Algorithm for Wearable Sensors Ably Measures Tremor Severity as Patients Go About Daily Life, Study Says

algorithm for tremor sensors

Researchers have developed algorithms that work with wearable sensors to continuously monitor tremor, and estimate total tremor, in Parkinson’s patients as they go about their daily routines.

Analyses of sensor results using one algorithm, in particular, were similar to an established test assessing tremor without being dependent on the time the test is given.

The study, “Wearable Sensors for Estimation of Parkinsonian Tremor Severity during Free Body Movements,” was published in Sensors.

Resting tremor, or the rhythmic shaking of muscles while relaxed, is among the motor symptoms of Parkinson’s disease (PD), and some patients also have active tremor, or shaking while engaged in voluntary muscle movement. Others motor symptoms are slowness of movement (bradykinesia), rigidity, and problems with posture, balance, and gait.

Currently, Parkinson’s motor symptoms are assessed using the Unified Parkinson’s Disease Rating Scale (UPDRS) Part III, scores of whose tests (like the finger-to-nose test) are evaluated by doctors. This test requires office visits where the tasks are performed, providing essentially only a snapshot of a person’s tremor experience in day-to-day life.

“A single, clinical examination in a doctor’s office often fails to capture a patient’s complete continuum of tremors in his or her routine daily life,” Behnaz Ghoraani, PhD, an assistant professor at Florida Atlantic University’s (FAU) Institute for Sensing and Embedded Network Systems (I-SENSE) and FAU’s Brain Institute (I-BRAIN), and lead author of the study, said in a press release.

“Wearable sensors, combined with machine-learning algorithms, can be used at home or elsewhere to estimate a patient’s severity rating of tremors based on the way that it manifests itself in movement patterns,” Ghoraani added.

Investigators developed two distinct machine-learning algorithms that, when combined with wearable sensors, could estimate total Parkinsonian tremor as patients performed a variety of free body movements.

In a collaboration between FAU, the Icahn School of Medicine at Mount Sinai and the University of Rochester Medical Center, researchers developed two algorithms: gradient tree boosting and long short-term memory (LSTM)-based deep learning. These tools can estimate tremor severity both in a resting and action state.  

A total of 24 Parkinson’s patients (10 women and 14 men; mean age, 58.9) had data on their movements recorded in two studies.

“In both protocols, the subjects stopped their medication the night before the experiment, and the experiment started in the morning. Yet, if the subjects were unable to withdraw their medication overnight, they came to the laboratory near the time of a scheduled dose of their PD medication,” the researchers noted.

For the experiment, doctors placed one motion sensor (consisting of a gyroscope and an accelerometer) on patients’ wrist and another on the ankle of the most disease-affected body side. Movement was recorded as they went about daily life activities.

Fifteen individuals were instructed to perform four rounds of specific activities, like walking, resting, eating, drinking, dressing, combing hair, putting groceries on a table, and cutting food. Motion data were recorded only while performing these activities.

Patients then took their routine “morning dose” of Parkinson’s medications. Later, they repeated the same activities at the start of every hour for up to four hours. For comparison purposes, standard UPDRS-based assessment were also given preformed every hour of the testing period before each round of daily life activities.

The other nine patients had their motion recorded continuously for the entire experiment. These people were instructed to cycle through six stations in a home-like setting, performing tasks like personal hygiene, dressing, eating, desk work, entertainment, and laundry. They took their medications after finishing a first round of activities, and when the treatment kicked in, they repeated the previous exercises. This set of activities lasted up to two hours, and the motor part of UPDRS (Part III) was assessed before and after the experiment.

“The data from the 15 subjects who performed rounds of specific [activities of daily living] was used to train the [artificial intelligence] models, and the data from the remaining nine subjects who performed continuous [daily life activities] were held out for testing the models,” the researchers wrote.

Results revealed the gradient tree boosting method estimated total tremor as well as resting tremor with high accuracy, and in most cases, with the same results found by doctors scoring UPDRS Part III.

Importantly, gradient tree boosting-based sensors were able to detect decreases in tremors after patients took their medication, even in cases where results did not match total tremor sub-scores from the UPDRS assessments. The LSTM-based algorithm was less effective in doing the same.

“These results indicate that our approach holds great promise in providing a full spectrum of the patients’ tremor from continuous monitoring of the subjects’ movement in their natural environment,” the researchers wrote.

“It is especially interesting that the method we developed successfully detected hand and leg tremors using only one sensor on the wrist and ankle, respectively,” said Murtadha Hssayeni, a study co-author and a PhD student at FAU’s Department of Computer and Electrical Engineering and Computer Science.

The new gradient tree boosting algorithm combined with wearable sensor technology resulted  “in the highest correlation … reported in the literature when using unconstrained body movements’ data,” the researchers wrote.

“This finding is important because our method is able to provide a better temporal resolution to estimate tremors to provide a measure of the full spectrum of tremor changes over time,” Ghoraani added.

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Do I Deserve a Pat on the Back for My 50th Column?

50th column

“Wow! Your 50th column. You should feel proud,” Neo exclaims over our shared breakfast ruminations. (Neo is my brain’s neocortex, which I’ve mentioned in previous columns.)

“Not really,” I reply without hesitating. “I feel humbled and awestruck. I have been writing about these topics for decades. To be given the honor of a column is a blessing, and I hope that I touch on issues that other people face.”

Neo pushes back a little, asking, “Don’t you think you deserve a pat on the back for all of your hard work?”

The concept of ego gratification pushes my emotional buttons. “A pat for what? I am merely following a calling and showing up well prepared. There’s no need for an ego massage.”

“That’s not what I mean,” Neo snaps back. “Your sister said the columns are very well written. They’ve helped her to feel better while dealing with her medical issues, and she looks forward to reading them each week. Other readers have said the same thing.”

Calmly, I reply, “I am very grateful for my readership, but their praise doesn’t dictate the writing. It can’t if the writing is to remain authentic to my life experiences.”

“So, you are going to let this 50th column pass by without a pat on the back?” Neo tersely asks. Receiving recognition for his achievements has been important to him since childhood. However, I know that the desire for praise can be a slippery slope. Facing and working through medical challenges and striving to establish a means of communication for fellow sufferers of Parkinson’s disease doesn’t fit well with such ego-driven goals.

Between sips of my morning juice, I counter, “It’s not about me. It has never been, nor should it be. It’s about the message of hope and crafting the best voice for sharing that message with all who wish to read it. Ego will only get in the way.”

Neo gazes out the window, sighs, and says, “So, you are going to do nothing then? Maybe you feel unworthy.”

I reply, “My worthiness is my own business and not subject to a culturally shaming guilt trip. This life owes me nothing; no entitlements or guarantees. I don’t write for expectations of rewards. Accolades come with feel-good attachments; like fame, they are illusory. Illusions cannot provide a sound foundation for authentic, hopeful writing.”

Neo, frustrated by my response, says, “I don’t get it. It’s normal to feel proud. It’s the 50th column you’ve written.”

I comfort him with a pat. “Normal has never been anything but a bell curve point for me,” I say. “No measure of normality can direct excellence or increase well-being. Pride is normal, but it is ego-driven, not guided by the message. Pride is defensive, superficial, quick to judge, and often built on a crumbling foundation of ignorance. It can’t direct my actions or thoughts.”

Neo responds, “I’m saying it’s OK to acknowledge your efforts. That isn’t false pride. It’s OK to show a little self-kindness. You deal with a lot of issues in your life, much of it medical or related to how you deal with symptoms. You have additional challenges with accessing medical care, disease progression, and family and friends who don’t always understand what is going on or can’t show the level of support you need at the moment. They don’t know how difficult it is to wake up every morning and try to keep going despite the setbacks. What they see is the result of all of your efforts. They notice how good you look and not what it takes every day to travel the path.”

He is right in his assertion that I can be too hard on myself sometimes. One thing that I’m proud of is my persistence in continually showing up well prepared, day after day, year after year. And for those days when either Parkinson’s or my vision causes my life to be upended or adjusted at a moment’s notice, I work through it the best I can and hope the next day will be a little better. If I can share any measure of hope through my experiences, or a sense of a shared community, then that is the best reward I can ever receive.

Neo agrees, “Yeah! That deserves a pat on the back.”


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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U.S. Defense Department Funds Research Into Parkinson’s and Exercise

The U.S. Defense Department has awarded researchers from Northeast Ohio Medical University (NOMU) and Michigan State University (MSU) about $1 million each to study the effect of exercise at different stages of Parkinson’s disease.

The three-year grant went to longtime collaborators Sheila Fleming, PhD, an assistant professor of pharmaceutical sciences at NOMU and Caryl Sortwell, PhD, a translational neuroscience professor at MSU.

“It’s a major award for both of us,” Fleming said in a news release. “We had been working together for many years because our interest and work are very complementary. Ultimately, it’s about a $2-million grant. She gets half and I get half.”

Fleming, who was awarded $954,566 by the U.S. Army Medical Research Acquisition Activity, said she will work on behavioral aspects of the study while Sortwell will handle pathological events.

The project, titled “Exercise Effects on Synuclein Aggregation, Neuroinflammation and Neurodegeneration,” will analyze the impact of exercise in an optimized preclinical disease model. That will include examining mechanisms associated with the central characterization of Parkinson’s — the buildup of toxic alpha-synuclein aggregates, neuroinflammation, and expression of certain molecules in the brain called trophic factors.

Using a progressive Parkinson’s disease animal model, Sortwell is charting the course and development over time of pathological events in the brain. Fleming is examining how the pathological occurrences relate to changes in motor and non-motor symptoms. Together, the researchers are examining the impact of introducing exercise at different stages of Parkinson’s progression.

Most scientists studying exercise in Parkinson’s have used what are called toxin models, which solely target the dopamine system, Fleming said. The chemical dopamine acts as a neurotransmitter and is essential in sending messages from the brain to direct muscle movement and coordination. As more dopamine-producing neurons die, dopamine levels slowly and progressively decrease until patients are unable to control normal movements.

But those models have issues related to reproducibility and a lack of understanding of the biological properties of alpha-synuclein pathology. Fleming and Sortwell are using a newer model supported by the Michael J. Fox Foundation called PFF — for pre-formed synthetic fibrils — to elucidate mechanisms of alpha-synuclein-induced pathology. In this model, fibrils are injected into animals, and researchers track the appearance of symptoms.

Studies have already shown the likelihood that alpha-synuclein clumping begins in the back of the brain and proceeds to the front, a pathology that may be related to non-motor Parkinson’s symptoms such as depression, anxiety, reduced sense of smell, and cognitive impairment.

Fleming and Sortwell will look at the effect of exercise on both non-motor and motor symptoms (such as problems walking) to determine what symptoms manifest and in what order. This information could lead to earlier diagnoses, and provide a non-pharmacological, low-cost therapeutic strategy for patients, including veterans.

Currently, Fleming said, by the time individuals first seek help for symptoms, they have typically already lost at least half their dopamine neurons.

“Slowing the progression of the disease could have a huge benefit, especially since patients aren’t usually diagnosed until between 50 and 60 years of age,” she said. “So, if you could slow it, that could have a potentially huge impact on the quality of life of patients.”

The scientists presented their project in October at the annual meeting of the Society for Neuroscience.

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Brain Circuit That Works to Control Impulsivity Identified in Rats, Study Suggests

impulsivity and Parkinson's

A particular signaling protein in the brain, called melanin-concentrating hormone (MCH), was seen to help regulate impulse control in rats, a study reports.

This finding may have implications for disorders where impulse behaviors manifest, from binge eating and drug addiction to Parkinson’s disease.

The study, “Hypothalamus-hippocampus circuitry regulates impulsivity via melanin-concentrating hormone,” was published in Nature Communications.

Impulsive behaviors are those done without thought to the long-term consequences. Such behaviors play obvious roles in diseases like addiction, and they often become dysregulated in conditions like Parkinson’s.

“We discovered the brain connections that keep impulsivity in check,” Scott Kanoski, MS, PhD, a study co-author and a professor at the University of Southern California, said in a press release. “The key to this system is a neuropeptide that we’ve been focusing on, melanin-concentrating hormone, in studies on appetite and eating.”

Researchers trained rats to press a lever in order to get a treat — a high-sugar, high-fat delicacy that Kanoski compared to a “little donut hole.” But there was a catch: the rats wouldn’t get the treat until 20 seconds after they had pressed the lever, and every time they pressed the lever, the countdown restarted.

This works as a test for impulsivity because more impulsive rats would be expected to hit the lever more frequently — even though it meant getting fewer treats in the end.

Melanin-concentrating hormone (MCH) is signaled by brain cells in the hypothalamus, an area of the brain that produces hormones which control several functions, such as body temperature, sex drive, and hunger.

The researchers found that, when they increased MCH signaling in the rats’ brains (via a variety of techniques, including injecting MCH and using viruses to genetically modify MCH-producing neurons), the rats hit the levers more frequently — again, indicating increased impulsivity.

Researchers then gave the rats a choice between two levers: one with the same 20-second delay per one treat, the other with a longer delay (30 to 45 seconds) that gave five treats. The rats with increased MCH signaling pressed the 20-second delay levers more often, suggesting an increase in delay discounting — that is, they wanted the reward sooner, even if waiting would mean a larger overall reward. Again, this is indicative of high impulsivity levels.

These experiments suggested that other behaviors could also be affected. For instance, the team wondered if increased MCH signaling made the rats more hungry for these particular treats. But when the researchers gave the rats free access to treats, they ate the same amount regardless of whether they had increased MCH signaling or not, discrediting this idea.

It is also conceivable that MCH helped regulate the rats’ internal clocks, making it harder for them to keep track of how long it had been since they last pressed the lever. But again, experiments that examined the rats’ ability to do other time-related tasks showed no differences.

Rats with increased MCH signaling also didn’t exhibit any difference in the frequency with which they hit levers that weren’t linked to a reward, suggesting that the observed difference in behavior wasn’t due to general hyperactivity.

By ruling out these other possible explanations, the researchers concluded that the change in behavior was specifically due to differences in impulse control.

These scientists then went the other way, decreasing MCH signaling using a technique called RNA interference, which ultimately blocks gene expression: the process by which information in a gene is synthesized to create a working product, like a protein.

They expected that this would have the opposite effect. But, interestingly, rats with lesser MCH signaling also hit the levers more frequently in the original task — these rats were more impulsive, too.

Additional tests and brain imaging scans suggested that most MCH signaling starts in a brain region called the ventral hypothalamus and ends up in the nucleus accumbens, both of which are associated with hunger and reward responses. The precise circuitry is still being worked out and will require future studies to fully understand.

“Surprisingly, our results [in the above experiment] showed that animals behaved more impulsively when MCHR1 [MCH receptor 1] levels were knocked down in the vHP [ventral hypothalamus], indicating an increase of impulsivity when vHP MCHR1 tone is perturbed in either direction,” the researchers wrote.

And, they added, “our results show that MCH signaling in the vHP increases impulsive responding and impulsive choice for a palatable food reinforcer but has no effect on food-motivated responding, locomotor activity, or clock speed timing. We conclude that the projection pathway from MCH neurons … to the vHP plays a role in mediating impulsivity.”

Emily Noble, MS, PhD, a professor at the University of Georgia and study co-author, noted that fully understanding how this signaling works may pave the way for future therapies for impulsivity-related diseases.

“We are not quite in a place where we can target therapeutics to specific brain regions yet,” Noble said, “but I think that day will come.”

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