High-Intensity Exercise May Be Feasible in Patients With Parkinson’s Disease

November 24, 2016

Merrill R. Landers, PT, DPT, PhD, OCS

PORTLAND, OR —High-intensity exercise is feasible and safe in patients with Parkinson's disease, according to trial results presented at the Fourth World Parkinson Congress. An eight-week high-intensity exercise and fall-prevention boot camp was well attended, and participants tolerated high-intensity aerobic, strength, and balance training exercises, researchers said. 

Most contemporary exercise programs for people with Parkinson's disease are low to moderate in intensity. Recent studies, however, suggest that older adults can safely tolerate high-intensity exercise programs and attain more meaningful benefits. "The optimal parameters of exercise for Parkinson's disease have not been thoroughly explored," said Merrill R. Landers, PT, DPT, PhD, OCS, Professor of Physical Therapy, and James Navalta, PhD, Associate Professor of Kinesiology, both at the University of Nevada in Las Vegas.

To test the feasibility and safety of a high-intensity exercise and fall-prevention boot camp in people with Parkinson's disease, Drs. Landers and Navalta conducted a phase II, pragmatic, randomized clinical trial. 

Twenty-seven participants were included in the study. Fourteen patients were randomized to the high-intensity exercise program, and 13 patients were randomized to a low-intensity control program (ie, Fitness Counts Exercise Program). Physiotherapists supervised the exercise programs at community exercise gyms. 

Patients had an average age of about 64 and disease duration of nearly five years. Nineteen men and eight women enrolled in the study. Most patients were Hoehn and Yahr stage 2. 

The high-intensity boot camp sessions consisted of 30 minutes of aerobic exercise (70% of heart rate maximum), 30 minutes of strengthening (50% to 80% of one-repetition maximum), 15 minutes of balance training, and 15 minutes of active rest and stretching. The control sessions consisted of 15 minutes of aerobic exercise (60% of heart rate maximum), 15 minutes of strengthening (less than 50% of one-repetition maximum), 10 minutes of balance training, 10 minutes of rest, and 10 minutes of stretching. There was not a significant difference in the rate of injuries, falls, or exercise side effects between groups. Adverse events were similar in the two arms. Compared with low-intensity exercise, high-intensity exercise produced greater improvements in balance, physical activity, parkinsonian symptoms, endurance, fatigue, and bone health. 

"These results warrant further investigation in a large-scale comparative effectiveness trial," the researchers concluded. 

—Jake Remaly

http://www.mdedge.com/neurologyreviews/article/113292/parkinsons-disease/high-intensity-exercise-may-be-feasible-patients?channel=249

HOW NEURONS ARE ABLE TO KEEP UP THE CHATTER

NEUROSCIENCE NEWSNOVEMBER 26, 2016

Summary: Researchers provide new insight into the mechanisms of neurotransmission. 

Source: Harvard.

Ultrafast signal transmission between neurons is vital for normal neurologic and cognitive function. In the brain, cell-to-cell communication occurs at the junction that connects two neurons—a structure known as a synapse. NeuroscienceNews.com image is adapted from the Harvard press release.

Neuroscientists have long known that brain cells communicate with each other through the release of tiny bubbles packed with neurotransmitters—a fleet of vessels docked along neuronal ends ready to launch when a trigger arrives.

Now, a study conducted in mice by neurobiologists at Harvard Medical School reveals that dismantling the docking stations that house these signal-carrying vessels does not fully disrupt signal transmission between cells.

The team’s experiments, described Aug. 17 in the journal Neuron, suggest the presence of mechanisms that help maintain partial communication despite serious structural aberrations.

“Our results not only address one of the most fundamental questions about neuronal activity and the way cells in the brain communicate with each other but uncover a few surprises too,” said Pascal Kaeser, senior author on the study and assistant professor of neurobiology at HMS.

“Our findings point to a fascinating underlying resilience in the nervous system.”

Ultrafast signal transmission between neurons is vital for normal neurologic and cognitive function. In the brain, cell-to-cell communication occurs at the junction that connects two neurons—a structure known as a synapse.

At any given moment, neurotransmitter-carrying vesicles are on standby at designated docking stations, called active zones, each awaiting a trigger to release its load across the synaptic cleft and deliver it to the next neuron.

Signal strength and speed are determined by the number of vesicles ready and capable of releasing their cargo to the next neuron.

Neuroscientists have thus far surmised that destroying the docking stations that house neurotransmitter-loaded bubbles would cause all cell-to-cell communication to cease. The HMS team’s findings suggest otherwise.

“Neurons appear to retain some residual communication even with a key piece of their communication apparatus missing.” – Shan Shan Wang

To examine the relationship between docking stations and signal transmission, researchers analyzed brain cells from mice genetically altered to lack two key building proteins, the absence of which led to the dismantling of the entire docking station.

When researchers measured signal strength in neurons with missing docking stations, they observed that those cells emitted much weaker signals when demand to transmit information was low. However, when stronger triggers were present, these cells transmitted remarkably robust signals, the researchers noticed.

“We would have guessed that signal transmission would cease altogether but it didn’t,” said Shan Shan Wang, a neuroscience graduate student in Kaeser’s lab and a co-first author of the study. “Neurons appear to retain some residual communication even with a key piece of their communication apparatus missing.”

Elimination of one active zone building block, a protein called RIM, led to a three-quarter reduction in the pool of vesicles ready for release. Disruption of another key structural protein, ELKS, resulted in one-third fewer ready-to-deploy vesicles. When both proteins were missing, however, the total reduction in the number of releasable vesicles was far less than expected. More than 40 percent of a neuron’s vesicles remained in a “ready to launch” state even with the entire docking station broken down and vesicles failing to dock.

The finding suggests that not all launch-ready vesicles need to be docked in the active zone when a trigger arrives. Neurons, the researchers say, appear to form a remote critical reserve of vesicles that can be quickly marshaled in times of high demand.

“In the absence of a docking sites, we observed that vesicles could be quickly recruited from afar when the need arises,” said Richard Held, an HMS graduate student in neuroscience and co-first author on the paper.

The team cautions that any clinical implications remain far off, but say that their observations may help explain how defects in genes responsible for making neuronal docking stations may be implicated in a range of neurodevelopmental disorders.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The work was funded by grants from the National Science Foundation (DGE1144152) and the National Institutes of Health (F31NS089077; RO1NS083898); and by the Nancy Lurie Marks Foundation, the Brain Research Foundation, the Harvard Brain Initiative and the Lefler Foundation.

Co-investigators included Man Yan Wong, Changliang Liu and Aziz Karakhanyan, all of Harvard Medical School.

Source: Ekaterina Pesheva – Harvard

Image Source: NeuroscienceNews.com image is adapted from the Harvard press release.

Original Research: Abstract for “Fusion Competent Synaptic Vesicles Persist upon Active Zone Disruption and Loss of Vesicle Docking” by Shan Shan H. Wang, Richard G. Held, Man Yan Wong, Changliang Liu, Aziz Karakhanyan, and Pascal S. Kaeser in Neuron. Published online August 17 2016 doi:10.1016/j.neuron.2016.07.005

Abstract

Fusion Competent Synaptic Vesicles Persist upon Active Zone Disruption and Loss of Vesicle Docking

Highlights

•Deletion of RIM and ELKS leads to loss of Munc13, Bassoon/Piccolo, and RIM-BP

•Synaptic vesicle numbers and the PSD remain unaltered after active zone disruption

•This disruption results in loss of vesicle docking and reduced release probability

•Fusion competent vesicles persist upon disruption of the active zone and docking

Summary

In a nerve terminal, synaptic vesicle docking and release are restricted to an active zone. The active zone is a protein scaffold that is attached to the presynaptic plasma membrane and opposed to postsynaptic receptors. Here, we generated conditional knockout mice removing the active zone proteins RIM and ELKS, which additionally led to loss of Munc13, Bassoon, Piccolo, and RIM-BP, indicating disassembly of the active zone. We observed a near-complete lack of synaptic vesicle docking and a strong reduction in vesicular release probability and the speed of exocytosis, but total vesicle numbers, SNARE protein levels, and postsynaptic densities remained unaffected. Despite loss of the priming proteins Munc13 and RIM and of docked vesicles, a pool of releasable vesicles remained. Thus, the active zone is necessary for synaptic vesicle docking and to enhance release probability, but releasable vesicles can be localized distant from the presynaptic plasma membrane.

“Fusion Competent Synaptic Vesicles Persist upon Active Zone Disruption and Loss of Vesicle Docking” by Shan Shan H. Wang, Richard G. Held, Man Yan Wong, Changliang Liu, Aziz Karakhanyan, and Pascal S. Kaeser in Neuron. Published online August 17 2016 doi:10.1016/j.neuron.2016.07.005

http://neurosciencenews.com/how-neurons-are-able-to-keep-up-the-chatter/

Benzodiazepine and related drug use increases hip fractures in persons with Alzheimer's disease

November 25, 2016

The use of benzodiazepines and related drugs increases the risk of hip fracture by 43% in persons with Alzheimer's disease, according to a new study from the University of Eastern Finland. The hip fracture risk was investigated in community-dwelling Finnish persons with Alzheimer's disease. The results of the study were published in the Journal of the American Medical Directors Association.

In total, 21% of persons with Alzheimer's disease initiated benzodiazepine and related drug use during the study. During benzodiazepine and related drug use, 2.5 hip fractures occurred per 100 person-years whereas without drug use, the incidence was 1.4 hip fractures per 100 person-years. The use of benzodiazepines and related drugs increased the hip fracture risk especially during the first six months of drug use. There was no difference within the drug group, as benzodiazepines increased the hip fracture risk as much as benzodiazepine-related drugs.

Additionally, long-term hospital stays exceeding four months after hip fracture were more common in persons with Alzheimer's disease who used benzodiazepines and related drugs at the time of hip fracture than in persons who did not use such drugs.

Treatment guidelines in different countries recommend that behavioral and psychological symptoms of dementia should be treated with nonpharmacological options. Benzodiazepines and related drugs can be used in infrequent or short-term treatment of symptoms. The results of this study highlight the importance of the guidelines to avoid adverse events associated with benzodiazepine and related drug use.

The study was based on the MEDALZ (MEDication use and ALZheimer's disease) cohort, including all Finnish persons diagnosed with Alzheimer's disease between 2005 and 2011, amounting to 70,718 persons. This study involved 46,373 persons who had no history of hip fractures and who had not used benzodiazepines and related drugs during the year preceding the study. The follow-up time in the study was up to five years.

Article: Risk of Hip Fracture in Benzodiazepine Users With and Without Alzheimer Disease, Saarelainen L, Tolppanen A-M, Koponen M, Tanskanen A, Sund R, Tiihonen J, Hartikainen S, Taipale H, Journal of the American Medical Directors Association, doi: 10.1016/j.jamda.2016.09.019, published online 12 November 2016.

http://www.medicalnewstoday.com/releases/314367.php

Dignity and life: UCSC pre-med students paired with patients for course in compassion

November 25, 2016

Dominican Oaks resident Raymond Millard gets regular visits from Hospice volunteer Eric Flores. (Dan Coyro -- Santa Cruz Sentinel)

SANTA CRUZ >> Ray Millard’s room in the retirement home has a great view of the cemetery.

The irony is not lost on the 82-year-old Navy veteran, who was diagnosed three years ago with Parkinson’s disease. In fact, he’s got a pretty good sense of humor about it.

One of Millard’s favorite jokes these days is about a man visiting the doctor’s office. The doctor says he’s stymied by the patient’s symptoms, so he sends him to the hospital. The hospital can’t figure out a treatment plan, so sends the man to a specialist.

“The specialist can’t do anything for you either, so he sends you across the street,” said Millard, pointing to the cemetery. “You’ve heard of one-stop shopping? This is one-stop living.”

Millard, who said he believes one reason he was put on Earth is to make people laugh, is one of about a thousand patients this year receiving care from Hospice of Santa Cruz County, a nonprofit whose vision for the community is for residents to live and die with dignity.

HOSPICE AND UCSC

In October, Hospice of Santa Cruz County was recognized for its Volunteer Visitor Pre-Med program, which recruits hospice volunteers from the Health Sciences internship program at UC Santa Cruz. The students, who now make up 10 percent of Hospice of Santa Cruz County’s volunteer base, provide companionship, run errands and hold bedside vigils for dying patients.

The students are also exposed to the process of dying, a topic rarely discussed in medical school. That’s an experience hospice workers hope will help future doctors consider more end-of-life options for patients, who may prefer to end treatments and die at home rather than a hospital bed.

“In the long run, if we can provide opportunities for future physicians to be at the bedside, conversations with dying patients and hospice referrals will come more naturally to them as physicians,” said Forbes Ellis, director of volunteer services at Hospice of Santa Cruz County.

Millard’s hospice volunteer, UCSC premed student Eric Flores Alvarez, says his studies so far have not included conversations about death, or dying with dignity.

“I guess it’s just too taboo, too sensitive to be talking about, and we don’t pay much attention to it,” said Alvarez ,who plans to study internal medicine and advocate for the uninsured and underinsured. “But hospice is a whole different story. In the training, we’d always talk about death, and how we can normalize the discussion, how we can sit down and engage with it.” 

BEING MORTAL

The program was inspired by the bestselling book “Being Mortal,” written by Dr. Atul Gawande, as well as the documentary by the same name. The works explore how patients and doctors struggle with the topic of death and dying, and advocate for the patient’s quality of life.

Last Thursday, Hospice of Santa Cruz County screened “Being Mortal” for the second time this year at the Del Mar Theater. The first screening, in October, was so well-attended that movie-goers were turned away for lack of seats. The film is also available on YouTube.

Alvarez visits Millard for four hours once a week, in addition to taking 14 units and working nine hours on campus. It’s clear their favorite thing to do together is play bingo for a buck a card with other seniors. 

“I can’t go anywhere without a chauffeur, so he pushes my wheelchair to bingo,” said Millard.

“He introduces me as his personal body guard,” said Alvarez.

Last week Millard won $29 at the bingo table, bringing his total winnings to more than $7,000 in the last four years. Alvarez, not so lucky, is going to keep his day job studying medicine.

Millard, born in Rochester, N.Y., is an upbeat guy, who has “enjoyed every job I ever had,” mostly working in union shops as a member of the United Auto Workers and the International Brotherhood of Electrical Workers. 

He served as an electrician in the Navy on a four-year cruise that began in 1953, keeping equipment running aboard the aircraft carrier USS Bon Homme Richard. He also worked as a lineman’s assistant for the city of Azusa’s power company. Later, he worked at the Chrysler plant in Norwalk, attaching motor numbers to engines and frames as Chryslers rolled by on an assembly line. He was a volunteer firefighter for 23 years in Washington.

One job that didn’t work out so well was at a Huffy bicycle plant, where he tested bicycles for sulfuric acid residue by sucking fumes through a straw, he said. “That’s when I got bounced for trying to get the union in. Only place I worked that wasn’t union,” he said.

GROWING OLD

His good nature aside, Millard said getting old and living with Parkinson’s disease — a degenerative condition that affects nerve cells in the brain — is frustrating. 

“I sit here talking, and my hand can start going like this,” he said, simulating a hand tremor, one of the disease’s signature symptoms. “And when I’m talking to you now, I miss so many words.”

Millard says he doesn’t think about death — “Never.” But then he tells a story about a friend at the retirement home who also had Parkinson’s, who already died at age 75.

“He lives across the street now,” he said, gesturing toward the cemetery.

Millard said when he was young, he never thought much about growing old. And now that he’s old, he is frustrated by basic things, such as not being able to choose where he sits to eat, and not being able to go outside to work crossword puzzles without asking the staff to assist him.

And while he says he doesn’t think about death, he talks about his wife, Joyce, dying in the same facility he’s in now. He keeps pictures of her seven children — his step children — on his refrigerator door. There’s a picture of Joyce there, too.

“She lives across the street now,” he said.

Alvarez says end-of-life processes are difficult for everyone around the patients, even the volunteers. Hospice provides grief support for family members, and is also at the ready to counsel volunteers whose lose a patient.

While in Oaxaca on a medical internship, one of Alvarez’s hospice patients was weighing on his mind, so he emailed Forbes, who advised thinking of the patient while meditating.

Alvarez says it brought him some peace.

Millard seems proud of Alvarez’s choice to pursue medical school.

“I hope he makes it. We need more doctors,” said Millard.

“Thanks, Ray,” Alvarez responded.

“He’s gotta learn to play bingo a little better, though,” Millard joked.

Hospice of Santa Cruz County was awarded the Outstanding Program Achievement Award by the California Hospice and Palliative Care Association in October.

Hospice volunteers commit to four hours a week visiting patients for a minimum of one year. To learn about becoming a volunteer, call 831-430-3045, email fellis@hospicesantacruz.org or visit www.hospicesantacruz.org.

Hospice care

Hospice care is a benefit offered by Medicare, available to patients expected to live six months or fewer. Patients are assigned to a hospice team, including a hospice physician, hospice nurse, hospice aide, social worker, chaplain, grief support and a volunteer, who all work with the patient’s personal physician.

Grief support is provided at no charge to family and friends for a year following a patient’s death.

Hospice also offers pet companions and faith outreach services.

Information: hospicesantacruz.org.

http://www.santacruzsentinel.com/health/20161125/dignity-and-life-ucsc-pre-med-students-paired-with-patients-for-course-in-compassion

Dementia risk declines: Big news for Alzheimer’s, Parkinson’s, stroke

November 25, 2016  Tabitha Powledge 

GIVING THANKS FOR LESS DEMENTIA

If, like me, you’ve been clawing urgently through recent events trying to find reasons to be thankful this Thanksgiving weekend, here’s a big one: As Star Lawrence observes at HEALTH’Sass, “Dementia decreasing–let us give thanks.”

Dementia has dropped dramatically in just a dozen years: from 11.6% of US adults over 65 in 2000 to 8.8% (and even a little lower, to 8.6%, among those over 85) in 2012. See Sharon Begley’s brief summary at STAT.  The paper, free to read, was published by JAMA Internal Medicine on Nov. 21.

Because the US dementia rate plunged after 2000, the researchers said, more than a million people who would have been affected have been spared.

“Dementia” is an umbrella term for loss of memory and thinking and problem-solving ability, often accompanied by startling personality changes. As Trevor Plunkett emphasizes at the BMJ Blog, dementia is not a disease. It is a symptom of disease, and varies with the disease.

Alzheimer’s disease is probably the highest-profile disorder manifesting dementia. But dementia can be a feature of other brain conditions, such as Parkinson’s disease. An estimated 1 out of 3 cases of dementia are due to blood vessel diseases. These include arteriosclerosis (the accumulation of plaque in arteries) and atherosclerosis (artery stiffness with increasing age) that block the oxygen-rich blood brain cells must have to survive.

As Julie Corliss explains at the Harvard Health Blog, dementia can result also from strokes that block blood flow and kill off brain tissue, including the very common “silent” strokes, small blockages deep within the brain. Loss of cognition seems to be more characteristic in Alzheimer’s, while loss of memory often accompanies vascular disease.

Chronic diseases like diabetes and cardiovascular disease (especially high blood pressure) are risk factors for dementia. Those conditions are increasingly likely to be treated, which may be one reason the dementia rate dropped.

But reports on this paper, like Ina Jaffe’s at Shots, often emphasized another factor, one that seems to reduce dementia risk: education. The more you have, the less likely you are to develop dementia. Study subjects in 2000 averaged 11.8 years of education. By 2012 the average, 12.8 years, included a bit of college.

Is this an example of correlation being interpreted as cause? Maybe not. One theory is that education increases “cognitive reserve.” It forces the brain to make more connections. The more complex our brain networks are, the more easily the brain can resist damage by finding ways around it, as Anna Almendrala explains at the Huffington Post.

Her post describes the study methodology, noting that this is not the first research to show that dementia has declined. It is the largest though, involving 21,000 people over 65. “We’re definitely not certain or even confident that the declining risk we saw over the last 25 years will continue to decline, level off, or start ticking back up,” the lead researcher told her.

WHICH BRINGS US TO THE BAD NEWS

In these parlous times, there was bound to be bad news. So, despite the percentage drop, an estimated 5 million people in the US are affected by dementia right now, and the numbers are inevitably  increasing. An estimated 14 million in 2050. And, gulp, 131 million worldwide. The US estimates are driven by the fact that the oldest members of the big post-WWII Baby Boomer population bulge have begun to turn 70. Dementia risk increases with age.

AND MORE BAD NEWS

Which brings us to the latest flop of a miraculous drug–about a hundred potential ones have been studied so far–for Alzheimer’s disease.At In the Pipeline, Derek Lowe is definitive:  “After years of work and untold amounts of money, Eli Lilly’s Alzheimer’s antibody, solanezumab, does not work. It does not help Alzheimer’s patients. No matter how many times you run the Phase III trials, or in which patient populations, they do not get better. No matter how many hopeful press articles you might have seen on its prospects and no matter how many statementsyou might have seen from the company itself, no matter how you may try to spin the results, it does not do anything useful when you give it to actual Alzheimer’s patients. The program is over. It is done, because it does not work.”

(Side note on the In the Pipeline blog. I completely missed the fact that it moved to Science Translational Medicine more than a year ago. Lowe, a medicinal chemist, notes modestly that his reliable and illuminating blog, which focuses mostly on pharma, is one of the oldest science blogs, perhaps even the oldest, having been started in January 2002. “I have never once worked on any compound that has made it all the way to the market, not in 26 years and counting. If you want to know how come your prescriptions cost so much, it’s me.”)

Alison Abbott and Elie Dolgin try to keep hope alive in a post at Nature News, arguing that the drug’s death doesn’t mean that the amyloid hypothesis of Alzheimer’s disease is dead too. The amyloid hypothesis is the idea that Alzheimer’s results from amyloid protein buildup in the brain, known as plaques. Solanezumab is an antibody that seeks and destroys amyloid in blood and cerebrospinal fluid.

Maybe, they suggest, solanezumab would work if you just gave it to patients earlier. . .

But the fact is that the future of solanezumab–and other amyloid-targeting drugs–has been doubtful for a while. See the On Science Blogs post from July 2015. There I noted, “Recent research is also showing that even if a splendid Alzheimer’s drug arrives, it may be splendid for only part of the population, owing to human diversity.”

Despite these continuing disappointments, will the hunt for a magic bullet against Alzheimer’s disease continue?

You bet.

Medicare is now spending around 20% of its funds on caring for Alzheiemer’s patients. Not to mention that the profit potential is ginormous.

http://blogs.plos.org/onscienceblogs/2016/11/25/dementia-risk-declines-big-news-for-alzheimers-parkinsons-stroke/

Further evidence that Parkinson's starts in the gut

November 24, 2016

New research shows that an abnormal protein normally found in brain cells affected in Parkinson's can move from the gut to the brain.

The discovery adds to growing evidence that suggests Parkinson's may start in the gut.

The findings come from an American research team at the annual meeting of the Society of Neuroscience ahead of publication.

Parkinson's protein travels from gut to brain

Lewy bodies are sticky protein clumps that form in brain cells affected by Parkinson's.

The discovery adds to growing evidence that suggests Parkinson's may start in the gut

They are mainly made up of abnormal alpha-synuclein, a protein thought to be important for the spread of Parkinson's.

Researchers from the University of Alabama used mice to study the movement of the alpha-synuclein protein and investigate if the protein could move from the gut to the brain.

They injected a synthetic form of alpha-synuclein into the gut of mice and then used a state of the art technique to track its movement. After 60 days, they found the protein had travelled to the part of the brain affected in Parkinson's.

The link between Parkinson's and the gut

Sophie Mclachlan, Parkinson's UK Research Communications Officer, said:

Understanding how this protein gets to the brain could be key to finding ways to stop the progression of Parkinson's

"We know that many people with Parkinson's experience problems in their digestion – such as constipation – often before movement symptoms appear.

"This research supports previous studies that suggest the first changes in Parkinson's may happen in the gut before spreading to the brain.

"We have much to learn about the origins of Parkinson's. If it does really start in the gut, understanding how this protein gets to the brain could be key to finding ways to stop its progression."

https://www.parkinsons.org.uk/news/24-november-2016/further-evidence-parkinsons-starts-gut

Film supports young children with parents with Parkinson’s disease

November 25, 2016 By Andrew Gould

A new film will help young children with parents with Parkinson's disease by informing teachers and other professionals of the issues (Could not copy original family photo)

The lives of a significant number of primary school-aged children and younger are thought to be affected by having a parent with Parkinson’s – and as a relatively newly recognised phenomenon there is little or nothing to support them or to inform the professionals who interact with them.

Parkinson’s disease is by no means a condition exclusive to the elderly, but as parents have children later in life so the risk of developing the disease while their children are still quite young increases.

As a consequence, little has been put in place to support young children who are struggling with the ramifications of a poorly parent and the complex issues and problems this disease imposes on a family. Families under stress, because of the condition, have little support from teachers, care workers and other professionals who have not been appropriately briefed to understand their needs.

A group of people with Parkinson’s in the South West who are members of the Peninsula Parkinson’s Excellence Network (PenPEN) have worked with Parkinson’s UK and Parkinson’s experts and researchers at Plymouth University to produce the first information resource for teachers and professionals who interact with young children. As well as providing expertise, Parkinson’s UK has also funded the resource, with additional support provided by the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care South West Peninsula (NIHR PenCLAHRC).

The catalyst for the project and project lead is Lyn Fearn, who has Parkinson’s disease and who is mum to Mael, 12 and Amy, seven. Lyn said: 

“I went to a PenPEN meeting and the discussions were very much about the disease and older people. I thought ‘what has this got to do with me?’ and actually asked that question. The conversation then moved to my family’s emotional and psychological experience: how Mael was taking responsibility for my welfare and how that was affecting his time at school; how Amy found it hard because I couldn’t do with her the things other parents could do; and how teachers, doctors and other professionals just didn’t understand our situation. I thought it was important that my children, and children like them, should have a voice and support. This is where our project has come from.”

Called “Listen to my Thoughts”, the resource consists of a film and accompanying text with links for useful information. The film follows the experiences of Jess, a primary school pupil whose mum has Parkinson’s. It shows some of what she has to deal with at home and at school, and ultimately indicates the mutual benefits when she, her parents and her teacher communicate and understand the enormous impact Parkinson’s has on life at home. The film includes quotes from Mael and Amy about their experiences, and an interview with Helen Young, a teacher at Lewannick Community Primary School in Cornwall.

Helen speaks of her experience of teaching children who are affected by living with a parent with Parkinson’s and explains how teachers and other professionals can help.

Leading the project from Plymouth University Peninsula Schools of Medicine and Dentistry is Dr Camille Carroll, an academic neurologist who specialises in Parkinson’s and who leads PenPEN. She said: 

“It is important to remember that Parkinson’s is not just a condition of the elderly. With the trend for people to have children later in life, a greater number of very young children are living lives touched by a parent with the condition.”

She added: 

“A diagnosis of Parkinson’s is stressful for anyone, but add to that the responsibility of raising young children with professionals and support services who, through no fault of their own, just don’t understand the issues involved, there is real potential for children and families to feel even more isolated and vulnerable. That’s why we were very pleased to work with Lyn, who has led this project on behalf of PenPEN, to ensure that the problem is addressed and that resources are created and made available to help professionals provide much-needed relevant support.”

Barbara Williams, Director of Support and Local Groups for Parkinson’s UK, said:

“For every one of the 127,000 people who have Parkinson’s in the UK, there are many loved ones who also have to get to grips with the implications of having someone close to them living with a progressive neurological condition. We welcome the focus of this film highlighting the impact that the condition has on children. Access to high quality information and support is critical for people with Parkinson’s themselves, but also families, friends and carers to ensure that questions can be answered and fears quashed. Parkinson’s UK has resources for young children to help explain Parkinson’s and for teachers and others to use to raise awareness and understanding.”

Parkinson's is a degenerative neurological condition, for which there currently is no cure. The main symptoms of the condition are tremor, slowness of movement and rigidity. It is estimated that one person in every 500 has Parkinson’s, about 127,000 people in the UK. Most people who get Parkinson's are aged 50 or over but younger people can get it too. It can be hard on children whose parents have Parkinson’s and Parkinson’s UK has a range of books to help explain the condition. It is always important to explain Parkinson’s and the circumstances with teachers, care workers and other professionals so that they can understand the needs of the child.

“Children need to be heard” – Lyn Fearn’s story

Lyn Fearn, lives in Cornwall with her husband Eifion (Eif) and children Mael, 12, and Amy, seven. Lyn was diagnosed with Parkinson’s four years ago.

"Parkinson’s caught up with me gradually. It started with losing my sense of smell, and then as a teacher I was finding it hard to write on the blackboard. I started to walk with a limp, and was having problems managing simple things like putting my feet into wellies or keys in locks and doing buttons for the children.

Like most people, and some of the health professionals I saw, Parkinson’s was the last thing in my mind as a reason for all this. Surely I was too young to have the condition? It took three years to get a diagnosis, and when it came it was a bombshell - we had even been told before by a neurologist it was not a serious problem, certainly nothing such as Parkinson’s.

We were having building work done to the house at the time. Eif and I had gone to see the consultant fully expecting to be told we had nothing to worry about. I came into the house and among the chaos, wheelbarrows of cement and workmen I simply burst into tears and fell apart.

I remember it was the October half term and we sat in our lounge which has glass doors. I know the workmen could see me in floods of tears, and the children could too. They didn’t understand what was going on and I remember being really scared – simply full of fear. Eif looked like he had been punched in the stomach and I felt confused, guilty and fearful.

We couldn’t think of what to say to the children. All they could see was us falling apart and we didn’t have the words. In fact, at the beginning we tried to hide it from them.

We got in touch with Parkinson’s UK who were brilliant and gave us some really use information and contacts. We were advised to tell the children, which we did.

Everyone makes plans and you think you’ll live forever and your future is bright, but it was like everything we were looking forward to, had gone. I was a relatively young woman with children, which is unusual for Parkinson’s. Life had to go on. The children had to go to school and Eif had to go to work.

The children had a hard time at school, not through anyone’s fault but because the teachers had received no training or briefing on what to do in a situation like ours. We told the school, but with staff changes the message just didn’t get passed on. Mael especially was struggling. He felt that he was responsible for me. He would go to school and worry all day and not learn anything. He got into trouble at school because no one understood what he was going through. There was no official support for him or for Amy.

As a teacher I realised that, at age four and eight, they simply didn’t have the language or the experience to explain how they felt or to process their feelings. Ours was a crisis for the children more than anyone – at that age they had no one in authority to turn to with the skills and expertise they needed.

It was then I really got that children of their age needed to be helped and that we needed to really think about the resources that would be required. There is little out there to explain Parkinson’s to young children, and what there is focuses on older relatives with the condition.

This created its own worries and concerns – why is this just about grannies? Are you getting older faster mum? Are you going to die soon? For children of Mael and Amy’s age with a parent with Parkinson’s the concepts and resources are so muddled.

It was then that I got involved with the Peninsula Parkinson’s Excellence Network (PenPEN). At the first meeting I went to everything was about older patients and medical advice and I really wondered, what am I doing here? How relevant is this going to be for me?

I raised this with the group and we got on to discussing my family’s situation – and it became apparent that we were not alone.

We decided that there was a need to develop resources not just for young children, but also for the professionals who interact with them. We wanted children to be heard, listened to and looked after.

So, we developed the “Listen to my Thoughts” film and leaflet (the name is actually something Mael said), with backing from Parkinson’s UK and invaluable input from PenPEN and Plymouth University and they are finally complete.

We’re really pleased with the results and we are hopeful that they will make a difference. We’re really grateful to Parkinson’s UK and Plymouth University for their support.

From now on there should be no reason for young children and their families to feel isolated or hopeless because a parent has Parkinson’s. When you are suffering from a condition which leaves you depressed, exhausted, emotionally drained and frustrated and physically ill so that you can’t be the parent you were or want to be to your children, having no support from the professionals involved with you and your family because they simply do not understand your situation and have not had it explained to them, is soul-destroying and damaging, isolating – not just for you but for your children and family relationships.

As more young children are faced with this situation, it is not a problem that is going to go away. In some small way I hope that our film is the first step to ensuring that this is a problem of the past, and that there is a brighter future ahead for families touched by Parkinson’s."

The film is available free of charge. The film can be view at https://drive.google.com/open?id=0B_MoJySrabBvWjVUWFNiMHYtZXM

https://www.plymouth.ac.uk/news/film-supports-young-children-with-parents-with-parkinsons-disease