Parkinson’s Medications Relieve Central Pain Better than Other Types of Pain, Study Finds

central pain, Parkinson's therapies

Treatment with standard Parkinson’s therapies, such as levodopa or dopamine agonists, can provide effective relief of central parkinsonian pain, but they may fail to manage motor symptoms in these patients, a study has found.

As many patients with Parkinson’s disease experience some type of pain, these findings suggest that clinicians should take an integrated approach to ensure adequate care for motor and non-motor symptoms in this population.

The study, “Unveiling the Relationship Between Central Parkinsonian Pain and Motor Symptoms in Parkinson’s Disease,” was published in the European Journal of Pain.

Pain is a common non-motor symptom in Parkinson’s patients, but little is known about its clinical characteristics and possible predictors.

Parkinson’s can affect the way patients experience pain, and it can lead to pain even in the absence of any evident cause for it. This is the case of central parkinsonian pain, which is characterized by a constant, aching type of pain affecting most of the body and is caused by Parkinson’s disease itself. This type of pain is poorly understood and can be difficult to treat.

Nuno Vila-Chã, MD, neurologist and researcher at Centro Hospitalar do Porto and the University of Porto, in Portugal, and his collaborators were interested in studying the prevalence and types of pain experienced by people with Parkinson’s. They examined the relationship between central pain and patient characteristics, as well as the impact of Parkinson’s targeted treatments on this type of pain.

They analyzed the clinical records, and performed interviews and neurological examinations of 292 patients with Parkinson’s, aged 63 to 79. The patients’ motor symptoms and degree of independence were assessed using different rating scales, while the patients were on medications (in the morning) or off medications. Anxiety, depression, and impulse control disorders (such as dopamine dysregulation syndrome) were also evaluated through patient-reported questionnaires.

Pain was categorized as central parkinsonian or non-central parkinsonian by a neurologist, based on the patients’ description of their pain. Central parkinsonian pain was defined as “burning, tingling, formication, or ‘neuropathic’ sensations, often relentless and bizarre in quality, not confined to root or nerve territory, and not explained by rigidity, dystonia, musculoskeletal, or internal lesion.”

Except for four patients, all (99%) were taking levodopa alone or combined with a dopamine agonist (taken by 39% of the patients), which included ropinirole (108 patients; brand name Requip, among others), pramipexole (two patients; sold as Mirapex and other names), and piribedil (three patients; sold as Trivastal, among other names).

Most patients (73%) reported feeling some sort of pain, which had lasted for a median time of five years. These patients classified it as either musculoskeletal (in 63% of the patients), dystonia-related (27%), central parkinsonian (22%), and/or radicular or neuropathic (9%).

About one-third (68 or 32%) of the patients reported that the pain developed before their Parkinson’s motor symptoms, and half (105 or 50%) said that they could achieve pain relief with antiparkinsonian therapy.

Many of them (78%) reported to have one type of pain, while some patients (22%) claim to experience two or more forms of pain. Many also complained of feeling pain everyday (63%) and rated it as moderate or severe (83%).

The team found that patients who experienced pain also were the ones with more comorbidities (particularly diseases affecting the bones and joints) and more severe motor symptoms.

These findings “confirmed that pain is a common non-motor symptom in Parkinson’s disease and that the presence of pain is associated with more severe motor manifestations of Parkinson’s,” the researchers wrote.

The researchers found that patients with central pain specifically had certain demographic and clinical characteristics. These patients were significantly younger, and their disease often started earlier, but had fewer comorbidities, compared with patients with non-central pain.

They also showed more disability related to pain and worse non-axial motor symptoms while on medications. Non-axial symptoms include all motor symptoms not related to speech, rigidity of the neck, posture and postural stability, and gait (which are considered axial symptoms).

The patients with central pain reported having greater relief in their pain with the medications they were taking for Parkinson’s, compared with those with non-central pain. Also, there was a tendency for more motor fluctuations in the subgroup of patients who took antiparkinsonian medication to relieve their pain.

“This set of demographic and clinical associations suggests the need for an integrated approach to motor and non-motor symptoms in the clinical care of Parkinson’s patients with central parkinsonian pain,” the researchers stated. Also, the association between pain and mood “appears to be weaker and even more complex in Parkinson’s” than in other diseases, they added.

Future studies should continue to search for a deeper understanding of central pain in Parkinson’s, the team noted, as “the improvement of central parkinsonian pain should be considered as a treatment outcome in Parkinson’s disease.”

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A Message to Readers: It’s Not Just the Parkinson’s Disease

PD Dr. C's Journey, loss of vision

In a previous column that I wrote about courage, I mentioned an eye disease I have for which I receive monthly eye injections. Yes, you read that correctly. I get a needle in my eye. Actually, I get two needles — one injection contains additional anesthetic medicine after the topical application of a numbing agent, while the second injection contains chemotherapy.

The disease is unstable and progressive. Treatment is not the same thing as a cure. My providers do their very best to keep things under control. Unfortunately, I recently had a dramatic decompensation that has left me close to legally blind. It’s not the Parkinson’s disease alone that makes life difficult, but rather all the other medical “stuff” that gets thrown on top of it. I will be seeing another specialist for assessment and more treatment. But right now, the loss of vision makes it much more difficult to do the quality columns I am so fond of writing for my readers. It’s hard to adjust when such events hit unexpectedly and steal away another part of my self-identity.

Having been through other traumatic events in my life (and counseled others through traumatic injury), I know there is a process. There is a grieving process that has famously been described by Elizabeth Kubler-Ross. There is also a recovery process. Not all will be as bad during the healing process as it initially appears. A flood of emotions needs to be taken in, understood, processed, and then let go so that the healing may continue. Time is needed to make life adjustments to the effects of the physical trauma. All of this takes time, patience, and a gentleness with me.

The first emotions I work through are anger: “Why me? It’s not fair!” Then comes the self-pity: “This is too hard. I just can’t handle it. I wish someone would come and make it all better.”

Anger is a normal response. But anger and I just don’t do well together. I can easily become “The Grouch.” I am an ugly grouch, mostly because of what I call “spilling out behavior.” It’s been a bad day and the anger needs to go somewhere, so it spills out onto those closest to me. Talk about unfair!  I have way too many skills to get into a verbal fight with those I care about.

Self-pity also spills out onto all of those around me. We may not realize it, but walking around with that dark cloud overhead casts a dark shadow on those closest to us. Clinging to the hope that someone will save us from our own fate if we just whimper and whine loud enough does nothing but create more suffering. The choice, then, is to accept that something bad happened and that is just the way it is. Time to pull it together and attack the new challenges.

Don’t get me wrong. I am not saying I feel all rosy and chipper about what has happened. I am upset and constantly reminded of the situation. Every time I open my eyes, I am forced to face head-on what has happened. If I let the emotions overwhelm me, I can’t move forward. If I can’t move forward, then my self-identity is headed for extinction. The choice is to accept the fact that something bad has happened, and it is time to figure out how to deal with it.

Part of figuring out how to deal with a dramatic loss of vision will involve all those changes and adaptations that need to be put in place in order to maintain a high quality of life. This new journey has just begun, and I will return to writing columns for this group of readers. Right now, though, I need to take a short break while I complete the medical procedures and then put into place any adaptations necessary for helping me to see the computer screen, to use pen and paper, and to explore other adaptive equipment.

Thanks to all my readers, editors, writers, and staff at BioNews Services for their kind words of support and encouragement. In the esteemed words of the former governor of California, “I’ll be 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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Singing Therapy Programs like ‘ParkinSong’ May Prevent Communication Impairment, Study Suggests

singing ParkinSong

Intensive singing interventions have the potential to increase vocal loudness, respiratory muscle strength, and voice-related quality of life in people with Parkinson’s disease, a study suggests.

The study, “ParkinSong: A Controlled Trial of Singing-Based Therapy for Parkinson’s Disease,” was published in Neurorehabilitation and Neural Repair.

Communication impairment is common among Parkinson’s patients. The neurodegenerative disorder not only affects the muscles needed for movement, but also the ones necessary to control communication capacity, including speech and facial expressions.

Around 90% of those living with Parkinson’s have voice and speech changes, but few seek medical advice. Patients’ voice can become difficult to hear due to throat muscle rigidity (stiffness).

There are known similarities between anatomical and neural requirements for both singing and speaking. Evidence suggests that singing may have the potential to ease some of the speech-motor changes associated with several neurological disorders.

Researchers from the University of Melbourne in Australia examined the impact of a singing-based therapeutic intervention, called ParkinSong, on voice, speech, respiratory function, and voice-related quality-of-life in people with Parkinson’s.

A total 75 patients, 46 men and 29 women with a mean age of 74.3 years, were included in the controlled trial (ACTRN12617000528358). Participants were randomly assigned to four groups, in which they engaged in singing-based intervention with different frequency. The ParkinSong weekly group comprised 20 individuals and the monthly group 27, while the control weekly counted 15 participants and the control monthly group had 13.

According to the investigators, this is the first controlled trial studying the efficacy of a singing-based therapeutic training program in Parkinson’s disease.

ParkinSong training consisted of 30 minutes of high-intensity music-based vocal exercises incorporating respiratory control, vocal loudness, pitch control, and speech clarification strategy activities. After that, participants underwent 60 minutes of singing popular and traditional songs and rounds, with a focus on loud voice projection and increased respiratory support. Patients then had 30 minutes of social interaction and conversation practice over morning or afternoon tea, where they were asked to use the strategies for generating loud voice that had been practiced during the training session. The intervention was delivered either once a week or once a month, for three months.

“Weekly control participants attended weekly painting, dancing, or tai chi sessions, and monthly control participants attended monthly peer support groups,” the researchers said.

The team found that patients in the ParkinSong sessions had significantly better vocal intensity, respiratory muscle strength (as measured by maximum expiratory pressure), and voice-related quality of life, compared with those in the control groups. Voice-related quality of life was scored by applying the Voice Activity and Participation Profile (VAPP) questionnaire, a reliable measure for assessing patients’ voice problems and degree of severity.

Comparison of weekly and monthly ParkinSong interventions revealed there was a higher vocal intensity in the weekly group, suggesting that the intensive approach positively affected speech characteristics.

After completion of the three months of therapeutic intervention, loudness decreased in both control groups, and there were no differences between the groups on the longest time patients could say a vowel, or on inspiratory muscle strength.

“Singing groups offer an engaging way to enhance voice and communication for people living with [mild to moderately severe] Parkinson’s disease as well as providing opportunities for socialization,” the researchers concluded.

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Abbott Partners with NIH on BRAIN Initiative to Use Neuromodulation Technologies

Abbott BRAIN NIH

Abbott is partnering with the National Institutes of Health (NIH) to explore the use of its neuromodulation technologies for treating chronic pain and progressive movement disorders, including Parkinson’s disease.

The partnership’s goal is to drive forward the Brain Research through Advancing Innovative Neurotechnologies initiative, known as BRAIN, which is working to accelerate neuroscience research.

With this collaboration agreement, Abbott will make its proprietary neuromodulation technologies available for research purposes. These include directional deep brain stimulation (DBS), spinal cord stimulation (SCS), and dorsal root ganglion (DRG) therapy, which have already been shown to be beneficial in treating several conditions affecting the central nervous system.

Researchers will now be able to explore ways to use these technologies to fill knowledge gaps in the field of neuroscience and, at the same time, find new strategies to apply them to treat chronic and progressive neurological disorders.

“The NIH is investigating the application of these devices for the treatment of a wide range of neurological and neuropsychiatric conditions and chronic pain,” Nick B. Langhals, PhD, program director for neural engineering in the division of translational research at the National Institute of Neurological Disorders and Stroke (NINDS), said in a press release.

“The neuromodulation technologies provided by Abbott will help us determine the inner workings of the nervous system to help fill gaps in our current knowledge of the brain and provide opportunities for exploring how the brain interacts with the human body in patients with neurological conditions,” Langhals added.

The  BRAIN initiative, launched in 2013, seeks to understand how the human brain works, especially in a context of disease, by taking advantage of innovative technologies. It also is working to establish new “out-of-the-box” applications for currently available technologies. Its goal is to show how individual cells and complex neural circuits interact in both time and space.

To date, the BRAIN initiative has gathered partners and contributors from diverse backgrounds, including federal agencies, public organizations, Congress, and even the media.

“Researchers at Abbott are continuously striving to better understand how neuromodulation technology can benefit people living with chronic pain or movement disorders,” said Keith Boettiger, vice president of neuromodulation at Abbott. “In addition to our own research efforts, including clinical and real-world studies, working together with world-class scientists at the NIH will help us further validate our neuromodulation therapies and explore new avenues where they may benefit patients affected by devastating neurological conditions.”

With the support of NINDS and the BRAIN initiative, researchers have developed an experimental DBS system that uses brain signals to fine tune its activity in response to signs of dyskinesia, or uncontrolled body movement. This approach may potentially represent a more refined way to ease motor problems in Parkinson’s patients.

During the 5th Annual BRAIN Initiative Investigators Meeting, recently held in Washington, D.C., partners from the BRAIN initiative discussed scientific advancements in the neuroscience field, and identified areas for collaboration and research coordination. 

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PatientPoint Launches Digital Support Network for Neurologists, Patients, and Caregivers

PatientPoint

PatientPoint, in collaboration with five U.S. patient advocacy organizations, has introduced a technology-driven point-of-care network for neurologists, neurology patients, and caregivers.

With a focus on neurological conditions such as Parkinson’s and Alzheimer’s disease, the comprehensive network hopes to promote improved communication between patients and physicians.

The new patient empowerment network, targeting the estimated 100 million U.S. residents with neurological diseases, emphasizes everyday living, symptom management, treatment regimens, advice for caregivers, and tailored content in physicians’ offices, and waiting and exam rooms. By year’s end, the network is expected to reach some 1,000 neurologists nationwide.

“We know that education can help decrease anxiety and provide a sense of control,” Kate Merz, executive vice president of content and creative of PatientPoint, said in a press release. “With that in mind, the inspiring and educational content offered on our new neurology network is designed to help patients live their best lives.”

Aiming to improve doctor-patient engagement, PatientPoint has established partnerships with the Parkinson’s Foundation, the Alzheimer’s Association, the International Essential Tremor Foundation, Migraine Again, and the National Multiple Sclerosis Society. Across the PatientPoint platform, the organizations will provide essential tools and educational information to all individuals involved or affected by neurological conditions.

“At PatientPoint we put the patient-doctor relationship at the center of everything we do, and our neurology network is no exception,” said Mike Collette, founder and CEO of PatientPoint. “We conducted extensive research in developing this new network, and we are confident that the resulting blend of empowering health education, lifestyle and partner content will meet the unique needs of neurology patients, and drive doctor-patient engagement in an important new medical specialty.”

For the neurology examination room, for example, diagnoses can be more clearly communicated through interactive touchscreens that offer condition-precise multimedia education and three-dimensional human body images. To further communication beyond doctor visits, touchscreen content also can be emailed and texted.

The new network also features back-office digital screens that can keep physicians and staff apprised on a host of topics, including real-time breaking news, industry trends, practice management, and self-care.

In addition to the neurology network, PatientPoint offers engagement networks in other specialties, including cardiology and primary care.

The Michael J. Fox Foundation for Parkinson’s Research estimates that, by next year, nearly 1 million Americans over age 45 will be diagnosed with the disease.

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Lysosome-targeting Therapies Can Potentially Reverse LRRK2 Effects in Parkinson’s, Study Suggests

LRRK2 mutations

Mutations in the LRRK2 gene, which have been linked to familial Parkinson’s disease, impair the activity of the waste clearance system inside nervous brain cells, contributing to their progressive degeneration, a study finds.

Using a compound called clioquinol, researchers could restore the activity of lysosomes — the core centers of waste degradation — that was blocked by mutated LRRK2. This finding highlights the potential for lysosome-targeting therapies as a strategy for treating people with Parkinson’s and other neurodegenerative disorders.

The study, “LRRK2 interacts with the vacuolar-type H+-ATPase pump a1 subunit to regulate lysosomal function,” was published in the journal Human Molecular Genetics.

Parkinson’s is a chronic and progressive neurodegenerative disease caused by the loss of dopamine-producing neurons in the substantia nigra, a brain region involved in the control of voluntary movements. It remains unclear why this particular group of brain cells is more sensitive, but researchers believe that the cells’ death is due to the accumulation of toxic protein aggregates.

Recent findings suggest that lysosomes, special compartments within cells that digest and recycle different types of molecules, may play a role in this mechanism of protein buildup. When the lysosomes don’t function properly, waste accumulates inside cells instead of being degraded and cleared out.

Increasing evidence also suggests that both genetic and sporadic cases of Parkinson’s are linked to lysosomes malfunction.

One of the most common genetic causes associated with familial forms of Parkinson’s are mutations in the leucine-rich repeat kinase 2 gene, known as the LRRK2, which provides instructions for making a brain protein called dardarin. Although mutated LRRK2 is believed to contribute to malfunctioning lysosomes, its underlying mechanism remains unclear.

Researchers from the University of Oxford tackled this question, using a genetically modified rat model carrying a mutated version of the LRRK2 gene, called R1441C, which has been found in human patients.

They analyzed the rats’ neurons — including the dopamine-producing neurons whose loss underlies Parkinson’s — and found that the R1441C mutation prevented the binding of LRRK2 to a lysosomal protein called vATPase a1. This protein has the particular role of regulating the acidity inside lysosomes that is necessary to degrade cell waste.

To further confirm the association between mutated LRRK2 and lysosome impairment, the team treated nerve cells with clioquinol, a compound previously reported to modulate lysosomes acidity by regulating the levels of vATPase. Treatment with clioquinol reversed the effect of the LRRK2-R1441C mutation in lysosomes, and restored the activity of the cells’ waste disposal system.

“Our work identifies for the first time the very important role of LRRK2 in regulating the acidity and the normal function of the protein recycling centre, the lysosome, and identifies a new way to target this therapeutically in Parkinson’s,” Richard Wade-Martins, PhD, professor of Oxford’s department of physiology, anatomy and genetics (DPAG), and the study’s senior author, said in a press release.

“The demonstration that small molecules which directly target lysosome dysfunction, such as clioquinol, have potential therapeutic benefit for Parkinson’s disease, fits closely with the emerging consensus from genetics on this critical area of cell biology,” the researchers said.

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Early Involvement of Caudate Brain Region Linked to Worse Prognosis in Parkinson’s Patients, Study Finds

caudate involvement

Almost half of people in the early stages of Parkinson’s disease already have signs of neurodegeneration in a brain region called the caudate, which was previously thought to affect mostly those at advanced disease stages, a study reports.

Early caudate involvement on both sides of the brain, as seen by DaTscan imaging of the brain, appeared to predict the risk for worse outcomes, including cognitive impairment, depression, and gait problems, over a four-year follow-up period.

These findings suggest that caudate involvement detected through DaTscan neuroimaging may serve as an early biomarker to identify patients at a greater risk of faster disease progression in the near future.

The study, “Clinical implications of early caudate dysfunction in Parkinson’s disease,” was published in the Journal of Neurology, Neurosurgery & Psychiatry.

Parkinson’s disease is believed to be caused by the impairment or death of dopamine-producing nerve cells (neurons) in a region of the brain called the substantia nigra, which controls the body’s balance and movement.

When the disease is established, or advanced, the degeneration of dopaminergic neurons and nerve fibers frequently extends to a brain region called the caudate nucleus. This region plays important roles in motor control as well as in various other non-motor tasks, such as learning and sleep.

In fact, the loss of dopaminergic function in this region is known to contribute to the hallmark symptoms of Parkinson’s including cognitive impairment, depression, sleep disorders, and gait problems.

Although less common, caudate dopaminergic dysfunction may also emerge in the early stages of the disease, in which case it could also contribute to the onset of non-motor symptoms. However, the frequency of this specific brain impairment in early Parkinson’s is unknown as are its clinical implications for patients.

To address this lack of knowledge, a team, led by researchers at the University of Milan in Italy and Newcastle University in England, investigated the prevalence of caudate dopaminergic dysfunction in people who were still in the very early stages of Parkinson’s.

By comparing the participants’ state at the beginning of the study and four years later, they also looked for associations between caudate involvement and an increased risk of disease progression.

They analyzed clinical data from 397 patients who had had a Parkinson’s diagnosis for two years or less, and were participating in the Parkinson’s Progression Markers Initiative (PPMI), an ongoing study attempting to identify biomarkers of disease progression. The team compared the collected clinical data from Parkinson’s patients with that of 177 healthy volunteers.

Caudate dysfunction was detected using 123I-FP-CIT single-photon emission computed tomography, commonly known as DaTscan. This is an imaging technique that depicts the levels of dopamine transporters in the brain that is often used to confirm a Parkinson’s diagnosis.

Based on DaTscan imaging data, the participants were divided into three groups: those who had no reduction of dopamine transporters, those who showed reduction in just one side of the brain, and those who had involvement of both sides of the brain.

Initial data showed that 51.6% of the patients had signs of normal caudate dopamine function, while 26% had caudate dopaminergic dysfunction on one side of the brain (unilateral), and 22.4% on both sides (bilateral).

Four years later, the patients who initially had bilateral caudate involvement were found to experience more frequent and worse cognitive impairment and depression, and more severe gait disability.

In general, after four years of follow-up, more patients showed a loss of dopaminergic nerve fibers in the caudate, compared with the study start, affecting 83.9% of patients (unilateral 22.5%, bilateral 61.4%).

“In this study, we have demonstrated a high frequency of early caudate dopaminergic dysfunction in patients with recently diagnosed [Parkinson’s disease],” the researchers wrote.

“Our study suggests that early bilateral caudate dopaminergic dysfunction is associated with an increased frequency of clinically significant depression and to worse depressive symptoms, regardless of age,” they added.

DaTscan parameters used to define the presence of early caudate dysfunction may be a “valid indicator of more rapid onset of such symptoms,” they said, which may help in “identifying patients at risk of clinical progression to cognitive impairment, depression, and gait problems in the near future.”

Assessment of caudate dopaminergic denervation may also assist clinicians in better predicting disease course at an early stage and identifying patients who may benefit the most from early, targeted disease-modifying therapies.

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Restless Legs Syndrome and Restlessness: A Bad Combination

sleep

Restless legs syndrome (RLS) is common in Parkinson’s disease (PD). So, too, is restlessness. However, the two symptoms are not the same. When you experience both, and add discomfort to the equation, you have a very uncomfortable person dealing with PD.

I can relate so well.

I have walked the floor many nights trying to get my legs to stop twitching. Once my restless legs begin their midnight dance, there is little else that will calm them down. So, I walk around my living room, sometimes singing softly or praying.

Restlessness and RLS can keep you awake and fidgety, but they don’t affect you in the same way. Restlessness creates anxiousness, and vice versa. It can affect anyone, not just those who are already struggling with Parkinson’s.

Another lesser-known symptom accompanies Parkinson’s: being uncomfortable. I am not referring to a feeling of awkwardness but rather a state of being.

It’s when you’re unable to find a comfortable chair to sit in and then can’t get into a restful position in that chair. The same goes for sleeping. Your bed may be the one Goldilocks would have chosen, but you can’t seem to find that sweet spot for yourself.

My husband has told me that sometimes I look like a puppy dog circling its bed in an attempt to find the most comfortable position. Sometimes I feel like a puppy in that respect! Just when I have lain down and reached the elusive “comfortable” spot of sleep, I think I need to visit the bathroom again. Upon returning, the comfort game begins again, which I usually lose.

What worsens my discomfort? Too much sugar or caffeine close to bedtime is an example. This happened the other night. 

I had a large cup of Diet Coke for lunch that I sipped on the rest of the day. I hadn’t had Diet Coke in what seemed like forever, and that one drink reduced my usual nine hours of sleep to a few more than two. Sugar has been known to keep me awake all night. Having Parkinson’s disease, you try everything you can to ensure the best possible night’s sleep — or you pay for it the next day.

I have noticed that when I am on my computer just before going to bed, it takes me longer to fall asleep. My mind keeps buzzing. So, because I must charge my deep brain stimulator battery each night, I have started reading during that time. Reading tends to quiet my mind and gets me ready to fall asleep sooner and more easily. Going to bed at a regular bedtime also seems to help.

Several things can hinder our attempts to sleep well. We can change some of these things. If you’re having a tough time getting a good night’s sleep, talk to your doctor about it and try some of my tips. It’s worth a shot.

***

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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Vulnerable, but Not Alone

vulnerability

Slow Is the New Fast

“People who know me know I’m strong, but I’m vulnerable.” — Catherine Deneuve

Oxford Dictionaries define vulnerability as: “The quality or state of being exposed to the possibility of being attacked or harmed, either physically or emotionally.”

Recently, I felt a level of extreme vulnerability that I don’t remember experiencing before. Potentially, this could be due to any of the following reasons:

  • I lack confidence and strength now because I have Parkinson’s disease.
  • I am old (although in my mind, I’m still 21).
  • I am a woman living alone.
  • A combination of the above.

Although, lately, I seem to blame everything on Parkinson’s — it’s a good scapegoat!

What happened?

At 7:15 one recent morning, as I looked out my kitchen window, I saw an unmarked van backing into my driveway. A man I did not know got out of the vehicle and rang my doorbell. When I didn’t answer, he tried to enter. I froze as I stood in my hallway and stared at the front door, watching the doorknob moving. My pet bunny started to thump, and I knew I wasn’t going to get any help from bunny. I think he was more frightened than I was.

Luckily, since I live in a retirement community, around-the-clock security is available. I called security, and within five minutes, someone arrived and confronted the person outside my front door.

All is well

It turns out that some construction workers went to the wrong address and rang my doorbell by mistake.

Although I felt so vulnerable in this situation, I am thankful to live in a community where I am not alone.

“I do have a vulnerable side. I think a lot of people have a misperception of me. They only see the tough, defensive, aggressive side. But every woman is vulnerable.” — Rihanna

***

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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Centogene Launches 2-Year Global ROPAD Study to Assess the Genetics of Parkinson’s Disease

ROPAD study, Parkinson's genetics

A two-year, global, observational study that will assess the contribution of genetic factors in the development of Parkinson’s disease has been launched by Centogene, in collaboration with the University of Lübeck.

The new study (NCT03866603), which is called “Rostock International Parkinson’s Disease Study” or ROPAD, seeks to enroll around 10,000 participants worldwide to get a representative snapshot of the genetic variability in a large population of patients with this progressive neurodegenerative disease.

Adult individuals, 18 or older, who have been clinically diagnosed with Parkinson’s disease are eligible to participate in the study, as well as individuals who are family members of a patient with LRRK2 parkinsonism or are at high risk of having the disease.

The main goal of the study is to pinpoint the specific genetic mutations and genes that may be associated with the development of Parkinson’s disease.

The study’s primary outcome will be to assess the number of patients carrying mutations in the LRRK2 gene, in which more than 100 different mutations associated with late-onset Parkinson’s disease have already been identified. The researchers will also assess, as the study’s secondary outcomes, the prevalence of mutations in other genes previously linked to Parkinson’s, such as GBA.

All the genetic analysis will be performed using the CentoCard, Centogene’s proprietary, CE-marked device that has been designed to collect and evaluate dried blood spot samples.

“Centogene is committed to bringing hope to patients and their families by shortening the diagnostic odyssey, and we are proud to be working on this important study that may have vast implications for the future diagnosis and treatment of Parkinson’s disease,” Arndt Rolfs, CEO and founder of Centogene, said in a press release.

“All too often clinical studies do not reflect the ethnic diversity of the world, and this study is unique in that we are working across all ethnicities worldwide and crosschecking the effect of environmental components and individual genetics. We are excited about the contribution that Centogene and our partners are making in discovering deeper insights into Parkinson’s disease genetics,” Rolfs added.

Patients carrying genetic mutations linked to the development of Parkinson’s disease will have the opportunity to participate in the “LRRK2 International Parkinson’s Disease Project (LIPAD),” a study led by professor Christine Klein at the University of Lübeck which is designed to document the frequency of all signs and symptoms of Parkinson’s disease among this particular population.

In addition, patients participating in ROPAD who are carriers of LRRK2 mutations will have the chance to enroll in future clinical studies led by Denali Therapeutics, Centogene’s study partner, which is currently working on a set of new investigational therapies for neurodegenerative disorders.

To know more about the ROPAD trial and how to participate, visit Centogen’s webpage or its ClinicalTrial.gov registry page.

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