Cognitive Impairment Tests to Assess Dementia Risk Can Be Easier, Study Shows

cognitive impairment test

A shorter, simpler version of testing to diagnose mild cognitive impairment in Parkinson’s disease is just as effective as a lengthier evaluation at predicting the risk of developing Parkinson’s disease dementia, a report shows.

The study, “Risk of Parkinson’s Disease Dementia Related to Level I MDS PD-MCI,” was published in Movement Disorders.

Both cognitive decline and dementia are recognized as non-motor complications of Parkinson’s with significant clinical impact. Evidence suggests that mild cognitive impairment is a risk factor for Parkinson’s disease dementia (PDD).

The International Parkinson and Movement Disorder Society (MDS) has formulated two levels of criteria for diagnosing Parkinson’s-related mild cognitive impairment. Levels 1 and 2 differ in their methods of assessment, level of diagnostic certainty, and extent of clinical characterization.

Level 1 is comprised of a simpler, shorter series of cognitive tests, while level 2 entails a more extensive neuropsychological evaluation.

One study has shown that using level 2 criteria to assess mild cognitive impairment — which considered age, sex, years of education, depression and the severity of motor symptoms — can be effective at confirming an increased risk of patients developing dementia.

The University of Amsterdam researchers evaluated the prognostic value of testing mild cognitive impairment, using level 1 criteria as indicators of PDD.

“Comprehensive neuropsychological testing is not always possible because of time, cost, or patients’ inability to cooperate with a long assessment,” they said.

Looking at eight international studies, totaling 1,045 patients, they analyzed demographic and clinical data including age, sex, years of education, disease duration and neuropsychological examinations, based on the Unified Parkinson’s Disease Rating Scale (UPDRS) part III (motor tests), the Movement Disorder Society (MDS)-UPDRS III score, the Hoehn and Yahr scale (used to measure symptom progression), and an indicator of patient depression.

Level 1 criteria were applied, with one test of each of the five cognitive domains: attention, executive function— the ability to manage and organize thoughts, actions, and feelings — memory, visuospatial function, and language.

Survival analysis evaluated how each factor contributed to the risk of PDD.

In an initial evaluation17% of the patients were diagnosed with mild cognitive impairment. Median follow-up was 2.8 years and 151 out of the 1,045 (14.4%) patients developed dementia.

Only 9% of those without cognitive impairment at the beginning of the study developed dementia during follow-up, compared to 77% in the mild cognitive impairment group.

Worse performance in level 1 testing was associated with a higher risk of developing PDD dementia.

The evaluation also revealed that increasing age, male sex, and the severity of Parkinson’s motor symptoms independently heighten this risk.

Importantly, the study found that both levels of criteria had similar discriminant ability, meaning that the less extensive level 1 testing was effective at determining PDD risk.

Researchers also reported that level 1 criteria identified fewer mild cases, and associated them with relatively higher risk ratios, which they said could be attributed to the rating system used.  Level 1 criteria measures greater cognitive decline, when using the same cutoff as level 2 criteria.  For example, in level 1, at least two out of five tests need to show impairment, compared to at least two out of 10 tests in level 2.

“In conclusion, level I PD-MCI [mild cognitive impairment] criteria classification, based on a brief neuropsychological assessment, confers an independent contribution to the hazard of PDD while taking age, sex, education, PD motor sign severity, and depression into account. This finding supports the role of level I PD-MCI as a risk factor for PDD,” they wrote.

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Gut Bacteria Affect Metabolism of Parkinson’s Therapy Levodopa, Study Shows

gut bacteria

Levodopa, one of the main medicines used to treat Parkinson’s symptoms, can be converted into dopamine by gut bacteria, researchers report.

The findings might explain why levodopa treatment is less effective in some patients.

The study, “Gut bacterial tyrosine decarboxylases restrict levels of levodopa in the treatment of Parkinson’s disease,” was published in Nature Communications.

Parkinson’s disease is characterized by low levels of dopamine, a chemical brain messenger essential for neurons involved in movement control.

In terms of treatment, patients cannot take dopamine directly, as the compound is broken down by the body before it reaches the brain. Levodopa crosses the blood-brain barrier and is taken up by dopaminergic neurons, which convert the chemical into dopamine, which helps manage disease-related motor symptoms.

Studies have suggested that gut bacteria can affect treatment effectiveness in several diseases; particularly in Parkinson’s, the amount of levodopa that reaches the brain varies among patients.

“It is well established that gut bacteria can affect the brain,” assistant professor in microbiology Sahar El Aidy, PhD, and this study’s lead investigator, said in a press release. “There is a continuous chemical dialogue between gut bacteria and the brain, the so-called gut-brain axis.”

However, it remains to be explained if inter-patient variations in gut bacteria composition and functionality contribute to treatment response fluctuations in Parkinson’s disease patients who require a higher daily treatment dosage regimen.

Researchers from the University of Groningen in The Netherlands analyzed the effect of levodopa metabolizing bacteria in the middle section of the small intestine (jejunum), where levodopa is absorbed.

Using rat jejunum bacteria samples, researchers saw that an enzyme called tyrosine decarboxylase, which normally converts tyrosine into tyramine, also efficiently converted levodopa to dopamine in the gut. Enterococcus bacteria, commonly found in the intestines, were responsible for such enzymatic activity.

To understand if they could somehow inhibit levodopa’s conversion, the Dutch team “fed” the bacteria with a high concentration of the amino acid tyrosine, the main substance that tyrosine decarboxylase acts on, but tyrosine’s abundance did not prevent levodopa’s metabolization.

As part of their treatment regimen, Parkinson’s patients are given a decarboxylase inhibitor, like carbidopa, to block peripheral metabolism of levodopa to dopamine, allowing a greater concentration of levodopa to reach the brain.

Scientists studied the effect of human decarboxylase inhibitors, including carbidopa, benserazide, and methyldopa, on the bacterial tyrosine decarboxylase. None of the tested inhibitor compounds blocked levodopa’s enzymatic transformation.

“It turned out that, for example, the inhibitor carbidopa is over 10,000 times more potent in inhibiting the human decarboxylase,” said El Aidy. This could be due to species-specific changes in carbidopa’s chemical structure, indicating that a more effective levodopa treatment could be achieved by co-administration of tyrosine decarboxylase inhibitor targeting both human and bacterial forms of the enzyme.

“[C]ommonly applied inhibitors of human DOPA [levodopa] [tyrosine] decarboxylase in levodopa combination therapy do not inhibit bacterial TDC [tyrosine decarboxylase] dependent levodopa conversion, implying levodopa/carbidopa (levodopa) combination therapy for PD [Parkinson’s disease] patients would not affect the efficacy of levodopa in situ [locally] by small intestinal bacteria,” researchers wrote.

These findings confirm the gut bacteria’s ability to influence local levels of levodopa treatment and suggest that the presence of tyrosine decarboxylase could reduce the amount of levodopa available in the bloodstream of Parkinson’s patients.

To test the latter hypothesis, investigators analyzed stool samples from patients who were on a normal or high dose of levodopa. They reported a strong positive correlation between the relative abundance of the bacterial gene encoding for tyrosine decarboxylase and the need for a higher levodopa/carbidopa treatment dose, as well as with disease duration.

To further understand the concept that the amount of tyrosine decarboxylase in jejunum’s bacteria affects bloodstream levels of levodopa/carbidopa and dopamine, scientists orally administered levodopa plus carbidopa to 18 wild-type (healthy) rats and analyzed animals’ blood 15 minutes after administration (time point when levodopa is at its higher concentration in rats).

Results showed that higher abundance of bacterial tyrosine decarboxylase in the rats’ jejunum decreased plasma levels of levodopa. The ratio between dopamine and levodopa/carbidopa levels in the small intestine positively correlated with bacterial enzyme amount.

Researchers then treated 10 rats with a subtype of Enterococcus bacteria known as Enterococcus faecalis that did not have the tyrosine decarboxylase gene and compared their levodopa/carbidopa plasma levels with 10 other rats that were given wild-type (normal, positive for the tyrosine decarboxylase gene) Enterococcus faecalis cells.

As expected, animals treated with wild-type cells had significant lower plasma levels of levodopa/carbidopa than the ones treated with mutant cells.

“Collectively, our data show that levodopa conversion by bacterial [tyrosine decarboxylase] in the small intestine should be considered as a significant explanatory factor for the increased levodopa/carbidopa dosage regimen required in a subset of [Parkinson’s disease] patients,” researchers wrote.

“This is considered to be a problem for Parkinson’s disease patients, because a higher dose will result in dyskinesia, one of the major side effects of levodopa treatment,” El Aidy said, referring to the involuntary, jerky movements patients experience.

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Cancer Patients Have Lower Risk of Developing Parkinson’s Disease, Study Suggests

cancer, Parkinson's risk

Cancer patients appear to have a lower risk of developing Parkinson’s disease, even when taking into account important risk factors and overall survival, a study has found.

The study, “Cancers Preceding Parkinson’s Disease after Adjustment for Bias in a Danish Population-Based Case-Control Study,” was published in Neuroepidimiology.

Previous studies have shown that cancer patients are less likely to develop Parkinson’s during their lifetime than the general population. However, it is unclear whether this could be caused by the negative association between Parkinson’s disease and smoking, when, for many cancers, smoking is a known risk factor, or simply by the fact that most cancer patients do not survive long enough to reach a stage in which they are more likely to develop Parkinson’s.

Researchers at the University of California Los Angeles carried out a large population-based case-control study in Denmark (PASIDA) to investigate if cancer correlated with a lower risk of Parkinson’s disease, even after normalizing important risk factors, such as smoking, physical activity, and survival bias.

The study involved a total of 1,813 patients with Parkinson’s disease and 1,887 age- and sex-matched individuals without Parkinson’s used as controls.

Demographic analysis showed the percentage of non-smokers was higher in the group of Parkinson’s patients (49.6%) than in controls (35.3%). Conversely, the incidence of cancer was lower among Parkinson’s patients (3.8%) than in controls (4.2%), a difference that was even more pronounced when comparing the incidence of smoking-related cancers (1.7% versus 2.2%).

Apart from skin and breast cancer, further analysis showed a negative correlation between Parkinson’s disease and all types of cancers, including those related and not related to smoking. Even after normalization for risk factors and cancer patients’ survival bias, the negative association between Parkinson’s disease and cancer remained the same.

“Since PD [Parkinson’s disease] cases stop smoking many years prior to PD diagnosis, one might say that ‘PD prevents smoking’ and thus reduces the risk of smoking-related cancers and mortality. [However,] in PASIDA adjustment for pack-years of smoking did not change the observed associations between cancer and PD, which suggested that smoking is unlikely to be a strong confounder between cancer and PD,” the researchers wrote.

“In conclusion, our study suggested a lower frequency of most cancers preceding PD diagnosis after adjustment for major lifestyle factors. Our bias analysis indicated that survival bias minimally impacts the observed associations,” they added.

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The Calm After the Parkinson’s Storm

calm

Sherri Journeying Through

This morning I read a Facebook post from a person who is in the early stages of being diagnosed with Parkinson’s disease. He listed some of his symptoms and said he was awaiting lab results. He asked whether it’s common for symptoms to differ from day to day and if so, why this happens.

Shortly afterward I checked in with my mother-in-law by text: “A few clouds but nothing like the storm that came down last night! Incredible rainfall and wind. And today, all is calm.” 

All was calm yesterday morning, and then the storm clouds began to gather. They hovered overhead all afternoon; no raindrops, just a gradual darkening of the sky. And then, last night while I was at my boxing class, duking it out with a punching bag, God began to duke it out outside with a horrid rainfall that, on my drive home, caused me to drift into the other lane a few times. I was traveling a good deal slower than the speed limit because of poor visibility and with the force of the wind blowing against me, it was a nail-biting ride.

And then the rain eased, and the wind began to abate. It was over — at least for another day.

While trying to formulate a response to the person with a Parkinson’s diagnosis, (don’t you remember those unsettling days?), I checked out the weather, which led me to the answer to his cry for help: Having this disease is like “living” the weather. Your doctor is the weather forecaster, but he can only make predictions because no one can foresee how your disease will progress or maybe even regress. Just as the weatherman can’t predict the next tornado or storm, your doctor can only give you an educated guess at what lies ahead.

You’ll probably have heard this one before: Each person’s experience with this disease is different. It’s true: the variations between symptoms, the severity of those symptoms, and the patient’s reactions to medications can be like night and day.

One day you may feel tossed about and nothing seems to help. At other times your meds kick in, and in 20 minutes, or an hour, a day, maybe even a week, you feel “normal” again — or as close to what you remember as normal. 

But there are other days, and thank God for the other days! Days of sunshine, playing with your grandchildren, working in your garden. Days of writing. Perhaps the reprieve lasts for mere hours or minutes, but you grasp every moment you can. Because — and I know you’ve heard this before — none of us are guaranteed today or tomorrow. And not because we have Parkinson’s, but because that is the nature of living. Parkinson’s is not a death sentence; it is an invitation to live your best now.

After the storm, there is calm. The trees have been stripped bare of their leaves by the fierce winds, and the neighbor’s trash cans have blown into your front yard. You stop to listen and realize that the wind no longer whistles as it passes your windowpanes.

It is still. You take a breath. You straighten things up and return the garbage cans that, thankfully, had been emptied before the storm hit. And you thank God the storm is over, if only for today.

***

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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Physical Activity, Coffee, Moderate Alcohol Consumption Protect Against Disease Progression, Study Reports

coffee, alcohol, lifestyle factors

Physical activity and participation in competitive sports, as well as coffee, caffeinated tea or moderate alcohol consumption before diagnosis, protect against worsening motor and cognitive function in Parkinson’s patients, according to a new population-based study.

In contrast, smoking and heavy alcohol consumption — or never consuming alcohol — correlated with higher risks of mortality and cognitive and motor decline.

The research, “The Association Between Lifestyle Factors and Parkinson’s Disease Progression and Mortality,” was published in the journal Movement Disorders.

Lifestyle factors such as coffee and moderate alcohol consumption, physical activity, and cigarette smoking have been linked with lower risk of Parkinson’s disease. Whether they affect disease progression remains undetermined, although small studies have shown that smoking and drinking coffee do not affect motor progression in Parkinson’s.

In turn, nonpaharmacologic approaches such as physical activity may benefit physical functioning, balance and gait, as well as protect against dementia.

Researchers at the UCLA Fielding School of Public Health and the David Geffen School of Medicine, in Los Angeles, California, assessed whether diverse lifestyle factors before a Parkinson’s diagnosis in adults affect motor progression, cognitive decline, and survival.

A total of 360 patients were enrolled within three years of diagnosis (average 2.1 years), as part of the population-based Parkinson’s Environment and Gene study in central California. The patients lived in one of three central California counties — Kern, Fresno or Tulare — and were followed from 2001 to 2016.

From the 252 patients not lost to follow-up (mean follow-up 5.3 years; 64 patients deceased, six were too ill, 17 withdrew, and 21 could not be contacted), 244 individuals — 139 men, mean age at diagnosis 66.9 years, mean duration of disease at baseline 2.1 years — provided data for analysis of disease progression.

The team also included 341 control participants from the same communities for analysis of mortality, who had been living in California for at least five years.

Telephone interviews were conducted to obtain self-reports of history of smoking, caffeinated coffee/tea or alcohol (beer, wine and liquor) consumption, overall physical activity level, and participation in competitive sports.

The participants were asked to report at what age they started and stopped drinking the beverages, as well as their average consumption per day during four age groups: 18-24, 25-44, 45-64, and 65 years or older.

Also, patients were asked about the average number of days per week and hours per day they participated in mild, moderate, or vigorous physical activity at the same age groups. Participation in competitive sports also was addressed, including basketball (20.6% of participants), baseball (18.1%), football (18.1%), track and field (12.5 %), and softball (8.3%).

Physical examinations were performed at each visit to assess motor function — Hoehn & Yahr (H&Y) stages — and cognition, with the Mini-Mental State Exam (MMSE). Cognitive decline was defined as a 4-point decrease from baseline MMSE examination.

In total, 209 patients (58%) and 67 controls (20%) died during follow-up. Fifty of the 244 patients (21%) assessed for progression experienced a 4-point or greater decline on the MMSE, while 77 (32%) progressed to H&Y stage 3 — transition from mild to moderate motor dysfunction, with loss of balance — or worse.

Coffee, caffeinated tea, moderate (below the median drinks per day), beer or liquor consumption, and participation in competitive sports were protective against mortality. In contrast, smoking and never drinking coffee or alcohol correlated with increased risk of mortality. Of note, the higher risk with smoking contrasts with prior studies showing protection against disease onset, the scientists noted.

In controls, alcohol and coffee consumption also were protective, while smoking conferred greater mortality risk.

The data further showed that engaging in competitive sports was associated with a history of head trauma in Parkinson’s patients, but not in controls. Head trauma also was linked with shorter time from diagnosis to death in this subset of patients.

Ever coffee consumption, participating in competitive sports and physical activity were protective against both motor function worsening and cognitive decline. Compared to moderate drinkers, patients who never drank liquor and those who drank more heavily were at greater risk for motor dysfunction. Also, never drinking and current cigarette smoking were associated with increased risk of cognitive decline.

Comparing patients who never drank coffee to those who have ever drank it, the findings also showed that never consuming coffee was associated with younger age at diagnosis (62.6 vs 67.6 years), longer disease duration at baseline (2.7 vs. 1.9 years) and less weekly alcohol consumption at some point (44% vs 69%).

“Although replication is needed,” researchers wrote, “our study suggests that multiple lifestyle factors potentially modify the rate of symptom progression.”

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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

river

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

protein

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 Parkinson.org, “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.

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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 Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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