Mission Impossible: Getting Dressed

clothes, dressing

“Your mission, should you choose to accept it … This tape will self-destruct in 10 seconds.” Mission: Impossible (TV series).

What is my problem?

At times, putting on my clothes in the morning can be an impossible mission. This is one of the unseen symptoms that some people with Parkinson’s may deal with on a daily basis. Although it is merely a nuisance at this point, feeling like a 4-year-old learning how to dress gets a little old after a while.

Since this is one of the more absurd Parkinson’s symptoms with which I am afflicted, I have to laugh at myself. I had a chuckle at a photo of me trying to put on a sports bra.

Pulling the garment over my head causes me to get “stuck” sometimes, so I bought a sports bra with a front closure. Well, that was not such a good solution. After much difficulty, I finally found the openings to slip my arms through. However, once I had accomplished that, I couldn’t fasten the front zipper and hook. I am now back to the “pull over my head style,” and hope I don’t get stuck for too long.

Columnist photo; Dressing, clothes
Struggling. (Photo by Lisa Bjelland)

It’s not just sports bras …

On more than one occasion, I have put my pants on backward or my sweater on inside out. It takes me forever to get dressed in the first place. Now when I don’t dress properly, I have to take the garment off and start all over again — adding another five minutes to the process. Sometimes it takes me almost 15 minutes just to get dressed in the morning.

Somedays I look at one of my shawl-collar cardigans and can’t figure out how to put it on or hang it up. Sometimes, my Parkinson’s symptoms of bradykinesia and loss of cognitive skills team up to thwart my efforts. When this happens, getting dressed can take me over 10 minutes, frustrate the heck out of me, and require my entire focus. Something I have done in less than a minute for over 60 years without a second thought can now overwhelm me.

I try to exercise every morning, so most days I wear tights or spandex leggings. These do not go on easily, and inevitably, my left foot freezes and gets stuck. Forget about it when I have to take them off to use the bathroom. It feels like I am trying to remove shrink-wrap from a package with no scissors to cut it, and I end up tripping over my own feet in a hurry to get to the bathroom in time. No more waiting for the last minute. Now, I must plan when to use the bathroom so that I allow myself enough time to peel off the tights.

One time I put my underwear on inside out, and when I told my friend who also has Parkinson’s, she laughed and said when that happens to her she leaves them that way. I am getting to that point now.

dressing, clothes
Stuck in a sports bra. (Photo by Lisa Bjelland)

What can I do about it?

For people with Parkinson’s, activities of daily living can become very frustrating. Here is a list of helpful tips that have eased my stress levels so that I don’t self-destruct when I am getting dressed. Keeping a sense of humor helps, too. 😊

So if you see me with my shirt on inside out and my pants on backward, you don’t need to comment. However, know that I am probably not having a good day.

To adapt a Heidi Rader quote: “I am a Parkinson’s warrior. I fight an ugly war inside my body every single day. I may not win this battle, but I will not go down without a fight!” 


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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Here’s a Primer on Common Parkinson’s Terms and Abbreviations

When you are new to something, it’s common to feel disconnected or out of place — especially when it comes to understanding the language. At church, newcomers may hear words that don’t make any sense. “Churchy” people (including me) tend to throw around big words.

It also occurs with abbreviations. I’ve seen it happen in the Parkinson’s community. It isn’t intentional, but it happens. Someone might read a post with the abbreviation “PWP” and ask, “What is PWP?” Some might even add an apology of sorts: “Sorry, I’m not very smart.”

Big words

Following is a list of common words and definitions that may be unfamiliar to a Parkinson’s newbie:

  • Akinesia: Inability to move spontaneously; loss of voluntary movement.
  • Ataxia: Impaired balance, coordination, and muscle control.
  • Bradykinesia: Slowed movement.
  • Carbidopa-levodopa: Medication used to relieve Parkinson’s disease symptoms.
  • Dopamine: Acts as one of the brain’s messengers to signal movement and maintain balance and coordination.
  • Rigidity: Muscle stiffness and resistance to movement.
  • Postural instability: A term with big words referring to balance issues.
  • Dyskinesia: Abnormal, involuntary movements.
  • Micrographia: Small, cramped, often illegible handwriting.
  • Facial masking: Facial muscles become immobilized, giving the patient a mask-like expression.

Did you know all those words and their meanings when Parkinson’s first arrived at your door? I know I felt out of place when someone would use “dyskinesia” to describe actor Michael J. Fox’s symptoms. It can be awkward when you don’t know.


The same is true when we throw around abbreviations such as:

  • DBS: Deep brain stimulation.
  • PD: Parkinson’s disease.
  • MDS: Movement disorder specialist, a neurologist who has training specific to Parkinson’s and other movement disorders.
  • PWP: Person (or people) with Parkinson’s disease.

Those may seem second nature to us, but not to someone who was just diagnosed.

The same holds true for the Michael J. Fox Foundation (MJFF), American Parkinson Disease Association (APDA), Parkinson’s Foundation (PF), and more. We tend to abbreviate them, forgetting that the majority of people don’t know what Parkinson’s disease is, let alone the abbreviations of its foundational and organizational names.

Keep it simple

We don’t need to dumb things down, we just need to keep them simple. Starting with the PWP who might be considering DBS as suggested by an MDS and are searching for information from the MJFF to help them understand.

That’s all.


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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PKG Wristwatch Device May Improve Clinical Decision-Making in Parkinson’s, Study Shows

PKG wearable monitoring device

A wrist-worn medical device — called the Personal KinetiGraph or PKG — that reminds people with Parkinson’s disease to take their medication, and records their movements to provide physicians with objective measurements of motor symptoms, showed great promise as a tool to improve clinical decision-making, a study found.

When worn for six days before a routine care visit, the device reported disease-related motor symptoms, like dyskinesiainvoluntary muscle movement — and bradykinesia, or the progressive slowness of movement over time, even when patients did not report such symptoms.

Overall, the device provided information for better treatment plans, allowed doctors to assess the efficacy of treatments, and improved doctor-patient communication.

The findings were reported in “PKG Movement Recording System Use Shows Promise in Routine Clinical Care of Patients With Parkinson’s Disease,” a study published in the journal Frontiers in Neurology.

The focus of Parkinson’s disease treatment is the relief, through medication, of symptoms like slow movements, rigidity, and tremor. However, such treatment regimens rely on patient self-reported symptoms, which often can be unreliable, even with validated assessments such as the Unified Parkinson’s Disease Rating Scale (UPDRS).

In addition, patients tend to do better during their appointments and clinical examination than at home.

The lack of objective data complicates treatment recommendations.

To overcome these problems, Global Kinetics Corporation (GKC) developed PKG, a watch-like device that objectively records movements and reminds patients to take their medication. The device was cleared for use by the U.S. Food and Drug Administration in September 2016. It weighs 35 grams, and is programmed and dispensed by clinical staff and worn by the patient for 6–10 full days.

The PGK uses accelerometers to monitor movement and a proprietary mathematical algorithm to convert the raw movement data into a PKG report — a graphical illustration of the patient’s movement that the clinician can analyze. That report provides “scores representative of dyskinesia and bradykinesia, compared to controls, throughout the day and from day to day,” the device’s website says.

To evaluate the clinical utility of the PKG, physicians at the University of California, Irvine (UCI) and University of California, Los Angeles (UCLA) now conducted a single-arm, open-label, observational study. The study included 63 people with Parkinson’s, ages between 46 and 83 years, who were responsive to dopaminergic therapy. In total, the patients had 85 routine care visits.

The main goal was to determine how often symptoms reported by patients disagreed with those in the PKG report. Secondary measures included the number of times the PKG report had findings that were treatable, how often doctors changed treatment based on the PKG report and how the report impacted patient care. Patients and caregivers’ satisfaction with the device also was measured.

The study’s participants wore the PKG for six continuous days before their appointments. Physicians then discussed symptoms with their patients and conducted a motor examination prior to uploading and reviewing the PKG report.

The team found that the PKG report demonstrated the presence of symptoms not reported by patients in 35% of the visits. Among these symptoms, bradykinesia was the most common finding of the PKG not picked up by the patient (50% of cases), followed by dyskinesia (33%). In contrast, 24% of patients reported a symptom that did not appear in the PKG report.

Regarding treatable symptoms, the device identified those individuals who could benefit from increases in levodopa doses or other treatments, including 47% of those with bradykinesia and 44% of those with dyskinesia.

In total, the report provided insights used to change treatment plans in 79% of participants, improved dialogue with the patient in 59% of visits, improved the ability to measure treatment impact in 38% of visits, and improved motor assessment in 33% of visits.

When surveyed at the end of the study, 82% of the participants agreed or strongly agreed that the PKG was easy to learn, easy to use, enabled them to confirm medication administration, and performed as expected. These patients said they would use the device again. In 39% of responses, participants also reported a very valuable impact on their care.

A 75-year-old women included in the trial “had difficulty reporting when she was off [when levodova effects wear out] and when she was dyskinetic,” the researchers said. “The PKG identified off times in the [morning] and dyskinesias in the afternoon. Based on the PKG data her regimen of carbidopa/levodopa dose was adjusted and her symptoms markedly improved.”

The researchers noted that the study was limited by the small number of patients. However, they said the results showed the usefulness of the new medical device.

“The PKG system provided clinical utility through improved characterization of motor manifestations of Parkinson’s disease, both the type and timing. This served to improve physician-patient dialogue and provide insight to clinicians and patients to inform treatment impact and decisions,” the team concluded.

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Impaired Backward Walking Linked to Motor Symptoms, Fear of Falling in Early Parkinson’s, Korean Study Suggests

backward walking

Backward walking is significantly impaired and associated with motor symptoms and fear of falling in newly diagnosed Parkinson’s patients, a small Korean study suggests.

These results point to backward walking parameters as potential biomarkers of Parkinson’s disease progression. The researchers called for future studies investigating the dynamics of backward walking in people with Parkinson’s, and its link to falls.

The study, “Backward Gait is Associated with Motor Symptoms and Fear of Falling in Patients with De Novo Parkinson’s Disease,” was published in the Journal of Clinical Neurology.

People with Parkinson’s are at a significant risk of falls due to gait (walking) and balance problems. Specifically, these patients show increased stride-to-stride variability and take shorter and slower steps.

While most gait studies in people with Parkinson’s have focused on walking forward, backward gait has been suggested to be even more impaired in these patients. It’s also been associated with freezing of gait, defined as not being able to start stepping forward, with no apparent cause.

Several studies have also shown that people with Parkinson’s have considerably more difficulties in walking while performing a secondary cognitive task, known as dual-task gait. Dual-tasking measures an individual’s ability to carry out a cognitive task — such as counting, or naming words that start with a particular letter — while engaging in a motor skill like walking.

However, since changes in walking parameters are closely associated with the progression of motor symptoms, most of what is known about walking difficulties in Parkinson’s patients comes from studies preformed in people at advanced stages of the disease.

Thus, understanding gait dynamics and difficulties in early-stage Parkinson’s disease remains largely unknown.

Now, a team of Korean researchers set out to determine which type of gait — forward, backward, or dual-task — was more strongly associated with motor symptoms or the risk of falling in people with de novo Parkinson’s disease, meaning they are newly diagnosed and still untreated.

The study involved 24 individuals with de novo Parkinson’s — 13 men and nine women, who had the disease for less than five years, were between 50 and 75 years old, and were able to perform various types of gaits. An additional 27 unaffected people, including 16 men and 11 women, were used as controls.

Clinical data for all participants was measured through several tests and scales, including the Korean version of the Montreal Cognitive Assessment, the Fear of Falling Measure (FFM) — a rating scale in which lower scores indicate greater fear of falling — and the Unified Parkinson’s Disease Rating Scale part II and III, which assesses motor symptoms.

The participants’ gait parameters were analyzed using the computerized GAITRite system with a 4.6-meters (16 foot) long, pressure-sensitive walkway mat. Each type of gait was tested 10 times while walking at a comfortable speed. Dual-task gait consisted of walking while subtracting serial sevens.

Results showed that de novo Parkinson’s patients had a slower walking speed and shorter stride in all three gaits, compared with unaffected people. However, backward gait showed the highest stride-to-stride variability in both stride time and length.

Dual-task gait also showed significant variability in stride length between the two groups of participants, while forward gait showed no significant differences.

When looking at the potential associations between gait speed, motor symptoms, and fear of falling in these patients, the team found that reduced backward gait speed was significantly associated with a wider range of motor symptoms. These included walking difficulties, bradykinesia (difficulty in body movement), postural instability, and total motor score. These individuals also had an increased fear of falling.

Reduced dual-task gait speed was specifically linked to worse bradykinesia and total motor score, while reduced forward gait speed was associated with reduced tremor score. That was consistent with previous studies suggesting that reduced gait speed is “more pronounced in non-tremor-dominant [Parkinson’s] patients,” the researchers said. None of these gaits’ speeds were associated with fear of falling.

“These results indicate that slow walking with a short stride is a clear feature of de novo PD regardless of the gait task being performed, and the earliest alterations of gait variability may first become apparent in [backward gait], followed by [dual-task gait] and then [forward gait],” the researchers said.

The team added that these findings suggest that backward walking speed is more strongly associated with the risk of falling and is “a potential surrogate marker for the progression of motor symptoms or gait impairment in PD.”

Future studies are required to confirm and better understand the association of backward gait and motor symptoms and to investigate the clinical relevance of stride-to-stride variability in the different types of gaits, the researchers said. They also called for additional studies into the link between backward walking and falls in people with Parkinson’s disease.

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Grants Will Establish Exercise Program for Parkinson’s Patients in Arkansas

exercise program

Grants totaling nearly $29,000 will enable the University of Arkansas for Medical Sciences (UAMS)  to establish a free exercise program for patients with Parkinson’s disease and Parkinson’s-like symptoms.

Some $13,924 from the Parkinson’s Foundation will go toward program staffing, training and other support. A $15,000 grant from the Philip R. Jonsson Foundation will pay for equipment. Classes start Aug. 20.

Designed to enhance patients’ overall quality of life, the program’s regimen will emphasize strength maintenance, balance improvement, and cognitive and social engagement.

“Treating Parkinson’s disease involves treating the whole person, and that means going beyond what we can accomplish during a clinical visit,” Rohit Dhall, MD, said in a press release. Dhall is director of neurodegenerative disorders in the UAMS department of neurology. “I am so happy that the central Arkansas Parkinson’s community will be able to benefit from this evidence-based, high-quality exercise program — all free of charge.”

Fitness instructors will receive Parkinson Wellness Recovery (PWR!) certification in PWR!Moves group and circuit class formats. The funding also will enable a physical therapist specializing in Parkinson’s disease to receive certification in research-based exercise approaches and task-specific training routines.

PWR!Moves is a Parkinson’s-specific skill-training program aimed at maintaining or restoring skills that deteriorate and interfere with everyday movements. Specifically, the program targets antigravity extension, weight shifting, axial mobility and transitions. The regimen aims to counteract Parkinson’s symptoms such as rigidity, bradykinesia (slowness of movement), lack of coordination, and loss of motor automaticity.

In the group class, patients will learn how to offset Parkinson’s symptoms and move “bigger and faster” during daily life. The course is designed to be fun and supportive, but physically and cognitively challenging.

The circuit will incorporate PWR!Moves into athletics, fitness and conventional gym activities such as coordination, strength, balance, agility, and flexibility training. Using different exercise stations — each with a specific focus — patients will work alone or with partners.

While each participant will receive personalized input regarding needs and goals, the program is crafted to benefit patients regardless of fitness and symptom levels. For instance, a new Solo-Step overhead track and harness system — in which a torso harness attaches to a room-length ceiling track — allows patients with concerns about balance or strength to exercise safely. Other grant-funded equipment will help participants with functions such as walking on uneven surfaces.

“Our approach combines the best of an individualized exercise experience with the social nature of group exercise,” said Chris Oholendt, program manager for UAMS outpatient physical therapy/occupational therapy. “We are thrilled to provide people with Parkinson’s and their care partners this unique program that will change the way they live with PD for the better.”

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Coupling of Brain Electrical Signals May Be Parkinson’s Biomarker, Way to Improve Deep Brain Stimulation, Study Suggests

cross-frequency coupling electrical signals

The coupling of electrical signals in the brain — as it responds to levodopa and is associated with motor improvements — may provide ways to better assess the clinical state of people with Parkinson’s disease, and improve the efficacy of deep brain stimulation (DBS), according to new research.

The researchers say coupling patterns may enable broader insight into Parkinson’s, and have potential use as a biomarker.

The study, “Distinct subthalamic coupling in the ON state describes motor performance in Parkinson’s disease,” appeared in the journal Movement Disorders.

The human brain displays repetitive patterns of neural activity, or electrical pulses, due to the communication between brain nerve cells (neurons). These are called brainwaves.

Measuring a type of electrical pulses called local field potentials (LFPs) from the subthalamic nucleus (STN) — a brain region hyperactive in Parkinson’s patients — has shown the existence of frequency bands, or wave oscillations, that correlate with motor impairment and respond to medication.

The interactions between high- and low-frequency brain waves — cross-frequency coupling — also has been increasingly studied. This is particularly evident in unmedicated patients. Yet, what these interactions mean is still scarcely understood.

A team at the University of Houston addressed how these bands are changed by medication, as well as their coupling, via a 24-hour monitoring period that included three trials. Those trials involved nine people (seven men, ages 39-70 years) with idiopathic Parkinson’s, meaning the disease with no known cause. The participants underwent local field potential recording three weeks after deep brain stimulation of the subthalamic nucleus. The recordings were then correlated with motor improvements over three treatment cycles.

Clinical and behavioral assessments were made within 30 minutes prior to taking levodopa, which controls Parkinson’s symptoms. Similar evaluations were then done within 30 minutes after the participants said they felt the medication kicking in, in terms of motor function (verbal on state).

Specifically, the clinicians used the Unified Parkinson’s Disease Rating Scale to assess numerous symptoms: hand and foot tremors (item 20); upper and lower extremity rigidity (item 22); and finger tapping, hand open and close, hand pronation and supination — which means flipping the palm face up or face down — and leg agility (items 23–26).

A computer-based task also was used, with a keyboard. Participants had to press the left and right arrow keys sequentially and as fast as possible, for 30 seconds, using the index and middle fingers. The total number of keypresses was then analyzed.

The results showed that bradykinesia — slowness of movement — and keyboard scores differed between “off” and “on” states, meaning the periods before and after taking levodopa and regaining motor control. However, these responses did not correlate in all patients. Two patients showed eased bradykinesia yet minimal-to-no improvement in the performance of the keyboard task.

The data also showed distinct peaks across different bands. In the off state, the activity of low-beta (13-22Hz) and high-frequency oscillations (200-300Hz) was higher than normal. It was either suppressed, or shifted to a different frequency, after taking levodopa. Among other findings, six patients also showed a peak in the gamma range (50–200 Hz).

The investigators also found that, in the off state, the amplitude or signal strength of high-frequency oscillations was coupled with a specific parameter — called phase — of low-beta bands in all participants.

After the transition to the on state, this coupling shifted to a different subset of beta bands (22-30Hz) and high-frequency oscillations (300-400Hz). It also was linked with more pronounced improvements in the keyboard task scores. Only two patients failed to show this coupling after taking levodopa. That could be due to suboptimal dose, the team said.

Overall, the findings show that cross frequency coupling also exists in treated patients. “So in effect we have ‘cleared coupling’s name’ and showed the frequencies involved in coupling impacts whether its effects are negative or positive,” Musa Ozturk, the study’s lead author, said in a press release.

“Together with the differences in the ON-state coupling according to the degree of motor improvement, our observations suggest that [cross-frequency coupling] patterns provide a broader insight into [Parkinson’s], and have potential utility as a biomarker for the clinical state of patients,” the researchers said.

One potential application is deep brain stimulation.

“We can now make the closed-loop stimulator adaptive to sense a patient’s symptoms, so it can make the adjustments to the fluctuations in real time, and the patient no longer has to wait for weeks or months until the doctor can adjust the device,” said Nuri Ince, PhD, the study’s senior author.

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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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Encephalitis Symptoms Masked as Worsening Parkinson’s Disease, Case Report Shows

encephalitis case report

Parkinson’s disease can sometimes mask the symptoms of other neurological disorders, according to a case report.

The report, titled “NMDAR encephalitis presenting as akinesia in a patient with Parkinson disease,” documents the case of a 71-year-old woman who was eventually diagnosed with encephalitis, the symptoms of which were first thought to be caused by a worsening of her Parkinson’s.

It was published in the Journal of Neuroimmunology.

The patient, who had a two-year history of Parkinson’s, had initially experienced some difficulty moving her left arm, a condition called bradykinesia, but was generally responding well to levodopa, a mainstay of Parkinson’s treatment.

Then, at the end of 2017, her symptoms started to worsen. Her bradykinesia increased to the point that she was unable to move her arm at all, defined as akinesia. In April 2018, she was admitted to a hospital due to difficulty moving and swallowing.

She stopped responding to levodopa treatment, and her condition continued to decline. She eventually became unresponsive; the authors described her state as being nearly catatonic.

Because the disease was continuing to progress and wasn’t responding to treatment, the doctors decided to examine her cerebrospinal fluid, the liquid that surrounds the brain and spinal cord.

After taking a sample of the patient’s cerebrospinal fluid and running a series of tests, they found antibodies against N-methyl-D-aspartate receptor (NMDAR). These antibodies are a hallmark of encephalitis, which occurs when there is inflammation in the brain — essentially, the body’s immune system attacks cells in or near the nervous system, which is not conducive to proper neurological function.

Typically, encephalitis presents as a severe disease with rapidly worsening symptoms. In this particular case, this was still true — but because the patient had Parkinson’s, which shares some similar symptoms, she was believed to be experiencing worsening Parkinson’s, and not an altogether separate disease.

“Our case should alert neurologists that NMDAR-E [encephalitis associated with antibodies against NMDAR] onset in PD [Parkinson’s] patients could manifest mainly as worsening of PD,” the researchers wrote.

After the correct diagnosis was made, appropriate treatment was swiftly given, and the patient responded well. She gradually regained her function and had completely recovered within three months, her symptoms returning to just bradykinesia of her left arm.

As is often the case in acute encephalitis, the patient has no memory of what occurred during the worst parts of the disease.

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Benefits of Exercise for Parkinson’s Patients Linked to Increased Dopamine Release, Study Suggests

exercise and Parkinson's

Engaging in regular exercise can help preserve the motor and non-motor function of Parkinson’s disease patients, most likely as a result of an increased release of dopamine in the brain, a small study suggests.

The study, “Habitual Exercisers Versus Sedentary Subjects With Parkinson’s Disease: Multimodal PET and fMRI Study,” was published in the journal Movement Disorders.

Exercise has been shown to ease both motor and non-motor symptoms of Parkinson’s disease, including bradykinesia (slowness of movement) and balance, as well as cognition and mood.

While the mechanisms underlying these benefits are largely unknown, researchers hypothesize that exercise may enhance dopamine release. The progressive degeneration and death of nerve cells in the brain that produce dopamine, called dopaminergic neurons, is one of the underlying causes of Parkinson’s disease.

In this study, researchers investigated how dopamine release and other clinical features of Parkinson’s disease differ between patients who exercise and those who remain sedentary.

A total of 17 patients with mild to moderate Parkinson’s disease were recruited, eight of whom engaged in regular exercise at least three times a week for more than three hours total, while nine were sedentary.

All patients underwent two positron emission tomography (PET) scans, one before and one after exercising on a stationary cycle, to determine whether exercise affects the release of natural dopamine in the dorsal striatum — a region of the brain involved in the control of movement. PET scans were performed after overnight withdrawal from dopaminergic medication.

Additionally, participants underwent functional magnetic resonance imaging (MRI) of the brain during a monetary reward task that required randomly selecting one of four cards.

“Subjects were explicitly informed about the probability of obtaining a monetary reward ($0.50) for selecting a winning card during each block. Subjects were also instructed that the task was purely chance (analogous to a slot machine), and there was no pattern to learn that could improve odds,” the researchers wrote.

However, for each selected card, subjects were provided visual (happy or sad face) and auditory (cheers or sighs) feedback, which could alter the card selection process, even though the success of each trial was by chance.

This test allowed researchers to evaluate possible behavioral differences in card selection between groups. Specifically, researchers measured the response of the brain’s ventral striatum, a region involved in the evaluation of rewards.

Participants also completed other tests to evaluate motor and non-motor function, including the Beck Depression Inventory to assess depression and the Starkstein Apathy Scale to measure apathy.

Results showed that habitual exercisers had an increased release of dopamine compared with sedentary patients. They also had greater activation of ventral striatum during the MRI reward task. Their apathy and bradykinesia scores were also lower than sedentary patients.

These results suggest that exercise is associated with improved motor and non-motor functions in Parkinson’s patients, which is likely linked to exercise-enhanced dopamine release.

“Although it appears that exercise plays a role in the clinical outcome of subjects with PD, future randomized control trials are needed to determine the cause-effect relationship between exercise and enhanced DA [dopamine] release, response to anticipation of reward, and clinical outcomes,” the researchers wrote.

“Future studies should also investigate other potential mechanisms of benefit from exercise,” they added.

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Specific Area of Brain Involved in Motor Issues, Slow Thinking in Parkinson’s, Mouse Study Shows

area of brain

Nerve cell damage in a specific area of the brain impairs motor function and slows thought, both of which are symptoms of Parkinson’s disease, a mouse study finds.

The study, “Loss of glutamate signaling from the thalamus to dorsal striatum impairs motor function and slows the execution of learned behaviors,” was published in NPJ Parkinson’s Disease.

Parkinson’s disease is caused by the progressive loss of brain nerve cells — in particular, those that produce dopamine, a molecule essential for nerve cell communication — as well as the abnormal accumulation of alpha-synuclein-containing Lewy bodies that induce nerve cell damage.

While a hallmark of Parkinson’s disease is the loss of dopamine-producing nerve cells in a brain area called the substantia nigra, known to be involved in motor function, increasing evidence shows that other areas of the brain are also impacted both at Parkinson’s onset and throughout the course of the disease.

Nerve cells in the substantia nigra send dopamine signals to the dorsal striatum, a region of the brain also involved in the control of movement. The loss of dopamine signaling in Parkinson’s disease leads to dorsal striatum dysfunction and to the motor problems seen in Parkinson’s patients.

However, the dorsal striatum also receives signals from other areas of the brain, such as the thalamus, which relays motor signals to the dorsal striatum through glutamate, another signaling molecule. The thalamus is also known to play a crucial role in memory, executive function, and attention.

Several studies have reported that Parkinson’s patients present with Lewy bodies, loss of nerve cells, and changes in the structure and activity of the thalamus.

These data suggest that nerve cell damage in the thalamus may be involved in the development of Parkinson’s symptoms.

Researchers have now evaluated whether the disruption of glutamate-dependent thalamus signaling to the dorsal striatum results in the cognitive and motor deficits characteristic of Parkinson’s.

The team generated genetically modified mice that allowed the induction of loss of glutamate signaling specifically between the thalamus and the dorsal striatum. A battery of motor and behavioral tests were performed in these mice to assess motor function, visuospatial function, executive function, attention, and working memory.

Modified mice showed significant motor coordination deficits, compared with healthy mice, suggesting that impaired thalamus-dorsal striatum signaling is involved in motor deficits.

In addition, while the disruption of thalamus-dorsal striatum signaling did not result in an apparent cognitive impairment, these mice took longer to process cues and new environments and were slower at carrying out tasks than healthy mice.

These results suggest that the loss of glutamate signaling between the thalamus and dorsal striatum led to slower processing reaction times, which resemble “bradyphrenia, the slowness of thought that is often seen in patients with PD and other neurological disorders,” the researchers wrote.

Slow thought can cause bradykinesia — slowness of movements or difficulty moving the body quickly on demand — which is also a symptom of Parkinson’s.

The team noted that the results highlight the involvement of glutamate-producing nerve cells in the thalamus that signal to the dorsal striatum in behaviors of mice that resemble slowness of thought and movement, indicating that the loss of function of these cells contribute to cognitive and motor deficits in Parkinson’s disease.

This may explain why some of the Parkinson’s therapies that target dopamine signaling have limited therapeutic effects in terms of patients’ cognitive function.

The researchers added that new therapies acting on other communication molecules besides dopamine are needed to target cognitive symptoms, and that their genetically modified mice may serve as a model to test those approaches.

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Source: Parkinson's News Today