Managing the Side Effects of Parkinson’s Disease

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.

http://www.healthline.com/health/parkinsons/side-effects#1

Game-Changers in 2015: Parkinson's Disease

 NEUROLOGY 12.29.2015

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

4. Sleep: SERVE-HF trial showing adaptive servoventilation (ASV) increased mortality

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.

http://www.medpagetoday.com/Neurology/ParkinsonsDisease/55449       

Was This the Real Condition Behind Robin Williams's Suicide?

Dec. 28, 2015

In my post, "The Tragic Side of Comedy: Where the Pain Lives," posted after Robin Williams's suicide , I suggested that his suicide might be attributed to a combination of factors-a mood disorder , substance abuse , and a recent diagnosis of Parkinson's Disease. 

More recently, in a revealing interview, Williams's widow, Susan Schneider Williams, said that it was not major depression that drove her husband to suicide but a rare brain disease called Lewy Body Dementia that can resemble Parkinson's and is often misdiagnosed as Parkinson'sIn my post, "The Tragic Side of Comedy: Where the Pain Lives," posted after Robin Williams's suicide, I suggested that his suicide might be attributed to a combination of factors—a mood disorder, substance abuse, and a recent diagnosis of Parkinson's Disease. More recently, in a revealing interview, Williams's widow, Susan Schneider Williams, said that it was not major depression that drove her husband to suicide but a rare brain disease called Lewy Body Dementia that can resemble Parkinson's and is often misdiagnosed as Parkinson's. She told in heart-wrenching detail about how she and Williams struggled for more than a year to figure out what was wrong with him.

As Psychiatric Times explained, it is a challenge not to miss a general medical cause when addressing symptoms that appear to be psychiatric, especially when looking at an already diagnosed psychiatric disorder. And Williams had suffered for years with substance abuse and a mood disorder; further, at the end of his life, was diagnosed with Parkinson's Disease, leading some to speculate that his depression resulted from Parkinson's.

Before his suicide, his medical doctors had been working up his Parkinson's diagnosis and searching for any other neurological disorders. His psychiatrist reportedly wanted to hospitalize him for more extensive neuropsychological testing, but Williams refused. More recently, a coroner’s report revealed that Williams suffered from Lewy body dementia, a rather rare, difficult-to-diagnose condition that can resemble Parkinson's.

When a patient is diagnosed with a slow developing dementia of any type, the most disturbing period is the interval between more “normal” cognition and no longer realizing that one's thinking is impaired, an interval of recognition that he is literally losing his mind (or more technically, part of the brain). When Parkinson's was diagnosed, undoubtedly Williams knew he was losing his ability to access his wonderfully creative brain, which may have led him to think that he should take his own life before this occurred. If this is so, then his decision to take his own life might be considered less of an act of depressive desperation.

This brilliant man who brought the joy of laughter into the lives of so many people is sorely missed.

https://www.psychologytoday.com/blog/the-mind-body-connection/201512/was-the-real-condition-behind-robin-williamss-suicide

Breakthrough in search for a cure for Alzheimer's and Parkinson's

By Plymouth Herald  |  Posted: December 29, 2015

A CURE for Alzheimer's and Parkinson's could be a step closer after a breakthrough discovery that toxic protein clumps kill neurons in motor neurone disease.

For the first time scientists have pinned down the structure of toxic clumps of a protein associated with incurable motor neurone conditions.

It could lead to new drugs to stop the protein clumps forming and stem the progression of the disease. Known as Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig's disease, it is a rare condition that progressively damages parts of the nervous system leading to muscle weakness.

It occurs when specialist nerve cells in the brain and spinal cord called motor neurones stop working properly. These are crucial to moving, speaking, swallowing, and breathing and as the disease progresses can be fatal. Motor neurone disease affects around two in every 100,000 people Britons each year and there are about 5,000 people living with the condition in the UK at any one time. Cures for motor neurone disease and other neurodegenerative diseases have long eluded researchers, largely because their causes have remained mysterious.

http://health.einnews.com/article/303820757/8RoxfiHtX1Wsh_sP

Read more: http://www.plymouthherald.co.uk/Breakthrough-help-cure-fatal-brain-diseases/story-28431667-detail/story.html#ixzz3vj2CByv6 
Follow us: @heraldnewslive on Twitter | theplymouthherald on Facebook

ULTRA EARLY DIAGNOSIS OF PARKINSON'S DISEASE

28th December 2015 - New research

Researchers determined the value of enhanced substantia nigra echo in the diagnosis of Parkinson's Disease by analyzing the intensity and area of substantia nigra echo using transcranial Doppler sonography (TCS). Transcranial Doppler sonography is a technique that uses a handheld, microprocessor-controlled, low-frequency, pulsed Doppler transducer to measure the velocity and pulsatility of blood flow within certain areas of the brain. 

People without Parkinson's Disease were compared to people with ultra early stage Parkinson's Disease using results of substantia nigra echo, which are graded I (the least) to V (the greatest). The sensitivity of substantia nigra echo in diagnosing Parkinson's Disease was 89% and the specificity was 93%. %). The levels were much higher in Parkinson's Disease.

The figures for those people with Parkinson's Disease compared to those who did not have it were Grade V (19% v none), Grade IV (33% v none), Grade III (36% v 6%), Grade II (11% v 40%), Grade I (none v 53%). High grades were only present in Parkinson's Disease. Low grades were only present when there was no Parkinson's Disease.

Analysis of substantia nigra echo is of practical use for the diagnosis of the ultra early stage Parkinson's Disease, and so can potentially improve the accuracy of clinical diagnosis to significantly enhance the early clinical prevention of disability.

information go to : http://pubs.rsna.org/doi/pdf/10.1148/radiographics.15.1.7899596

Reference : European Review of Medical and Pharmacologial Sciences [2015] 19 (23) : 4621-4626 (J.J.Zhuang, Y.H.Zheng, X.W.Xu, L.Zhou)

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/26698260

http://www.viartis.net/parkinsons.disease/news/151228.pdf mail@viartis.net

©2015 Viartis 

Discovery puts designer dopamine neurons within reach

Parkinson's disease researchers discover a way to reprogram the genome

Date:

December 7, 2015

Source:

University at Buffalo

Summary:

Parkinson's disease researchers have developed a way to ramp up the conversion of skin cells into dopamine neurons. They have identified -- and found a way to overcome -- a key obstacle to such cellular conversions.

Image shows a protein found only in neurons (red) and an enzyme that synthesizes dopamine (green). Cell DNA is labeled in blue.

Credit: Jian Feng, University at Buffalo

For decades, the elusive holy grail in Parkinson's disease research has been finding a way to repair faulty dopamine neurons and put them back into patients, where they will start producing dopamine again. Researchers have used fetal material, which is difficult to obtain and of variable quality. Embryonic stem cells represented a tremendous innovation, but making dopamine neurons from stem cells is a long process with a low yield.

These issues have driven researchers to try to develop ways to turn cells that are easy to obtain, such as skin cells, into dopamine neurons, which are normally hidden in the brain. But here, too, it has been difficult to obtain sufficient quantities of neurons.

Now, Parkinson's disease researchers at the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo have developed a way to ramp up the conversion of skin cells into dopamine neurons. They have identified -- and found a way to overcome -a key obstacle to such cellular conversions. At the same time, the researchers say the finding has profound implications for changing the way scientists work with all cells.

A cellular 'gatekeeper'

The new research, published Dec. 7 in Nature Communications, revolves around their discovery that p53, a transcription factor protein, acts as a gatekeeper protein.

"We found that p53 tries to maintain the status quo in a cell, it guards against changes from one cell type to another," explained Jian Feng, PhD, senior author and professor in the Department of Physiology and Biophysics in the Jacobs School of Medicine and Biomedical Sciences at UB. "We found that p53 acts as a kind of gatekeeper protein to prevent conversion into another type of cell. Once we lowered the expression of p53, then things got interesting: We were able to reprogram the fibroblasts into neurons much more easily."

The advance has importance to basic cell biology, Feng said. "This is a generic way for us to change cells from one type to another," he said. "It proves that we can treat the cell as a software system, when we remove the barriers to change. If we can identify transcription factor combinations that control which genes are turned on and off, we can change how the genome is being read. We might be able to play with the system more quickly and we might be able to generate tissues similar to those in the body, even brain tissue.

"People like to think that things proceed in a hierarchical way, that we start from a single cell and develop into an adult with about 40 trillion cells, but our results prove that there is no hierarchy," he continued. "All our cells have the same source code as our first cell; this code is read differently to generate all types of cells that make up the body."

Generating new dopamine neurons via cellular conversion

Timing was key to their success. "We found that the point in the cell cycle just before the cell tries to sense its environment to ensure that all is ready for duplicating the genome, is the prime time when the cell is receptive to change," said Feng.

By lowering the genomic gatekeeper p53 at the right time of cell cycle, they could easily turn the skin cells into dopamine neurons, with transcription factor combinations discovered in previous studies. These manipulations turn on the expression of Tet1, a DNA modification enzyme that changes how the genome is read.

"Our method is faster and much more efficient than previously developed ones," said Feng. "The best previous method could take two weeks to produce 5 percent dopamine neurons. With ours, we got 60 percent dopamine neurons in ten days."

The researchers have done multiple experiments to prove that these neurons are functional mid-brain dopaminergic neurons, the type lost in Parkinson's disease.

The finding enables researchers to generate patient-specific neurons in a dish that could then be transplanted into the brain to repair the faulty neurons. It can also be used to efficiently screen new treatments for Parkinson's disease.

---

Story Source:

The above post is reprinted from materials provided by University at Buffalo. The original item was written by Ellen Goldbaum. Note: Materials may be edited for content and length.

---

Journal Reference:

1. Houbo Jiang, Zhimin Xu, Ping Zhong, Yong Ren, Gaoyang Liang, Haley A. Schilling, Zihua Hu, Yi Zhang, Xiaomin Wang, Shengdi Chen, Zhen Yan, Jian Feng. Cell cycle and p53 gate the direct conversion of human fibroblasts to dopaminergic neurons. Nature Communications, 2015; 6: 10100 DOI: 10.1038/ncomms10100

http://www.sciencedaily.com/releases/2015/12/151207081821.htm

Dyskinesia Drug a Step Closer to FDA Approval with Positive Phase III Results

FoxFeed Blog

Posted by  Maggie McGuire Kuhl, December 28, 2015

Dyskinesia can be confusing. These involuntary movements can look like smooth tics or an uncoordinated dance, and may be part of how people think of Parkinson’s disease. But they are not part of the disease itself. Dyskinesia is a side effect of levodopa — the gold standard medication for Parkinson’s motor symptoms tremor and rigidity — and can significantly impact quality of life.

“If we could control dyskinesia, it would probably be the biggest change in terms of how we treat patients,” said Susan Bressman, MD, chair of the Department of Neurology at Beth Israel Medical Center in New York City, in an MJFF video on dyskinesia.

Physicians have long thought that dyskinesia arose with long-term use of levodopa, so patients may delay starting medication and live with disabling symptoms in an attempt to “save” the window of efficacy before dyskinesia begins. While more recent research is showing that levodopa-induced dyskinesia may be influenced more by stage of disease than length of medication use, a treatment for this side effect would be a game-changer for many patients.

Last week pharmaceutical company Adamas announced it is a step closer to such a therapy with positive findings from a Phase III study of extended-release amantadine. People who took the drug (called ADS-5102) showed a 23 percent reduction in dyskinesia compared to people who received a placebo.

To measure the effect of ADS-5102, researchers used the Unified Dyskinesia Rating Scale, a critical tool validated with funding from The Michael J. Fox Foundation. In 2012 MJFF supported a study of the scale to determine its utility in testing dyskinesia treatments. The validation of the rating scale shows it is a solid measure of a drug’s impact, and may help the U.S. Food and Drug Administration assess the utility of ADS-5102 when deciding on approval.

Interestingly, researchers used amantadine (the same compound as ADS-5102) to validate the rating scale. Amantadine is approved as a treatment for influenza, but physicians have used it treat dyskinesia. The drug blocks receptors of neurotransmitter glutamate, which scientists believe is involved in causing this side effect. This extended-release formulation could help control dyskinesia throughout the day.

https://www.michaeljfox.org/foundation/news-detail.php?dyskinesia-drug-step-closer-to-fda-approval-with-positive-phase-iii-results

Possible Parkinson’s Treatment for Levodopa-Induced Dyskinesia Gets US Patent Protection

Amarantus BioScience's eltoprazine, in clinical testing, is covered through 2027

Dec. 22,  2015

Amarantus BioScience Holdings, Inc. (AMBS) received a Notice of Allowance from the U.S. Patent and Trademark Office covering the use of 5HT1A in combination with 5HT1B agonists, including the clinical Phase 2b stage drug eltoprazine, to treat levodopa-induced dyskinesia (PD-LID) in Parkinson’s disease (PD). The office issues such a notice after determining that a patent should be issued based on examination of the filing.

This Notice of Allowance was received for a patent application filed as a continuation, in part, to a previously issued patent (No. 9,066,903), and reinforces Amarantus’ intellectual property protection for the potential combination 5HT1A/1B receptor agonist against competitors also targeting PD-LID. For eltoprazine, the notice provides further protection through 2027.

Eltoprazine is a small molecule in clinical development for the treatment of levodopa-induced dyskinesia in Parkinson’s patients and for adult attention deficit hyperactivity disorder (ADHD). Patient enrollment for the current Phase 2b trial is momentarily stopped, as Amarantus expects a decision from the U.S. Department of Food and Drug Administration (FDA) regarding an orphan drug application submitted for PD-LID that may change the company’s development plan.

Levodopa-induced dyskinesia, a form of dyskinesia associated with the drug levodopa used to treat PD, often involves hyperkinetic movements, including chorea, dystonia, and athetosis. In the context of PD, dyskinesia is often the result of chronic L-DOPA (levodopa) therapy. These motor fluctuations occur in more than half of PD patients after 5–10 years of L-DOPA treatment, with the percentage of affected patients increasing over time.

“This Notice of Allowance for eltoprazine in Parkinson’s disease levodopa-induced dyskinesia significantly strengthens the company’s intellectual property position by creating an additional barrier to entry for the 5HT1A/1B receptor agonist field for the treatment of PD-LID,” said Gerald E. Commissiong, president and CEO of Amarantus, in a recent press release. “As we await a decision from the US FDA on the orphan drug designation for treating PD-LID, we are currently evaluating alternative clinical pathways by which to accelerate our commercialization timeline, while also evaluating strategic interest in the overall eltoprazine program which includes Alzheimer’s aggression and adult ADHD.”

To date, eltoprazine has been assessed in more than 680 patients, and has a known safety profile. The drug initially entered clinical development at Solvay Pharmaceuticals to treat aggression, but the clinical program was out-licensed to PsychoGenics when Solvay merged with Abbott Pharmaceuticals. Eltroprazine was then licenced to Amarantus after positive proof-of-concept clinical trials in PD-LID as well as in adult ADHD.

http://parkinsonsnewstoday.com/2015/12/22/amarantus-gets-us-patent-covering-method-of-treating-parkinsons-disease-levodopa-induced-dyskinesia/?utm_source=PAR+E-mail+List&utm_campaign=bc04872f63-RSS_WEEKLY_EMAIL_CAMPAIGN&utm_medium=email&utm_term=0_62dd4fb5e3-bc04872f63-71459285

Can ballet ease Parkinson's symptoms

26 December 2015 Last updated at 09:29 GMT 

It is a disease characterised by tremors, slow movements and stiff muscles - but new research has found an unusual method of easing the symptoms of Parkinson's.

Academics from the University of Roehampton have found that ballet can have significant physical and emotional benefits for patients. 

Jayne McCubbin joined a class in Liverpool to see the effects.

http://health.einnews.com/article/303494282/IAjnRVkhOnfGOU3i

Elastic Abdominal Binders May Prevent Dizziness on Standing

- Dec 21 2015

Wearing an elastic abdominal binder (a medical version of a girdle available in most drugstores) may help prevent low blood pressure on standing in people with Parkinson’s disease (PD), according to research published in the November 27 online edition of Movement Disorders Clinical Practice.

Many people with mid- and late-stage PD experience a sharp drop in blood pressure when standing up from a sitting position. This symptom is also common among people living with the atypical parkinsonism known as multiple system atrophy (MSA). The medical term for it is neurogenic orthostatic hypotension (nOH), and it can make a person feel dizzy, lose their balance and fall or even lose consciousness. Treating orthostatic hypotension with drugs that raise blood pressure is tricky — the medicines can prevent dizziness when standing up, but can make blood pressure too high when lying down.

Studies in people with other conditions that lead to orthostatic hypotension, including diabetes, have suggested that wearing an elastic abdominal binder — a wide elastic band that supports the stomach — helped them maintain a steady blood pressure.

Researchers led by Klaus Seppi, M.D., at the Innsbruck Medical University in Austria tested the treatment in 15 study participants who had PD and orthostatic hypotension. First, they monitored each study participant’s blood pressure during a “tilt test,” during which participants lay on a flat examining table, which is then raised to a seated position. Then participants wore either an elastic abdominal binder or a placebo binder — one that did not put pressure on the abdomen — for two hours and repeated the test. On a different day the participants switched binders and were tested again. Then all participants wore the elastic binders a few hours a day for four weeks and were assessed again.

Results

• On average, blood pressure was about 10 mm Hg higher when participants sat up wearing the elastic abdominal binder versus the placebo binder.
• Lying-down blood pressure remained the same no matter which binder the participants wore.
• Using an elastic abdominal binder daily for four weeks improved symptoms of orthostatic hypotension.

What Does It Mean?

The study authors conclude that elastic abdominal binders may provide a simple tool to alleviate the troublesome PD symptom of orthostatic hypotension. For some, it may be worth trying because it involves no drugs that might interact with other PD medications, and there is no risk of raising overall blood pressure in people whose blood pressure is already generally high.  

Limitations of the study include the fact that the number of study participants was small and the study was not double blinded (participants knew which group they were in).

In addition, one side effect that remains to be investigated is the possibility that abdominal binders exacerbate varicose veins in the legs. Therefore, a larger, controlled trial will likely need to be performed before abdominal binders receive broad endorsement. In the meantime, talk with your physician to see if you might benefit from this simple tool to help manage orthostatic hypotension.

http://www.pdf.org/en/science_news/release/pr_1450734465