I HAVE PARKINSON'S DISEASES AND THOUGHT IT WOULD BE NICE TO HAVE A PLACE WHERE THE CONTENTS OF UPDATED NEWS IS FOUND IN ONE PLACE. THAT IS WHY I BEGAN THIS BLOG.
I COPY NEWS ARTICLES PERTAINING TO RESEARCH, NEWS AND INFORMATION FOR PARKINSON'S DISEASE, DEMENTIA, THE BRAIN, DEPRESSION AND PARKINSON'S WITH DYSTONIA. I ALSO POST ABOUT FUNDRAISING FOR PARKINSON'S DISEASE AND EVENTS. I TRY TO BE UP-TO-DATE AS POSSIBLE.
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Parkinson's disease is characterised by motor and non-motor clinical features. The latter may
present as pre-motor symptoms several years before the onset of motor symptoms. Pre-motor
symptoms have been found to be associated to a later motor onset of Parkinson's Disease.
The overall frequency of pre-motor symptoms was 76%. Among the most prevalent
symptoms were depression (38%), sleep disorders (37%) and anxiety (36%). The time prior
to motor onset was greatest for constipation (9 years) and pain (8 years).
People with more than two pre-motor symptoms had a later age
at motor onset when compared to people without pre-motor
symptoms (56 v 52). Late onset patients had a higher frequency
of pre-motor symptoms (79% v 65% in early onset) and worse
symptoms than early onset. Females reported a higher number
of pre-motor symptoms (1.9 v 1.4). Anxiety lead-time was
greater in tremor-dominant compared to bradykinetic-rigid
patients (3 years).
Pre-motor symptoms load is associated to a later motor onset of PD. Pre-motor symptoms are
more frequent in subjects with late onset Parkinson's disease. Female subjects report a higher
number of pre-motor symptoms, depression and anxiety being the most common.
Reference : Journal of Parkinson's Disease [2015] Dec 10 [Epub ahead of print] (M.
Rodríguez-Violante, A.J.de Saráchaga, A.Cervantes-Arriaga, R.Millán-Cepeda, R.Leal-
Ortega, I.Estrada-Bellmann, C.Zuñiga-Ramírez)
Please click on Healthy Living: Preventing to see video Posted: Dec 30, 2015 11:59 AM EST
As many as one-million Americans are living with Parkinson’s disease, a progressive movement disorder with no cure.
Medications may help control the symptoms for a period of time, but eventually, they lose their punch.
Researchers now say they've found a way to prevent Parkinson’s from developing in animals, a huge step toward eliminating the disease in people.
Dr. Burton says a clinical trial of gene therapy in humans is only two to three years away.
He says the therapy needs to be tested in other animals and researchers need to assess the long-term effects before it could move to human trial. http://www.9and10news.com/story/30853901/healthy-living-preventing-parkinsons#.VoVKPLs7IrE.blogger
PeggyWillocks was 44 when she was diagnosed with Parkinson’s disease. It progressed quickly, forcing her to retire four years later from her job as a primary-school principal in Elizabethton, Tennessee. Soon, her condition had deteriorated so much that she was often unable to dress and feed herself, take care of basic hygiene or walk unaided across a room.
Willocks enrolled in a trial for an experimental therapy called Spheramine, developed by Titan Pharmaceuticals, a biotechnology company in South San Francisco, California. Spheramine consists of cultured human retinal epithelial cells bound to specialized man-made carrier molecules. The cells are implanted into the brain, where it is hoped that they will produce the dopamine precursor levodopa, which can reduce the symptoms of Parkinson’s disease. In August 2000, Willocks became the second person ever to receive the treatment. After having a steel halo — a stereotactic frame — bolted to her skull, she was put under general anaesthesia. Surgeons then used the frame and coordinates obtained from numerous magnetic resonance imaging (MRI) scans to pinpoint the location at which to drill. They then snaked a catheter through her brain’s white matter to deliver the cells into the striatum.
At first there was no effect, but Willocks says that after 6–8 months she began to feel better. The changes were always moderate and gradual, except for once, about nine months after her surgery, when she showed what her doctor called a “radical” improvement in balance. By a year after the treatment, she and the five other patients in the phase I trial showed an improvement in motor ability of 48%, and those gains largely held 4 years later1.
Ten years on, she says she notices her condition worsening, but is still doing much better than she was before her operation. She has no doubt that the treatment works. Investigators disagree: Spheramine was shelved in 2008 after a follow-up phase II, double-blind study found that it was no more effective than placebo2. This time, the researchers compared the treatment with a ‘sham’ brain surgery that copied almost every aspect of the procedure Willocks received, short of injecting cells into the brain.
For many investigators aiming to treat Parkinson’s and other neurological diseases invasively, using sham brain surgery as a control is, well, a no-brainer. And the practice is likely to expand in coming years, as researchers continue to develop experimental tissue transplants, gene therapies and stem-cell treatments. Small safety trials such as the one in which Willocks was enrolled may hint at the efficacy of a treatment, but they are not designed to prove it. And because they are ‘open label’ — both the investigators and the participants know that the drug is being administered — they are riddled with biases that can skew results. “It is so clear that open-label studies provide information that is not reliable,” says Warren Olanow, a neurologist at New York’s Mount Sinai Medical Center who has worked on cell-based neurosurgical therapies in Parkinson’s for more than two decades. “It’s almost impossible for me to imagine how a serious scientist can not desire their data or hypothesis to be tested in double-blind studies.”
Other scientists, however, say that sham brain surgery is an expensive, potentially dangerous and possibly unethical bit of biomedical theatrics. It may also be unnecessary. Clinical neuroscientist Roger Barker at the University of Cambridge, UK, contends that because there is huge variation in how these therapies are administered and in how patients respond, the protocols need to be refined in an open-label setting before going on to the next stage of development. And because cost, complexity and the small number of people eligible for such invasive therapies limit the size of the studies, a sham control provides results of limited statistical utility. Barker and his colleagues across Europe are currently enrolling patients in a €12-million (US$17-million) multicentre trial of a fetal dopaminergic nerve-cell treatment for Parkinson’s disease. The treatment may never be tested against a sham-surgery control. “There’s a sort of historical precedent” for using placebo controls, but it may not apply to neurosurgical trials, he says. Willocks and other patients go further. Placebo-controlled studies aren’t just unnecessary, they say, they are actually causing the downfall of potentially valuable treatments.
A complicating control
During the past 25 years, surgical therapies for Parkinson’s disease have travelled a rocky road. In 1987, a report by Mexican surgeons3 described seemingly miraculous effects in two patients with severe Parkinson’s who received transplants of tissue from the adrenal gland, which produces dopamine. In the next several years, hundreds of patients received the treatment, but some autopsies later showed that the cells didn’t in fact survive4. Around the same time, researchers started to test fetal nerve-cell transplants (similar to those in Barker’s trial) in small-scale studies, finding mixed but promising results. Two studies5,6 comparing the treatment to sham surgery concluded, however, that the transplants were not only ineffective, but also often caused dyskinesia — the movement disorder that plagues people with Parkinson’s disease. In the past seven years, three experimental treatments (including Spheramine) that showed promise in small, open-label studies1,7,8 failed in phase II trials2,4,9 comparing them with a sham control (see ‘The sham wall’).
Sham brain surgery is no sugar pill. After the stereotactic frame is affixed to the skull, the patient is usually anaesthetized and surgeons drill into the skull. In most cases, the burr holes stop at the dura mater, a protective membrane covering the brain, but they sometimes go deeper: in a phase II trial testing the nerve growth factor GDNF, investigators catheterized the brain in all participants but infused saline, rather than GDNF, into the controls9.
“We have to stage the whole thing such that from the outside it’s completely indistinguishable” from the real thing, says Joao Siffert, chief medical officer of Ceregene, a company in San Diego, California, that is working on a therapy that delivers a gene for another nerve growth factor, called neurturin, using a viral vector. For many sham treatments, everyone in the operating room, from surgeons to nurses’ assistants, must pretend that they are busily performing the complete operation — in some cases, turning on machines to elicit appropriate noises. An extremely complex protocol ensures that no one outside the surgical team knows who got what treatment. “It’s very complicated, there are a lot of moving parts,” Siffert says. All that ratchets up the cost of a trial; Siffert estimates that between operating-theatre costs, follow-up and the unwieldy infrastructure required for data management, a 50-patient study would cost more than $10 million.
Still, at least in North America, Parkinson’s disease investigators overwhelmingly support the use of sham surgery — at a rate of 94%, according to a 2004 survey10. Around 20% said that penetrating the brain is justifiable. And proponents say the procedure is relatively safe. Although sham brain surgery has definite risks, most notably those associated with general anaesthesia, supporters note that adverse events are almost unheard of, unlike the risks of the actual treatments. And participants in the sham groups are generally promised the treatment if it is ultimately approved; in that event, they will already have the burr holes in their skulls through which it would be administered.
Sham treatments help to tease out the placebo effect and biases. In Parkinson’s disease, the placebo effect is especially strong. One reason is that patients’ expectations that they will benefit from a treatment induce the release of dopamine11, the neurotransmitter that is lacking in the disease. “The placebo effect is real, it’s huge and it’s got a physiological basis,” says Jon Stoessl, a neurologist at the University of British Columbia in Vancouver, Canada, who studies Parkinson’s and the placebo effect. In one double-blind study of fetal nerve-cell transplants, patient improvement correlated with whether they believed they had received the treatment, irrespective of whether they actually had12. And the effect can last as long as two years, Stoessl says, citing an unpublished study by his colleagues.
“There’s a historical precedent for using placebo controls, but it may not apply to neurosurgical trials.”
Many regard bias as a more significant confounder. “Investigators have a tremendous vested interest in seeing that their treatment is effective,” says Anthony Lang, a neurologist at the University of Toronto in Canada who has participated in several neurosurgical trials for experimental Parkinson’s therapies. In any trial, bias can affect how researchers assess patient responses and may inflate the patients’ expectations, further enhancing the placebo effect. Compounding the problem for Parkinsons’ research is the fact that there are no objective measures for how well a patient is doing. “It’s just a sort of perfect storm conspiring against our ability to see definitive changes in the underlying disease,” says Steven Piantadosi, a clinical-trials methodologist at Cedars-Sinai Medical Center in Los Angeles, California. “Sham surgery, properly done, can control for that.”
Barker counters that it is possible to control for investigator bias in an open-label trial by taking steps such as having blinded raters assess patients. His position is in some ways unsurprising; in Europe, sham surgery is deemed much less acceptable than it is in the United States. It has never been used in the United Kingdom. Barker is categorical about his belief that transplantation of fetal tissue works, at least for some people. “I don’t need sham surgery to show that,” he says, pointing instead to a paper13 published last year describing two patients treated 13 and 16 years previously who were still benefiting from the treatment, and whose brains showed functional dopamine-producing neurons at the transplant site. He attributes the mixed results in past studies to variation in the patients selected for treatment, the characteristics of the tissue being implanted and the methods used to implant it. His trial will have to demonstrate efficacy without eliciting some of the side effects found in the two sham-controlled studies. That will require some type of control study, he says, but it might take the form of comparison to an approved therapy that is known to work, such as deep brain stimulation.
But time, says Barker, will best establish efficacy. In most trials the end point is no more than a year after the treatment. That may not be long enough: implanted cells or injected growth factors might take longer than this to become fully functional, and the placebo e
effect may not have had time to dissipate. “We want a 3–5-year endpoint,” says Barker.
There are hints from some of the failed phase II trials that patients followed up beyond study endpoints might tell a more positive story4. Some say, therefore, that sham controls are sinking the prospects of valuable drugs. Anders Björklund, a neuroscientist at Lund University in Sweden who is collaborating with Barker, says that sham surgery can lead researchers to throw out a strategy prematurely if the trial fails because of technical or methodological glitches rather than a true lack of efficacy.
Advocacy and frustration
According to Perry Cohen, who leads a network of patient activists called the Parkinson Pipeline Project, that’s exactly what is happening. He had always questioned the need for sham surgery, he says, but after the string of phase II failures, “We started saying, ‘Hey, this is a problem. These trials failed, but we know they are working for some people.'”
For researchers, it is easy to dismiss patients’ concerns as being driven by emotion. “Patients want cures,” says Lang, “and they will often be convinced that the more aggressive, surgical therapies are more likely to be curative.” But Cohen counters that patients have different priorities and that researchers must take these into account. Researchers use placebo controls to weed out false positives. But for patients, the real ogre is the false negatives — which can sink a therapy before it has been optimized. The better a trial is at stamping out the former, the higher the rate of the latter — which means at best delays, and at worst dead ends. Spheramine, for example, “is still on a shelf somewhere”, Cohen says. Then there’s Amgen’s phase II trial of GDNF. The trial was halted in 2004 amid lacklustre results and potential safety concerns, which some have attributed to Amgen’s procedure, rather than to the therapy itself. Now researchers are taking a renewed interest in the molecule, but although Cohen is glad it is getting a second chance, “we lost 6 years on it”, he says.
Patients also have different perspectives on risk from researchers, Cohen says. He offers the story of Tom Intili, who had had Parkinson’s for 10 years when, at the age of 50, he signed on to the double-blind, placebo-controlled trial of neurturin. At first, Intili improved dramatically. But when the results were unblinded, he learned that he had received the sham. His condition plummeted, leaving him more debilitated than he had been before the trial. “We just don’t know what the psychological effects of unblinding are,” Cohen says.
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Moreover, trying to exclude the placebo effect is simply misguided, Cohen argues. “I don’t want to subtract out the placebo effect — I want to keep it, because in real life it’s part of the treatment,” he insists. Because psychological factors are so salient in Parkinson’s, a placebo response might actually potentiate a therapy, he explains. “I want to be convinced that sham surgery is necessary. I’m looking for arguments that might change my mind, but I haven’t found any yet,” he says.
Willocks says that she is living proof that many of the recently shelved therapies are in fact salvageable. Of course from a scientific perspective, her story is an anecdote, not data. In May, the failed phase II study of Spheramine — the therapy she received a decade ago — was finally published2. The paper closes with a warning about the dangers of the placebo effect and stresses the importance of controlling for it with a double-blind design. “That last paragraph bothered me,” Willocks says. “I just don’t see how they can call it a placebo effect after ten years.”
The worst day of this disease was the day I was diagnosed. The best day was when I understood that I could do something about it. It gave me back a sense of control in my life, and some power.” –Phyllis, 63, five years after diagnosis
If you or someone close to you has recently been diagnosed with Parkinson’s disease (PD), you are likely experiencing many emotions and have many concerns and questions.
Remember that you are not alone. As many as one million people in the US and an estimated seven to 10 million worldwide live with Parkinson’s disease. These estimates do not account for cases of PD that are unreported, undiagnosed or misdiagnosed.
With a diagnosis now in hand and the freedom to learn at your own pace, you can begin to understand PD and its treatments and the role they will play in your life. Your diagnosis can be the first step to taking charge of your life with Parkinson’s disease. What are some next steps?
Hear Real Stories from People with PD:
It is common for many people to experience a wide range of emotions upon diagnosis from shock, to anger and even to sometimes a sense relief at being able to name symptoms (perhaps a small tremor or weaknesses) that have gone unexplained or misdiagnosed for years. Hear from others who may have had an experience similar to yours.
Inform Yourself about PD:
You will need time to adjust to the new diagnosis, so educate yourself about PD – slowly. PDF provides educational publications and website, a HelpLine, suggestions of local support groups and doctors and online and video resources to help you and your loved ones to cope and become informed.
This fact sheet offers in-depth information and practical tips on choosing the right doctor. It includes facts about why it’s important to see a Parkinson’s specialist. Also offered in: Spanish.
In 2009, Andrew Johnson, 35, was diagnosed with early onset Parkinson’s disease. Last November, and again in February, he underwent a procedure, during which surgeons implanted a device in his brain that controls his tremors. Today, you’d never guess he suffers from Parkinson’s – but watch what happens when he turns his new implant off.
Johnson flips the switch on his device at the 2:00 mark, but for the full effect you’ll want to watch from the beginning. When his hands and head are at rest, you’re witnessing the stunning effects of a procedure known as deep brain stimulation (DBS). The surgery involves the implantation of a brain pacemaker. Like the artifical pacemaker you might find attached to someone’s heart, a brain pacemaker is used to generate electrical impulses, only instead of targeting heart muscles it targets specific regions of the brain. In patients suffering from Parkinson’s disease, DBS is used to treat motor symptoms when other forms of therapy fail.
As Johnson points out on his blog, DBS is not a miracle cure – it’s an FDA-approved surgical procedure that’s been cleared for the treatment of Parkinson’s disease for over a decade now. That being said, Johnson has responded to the treatment extraordinarily well, as you can clearly see in the video above. http://www.infocreations.org/2015/12/30/vanishing-parkinsons-disease
First Clinical Efficacy Study Investigating ND0612H Subcutaneously Delivered Liquid Levodopa/Carbidopa for the Treatment of Advanced Parkinson's Disease
ET|Source:NeuroDerm Ltd.
REHOVOT, Israel, Dec. 30, 2015 (GLOBE NEWSWIRE) -- NeuroDerm Ltd. (Nasdaq:NDRM), a clinical stage pharmaceutical company developing drugs for central nervous system (CNS) disorders, today announced the start of patient enrollment in a first efficacy trial of ND0612H, the company’s continuously administered subcutaneous levodopa/carbidopa solution. This treatment is intended to be an alternative to current treatments for patients with advanced Parkinson’s disease that require surgical intervention. The multicenter international phase II clinical study will compare the efficacy, safety and tolerability of ND0612H to the baseline oral standard of care. ND0612H, administered through a belt pump, is designed to deliver steady LD/CD levels and improve motor fluctuations that cannot be adequately controlled with oral therapy and might otherwise require surgical intervention.
"Previous studies demonstrated that continuous subcutaneous delivery of ND0612H has the capacity to produce stable plasma levodopa levels that currently can be reached and maintained only by treatments that require invasive surgery. In other studies the company demonstrated that continuous subcutaneous delivery of the low dose product, ND0612L, as an add-on, can improve motor fluctuations without causing an increase in dyskinesia, benefits that are similar to those obtained with invasive therapy such as deep brain stimulation and LD/CD intestinal gel, but avoiding the potentially serious side effects associated with those procedures,” said C. Warren Olanow, MD, Professor of Neurology and of Neuroscience at the Mount Sinai School of Medicine in New York City. “This trial is intended to produce additional evidence that ND0612H is a viable alternative for advanced Parkinson’s patients who suffer motor complications that can no longer be satisfactorily controlled with current optimized therapies.”
This 28 day multicenter, parallel-group, rater-blinded, randomized pilot phase II study (designated 006) will investigate the efficacy, safety, tolerability and pharmacokinetics of two dosing regimens of ND0612H and compare them to the baseline oral standard of care. The study is expected to enroll a total of 36 advanced Parkinson’s disease patients.
This first efficacy trial of ND0612H marks an important milestone in its clinical development. Advanced Parkinson’s disease patients who suffer motor complications that cannot be adequately controlled with current therapy face limited treatment options that include surgical intervention that may be associated with serious adverse effects and death. NeuroDerm is committed to provide advanced stage patients with a new therapy option that will be a safe, simple and effective alternative to current surgical treatments,” said Oded S. Lieberman, PhD, MBA, CEO of NeuroDerm.
The Company is proceeding on track in Europe with a head-to-head pharmacokinetic (PK) comparison study of ND0612H and DUODOPA®, the results of which are expected in Q2 2016. The Company is also planning to initiate a Phase III pivotal efficacy trial for its ND0612L treatment for patients with moderate to severe Parkinson’s disease as well as a long-term safety follow-up in the first half of 2016.
ND0612H and ND0612L ND0612H and ND0612L are designed to significantly reduce motor complications in Parkinson's disease patients through continuous, subcutaneous delivery of LD/CD solution. Previously completed Phase II trials demonstrated that ND0612L maintained steady, therapeutic levodopa plasma concentrations that were associated with major changes in several clinical parameters including "off time" reductions when added to optimized oral standard of care. ND0612H, intended for severe Parkinson's disease patients, was shown to reach even higher levodopa steady plasma levels, indicating that it may provide an effective therapy alternative to current treatments requiring surgery such as deep brain stimulation and LD/CD Intestinal Gel.
About Parkinson's disease Parkinson's disease is a progressive neurodegenerative illness characterized by reduced dopamine in the brain, resulting in a debilitating decrease in the patient's motor and non-motor functions. Its symptoms, such as trembling in the extremities and face, slowness of movement and impaired balance and coordination, worsen over time and gravely impact the patient's quality of life. Levodopa is the most effective treatment for Parkinson’s disease. However, chronic oral levodopa treatment is associated with fluctuations in motor response as result of which, despite the benefits of the drug, patients can experience periods of impaired motor and non-motor functions, also referred to as "off" time. In addition, mainly as a result of excessive/intermittent oral doses of levodopa aimed at treating the "off" time, some patients experience involuntary movements, or dyskinesia. The "off" time and dyskinesia affect the majority of levodopa-treated Parkinson's disease patients and can interfere with day-to-day functions, causing patients to become severely disabled. Current evidence suggests that intermittent dosing with standard oral formulations of levodopa contributes to the development of these motor complications. By contrast, it has been shown that continuous administration of levodopa can effectively treat motor fluctuations in Parkinson's disease patients without increasing troublesome dyskinesias; however, a convenient route for continuous administration has not been introduced to date.
AboutNeuroDerm NeuroDerm is a clinical-stage pharmaceutical company developing central nervous system (CNS) product candidates that are designed to overcome major deficiencies of current treatments and achieve enhanced clinical efficacy through continuous, controlled administration. The company has three product candidates in different stages of development which offer a solution for almost every Parkinson's disease patient from the moderate to the very severe stage of the disease. The company has developed a line of LD/CD product candidates administered through small belt pumps that deliver a continuous, controlled dose of LD/CD. The LD/CD line of product candidates includes: ND0612L and ND0612H, delivered subcutaneously, for moderate and for advanced Parkinson's disease patients, respectively. In addition, NeuroDerm is developing ND0701, a novel subcutaneously delivered apomorphine formulation for patients who suffer from severe Parkinson's disease and who do not respond well to LD/CD. NeuroDerm is headquartered in the Weizmann Science Park in Rehovot, Israel.
NeuroDerm Contact:
Oded S. Lieberman, PhD, MBA, CEO oded@neuroderm.com Tel.: +972-8-946 2729; Cell: +1-617-517 6077
U.S. Investor Contact:
David Carey Lazar Partners Ltd. dcarey@lazarpartners.com +212-867-1762
U.S. Media Contact:
Erich Sandoval Lazar Partners Ltd. esandoval@lazarpartners.com +917-497-2867
Service dogs are specialty trained to help and protect people with vision, hearing, physical and emotional challenges. Some of the earliest and well-known use of service dogs is the use of guide dogs for blind or visually challenged persons. The majority of people with PD use a Mobility Assistance Dog.
Sometimes a special harness is worn by a Mobility Assistance Dog made for pulling objects, such as wheelchairs.
Service dogs can help a person with Parkinson’s disease in many ways. Here are just a few of the ways:
Help with physical tasks around the house such as turning on light switches, opening and closing doors, picking up objects.
Assist with walking by helping with balance, act as a support or help a person get up.
Hold a person up if they are dizzy.
Overcome freezing of gait. This can be done by clearing the way in crowded areas, by using gentle pressure on a person’s leg or leading a person away from a hectic and stressful area that can exacerbate freezing.
Exert a calming effect at times of stress and anxiety
Remember these are service dogs and not pets nor a guard dog. They are wonderful and amazing animals that can help you live better. Contact the following sources for more information:
Written by Kimberly Holland | Published on May 30, 2012
This continues to be true, so I placed it here for all
Parkinson’s disease is a progressive disease, and while treatments for it are becoming more advanced every day, it’s still a disease that cannot be cured. It starts silently—often with a minor tremor or difficulty moving as quickly as you once did. Over time, however, the disease will affect everything from your speech to your ability to walk and express emotions on your face. For that reason, an important part of a successful Parkinson’s treatment plan is recognizing and managing secondary symptoms, those that affect your day-to-day life. Here are a few of the more common secondary symptoms and what you can do to help make them more manageable.
Depression
Depression among people with Parkinson’s disease is not at all uncommon. In fact, by some estimates at least 50 percent of people with Parkinson’s disease will experience depression. Facing the reality that your body and life will never be or act the same can take a great toll on your mental and emotional health. Symptoms of depression include feelings of sadness, worrying, or loss of interest. It’s imperative that you talk with a doctor or licensed psychologist if you think, or if a family member suggests, you may be struggling with depression. Depression is usually treated successfully with antidepressant medications.
Difficulty Sleeping
Individuals with Parkinson’s disease may have difficulty falling asleep. You may also experience restless sleep, where you wake up frequently during the night. More than 75 percent of people with Parkinson’s disease report sleep problems. You may also experience sleep attacks—episodes of sudden sleep onset—during the day. Talk with your doctor about taking an over-the-counter or prescription sleep aid to help you regulate your sleep.
Constipation and Digestive Issues
As Parkinson’s disease progresses, your digestive tract will slow down and no longer function as efficiently as it once did. This lack of movement may lead to increased bowel irritability and constipation. In addition, certain medications often prescribed to patients with Parkinson’s disease, such as anticholinergics, can cause constipation. Combat constipation by eating a well-balanced, nutritious diet that contains plenty of vegetables, fruits, and whole grains. In addition to offering vitamins, minerals, and nutrients, fresh produce and whole grains also contain a great deal of fiber, which can help prevent constipation. Fiber supplements and powders are also an option for many Parkinson’s patients. Be sure to ask your doctor how to gradually add fiber powder to your diet so that you don’t begin with too much too quickly and make your constipation problem worse. Eat a variety of fish and seafood, too—this food group contains omega-3 fatty acids, which may have additional benefits for people with Parkinson’s disease.
Urinary Problems
Just as your digestive tract may become weaker, so can the muscles of your urinary tract system. Parkinson’s disease and medications often prescribed to treat it can cause your autonomic nervous system (often referred to as your involuntary nervous system) to stop functioning properly. When that happens, you may begin experiencing urinary incontinence or difficulty urinating.
Difficulty Eating
In the later stages of the disease, the muscles in the throat and mouth may work less efficiently, which may make chewing and swallowing difficult. This same problem can also increase the likelihood of drooling or choking while eating. Fear of choking and other eating problems may put you at risk for inadequate nutrition. However, working with an occupational therapist or speech-language therapist may help you regain some control of your facial muscles.
Decreased Range of Movement
Exercise is important for everyone, but it is an especially important part of treatment for patients with Parkinson’s disease. Physical therapy or exercise can help improve mobility, muscle tone, and range of motion—physical capabilities often greatly affected by the disease. Increasing and maintaining muscle strength may be especially important as muscle tone is lost; in some cases, it can act as a buffer, countering some of the disease’s more harmful effects. Additionally, massage helps you reduce muscle stress and relax, which is especially beneficial to people with Parkinson’s disease.
Increased Falls and Loss of Balance
Parkinson’s disease can alter your sense of balance and make simple tasks such as walking seem more dangerous than they once were. When you’re walking, be sure to move slowly so your body can rebalance itself. Don’t try to turn around by pivoting on your foot—you may not have adequate balance and control, and you increase your risk of falling. Instead, turn yourself around by walking in a U-turn pattern. Also, don’t carry things while walking. Your hands are needed to steady you and help your body balance. Prepare your home and remove any fall hazards by arranging furniture with wide spaces between each piece so there is ample room to walk; position furniture and lighting so that no extension cords are needed; and install handrails in hallways, entryways, and stairwells and along walls.
Sexual Problems
Another common secondary symptom of Parkinson’s disease is decreased libido. Doctors are not certain what causes this, but it’s suspected that a combination of physical and psychological factors may contribute to the drop in sexual desire. The good news is the problem is often treatable with medications and counseling.
Hallucinations
Medicines prescribed to treat Parkinson’s disease may cause unusual visions, vivid dreams, or even hallucinations. If these side effects do not improve or go away with a change in prescription, your doctor may prescribe an antipsychotic drug.
Pain
The lack of normal movement associated with Parkinson’s disease can increase your risk of having sore, aching muscles and joints, and may lead to prolonged pain. Prescription drug treatment can help relieve some of the pain, but exercise has also been found to help relieve muscle rigidity and pain.
Medications prescribed to treat Parkinson’s disease may have additional side effects, such as involuntary movements (or dyskinesia), nausea, hypersexuality, compulsive gambling, and compulsive overeating. Many of these side effects can be resolved with a dose correction or change in medicine. However, it’s not always possible to eliminate the side effects and still treat the Parkinson’s disease effectively. Do not stop taking or self-adjust medications without talking to your doctor first.
Debate over importance of new carbidopa-levodopa agents
New therapies that offer a better
way of delivering carbidopa/levodopa were the biggest clinical advance in
Parkinson's disease, according to a plurality of experts contacted by MedPage
Today. But the responses fell short of a consensus.
Rytary, an extended release form
of carbidopa/levodopa, and Duopa, which delivers these agents using a small
portable infusion pump, was approved by the FDA in January 2015.
The new therapies were chosen as
part of the responses of 55 neurologists asked to pick a
"game-changer" in their subspecialty. The most popular selections (or
lack, in one case) in each of five major neurology fields were:
1. MS: Ocrelizumab results in
ORATORIO and OPERA I and II
2. Stroke: Publication of five
trials confirming the efficacy of neurothrombectomy for acute ischemic stroke
3. Parkinson's disease: New
formulations for delivering carbidopa/levodopa
5. Alzheimer's disease: no
clinical advance stood out
Several of the specialists we
contacted agreed that Rytary was a significant advance. "Substituting
Rytary, a long-acting form of carbidopa-levodopa, for standard
carbidopa-levodopa, reduces fluctuations and 'off' time, keeping people in the
'on' state for more of the time," said Stephen G. Reich, MD,
the Frederick Henry Prince Distinguished professor in Neurology, University of
Maryland School of Medicine.
Robert A. Hauser, MD, MBA,
director, Parkinson's Disease and Movement Disorders Center at the University
of South Florida, said patients "may benefit from a small levodopa dose as
the capsules can be opened and the beads mixed in with food such as
applesauce."
Some felt there are
pharmacological advances to Rytary because, as Jacci Bainbridge, PharmD,
professor of clinical pharmacy at the University of Colorado, put it, the
product "allows for continuous smoother serum concentrations as opposed to
immediate release formulations... (which) keeps (the) drug in the therapeutic
window."
Duopa, an enteral suspension for
the treatment of motor fluctuations for people with advanced Parkinson's
disease, was called a "fundamentally new therapy" by David G. Standaert, MD, PhD,
John N. Whitaker professor and chair of neurology at the University of Alabama
at Birmingham. "I and others have seen some very dramatic improvements
with this approach -- it is often equivalent to what you might see with deep
brain stimulation," he said.
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Both of these treatments, in the
view of a number of experts, improve their ability to minimize "off"
time for patients. "It's a particularly welcome addition to our
armamentarium for managing motor fluctuations in PD patients who are not (or
are not yet) DBS candidates," added Matthew Swan, MD, of
Albert Einstein College of Medicine and Montefiore Medical Center in New York.
However, a number of experts were
not enthusiastic about Rytary. Alessandro Di Rocco, MD,
chief of NYU Langone Medical Center's movement disorders division, said the
clinical effect of the drug was "less than ideal" because of
"complex dose conversion tables that were often unhelpful in difficulty
identifying the correct dose." He said the "off" periods for
many patients fluctuated and were not predictable. "Many of the patients
[who] started on Rytary were later switched back to their previous older L-dopa
formulation, and often patients emphatically asked to return to their previous
drugs," he said.
And Sanjay Iyer, MD,
medical director of neurology at Carolinas HealthCare System's Neurosciences
Institute, noted a lack of data "to suggest that extended release versions
have fewer complications than immediate release levodopa, especially as it
relates to potential to develop dyskinesia, or abnormal involuntary movements,
such as writhing, and squirming."
Another advance for the year
included a 2013 finding that one expert said had made its way into practice
this year. Padraig O'Suilleabhain, MD,
of UT Southwestern Medical Center in Dallas, cited "the finding that doing
DBS surgery earlier rather than later is better in terms of quality of life and
likely overall cost, in a patient who develops motor fluctuations in their
first 5 years of PD."
Also mentioned was a small trial
with the leukemia drug nilotinib (Tasigna). Mark A. Stacy, MD, vice dean for
clinical research at Duke University School of Medicine, pointed to the small study conducted at
Georgetown, which found a benefit in multiple domains of the
disease.
