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Saturday, March 9, 2019

Learning About Pot and Parkinson's With Dr. James Beck

March 8, 2019



Westword checked in with Dr. James Beck, chief scientific officer for the Parkinson's Foundation, to learn more about what the organization hopes to gain from its time in Denver, as well as what kind of studies need to be done going forward so that medical professionals can properly evaluate the effects of cannabis on Parkinson's.

Westword: Why choose Denver for the foundation’s first conference about medical marijuana?

Dr. James Beck: We needed a location that is centrally located to ensure that experts from academia, clinics, industry, government and the Parkinson's disease (PD) community can easily get to our first-ever medical marijuana and PD conference.

Being that the conference is invite-only, is there any way that patients or those interested in medical marijuana and Parkinson's disease can learn more after the conference? 

In addition to Parkinson’s specialists, seven Parkinson’s advocates living with PD will participate in the conference to provide their perspective. The foundation will publish more information and research recommendations for marijuana and PD following the conference this summer on our website, at Parkinson.org/marijuana.

Dr. James Beck


Is medical marijuana a popular form of self-medication for Parkinson's disease? If so, why?

In a study we did with Northwestern University, 95 percent of neurologists have been asked to recommend medical marijuana. While it’s never supposed to be used as a substitute to medication, marijuana is a popular topic in the PD community. People with Parkinson’s have reported improvement in pain management, sleep dysfunction, weight loss and nausea after using marijuana. 

However, clinical studies have not proven that cannabis can directly benefit Parkinson’s symptoms.

Has there been enough research on medical marijuana and its effects on Parkinson's disease to form an opinion?
Unfortunately, no. Studies have not clearly supported the use of marijuana for PD, and are often not conducted on a large enough scale; some studies have as few as five subjects. While some study results have been positive, others show the downsides for people with Parkinson’s, like impaired cognition, dizziness and loss of balance. The Parkinson’s Foundation believes in research. Through this conference, we hope to find out if and how medical marijuana can make life better for people with Parkinson’s. Getting experts together in one room can get us on the path to make research recommendations that can lead to answers.
What specific areas of research regarding Parkinson's disease and medical marijuana need to be expanded upon most?
We need research to help us determine how medical marijuana should be administered and how its long-term use can affect PD symptoms. There are hundreds of strains and various ways to use medical marijuana, and it can all differ from state to state. To ensure safety for people who use medical marijuana, states that legalize medical marijuana will eventually need to develop training programs for doctors and medical teams that prescribe medical marijuana.
https://www.westword.com/marijuana/colorado-leaning-on-new-approaches-and-pot-industry-partnerships-to-fight-stoned-driving-11258142

The radical drug trial hoping for a miracle Parkinson's cure

March 9, 2019





Tom Isaacs was diagnosed with Parkinson's aged 27. And for 17 years he's been desperate to find a cure. 

Now along with 41 others he's volunteered for a ground-breaking medical trial of a drug called GDNF. He will undergo complex brain surgery, and then months of drug infusions via a port embedded in his skull. And he doesn't even know if he's been given the drug or just a placebo. 

Over six years we follow Tom and the volunteers hoping they will be be cured, and the doctors who believe they have found a breakthrough drug. 

Will this be the miracle that millions of Parkinson's patients around the world have been waiting for?

You can watch the two-part documentary The Parkinson's Drug Trial: A Miracle Cure? on iPlayer.

Video:


https://www.bbc.com/news/av/stories-47483307/the-radical-drug-trial-hoping-for-a-miracle-parkinson-s-cure

Patients experiment with prescription drugs to fight aging

March 8, 2019    by Marisa Taylor


Metformin 500mg tablets. Credit: public domain


Dr. Alan Green's patients travel from around the country to his tiny practice in Queens, N.Y., lured by the prospect of longer lives.
Over the past two years, more than 200 patients have flocked to see Green after learning that two drugs he prescribes could possibly stave off aging. One 95-year-old was so intent on keeping her appointment that she asked her son to drive her from Maryland after a snowstorm had closed the schools.
Green is among a small but growing number of doctors who prescribe drugs "off-label" for their possible anti-aging effects. Metformin is typically prescribed for diabetes, and  prevents organ rejection after a transplant, but doctors can prescribe drugs off-label for other purposes—in this case, for "aging."
Rapamycin's anti-aging effects on animals and 's on people with diabetes have encouraged Green and his patients to experiment with them as anti-aging remedies, even though there's little evidence healthy people could benefit.
"Many of (my patients) have Ph.D.s," said Green, who is 76 and has taken the drugs for three years. "They have read the research and think it's worth a try."
In fact, it's easier for patients to experiment with the drugs—either legally off-label or illegally from a foreign supplier—than it is for researchers to launch  that would demonstrate they work in humans.
No rigorous large-scale clinical trials have been conducted aimed at aging. The FDA so far has not agreed that a treatment could be approved for delaying the onset of aging or age-related diseases, citing questions about whether research can demonstrate an overall effect on aging rather than just on a specific disease.
Given such reservations, pharmaceutical companies have little incentive to fund costly, large-scale trials. Also, both metformin and rapamycin are generic and relatively cheap.
"There's no profit," said Matt Kaeberlein, a professor of pathology at the University of Washington medical school whose team received a $15 million grant from the National Institutes of Health to study the effects of rapamycin in dogs, but has noted the lack of funds for studies in people. "Without profit, there's no incentive."
Supplements with purported anti-aging effects routinely enter the market with little scrutiny and less evidence.
Yet, late last year, the NIH rejected a $77 million grant proposal by a prominent group of researchers to determine whether metformin could target multiple age-related diseases at once. It was the second rejection of the ambitious but unorthodox bid.
"We're going to keep trying," said a lead author of the metformin proposal, Stephen Kritchevsky, a co-director of the Sticht Center for Healthy Aging and Alzheimer's Prevention. "These things take time."
Less is known about rapamycin's anti-aging effects and its possible side effects in the general population, including the possibility it could lead to insulin resistance. Yet a litany of studies show that rapamycin extends animal life spans. It also has been shown in such studies to stave off age-related diseases, from cancer to cardiovascular diseases to cognitive diseases.
"There should have been a clinical trial for rapamycin and Alzheimer's disease years ago," said Kaeberlein, who has publicly urged NIH to use a historic boost in Alzheimer's funding to study the drug's effects. "But the fact is, the clinical trials are really hard and expensive."
Alexander Fleming, a former FDA official and advocate for the metformin proposal, said he believed it was difficult for regulators and funders to grasp that aging can be tackled as a whole—not just one disease at a time.
In fact, NIH reviewers who rejected the metformin proposal cited problems with the project's aim of testing multiple age-related diseases at once. The researchers considered appealing the decision, asserting those reviewers were biased against studying aging as a whole. NIH, which declined to comment, discouraged the attempt.
Dr. Evan Hadley, director of the National Institute on Aging's division of geriatrics and clinical gerontology, told Kaiser Health News that NIH is not ruling out funding projects that target aging, saying such proposals are still "of interest."
The FDA also is open to considering such efforts "based on the presented to us," said FDA spokeswoman Amanda Turney.
Fleming, who oversaw the controversial FDA approval of metformin for Type 2 diabetes, said an argument could be made that it could approve a drug like metformin for preventing  instead of just treating them. He points to now widely used statins, which were approved to prevent heart disease.
"There is some kind of belief that the FDA can't approve a therapy to reduce the progress of aging or age-related conditions," said Fleming, an endocrinologist. "It's just not true."
Given the lack of consensus, other researchers have moved ahead with clinical trials focused on specific age-related conditions.
Researchers have shown that a "cousin" of rapamycin boosts the effectiveness of flu shots and lowers the incidence of upper respiratory infections in seniors by up to 30 percent. This group, led by Dr. Joan Mannick, has licensed it from Novartis and is now working on getting approval to target Parkinson's disease.
"We're trying to be pragmatic," Mannick said of her team's approach.
Some doctors and patients have decided not to wait. At a recent scientific forum on aging, one of the researchers on the NIH proposal asked the 300 or so people in attendance to raise their hands if they were already taking metformin for aging.
"Half the audience raised their hands," recalled the researcher, Dr. Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine, who said a pharmaceutical rep recently estimated that metformin sales are up 20 percent.
Barzilai is concerned about the off-label trend, although he sees metformin as promising. He contends that researchers in the longevity field first need to set up a framework for testing in clinical trials. Even if metformin doesn't pan out as the most effective drug, he asserts a model like the metformin proposal is needed for any major clinical trial to proceed. His group is now trying to secure about half the amount of funding it requested from NIH from a mix of nonprofit and private investment.
"Much of the aging field is charlatans," Barzilai said. "They tell you take this or that and you'll live forever. But you have to do a clinical trial that is placebo-controlled and only then can you say what it really is and whether it's safe."
Green nonetheless said he plans to continue prescribing. He estimates about 5 percent of his patients are doctors themselves. Others have backgrounds in science or are in the upper-income bracket. According to his website, he charges $350 for an initial visit and does not accept insurance.
"They fly to see me on their own planes," he said.
But other doctors who are open to prescribing metformin are holding off on rapamycin, given side effects in higher doses in sick patients.
I need to see more evidence," said Dr. Garth Denyer, a doctor in The Woodlands, a wealthy Houston suburb, who said he prescribed metformin to a small number of patients but is waiting on rapamycin. "I'm hoping to see more data on safety."
Michael Slattery, who has been HIV-positive since 1983, said he is taking both drugs because the virus is likely to shorten his life expectancy.
So far, he has not noticed any side effects or benefits. His partner, however, who is also HIV-positive, stopped taking rapamycin after getting kidney infections.
"I feel I have nothing left to lose," said Slattery, a retired biotech consultant.
Other patients remain hopeful, even though the evidence is unlikely to be definitive anytime soon.
Linda Mac Dougall, 70, of Port Hueneme, Calif., said she participated in a small study that did not have a placebo control. She's uncertain whether it had any effect on her.
"I really haven't noticed anything, but that doesn't mean it didn't work," said Mac Dougall, a massage therapist for seniors. She has slightly more confidence in the wide array of supplements she takes, she said: "If I live until I'm 110, we'll know."
https://medicalxpress.com/news/2019-03-patients-prescription-drugs-aging.html

Identification of potential target protein aggregates for treating Alzheimer's

March 8, 2019   by CEA







The aggregation of alpha-synuclein proteins in Parkinson's disease and tau proteins in Alzheimer's disease is intimately linked to the progression of these neurodegenerative diseases. These aggregates propagate from one neuronal cell to another, attaching themselves to the cells.

They multiply during this propagation. It has already been shown that the propagation and amplification of these protein aggregates are harmful and contribute to the progression of these diseases.
Understanding the formation of these aggregates, their propagation and their multiplication in the  of the central nervous system offers potential for treatments: it would make it possible to target these processes and to act on their consequences.
Protein propagation
The key step in the propagation of the pathogenic aggregates is the attachment of aggregates released from affected neuronal cells to the membranes of unaffected cells. Having already identified the targets of pathogenic aggregates of the alpha-synuclein protein (Shrivastava et al., 2015 EMBO-J), the team at the Neurodegenerative Diseases Laboratory (CNRS/CEA/Université Paris-Sud , MIRCen, Fontenay-aux-Roses), in collaboration with the Ecole normale supérieure, Sorbonne University and Inserm, has just identified the targets of tau protein aggregates. The targets are the sodium / potassium pump and glutamate receptors, two essential proteins for the survival of neurons The experiment was carried out on mouse neurons in culture.
Neuron membrane modification
The researchers also showed that the pathogenic aggregates modify the neuron membranes by redistributing the  proteins. The integrity of the membrane—and particularly of the synapses, the essential nodes for communication between neurons—is affected. These changes have a deleterious effect on the neurons because they cause abnormal communication between the neurons, as well as their degeneration.
This work therefore explains the early malfunctioning of the synapses and the degradation of normal communication observed in the neuronal networks as the  progresses.
Toward new treatments
It also paves the way for the development of new treatment strategies based on protecting the integrity of the synapses, restoring the activity of the tau protein membrane receptors through the use of decoys to prevent harmful interaction between the pathogenic tau  aggregates and their neuron membrane targets. These therapeutic approaches could be developed using human , since researchers at the laboratory have just developed cultures of this type in collaboration with the I-Stem (Institute for Stem Cell Therapy & Exploration of Monogenic Diseases, AFM-Téléthon/Insem/Génopole/University of Evry-Val-d'Essonne) laboratory and Sorbonne University. This latter study is also published on 10 January 2019, in Stem Cell Reports.
https://medicalxpress.com/news/2019-03-identification-potential-protein-aggregates-alzheimer.html

Scientists report new modeling of brain signaling

March 8, 2019   by Bill Snyder, Vanderbilt University





The release of neurotransmitters and hormones in the body is tightly controlled by complex protein machinery embedded in cell membranes.

Manipulating that machinery with drugs could improve treatment of disorders ranging from diabetes to Parkinson's disease. Progress has been slow, however, because of the lack of an animal model to test the effects of potential drugs. Until now.
Last week Vanderbilt University pharmacologist Heidi Hamm, Ph.D., and her colleagues reported the first animal model of an important feedback mechanism, essentially a "shut-off valve" for neurotransmitter and hormone release through SNARE complex-mediated membrane fusion.
In a paper featured on the cover of the journal Science Signaling, the researchers reported that when they disabled the shut-off valve in  in the brains of mice through genetic manipulations, the animals exhibited significant deficits in motor coordination, cognitive and other behaviors.
Scientists know how to modulate SNARE and turn on the neurotransmitter "spigot." But until now, they had no idea what might happen if they did.
"We can now investigate that more thoroughly with this animal model," Hamm said. "So many things that couldn't be looked at before or were really hard to (study)—now they're going to be easier to look at."
Hamm is the Aileen M. Lange and Annie Mary Lyle Professor of Cardiovascular Research in the Vanderbilt University School of Medicine. Former chair of the Department of Pharmacology, she also is a professor of Ophthalmology & Visual Sciences and of Orthopaedic Surgery & Rehabilitation.
During her career she has made several important discoveries about G-protein coupled receptors (GPCRs). Embedded in the membranes of nearly every cell, GPCRs are the most common conduit for signaling pathways found in nature. Two-thirds of all drugs target them.
GPCRs are turned on and off by G-proteins inside the cell. G proteins consist of two subunits—alpha and beta/gamma—both of which can stimulate independent signaling pathways.
Several years ago, Hamm and colleagues including Simon Alford, Ph.D., at the University of Illinois at Chicago, showed how the beta/gamma subunit of an inhibitory G protein prevents intracellular vesicles containing neurotransmitters from fusing to the  and spilling their contents into the extracellular space between nerve —the synapse.
It does this in two ways: by preventing the flow of calcium through "calcium channels" from allowing vesicles to fuse to the membrane and by "switching off" the SNARE receptor complex.
Hamm wanted to know why there are two separate mechanisms for "damping down" neurotransmitter release. "We studied this regulation through SNARE intensively in cell culture," she said, but didn't know how it functioned in living organisms.
Using a genome editing technology called CRISPR/Cas9, Zack Zurawski, then a graduate student in Hamm's lab, introduced a mutation that didn't let the beta-gamma subunit turn off the SNARE machinery anymore. The mutation turned on the "spigot."
"It's amazing that it worked the first time," Hamm said. "It used to take two or three years to make such a mouse and we did it in three months. It was really a great achievement."
Zurawski, the first author on the paper, has since earned his Ph.D. and is conducting post-doctoral research at the University of Illinois with Alford, a senior co-author.
The researchers also discovered that the two mechanisms for preventing vesicle fusion, one that acts on calcium channels and the other on SNARE, are synergistic. Blocking both results in a more powerful inhibition of  release than blocking one or the other separately.
"I think this means that these two different mechanisms are probably a lot more important than people think," Hamm said.
More information: Zack Zurawski et al. Disabling the Gβγ-SNARE interaction disrupts GPCR-mediated presynaptic inhibition, leading to physiological and behavioral phenotypes, Science Signaling (2019). DOI: 10.1126/scisignal.aat8595
Provided by Vanderbilt University
https://medicalxpress.com/news/2019-03-scientists-brain.html

Others Provide Support and a Mirror Within the ‘Compassion Space’

 MARCH 8, 2019 DR. C 



The “O” in the CHRONDI Creed stands for “others” — the other people around us who support, teach, and love us, and who pray and care for us. Other people can also provide a mirror that helps us to see how others perceive our actions. If we can objectively view this reflection, we can gain wisdom about the consequences of our actions and then make informed choices that will affect how we interact with others.
The relationships we have with other people provide support and a mirror seen clearly within the compassion space (see diagram below).
Columnist Sherri Woodbridge has written about relationships while dealing with Parkinson’s disease, saying that we need to work on keeping relationship magic alive. She advises readers to seek help with relationship issues rather than ignoring them. It takes work to keep relationships healthy and growth-promoting. We don’t put our foot into the stream of life the same way twice — our lives continuously change, and our relationships need to adjust to these changes.
Growth-promoting relationships with others happen within what I call the “compassion space.” It is a shared space between the self and the other and our well-being possibility. Movement also takes place within this space. Reaching out to the other and then retreating to self (“push the person away” and then later “seek to get closer”) is one of the most common relationship dances.
A similar dance happens when we seek to help someone achieve well-being or receive assistance with our own health. It is a dance of getting closer to well-being and then retreating from the experience. I have termed this “compassion space resistance,” and it is the primary source of compassion fatigue. The latter does not arise from successful compassion that leaves one with more energy than it takes. Compassion space resistance can drain emotional energy and lead to caregiver burnout.
Imagine that your lifelong partner has a chronic illness. You want to help your partner move toward a place with less suffering. But compassion resistance can happen if you spend days arguing, your partner neglects his rehabilitation plan, or neither of you is willing to take responsibility for your half of the well-being journey. 
Successful movement within the compassion space involves a shift toward well-being. When the self and the other are in the compassion space where this shift occurs, they experience a special type of growth-promoting relationship called the healing relationship. This relationship is often interpreted as sacred or a gift, and something that is allowed and not grasped.
Once the healing relationship is established, then the shift toward well-being becomes a stepping stone for the other to use in his or her journey toward maintaining an improved quality of life. The self then becomes a witness stepping stone, using supportive words such as, “Remember I was there with you.” Then, as a witness, he asks the other person to recall how much better she felt after the event. This witnessing happens within the support relationship where both parties discuss how each person can follow his or her path to well-being.
Growth-promoting relationships involve entering the compassion space in the roles of the self and the other. If we can understand the dance that takes place inside that space — the dance in which the relationship changes from healing to support, to resistance, and then back again — then we can more clearly envision our own path to well-being.
Growth-promoting relationships are fundamental to success in the battle against chronic disease. Healthy relationships depend upon the successful communication of our needs to each other. If you are waiting for the other person to read your mind and recognize your needs, then you will be disappointed.
Much of the suffering in the world happens when people do not enter the compassion space. Instead, they throw words at each other from inside their personally constructed self-bubbles. We think that we are safe inside our self-bubbles. But we can’t hear the needs of the others in our lives from inside our bubbles and this hinders our ability to develop growth-promoting relationships.
Our caregivers need our attention and compassion. The others in our lives help us to mirror ourselves and provide us with support in our battle against our chronic illness. Use of the compassion space helps us to express our individual needs and feel heard. It takes practice to move around in the compassion space, and the CHRONDI elements help us with this practice.
Have you had experiences within the compassion space? Did you like anything that was expressed in this column? Please share your thoughts in the comments to help other readers gain a broader perspective on helping and receiving help from others.
***
Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.
https://parkinsonsnewstoday.com/2019/03/08/others-support-mirror-compassion-space/

Scientist Lands $5M Grant to Study Link Between Pesticides, Smell and Parkinson’s

MARCH 8, 2019 BY MARY CHAPMAN 


The National Institutes of Health (NIH) has granted a Michigan State University scientist $5 million to study a possible link between pesticides, a diminished sense of smell, and early symptoms of diseases such as Parkinson’s among older farmers.
The investigator is Honglei Chen, MD, PhD, a professor of epidemiology whose research focuses on neurodegenerative disorders. His primary scientific interests include environmental and genetic risk factors for Parkinson’s disease.
“Our battle against Alzheimer’s and Parkinson’s may depend on early disease identification and intervention, and poor olfaction [sense of smell] has been identified as an early warning for these diseases,” he said in a press release.
“This grant will allow us to connect the dots by identifying factors that contribute to poor olfaction among older adults, and evaluating how this sensory deficit may progress to early stages of neurodegenerative diseases,” Chen said.
Early analyses, published in the journal Environmental Health Perspectives, revealed a link between high pesticide exposure and a self-reported impaired sense of smell.
The team studied more than 11,200 farmers, of whom 16% experienced a high pesticide exposure event, over a 20-year period. At the end of the study, participants were asked if they suffered a partial-to-complete loss of sense of smell. Those who were exposed to high pesticide levels were 50% more likely to report a poor sense of smell. Importantly, an immediate washing with soap and water after a large amount of pesticide contacting the body, for example, could lower this risk.
study published last December in the Journal of Neurology suggested that an impaired sense of smell or taste can raise an individual’s risk of developing Parkinson’s disease 2.5 times. Presently, Parkinson’s is diagnosed chiefly through assessment of motor symptoms and their severity. However, non-motor symptoms have gained attention due to their potential to predict Parkinson’s-related motor symptoms.
Chen and his team will use the grant to measure the ability to smell among roughly 2,200 farmers. After using a scratch-and-sniff method to try to identify a dozen common smells — smoke, lemon and cinnamon, for example — some 450 farmers will get a home visit from researchers who will test the farmers’ cognitive function and motor symptoms.
Researchers are using resources from the Agricultural Health Study (AHS) and its NIH scientists, along with research assistance from partners at Duke University, the University of Chicago and Penn State University.
A collaboration of the National Institute of Environmental Health Sciences (NIEHS), the National Cancer Institute (NCI), the Environmental Protection Agency (EPA) and the National Institute for Occupational Safety and Health (NIOSH), the AHS is a prospective investigation of licensed pesticide applicators from North Carolina and Iowa who were recruited for the study from 1993 to 1997.
Through 2014, after rounds of questionnaires, a telephone interview, and collecting a buccal-cell DNA sample, follow-up is ongoing to see what, if any, diseases develop among study subjects.
In addition, researchers annually link the study group to state cancer registries and vital records to monitor cancer incidence and mortality.
The AHS is believed to be the world’s largest study of farmers and their families.
https://parkinsonsnewstoday.com/2019/03/08/grant-study-link-pesticides-smell-parkinsons/

Freedom of Movement May Be Misinterpreted as Balance Instability, Parkinson’s Study Suggests

 MARCH 8, 2019 BY CATARINA SILVA 




Antiparkinsonian medicines may allow patients with mild to moderate Parkinson’s disease to experience freedom of movement, which could be confused with balance issues if measured by traditional postural stability testing, researchers suggest.
Their findings were published in the study, “The influence of dopaminergic medication on balance automaticity in Parkinson’s disease,” in the journal Gait & Posture.
Dopaminergic medications can help control Parkinson’s motor symptoms, but as the disease progresses, patients typically need to gradually increase the treatment dose for maximum benefit. Even after increasing the dose, they might sometimes experience a reappearance or worsening of symptoms (off periods) due to the diminishing effects of the therapy.
It is known that Parkinson’s patients have difficulty performing learned motor skills automatically, a phenomenon referred to as decreased motor automaticity. Automaticity is the ability to perform movements without having to pay attention to the details of the movement, particularly for actions that require low levels of precision or for movements that are frequently made.
Studies also report that the ability to perform two or more tasks at the same time, called dual-tasking, is impaired in Parkinson’s disease.
“Dual-tasking involves performing a primary motor task (e.g., standing) and a secondary task (e.g., conversing) simultaneously and is the primary means of assessing the automaticity of a given motor task,” the researchers wrote.
In theory, if a primary task is automatic, performing another task simultaneously should not interfere with the first one.
Although dopaminergic medication seems to improve dynamic balance (the ability to maintain postural stability while in motion), there is still little evidence on how it influences standing balance (the ability to maintain the body in a fixed posture).
University of Houston researchers set out to evaluate how dopaminergic medication influenced long-duration standing balance with the eyes open or closed while dual-tasking in Parkinson’s disease.
They recruited 16 Parkinson’s patients with mild to moderate disease (four women and 12 men, with a mean age of 67.1 years) for the study.
Before dual-task testing, the participants underwent a minimum 12-hour overnight medication withdrawal, so that researchers could assess patients’ status in an off state.
Single- and dual-task tests were conducted. For dual-task testing, patients had to stand in silence (primary task), both with their eyes open and then with them closed, while listening on headphones to a pre-recorded unfamiliar speech and mentally counting the number of times a specific word occurred (secondary task). This is known as phoneme monitoring. They also had to listen to the details of the story so that they could answer a few questions about it at the end of the testing session.
Under the protocol, participants were asked to perform the following tasks in random order: 1) phoneme monitoring while seated comfortably in a quiet room, 2) single-task standing eyes open, 3) single-task standing eyes closed, 4) dual-task standing eyes open, and 5) dual-task standing eyes closed.
“After the [off] trials were completed, the subjects took their dopaminergic medication as prescribed for their first/morning dose and waited until they achieved a stable ‘on’ feeling (minimum of 45 [minutes]) before commencing the on-medication testing,” the researchers said.
Every trial session was performed once for three minutes, and participants were given at least a minute between sessions to sit down and rest.
Data on motor variables of interest were obtained by the NeuroCom Balance Master, a system that uses a fixed force plate to measure the vertical forces exerted through the patient’s feet to measure the center of gravity position and postural control.
Results revealed that antiparkinsonian medicines significantly increased center of pressure movement. The center of pressure is a point, inside or outside the body, where the resulting vector of all forces (including gravity) acting on the body is considered to act.
Patients’ performance in the secondary task was reduced after they took the medications.
Additionally, having the eyes closed or open significantly increased the patients’ back and forth plus lateral sway velocities and the integrated time to boundary.
In biomechanics, time to boundary estimates the time required for the center of pressure to reach the boundary of the base of support if it were to continue its instantaneous trajectory and velocity. Higher integrated time indicates poorer balance.
Postural sway was also increased during the on state. Scientists often interpret increases in sway velocity and integrated time to boundary as indications of impaired balance; however, the researchers suggest that their findings could indicate an increase in freedom of movement rather than compromised stability.
Importantly, medication did not improve balance automaticity.
“The data did not support a medication-induced improvement in automaticity, as measured by significant medication by task interactions. An alternate interpretation for medication-induced balance changes in PD [Parkinson’s disease] includes an increase in maneuverability without sacrificing stability after taking dopaminergic medication,” the researchers concluded.
https://parkinsonsnewstoday.com/2019/03/08/freedom-movement-misinterpreted-impaired-balance/