Your brain on mesh: Injectable flexible probe melds with neurons, causes little or no chronic immune response

July 5, 2017 by Stuart Mason Dambrot

Fig. 1. Schematics of mesh electronics. (A) Schematics of the mesh electronics structure in 2D. (I) Overall design of mesh electronics structure, where the blue lines highlight the overall mesh structure, the black filled circles at left indicate I/O pads, and the red filled circles indicate recording electrodes. (II) A single unit cell of mesh electronics, where the orange lines, which are shown without top polymer layer, highlight the metal interconnects and blue lines correspond to polymer passivation layer; w1, w2, and wm indicate the widths of the longitudinal polymer, transverse polymer, and metal lines, respectively. The schematic in the green dashed box highlights the cross-section view, which shows the polymer encapsulated metal structure, at the position indicated by the green dashed line. (B) Schematic of free-standing mesh electronics floating in aqueous solution and ready to be loaded into a glass needle. (C) Schematic of mesh electronics injected into mouse brain, with part of the mesh sagging between the brain and the needle. (D) Schematic of mesh electronics implanted in brain tissue with horizontal (yellow plane) and sagittal (green plane) sectioning directions highlighted in the inset. (E) Schematics of the interface between mesh electronics and the brain tissue (Left, cross-section view) and that between flexible thin-film and the brain tissue (Right, cross-section view). Mesh elements and the flexible thin-film are highlighted in blue, neurons are in purple, and glial scar is in yellow. Credit: Zhou T, Hong G, Fu T-M, Yang X, Schuhmann TG, Robert D. Viveros, RD, Lieber CM (2017) Syringe-injectable mesh electronics integrate seamlessly with minimal chronic immune response in the brain. Proc Natl Acad Sci USA 114(23):5894-5899.

Phys.org)—Neuroprostheses, neural probes and other intraneural tissue implants have offered remarkable benefits to recipients in a number of areas in neuroscience research and biomedical applications, therapeutic examples being not only Alzheimer's Disease, Parkinson's Disease, epilepsy, traumatic brain injury, and other neurological/neurologically-related conditions, as well as cognition, memory, and sensorimotor disorders. However, current neural implants have several drawbacks, including neural tissue inflammation or scarring due to device micromotion, as well as longevity and the potential need for removal, and high power requirements. Devising electrical probes that seamlessly integrate within neural tissue has therefore been a coveted goal. To that end, scientists at Harvard University have reported the successful implantation of a neuromorphic (that is, having a structure similar to brain tissue) ultraflexible open mesh electronics neural probe that is delivered to specific brain regions via syringe injection (a protocol they published in 2015 in Nature Nanotechnology)1.

The probe—which does not require a power supply—directly records neural voltage changes by being able to interface with all regions of the brain from the level of single neuron through circuits and networks, in which the mesh recording electrode is connected by passivated metal lines (that is, having a protective coating applied to its surface) to input/output pads located at the opposite end of the mesh structure. These I/O pads, in turn, are then connected to Flat Flexible Cables (FFC) and plugged in external system for recording. The researchers also conducted systematic post-implantation studies, finding minimal or absent neural immune responses, and moreover that brain tissue had penetrated and merged with the mesh probe. The scientists note that the mesh implant may never require removal—but if it does, doing so would be a straightforward if not issue-free procedure. They conclude that most areas of fundamental neuroscience research could benefit from mesh electronics providing long-term stability and single-neuron resolution—unique capabilities not found in conventional neuroprosthetics—and state in their paper that ultraflexible open mesh electronics probes could in the future enable a wide range of opportunities for in vivo chronic recording and modulation of brain activity.

Chemical Biology Mark Hyman Jr. Professor of Chemistry Charles Lieber discussed the paper that he, Lead author Graduate Student Tao Zhou, Postdoctoral Fellow Guosong Hong, and their colleagues published in Proceedings of the National Academy of Sciences. "The main challenge of designing and implanting an injectable ultraflexible open mesh probe is ensuring the design has four key features," Lieber tells Phys.org. These factors are mesh openings larger than cell bodies to facilitate neuron penetration; mesh element features that are the same size or smaller than neurons; flexibility that in this study was many orders of magnitude greater than that of neurons; and mesh electronics that can be easily injected through very high-gauge needles to precisely control the mesh position. "By designing the mesh electronics such that all key properties are neuromorphically similar to neural tissue, we eliminate chronic immune response that is found with all other probes and medical implants, which are more like thorns in your tissue."

As mentioned earlier, the scientists' 2015 paper initiated the concept of syringe injectable electronics, which Lieber notes opens up a new field with many opportunities awaiting further studies—an example being co-injection of electronics and cells where mesh electronics also functions as a tissue growth scaffold relevant to regenerative medicine. "In the paper being discussed herein we report systematic time-dependent chronic histology studies of the tissue-mesh interface after the mesh probes were implanted into rodent brains. Both horizontal (which contains cross-sections of implanted mesh probes) and sagittal (which contains nearly the entire implanted mesh probes) brain slices were used for immunohistochemistry and were stained with antibodies that can target neuron somata, axons, astrocytes and microglia. The results in this paper reveal the uniqueness of mesh probes in terms of minimal or absence of tissue response and neuron penetration when chronically implanted in the brain.

Fig. 2. Time-dependent histology of horizontal tissue slices containing implanted mesh electronics and flexible thin-film probes. Confocal fluorescence microscopy images of horizontal tissue slices containing mesh electronics/flexible thin-film probes at 2 wk (A and D), 4 wk (B and E), and 3 mo (C and F) postimplantation. In all of the panels the image labels were NeuN (I, green), NF (II, red), GFAP (III, cyan), and NeuN, NF, GFAP composite (IV). The mesh electronics and flexible thin-film cross-sections are pseudocolored blue. (Scale bars in all images, 100 μm.) Credit: Zhou T, Hong G, Fu T-M, Yang X, Schuhmann TG, Robert D. Viveros, RD, Lieber CM (2017) Syringe-injectable mesh electronics integrate seamlessly with minimal chronic immune response in the brain. Proc Natl Acad Sci USA 114(23):5894-5899.

The researchers used standard photolithography to fabricate the mesh electronics probes using a polyimide-based photoresist (polyimides are biocompatible) in a three-layer structure;

1. the bottom mesh structure (typically ~400 nm thick) is defined per the specific design

2. the metal interconnects, input/output pads, and brain electrodes are defined, these being ~100 nm thick

3. the top layer of polyimide resist is defined such that all metal is encapsulated except for the I/O pads and electrodes, where the approach and subsequent polymer processing leads to a robust near-monolithic structure <1 um in thickness

Lieber points out that the neuromorphic nature of the mesh electronics probes is related to the above three points, the bio/neural compatibility of the polyimide polymer used for the mesh, and the post-implantation open three-dimensional mesh structure. Together, he adds, these features make the injected mesh electronics quite similar to neural networks that comprise brain tissue, and therefore quite distinct from conventional probes.

Fig. 4. Histology of a sagittal tissue slice containing nearly the full implanted mesh electronics probe. (A and B) Confocal fluorescence microscopy images of a sagittal tissue slice including the mesh electronics probe at 3 mo postimplantation. Each of the images are 3×3 composite images recorded directly in the Tile Scan mode, where each component image of the Tile Scan had a field of view of 425 μm × 425 μm. The tissue slice was stained with antibodies for NeuN (green), NF (red), and GFAP (cyan); the mesh is shown as pseudocolored blue. The images were recorded at an optical focal plane ca. 5 μm below the surfaces of side-A (A) and side-B (B). (C) Fluorescence intensity as a function of distance from the boundary of the mesh electronics in images of side-A (A) and side-B (B). The pink shaded regions indicate interior of mesh electronics on each side. The NF and GFAP fluorescence intensity was analyzed based on the entire images, and the NeuN fluorescence intensity was analyzed based on the regions shown in yellow dashed boxes in A and B. Error bars represent SEM. Credit: Zhou T, Hong G, Fu T-M, Yang X, Schuhmann TG, Robert D. Viveros, RD, Lieber CM (2017) Syringe-injectable mesh electronics integrate seamlessly with minimal chronic immune response in the brain. Proc Natl Acad Sci USA 114(23):5894-5899.

"The main challenges of demonstrating that the probes do not elicit inflammation or scarring—unlike the typical chronic tissue response—is to characterize the tissue-mesh interface at different times post-implantation," Lieber explains. To accomplish this, without removing implanted mesh probes the researchers sectioned mouse brains into both cross-sectional and longitudinal or sagittal (left/right) slices. "Investigations of both cross and longitudinal sections with the implanted mesh electronics probe provided detailed and global views, respectively, of probe/tissue interaction," he notes, stressing that in most cases conventional probes must be removed from tissue before sectioning, resulting in loss of some critical interface information.

"The horizontal and sagittal brain slices—which contain cross-sections of implanted mesh probes, and nearly the entire implanted mesh probe, respectively—were stained with antibodies that can target neuron somata, axons, astrocytes and microglia," Lieber continues, Moreover, he points out that these studies demonstrated that unlike conventional probes, neuron somata and axons around mesh probes were not harmed, and led to natural tissue levels at the mesh probe surface. "Similarly, the markers for immune response inflammation highlighting astrocytes and microglia showed that these species became background level after only a couple of weeks in the mesh electronics—but they proliferated and accumulated at the interfaces of conventional probes." The scientists also found that the ability of allowing the neurons and mesh to interpenetrate is universal for all meshes they injected and imaged at 6~12 weeks post injection, prompting them to initiate additional experiments to find out how the size of mesh electronics structural elements and other parameters might be tuned to enhance the capability of neuron interpenetration.

It should be noted, Lieber tells Phys.org, that the researchers are being conservative when in their paper they write a minimal immune response pending more detailed marker analyses. "In fact, we believe there is no immune response from the mesh because our results show that any initial enhancement in astrocyte and microglia return to background with no measureable difference proximate or distal to the probe at 12 weeks—and, as shown in our 2016 Nature Methods paper1—up to at least one year. We thus believe that the response is due to acute damage that occurs when inserting the needle (or for that matter, any probe) into the brain—but given the lack of immune response from the mesh probe, this acute damage all heals over time, as opposed to worsening, as is the case with conventional probes."

Fig. S2. Time-dependent histology of chronically implanted mesh electronics (A–C) and flexible thin-film probes (D–F) in mice brains (horizontal sections). Tissue slices are labeled with Iba-1 (magenta) to highlight microglia; mesh electronics and flexible thin-film probes were imaged by DIC and are pseudocolored blue. (Scale bars in all images, 100 μm.) Credit: Zhou T, Hong G, Fu T-M, Yang X, Schuhmann TG, Robert D. Viveros, RD, Lieber CM (2017) Syringe-injectable mesh electronics integrate seamlessly with minimal chronic immune response in the brain. Proc Natl Acad Sci USA 114(23):5894-5899.

The minimal, recoverable acute damage and the absence of an immune response support the possibility that mesh electronics may be permanently viable. "According to our past and ongoing studies thus far, mesh probes can maintain a stable recording/stimulation interface with the brain tissue for at least one to two years," Lieber says. "However, this time period does not represent the achievable life expectancy since ongoing studies are currently under way to demonstrate even longer-term stability." Due to the limitation of the rodent two- to three-year lifetime, the scientists expect to find more extensive stability in longer-living mammals such as rhesus macaques and in studies currently under way. "In the case with absent immune response as demonstrated in our recent paper, the life expectancy of mesh electronics should only be determined by biocompatibility and lifetime of the materials, including the metal electrodes (gold and platinum, which are both inert), and the passivating polymer that has been studied extensively in previous publications (such as Nemani et al 2) to show long-term stability in physiological conditions). Therefore, we remain confident that mesh electronics will likely have a life expectancy with stable neural interface and recording/stimulation functions for years, and envision the mesh ultimately as lifetime implant."

However, Lieber adds, should the mesh need to be removed, it can be directly extracted with minimum force and damage to the brain. "While this could cause a small amount of damage due to seamless integration with neural tissue, we believe the unprecedented stability and absence of chronic immune response of our neural tissue-like mesh electronics will lead to a paradigm change where the probe is a lifelong implantation that does not require removal."

Moving forward, Lieber says that they are conducting ongoing studies of new mesh designs having high large numbers of electrodes and multisite injections. "Moreover, our next steps include implantations of mesh electronics into tissues and organs other than the brain—for example, in the eye for in vivo recording of single retinal ganglion cells, in the spinal cord, in the muscle for studying signal propagation at the neuromuscular junction, and so on. We're also beginning studies exploiting the unprecedented stability and absence of chronic immune response of the mesh electronics in Alzheimer's and Parkinson's disease models, and are working on implantation of mesh electronics in non-human primates subjects and human patients."

They also see a wide range of current and potential applications benefitting from the use of their mesh probe, including spinal cord and neuromuscular junction implants, brain–machine interfaces, cyborg animals, natural and pathological aging (such as Alzheimer's disease) with insight on how spatial memory and learning evolve as a function of age and disease stage. Moreover, by adding stimulation electrodes, being able to enable fine level feedback that can ameliorate or overcome the cognitive declines associated with aging and other neurodegenerative diseases.

As to other areas of research that might benefit from their study, Lieber says that in general, most areas of fundamental neuroscience research could benefit from mesh electronics' unique capabilities of long-term stability and single neuron resolution. "In addition, almost any clinical/medical application that involves electrical recordings and/or stimulations will benefit from our studies. In addition to that mentioned above," he concludes, "the mesh electronics should provide unique opportunities for brain-machine interfaces for tetraplegic patients, deep brain stimulations for the treatment of Parkinson's disease, and neural prosthetics in general."

More information: Syringe-injectable mesh electronics integrate seamlessly with minimal chronic immune response in the brain, Proceedings of the National Academy of Sciences (2017) 114(23):5894-5899, doi:10.1073/pnas.1705509114

Journal reference: Nature Nanotechnology

Proceedings of the National Academy of Sciences 

Nature Methods

https://phys.org/news/2017-07-brain-mesh-flexible-probe-melds.html

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First-ever Definitive Test for Parkinson’s Developed in Israel

Ruth Schuster Jul 05, 2017

Magnetic resonance image (MRI) of Parkinson's Disease, a degenerative disorder of the central nervous system. REUTERS/Neil Hall

The good news about Parkinson’s is that a scientist in Jerusalem has developed a test that detects the degenerative brain disease both definitively and earlier, hopefully improving the prognosis for patients.

The bad news is that the Mayo Clinic has noticed an association between Parkinson’s and melanoma, a deadly form of skin cancer. They can’t explain it, but a significant association has been found.

Parkinson’s disease is the second most prevalent degenerative brain disorder in the elderly, after Alzheimer’s. But by the time one knows one has the condition, it may be spiraling out of control. 

By the time patients are symptomatic, around two-thirds of the brain cells that make dopamine (the substantia nigra part of the brain) are already dead, says Suaad Abd-Elhadi of Hebrew University of Jerusalem, winner of the Kaye Innovation Award for inventing the method to – finally – achieve categorical diagnosis of Parkinson’s. Not only that, but at an early stage of the disease.

Earlier diagnosis means identifying Parkinson’s before the dopamine cells die off en masse and symptoms appear (motor or cognitive or both). True, PD remains incurable. Even so, “Earlier diagnosis can help by seeing how a given drug affects the progress of the disease, for example,” says Abd-Elhadi.

A big problem is that early PD looks just like other neurodegenerative diseases, which hinders appropriate care, she explains. A great deal of effort is presently being put into delaying the progress of PD, for which purpose, one needs to know that one has it.

Definitely locating

Using the kit invented by Abd-Elhadi, now one can know it, even before becoming asymptomatic. Which begs the question of under what circumstances one would check if one isn’t showing symptoms.

“PD isn’t as common as cancer, for instance,” she says. “But there is a not-small percentage of people who have PD in the family, and if one has it in the family, it pays to go get checked.”

But how to know definitively that one has PD, not Alzheimer’s for instance, or some other disease of the nervous system? The definitive test Abd-Elhadi developed is based on the fact that PD is associated with a weird protein called alpha-synuclin.

According to recently-published research, the pathological form of alpha-synuclin appears first in peripheral nerves, usually in the digestive system, and only appears in the brain at later stages of Parkinson’s, says Abd-Elhadi. “It’s known that patients with early-stage PD have problems with their digestive systems, even with swallowing,” she says. “Only later in the disease does the pathology reach the brain.”

Alpha-synuclin binds to fat molecules, called lipids, on cell membranes, Abd-Elhadi explains. What she did is identify the lipid types, originating in both peripheral tissues and brain cells, to which alpha-synuclin binds best.

Using these lipids, she invented a minimally invasive, highly sensitive kit to test for Parkinson’s, called “lipid ELISA” (ELISA stands for “enzyme-linked immunosorbent assay.”) She achieved proof of concept – that the invention works in people with different stages of PD, and people without the disease.

Obviously this isn’t a home kit for the perennially perturbed. This is an invention for hospitals, or possibly for groups of workers exposed to industries that are high-risk for PD, such as agriculture. Pesticides have an unfortunate association with the development of the disease, Abd-Elhadi points out.

As for the melanoma association, causality remains a mystery. But the Mayo Clinic found that melanoma patients had a fourfold higher risk of developing Parkinson’s, and people with Parkinson’s had a fourfold higher risk of having preexisting melanoma (which means they had it in their medical history).

“There appears to be an association between melanoma and PD,” the Mayo clinicians wrote cautiously in a paper by author Lauren Dalvin and the team. Their conclusion: Doctors should warn their melanoma and Parkinson’s patients to keep an eye out for the other disease.

http://www.haaretz.com/science-and-health/1.799726

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Link between Parkinson's and melanoma runs both ways

By Tim Newman   July 5, 2017

Melanoma is a common form of skin cancer and appears to be linked with Parkinson's disease.

A study published this week in Mayo Clinic Proceedingsconfirms that Parkinson's disease can, perhaps surprisingly, increase the risk of melanoma. The researchers also show that the link is a two-way relationship, with melanoma also suspected to increase the risk of Parkinson's.

Parkinson's disease is a neurodegenerative condition that affects around 1 million people in the United States. At first glance, it seems entirely removed from cancer.

However, melanoma - a type of skin cancer with more than 80,000 new diagnoses each year in the U.S. - seems to be entwined with the condition.

Studies carried out over recent decades have clearly demonstrated this interaction. For instance, a study published in JAMA Neurology in 2010 concluded that, "Melanoma prevalence appears to be higher in patients with PD [Parkinson's disease] than in the general population. [...] the study supports increased melanoma screening in patients with PD."

Similarly, a paper published in Translational Neurodegeneration in 2015 came to a similar conclusion, stating, "An association between PD and melanoma was confirmed. Most of the evidences were of high quality, and the conclusion was robust."

Although the link seems clear, there has been debate regarding the reasons for this interaction. Some researchers have theorized that a frequently used Parkinson's drug called levodopa might be the reason for the increase in melanoma incidence in people with the neurodegenerative condition.

In fact, the first research to point the finger at levodopa was an article called "Multiple primary melanoma following administration of levodopa," which was published in the journal Archives of Pathology in June 1972.

Recently, researchers from the Mayo Clinic set out to investigate the relationship between Parkinson's disease and melanoma in more detail. Firstly, they wanted to understand whether or not levodopa was, in fact, the pivotal factor. They also wanted to work out whether the interaction could go both ways.

Probing Parkinson's and melanoma links

The team took data from the Rochester Epidemiology Project medical records database. They collated all neurologist-confirmed Parkinson's disease cases in Olmsted County, MN, from January 1976 to December 2013. Within this 974 subject-strong group, they checked the prevalence of melanoma and compared it with a control group of 2,922 people without Parkinson's.

Next, the team identified 1,544 melanoma cases over the same period of time to determine the subjects' 35-year risk of developing Parkinson's, and they compared that with 1,544 people without melanoma.

The analysis showed that individuals with Parkinson's disease were four times more likely to have a history of melanoma. Additionally, people with melanoma had four times the risk of developing Parkinson's.

The study not only reconfirms the links between the conditions, but it also argues against levodopa being the cause, as do some of the other more recent studies to investigate this phenomenon.

However, aside from being able to discount Parkinson's drugs as the cause, the reasons behind the relationship are no clearer. The authors believe that the causal factors could potentially include shared genetic, environmental, or immune system irregularities. More work is needed.

First author Dr. Lauren Dalvin, Mayo Foundation Scholar in ocular oncology, says, "Future research should focus on identifying common genes, immune responses, and environmental exposures that may link these two diseases."

"If we can pinpoint the cause of the association between Parkinson's disease and melanoma, we will be better able to counsel patients and families about their risk of developing one disease in the setting of the other."

So, regardless of the causal factors, the take-home message centers on awareness. According to the authors, a patient with either condition should be closely monitored for the other. Further research will be needed to ultimately tease out the factors involved in this unexpected and intriguing link.

http://www.medicalnewstoday.com/articles/318245.php

New drug target for Parkinson's disease found

By Ana Sandoiu, July 4, 2017

A new study may have found a target for a potential drug for Parkinson's disease

A new study has found an enzyme that drives neurotoxicity in both Alzheimer's and Parkinson's disease. Blocking the action of this enzyme may prevent these conditions from developing, so the research may have found a new drug target. 

It is currently estimated that more than 5 million people in the United States are living with Alzheimer's disease, and as many as 1 in 3 elders are said to die with the condition, or another form of dementia. Parkinson's disease also affects approximately 60,000 U.S. adults every year. 

Both diseases are neurodegenerative, meaning that brain cells progressively and irreversibly degenerate until they eventually die.

Even though there are various differences between the two conditions on a genetic and structural level, a team of scientists at Emory University in Atlanta, GA, may have found an enzyme that triggers both of them. This newly discovered enzyme could be a target for a potential drug for Parkinson's disease. 

The new study was led by Keqiang Ye, Ph.D., and the findings were published in the journal Nature Structural and Molecular Biology.

The tau and alpha-synuclein proteins

One aspect shared by the two conditions regards disease formation: both conditions are characterized by a clumpy protein capable of killing brain cells. This protein is called alpha-synuclein in Parkinson's disease, and tau in Alzheimer's disease. 

In Parkinson's disease, it is believed that alpha-synuclein aggregates and forms clumps called Lewy bodies. These clumps can be found in the outer layer of the cerebrum, as well as deeper inside the midbrain. 

In Alzheimer's disease, an excess production of tau forms tangles that can obstruct the transportation of nutrients to neurons, which die as a result of this starvation.

Previous research carried out by Dr. Ye and colleagues found an enzyme called asparagine endopeptidase (AEP), which makes tau clumpier and more toxic. The new research hypothesized that AEP would have the same enhancing effect on alpha-synuclein.

"

In Parkinson's, alpha-synuclein behaves much like tau in Alzheimer's. We reasoned that if AEP cuts tau, it's very likely that it will cut alpha-synuclein too." 

Keqiang Ye, Ph.D.

This is a Parkinson’s disease brain sample, stained with an antibody that only recognizes the N103 chunk of alpha-synuclein, which is generated through cleavage by AEP. NeuroscienceNews.com image is credited to From Zhang et al NSMB (2017).

 

AEP and neurotoxicity in Parkinson's

As expected, Dr. Ye and team found that AEP drives the aggregation of alpha-synuclein and increases its neurotoxicity. In the mouse model designed by the researchers, AEP-induced neurotoxicity lead to a loss of neurons and motor deficits.

The researchers also found that AEP has a scissor-like, "cleaving" effect on human alpha-synuclein. Cleaved fragments of alpha-synuclein were found to be likelier to form clumps than the full-length form of the protein. When introduced in the cells or brains of mice, the neurotoxicity of the cleaved protein was higher. 

Additionally, the researchers mutated the protein so that AEP could not cleave it, and they found that the uncut protein was less toxic. 

Furthermore, Dr. Ye and colleagues found cleaved fragments of alpha-synuclein in brain tissue samples from people with Parkinson's disease, but not in samples from healthy controls. 

In the healthy control samples, the researchers found AEP exclusively in lysosomes, which are tiny organelles within the cell that act as its "digestive system." But in the tissue samples of people with Parkinson's disease, AEP overflowed into other parts of the cell. 

These findings could point to a new target for a potential anti-Parkinson's drug.  Trials in animal models have already shown that an AEP-inhibiting drug preserves memory and may have a preventive effect against Alzheimer's disease. 

Although the researchers note that AEP is not the only enzyme that breaks down alpha-synuclein, thus making it more toxic, Dr. Ye and team are also planning to test AEP-inhibiting drugs in animals with Parkinson's disease. 

http://www.medicalnewstoday.com/articles/318257.php

Yoga can cause musculoskeletal pain

 By Honor Whiteman Published July 2, 2017

While yoga can help to alleviate pain, research shows that it can also cause it.

Yoga is often hailed as an effective practice for pain relief. A new study, however, notes that yoga can also cause pain, and yoga-related injuries are much more common than one may think.

The research suggests that every year, more than 10 percent of people who practice yoga in a recreational capacity experience musculoskeletal pain, particularly in the upper limbs, as a result.

What is more, the study found that yoga actually worsens more than a fifth of existing injuries.

Lead study author Prof. Evangelos Pappas, of the Faculty of Health Sciences at the University of Sydney in Australia, and colleagues recently reported their findings in the Journal of Bodywork and Movement Therapies.

Yoga is one of the most common mind and body practices in the United States, and its popularity is increasing. According to a survey conducted by Yoga Alliance last year, around 37 million U.S. adults practice yoga, a significant rise from 20 million in 2012.

But why is yoga so appealing? Aside from its stress-relieving effects, one reason why people are attracted to yoga is its ability to ease pain. A recent study reported by Medical News Today found that for low back pain, yoga is just as beneficial as physical therapy.

However, the new study from Prof. Pappas and team suggests that caution should be applied when practicing yoga, as it could do more harm than good.

Upper limb pain most common

For their study, the researchers analyzed the data of 354 adults who engaged in recreational yoga.

Participants completed two electronic questionnaires 1 year apart, which gathered information on any musculoskeletal pain they might have, where in the body this pain occurred, and pain severity.

The data revealed that 10.7 percent of participants experienced musculoskeletal pain as a result of yoga.

"In terms of severity, more than one third of cases of pain caused by yoga were serious enough to prevent yoga participation and lasted more than 3 months," notes Prof. Pappas.

Pain in the upper extremities - including the shoulder, elbow, wrist, and hand - was the most common type of pain caused by yoga, which Prof. Pappas speculates may be down to "postures that put weight on the upper limbs," such as the downward dog.

For subjects with pre-existing musculoskeletal injuries, around 21 percent of these injuries were exacerbated by yoga participation, the team reports. Pre-existing upper limb pain was most affected by yoga.

Injury rate higher than previous reports

However, the study also brought some positive news; around 74 percent of participants reported that their pre-existing musculoskeletal pain had improved as a result of yoga.

Still, the researchers believe that their findings highlight the need for caution when it comes to practicing yoga, especially for people who already have musculoskeletal pain.

"Our study found that the incidence of pain caused by yoga is more than 10 percent per year," says Prof. Pappas, "which is comparable to the injury rate of all sports injuries combined among the physically active population."

“However people consider it to be a very safe activity. This injury rate is up to 10 times higher than has previously been reported."

Prof. Evangelos Pappas

The researchers say that their findings may help both healthcare professionals and patients to compare the risks of yoga with other types of physical activity, allowing them to make informed decisions about which form of exercise is best.

"We recommend that yoga teachers also discuss with their students the risks for injury if not practiced conscientiously, and the potential for yoga to exacerbate some injuries," adds Prof. Pappas.

"Yoga participants are encouraged to discuss the risks of injury and any pre-existing pain, especially in the upper limbs, with yoga teachers and physiotherapists to explore posture modifications that may result in safer practice."

http://www.medicalnewstoday.com/articles/318160.php?utm_source=newsletter&utm_medium=email&utm_campaign=daily-us 

40 attend Hagerstown Parkinson’s Support Group picnic

July 1, 2017

The Hagerstown, Maryland Parkinson’s Support Group held its summer picnic on June 16.

Forty people associated with Parkinson’s disease enjoyed the day at Martin L. "Marty" Snook Memorial Park in Halfway. The group ate fried chicken from AC&T accompanied by a variety of dishes and desserts provided by participants.

The host, Art Guyer, recognized the absence of Frank and Vi McConnell; Frank died late last month.

Dean Cook, co-host, conducted a couple of “memory” quizzes, giving away a $10 gift certificate to the winner. Cook also called bingo for the group, giving away about 50 wrapped prizes brought by the members. Chuck Bihun entertained the group with some banjo strumming.

In attendance were Art and Doris Guyer; Dean and Carol Cook; Mike and Marci Saterbak; Harry and Phyllis Davis; Hugh and Rayetta Schindel; Diane and Sherwood Bair; Becky and Paul Corderman; Bill and Marquita Storms; Jay and Betty Stouffer; Harry and Janet Taylor; Barbara and Jerry Harrell; Lu and Jim Mattern; Chuck and Aura Bihun; Bonnie Embly; Paul and Linda Embly; Belinda Neff and son Dylan; Marie Fogarty; Talia Valencia; Charles and Betty Martin; Edie Johnston; Peg Hayzlett; and Gloria and Carl Rith.

The Hagerstown Parkinson’s Support Group will hold another picnic Friday, Sept. 15, at the same place.

The group meets on the first Thursday of every month at 11:45 a.m. at the Western Sizzlin’ restaurant in Halfway. Anyone associated with Parkinson’s and those interested in learning about the disease are welcome to attend. A variety of speakers help educate members throughout the year.

In addition to the regular monthly meetings, the group holds a caregivers’ breakfast on the third Monday of every month at Hagerstown Family Diner, bowls once a month and hosts other activities.

For more information, go to www.fareshare.net/Parkinsons; email 4Parkinsons@gmail.com; or call 240-625-2722.

http://www.heraldmailmedia.com/life/health/attend-hagerstown-parkinson-s-support-group-picnic/article_39cb73c2-6313-5bd1-88bf-f54c0ae58242.html

Parkinson’s Disease: Live It with Vitality

JULY 2, 2017 BY SHERRI WOODBRIDGE

I received an email from someone concerned that they may have the beginnings of Parkinson’s. I have met others with the disease, but not someone wondering if the symptoms they are experiencing are from it.

I keep thinking about him. His worries take me back to the days before my diagnosis, when I was wondering what was going on with my brain and my body. I can relate to what he is going through and can understand it all too well.

He is scared, he tells me. I remember when I was where he is now: scared, uncertain, and desperate for an answer. The right answer. I now see that, even though my future is still uncertain, I was blessed with a wonderful doctor, the support of good friends, and a caring, loving, faithful family. 

One of the biggest blessings? I have the opportunity to encourage others. That’s because I am further along on this journey than those just diagnosed. I was unable to see any good in it back then because fear of the future was overwhelming, as was a sense of hopelessness. I am still unable to see the good in it on the hard days. But when my vision and emotions are clear, I can.

In reality, isn’t the future uncertain for all of us, whether we have been diagnosed with a disease or not? None of us knows how things will turn out, when will be the last time we tuck our babies in bed at night, or what diagnosis we may be handed tomorrow.

When I think about this, I remember one of my favorite quotes: “Dance as if no one were watching, sing as if no one were listening, and live every day as if it were to be your last.”

That is how I want to live each day, whether I am fighting Parkinson’s or making peace with it. I want to dance without reserve, even if I stumble. I want to sing at the top of my lungs, even if others think I’m only whispering. And I want to live each day as if it were my last opportunity to do something, even if I am given a tomorrow.

It is hard to live like that, of course. There are so many distractions, so many reminders that our bodies are broken. Despite the distractions and the constant reminders that our bodies are struggling against disease, we can decide to live life to the fullest and enjoy the journey.

I read a tweet the other day about Tom Isaacs, a tireless Parkinson’s advocate. He died several weeks ago, leaving a hole in the community that is fighting for a cure. “The loss of Tom [Isaacs] is felt so keenly because he demonstrated a vitality that many think PD robs one of,” the tweet said. Most would not connect Parkinson’s with vitality, but I think the choice of words was spot on.

Vitality: endurance, stamina, strength, vigor, continuity, exuberance.

The word describes someone who knows how to live life, regardless of the path they’re on. It may not be the journey we would have chosen, but there will be good in it. We can despair over that journey or, like Tom Isaacs, live it with vitality.

It’s always better to wear a face of hope than of despair, I believe. This applies to all of us — but especially to ourselves.

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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 Todayor its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s Disease. 

https://parkinsonsnewstoday.com/2017/07/02/parkinsons-patients-sherry-woodridge-calls-for-living-the-disease-with-vitality/