By Steven Marsh
Patients who have been diagnosed with Parkinson’s disease (PD) may have relief from symptoms associated with the condition in the near future, according to a study presented at the 2010 American Society for Stereotactical and Functional Neurosurgery.
In an effort to find potential treatments for individuals with the nervous system disorder, a team of researchers at Rhode Island Hospital conducted a series of exercises that stimulated the spinal cord on an animal model, which showed signs of PD. Because the findings displayed better motor function in the animal, the investigators tested the treatment with spinal cord simulation on a male patient aged 82 years.
While the individual wasn’t receiving any form of medication as treatment for the disorder, researchers used different frequencies of stimulation to determine if a human would experience similar results compared to the animal model.
The researchers discovered that high stimulation frequencies made it easier for the patient to walk, while low frequencies worsened PD side effects.
While the results of the study did give investigators some insight as to how to treat PD patients, clinical trials with a larger group of patients would be more beneficial to developing treatment.
Finding therapies for this disorder is growing in interest throughout the medical world, as QR Pharma and Massachusetts General Hospital have launched research to determine a way to block a protein associated the development of PD.ADNFCR-1960-ID-19845071-ADNFCR
Showing posts with label tremor. Show all posts
Showing posts with label tremor. Show all posts
Tuesday, June 22, 2010
Saturday, June 13, 2009
Treatments and drugs
Your initial response to Parkinson's treatment can be dramatic. Over time, however, the benefits of drugs frequently diminish or become less consistent, although symptoms can usually still be fairly well controlled. Your doctor may recommend lifestyle changes, such as physical therapy, a healthy diet and exercise, in addition to medications. In some cases, surgery may be helpful.
Medications
Medications can help manage problems with walking, movement and tremor by increasing the brain's supply of dopamine. Taking dopamine itself is not helpful, because it is unable to enter your brain.
*
Levodopa. The most effective Parkinson's drug is levodopa, which is a natural substance that we all have in our body. When taken by mouth in pill form, it passes into the brain and is converted to dopamine. Levodopa is combined with carbidopa to create the combination drug Sinemet. The carbidopa protects levodopa from premature conversion to dopamine outside the brain; in doing that, it also prevents nausea. In Europe, levodopa is combined with a similar substance, benserazide, and is marketed as Madopar.
As the disease progresses, the benefit from levodopa may become less stable, with a tendency to wax and wane ("wearing off"). This then requires medication adjustments. Levodopa side effects include confusion, delusions and hallucinations, as well as involuntary movements called dyskinesia. These resolve with dose reduction, but sometimes at the expense of reduced parkinsonism control.
*
Dopamine agonists. Unlike levodopa, these drugs aren't changed into dopamine. Instead, they mimic the effects of dopamine in the brain and cause neurons to react as though dopamine is present. They are not nearly as effective in treating the symptoms of Parkinson's disease. However, they last longer and are often used to smooth the sometimes off-and-on effect of levodopa.
This class includes pill forms of dopamine agonists, pramipexole (Mirapex) and ropinirole (Requip), as well as a patch form, rotigotine (Neupro). Pergolide (Permax) has been withdrawn from the market because of its association with heart valve problems. A short-acting injectable dopamine agonist, apomorphine (Apokyn), is used for quick relief.
The side effects of dopamine agonists include those of carbidopa-levodopa, although they're less likely to cause involuntary movements. However, they are substantially more likely to cause hallucinations, sleepiness or swelling. These medications may also increase your risk of compulsive behaviors such as hypersexuality, compulsive gambling and compulsive overeating. If you are taking these medications and start behaving in a way that's out of character for you, talk to your doctor.
* MAO B inhibitors. These types of drugs, including selegiline (Eldepryl) and rasagiline (Azilect), help prevent the breakdown of both naturally occurring dopamine and dopamine formed from levodopa. They do this by inhibiting the activity of the enzyme monoamine oxidase B (MAO B) — the enzyme that metabolizes dopamine in the brain. Side effects are rare but can include serious interactions with other medications, including drugs to treat depression and certain narcotics.
* Catechol O-methyltransferase (COMT) inhibitors. These drugs prolong the effect of carbidopa-levodopa therapy by blocking an enzyme that breaks down levodopa. Tolcapone (Tasmar) has been linked to liver damage and liver failure, so it's normally used only in people who aren't responding to other therapies. Entacapone (Comtan) doesn't cause liver problems and is now combined with carbidopa and levodopa in a medication called Stalevo.
* Anticholinergics. These drugs have been used for many years to help control the tremor associated with Parkinson's disease. A number of anticholinergic drugs, such as trihexyphenidyl and benztropine (Cogentin), are available. However, their modest benefits may be offset by side effects such as confusion and hallucinations, particularly in people over the age of 70. Other side effects include dry mouth, nausea, urine retention — especially in men with an enlarged prostate — and severe constipation.
* Antivirals. Doctors may prescribe amantadine (Symmetrel) alone to provide short-term relief of mild, early-stage Parkinson's disease. It also may be added to carbidopa-levodopa therapy for people in the later stages of Parkinson's disease, especially if they have problems with involuntary movements (dyskinesia) induced by carbidopa-levodopa. Side effects include swollen ankles and a purple mottling of the skin.
Physical therapy
Exercise is important for general health, but especially for maintaining function in Parkinson's disease. Physical therapy may be advisable and can help improve mobility, range of motion and muscle tone. Although specific exercises can't stop the progress of the disease, improving muscle strength can help you feel more confident and capable. A physical therapist can also work with you to improve your gait and balance. A speech therapist or speech pathologist can improve problems with speaking and swallowing.
Surgery
Deep brain stimulation is the most common surgical procedure to treat Parkinson's disease. It involves implanting an electrode deep within the parts of your brain that control movement. The amount of stimulation delivered by the electrode is controlled by a pacemaker-like device placed under the skin in your upper chest. A wire that travels under your skin connects the device, called a pulse generator, to the electrode.
Deep brain stimulation is most often used for people who have advanced Parkinson's disease who have unstable medication (levodopa) responses. It can stabilize medication fluctuations and reduce or eliminate involuntary movements (dyskinesias). Tremor is especially responsive to this therapy. Deep brain stimulation doesn't help dementia and may make that worse.
Like any other brain surgery, this procedure has risks — such as brain hemorrhage or stroke-like problems. Infection also may occur, requiring parts of the device to be replaced. In addition, the unit's battery beneath the skin of the chest wall must be surgically replaced every few years. Deep brain stimulation isn't beneficial for people who don't respond to carbidopa-levodopa.
Medications
Medications can help manage problems with walking, movement and tremor by increasing the brain's supply of dopamine. Taking dopamine itself is not helpful, because it is unable to enter your brain.
*
Levodopa. The most effective Parkinson's drug is levodopa, which is a natural substance that we all have in our body. When taken by mouth in pill form, it passes into the brain and is converted to dopamine. Levodopa is combined with carbidopa to create the combination drug Sinemet. The carbidopa protects levodopa from premature conversion to dopamine outside the brain; in doing that, it also prevents nausea. In Europe, levodopa is combined with a similar substance, benserazide, and is marketed as Madopar.
As the disease progresses, the benefit from levodopa may become less stable, with a tendency to wax and wane ("wearing off"). This then requires medication adjustments. Levodopa side effects include confusion, delusions and hallucinations, as well as involuntary movements called dyskinesia. These resolve with dose reduction, but sometimes at the expense of reduced parkinsonism control.
*
Dopamine agonists. Unlike levodopa, these drugs aren't changed into dopamine. Instead, they mimic the effects of dopamine in the brain and cause neurons to react as though dopamine is present. They are not nearly as effective in treating the symptoms of Parkinson's disease. However, they last longer and are often used to smooth the sometimes off-and-on effect of levodopa.
This class includes pill forms of dopamine agonists, pramipexole (Mirapex) and ropinirole (Requip), as well as a patch form, rotigotine (Neupro). Pergolide (Permax) has been withdrawn from the market because of its association with heart valve problems. A short-acting injectable dopamine agonist, apomorphine (Apokyn), is used for quick relief.
The side effects of dopamine agonists include those of carbidopa-levodopa, although they're less likely to cause involuntary movements. However, they are substantially more likely to cause hallucinations, sleepiness or swelling. These medications may also increase your risk of compulsive behaviors such as hypersexuality, compulsive gambling and compulsive overeating. If you are taking these medications and start behaving in a way that's out of character for you, talk to your doctor.
* MAO B inhibitors. These types of drugs, including selegiline (Eldepryl) and rasagiline (Azilect), help prevent the breakdown of both naturally occurring dopamine and dopamine formed from levodopa. They do this by inhibiting the activity of the enzyme monoamine oxidase B (MAO B) — the enzyme that metabolizes dopamine in the brain. Side effects are rare but can include serious interactions with other medications, including drugs to treat depression and certain narcotics.
* Catechol O-methyltransferase (COMT) inhibitors. These drugs prolong the effect of carbidopa-levodopa therapy by blocking an enzyme that breaks down levodopa. Tolcapone (Tasmar) has been linked to liver damage and liver failure, so it's normally used only in people who aren't responding to other therapies. Entacapone (Comtan) doesn't cause liver problems and is now combined with carbidopa and levodopa in a medication called Stalevo.
* Anticholinergics. These drugs have been used for many years to help control the tremor associated with Parkinson's disease. A number of anticholinergic drugs, such as trihexyphenidyl and benztropine (Cogentin), are available. However, their modest benefits may be offset by side effects such as confusion and hallucinations, particularly in people over the age of 70. Other side effects include dry mouth, nausea, urine retention — especially in men with an enlarged prostate — and severe constipation.
* Antivirals. Doctors may prescribe amantadine (Symmetrel) alone to provide short-term relief of mild, early-stage Parkinson's disease. It also may be added to carbidopa-levodopa therapy for people in the later stages of Parkinson's disease, especially if they have problems with involuntary movements (dyskinesia) induced by carbidopa-levodopa. Side effects include swollen ankles and a purple mottling of the skin.
Physical therapy
Exercise is important for general health, but especially for maintaining function in Parkinson's disease. Physical therapy may be advisable and can help improve mobility, range of motion and muscle tone. Although specific exercises can't stop the progress of the disease, improving muscle strength can help you feel more confident and capable. A physical therapist can also work with you to improve your gait and balance. A speech therapist or speech pathologist can improve problems with speaking and swallowing.
Surgery
Deep brain stimulation is the most common surgical procedure to treat Parkinson's disease. It involves implanting an electrode deep within the parts of your brain that control movement. The amount of stimulation delivered by the electrode is controlled by a pacemaker-like device placed under the skin in your upper chest. A wire that travels under your skin connects the device, called a pulse generator, to the electrode.
Deep brain stimulation is most often used for people who have advanced Parkinson's disease who have unstable medication (levodopa) responses. It can stabilize medication fluctuations and reduce or eliminate involuntary movements (dyskinesias). Tremor is especially responsive to this therapy. Deep brain stimulation doesn't help dementia and may make that worse.
Like any other brain surgery, this procedure has risks — such as brain hemorrhage or stroke-like problems. Infection also may occur, requiring parts of the device to be replaced. In addition, the unit's battery beneath the skin of the chest wall must be surgically replaced every few years. Deep brain stimulation isn't beneficial for people who don't respond to carbidopa-levodopa.
Sunday, May 10, 2009
Mayo Clinic Study Finds Anemia Might be Associated With Development of Parkinson's Disease
Mayo Clinic Study Finds Anemia Might be Associated With Development of Parkinson's Disease
ROCHESTER, Minn. — Results of a new Mayo Clinic study support an association between anemia experienced early in life and the development of Parkinson's disease many years later. The findings will be presented at the American Academy of Neurology Annual Meeting in Seattle on April 30, 2009.
"We were surprised to discover that chronic anemia or low levels of hemoglobin were linked to the risk of Parkinson's disease 20-30 years later," says Walter Rocca, M.D. an author of the study and a neurologist at Mayo Clinic.
Hemoglobin is the protein that transports oxygen in the blood, an essential element for life. "We looked at both anemia as diagnosed by a physician and low hemoglobin values," Dr. Rocca says. "Both were associated with an increased risk of Parkinson's disease. This might indicate that Parkinson's disease actually starts 20--30 years before we see any motor changes in the body."
The case-control study included 196 people who developed Parkinson's disease in Olmsted County, Minn., from 1976 through 1995. Each case was matched by age and sex to a general population control subject who was not affected by Parkinson's disease. The medical records of cases and controls were reviewed using the resources of the Rochester Epidemiology Project to determine if there was a link between anemia or low hemoglobin levels and the risk of developing Parkinson's disease many years later. Anemia was significantly more common in the history of cases than in the history of controls.
Dr. Rocca and his team hope to replicate these results in another population group. "We first need to confirm the study results. If the findings are replicated, we will try to understand what are the underlying mechanisms. Understanding the mechanisms may lead to new ways to prevent or treat Parkinson's disease," Dr. Rocca says.
Other members of the Mayo Clinic research team included Rodolfo Savica, M.D.; Justin Carlin; Brandon Grossardt; James Bower, M.D.; and Demetrius Maraganore, M.D.
ROCHESTER, Minn. — Results of a new Mayo Clinic study support an association between anemia experienced early in life and the development of Parkinson's disease many years later. The findings will be presented at the American Academy of Neurology Annual Meeting in Seattle on April 30, 2009.
"We were surprised to discover that chronic anemia or low levels of hemoglobin were linked to the risk of Parkinson's disease 20-30 years later," says Walter Rocca, M.D. an author of the study and a neurologist at Mayo Clinic.
Hemoglobin is the protein that transports oxygen in the blood, an essential element for life. "We looked at both anemia as diagnosed by a physician and low hemoglobin values," Dr. Rocca says. "Both were associated with an increased risk of Parkinson's disease. This might indicate that Parkinson's disease actually starts 20--30 years before we see any motor changes in the body."
The case-control study included 196 people who developed Parkinson's disease in Olmsted County, Minn., from 1976 through 1995. Each case was matched by age and sex to a general population control subject who was not affected by Parkinson's disease. The medical records of cases and controls were reviewed using the resources of the Rochester Epidemiology Project to determine if there was a link between anemia or low hemoglobin levels and the risk of developing Parkinson's disease many years later. Anemia was significantly more common in the history of cases than in the history of controls.
Dr. Rocca and his team hope to replicate these results in another population group. "We first need to confirm the study results. If the findings are replicated, we will try to understand what are the underlying mechanisms. Understanding the mechanisms may lead to new ways to prevent or treat Parkinson's disease," Dr. Rocca says.
Other members of the Mayo Clinic research team included Rodolfo Savica, M.D.; Justin Carlin; Brandon Grossardt; James Bower, M.D.; and Demetrius Maraganore, M.D.
Saturday, May 2, 2009
Parkinson's Disease: More Than Shaking Going On Researchers discovering non-motor symptoms may happen first
Parkinson's Disease: More Than Shaking Going On Researchers discovering non-motor symptoms may happen first
(live-PR.com) - TORONTO, ONTARIO -- (Marketwire) -- 04/21/09 -- Parkinson's is much more than a tremor. That's a message Parkinson Society Canada hopes to drive home this April during Parkinson's Awareness Month.
In Parkinson's, the most common symptoms are movement-related: tremor, slowness, muscle stiffness and balance problems. However, by the time Parkinson's is diagnosed, people have already lost 60 to 70 percent of the dopamine-producing cells. Now researchers are discovering that non-motor symptoms such as sleep problems, depression and smell loss may represent the earliest signs of Parkinson's, for some people, and may appear years before the diagnosis.
In research at Montreal's Sacre-Coeur Hospital, Dr. Ronald Postuma, assistant professor of neurology at McGill University found that people with a rare sleep disorder where they physically acted out their dreams had a 50% risk of developing Parkinson's disease or dementia within 12 years. The patients had REM-sleep behaviour disorder, which Postuma describes as "punching and yelling or kicking out while asleep. It mostly affects people in their 60s and 70s, almost always men." Not all will develop a neurodegenerative disease but Postuma says, "Patients with true REM-sleep behaviour disorder have a considerable risk of developing Parkinson's disease."
Depression and anxiety can surface early in Parkinson's. "Many people, as they're starting to lose their dopamine, may not yet have developed a tremor, slowness or trouble walking, but may feel anxious and depressed," says Dr. Susan Fox, assistant professor of neurology at University of Toronto. "Depression is also part of Parkinson's disease itself and not just a reaction to having a chronic neurological disorder." Fox notes untreated depression can reduce quality of life.
Smell loss is a common occurrence. "The general consensus is that the changes in olfaction (sense of smell) occur about five years before the Parkinson's diagnosis." says Dr. Harold Robertson, a professor in the Brain Repair Centre and Department of Pharmacology at Dalhousie University in Halifax. "That could give us enough lead time to try to stop the process."
Joyce Gordon, Parkinson Society Canada President and CEO says "The more dollars we can put towards Parkinson's research, the sooner we may be able to establish if there is a definite link to Parkinson's when a person has sleep problems, depression or loss of smell. This would lay the groundwork for developing treatments to delay or stop this debilitating disease in its tracks. The answers can't come soon enough for the 100,000 Canadians who have Parkinson's disease and those who are unknowingly at risk."
In the meantime, the first step for anyone experiencing difficulties with sleep or mood is to see a doctor for a proper diagnosis. REM sleep behaviour disorder and depression are treatable. Smell loss is not currently treatable but is worth mentioning to the doctor, during a routine visit, as it may be due to a variety of causes.
Parkinson's is a progressive neurological disease for which there is no known cause or cure. When cells in the brain that normally produce a chemical called "dopamine" die, symptoms of Parkinson's appear. The most common symptoms are: tremor (shaking), slowness in movements, muscle stiffness and problems with balance. Other symptoms that may also occur for some people include fatigue, difficulties with speech and writing, sleep disorders, depression and cognitive changes.
For over 40 years, Parkinson Society Canada (PSC) has been the national voice of people living with Parkinson's disease. PSC has over 230 chapters and support groups. PSC's mission is to fund research, support services, advocacy and education.
For more information on Parkinson's disease and Parkinson Society Canada, visit the PSC website at www.parkinson.ca : www.parkinson.ca or call 1-800-565-3000.
Contacts:
Parkinson Society Canada
John Provenzano
416-227-3399 or 1-800-565-3000 ext 3399
John.provenzano@parkinson.ca : John.provenzano@parkinson.ca
(live-PR.com) - TORONTO, ONTARIO -- (Marketwire) -- 04/21/09 -- Parkinson's is much more than a tremor. That's a message Parkinson Society Canada hopes to drive home this April during Parkinson's Awareness Month.
In Parkinson's, the most common symptoms are movement-related: tremor, slowness, muscle stiffness and balance problems. However, by the time Parkinson's is diagnosed, people have already lost 60 to 70 percent of the dopamine-producing cells. Now researchers are discovering that non-motor symptoms such as sleep problems, depression and smell loss may represent the earliest signs of Parkinson's, for some people, and may appear years before the diagnosis.
In research at Montreal's Sacre-Coeur Hospital, Dr. Ronald Postuma, assistant professor of neurology at McGill University found that people with a rare sleep disorder where they physically acted out their dreams had a 50% risk of developing Parkinson's disease or dementia within 12 years. The patients had REM-sleep behaviour disorder, which Postuma describes as "punching and yelling or kicking out while asleep. It mostly affects people in their 60s and 70s, almost always men." Not all will develop a neurodegenerative disease but Postuma says, "Patients with true REM-sleep behaviour disorder have a considerable risk of developing Parkinson's disease."
Depression and anxiety can surface early in Parkinson's. "Many people, as they're starting to lose their dopamine, may not yet have developed a tremor, slowness or trouble walking, but may feel anxious and depressed," says Dr. Susan Fox, assistant professor of neurology at University of Toronto. "Depression is also part of Parkinson's disease itself and not just a reaction to having a chronic neurological disorder." Fox notes untreated depression can reduce quality of life.
Smell loss is a common occurrence. "The general consensus is that the changes in olfaction (sense of smell) occur about five years before the Parkinson's diagnosis." says Dr. Harold Robertson, a professor in the Brain Repair Centre and Department of Pharmacology at Dalhousie University in Halifax. "That could give us enough lead time to try to stop the process."
Joyce Gordon, Parkinson Society Canada President and CEO says "The more dollars we can put towards Parkinson's research, the sooner we may be able to establish if there is a definite link to Parkinson's when a person has sleep problems, depression or loss of smell. This would lay the groundwork for developing treatments to delay or stop this debilitating disease in its tracks. The answers can't come soon enough for the 100,000 Canadians who have Parkinson's disease and those who are unknowingly at risk."
In the meantime, the first step for anyone experiencing difficulties with sleep or mood is to see a doctor for a proper diagnosis. REM sleep behaviour disorder and depression are treatable. Smell loss is not currently treatable but is worth mentioning to the doctor, during a routine visit, as it may be due to a variety of causes.
Parkinson's is a progressive neurological disease for which there is no known cause or cure. When cells in the brain that normally produce a chemical called "dopamine" die, symptoms of Parkinson's appear. The most common symptoms are: tremor (shaking), slowness in movements, muscle stiffness and problems with balance. Other symptoms that may also occur for some people include fatigue, difficulties with speech and writing, sleep disorders, depression and cognitive changes.
For over 40 years, Parkinson Society Canada (PSC) has been the national voice of people living with Parkinson's disease. PSC has over 230 chapters and support groups. PSC's mission is to fund research, support services, advocacy and education.
For more information on Parkinson's disease and Parkinson Society Canada, visit the PSC website at www.parkinson.ca : www.parkinson.ca or call 1-800-565-3000.
Contacts:
Parkinson Society Canada
John Provenzano
416-227-3399 or 1-800-565-3000 ext 3399
John.provenzano@parkinson.ca : John.provenzano@parkinson.ca
Sunday, April 26, 2009
Studies Show 3 out of 4 Parkinson's Disease Patients Can Improve Walking and Quality of Life Within 2 Weeks
Studies Show 3 out of 4 Parkinson's Disease Patients Can Improve Walking and Quality of Life Within 2 Weeks
Newly released virtual reality gait training device shown to improve quality of life for Parkinson's disease and other movement disorders.
Haifa, Israel (PRWEB) April 13, 2009 -- Parkinson's disease patients are discovering first-hand that daily exercise with a new virtual reality device, the GaitAid, has a positive effect on their walking ability, minimizing balance problems and freezing, and improving quality of life. The GaitAid offers a drug free, non RX alternative with no side effects.
As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!
Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD.
Daniel Neal, a Parkinson's disease patient from Palm Springs, CA., commented after receiving his GaitAid, "As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!"
Yoram Baram, a computer science professor and incumbent of the Roy Matas / Winnipeg Chair in Biomedical Engineering at the Technion, Israel Institute of Technology has collaborated with several neurologists specializing in treating Parkinson's disease, Multiple Sclerosis and other movement disorders, in developing and testing a new, non-invasive training device designed to proactively minimize freezing and balance problems during walking. The noticeable physical and mental improvement of patients participating in clinical studies led Baram to bring the GaitAid device to market as a FDA registered medical device and is offering the device for a no risk trial period on his company's website (www.medigait.com).
Alberto J. Espay, MD, from the Neuroscience Institute, Department of Neurology, Movement Disorders Center, University of Cincinnati, specializes in research and clinical treatment of movement disorders. After offering the GaitAid to a group of his Parkinson's disease patients to use at home, Dr. Espay states, "Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD."
The easy to use device includes special glasses and earphones which provide sensory feedback in response to the patient's movements. A practice session involves walking with the device for up to twenty minutes with no special training needed. These practice sessions soon start to evoke a lasting improvement for most Parkinson's disease patients. The degree of improvement varies, some patients use the GaitAid only occasionally after a few months while others make a short session a part of their daily routine to keep their results.
Parkinson's disease remains a mystery of medical science. For reason's unknown, certain brain cells stop producing a substance called Dopamine, which affects an individual's movement, strength and balance. There is currently no cure, though stem cell research offers future promise.
Emerging scientific evidence confirms that movement lessens neurological deterioration that contributes to Parkinson's Disease progression.
The device is available for a no risk trial period of 60 days:
online www.medigait.com
email: support (at) medigait (dot) com
or by phone 888-777-9906.
Newly released virtual reality gait training device shown to improve quality of life for Parkinson's disease and other movement disorders.
Haifa, Israel (PRWEB) April 13, 2009 -- Parkinson's disease patients are discovering first-hand that daily exercise with a new virtual reality device, the GaitAid, has a positive effect on their walking ability, minimizing balance problems and freezing, and improving quality of life. The GaitAid offers a drug free, non RX alternative with no side effects.
As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!
Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD.
Daniel Neal, a Parkinson's disease patient from Palm Springs, CA., commented after receiving his GaitAid, "As soon as I tried it my mobility improved tremendously! For the first time in over a year I am already walking without a cane. I am so impressed and so grateful. I was dreading my planned trip out of the country until I received your glasses. I cannot wait to share the miracle with my friends who suffer from PD. Thank you!"
Yoram Baram, a computer science professor and incumbent of the Roy Matas / Winnipeg Chair in Biomedical Engineering at the Technion, Israel Institute of Technology has collaborated with several neurologists specializing in treating Parkinson's disease, Multiple Sclerosis and other movement disorders, in developing and testing a new, non-invasive training device designed to proactively minimize freezing and balance problems during walking. The noticeable physical and mental improvement of patients participating in clinical studies led Baram to bring the GaitAid device to market as a FDA registered medical device and is offering the device for a no risk trial period on his company's website (www.medigait.com).
Alberto J. Espay, MD, from the Neuroscience Institute, Department of Neurology, Movement Disorders Center, University of Cincinnati, specializes in research and clinical treatment of movement disorders. After offering the GaitAid to a group of his Parkinson's disease patients to use at home, Dr. Espay states, "Gait velocity and stride length were improved in PD patients after training with a visual-and-auditory virtual cueing system, with a marked residual effect. Devices utilizing closed-loop visual feedback system are desirable non-pharmacologic interventions to improve walking in PD."
The easy to use device includes special glasses and earphones which provide sensory feedback in response to the patient's movements. A practice session involves walking with the device for up to twenty minutes with no special training needed. These practice sessions soon start to evoke a lasting improvement for most Parkinson's disease patients. The degree of improvement varies, some patients use the GaitAid only occasionally after a few months while others make a short session a part of their daily routine to keep their results.
Parkinson's disease remains a mystery of medical science. For reason's unknown, certain brain cells stop producing a substance called Dopamine, which affects an individual's movement, strength and balance. There is currently no cure, though stem cell research offers future promise.
Emerging scientific evidence confirms that movement lessens neurological deterioration that contributes to Parkinson's Disease progression.
The device is available for a no risk trial period of 60 days:
online www.medigait.com
email: support (at) medigait (dot) com
or by phone 888-777-9906.
Sunday, April 19, 2009
Shedding some light on Parkinson's treatment
Shedding some light on Parkinson's treatment
EUREKALERT
Contact: Lisa Van Pay
lvanpay@nsf.gov
703-292-8796
National Science Foundation
Scientists use optical approach to study deep brain stimulation
A research team lead by Karl Deisseroth in the bioengineering department at Stanford University has developed a technique to systematically characterize disease circuits in the brain. By precisely controlling individual components of the circuit implicated in Parkinson's disease, the team has identified a specific group of cells as direct targets of deep brain stimulation (DBS), a Parkinson's treatment.
Termed optogenetics, the NSF-funded technology uses light-activated proteins, originally isolated from bacteria, in combination with genetic approaches to control specific parts of the brain. The technique is a vast improvement over previous methods because it allows researchers to precisely stimulate neurons and measure the effect of treatment simultaneously in animals with Parkinson's-like symptoms.
Published in the April 17 issue of Science, Deisseroth's team found they could reduce disease symptoms by preferentially activating neurons that link to the subthalamic nucleus region of the brain. First, these specific cells were treated in a way that made them sensitive to stimulation by blue light, then the team implanted an optical fiber in the brain.
When researchers rapidly flashed blue light inside the animals' brains the disease symptoms improved. In contrast, treating with slower flashes of light actually made the symptoms worse, and targeting other kinds of cells had no effect at all, indicating both proper cell type and stimulation frequency are crucial components of effective treatment. Flashing blue light on portions of the same neurons found closer to the outer surface of the brain had an effect similar to treatment deep within the brain, raising the possibility that researchers may be able to develop treatments that are less invasive than current options.
Approved as a medical treatment in 1997, DBS remains controversial because it doesn't work on all patients. Used to treat Parkinson's disease, depression and movement disorders, DBS involves surgical implantation of a brain pacemaker, which sends electrical impulses into the brain. In the past, researchers have been unable to understand the effective mechanism of DBS because the electrical signal emitted by DBS devices interferes with the ability to observe brain activity.
Explains Deisseroth, "The brain is an electrical device, but it is a very complicated device. Think of it as an orchestra without sections: all of the types of instruments, or cells, are mixed together. Treatments like DBS are unrefined, in that they stimulate all of the cells or instruments. The optogenetic approach allows us to control stimulation of specific cells in the brain on the appropriate timescale, much like a conductor directing specific sections of an orchestra at the appropriate time."
Production of new therapies is always a long-term goal, but for now Deisseroth and his group are focused on mapping disease circuits and understanding brain function. "We need to understand the players before we can develop effective treatment strategies," he stated.
EUREKALERT
Contact: Lisa Van Pay
lvanpay@nsf.gov
703-292-8796
National Science Foundation
Scientists use optical approach to study deep brain stimulation
A research team lead by Karl Deisseroth in the bioengineering department at Stanford University has developed a technique to systematically characterize disease circuits in the brain. By precisely controlling individual components of the circuit implicated in Parkinson's disease, the team has identified a specific group of cells as direct targets of deep brain stimulation (DBS), a Parkinson's treatment.
Termed optogenetics, the NSF-funded technology uses light-activated proteins, originally isolated from bacteria, in combination with genetic approaches to control specific parts of the brain. The technique is a vast improvement over previous methods because it allows researchers to precisely stimulate neurons and measure the effect of treatment simultaneously in animals with Parkinson's-like symptoms.
Published in the April 17 issue of Science, Deisseroth's team found they could reduce disease symptoms by preferentially activating neurons that link to the subthalamic nucleus region of the brain. First, these specific cells were treated in a way that made them sensitive to stimulation by blue light, then the team implanted an optical fiber in the brain.
When researchers rapidly flashed blue light inside the animals' brains the disease symptoms improved. In contrast, treating with slower flashes of light actually made the symptoms worse, and targeting other kinds of cells had no effect at all, indicating both proper cell type and stimulation frequency are crucial components of effective treatment. Flashing blue light on portions of the same neurons found closer to the outer surface of the brain had an effect similar to treatment deep within the brain, raising the possibility that researchers may be able to develop treatments that are less invasive than current options.
Approved as a medical treatment in 1997, DBS remains controversial because it doesn't work on all patients. Used to treat Parkinson's disease, depression and movement disorders, DBS involves surgical implantation of a brain pacemaker, which sends electrical impulses into the brain. In the past, researchers have been unable to understand the effective mechanism of DBS because the electrical signal emitted by DBS devices interferes with the ability to observe brain activity.
Explains Deisseroth, "The brain is an electrical device, but it is a very complicated device. Think of it as an orchestra without sections: all of the types of instruments, or cells, are mixed together. Treatments like DBS are unrefined, in that they stimulate all of the cells or instruments. The optogenetic approach allows us to control stimulation of specific cells in the brain on the appropriate timescale, much like a conductor directing specific sections of an orchestra at the appropriate time."
Production of new therapies is always a long-term goal, but for now Deisseroth and his group are focused on mapping disease circuits and understanding brain function. "We need to understand the players before we can develop effective treatment strategies," he stated.
Sunday, April 12, 2009
Arrayit Corporation and The Parkinson's Institute Announce New Research Collaboration
Arrayit Corporation and The Parkinson's Institute Announce New Research Collaboration
ARYC 2.63, -0.37, -12.5%) , a proprietary life sciences technology leader, announces a new research collaboration with The Parkinson's Institute of Sunnyvale, California to discover biomarkers for Parkinson's disease. This unique study involves the prospective collection of samples from well-characterized Parkinson's patients combined with Arrayit's new H25K microarray technology. The first experiments have enabled rapid and efficient sample preparation of specimens from Parkinson's disease patients, an important step in the discovery of molecular markers for Parkinson's disease.
"This collaboration provides an important first step towards unraveling the mysteries of Parkinson's disease," stated Dr. Mark Schena, Ph.D., Arrayit President. "We look forward to working with The Parkinson's Institute to decipher the molecular basis of the disease," he continued. The Parkinson's Institute Assistant Professor Dr. Birgitt Schuele, M.D. added, "Parkinson's disease represents a serious and challenging medical condition. We are pleased to be deploying Arrayit technology to combat this illness."
About Arrayit Corporation
Arrayit Corporation, headquartered in Sunnyvale, California, leads and empowers the genetic, research, pharmaceutical, and diagnostic communities through the discovery, development and manufacture of proprietary life science technologies and consumables for disease prevention, treatment and cure. It now offers over 650 products to a customer base of more than 2,500 laboratories worldwide, including most every major university, pharmaceutical and biotech company, major agricultural and chemical company, government agency, national research foundation and many private sector enterprises. Please visit www.arrayit.com for more information.
About The Parkinson's Institute
The Parkinson's Institute and Clinical Center (PI) is America's only independent non-profit organization that provides basic and clinical research, clinical trials and a comprehensive movement disorder patient clinic for Parkinson's disease (PD) and related neurological movement disorders, all under one roof. Our mission is to find the causes, provide first class patient care and discover a cure. Our unique freestanding organization supports a strong collaboration of translational medicine designed to more directly connect research to patient care -- from the "bench to bedside." Please visit www.thepi.org for more information.
Safe Harbor Statement
Except for historical information contained herein, statements made in this release that would constitute forward-looking statements may involve certain risks and uncertainties. All forward-looking statements made in this release are based on currently available information and the Company assumes no responsibility to update any such forward-looking statement. The following factors, among others, may cause actual results to differ materially from the results suggested in the forward-looking statements. The factors include, but are not limited to, risks that may result from changes in the Company's business operations; our ability to keep pace with technological advances; significant competition in the biomedical business; our relationships with key suppliers and customers; quality and consumer acceptance of newly introduced products; market volatility; non-availability of product; excess inventory; price and product competition; new product introductions, the outcome of our legal disputes; the possibility that the review of our prior filings by the SEC may result in changes to our financial statements; and the possibility that stockholders or regulatory authorities may initiate proceedings against Arrayit and/or our officers and directors as a result of any restatements. Risk factors associated with our business, including some of the facts set forth herein, are detailed in the Company's Form 10-K for the fiscal year ended December 31, 2007 and Form 10-Q/A for the fiscal first quarter ended March 31, 2008 and Form 10-Q for the fiscal second quarter ended June 30, 2008.
ARYC 2.63, -0.37, -12.5%) , a proprietary life sciences technology leader, announces a new research collaboration with The Parkinson's Institute of Sunnyvale, California to discover biomarkers for Parkinson's disease. This unique study involves the prospective collection of samples from well-characterized Parkinson's patients combined with Arrayit's new H25K microarray technology. The first experiments have enabled rapid and efficient sample preparation of specimens from Parkinson's disease patients, an important step in the discovery of molecular markers for Parkinson's disease.
"This collaboration provides an important first step towards unraveling the mysteries of Parkinson's disease," stated Dr. Mark Schena, Ph.D., Arrayit President. "We look forward to working with The Parkinson's Institute to decipher the molecular basis of the disease," he continued. The Parkinson's Institute Assistant Professor Dr. Birgitt Schuele, M.D. added, "Parkinson's disease represents a serious and challenging medical condition. We are pleased to be deploying Arrayit technology to combat this illness."
About Arrayit Corporation
Arrayit Corporation, headquartered in Sunnyvale, California, leads and empowers the genetic, research, pharmaceutical, and diagnostic communities through the discovery, development and manufacture of proprietary life science technologies and consumables for disease prevention, treatment and cure. It now offers over 650 products to a customer base of more than 2,500 laboratories worldwide, including most every major university, pharmaceutical and biotech company, major agricultural and chemical company, government agency, national research foundation and many private sector enterprises. Please visit www.arrayit.com for more information.
About The Parkinson's Institute
The Parkinson's Institute and Clinical Center (PI) is America's only independent non-profit organization that provides basic and clinical research, clinical trials and a comprehensive movement disorder patient clinic for Parkinson's disease (PD) and related neurological movement disorders, all under one roof. Our mission is to find the causes, provide first class patient care and discover a cure. Our unique freestanding organization supports a strong collaboration of translational medicine designed to more directly connect research to patient care -- from the "bench to bedside." Please visit www.thepi.org for more information.
Safe Harbor Statement
Except for historical information contained herein, statements made in this release that would constitute forward-looking statements may involve certain risks and uncertainties. All forward-looking statements made in this release are based on currently available information and the Company assumes no responsibility to update any such forward-looking statement. The following factors, among others, may cause actual results to differ materially from the results suggested in the forward-looking statements. The factors include, but are not limited to, risks that may result from changes in the Company's business operations; our ability to keep pace with technological advances; significant competition in the biomedical business; our relationships with key suppliers and customers; quality and consumer acceptance of newly introduced products; market volatility; non-availability of product; excess inventory; price and product competition; new product introductions, the outcome of our legal disputes; the possibility that the review of our prior filings by the SEC may result in changes to our financial statements; and the possibility that stockholders or regulatory authorities may initiate proceedings against Arrayit and/or our officers and directors as a result of any restatements. Risk factors associated with our business, including some of the facts set forth herein, are detailed in the Company's Form 10-K for the fiscal year ended December 31, 2007 and Form 10-Q/A for the fiscal first quarter ended March 31, 2008 and Form 10-Q for the fiscal second quarter ended June 30, 2008.
Saturday, March 21, 2009
Early Parkinson's Treatment With Rasagiline Safe, Well Tolerated, and Effective Versus Placebo
Early Parkinson's Treatment With Rasagiline Safe, Well Tolerated, and Effective Versus Placebo: Presented at ADPD
By Chris Berrie
PRAGUE, Czech Republic -- March 14, 2009 -- Rasagiline monotherapy is safe and well tolerated, with clinical benefits versus placebo in patients with early, previously untreated Parkinson's disease (PD), researchers noted here at the 9th International Conference on Alzheimer's and Parkinson's Diseases (ADPD).
Early initiation of treatment with rasagiline 1 mg/day also provided significant clinical benefits over later initiation.
A prospective, multicentre study entitled Attenuation of Disease Progression With Azilect Given Once-Daily (ADAGIO) was presented here on March 13 by principal investigator Olivier Rascol, MD, Toulouse University Hospital, Toulouse, France.
"A treatment that slows or halts the progression of disease is a key unmet need in Parkinson's disease," Dr. Rascol stated. He and his colleagues utilised a delayed-start design in their randomised, double-blind, placebo-controlled trial to allow separation of disease-modifying effects from symptomatic effects in the examination of patients with moderate to advanced PD taking rasagiline monotherapy and combination therapy with levodopa.
Patient diagnosis was for cardinal PD signs -- resting tremor, bradykinesia, and rigidity -- with inclusion requiring a disease duration of less than 18 months from diagnosis and investigator judgement of no requirement for additional anti-PD treatment in the following 9 months.
The 1,176 patients enrolled were 61.1% male, with mean baseline characteristics as follows: age, 62.2 years; PD duration, 4.5 months; total Unified PD Rating Scale (UPDRS) score, 20.4; motor-UPDRS score, 14.2; and modified Hoehn and Yahr score, 1.5.
The study followed 2 phases: a 36-week placebo-controlled phase 1, followed by a 36-week full active-treatment phase 2. Randomisation was to 4 groups -- 2 of placebo followed by rasagiline 1 or 2 mg/day for delayed-start treatment (n = 595) and 2 of rasagiline 1 mg/day (n = 288) or 2 mg/day (n = 293) for the full 72 weeks. There were no significant baseline differences across these groups.
With rasagiline 1 mg/day, the 3 specific primary efficacy endpoints were met:
A. The slope in weeks 12-36 of phase 1 was significantly superior with active treatment versus placebo (difference, -0.05; 95% confidence interval [CI], -0.08 to -0.01; P = .0133).
B. Results from the early-start group were significantly superior to those of the late-start group at week 72 (difference, -1.7; 95% CI, -3.15 to -0.21; P = .025).
C. The noninferiority of the slope of early versus late start was met (difference, 0.0; 90% CI, -0.04 to 0.04; P < .0001).
The rasagiline 2-mg/day treatment showed significant benefit in phase 1 versus placebo (P < .001), but did not show superiority versus the delayed start at the end of phase 2.
The secondary endpoint for changes in total UPDRS score from baseline to week 36 for each rasagiline group was met for rasagiline 1 and 2 mg/day, as adjusted effect sizes of -3.0 (95% CI, -3.9 to -2.2; P < .0001) and -3.2 (95% CI, -4.0 to -2.3; P < .0001) respectively.
Rasagiline monotherapy was deemed safe and well tolerated, with few treatment-related adverse events and few discontinuations (placebo, 2.9%; rasagiline 1 mg/day, 3.1%; rasagiline 2 mg/day, 3.8%).
The researchers concluded that this early treatment with rasagiline 1 mg/day is consistent with disease-modifying effects, noting, "ADAGIO also confirms the symptomatic efficacy of rasagiline monotherapy versus placebo in patients with early [Parkinson's] disease."
Funding for this study was provided by Teva Pharmaceutical Industries Ltd. and Teva Neuroscience, Inc.
[Presentation title: The ADAGIO Delayed-Start Study Demonstrates That Early Rasagiline Treatment Slows UPDRS Decline. Abstract P1-423]
By Chris Berrie
PRAGUE, Czech Republic -- March 14, 2009 -- Rasagiline monotherapy is safe and well tolerated, with clinical benefits versus placebo in patients with early, previously untreated Parkinson's disease (PD), researchers noted here at the 9th International Conference on Alzheimer's and Parkinson's Diseases (ADPD).
Early initiation of treatment with rasagiline 1 mg/day also provided significant clinical benefits over later initiation.
A prospective, multicentre study entitled Attenuation of Disease Progression With Azilect Given Once-Daily (ADAGIO) was presented here on March 13 by principal investigator Olivier Rascol, MD, Toulouse University Hospital, Toulouse, France.
"A treatment that slows or halts the progression of disease is a key unmet need in Parkinson's disease," Dr. Rascol stated. He and his colleagues utilised a delayed-start design in their randomised, double-blind, placebo-controlled trial to allow separation of disease-modifying effects from symptomatic effects in the examination of patients with moderate to advanced PD taking rasagiline monotherapy and combination therapy with levodopa.
Patient diagnosis was for cardinal PD signs -- resting tremor, bradykinesia, and rigidity -- with inclusion requiring a disease duration of less than 18 months from diagnosis and investigator judgement of no requirement for additional anti-PD treatment in the following 9 months.
The 1,176 patients enrolled were 61.1% male, with mean baseline characteristics as follows: age, 62.2 years; PD duration, 4.5 months; total Unified PD Rating Scale (UPDRS) score, 20.4; motor-UPDRS score, 14.2; and modified Hoehn and Yahr score, 1.5.
The study followed 2 phases: a 36-week placebo-controlled phase 1, followed by a 36-week full active-treatment phase 2. Randomisation was to 4 groups -- 2 of placebo followed by rasagiline 1 or 2 mg/day for delayed-start treatment (n = 595) and 2 of rasagiline 1 mg/day (n = 288) or 2 mg/day (n = 293) for the full 72 weeks. There were no significant baseline differences across these groups.
With rasagiline 1 mg/day, the 3 specific primary efficacy endpoints were met:
A. The slope in weeks 12-36 of phase 1 was significantly superior with active treatment versus placebo (difference, -0.05; 95% confidence interval [CI], -0.08 to -0.01; P = .0133).
B. Results from the early-start group were significantly superior to those of the late-start group at week 72 (difference, -1.7; 95% CI, -3.15 to -0.21; P = .025).
C. The noninferiority of the slope of early versus late start was met (difference, 0.0; 90% CI, -0.04 to 0.04; P < .0001).
The rasagiline 2-mg/day treatment showed significant benefit in phase 1 versus placebo (P < .001), but did not show superiority versus the delayed start at the end of phase 2.
The secondary endpoint for changes in total UPDRS score from baseline to week 36 for each rasagiline group was met for rasagiline 1 and 2 mg/day, as adjusted effect sizes of -3.0 (95% CI, -3.9 to -2.2; P < .0001) and -3.2 (95% CI, -4.0 to -2.3; P < .0001) respectively.
Rasagiline monotherapy was deemed safe and well tolerated, with few treatment-related adverse events and few discontinuations (placebo, 2.9%; rasagiline 1 mg/day, 3.1%; rasagiline 2 mg/day, 3.8%).
The researchers concluded that this early treatment with rasagiline 1 mg/day is consistent with disease-modifying effects, noting, "ADAGIO also confirms the symptomatic efficacy of rasagiline monotherapy versus placebo in patients with early [Parkinson's] disease."
Funding for this study was provided by Teva Pharmaceutical Industries Ltd. and Teva Neuroscience, Inc.
[Presentation title: The ADAGIO Delayed-Start Study Demonstrates That Early Rasagiline Treatment Slows UPDRS Decline. Abstract P1-423]
Saturday, March 14, 2009
Long Term Results Similar in Two Parkinson's Medications
By Will Dunham
WASHINGTON, March 9 (Reuters) - People with Parkinson's disease may worry over which of two kinds of medications to use when first starting treatment, but a study published on Monday indicates the results are similar either way.
Researchers compared disability levels and quality of life after six years for people who started out taking either the standard generic drug levodopa or privately held German drug maker Boehringer Ingelheim's Mirapex, also called pramipexole.
The two drugs are generally employed as the first line of treatment for Parkinson's disease. In different ways, they address the decline in production of the brain chemical dopamine that occurs with the disease.
Parkinson's undermines control over movements and speech. Patients can have stiffness or rigidity of the arms and legs, slowness or lack of movement, and walking difficulties, along with tremors in their hands, arms, legs, jaw or face.
Levodopa is seen as better to deal with mobility issues and tremors. But it can cause involuntary movements known as dyskinesia, and its effectiveness also may wear off over time.
Mirapex may be less effective at handling motor control symptoms and can cause sleepiness. But it is less likely to cause involuntary movements or lose effectiveness over time.
"Despite a little bit of variations in how people were doing in specific areas, in terms of overall quality of life and disability measurements, the two groups looked the same," University of Rochester Medical Center neurologist Dr. Kevin Biglan, one of the researchers, said in a telephone interview.
"Then it becomes more of an individual decision in terms of short-term issues and individual preferences about some of these complications, potentially," he said.
Mirapex is in a class of drugs called dopamine agonists that also includes GlaxoSmithKline's (GSK.L) (GSK.N) Requip, or ropinirole.
The researchers tracked 222 patients in the study published in the journal Archives of Neurology.
Of those who started on Mirapex, 90 percent of them ended up also taking levodopa, a drug that has been around for more than four decades, Biglan said. But the side effects differed depending on which drug they started on, he added.
"There's been all this research trying to address what's the better initial treatment strategy. And patients have struggled with whether they were making the right decision in terms of what treatment to go with initially," Biglan said.
"So they could probably make a decision regarding either treatment without being overly worried about the long-term implications," he added. Boehringer funded the study. (Editing by Julie Steenhuysen)
WASHINGTON, March 9 (Reuters) - People with Parkinson's disease may worry over which of two kinds of medications to use when first starting treatment, but a study published on Monday indicates the results are similar either way.
Researchers compared disability levels and quality of life after six years for people who started out taking either the standard generic drug levodopa or privately held German drug maker Boehringer Ingelheim's Mirapex, also called pramipexole.
The two drugs are generally employed as the first line of treatment for Parkinson's disease. In different ways, they address the decline in production of the brain chemical dopamine that occurs with the disease.
Parkinson's undermines control over movements and speech. Patients can have stiffness or rigidity of the arms and legs, slowness or lack of movement, and walking difficulties, along with tremors in their hands, arms, legs, jaw or face.
Levodopa is seen as better to deal with mobility issues and tremors. But it can cause involuntary movements known as dyskinesia, and its effectiveness also may wear off over time.
Mirapex may be less effective at handling motor control symptoms and can cause sleepiness. But it is less likely to cause involuntary movements or lose effectiveness over time.
"Despite a little bit of variations in how people were doing in specific areas, in terms of overall quality of life and disability measurements, the two groups looked the same," University of Rochester Medical Center neurologist Dr. Kevin Biglan, one of the researchers, said in a telephone interview.
"Then it becomes more of an individual decision in terms of short-term issues and individual preferences about some of these complications, potentially," he said.
Mirapex is in a class of drugs called dopamine agonists that also includes GlaxoSmithKline's (GSK.L) (GSK.N) Requip, or ropinirole.
The researchers tracked 222 patients in the study published in the journal Archives of Neurology.
Of those who started on Mirapex, 90 percent of them ended up also taking levodopa, a drug that has been around for more than four decades, Biglan said. But the side effects differed depending on which drug they started on, he added.
"There's been all this research trying to address what's the better initial treatment strategy. And patients have struggled with whether they were making the right decision in terms of what treatment to go with initially," Biglan said.
"So they could probably make a decision regarding either treatment without being overly worried about the long-term implications," he added. Boehringer funded the study. (Editing by Julie Steenhuysen)
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