Deep Brain Stimulation Technique Lessens Parkinson’s Dyskinesia, Study Finds

deep brain stimulation, dyskinesia

Using a parameter called interleaving stimulation (ILS) in deep brain stimulation (DBS) eased dyskinesia — involuntary, jerky movements — in patients with Parkinson’s, according to a new study.

In contrast, the benefits in people with tremor or dystonia — abnormal muscle tone — or in mitigating DBS-induced adverse side effects were not as evident.

The study, “Interleaving Stimulation in Parkinson’s Disease, Tremor, and Dystonia,” was published in the journal Stereotactic and Functional Neurosurgery.

DBS is a surgical treatment for Parkinson’s motor symptoms that involves implanting a device to stimulate specific brain regions using electrical impulses generated by a battery-operated neurostimulator.

ILS is a variant of DBS that enables alternating stimulation with two contacts on different brain regions set with specific measures — amplitude, or wave height, and pulse width. ILS may be applied to lessen stimulation-induced adverse side effects and to simultaneously target different brain regions to ease specific symptoms.

Researchers assessed the applications and outcomes of ILS in clinical practice for patients with Parkinson’s, tremor, and dystonia. The team conducted a review through June 2015, by searching the electronic database at Toronto Western Hospital for all patients receiving DBS and ILS.

ILS was preformed in 50 patients — 27 with Parkinson’s (19 men), seven with tremor (three men), and 16 with dystonia (three men). Mean age at diagnosis was 48 for patients with Parkinson’s, 48.6 for people with tremor, and 23.8 for those with dystonia. Age at surgery was 58, 57.8 and 37.8, respectively.

Pre- and post-operative assessments (at six months) were performed with validated scales, including the Unified Parkinson’s Disease Rating Scale part III (motor section), the Fahn-Tolosa-Marin Tremor Rating Scale for patients with tremor, and the Toronto Western Spasmodic Torti-collis Rating Scale and the Burke-Fahn-Marsden Dystonia Rating Scale specifically for those with dystonia.

Twenty-nine patients underwent ILS to manage stimulation-induced adverse effects, mainly to reduce the volume of activated tissue (the amount of brain tissue that is stimulated by electrical activity in DBS). Nineteen participants — 14 with Parkinson’s, two with tremor and three with dystonia — experienced a reduction of symptoms, while 10 (seven with Parkinson’s, one with tremor and two with dystonia) saw no change.

Overall, the benefit of using ILS was predominantly noted in the lessening of dyskinesia — the involuntary, jerky movements — in patients with Parkinson’s disease, and occurred soon after the switch. The average duration of ILS in the six Parkinson’s patients who continued on this approach was 206 days.

Six additional patients also experienced easing of dyskinesia but discontinued the therapy due to worsened pain or mood, temporary benefit, and worsened motor function.

Of the nine Parkinson’s patients receiving ILS for other stimulation-induced adverse effects, only one who tried ILS for dysarthria (slurred or slow speech) continued the treatment with further improvement in parkinsonism.

Three patients with tremor and five with dystonia were receiving ILS for stimulation-induced adverse events. Among these, the approach had mixed results, with only three participants with dystonia showing improvements.

A total of 21 participants tried ILS to improve DBS clinical effectiveness (six Parkinson’s; four tremor; 11 dystonia). Of these, all six Parkinson’s patients and three with dystonia demonstrated benefits. Of the patients with Parkinson’s (mean ILS duration 420 days), four had ILS to reduce tremor, one to lower bradykinesia (slowness of movement), and one to lessen freezing of gait. ILS was not effective in people with tremor and only two patients with dystonia continued with the treatment.

“We identified 2 reasons for attempting ILS: to mitigate adverse effects and to improve disease signs and symptoms,” researchers wrote. “The most impressive finding was improvement of dyskinesias with ILS …  In tremor and dystonia, marginal effects in terms of mitigation of adverse effects and improvement of clinical outcomes were evident,” they added.

“Overall, ILS appears to have limited benefits in the treatment of other stimulation-induced adverse effects potentially due to minimal adjustment of the VAT [volume of activated tissue] and would unlikely be effective to salvage a misplaced electrode,” they concluded.

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Finding the River of Life in Parkinson’s Disease


Sherri Journeying Through

I felt different.

With Parkinson’s disease, that can mean many different things. I may be behind on my anti-depressant and can’t decide whether to laugh or cry. Or I’m behind on my Sinemet (carbidopa-levodopa) and feel shakier than usual. There’s no sense in listing all the ways and reasons I might feel different as a person with PD, other than to say I just feel different.

Sometimes I wake up one day and nothing has changed except my mood. I feel dry, or worse, dried up. I am thirsty for something more. Something greater. I am uninspired, emotionless; emotionally and spiritually dehydrated and thirsty for something to fill up the empty spaces and refresh the parched. This can be borderline depression. It is not a place I wish to go. It is not a place I wish to be.

A while ago, I spent two weeks up in Montana visiting my parents. They live right on the banks of the Kootenai River in a little town tucked in the upper northwest corner of the state. While it can be unsafe to get in the local river there, one can sit at the water’s edge and enjoy it any time and for as long as preferred. The peaceful lapping of water against the colorful boulders at the river’s edge is rejuvenating.

I spent several moments of my day at the water’s edge, sitting on a rock and watching the sunset, thinking about different things, or waiting for my dad’s boat to come around the corner. As I sat there, I wondered why I had felt so dry lately. I had been craving to be filled up, drenched with the spirit of God. Then I realized: Sometimes the dry times are when I find more of God. The times when I feel withered and run out of juice. The times when there is absolutely nothing I can do to get filled up, except to rest in Him and trust Him to bring me through that very empty and very lonely place and into a place of spiritual abundance.

It is often suggested that when writers are in the throes of writer’s block, the best thing to do is just to keep writing, regardless of emotional capacity. Get something on paper. Eventually, writers get back in the saddle to write once again. 

Walking through spiritual deserts is similar. I must keep putting one foot in front of the other, knowing that it won’t be an oasis I’ll find in one of my tomorrows, but eventually, I will find the river of life. How much more refreshing is a river or body of water after having just come from the desert? How much more it is appreciated! It is a river where a person can be drenched with cool, dripping water that saturates the dry places and leaves one refreshed.

If in a “dry” place today, for whatever reason, keep walking the path of this journey He has set. A refreshing river may be just around the corner where God is waiting to refresh spirits.


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.

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Inexpensive Hand-Tracker Accurately Measures Bradykinesia in Parkinson’s Patients, Small Study Suggests

bradykinesia, hand-tracker, Parkinson's

An inexpensive off-the-shelf hand-tracker can objectively and reliably measure Parkinson’s disease-related slowness of movement (bradykinesia) over time, both in a clinical setting or at a patient’s home, researchers report.

The study, “Objective evaluation of bradykinesia in Parkinson’s disease using an inexpensive marker-less motion tracking system,” was published in Physiological Measurement.

Accurately assessing bradykinesia, or the progressive slowness of movement over time, is key in the management of Parkinson’s disease and allows clinicians to adjust therapies throughout disease progression.

Bradykinesia is usually assessed using part of the Movement Disorders Society – Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). This rating scale requires patients to perform a series of repetitive movements, which are then evaluated by a clinician from 0 (normal) to 4 (severe) to reflect a patient’s level of motor impairment.

However, this scoring method is not sufficiently sensitive, and is dependent on a particular clinician’s experience, making it subject to evaluator variability.

“Furthermore, patients residing in remote communities lack access to specialist clinics leading to a growing demand for objective monitoring systems that can be deployed in the absence of a movement disorders expert,” the researchers wrote.

There is an urgent need for developing objective, effective, and convenient measurements to help clinicians accurately identify bradykinesia.

“Although various technologies have been developed for assessing bradykinesia in recent years, most still require considerable expertise and effort to operate,” they added.

Therefore, a team of Australian researchers aimed to quantify the overall severity of bradykinesia in Parkinson’s disease patients using an inexpensive off-the-shelf hand-tracker, also known as a leap motion controller (developed by Leap Motion).

The leap motion controller is a small USB device that plugs into a computer. Using miniature infrared cameras and built-in image recognition algorithms, the technology scans the area between the subject and the computer, and tracks both hands and all 10 fingers as they move through space.

Researchers also investigated whether there was the need to perform a variety of hand tasks, or if just one was enough to characterize symptom severity.

The team evaluated 8 patients with Parkinson’s disease (from 44 to 60 years old, and 75% male), who were responsive to levodopa therapy (mean disease duration was 10.3 years) and receiving deep brain stimulation (DBS) for at least six months. Participants arrived off-medication, which continued throughout the study. Patients were assessed on and off DBS stimulation.

The software captured patients’ ability to rotate their palms down (pronation) or up (supination), open and close their hands, and tap their fingers, following MDS-UPDRS recommendations. At the same time, the participants’ movements were also scored by three clinicians.

“A total of 144 trials were recorded (8 subjects x 2 hands x 3 therapeutic conditions x 3 tasks),” the researchers wrote. Measurements were taken when DBS was “on” at the beginning of the study, 60 minutes after turning “off” DBS, and 30 minutes after turning back “on” DBS.

The software showed bradykinesia scores strongly correlated with clinical scores, indicating that the extracted motion data (amplitude, frequency, and velocity) can detect differences in the severity of slowness of movement.

Contrary to wrist and hand tasks, finger-tapping did not significantly predict bradykinesia severity, as the software often failed to track finger movement.

The motion tracking system was also able to differentiate between “on” and “off” DBS states, and, as expected, no difference was observed between both “on” periods.

“The results suggest that the prediction model produces a consistent and reliable score, which supports its use in clinical assessments,” the researchers said. “An objective assessment tool, such as the one proposed here, is therefore advantageous and may not only improve patient care, but also the accuracy and reliability of symptom severity reported in clinical trials.”

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Onstryv Now Approved for Parkinson’s Patients in Canada

Onstryv approval Canada

Onstryv (safinamide) has been approved for the treatment of Parkinson’s disease in Canada, where roughly 100,000 individuals live with the disorder.

The announcement was made by Quebec-based Valeo Pharma and Italian pharmaceutical conglomerate Zambon, the commercialization partner of Newron Pharmaceuticals, a biopharmaceutical company focused on the development of therapies for diseases of the central and peripheral nervous system.

The agreement with Zambon calls for Valeo Pharma, a specialty pharmaceutical company dedicated to commercializing innovative prescription products, to be responsible for all regulatory requirements, quality, sales and marketing, and drug distribution. Onstryv is expected to be available in Canada by June.

”The approval of safinamide in Canada is a step forward for patients who need new treatment options for Parkinson’s disease,” Roberto Tascione, Zambon’s CEO, said in the press release. “Our mission is to make this medication available to as many [Parkinson’s disease] patients worldwide as possible.”

Known as Onstryv in Canada and Xadago in the rest of the world, this compound is an oral, once-a-day, add-on therapy developed by Newron, and approved in the United States in March 2017 by the U.S. Food and Drug Administration to improve motor function in Parkinson’s patients who experience “off periods” while on treatment with levodopa and/or Lodosyn (carbidopa).

While partially effective, therapy using either or both levodopa and carbidopa results in debilitating fluctuations between a state of normal motor function (known as “on episodes”) and reduced motor function (“off periods”) as the treatment’s effectiveness wears off. What’s more, the increased doses necessary as the disease progresses frequently cause uncontrolled involuntary movements, a condition known as dyskinesia.

Onstryv raises the level and function of dopamine in the brain, both through the reversible blockage of the enzyme monoamine oxidase B that normally breaks down this chemical, and by inhibiting transporters responsible for its absorption and retention. In addition, the medicine inhibits the excessive release of the signaling molecule glutamate.

Following four randomized, double-blind, placebo-controlled Phase 3 trials, published results indicated that the addition of Onstryv increased the frequency of on episodes, decreased off periods, and improved motor function in levodopa-treated patients.

In 2017, Valeo and Zambon announced a partnership granting Valeo exclusive Canadian rights to commercialize Onstryv. In addition to Canada and the U.S., the medicine is approved in the European Union and Switzerland and was recently approved in Australia.

“There is a growing need for new treatments to manage Parkinson’s disease, and Onstryv provides an important option for patients that require better control of their symptoms,” said Steve Saviuk, Valeo’s CEO. “We look  forward to launching the first new oral treatment for Parkinson’s disease in over a decade to Canadian patients in need of a new therapeutic choice.”

In recent related news, a review study found that, along with cannabinoids and opioids, Onstryv may relieve Parkinson’s patients’ pain, a frequent non-motor symptom.

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‘Bananas and Beans, not Burgers’: High-Protein Meals and Levodopa


No one told me that breakfast bacon, ham, or sausage would make me feel awful!

I had seen my off-periods worsen after a heavy meat meal, but I shrugged it off as “just a bad off-period.” Now, after being on levodopa for five years, I am positive that animal protein meals are a serious issue. Overlapping a high meat meal with levodopa can result in not just an off-period, but also one that lasts much of the day.

“Bananas and beans, not burgers” is the mantra to remind me that diet is very important in the development of a rehab plan for folks with PD. I am not a nutritionist. I am writing from the perspective of a PD patient warrior and rehab clinician.

Research suggests that changes to your diet could help alleviate some symptoms of your PD. The American Parkinson Disease Association (APDA) notes that levodopa crosses the wall of the small intestine via molecules in the intestinal wall that transport amino acids. When dietary protein (beef, chicken, pork, fish, eggs, nuts, and dairy) is also present in the small intestine, fewer transporters are available for levodopa to use. We may experience the “protein effect” when the medication competes with a high-protein meal.

One of the most compelling statements in a 2014 study published in Frontiers in Aging Neuroscience is that a “growing body of evidence suggests that nutrition may play an important role in PD.”

The study “Irregular gastrointestinal drug absorption in Parkinson’s disease” in the journal Expert Opinion on Drug Metabolism & Toxicology states that levodopa transit time in the small intestine is approximately three hours. Therefore, gastric emptying is a major determining factor for the onset of symptom relief. When PD delays gastric emptying, it has the potential to cause motor fluctuations, known to us as off-periods.

Research also shows that with your microbiome (the microorganisms in your body), a relationship exists between Parkinson’s disease and improved gut health. In “Parkinson’s disease and bacteriophages as its overlooked contributors,” published in the journal Scientific Reports, George Tetz and his colleagues examined the viruses that live in the gut, as well as the role the microbiome may play in Parkinson’s disease. According to, “this has sparked the idea that we might be able to improve the symptoms if we change the microbiome through diet or other ways. … These bacteria play a role in the processes that produce dopamine and affect the intestine’s ability to absorb.”

Like many aspects of Parkinson’s symptoms, the protein effect is highly variable. Some people do not experience it at all. Others are extremely sensitive to protein’s effect on medication absorption. This diet concern was presented at my local PD support group, and the group’s PD warriors and caregivers agreed almost unanimously with having experienced or witnessed the adverse effects.

It typically becomes more of an issue as PD progresses. The APDA suggests that if someone experiences the protein effect, two potential strategies might help. One is to refrain from eating protein during the day, eating it at night instead, when the medication’s effect is less critical. The second is to distribute protein intake evenly throughout the day so that medication absorption is enhanced during that time.

The solution I have found that works best for me has two parts. First, I space the levodopa dosing so that it occurs between meals to minimize absorption issues. Second, I eat the day’s moderate meat meal at lunch, not dinner or breakfast.

Reducing meat in your diet may be beneficial not just to levapoda absorption. An amazing study on diet and overall health by Thomas Campbell and T. Colin Campbell, called “The China Study,” clearly showed that decreasing meat intake is a good change for all of us. Bananas and beans, not burgers.

What diet changes have you found to be helpful? Share in the comments below.


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.

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Mutations in Gene Associated With Hereditary Parkinson’s Disease Lead to Toxic Accumulation of Manganese

SLC30A10 study

Researchers have found that mutations in a gene linked to hereditary forms of Parkinson’s disease — SLC30A10 — cause accumulation of toxic levels of manganese inside cells, which disturbs protein transport and alters nerve cell function, leading to parkinsonian symptoms.

The study “SLC30A10 Mutation Involved in Parkinsonism Results in Manganese Accumulation within Nanovesicles of the Golgi Apparatus” was published in the journal ACS Chemical Neuroscience.

Manganese is an essential metal that helps enzymes carry out their functions in the body. However, too much manganese is toxic, especially for the central nervous system (brain and spinal cord), where its accumulation can lead to parkinsonian-like syndromes.

The SLC30A10 gene encodes an important manganese transport protein, which sits at the membrane of cells and pumps out manganese, to protect cells against this metal’s toxicity. However, mutations in the SLC30A10 gene block the protein’s pumping activity, resulting in manganese accumulation.

Mutations in this gene have been identified as the cause of new forms of hereditary Parkinson’s disease.

“Understanding the means by which mutations in SLC30A10 alter cellular Mn [manganese] homeostasis [manganese equilibrium] is expected to enhance understanding of the principles underlying Mn toxicity itself,” researchers wrote, which may render important information to fight certain forms of familial Parkinson’s disease.

A team of French researchers used advanced imaging techniques to find where manganese accumulates inside cells (cell lines available for laboratory research) carrying disease-causing SLC30A10 mutations versus cells carrying a normal, functional SLC30A10 gene (control cells).

Intracellular manganese levels were undetectable in control cells, confirming cells’ ability to expel the metal and avoid its toxicity. On the contrary, manganese levels were higher in cells carrying disease-causing SLC30A10 mutations.

The team then looked at cells that lacked SLC30A10 and were exposed to increasing levels of manganese. Researchers found that manganese accumulated in an organelle, called the Golgi apparatus, that works as the cell’s dispatching center for proteins. The same was true for cells carrying disease-causing SLC30A10 mutations.

Mutant SLC30A10 proteins lost their ability to expel manganese out of the cells, with cells behaving as if they had no SLC30A10 protein at all.

Using the an imaging technique known as Synchrotron X-ray fluorescence spectrometry, which allows researchers to look deeper into cells and their smaller structures, the team discovered that the main compartment for manganese accumulation in SLC30A10 mutated cells were tiny vesicles released from the Golgi apparatus.

These vesicles are important mediators of communication inside the cell. Researchers believe that disturbing this vesicular trafficking is probably the root of the toxicity induced by the disease-causing mutations of SLC30A10.

“It would be interesting to investigate whether Mn causes defects in Golgi vesicular trafficking and consequently on neurotransmitters,” researchers wrote.

Moreover, these results suggest that small molecules targeting the mutated SLC30A10 protein at the cell surface could become a potential therapeutic strategy.

Future experiments will show if a similar pattern of manganese accumulation is seen in animal models of Parkinson’s disease.

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Subjective Cognitive Decline Could Help Predict Parkinson’s Dementia, Study Contends

cognitive decline

Subjective cognitive decline in Parkinson’s disease could predict the development of dementia. As such, a suitable cognitive screening test could help provide an accurate diagnosis and prognosis.

The study with those findings, “Subjective cognitive decline and progression to dementia in Parkinson’s disease: a long-term follow-up study,” was published in Journal of Neurology.

Even during the early stages of disease, mild cognitive impairment can affect non-demented Parkinson’s patients, and is considered a risk factor for the development of dementia (PDD).

In fact, the prevalence of PDD increases as the disease progresses: from 28% after five years of evolution to 80% after 20 years of the disease.

Subjective cognitive decline — self-reported acquired difficulties with cognitive functioning — is common in the elderly and can be used as a predictor of dementia. In Alzheimer’s disease, subjective cognitive decline has been linked to disease-related tissue/molecular changes and a higher risk for dementia development. However, the predictive value of this type of cognitive status impairment has not been demonstrated yet in Parkinson’s disease.

Scientists from the University of La Laguna, Spain, investigated the neuropsychological profile of subjective cognitive decline in Parkinson’s disease and explored which components could better predict the development of PDD. The team also compared different screening tests to assess subjective cognitive complaints.

A total of 43 Parkinson’s patients and 20 healthy subjects were subjected to neuropsychological examination using a battery of cognitive tests. All patients were being medicated for Parkinson’s and were evaluated during their “on” state — when they are responding to medication and have reduced symptoms.

Subjective cognitive decline was diagnosed using two distinct approaches. A semi-structured interview in which the patient provided his/her subjective opinion on his/her attention, memory, spoken language, naming, written language, visuospatial skills and executive functions; diagnosis was considered when the patient had at least one cognitive complaint. Additionally, a subjective cognitive decline diagnosis also was established on the basis of the interview question concerning memory complaint.

For a mild cognitive impairment diagnosis, investigators followed the criteria proposed by the Movement Disorder Society (MDS)

Based on the results of the interview and on the MDS Task Force criteria, patients were diagnosed as having either subjective cognitive decline or mild cognitive impairment. Of the 43 patients, 13 (30.2%) were diagnosed with subjective cognitive decline, 22 (51.2%) with mild cognitive impairment and 8 (18.6%) had no subjective cognitive complaints. Difficulties in naming and memory were the most frequent cognitive complaints.

Based on memory complaints alone 10 patients (23.25%) were diagnosed with subjective cognitive decline. Interestingly, 10 of the 22 (45.45%) who had been diagnosed with mild cognitive impairment reported no memory complaints.

Mild cognitive impairment subjects performed poorer in the processing speed (the time it takes a person to do a mental task), executive functions (a set of mental skills that helps with organization and regulation), visuospatial skills, memory, and language domains, compared to the other groups.

There were no significant differences between healthy participants (controls)  and Parkinson’s disease patients with subjective cognitive decline in any of the neuropsychological measures.

The team also assessed how many patients diagnosed with subjective cognitive decline progressed to dementia after a mean follow-up of 7.5 years. Fifty percent of mild cognitive impairment patients, 33.3% of individuals diagnosed with subjective cognitive decline, and 14.3% of patients without subjective cognitive complaints developed dementia, which was found to be associated with a poor performance in verbal and visuospatial memory and naming at the beginning of the study.

Additionally, both the language and memory domains were good predictors of dementia development.

“These results are highly relevant for future investigations and also for clinicians: the [subjective cognitive decline] assessment is frequently the first step of cognitive examination and can influence future decisions (e.g., to administer a screening test or a comprehensive neuropsychological assessment),” researchers wrote.

“Assessments that do not include procedures to adequately explore cognitive complaints may underestimate the proportion of [Parkinson’s-related subjective cognitive decline] and, therefore, [mild cognitive impairment] and thus misclassify patients as [Parkinson’s disease] with normal cognition, especially when brief cognitive examinations are chosen,” they concluded.

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Forced Exercise Improves Mobility, Mood in PD Patient, Study Finds


A collaboration between Theracycle and Virginian Outpatient Therapy will replicate a forced exercise regimen on a motorized bicycle with evidence of easing Parkinson’s symptoms, including rigidity, loss of balance and tremor.

In a 2009 study conducted by the Cleveland Clinic, an eight-week program of forced exercise with a trainer on a stationary tandem bicycle — in which patients’ bodies move beyond the extent they can do so themselves — was compared to voluntary exercise on a stationary single bicycle. Ten patients (eight men) with mild to moderate idiopathic Parkinson’s were included, five patients in each group.

The results showed that the patients on forced exercise (mean age 58 years, disease duration 7.9 years) had a 35% improvement in motor scores — as assessed with the Unified Parkinson’s Disease Rating Scale (UPDRS; higher scores mean more impairment) — as well as improved control and coordination of grasping during a bimanual dexterity task. Such improvements were not observed with voluntary exercise, although both groups had greater aerobic capacity.

The benefits in rigidity, bradykinesia — slowness of movement — and hand dexterity were maintained four weeks after stopping forced exercise, in which the patients pedaled at a rate 30% greater than their preferred voluntary rate.

In 2018, Shirlea Hennessy, Virginian Outpatient Therapy’s assistant director of rehabilitation, replicated the Cleveland Clinic study in a Parkinson’s patient. The patient’s wellness program was supplemented with an hour of forced exercise on the Theracycle three times a week for eight weeks.

This approach led to an improvement in the UPDRS score from 36 to 6 in 12 weeks, loss of 10 pounds, more joy in daily activities — including tai chi, yoga, Bible study, and visits with his grandchildren — and regaining the confidence to drive.

“To see such substantial improvements in his mobility symptoms in as little as eight weeks was remarkable,” Hennessy, who is also a board-certified geriatric clinical specialist, said in a press release.

Similar to the 2009 study, the patient maintained his improvements for four weeks after stopping the program, “revealing that a little effort can go a long way in establishing greater freedom and independence,” Hennessy said. “That freedom and independence is all that [Parkinson’s] patients strive for as they face their diagnosis and symptoms.”

Peter Blumenthal, Theracycle’s CEO, said that “to see Virginian Outpatient Therapy replicate the Cleveland Clinic study with its own patient and produce equally impressive results is inspiring.”

Hennessy will keep implementing forced exercise with a Theracycle for Parkinson’s patients at the outpatient physical therapy provider and expects to see benefits across the board.

A recent survey conducted by Theracycle revealed that 80% of its customers had improved walking, balance, and gait. Also, 73% reported an improvement in overall mood and 64% had a reduction in tremors or involuntary movements. Full results of the survey can be found here.

“At Theracycle, we understand how life-changing forced exercise can be for [Parkinson’s] patients,” Blumenthal said. “We’re honored to make a positive impact on the lives of those living with [Parkinson’s].”

Besides Parkinson’s, Theracycle provides motorized exercise bicycles to ease symptoms of multiple sclerosis, paraplegia, stroke, Down syndrome, traumatic brain injury, and other degenerative neurological disorders.

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Parkinson’s Subtypes May Predict Disease Course and Survival, Study Suggests

Parkinson's subtypes

Subtyping Parkinson’s disease at diagnosis may predict disease course and survival, providing both doctors and patients with a more accurate prognosis, a study suggests.

The study, “Prognosis and Neuropathologic Correlation of Clinical Subtypes of Parkinson Disease,” was published in JAMA Neurology.

Parkinson’s disease is characterized by clinical diversity, and many attempts have been made to identify distinct clinical syndromic patterns. The presence of not only motor but also non-motor symptoms is increasingly being used to categorize the disease into different clinical subtypes.

However, “classification of patients with [Parkinson’s disease] is purely based on data association and may not reflect underlying [physiological processes associated with disease] driving clinical heterogeneity,” the researchers wrote.

Although very little is known about the correlation between brain tissue molecular/cellular changes and Parkinson’s subtypes, some studies suggest that motor severity, cognitive impairment, autonomic dysfunction — when the nerves of the system that controls basic bodily functions are damaged — and rapid eye movement (REM) sleep behavior disorder need to be taken into consideration during clinical subtyping. (REM is a sleep stage in which the eyes move rapidly in various directions.)

Moreover, the predictive value of Parkinson’s-related subtype classification remains to be confirmed.

For this purpose, investigators from the University College London Queen Square Institute of Neurology gathered life-course clinical and brain tissue analysis data and correlated it with Parkinson’s disease subtypes.

They analyzed the clinical records of 111 Parkinson’s patients, 60.4% of whom were men, who were regularly assessed throughout their disease and had their diagnosis confirmed by autopsy.

According to the severity of their motor symptoms, REM sleep behavior disorder, cognitive performance, and autonomic function at diagnosis, the patients were classified into three subtypes: mild-motor predominant (meaning they had mild motor and non-motor symptoms), diffuse malignant (severe symptoms), or intermediate (where they did not meet the criteria for the other two subtypes).

Researchers calculated the time it took patients to achieve specific disease milestones (recurrent falls, wheelchair dependence, dementia, and care home placement) and compared them between subtypes. They also assessed time from diagnosis to death.

In addition, post-mortem analysis of brain tissue was performed to assess the severity and distribution patterns of Lewy bodies — abnormal deposits of alpha-synuclein protein — and Alzheimer’s disease-related tissue changes.

Of the 111 participants, 54 were classified as mild-motor predominant, 39 as intermediate, and 18 as diffuse malignant.

Patients with the mild-motor predominant subtype were significantly younger at diagnosis, had a better response to levodopa, and received a higher levodopa equivalent dose. In contrast, those with the diffuse malignant subtype were older, had a poorer response to levodopa, and were more frequently misdiagnosed as having an atypical parkinsonian syndrome during their lifetime.

Age at diagnosis was significantly different across Parkinson’s subtypes: mild-motor predominant — 58.2 years, intermediate — 65 years, and diffuse malignant — 70.3 years.

Patients’ ages at diagnosis were also associated with faster disease progression and reduced survival: The later they were diagnosed, the faster the disease progressed.

All Parkinson’s subtypes showed different rates of deterioration, “with the diffuse malignant subtype reaching all prognostic milestones earlier in the disease course and having the shortest survival,” according to the researchers.

Additionally, all subtypes “reached advanced stages, with 105 of 111 patients (94.6%) reaching at least one disease milestone,” they said.

Brain tissue analysis revealed distinct progression rates of Lewy body and Alzheimer’s disease-related pathologies, which were found to be associated with age at death. However, there were no significant differences across subtypes regarding severity of Lewy pathology.

“Clinical subtyping of [Parkinson’s disease] … is feasible in clinical practice and provides accurate long-term estimation of disease progression and survival. Different pathologies with differing rates of progression are important determinants of clinical subtypes, and age at diagnosis should be included in future subtype classification systems,” the researchers concluded.

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Being Still Reveals Many Treasures

winter treasures, snow angels

Sherri Journeying Through

It is quiet behind our house this time of year. Not many people are using the pathway that stretches from one town to another. It is cold outside and it pierces my flesh, leaving me shivering as Ip stand and wait. In the silence, I can hear my teeth chatter.

So, what compels me to stand out in the cold and wet of winter?

Nothing. And everything.

I walk the icy pathway. Barren trees lift their branches high into the blue sky above. This is a cotton-candy-blue-sky morning. I almost could forget I have Parkinson’s disease.

The birch tree, with its white bark, stands tall beside me. It almost glows as the sun radiates its light on trunk and limbs. And I see utmost beauty. I stand speechless. It is a beautiful, frosty, winter-morning sight.

Taking a small respite from writing during the holidays, I have learned many lessons this past month from the silence of the keyboard. The rattling of its keys has been minimal. Social conversations via internet sites have not occurred. The telephone has been in the hands of another, and one-on-one phone conversations via satellites and modern technology have been almost nil.

Through the silence, through the barrenness of winter — this dark season of life — God has spoken. A mere whisper perhaps, but He has been there.

One who lately seemed so terribly far away still walks beside me in my struggles with this illness and life itself. In reality, Parkinson’s is much of my life.

But in silence He is teaching me that the faster I walk, the less I see, the less I hear. The faster I live, the more I am lifeless.

I miss the surprises.

I miss the beauty.

I miss the Creator.

I stand on the path. A man on a bike stops to ask what I am taking pictures of. I tell him salmon in the creek. A woman stops, repeating the same question. I tell her downy woodpeckers. They both look — one up into blue and one down into murky waters. They smile politely and continue on their way. They can’t see. They are hurried in their experiencing of life and in their hurry, they miss it.

I listen to the sounds of birds that are wintering over and have found sustenance at my bird feeders. Filled with black sunflowers, thistle seeds, and suet, they sing with thanksgiving before they dive down for another bite.

This — all of this — is a wonderful gift God has given. Regrettably, I too have often walked dark winter’s path without looking up into barren branches. To my regret, I have missed the surprises that are hidden for those who have learned to be still. For those who have learned who God is. For those who are still and not consumed by worry over things they cannot control.

I stand in the cold, warmed by knowing He is gently leading me back — back to a fullness in Him. A fullness that once discovered, once experienced no other can fill, no illness can take.

I stand there, taking in a deep breath of icy air surrounding my face. As my lungs fill with a cleansing cold, I see it and it sees me. There, in the high limbs, a hawk is perched, watching, observing, following me where I move.

I lift the camera and point in his direction and shoot. He is annoyed and removes his talons from tightly held limbs and takes off into flight. As I stand in stillness, I watch with held breath. I want to remember this moment forever. I want to remember this lesson He teaches me. How His wings protect and shelter us underneath. I want to remember in stillness there is greater sight.

I want to remember to live. Unhurried. Full of life. Full of thankfulness. Full of gratitude. I want to be a grace extender. I want to live in stillness, knowing deep in my being just who God is in my life: Hope-maker. Fear-taker. Peace-giver. Illness-comforter. Grace-coverer. Stillness-trainer. Life-sustainer. Soul-redeemer. Silence-creator. 

Day after day after day.


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