Rare sleep disorder common among veterans with PTSD

OCTOBER 11, 2019     by Erik Robinson, Oregon Health & Science University

Military veterans with post-traumatic stress disorder or concussion suffer from a thrashing form of sleep behavior at a rate that is far higher than the general population, according to a new study by researchers at the VA Portland Health Care System and Oregon Health & Science University. The finding was published online this week in the journal Sleep.

Researchers next want to probe whether the disorder, known as REM sleep behavior disorder, or RBD, might provide an early signal of the development of neurodegenerative conditions such as Parkinson's disease.

Normally during sleep that coincides with rapid eye movement, or REM sleep, muscles are effectively paralyzed. In cases of RBD, brain control of muscle paralysis is impaired, resulting in people acting out dreams during REM sleep, sometimes causing injuries to themselves or their partners. It is estimated to effect less than 1% of the general population.

That proportion rose to 9% of the 394 veterans in this study, and further swelled to 21% among those with PTSD.

"This is important because, in the general population, RBD has been linked to Parkinson's disease, and RBD often precedes classic symptoms of Parkinson's by years," said senior author Miranda Lim, M.D., Ph.D., a staff physician at the VA and assistant professor of neurology, medicine and behavioral neuroscience in the OHSU School of Medicine. "We don't know whether veterans who have PTSD and higher rates of RBD will go on to develop Parkinson's, but it is an important question we need to answer."

Researchers suspect chronic stress on the brain may play a role in causing the sleep disorder in veterans with PTSD, as many veterans have been exposed to concussion which potentially accelerates neurodegenerative processes.

Each study participant underwent an overnight sleep study at the VA Portland Health Care System between 2015 and 2017 to determine the presence of dream enactment during episodes of REM sleep. Muscle activity was monitored continuously during the 8 hours of the study in order to diagnose RBD. The study found that those with PTSD had over 2-fold increased odds of RBD compared to veterans without PTSD.

"RBD seems to be highly prevalent in veterans with a history of trauma," said lead author Jonathan Elliott, Ph.D., a research physiologist at the Portland VA and assistant professor of neurology in the OHSU School of Medicine.

Doctors involved in the study, including co-authors Kristianna Weymann, Ph.D., R.N., a clinical assistant professor in OHSU School of Nursing, and Dennis Pleshakov, a student at the OHSU School of Medicine, will continue to track research participants with RBD, looking for early signs of Parkinson's or other neurodegenerative conditions.

Although there are several therapies to ease some of the symptoms of Parkinson's, including tremor and fatigue, so far there has been no definitive therapy to prevent it.

Clinical trials for promising therapies are usually conducted well after patients have been diagnosed with Parkinson's, at a stage which may be too late to reverse the symptoms. Lim said that identifying patients with RBD presents an opportunity to identify people earlier in the disease course, and potentially provides a more viable window to test promising interventions.

"By the time a patient shows classic symptoms of Parkinson's, it may be too late," Lim said. "If you could intervene when people first start to show RBD, maybe you could prevent later symptoms of Parkinson's."

More information: Jonathan E Elliott et al, Post-traumatic stress disorder increases odds of REM sleep behavior disorder and other parasomnias in Veterans with and without comorbid traumatic brain injury, Sleep (2019).  DOI: 10.1093/sleep/zsz237

Journal information: Sleep 
Provided by Oregon Health & Science University 

https://medicalxpress.com/news/2019-10-rare-disorder-common-veterans-ptsd.html

Deciphering the early stages of Parkinson's disease is a matter of time

OCTOBER 11, 2019    by Instituto Nacional de Ciência e Tecnologia de Biologia Estrutural e Bioimagem (INBEB)

Electron micrograph of mature alpha-synuclein filaments. Credit: Guilherme A. P. de Oliveira

One of the biggest difficulties in treating Parkinson's disease, a progressive neurodegenerative disorder, is the understanding of when it starts. Now, a study published in Communications Biology by researchers at the Federal University of Rio de Janeiro, Brazil, and the University of Virginia School of Medicine, USA, may help to clarify that puzzle. For the first time, scientists observed how variants of the Parkinson's disease-associated protein alpha-synuclein change over time and were able to identify the initial stages of protein aggregates linked to early onset of familial cases of the disease.

The characterization of these structures and their organization is fundamental to identify the early stages of the disease. It is already known that the degeneration of neurons leading to the onset of symptoms such as tremors is linked to alpha-synuclein aggregates, also called amyloid filaments, in the brain. Before forming such filaments, proteins undergo an intermediate stage, the oligomers, which are also present in the brains of Parkinson's patients. However, there is no consensus on what mechanisms trigger aggregation, neuronal cell loss, and degeneration, neither how toxic the aggregates and the oligomers are to the cells. That is what the study tries to understand.

"A person develops Parkinson's disease over his lifetime. The conversion from one proteinstage to the other takes place slowly. The intermediate structures and the amyloid aggregates accumulate over time in the brain. So far, we don't know which species cause the symptoms and toxicity to cells," says the lead author of the research Guilherme A. P. de Oliveira, researcher at the University of Virginia and professor at the UFRJ. "If we understand the protein species forming during the early stages of disease conversion, we can propose new therapies for disease detection before the symptoms appear," he adds.

During the study, scientists compared the conversion of four variants of alpha-synuclein over time, three of them linked to early cases of the disease and the wild-type, present in cases of aging. Then, they observed significant differences in the aggregation processes of each protein and found that oligomers develop at a much greater rate in early onset cases than in aging cases of Parkinson. Such results may explain the early onset of symptoms in patients bearing these variants.

The researchers also found evidence of which protein species are important for the amyloid filaments growth. Moreover, they observed that the filaments have distinct structures depending on the protein mutation from which they originate. "Most intriguing is that not only the initial association steps are different, but also some mature filaments of hereditary cases. These filaments can twist differently depending on which mutation is present," explains Jerson Lima Silva, second co-author and professor at UFRJ.

To perform the study, the researchers used cutting-edge bioimaging techniques. First, they used a fluorescent probe that allowed them to visualize each protein association step over time. Researchers optimized conditions in the wet lab to detect structures that were not previously shown during the course of alpha-synuclein association. Typically, the probe allows scientists to see only two stages: dark, when there is no aggregation, and light, when aggregation is present. Creating the right conditions, Oliveira and Silva managed to handle the luminosity steps and, thus, to observe the intermediate species participating on alpha-synuclein association, which would not appear in other circumstances.

The use of cryo-electron microscopy, a technique awarded with the 2017 Nobel Prize in Chemistry, was also important for the study. By allowing the visualization of biomolecules at near-atomic resolution, the scientists observed the structural organization of the amyloid filaments. According to Oliveira, the possibility of seeing such structures contributes to the development of new treatments against the disease. "By plunge freezing these samples and acquiring advanced electron microscope images, we are able to better understand these wrong protein associations in their native environment and ways to avoid their formation. I am glad that Brazil is now making part of this S&T venture," he says.

The paper "Alpha-synuclein stepwise aggregation reveals features of an early onset mutation in Parkinson's disease," is published in Communications Biology.

https://medicalxpress.com/news/2019-10-deciphering-early-stages-parkinson-disease.html

Potential Treatment to Prevent Toxic Protein Clumping Enters Phase 1 Trial, Yumanity Announces

 OCTOBER 10, 2019     BY ALICE MELÃO 

Yumanity Therapeutics announced the start of a Phase 1 clinical study in healthy volunteers that will assess the safety and tolerability of YTX-7739, a potential disease-modifying therapy for Parkinson’s disease.

Trial results are expected to be announced in the first quarter of 2020.

YTX-7739 is designed to cross the blood-brain-barrier — a semipermeable membrane that protects the brain and spinal cord from the external environment — to inhibit the activity in the brain of an enzyme called stearoyl-CoA desaturase (SCD) .

This enzyme is known to play a key role in the production of certain fat molecules, called unsaturated fatty acids, that mediate the neurotoxic effects of alpha-synuclein protein accumulation — a key constituent of Lewy bodies, the toxic protein clumps that are a Parkinson’s hallmark.

In cell and animal disease models, the investigational medicine was shown to protect neurons against alpha-synuclein-derived toxicity and improve their survival.

“We advanced YTX-7739, an orally-active SCD inhibitor, into clinical development because of recent evidence established at Yumanity Therapeutics demonstrating its promise to protect cells from a-synuclein toxicity,” said Kenneth Rhodes, PhD, the company’s chief scientific officer, said in a press release.

“We look forward to fully characterizing the potential clinical use of YTX-7739, which is clearly differentiated from currently available Parkinson’s disease therapies that only address the symptoms, not the underlying causes.”

The Phase 1 trial is expected to enroll about 40 healthy volunteers, who will be randomly assigned to increasing doses of oral YTX-7739 or dose-matching oral placebo. Collected data will assess YTX-7739’s safety and tolerability, as well as its stability and metabolization (pharmacokinetics) inside the body: essentially, how the body affects a medicine.

If results are promising, Yumanity plans to advance YTX-7739 into a Phase 1b proof-of-concept clinical trial in patients, possibly in the second half of 2020.

“This Phase 1 trial will provide important validation for the broad application of our technology to help address arguably the most important therapeutic challenges of our time,” like that of “protect[ing] cells from neurodegeneration,” said Richard Peters, MD, PhD, Yumanity’s CEO.

https://parkinsonsnewstoday.com/2019/10/10/ytx-7739-potential-lewy-body-treatment-enters-phase-1-trial-yumanity-says/

MIT Scientists Building Artificial Gut to Study Bacteria’s Influence on Parkinson’s, Other Diseases

OCTOBER 10, 2019  BY CATARINA SILVA, MSC 

MIT Lincoln Laboratory researchers are developing an artificial gut to study how the human microbiome — the trillions of microorganisms and their genetic material that live within our body, and are as unique to a person as fingerprints — influences the onset and progression of diseases linked to changes in gut bacterial constitution, such as Parkinson’s disease.

The so-called “gut-brain axis” is a highly complex and interactive network between the gut and the brain, composed of endocrine (hormonal), immunological, and neural mediators. Dysregulation of “cross-talk” within this axis has been associated with metabolic syndrome, depression, anxiety and autism, as well as to neurodegenerative diseases like Parkinson’s, and Alzheimer’s.

By manipulating the gut microbiome in Parkinson’s patients, researchers could study its effects on neurodegenerative processes.

“Until now, no one has been able to culture a microbiome sample and maintain it,” David Walsh, a PhD with the Biological and Chemical Technologies Group at MIT who led the prototype device’s development and fabrication, said in a university news story by Anne McGovern. Further refinements are still being made.

“The question from the mechanical side is, how do you emulate the colon?” said Todd Thorsen, PhD, the project’s principal investigator and an assistant professor with the MIT group.

“Bacteria in the colon occupy lots of ecological niches,” Thorsen added. This means that all bacteria living in the colon have organism-specific demands for survival, including nutritional and environmental requirements. For instance, some are oxygen-dependent and others not.

To mimic the intestinal microenvironment, Lincoln Laboratory investigators are developing an easily accessible and cost-effective platform made of permeable silicon rubber and other plastics, like polystyrene. Importantly, in this “artificial gut,” scientists can regulate oxygen and mucus concentrations within microculture chambers, modeling the human colon. Because it can be easily replicated, it might also be of use to others studying the gut microbiome, and the impact of disease or treatment on it.

“If we can maintain a culture, we can do things like add toxins and therapeutics to see how they change the culture over time,” Walsh said. Such an ability could move research a step closer to tackling real-world problems, including bacterial resistance.

Using gut microbiome samples from Parkinson’s patients and healthy people, the scientists plan to use their device to study intestinal bacteria’s influence on the neurodegenerative processes seen in Parkinson’s.

Experiments are expected to begin soon, in collaboration with researchers at the University of Alabama at Birmingham, Northeastern University, and the University of California at San Francisco.

The team also plans to build a tube-shaped origami-like gut that rolls up during assembly to simulate the colon and the surrounding vascularized tissue, and to develop modeling software to predict how different bacterial communities change over time.

https://parkinsonsnewstoday.com/2019/10/10/mit-scientists-building-artificial-gut-study-gut-bacteria-influence-in-disease/

With $20 Million NIH Grant, Penn Researchers to Develop a Tool to Help Diagnose, Track Parkinson’s Disease

October 10, 2019

A special type of PET scan used for imaging the brains of patients with Parkinson’s could be revolutionary for drug development and treatment

PHILADELPHIA – Researchers in the Perelman School of Medicine at the University of Pennsylvania will lead a multi-institutional effort in pursuit of developing a critical tool for imaging the brains of patients with Parkinson’s and other neurodegenerative diseases. The Center Without Walls — a collaboration between Penn Medicine, Washington University-St. Louis, the University of Pittsburgh, the University of California-San Francisco, and Yale University — has received a five-year $20 million grant from the National Institute of Neurological Disorders and Stroke (NINDS) to pursue this work. 

“The NINDS set an incredibly ambitious goal that required an equally ambitious project,” said the Center’s principal investigator Robert H. Mach, PhD, the Britton Chance Professor of Radiology at Penn Medicine. “At the end of five years, we hope to have a radioactive tracer that will be able to detect Parkinson’s early on and provide detailed information about the disease’s progression, which is critical for discovering and testing new treatments.”

Parkinson’s disease, a progressive nervous system disorder, affects 10 million people worldwide and 500,000 in the United States. There is no single test available to diagnose the disease, and it can go undetected or misdiagnosed until its symptoms — tremors, changes in speech, and balance issues — become severe. The drug Levodopa, which was approved by the U.S. Food and Drug Administration for the treatment of Parkinson’s over 50 years ago and remains the gold standard of treatment, can become less effective as the disease progresses and is often accompanied by severe side effects. 

Identifying a Parkinson’s imaging biomarker, or indicator of the disease process, would be a critical step for detecting the disease early, before irreversible damage to the brain occurs. Not only could a biomarker aid in early diagnosis, but it could allow researchers to speed clinical trials of new therapies, according to study co-investigator Andrew Siderowf, MD, MSCE, the Hurtig-Stern Professor of Neurology at Penn. 

“Currently, when testing new drugs for Parkinson’s, assessing the patient’s clinical symptoms is the only way to measure whether or not the treatment is working, but clinical features evolve very gradually,” Siderowf said. “Having an imaging biomarker that is sensitive to changes in a Parkinson’s pathology could greatly accelerate drug development.” 

Robert H. Mach, PhD

A positron emission tomography (PET) scan is an imaging test that uses a radioactive drug (tracer) that binds to certain proteins or sugars, in order to show areas of the body that have higher levels of chemical activity, indicating disease. It was just under a decade ago that researchers first identified a radiotracer that could be used to detect the presence of amyloid protein plaques in the brain, which are a hallmark of Alzheimer’s disease. Though the search for a successful Alzheimer’s drug remains elusive, PET scans have revolutionized how the disease is diagnosed and monitored.  

Now, Mach and his team at the Center Without Walls are pursuing a similar outcome for Parkinson’s and a handful of other diseases that are characterized as “proteinopathies,” which occur when certain proteins “misfold” and structurally abnormal. With this funding, the researchers plan to develop two different radiotracers: one that will bind to a protein in the brain known as alpha-synuclein for the imaging of Parkinson’s and multiple system atrophy, and the other that will bind to the protein 4R tau for imaging frontotemporal degeneration and progressive supranuclear palsy. 

Identifying compounds that are able bind to the proteins alpha-synuclein and 4R tau is akin to “finding a needle in a haystack,” Mach said. To accomplish this undertaking, a research group within the Center Without Walls — led by E. James Petersson, PhD, an associate professor of Chemistry — will use a technology that can computationally screen for molecules, synthesize them, and interpret binding data based on crosslinking.

“Finding a needle in a haystack is much easier when you have a machine made to find needles,” Siderowf said. 

The research team will also draw from the expertise of John Q. Trojanowski, MD, PhD,the William Maul Measey-Truman G. Schnabel, Jr. Professor of Geriatric Medicine and Gerontology in Pathology and Laboratory Medicine, and Virginia Man-Yee Lee, PhD, MBA, the John H. Ware 3rd Endowed Professor in Alzheimer's Research. Trojanowski and Lee are also co-investigators on a separate project, funded recently by an $18 million NIH grant, to study the mechanisms of and connections between Alzheimer’s disease, dementia and Parkinson’s. 

Mach says that a successful outcome from the Center Without Walls could not only change the course of Parkinson’s disease research, but could have a much wider impact. 

“That would be a true paradigm shift in the way we develop molecular imaging probes to study neurological disease,” he said. 

The Center Without Walls is funded by the National Institutes of Health (U19NS110456). Other Penn investigators include: David Mankoff, Ilya Nasrallah, Kelvin Luk, Vera Moiseenkova-Bell, Hsiaoju Lee, Robert Doot, Erin Schubert, Catherine Hou and Chia-Ju Hsieh.

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Neurology and Neurosurgery

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Penn Medicine is one of the world’s leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation’s first medical school) and the University of Pennsylvania Health System, which together form a $7.8 billion enterprise.

The Perelman School of Medicine has been ranked among the top medical schools in the United States for more than 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $425 million awarded in the 2018 fiscal year. 

The University of Pennsylvania Health System’s patient care facilities include: the Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center—which are recognized as one of the nation’s top “Honor Roll” hospitals by U.S. News & World Report—Chester County Hospital; Lancaster General Health; Penn Medicine Princeton Health; and Pennsylvania Hospital, the nation’s first hospital, founded in 1751. Additional facilities and enterprises include Good Shepherd Penn Partners, Penn Home Care and Hospice Services, Lancaster Behavioral Health Hospital, and Princeton House Behavioral Health, among others.

Penn Medicine is powered by a talented and dedicated workforce of more than 40,000 people. The organization also has alliances with top community health systems across both Southeastern Pennsylvania and Southern New Jersey, creating more options for patients no matter where they live.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2018, Penn Medicine provided more than $525 million to benefit our community.

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https://www.pennmedicine.org/news/news-releases/2019/october/with-20-million-nih-grant-penn-researchers-develop-tool-help-diagnose-track-parkinsons-disease

Existing blood thinner delays Alzheimer's disease in mice

8 October 2019    By Maria Cohut, Ph.D.

An existing blood thinner — used to prevent the formation of blood clots in people at risk of stroke — could help delay the development of Alzheimer's disease, according to a new study in a mouse model.

Alzheimer's disease is the most common form of dementia, a neurodegenerative condition in which people experience progressive memory loss.

Some treatments can help people with Alzheimer's disease manage this symptom and others to a certain extent.

However, there is currently neither a cure nor a tried and true method of preventing the condition.

This is why researchers worldwide continue to search for strategies and therapies that could at least delay the onset of Alzheimer's symptoms.

This is also what a team of investigators — many from the Centro Nacional de Investigaciones Cardiovasculares (CNIC), in Madrid, Spain, and The Rockefeller University, in New York — has recently investigated.

In a new study, coordinated by Marta Cortés Canteli, Ph.D., the team has used a known anticoagulant, a drug that prevents blood clots, to slow the onset of Alzheimer's disease symptoms in a mouse model.

The researchers took this approach because previous studies have shown that individuals with this condition also tend to have poor circulation in the brain.

In the new study paper — which appears in the Journal of the American College of Cardiology — Cortés Canteli and colleagues explain that just 1 year's treatment with this drug resulted in no memory loss and no reduction in cerebral blood flow in a mouse model of the disease.

"This discovery marks an important advance toward the translation of our results to clinical practice to achieve an effective treatment for Alzheimer disease," says Cortés Canteli.

Significant reduction in Alzheimer's markers

In the current study, the researchers worked with female mice that they had bioengineered to become prone to developing Alzheimer's-like symptoms later in life.

To these mice and a control group, the investigators administered either a placebo or dabigatran etexilate, a blood thinning drug, mixed with regular chow over a period of 1 year.The researchers calculated that each mouse in the treatment group received an average dose of around 60 milligrams of dabigatran per kilogram of body weight over 24 hours.

Mice that received this treatment for 1 year developed no memory loss and maintained normal cerebral blood flow.

Moreover, the researchers found a significant reduction in typical biological markers of Alzheimer's disease in the mice that had received the drug. 

Specifically, these mice had a 23.7% reduction in the extent of amyloid plaques, which are buildups of toxic protein. The researchers also found a 31.3% reduction in aggressive immune brain cells called phagocytic microglia and a 32.2% reduction in infiltrated T cells, another type of immune cell.

These reductions indicate lower rates of inflammation and blood vessel injury in the brain, as well as less protein buildup that disrupts normal communication between brain cells.

"Winning the battle against Alzheimer disease will require individualized combination therapy targeting the various processes that contribute to this disease," notes Cortés Canteli.

"One goal is to improve the cerebral circulation, and our study shows that treatment with oral anticoagulants has the potential to be an effective approach in Alzheimer patients with a tendency to coagulation," she adds.

Dabigatran is all the more promising as a potential new treatment for Alzheimer's because it has already been approved as a treatment for other conditions and health events, and it reportedly has fewer side effects than other anticoagulant drugs.

Future studies, the researchers suggest, should develop better ways of finding out which people with Alzheimer's disease are also prone to developing blood clots. This cohort, they explain, may benefit most from a treatment that includes anticoagulants such as dabigatran.

An individualized treatment strategy such as this will first require the development of a diagnostic tool to identify those Alzheimer patients with a tendency to coagulation. This will be an important line of research in the coming years."Marta Cortés Canteli, Ph.D.

"Neurodegenerative diseases are very closely linked to disease in the cerebral blood vessels," lead author and general director of CNIC Dr. Valentín Fuster notes.

"The study of the links between the brain and heart is the major challenge for the next 10 years," he predicts.

https://www.medicalnewstoday.com/articles/326594.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&apid=&utm_campaign=MNT%20Weekly%20News%202019-10-09&utm_term=MNT%20Weekly%20News

A Surprising Reason to See the Dentist: Oral Hygiene & Parkinson’s

By TK Sellman · October 3, 2019

People with Parkinson’s disease, especially in later stages, can experience a wide array of oral hygiene issues.1

• Excessive saliva, or its opposite symptom, dry mouth
• Swallowing dysfunction
• Pain in the face or jaw, or “Burning mouth syndrome”

Oral hygiene and Parkinson’s

These symptoms may make it really hard for someone with PD to keep their teeth or dentures to clean, not mention willingly visit their dentist.1

For instance, they might forget to brush daily, or they may have facial pain that is an obstacle to practicing oral hygiene, or they could fall into depression—which can lead to inadequate self-care.1

A person with PD may also struggle to endure a dental visit because of their lack of control with movement and coordination, and bad experiences with dental professionals who aren’t experienced in treating patients with PD can make a future visit something to dread.1

However, poor oral hygiene can lead to a path of additional pain and problems. Obvious concerns are tooth loss and cavities. Sometimes people with PD who have oral pain will also avoid eating or will make poor nutrition choices to avoid pain.1

One serious oral health problem related to PD that may not be apparent—but requires checking by a dental professional—is nocturnal bruxism.

What is nocturnal bruxism?

Nocturnal bruxism describes nighttime tooth clenching or grinding. Like many of the movement behaviors in PD, nocturnal bruxism is an involuntary behavior and not simply the result of stress.2 It’s considered both a symptom of PD and a free-standing sleep disorder.

It’s interesting to note that, while bruxism can happen at any time of day, daytime versions are seldom a complaint in someone with PD.3

Caregivers might notice the actual sound of tooth grinding coming from their loved ones as they sleep. Or it not might be apparent at all. Clenching of the jaw is another form of bruxism that, while silent, can be just as damaging.

Complaints of morning jaw pain, or the discovery of loosened or even broken teeth, may signal a case of nocturnal bruxism. Tight or sore neck muscles are also common. It might be easy to blame the pillow or agingfor these problems, but it would be better to rule out bruxism first, as it can be treated.

Why treat nocturnal bruxism?

The involuntary movements of the jaw in PD, such as nocturnal bruxism, can lead to cracked teeth, the wearing away of tooth enamel—exposing nerve endings—and even changes in the fit and wear of dentures.4

Add these to the long list of other oral hygiene problems that occur as the result of PD and one can only expect to experience more and worsening dental problems—and more of those dreaded dental appointments.

Treatments

Since nocturnal bruxism is a movement disorder, it is treated in much the same way as PD.

Oral drugs such as muscle relaxants or anticholinergic drugs (especially trihexyphenidyl) can provide relief, but they do have side effects such as drowsiness and dry mouth.1

For people with PD who have extreme bruxism, it may become so severe that they cannot open their mouths to chew food; in this case, Botox injections, which paralyze specific muscles in the jaw, can be effective.3

How to ensure success at a dental visit

The Parkinson’s Foundation offers these tips for treating dental concerns in those with PD:4

• Alert the dentist of your (or your loved one’s) PD symptoms, if you haven’t already. Or, if you have, and the visits have not gone well, consider switching to a clinic where the hygienists and dentists specialize in treating PD patients. (Note: If you aren’t sure of PD severity, it may be determined by a dentist specializing in PD according to the modified Hoehn and Yahr scale.)5
• Consider the time of the day when reserving a time slot. When are PD symptoms best controlled during the day? Try for an appointment then.
• The dentist will need to know about any PD-related medications, as some of them can interact with anesthetic drugs used in dental procedures.
• If PD is in an early stage, this is the optimal time to take care of replacements of old dental work (bridges, crowns, or fillings) or poorly fitting mouthguards or dentures. It’s much harder to perform these important dental care procedures in people with later-stage PD.

https://parkinsonsdisease.net/living/oral-hygiene-dentist/?utm_source=weekly&utm_medium=email&utm_campaign=44e0743a-a4b2-4824-aaab-eddaee17ace5&utm_confid=sovjvgl57&aGVhbHRoIHVuaW9uIGJsYWg=b01df4d4845e4be5b0f0c4c755d0cd9e12cc4ea697f57c0fa932d3aa8e10a2ad