Young-onset Patients, Like This 34-Year-Old Mom, Focus of Parkinson’s Foundation and Awareness Month

Korines family

Christina Korines was 22 — a recent college graduate and a newly minted Spanish teacher — when she noticed a tremor in her right foot. That tremor soon progressed into a pronounced limp, and an arm that didn’t swing when she walked.

Something was terribly wrong, she just didn’t know what. Neither did her doctors.

”It was exhausting. It was like my leg wouldn’t listen to my body,” Korines told Parkinson’s News Today by phone from River Vale, New Jersey. “It was like something had sliced me right down the middle.”

Her heart told her it was multiple sclerosis, but that illness was ruled out. One specialist fingered essential tremor; another, generalized anxiety disorder. Still another misdiagnosed her with Huntington’s disease. Next, it was Wilson’s disease.

“My husband said ‘let’s keep looking,’” said the mother of two girls, ages 3 and 7. “So I kept fighting.”

She also kept teaching. But her handwriting had become so small, it was nearly illegible for her students. Her voice turned softer and quieter. She made excuses to avoid walking in her middle-school classroom, and even enlisted the help of an aide.

Still, not knowing what was happening was the most frustrating thing.

One doctor off-handedly broached Parkinson’s disease (PD), but dismissed the prospect because of her age, and she had no known family history of the disorder. But the seed had been planted.

One fateful day in late 2017, she went online and looked up Parkinson’s. Soon, she had an appointment with a movement specialist at NYU Langone Health. What came next was a minor miracle: after 10 years, five neurologists, four MRIs, and seemingly rivers of drawn blood, she finally had a diagnosis: young-onset Parkinson’s disease.

Young-onset PD, relatively rare

“I was totally shocked, but in the most weird way relieved,” said Korines, who immediately began treatment, and quickly noticed improvement. “I feel like that was the start of the rest of my life that day. I knew that I could take control as much as I could, and make a game plan.”

The average age for Parkinson’s onset is typically 60. Only around 4 percent of patients are diagnosed before age 50; the disease is considered young-onset in people diagnosed before the age of 40. And while the youngest known Parkinson’s patient was diagnosed at 12, Korines has yet to meet a patient under age 72. In her online social media groups, she has come to know a few 40-year-olds.

Christina Korines, a young-onset PD patient, and her family. (Photo courtesy of Christina Korines)

After she was diagnosed and subsequently retired, her husband — a law enforcement sergeant and her high-school sweetheart — persuaded her to sell their house and move with the family to her parents’ home. He wanted to make sure she’d be looked after while he worked.

These days, Korines, 34, is mostly doing OK. While she had no athletic proclivity prior to PD, she’s now totally into non-contact boxing to help manage symptoms.

“When you hit those mitts, the wires aren’t crossed anymore,” she said. “When I walk out, you wouldn’t even know I was sick.”

She does have symptom flair-ups each month, although her tremors are controlled. She tries to lay down during “off periods,” when her medications are wearing off and it’s not yet time for a new dose. Korines also regularly deals with dystonia — repetitive muscle cramping — in one of her feet.

She has problems with comprehension when trying to multitask, she said. But it’s anxiety that really gets her down. Along with depression, the condition is caused in some patients by chemical changes in the brain.

“I’d take any amount more of the physical pain than a second of the anxiety, because of how crippling it is,” Korines said. “It’s ridiculous, it’s absurd, but it’s there.”

Foundation takes the lead

Korines has found fellowship in the Parkinson’s Foundation, which aims to make life better for people with PD by improving care and advancing research toward a cure. Her story, along with other patient narratives, is featured on the organization’s website.

”When you’re so young with Parkinson’s you feel a little lost, but they provided me with support, and just really embraced me,” she said.

John L. Lehr has been the nonprofit’s president and CEO for just over two years.  The organization is gearing up for April, Parkinson’s Awareness Month. Toolkits and PD community tips are

John Lehr
John Lehr (Photo courtesy of Parkinson’s Foundation)

ready, as are opportunities for patients to share, via videos and photos, inspirational tips and messages. Highlighting the importance of disease awareness, the theme for this year is #KeyToPD.

Some 1 million Americans are thought to have Parkinson’s; Lehr expects that number to reach up to 1.2 million within 10 years. About 10 million people have PD worldwide, he said in a phone interview.

The hiring of Lehr, who has more than two decades of nonprofit fundraising and management experience, followed the merger of two legacy organizations: the National Parkinson Foundation and the Parkinson’s Disease Foundation. On his watch, the newly formed, 100-employee Parkinson’s Foundation has enhanced programming and seen revenue rise by 40 percent.

”What’s so important is the reinvestment in mission programs,” Lehr said. “You always want to do right by the community. It’s a very idiosyncratic disease — no two people have the same course — so we want to make sure it’s not one-size-fits-all.”

About 60,000 new Parkinson’s cases appear annually, he said, much of that owing to better diagnostics. To help address this, the foundation will launch a “newly diagnosed” initiative during April focusing on its 45 Centers of Excellence around the world, including 31 U.S. centers. Beyond setting standards globally, the centers provide expert care to more than 145,000 people.

“It’s going to be a full-court press, including with social media,” he said. “We want engagement early and often.”

The importance of exercise

Lehr said patients with young-onset PD, like Korines, are looking at many years of coping because of the disease’s progressive nature. Those diagnosed in their 60s can live several decades and longer, he said, if they’re proactive.

Still, major science hurdles abound.

“The last 20 to 30 years, we’ve learned a lot,” he said. “But there’s no real therapy, let alone a cure. We don’t know what causes it — genetics, the environment, or some combination. Answers to those big questions will prevent, slow, or even halt the disease.”

One of the foundation’s biggest efforts is its Genetics Initiative, dedicated to using genes to uncover mechanisms responsible for hindering or stopping the disease’s progression. Announced last year, it’s the first national Parkinson’s study to offer free genetic testing plus counseling for Parkinson’s-related genes, including the GBA and LRRK2 mutations.

Its goal is to track the genetic makeup of 15,000 PD patients across 50 U.S. sites within a year, with the first patients expected to be enrolled at six sites in April.

The pilot is an expansion of the Foundation’s ongoing 10-year-old Parkinson’s Outcomes Project. With more than 12,000 participants in five countries, it’s the largest clinical study of PD to date, and acts to help patients better manage their disease and receive better care. It also tracks and reports on research findings, and expects that those enrolled might be more interested in participating in clinical trials.

Along with its array of patient and caregiver support and fundraising efforts, the Parkinson’s Foundation has been busy on other fronts, recently hosting its first medical marijuana and Parkinson’s conference, and creating its first patient-centered research agenda for women.

The most significant Parkinson’s development during his tenure so far, Lehr said, has not been drug or even diagnostic discovery, but rather the heightened awareness of exercise.

“There will always be advancements in therapeutics,” he said. “But the importance of staying active — be it walking, boxing, dancing — and how it functions as good as a drug, has been the biggest news.”

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A Healthy New Identity Helps When Battling a Chronic Disease


Identity, the “I” in CHRONDI Creed, refers to the process of finding a health-fostering identity in the face of a chronic disease that has stolen things we loved to do and caused the death of self. When everything I loved to do was taken from me, all that was left was the time and energy I was putting into managing the disease.

Dealing with chronic disease consumes a large amount of time, and conversations about me were now connected to the disease, including my own self-talk. Without even knowing how, and thinking I should know better, the disease had filled that void created by the death of self. The disease had become my identity, and I hated it. I had to find a healthy new identity to help when battling a chronic disease.

Trying to “find yourself” is tied to one of those great philosophical questions: “What is the nature of human existence?” I have written about this philosophical quest and I thought I had a handle on things, a strong identity of scientist, teacher, and healer. But when the roles I used to make meaning of my existence were stripped from me, I discovered that my intellectual writings provided a thin tether out of the dark void created by the death of self. The actions in my life, the conversations, did not match my identity roles of scientist, teacher, and healer. I needed to reconstruct these identity roles — trying on new hats, looking for one that helps me build a new healthy identity. I needed this new healthy identity to succeed in my battle with a chronic disease.

Getting one’s actions in life, the roles we take on, to match the true self is not an easy thing to do in the face of chronic disease. It takes a commitment of personal resources, courage, and persistence to create new healthy roles to fill the void left after the death of self. It also helps to have support from peers, friends, and family.

But most importantly, you need a fire in the belly, a passion, a purpose that brings meaning from these action roles you will be creating. Then you need to do something every day that will move you one step closer to that purpose-driven life and a healthy identity matching the true self.

I started working on creating these new roles in 1999 when I left all that was my life (home, career) to pursue a PhD — the second-hardest challenge I have faced in my life. I also retrained myself to use the computer as a way of teaching and for a tool in aiding scientific inquiry. In 2006 I applied those skills to a science research project, which, after 13 years, has yielded new discoveries ready to share with the public.

I is for identity
(Courtesy of Dr. C)

I have also forced myself to become a writer in the humanities by writing as often as time allowed. I forced myself to become a computer-aided graphic artist and taught myself how to design a website. These skills — web design, writing, and graphic arts — helped me to re-establish the multimodal teacher role.

In 2018 I became a column writer for BioNews Services, giving me the opportunity to put the multimodal teacher into action more frequently, hopefully as a role model. Recreating the roles of scientist and teacher, after the death of self, is ongoing for me. Every day is a commitment to these re-created healthy roles as part of building a new identity. It is hard work, but worth it.

The one part of my identity that is still trapped in the void after the death of self is my role of healer. It is a role that is closest to my true nature, my soul. I have received written testimonials from dozens of people who stated that their lives were changed through encounters with this healer role. I miss that contribution to the well-being of individuals and to the collective well-being of society. I am going to try a different hat. It’s a hat with which holding the compassion space for others is expected, and in some ways embraced, so I can bring my experience in doing that and use it — hopefully.

I don’t know what will happen while wearing this new hat. I am just opening the door to new possibilities.

What new hats are you trying? Share your experiences in the comments so others may benefit.


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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ITI-214 Safe, Well-tolerated in Mild to Moderate Parkinson’s Patients, Phase 1/2 Trial Shows


Treatment with the experimental oral therapy ITI-214 was safe and well-tolerated in patients with mild to moderate Parkinson’s disease, according to a Phase 1/2 clinical trial.

Trial findings also suggested that ITI-214 may ease motor symptoms in these patients.

The study, “A Phase I/II Clinical Study of  ITI-214, a Novel Phosphodiesterase-I (PDE1) Inhibitor, for the Treatment of Parkinson’s Disease (PD),” was presented during AD/PD 2019 — The 14th International Conference on Alzheimer’s and Parkinson’s Diseases, taking place March 26-31 in Lisbon, Portugal.

ITI-214 is a selective blocker of an enzyme called phosphodiesterase 1 (PDE1), implicated in the breakdown of cAMP and cGMP. These two messenger molecules act within cells of the nervous system in response to diverse signals. Because altered PDE1 activity has been reported in both neurological and cardiovascular diseases, blockers such as ITI-214 are intended to restore its normal function.

Work in rodent models suggested that ITI-214, being developed by Intra-Cellular Therapies, may relieve motor and non-motor symptoms of Parkinson’s. In preclinical studies, the investigational therapy also reduced neuroinflammation through its effect on microglia — key immune cells in the central nervous system — and prevented neurodegeneration.

Data from four Phase 1 trials in healthy volunteers showed that treatment with ITI-214 was generally well-tolerated and safe.

Researchers are now presenting clinical data from the randomized, double-blind, placebo-controlled Phase 1/2 trial (NCT03387215) that primarily evaluated the safety and tolerability of increasing doses of ITI-214 in patients with mild to moderate Parkinson’s.

As secondary goals, the seven-day Intra-Cellular Therapies-sponsored study assessed the compound’s pharmacokinetics — its absorption, distribution, metabolism, and excretion in the body — as well as biomarkers of inflammation, and motor and non-motor effects through the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale.

The 40 participants (50 years and older) were maintained on stable Parkinson’s therapy. All five doses of ITI-214 — 1, 3, 10, 30, and 90 mg — were found safe and generally well-tolerated. In addition, the findings showed signals of less motor dysfunction and dyskinesia — involuntary, jerky movements — with some of the administered doses.

“Clinical data indicate that ITI-214 is safe and generally well tolerated across a range of doses in patients with mild to moderate [Parkinson’s],” the scientists wrote.

Noting that the signals of clinical improvement warrant further evaluation, the team added that “selective PDE1 inhibition may represent a novel approach for the treatment of motor and non-motor symptoms associated with [Parkinson’s].”

Of note, all seven of the study’s authors are employees of Intra-Cellular.

Besides Parkinson’s, ITI-214 is being evaluated in a Phase 1/2 trial (NCT03387215) in patients with heart failure, which is supported by results showing increased heart contraction strength in dogs and rabbits.

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Parkinson’s Patients with Diabetes at Higher Risk of Impulse Control Disorders, Other Issues, Study Suggests

diabetes, Parkinson's

Untreated Parkinson’s patients who also have type 2 diabetes mellitus may be at a higher risk of developing impulse control disorders, severe depression, apathy, and sleep problems, research suggests.

The study, “Preexisting Diabetes Mellitus is Associated with More Frequent Depression and Impulse Control Disorders in Drug Naïve Parkinson’s Disease” will be presented during the 14th​ International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders March 26-31 in Lisbon, Portugal.

Higher doses of dopamine agonists — which act as a substitute for (or mimic) dopamine in the brain — and longer treatment periods have been seen to make Parkinson’s patients more prone to developing impulse control disorders, including gambling, compulsive shopping, over-eating, and compulsive sexual behaviors.

Evidence indicates that type 2 diabetes increases the risk of developing Parkinson’s disease. Interestingly, an association among type 2 diabetes, depression, and impulse control behaviors has also been suggested.

Researchers from the University of Pécs in Hungary sought to study the impact of pre-existing type 2 diabetes mellitus on Parkinson’s-related non-motor symptoms and on impulse control behaviors in people with Parkinson’s not yet taking prescribed antiparkinsonian medications.

The team performed detailed neurological and neuropsychological examinations on 299 newly diagnosed Parkinson’s patients who were not on any medication.

Of these Parkinson’s patients, 77 (25.8%) had pre-existing type 2 diabetes. Diabetic Parkinson’s patients were older, heavier (with a higher body mass index) and included more men. Importantly, and in comparison to non-diabetic Parkinson’s patients, diabetic patients had more severe depression, apathy, sleep problems and more severe non-motor symptoms, measured by the Non-Motor-Experiences of Daily Living part of the Movement Disorders Society-sponsored Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) and the Non-motor Symptoms Scale.

Scientists also reported that 40.3% of Parkinson’s patients with diabetes had impulse control behaviors, which was significantly different from the 22.3% observed in the non-diabetic sample.

Untreated Parkinson’s patients with diabetes were 3.58 times more likely to have impulse control disorders. Due to this, type 2 diabetes mellitus was considered to be an independent predicting factor for the development of these behavior disorders.

Preexisting diabetes may be a risk factor for more frequent impulse control disorders and more frequent and more severe depression, apathy and sleep problems in drug naïve PD patients. However, further prospective longitudinal studies are warranted to study its effects on the disease course,” the researchers concluded.

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Mouse Studies Suggest Protective Effects of Caffeine in Parkinson’s Disease

caffeine and Parkinson's

Two new studies in mice suggest that caffeine might have protective effects in the brains of Parkinson’s disease patients.

The studies, “Chronic Caffeine Treatment Modulates  Disease Progression in a Transgenic Alpha-Synuclein Prion-Like Spreading Mouse Model of Parkinson’s Disease,” and “Chronic Caffeine Treatment Reverses A-Synuclein-Induced Cognitive Impairment With Enhanced Dendritic Spine Density and Morphology in Mice,” will be presented during the 14th​ International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders, March 26-31 in Lisbon, Portugal.

Previous epidemiological studies have suggested that consuming caffeine might protect against the development of Parkinson’s. These more-recent studies set out to test this premise more directly in an animal model.

Both studies used mouse models of Parkinson’s that involved injecting mice with alpha-synuclein. This protein is a major component of Lewy bodies, irregular “clumps” in brain cells that are a hallmark of Parkinson’s pathology. Specifically, both research teams used a mutant form of the protein called A53T, which forms these clumps even more effectively than the wild-type protein.

In both studies, injection with A53T led to changes characteristic of Parkinson’s disease, such as impaired motor function and memory, as well as changes in brain physiology, like the development of the aforementioned Lewy bodies and loss of dendritic spines (parts of neurons involved in making connections in the brain).

However, when the mice were given caffeine in their drinking water, these effects were lessened. Both studies showed similarly beneficial results, though the exact parameters that were measured were different.

In the first study, researchers at Aarhus University, Denmark, report that mice given caffeine had less alpha-synuclein in their brains. Caffeine also caused a three–week delay in the onset of clasping, which is a behavior mice do with their hind limbs that is indicative of brain damage. Furthermore, caffeine-treated mice lived, on average, 40% longer than their counterparts who weren’t given caffeine.

In the second study, researchers at Wenzhou Medical University, China, reported that mice given caffeine had fewer memory problems and more dendritic spines than their untreated counterparts.

Both studies support the previous epidemiological evidence that caffeine can be protective for Parkinson’s disease, although there is the usual caveat that experiments in animal models are never a perfect replica of actual human disease.

It also is not clear why or how caffeine might have such protective effects, and further research will be needed to figure out just how caffeine might benefit Parkinson’s patients.

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Is a Parkinson’s Life a Poem in Disguise?



Sherri Journeying Through

I’ve rarely had the thought, “Why me?” Does this mean that I’ve signed my life over to Parkinson’s disease? Is it a sign that I’ve given up?

Last week at my boxing class, I was punching a bag when I heard laughter coming from the other side of the half-wall. Behind the divider were our caregivers, family members, and friends who come to watch and cheer us on. However, I’m not convinced that their sole reason for coming is to encourage us; I think they enjoy the camaraderie with each other even more than watching their loved ones do forward lunges and situps. 

You could call it a caregiver support group. While we are jogging, tripping, punching, or attempting to rise from where we lie exhausted on the mat, they are on the other side of the wall sharing stories. The outburst of laughter caught my attention as I punched the bag, and I thought, “It’s not fair. Why me?” And as soon as the thought appeared, I reprimanded myself for indulging in such notions.

I want to be able to walk and run without inhibition; to eat my dinner without choking; to write legibly or type more than one letter every 30 minutes. I want my brain to do as I command and not stop me in my tracks.

The next train of thought went something like this: 

Yes, why not me? Would I instead prefer that a friend be afflicted with trembling, choking, and pain? My immediate response was “no!” Still, I’d rather not have this bruising of a blessing that appears as a curse in disguise. But just because I don’t want it doesn’t mean I’m going to get my way and be healed by the mighty hand of God — a God who sometimes, in my captivity with this disease, seems far away. 

During the night hours, I realize that my pain, sleeplessness, and cramping are not reasons to whine and wail but are part of a plan to complete His workmanship in my life. 

The word “poem” comes from the Greek word “poiēma,” which means “that which is made” or “workmanship.” Think about that for a moment.

We are a beautiful poem that is being written by the hand of God.

We are a poem written to inspire and encourage those who watch and read our lives. Knowing that, how could we ever again say, “Why me?”


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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MJFF Grant Will Help Inflazome Develop Brain-imaging Probe for Parkinson’s Research

Inflazome, funding

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) has granted more than $1 million to Inflazome to fund the development of a brain-imaging probe that may help track progression of Parkinson’s and develop new therapies for the disease.

The funding will help develop a positron emission tomography (PET) tracer specific to a cellular sensor of stress known as the NLRP3 inflammasome, and may enable quick, accurate and non-invasive imaging of brain inflammation, according to Inflazome.

Such a tool could increase the likelihood of success in clinical trials by  helping to select suitable patients at the appropriate disease stage, and providing a way to determine whether a treatment candidate binds to the target of interest in the brain, the company believes. The tracer also will help Inflazome determine what doses are needed in clinical trials.

The NLRP3 inflammasome is a multiprotein complex believed to drive chronic inflammation in Parkinson’s and other neurodegenerative diseases. A recent study in postmortem brains from Parkinson’s patients and mouse models of the disease showed that this inflammasome is activated by aggregated alpha-synuclein, the main component of Lewy bodies, and loss of dopamine-producing nerve cells. Both Lewy bodies and death of dopaminergic neurons are hallmarks of Parkinson’s.

Then, the researchers found that MCC950, an oral small-molecule blocker of the NLRP3 inflammasome, completely suppressed inflammasome activation in microglia, a key cell type in immune responses in the central nervous system (brain and spinal cord). MCC950 also inhibited alpha-synuclein clumping, prevented the loss of nerve cells, and eased motor deficits in a mouse model of Parkinson’s disease.

In a press release, Matthew Cooper, Inflazome’s co-founder and CEO, said The Michael J. Fox Foundation is a fantastic organization with a passionate commitment to new science, science translation and candidate therapies for Parkinson’s.”

Cooper, a co-author of the preclinical study and the principal investigator in the newly funded project, also mentioned that Inflazome and MJFF “are fully aligned” to help people with Parkinson’s and other neurodegenerative diseases with unmet medical needs. “Their support will help us advance and hopefully validate our disruptive approach to diagnose and then treat patients by focusing on neuroinflammation.”

Jamie Eberling, director of research programs at MJFF, said that having a tool to visualize brain inflammation “may help investigate Parkinson’s onset and progression as well as evaluate new treatments that could alter the course of the disease.” Eberling also said that MJFF “is investing in this research due to the significant potential impact on drug development and patient lives.”

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Milk Linked to Greater Risk of Parkinson’s, Swedish Study Shows

milk risk factor

Consumption of more than 40 milliliters (1.3 ounces) of milk per day is associated with an increased risk of developing Parkinson’s disease. Still, dietary intake of yogurts or soured milk does not pose a risk, results from a large-scale Swedish study show.

The study “Milk, Yogurt, and Soured Milk Consumption and Risk of Parkinson’s Disease,” will be presented Erik Olsson, PhD, an associate professor at Uppsala University, during the 14th International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders, March 26-31, in Lisbon, Portugal.

Dairy products are widely consumed worldwide and could be important contributors for the development of human disease.

Previous studies have suggested consuming dairy products could be linked to an increased risk of Parkinson’s disease, particularly among men.

More recently, a study has shown that total dairy intake was not associated with a significant risk of Parkinson’s. However, daily consumption of low-fat or skim milk instead of full-fat milk was linked to a 39% higher chance of Parkinson’s disease.

To further explore this issue, Swedish researchers reviewed the incidence of Parkinson’s disease in 81,889 adults during a mean follow-up period of 13.9 years. None of the participants had Parkinson’s when the study started in 1997, and they all answered a questionnaire about dietary regimens and food intake frequency.

A total of 1,251 cases of Parkinson’s disease were reported among this population, according to information from the Swedish National Patient and Cause of Death Registers.

Analysis of the dietary patterns of this population revealed that people who consumed 40 milliliters (ml) or more of milk per day had increased risk of having Parkinson’s disease.

In particular, individuals who drank 40 to 159 ml per day of milk had a 30% higher risk of developing Parkinson’s, compared to people who had low daily milk intake (less than 40 ml per day). The risk increased similarly for people who consumed even higher amounts of milk, with 25%, 33%, and 33% higher risk for 160-200 ml, 201-400 ml, or more than 400 ml per day of milk.

In contrast, researchers did not find any significant association between intake of yogurt or soured milk and long-term risk of developing Parkinson’s disease.

These risk estimates did not change when the team analyzed the data according to participants’ gender, with no differences found between men and women.

“Findings from this cohort study indicate that consumption of milk, but not soured milk and yogurt, is associated with an increased risk of Parkinson’s disease,” researchers concluded.

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Review Study Provides Update on Treatments for Parkinson’s Non-motor Symptoms

non-motor symptoms, Parkinson's

Although there are now more treatment options available for non-motor symptoms in Parkinson’s disease, a lack of evidence on their effectiveness and safety means that more studies and new therapeutic strategies are needed, according to a review study.

The study, “Update on Treatments for Nonmotor Symptoms of Parkinson’s Disease — An Evidence‐Based Medicine Review,” appeared in the journal Movement Disorders.

The International Parkinson and Movement Disorders Society Evidence-Based Committee reviewed research published from 2011 through 2016 on Parkinson’s non-motor symptoms to help physicians select the most effective treatments and provide an update to a 2011 study.

Two online databases were searched, resulting in the inclusion of 37 studies with 20 patients or more. In all of the included studies, treatment lasted a maximum of six months, except for one low-quality safety study, meaning the recommendations do not cover long-term symptom management, the team noted. The studies included pharmacological, surgical, and nonpharmacological interventions, which had to be available in at least one country.

According to their level of evidence, the different approaches were classified as efficacious, likely efficacious, unlikely efficacious, non-efficacious, or with insufficient evidence. To address practice implications, the team also rated the interventions as clinically useful, possibly useful, and unlikely useful, not useful, or investigational.

Christopher G. Goetz, MD, president of the International Parkinson and Movement Disorders Society, noted the differences between this approach and practice guidelines issued by medical associations such as the American Academy of Neurology. In a Neurology Today article written by Susan Fitzgerald, titled “Which are the Most Efficacious Therapies for Nonmotor Parkinson Disease Symptoms?” he said that “guidelines are really culturally based,” and take into account “regulatory issues, access issues, and insurance issues.”

“With evidence-based methodology, we are strictly looking at the published evidence. We don’t tell you whether we recommend it (a specific therapy),” he added.

No clinical trials met the inclusion criteria for the treatment of anxiety disorders, excessive sweating, rapid eye movement behavior disorder, and olfactory or ophthalmologic dysfunction.

Six new studies were reviewed for depression. One addressed venlafaxine, characterized as efficacious, with an acceptable safety risk and no need for specialized monitoring, and clinically useful. This contrasted to amitriptyline, which has insufficient efficacy evidence to treat depression in Parkinson’s patients and was rated as possibly useful. Paroxetine, citalopram, fluoxetine and sertraline, all selective serotonin reuptake inhibitors (SSRIs), were categorized in a similar way.

Rotigotine, marketed as Neupro, was found unlikely efficacious based on the results of one study, and rated as investigational regarding practice implications. Rasagiline, marketed as Azilect, also showed insufficient evidence of efficacy and was classified as investigational as well.

As for nonpharmacological interventions, two studies on repetitive transcranial stimulation showed inconsistent effects on depression. However, its benefits in the general population and in specific measures in people with depression make this approach possibly useful for short-term treatment of Parkinson’s.

Cognitive-behavioral therapy (CBT) could only be rated as likely efficacious and has insufficient safety evidence in the treatment of depression in Parkinson’s due to the lack of replication of its benefits, the investigators cautioned.

Treatments for apathy were also evaluated. Rivastigmine, marketed as Exelon, was found efficacious in one study, but its small group of patients mean that this medication is only possibly useful in the clinic. A similar conclusion was reached for piribedil following deep brain stimulation. In contrast, Neupro was classified as unlikely efficacious based on one trial.

As for the treatment of impulse control disorders, naltrexone, marketed as ReVia, showed insufficient efficacy and safety evidence, while CBT was rated as likely efficacious and possibly useful clinically based on one new study.

Regarding dementia, Aricept (donepezil) and Razadyne (galantamine) still have insufficient efficacy evidence, but were rated possibly useful in clinical practice due to their established benefits outside Parkinson’s.

Both rasagiline and rivastigmine have insufficient efficacy evidence to treat cognitive impairment. A similar conclusion was reached for transcranial direct current stimulation and for cognitive rehabilitation in patients on computer-based cognitive training.

Three new studies were evaluated for psychosis. While olanzapine, marketed as Zyprexa, is not efficacious and therefore not useful from a clinical perspective, Nuplazid (pimavanserin) was characterized as efficacious over six weeks and clinically useful. Seroquel (quetiapine) has insufficient evidence though it is possibly useful in the clinic.

Studies of sleep disorders indicated that Lunesta (eszopiclone) and melatonin have insufficient evidence for the treatment of insomnia, but are possibly useful. Modafinil, marketed as Provigil, is also possibly useful for excessive daytime somnolence and sudden onset of sleep in people with Parkinson’s. Continuous positive airway pressure was considered likely efficacious and possibly useful in lessening daytime sleepiness in patients with obstructive sleep apnea, and Neupro was rated the same for improving sleep quality in Parkinson’s patients.

Assessed treatments of orthostatic hypotension — defined as a drop in blood pressure when standing up — included midodrine and fludrocortisone, marketed as Florinef. Although both have insufficient efficacy evidence, they are classified as possibly useful in the clinic due to benefits seen in clinical trials.

The only trial concerning urinary dysfunction addressed solifenacin, marketed as VESIcare, as a treatment for overactive bladder. It showed that this medication has insufficient evidence on efficacy, but is possibly useful in clinical practice due to benefits observed outside Parkinson’s, while having an acceptable safety risk without specialized monitoring.

One other study addressed erectile dysfunction. Viagra (sildenafil) was considered efficacious and clinically useful, with data in the general population indicating an acceptable safety risk.

Similar efficacy and clinically utility conclusions were presented for botulinum toxin B as a therapy for drooling. Both botulinum toxin type A and B should be administered by well-trained physicians with access to specialized monitoring tools, the researchers emphasized.

Three studies evaluated approaches for gastrointestinal dysfunction. Results of one trial led to lubiprostone, marketed as Amitiza, being considered likely efficacious and possibly useful to treat constipation in people with Parkinson’s. Its safety data in the general and elderly populations indicate that lubiprostone has an acceptable risk in Parkinson’s patients.

Probiotics were categorized as efficacious and clinically useful, which support their over-the-counter use and lack of safety concerns. In contrast, abdominal massages with lifestyle advice have insufficient evidence on safety and efficacy to ease constipation.

Rasagiline was also evaluated as an approach for fatigue, considered efficacious and possible useful based on one small study. One trial analyzed acupuncture in Parkinson’s, but although benefits were found, this approach still has insufficient efficacy evidence.

For pain, prolonged-release oxycodone-naloxone has insufficient evidence, but is possibly useful for Parkinson’s patients with chronic pain, with an acceptable safety risk without specialized monitoring. Rotigotine also has insufficient evidence as a way to lessen pain in Parkinson’s patients, despite benefits seen in one trial.

Overall, despite the substantial growth in the evidence base of approaches for non-motor symptoms in Parkinson’s, this update shows that treatment options remain limited, making the development and testing of new therapies “a top priority,” the team said.

According to Daniel Weintraub, MD, research on Parkinson’s psychiatric and cognitive symptoms is key due to the specificity of the disease compared with the same manifestations found in the general population. He also said this update may help investigators spot areas in need of clinical trials, such as anxiety.

Laura Marsh, MD, a professor of psychiatry and neurology at Baylor College of Medicine, cautioned that although the new review provides “a useful analysis for clinicians to consider,” they still have to practice “the art of medicine.” This involves challenges such as evaluating if dopaminergic therapies for motor function are causing non-motor side effects and what symptom to address first in people with more than one of these complications, she said.

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For Parkinson’s Patients, the Sense of Loss Is Relentless

disease of loss

I fight for my health every day in ways that most people don’t understand. I’m not lazy. I’m a warrior!” –Unknown

Parkinson’s disease (PD) is a disease of loss. It chips away one’s ability to perform seemingly mindless tasks.

Examples of what I have lost to Parkinson’s disease

The list of things I can no longer do, or no longer do without a lot of effort, may seem inconsequential:

  • Putting a letter or card in an envelope
  • Keeping a slipper or clog on my left foot
  • Opening a sealed envelope
  • Picking up a thread on the floor
  • Turning the pages of a book
  • Tying my shoes
  • Rolling over in bed or on the floor
  • Opening up packages
  • Shaving my underarms
  • Rolling a yoga mat
  • Folding laundry
  • Washing the hair on the left side of my head
  • Holding a handbag close to the left side of my body
  • Finding the edge of the toilet paper on the roll
  • Slipping on a sports bra
  • Trying to put on pants while standing on one leg
  • Putting on pierced earrings
  • Writing legibly
  • Walking without fear of my left foot dragging and tripping me

“…[I]f opening your eyes, or getting out of bed, or holding a spoon, or combing your hair is the daunting Mount Everest you climb today, that is okay.” –Carmen Ambrosio

What is the most troubling loss for me?

A more disturbing concern is that I can’t be trusted to hold on to something firmly with my left hand, whether it is a cup of coffee or giving my rabbit his medication.

As an example, while giving medicine to my bunny, I was holding the bottle in my left hand and used an eyedropper with my right hand to administer the medication. Next thing I know, I looked down and saw pink medicine all over my rabbit’s fur. I was unaware that my left hand was tipping the bottle. So, not only did I waste the medicine, I also had to clean the rabbit.

I once spilled hot paraffin wax all over the kitchen floor, counter, and cabinets because I could not hold on to the paraffin container while trying to empty it. It took me almost two hours to clean up the mess.

The loss of my left-handed grip is a problem in itself, but the extra work and cleanup I have to do when it fails me are even more troubling.

PD is progressive

Just when I think I can deal with what I have lost, something else that I used to perform with ease now eludes me. It almost feels like a death by a thousand paper cuts.

While the loss of the ability to perform each activity is no big deal, it is the daily, collective, and continuing loss of other activities that serves as a constant reminder that I have an incurable and progressive disease. Day after day, this wears me down, and it seems the list of lost functionalities grows on a monthly basis.

Sometimes you will be in control of your illness and other times you’ll sink into despair, and that’s OK! Freak out, forgive yourself, and try again tomorrow.” –Kelly Hemingway

What’s the big deal?

While it may be easy to find a workaround now, PD is relentless, and someday it may get to the point where I don’t have an alternative way to accomplish a task. This is when independence is lost. Facing new failings every day, no matter how insignificant, is daunting and can fuel a sense of despair and hopelessness.

How can I best combat PD?

Keeping my sense of humor about some of the ridiculous things PD does to my body will be my salvation. Laughter will be one of the most effective weapons in my arsenal while I battle this insidious disease.

You either get bitter or you get better. It’s that simple. You either take what has been dealt to you and allow it to make you a better person, or you allow it to tear you down. The choice does not belong to fate, it belongs to you.” –Josh Shipp


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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