating oxidative damage of nerve cells to PD, some researchers are studying antioxidants. A 2002 study focused on the potential antioxidant Coenzyme Q10 (CoQ10), which is believed to play an important role in mitochondria health. Mitochondria are the "powerhouses" of a cell, and some scientists think that abnormalities of mitochondrial function may play a role in Parkinson's. A recent clinical trial found that high doses of CoQ10 (up to 1200 mg) showed a possible slowing of disease progression in a small number of subjects. These results are promising but researchers have not studied CoQ10 extensively enough to recommend it to Parkinson's patients.
Scientists have also examined Vitamin E, Vitamin C and health foods to evaluate their oxidative properties. Vitamin E can fight damage in the brain caused by free radicals, and has been suggested to lower the risk of PD. However, researchers conducted an extensive and thorough study over 10 years ago ( the DATATOP trial) and failed to find any evidence that Vitamin E slows the progression of Parkinson's or manages symptoms. Since Vitamin E has very few side-effects, many Parkinson's patients continue to take it in high doses of 400 IU or more. Researchers are also examining health foods, such as fermented papaya and blueberries, to determine their role in slowing nerve cell death. Scientists are optimistic about the research but do not have enough conclusive data to recommend these supplements to treat Parkinson's disease.
Creatine is another compound of scientific interest that increases levels of phosphocreatine (an energy source in muscle and the brain). The National Institute of Neurological Disorders and Stroke (NINDS) is conducting a multi-center clinical trial to determine if creatine protects against nerve cell damage. Researchers have also studied a compound called glutathione to determine its effect on nerve cell metabolism and its power as an antioxidant. Both compounds show promise, but the appropriate dosing is unclear, as are the most effective method of administration, side-effects and long-term dosing risks.
Although nutritional supplements have shown some promising results in preliminary studies, it is important to remember that there is not sufficient scientific data to recommend them for Parkinson's disease. Over-the-counter medications can and do have side-effects and interactions with other drugs. They tend to be expensive and they vary with different manufacturers. Before taking any over-the-counter medication, it is very important that a person with Parkinson's discuss the addition of these supplements with their doctor.

Managing Your Medications
Taking medications for Parkinson's disease is straightforward for most people during the first several years of treatment. The effect of each dose usually lasts well into the period after the next dose, and delaying a dose even by an hour does not disrupt the effective coverage of symptoms.
The situation is different for many people who have been taking Parkinson's medications for several years (usually five years or more). In these stages of the disease, effective relief from symptoms can depend on carefully following a regular schedule of medication doses. There are several ways for Parkinson's patients to achieve the greatest possible benefit from their medications. Since in the more advanced stages of Parkinson's disease the symptoms are often unpredictable and can fluctuate daily, it is important to take an active role in finding a routine that is tailor-made and makes the most of the medicine. A person should ask themselves how long it takes for a pill to work and how long its positive effects remain. Note if the pills should be taken with food, between meals or on an empty stomach and how it feels when medication starts to wear off. The answers to these questions can help explain how the pill works and possibly increase "on" time.
People with Parkinson's must know what medications they are taking, when and why. This can be achieved by working with one pharmacist. A pharmacist will note all of the medications a person is taking in a computer, which safeguards them from any interactions. Another way to obtain this information is by constructing a medication chart (to download a sample chart, click here). The chart should include information such as the medication's name, the strength and a time schedule of when it should be taken. This chart can help the patient and/or caregiver easily recognize the medication and decreases the chance of a missed dose. People with Parkinson's can also share this chart with a neurologist to make sure both parties are clear on what is being taken and why.
Organization is a key factor in getting the most from Parkinson's medications. Since several medications will probably be taken at different times of the day, a timing device can be crucial in avoiding missed doses. Talking systems, beeping watches and multi-alarm timers are widely available. These systems can be both discreet and loud, with vibrating and sound features. In addition, pill dispensers organize pills by day and time to eliminate carrying several large prescription bottles.
These tips can help people with Parkinson's manage their medications and develop a personal routine to suit their lifestyles and needs.

Saving on Medications
The substantial cost of Parkinson's medications is often a burden for many people. Several pharmaceutical companies feature programs to help eligible applicants reduce their medication costs. These programs are usually limited to the company's brand-name medications, and will most likely have specific requirements including age and income. Visit drug makers' websites or call the company's toll-free hotline for more information on money-saving assistance programs. These programs are often best accessed with the help of your doctor and healthcare team.
Researching the various drug assistance programs can be a great deal of work. An organization called The Partnership for Prescription Assistance (PPRA) may be able to help navigate these systems to find the best options. PPRA brings together America's pharmaceutical companies, doctors, other health care providers, patient advocacy organizations and community groups to help qualifying patients who lack prescription coverage get the medicines they need through public or private programs. PPRA's website, http://www.pparx.org/, provides access to more than 275 public and private patient assistance programs, including more than 150 programs offered by pharmaceutical companies. PPRA can also be contacted by calling (888) 477-2669.

The role of the Patient

The Role of the Patient
The Role of the Patient
Treating Parkinson's disease is not exclusively the doctor's job; there are many things a person with Parkinson's can do to contribute. Regular exercise, joining a support group, maintaining a healthy diet and taking part in a clinical trial are just some of the things you might consider.
A Healthy Patient/Doctor Relationship
Exercise
Support Groups
Diet
Physical, Speech and/or Occupational Therapy
Clinical Trials
A Healthy Patient/Doctor Relationship: Making an accurate diagnosis of Parkinson's - specifically in its early stages - is difficult, but a skilled practitioner can come to a reasoned conclusion that it is Parkinson's. Every person diagnosed with Parkinson's should consider getting a second opinion from a neurologist who specializes in movement disorders and is up-to-date on research and approaches to therapy.
Locating a qualified physician is a first step; next is considering whether the physician is the right one. A person with Parkinson's will work with a physician for many years. Consider these questions:
Are you comfortable speaking with your physician?
Do you feel respected by your doctor?
Are questions answered to your satisfaction or do you come away from a visit feeling that you have not been taken seriously?
Can you get in touch with the doctor between visits?
To find a neurologist or movement disorder specialist in your area:
Ask your primary care physician for a referral
Seek referrals from other living with Parkinson's
Contact your insurance provider for a list of neurologists or movement disorder specialists in your network
Contact PDF for a referral.

Exercise: For people with Parkinson's, regular exercise or physical therapy is crucial for maintaining and improving mobility, flexibility, balance, range of motion and for warding off many of the disease's secondary symptoms such as depression and constipation. PDF offers Motivating Moves for People with Parkinson's, a unique program of 24 seated and stimulating exercises that were created especially for people with Parkinson's. Copies are available for ordering through the website, or you can call or email PDF for more information. As with every aspect of your care, always consult your doctor before starting an exercise program.
Support groups: For many people, support groups play an important role in the emotional well-being of patients and families. They can provide a caring environment for asking questions about Parkinson's, for sharing stories and advice and for creating friendships with people who have experienced similar problems. To find a support group in your area, please call or email PDF. In addition to in-person support groups, many people also find online groups and list servs helpful. For a listing of list servs that serve the Parkinson's community, please request our publication, Web Resources for People with Parkinson's Disease.
Diet: Many people with Parkinson's lose weight because of poor appetite and inadequate food intake. It is recommended to maintain a full diet that contains all the daily nutritional requirements, including extra fresh fruits and vegetables for fiber to help prevent constipation and plenty of fluids to keep hydrated.
Some people who take levodopa find that protein may interfere with the medication's effect. Limiting protein intake or staggering the medication dosing to avoid conflicts with meals can help this problem. However, adjustments in protein intake are only worthwhile for those very few people whose response to levodopa is indeed sensitive to dietary protein.
People with Parkinson's who lose weight for no clear reason should discuss this with a physician.
Physical, Speech and/or Occupational Therapy: These therapies can help Parkinson's patients control their symptoms and make daily life easier. Physical therapy may increase muscle strength and flexibility and decrease the incidence of falls. Speech therapy can increase voice volume and assist with word pronunciation. The Lee Silverman technique is a special speech therapy that can be very beneficial to people with Parkinson's - for further information see www.lsvt.org.
Occupational therapy gives people alternative methods of doing tasks that they can no longer perform with ease. These options may provide a stronger sense of control when living with Parkinson's disease. A neurologist should be able to provide recommendations for these therapies and, if needed, a referral. These therapies may or may not be covered by insurance.
Clinical Trials: Clinical trials (also called medical research, clinical research or a clinical study) help researchers answer specific questions about the safety and efficacy of new treatments by studying its effects in people. They are an essential and necessary component of the scientific research process. Simply put, there is no other way for research to show that a proposed treatment works. In addition to contributing to research, joining a clinical trial can provide a person with early access to potentially-helpful Parkinson's treatments and drugs that are not yet on the market.
The lack of participation by people with Parkinson's disease has resulted in some trials being unnecessarily delayed. For more information on clinical trials and how you can get involved, visit www.PDtrials.org. PDtrials is a community-wide initiative of the major Parkinson's advocacy groups whose goal is to accelerate the development of new treatments for Parkinson's. This project is led by the Parkinson's Disease Foundation, in collaboration with the following organizations: American Parkinson Disease Association, Inc, The Michael J. Fox Foundation for Parkinson's Research, National Parkinson Foundation, Parkinson's

What is Parkinson's disease?

Parkinson's Disease: An Overview
What is Parkinson's disease?
Parkinson's disease is a movement disorder that is chronic and progressive, meaning that symptoms continue and worsen over time. As many as one million Americans suffer from Parkinson's disease. While approximately 15 percent of people with Parkinson's are diagnosed before the age of 50, incidence increases with age. The cause is unknown, and although there is presently no cure, there are many treatment options such as medication and surgery to manage the symptoms. (For more statistics on Parkinson's disease, read our fact sheet, General Facts on Parkinson's Disease).
Parkinson's disease occurs when a group of cells in an area of the brain called the substantia nigra begin to malfunction and die. These cells in the substantia nigra produce a chemical called dopamine. Dopamine is a neurotransmitter, or chemical messenger, that sends information to the parts of the brain that control movement and coordination. When a person has Parkinson's disease, their dopamine-producing cells begin to die and the amount of dopamine produced in the brain decreases. Messages from the brain telling the body how and when to move are therefore delivered more slowly, leaving a person incapable of initiating and controlling movements in a normal way.
Parkinson's disease can also cause several different symptoms. The specific group of symptoms that an individual experiences varies from person to person. Some of the most common symptoms of Parkinson's disease are:
tremor of the hands, arms, legs, jaw and face
rigidity or stiffness of the limbs and trunk
bradykinesia or slowness of movement
postural instability or impaired balance and coordination
If you have a question about Parkinson's disease, please submit it to our Ask the Expert service to receive an email reply within 10 working days. You can also visit the Expert Resource Center to find answers to hundreds of frequently-asked questions about Parkinson's.
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What casues Parkinson's?

Causes
What causes Parkinson's?
Why an individual develops Parkinson's disease remains unclear. The cause is probably a combination of genetic and environmental factors, and may vary from person to person. Although the cause of Parkinson's remains unknown, scientists have identified factors that contribute to Parkinson's in some patients. For example, people over age 60 have a two-to-four percent risk of developing Parkinson's disease, compared with the one-to-two percent risk in the general population.
Below is information on the two factors that scientists think are most likely to cause Parkinson's disease.
Genetics About 15 to 25 percent of people with Parkinson's report having a relative with the disease. In large epidemiological studies (studies that deal with incidence, distribution and control of disease in a population), researchers have found that people with an affected first-degree relative, such as a parent or sibling, have a two-to-three fold increased risk of developing Parkinson's, as compared to the general population. This means that if your parent has Parkinson's, your chances of developing the disease are slightly higher than the risk in the general population.The vast majority of Parkinson's cases are not directly inherited, but researchers have discovered several genes that can cause the disease in a small number of families. Some of these genes involve proteins that play a role in dopamine cell functions. Because genetic forms of a disease can be studied in great detail in the laboratory, and because understanding the rare genetic forms of Parkinson's disease may help to understand more common forms of the disease, genetic aspects of PD are currently the subject of intense research.
Environmental Factors Some scientists have suggested that Parkinson's disease may result from exposure to an environmental toxin or injury. Epidemiological research has identified several factors that may be linked to PD, including rural living, well water, herbicide use and exposure to pesticides. Also, a synthetic narcotic agent called MPTP can cause immediate and permanent parkinsonism if injected. These environmental factors are not useful in diagnosing the cause of Parkinson's disease in individual people. In fact, there is no conclusive evidence that any environmental factor, alone, can be considered a cause of the disease. However, these environmental factors have been helpful in studying laboratory models of Parkinson's disease. Scientists are continuing to pursue these clues to establish more concrete linkages.
Most experts share the opinion that Parkinson's is caused by a combination of genetic and environmental factors. However, no one yet knows what this combination is. For more information on genetic and environmental factors in causing Parkinson's disease, read the PDF News & Review article Nature Versus Nurture: What Causes PD?