Depression Diagnosis Increases Your Risk Of Parkinson’s Disease

 November 17, 2015

Parkinson’s disease belongs to a group of conditions called motor system disorders. Symptoms include tremor, rigidity, slowness of movement, and impaired coordination. A comprehensive study from Sweden finds people with depression are more likely to develop this disease.

Beginning at the end of 2005, researchers looked at the records of all Swedish citizens age 50 or older. Then, they identified 140,688 people who’d been diagnosed with depression and matched each of these with three control participants (without depression) of the same sex and birth year. Going forward, the researchers tracked the depressed participants and their controls while also retroactively examining medical records.

During the study period, 1,485 people with depression developed Parkinson’s disease, while 1,775 people of those who did not have depression similarly developed the disease. This amounts to 1.1 percent compared to 0.4 percent.

Analyzing the data further, the researchers found Parkinson’s disease was diagnosed 4.5 years, on average, after the study began. Generally, the likelihood of developing Parkinson’s disease decreased over time. Depressed people were 3.2 times more likely to develop Parkinson’s disease within a year of the study’s start date than controls. At 15 to 25 years after the start date, depressed people were about 50 percent more likely to develop the disease.“We saw this link between depression and Parkinson’s disease over a timespan of more than two decades, so depression may be a very early symptom of Parkinson’s disease or a risk factor for the disease,” Dr. Peter Nordström of Umeå University stated in a press release.

Elusive Cause

Parkinson’s is a result of the loss of dopamine-producing brain cells, yet scientists do not understand what causes the brain changes that lead to Parkinson’s disease. Generally, it is known that men are more likely than women to develop the disease. It also is known that the disease usually begins after age 60. Having a close relative with the disease and ongoing exposure to herbicides and pesticides increases your risk of developing the illness. For these reasons, scientists speculate a blend of genetic and environmental factors contribute to the disease.

In the Swedish study, the seriousness of depression impacted participants’ risks of Parkinson’s. Anyone who had been hospitalized for depression was 3.5 times more likely to develop Parkinson’s disease than depressed people treated only as outpatients. And, compared to those hospitalized for depression just once, people with major depression and hospitalized five or more times were 40 percent more likely to develop Parkinson’s.

When researchers adjusted for other conditions related to depression, such as traumatic brain injury, stroke, and alcohol and drug abuse, the link between this form of mental illness and Parkinson’s disease did not change. The researchers also examined siblings. Here, they found no link between one sibling having depression and the other having Parkinson’s disease.

“If the diseases were independent of each other but caused by the same genetic or early environmental factors, then we would expect to see the two diseases group together in siblings, but that didn’t happen,” said Nordström

http://healthcaresolutionsplus.org/depression-diagnosis-increases-your-risk-of-parkinsons-disease/

New saliva gland test may better diagnose patients with Parkinson’s Disease

Nov.18, 2015

It’s difficult for patients to absolutely know if they have Parkinson’s disease.

To date, the only way to diagnose someone with Parkinson’s is to do a clinical exam to access his or her symptoms. And in order to definitively get an answer, an autopsy is performed on the brain – only after the person has died.

But now, a conclusive clinical test may soon be available. Researchers from the examining a specific portion of a person’s saliva gland may be able to diagnose someone with Parkinson’s.

The idea to focus on such a small part of the human body came when lead author Dr. Charles Adler conducted a long-term study, examining people for Parkinson’s and dementia – for the course of their lives. Once the patients in the study had died, Adler and his team would perform whole body autopsies, looking at all the organs in the body.

“[During the autopsy] you can see the protein alpha-synuclein” – an abnormal protein associated with Parkinson’s disease – “and we find that in multiple areas of the body as well,” Adler, with the Mayo Clinic Arizona and a fellow of the American Academy of Neurology, told FoxNews.com. “However, the area that seemed to be most dense in the body was the submandibular gland – the salivary gland right under the jaw.”

Currently, the way to determine through autopsy if a person has Parkinson’s is to look for an aggregate of proteins called Lewy bodies in the mid-section of the brain. One of the proteins located in the Lewy bodies is the alpha-synuclein protein. Because of the protein’s association with Parkinson’s, Adler felt confident the protein’s location in the gland was specific to the disease.After identifying the salivary gland to be significant for Parkinson’s patients, Adler conducted another experiment, examining all of the submandibular glands of his autopsy patients. Of his already pre-determined Parkinson’s patients, all 28 of them had the alpha-synuclein protein in their submandibular glands.

Moving on to the third phase of his research, Adler decided to do biopsies on the submandibular glands of living Parkinson’s patients, to determine if this test made sense to do in living individuals.

“In the study we’re reporting now, we biopsied 15 living patients,” Adler said. “Unfortunately, in four of those cases, there was not enough gland tissue – so we had 11 cases to analyze. Of those 11 cases, nine of the 11 had that abnormal protein. So that’s 82 percent, which is pretty exciting.”

According to Adler, an 82 percent positive diagnosis is significant because the accuracy of Parkinson’s diagnosis to date is only about 80 percent of living individuals. Even if a patient is determined to have Parkinson’s during their lifetime, 20 percent of them turn out not to have the condition; they actually had a Parkinson’s –like illness instead.

“It definitely proves the concept that by doing a biopsy of living people with Parkinson’s, we have the opportunity to better diagnose the disease while their alive,” he added.

http://www.caringcare.info/?p=1160

THE IMPACT OF DATSCAN ON PARKINSON'S DISEASE DIAGNOSIS

18th November 2015 - New research

The aim of this study was to evaluate the impact of DaTscan in people with and without Parkinson's Disease in order to assess the degree of confidence in the diagnosis of Parkinson's Disease. DaTscan is the name of a clear colourless solution used for injection in SPECT scans. A SPECT scan uses a radioactive substance and a special camera to create three dimensional images that show how the organs work. The patient is positioned on a table in the room where they undergo the SPECT scan. For more information go to : http://www.mayoclinic.org/tests-procedures/spect-scan/basics/definition/prc-20020674

When a DaTscan was carried out on people with definite Parkinson's Disease, the DaTscan was markedly abnormal in 92% of people with Parkinson's Disease and normal in the remaining 8%. Each of the sensitivity and positive predictive values of DaTscan in patients who had a clinical diagnosis of Parkinson's Disease is therefore 92%. In people with an uncertain diagnosis of Parkinson's Disease, 48% had remarkably abnormal scans, 16% had mild abnormalities, and 36% had normal scans.

A markedly abnormal DaTscan is confirmed as the diagnostic pattern for Parkinson's Disease but not in all people with Parkinson's Disease. Remarkably abnormal scans can also occur in people who did not have a certain diagnosis of Parkinson's Disease. Therefore, even though the DaTscan is one of the most accurate methods of diagnosing Parkinson's Disease no method of diagnosis provides complete certainty.

Reference : Clinical Nuclear Medicine [2015] 40 (5) : 390-393 (I.Gayed, U.Joseph, M. Fanous, D.Wan, M.Schiess, W.Ondo, K.S.Won)

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/25783511

http://www.viartis.net/parkinsons.disease/news/151118.pdf mail@viartis.net

©2015 Viartis 

10 Unusual Facts About Parkinson’s Disease You Never Knew About

Nov.17, 2015

The unfortunate revelation that the late Robin Williams may have committed suicide due to a diagnosis of the neurological disease Parkinson’s has created an uptick in interest in finding out all about the dreaded condition. Here are 10 facts you have likely never heard of before.

10. Adolf Hitler Had Parkinson’s Disease

Getty Images

The German tyrant and dictator suffered from Parkinson’s, but it was well hidden from the general public in photographs, films and propaganda.

I daresay I’m not the only one who thinks it’s too bad the disease didn’t strike him down and dead BEFORE he began his reign of terror and Holocaust against any group of people he didn’t deem fit to live.

9. Parkinson’s Costs More Than You Think

Between treatments, preventative measures, lost income and wages amongst other money-eating problems, Parkinson’s Disease costs victims ,000 a year.

• The combined direct and indirect cost of Parkinson’s, including treatment, social security payments and lost income from inability to work, is estimated to be nearly $25 billion per year in the United States alone.
• *Medication costs for an individual person with PD average $2,500 a year, and therapeutic surgery can cost up to $100,000 dollars per patient.*
• (* Per Parkinson's Disease Foundation)

Of course, such treatments wouldn’t cost an arm and a leg if the government wasn’t beholden to the special interests and insurance companies that put profit over proper health coverage. Until that day, we plebeians find our wallets and bank accounts drained.

8. Please Don’t Pass the Batwing Casserole

A strange but incredibly true fact is that many who reside in Guam that love to dine on bats for dinner have developed Parkinson’s Disease. Apparently bats dine on plants and animals that contribute to a heavy buildup of neurotoxins that wreak havoc on whoever eats them.

So, the Addams Family and the Munsters may want to rethink their menu sometime soon.

7. Woody Allen was right?

In his comedy smash Sleeper, Woody Allen made a joke that high cholesterol diets and vices such as smoking and drinking were actually good for the human body. Research claims that a person is less likely to get Parkinson’s if they smoke, drink too much coffee, have high cholesterol and drink booze.

Since I avoid all of the above, I guess my Parkinson’s-free life goal isn’t looking too good.

6. Poison is Used to Treat the Disease

That’s right, a poisonous plant is used for Parkinson’s medication. Nightshade, a plant so lethal that a mere bite of a leaf can kill a normal sized human, is the basic ingredient of known Parkinson’s meds.

I can hear this being used as an excuse in a murder trial: “Your honor, my client wasn’t trying to poison his wife. He realized she had early signs of Parkinson’s disease and was just trying to treat her with a homeopathic plant!”

5. One Battle of the Sexes Men Wish They Weren’t Winning

Men are twice as likely to be diagnosed with Parkinson’s than women are.

I’m pretty sure even the most repulsive, obnoxious and stubborn male chauvinist on earth wouldn’t do a victory lap over this one.

4. There is no known cause

There is no one thing that causes Parkinson’s. So far, research has determined that such variables as environmental factors, viral infections and drug abuse are amongst the various things that can set off the disease.

Unfortunately, we are no closer to figuring out a root cause now than we were a century ago. Just where is that research money going?

3. Even children can get Parkinson’s

The youngest known person ever diagnosed was a three-year-old boy in 1875. Currently, the youngest living person diagnosed with Parkinson’s Disease was 12 years old.

So if you’re a teacher who notices a young student trembling and moving oddly, don’t assume they are merely goofing off for attention. He or she just may be one of the few children with this disease.

2. There is no definitive test to diagnose it

Getty Images

There is no blood test or lab procedure to diagnose it. Currently, one has to rely on a doctor’s evaluation of your symptoms and a series of motor skill tests. Our governments can’t find the money to fund development of a definitive diagnostic test, yet they seem to find enough money to pay for their golf outings, parties, perks and fancy receptions.

1. The disease truly doesn’t discriminate

It doesn’t matter what your race, creed, earning status or gender is. Parkinson’s Disease doesn’t discriminate as to who it afflicts itself upon.

Think about that one next time you’re feeling entitled and invincible while reading about another person’s misfortunes. It’s a most sobering feeling.

by Bill Treadway

http://www.mymedclinic.info/2015/11/17/10-unusual-facts-about-parkinsons-disease-you-never-knew-about-2/

Living with an ailment that puts one's survival instincts into play

Opinion: The never-ending tests of Parkinson's disease

Saturday November 14, 2015

Living with an ailment that puts one's survival instincts into play
Ken Thurman

Times Union - I fell again last week. That's been happening a lot lately.

In January, I took a leave of absence from my job to battle Parkinson's disease, a debilitating neurological malfunction in a part of the brain that basically controls one's balance and ability to walk.

At the time, I didn't know what to expect or even if I'd ever be well enough to return to work as an editor at the Times Union. Unfortunately, retirement became my best option and, on Aug. 28, I called it a career after more than 30 years as a journalist.

For me, each day brings a mixture of personal victories and defeats that may seem like no big deal to most people. Some days, for example, I get excited if I can just stand up long enough to brush my teeth or pour myself a bowl of cereal for breakfast.

Then there are days when I feel "normal" and, for an hour or so, I forget that I'm sick. But, as the cocktail of prescribed drugs — totaling nearly 30 pills a day — begins to wear off, the reality of PD's presence in my life returns.

Medically, PD is considered a movement disorder because signals from the brain to other parts of the body (especially the arms and legs) are interrupted as millions of brain cells die off prematurely. Scientists aren't sure why this occurs, but PD usually strikes people in their 50s or 60s. I was in my mid-50s when I was diagnosed. That was four years ago when I noticed a subtle twitch in my right hand when I used the computer at work.

At the time, all I knew about PD was that it made its victims shake uncontrollably, and that boxing legend Muhammad Ali and actor Michael J. Fox were among those who have it. I've since learned that PD is quite complex and how it manifests varies from patient to patient. The type I have often leaves me struggling just to lift a leg or foot a couple of inches, like the rusted Tin Man in the "Wizard of Oz." There are also times when my feet feel as if they are encased in concrete. This limits my mobility, and turning around in a narrow room or space can be a real challenge.

My biggest fear is falling and breaking an arm or a leg — or worse.

Parkinson's disease makes no apologies for what it steals from you, and it forces you to check your dignity at the door. I've lost track of the number of times my neighbor has had to help me get dressed. The Schenectady Fire Department has been to my home more than once, including an assistance call I made in July when I broke two toes by kicking a wall during an apparent nightmare related to my cocktail of medications. Each time I stumble or fall I learn a lesson about a progressive disorder that will continue to test me as it advances.

The classroom is inside my head where there are mood swings, periods of psychological paralysis, tremors and vertigo. I also get frustrated if I cannot perform simple tasks such as being able to walk across the room to answer the phone before it stops ringing.

I often feel like I am living in a basement apartment in a world where "life" begins on the first floor.

To slow the progression of the disease, I use a regimen of exercise, meditation and music. My day usually begins about 9 a.m. with AC/DC blasting away on the stereo and me wildly jumping up and down. This is my self-prescribed cup of black coffee, which I count on to release endorphins needed to get moving.

Time also takes on a whole new dimension and things seem to move a lot slower because the disease often impacts your fingers and hands. I'm still trying to get used to the reality that it can take me up to three hours to get dressed. Just putting on my socks took almost 20 minutes the other day; pants, shirt and shoes easily took another hour — and that doesn't include showering and grooming.

If necessity is the mother of invention, I can honestly say that my survival instincts have been pressed into duty. For example, when I'm home alone and unable to walk, I carefully map out my trek through my home before setting out on a pillow, which I use to scoot across hardwood floors. To avoid getting stuck in a corner, I study angles and objects such as door frames and radiators that can serve as leverage points with the handle of my cane — nicknamed "Excalibur."

At first, I used my cane to help me keep my balance while I walked or stood in line at a grocery store or bank. Today, I use it to turn on the stereo (and adjust the volume or radio station). I can also turn on the television and lights. It took a lot of patience and practice, but I can even use it to take a phone off the hook or table and dial 911. Next up is the kitchen sink water faucets. I'm currently working on incorporating use of the stove, microwave and even the telephone answering machine.

But don't feel sorry for me. Instead, feel empathy for the more than 1 million people in the United States who grapple to live with this mysterious and progressive disease. By sharing my personal experiences, I hope to raise awareness of PD, which affects some 55,000 more people each year.

The writer is a Schenectady resident and recently retired Times Union editor.

http://www.timesunion.com/tuplus-opinion/article/The-never-ending-tests-of-Parkinson-s-disease-6632549.php

https://nwpf.org/stay-informed/news/2015/11/the-never-ending-tests-of-parkinsons-disease/

Ask the MD: FAQs on Lewy Body Dementia

The terms Lewy body dementia and Dementia with Lewy bodies are used interchangeably, as are the abbreviations LBD and DLB.

Posted by  Rachel Dolhun, MD, November 17, 2015

1.       What is Lewy body dementia?

Lewy body dementia (LBD) is a form of dementia, which is a broad term for a disease of memory, thinking and/or social abilities that are severe enough to interfere with everyday activities. LBD is also a form of Parkinsonism, meaning that it causes some or all of the motor symptoms of Parkinson’s disease (tremor, stiffness, slowness, and walking/balance problems). Additionally, LBD causes visual hallucinations (seeing things that aren’t there) and unpredictable fluctuations in a person’s level of attention or alertness. Many people will also exhibit changes in mood (such as depression) and alterations in behavior or personality (including agitation or aggression). REM sleep behavior disorder (a condition in which people act out their dreams), fainting spells and low blood pressure can also be associated. Symptoms of LBD may seem to arise in the course of several months or may be more gradual in onset. The symptoms do, unfortunately, worsen and people with LBD will require progressively more assistance over time.  

2.       What is the difference between Lewy body dementia and Alzheimer’s?

Lewy body dementia (LBD) and Alzheimer's dementia (AD) are both types of dementia, meaning that they cause problems with memory, thinking and/or social abilities that are severe enough to interfere with everyday activities. Both of them affect “cognition” or thinking capabilities. In general, AD affects memory more significantly (causing forgetfulness) whereas LBD impacts executive function (planning and processing information) and the ability to understand visual information. LBD also causes some or all of the motor symptoms of Parkinson’s (tremor, slowness, stiffness, and walking/balance problems). People with AD may develop these symptoms too but if so, it’s typically much later in the disease course. Visual hallucinations (seeing things that aren’t there) and fluctuating levels of alertness and attention are more characteristic of LBD than AD. While every individual’s course is different, AD usually progresses a bit slower than LBD.

3.       What is the difference between Parkinson’s disease and Lewy body dementia?

Parkinson's disease (PD) is characterized by motor symptoms, including resting tremor, stiffness, slowness, and walking/balance problems. The diagnosis of PD relies on the presence of slowness plus tremor and/or stiffness. Many people with PD will experience cognitive (memory or thinking) problems, which can range from mild — “mild cognitive impairment” — to severe — “dementia.” However, not everyone with PD will have memory problems; not everyone with memory problems will have dementia; and not everyone with dementia will be classified as having Lewy body dementia (LBD). Even in people with PD, other types of dementia (Alzheimer’s dementia, vascular dementia — that due to multiple strokes, etc.) can occur. Lewy body dementia typically causes some or all of the motor symptoms of PD, memory/thinking problems, visual hallucinations, and fluctuating levels of attention or alertness.

4.       I have Parkinson’s disease. Am I more likely to get Lewy body dementia?

Some studies suggest that having Parkinson’s disease increases your risk of developing Lewy body dementia but having Parkinson’s certainly isn’t a guarantee that you will develop the condition.

 5.       Is there a test to diagnose Lewy body dementia?

There is no test that can diagnose Lewy body dementia (LBD). Imaging studies (brain PET, SPECT, DaT scans) are being researched to determine if they might be able to accurately diagnose LBD. At the present time, doctors make the diagnosis based on your medical history and their physical examination. Blood work and standard imaging tests (MRI or CT scans) may be done to exclude other medical conditions. Detailed memory testing is sometimes performed to support a doctor’s diagnosis or establish a baseline for comparison to future testing. Movement disorders specialists (the same physicians who treat Parkinson’s) or cognitive specialists (doctors who treat dementia) typically manage LBD.

6.       Are there any treatments for Lewy body dementia?

There is currently no medication that slows or stops the progression of Lewy body dementia (LBD). However, there are many medications that can help with the symptoms. 

For memory and thinking problems, medications called acetylcholinesterase inhibitors (e.g., donepezil, galantamine and rivastigmine), which are also used for Alzheimer’s dementia, are commonly prescribed. These drugs sometimes help control behavior problems and hallucinations as well. 

The motor symptoms that are similar to those of Parkinson’s disease (tremor, slowness and stiffness) can be treated with levodopa. Because people with LBD are usually a little more sensitive to the side effects of this medication, doctors use the lowest dosage possible.  

If visual hallucinations are frightening or disturbing, or if delusions (false beliefs) or paranoia occur, medications called atypical antipsychotics (e.g., quetiapine or clozapine) may be prescribed. These are used cautiously in select cases because they can potentially worsen the symptoms of LBD. Medication might be avoided, at least for a while, if hallucinations aren’t severe and a person can be reassured regarding them. A visual examination should also be performed as vision problems (the need for corrective lenses, for example) can trigger or worsen hallucinations. 

If REM sleep behavior disorder (a sleep disorder in which a person acts out their dreams) is present, melatonin or clonazepam may be helpful.

7.       Is there anything that can be done to prevent Lewy body dementia?

No therapies or behavioral changes have been identified that can prevent Lewy body dementia (LBD). However, some strategies have been suggested to help stave off memory problems in general, and since these don’t have side effects and are good for overall well-being and quality of life, they are worth a try. Recommendations include eating a healthy, balanced diet; exercising regularly; interacting with others socially; and doing activities to stimulate memory and thinking (e.g., reading, completing crossword puzzles, playing a musical instrument, etc.). Decreasing stress and getting enough sleep — easier said than done! — are also beneficial for everyone, of course.

8.       Are there genetic risks for Lewy body dementia?

There are no clear genetic factors that increase one’s risk for Lewy body dementia (LBD). It is worth mentioning, though, that several genetic risk factors do exist that increase risk for Parkinson’s disease, and Parkinson’s may increase risk for LBD.

9.       Do all people with Parkinson’s have Lewy bodies? Do Lewy bodies always cause dementia? How do you know if you have Lewy bodies? 

The vast majority of people with Parkinson’s disease (other than a rare subset with a certain genetic mutation) have Lewy bodies — clusters of abnormally folded proteins, including alpha-synuclein, which are found in the nerve cells in the brain. Not everyone with Parkinson’s disease who has Lewy bodies gets dementia. 

There is no way to know if you have Lewy bodies because the only way we can see them at the current time is to study the brain at autopsy (although some imaging tests are being done in research settings). We are also working on ways to measure alpha-synuclein (which could indirectly tell us about Lewy bodies) with brain imaging and other testing.

10.   What resources are available for people with Lewy body dementia and their caregivers?

The Lewy Body Dementia Association has an abundance of educational materials, caregiver resources and information about ongoing clinical trials. Your doctor can also connect you to local support groups and staff — social workers and physical and occupational therapists — who can help you navigate the symptoms and course of LBD.

https://www.michaeljfox.org/foundation/news-detail.php?ask-the-md-faqs-on-lewy-body-dementia

PROLONGED-RELEASE OXYCODONE–NALOXONE FOR TREATMENT OF SEVERE PAIN IN PATIENTS WITH PARKINSON'S DISEASE

PROLONGED-RELEASE OXYCODONE–NALOXONE FOR TREATMENT OF SEVERE PAIN IN PATIENTS WITH PARKINSON'S DISEASE (PANDA): A DOUBLE-BLIND, RANDOMISED, PLACEBO-CONTROLLED TRIAL

December 2015 

Prof Claudia Trenkwalder, MDcorrespondenceemail, Prof K Ray Chaudhuri, FRCP, Pablo Martinez-Martin, MD, Prof Olivier Rascol, MD, Reinhard Ehret, MD, Martin Vališ, PhD, Maria Sátori, MD, Prof Anna Krygowska-Wajs, MD, Prof Maria J Marti, MD, Prof Karen Reimer, MD, Alexander Oksche, MD, Mark Lomax, MSc, Julia DeCesare, MSc, Michael Hopp, MD for the PANDA study group 

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Background Pain is a common non-motor symptom of Parkinson's disease. We investigated the analgesic efficacy of prolonged-release oxycodone–naloxone (OXN PR) in patients with Parkinson's disease and chronic, severe pain. 

Methods We did this phase 2 study in 47 secondary care centres in the Czech Republic, Germany, Hungary, Poland, Romania, Spain, and the UK. We enrolled patients with Hoehn and Yahr Stage II–IV Parkinson's disease, at least one type of severe pain, and an average 24-h pain score of at least 6 (assessed on an 11-point rating scale from 0=no pain to 10=pain as bad as you can imagine). Participants were randomly assigned (1:1) with a validated automated system (block size four) to either oral OXN PR or placebo for 16 weeks (starting dose oxycodone 5 mg, naloxone 2·5 mg, twice daily). Patients and investigators were masked to treatment assignment. The primary endpoint was average 24-h pain score at 16 weeks in the full analysis population. This study is registered with EudraCT (2011-002901-31) and ClinicalTrials.gov (NCT01439100). 

Findings We enrolled 202 patients; 93 were assigned to OXN PR and 109 to placebo; the full analysis population consisted of 88 patients versus 106 patients. Least squares mean average 24-h pain score at 16 weeks in the full analysis population was 5·0 (95% CI 4·5 to 5·5) in the OXN PR group versus 5·6 (5·1 to 6·0) in the placebo group (difference −0·6, 95% CI −1·3 to 0·0; p=0·058). Similar proportions of patients in each group had adverse events (60/92 [65%] vs 76/109 [70%]), treatment-related adverse events (52/92 [57%] vs 62/109 [57%]), and serious adverse events (5/92 [5%] vs 7/109 [6%]). Treatment-related nausea was more common in the OXN PR group than in the placebo group (16/92 [17%] vs 10/109 [9%]), as was treatment-related constipation (16/92 [17%] vs 6/109 [6%]). 

Interpretation The primary endpoint, based on the full analysis population at week 16, was not significant. Nonetheless, the results of this study highlight the potential efficacy of OXN PR for patients with Parkinson's disease-related pain and might warrant further research on OXN PR in this setting.

http://www.epda.eu.com/en/research-papers/2015/lancet/12-01-lancetneurol/

Intel and Michael J. Fox Foundation present update on Apache Spark research

NOVEMBER 16, 2015 BY CHARLES MOORE

At the first Spark Summit Europe, a presentation by Intel researchers in cooperation with the Michael J. Fox Foundation  proposed that Big Data could be the key to unlocking the mysteries of Parkinson’s disease. Summit Europe is the premier event bringing together the community known as Apache Spark, a fast and general Open Source engine for big data processing, with built-in modules for streaming, SQL, machine learning and graph processing.

Summit attendees convened from Tuesday, Oct. 27, through Thursday, Oct. 29, meeting in celebrated Dutch architect Berlages magnum opus Beurs Van Berlage in Amsterdam. They heard from leading production users of Spark, Spark SQL, Spark Streaming and related projects, discovered where project development is going, and learned how to use the Spark stack in a variety of applications.

Big Data analytics’ architect and development manager Ido Karavany, with Intel’s Advanced Analytics group, addressed the Summit on leading edge technology projects within Intel involving Big Data & Stream analytic solutions in the Internet of Things (IoT) and in Parkinson disease (PD) research. Mr. Karavany has more than eight years of experience in software development in the domains of data analytics and distributed computing solutions.

In his Oct. 28 presentation entitled “Using Spark in an IoT Analytics Platform Enable breakthroughs in Parkinson Disease Research,” Mr. Karavney presented a partnership-developed approach that may enable breakthroughs in Parkinson’s disease research by leveraging wearable sensors, smartphones and big data analytics to monitor PD patients’ motor movements 24/7.

He explained that the research team has built an IoT Big Analytics platform (on Amazon Cloud Drive) based on open source technologies, such as Cloudera Distribution for Hadoop, to enable collection and processing of high data streams (up to 1 GB per patient per day). Mr. Karavney noted that the platform has been successfully used in multiple clinical trials and the project has started ramping up to connect thousands of patients 24/7 by the end of 2015.

The platform uses HBase & HDFS as its main scalable storage layer. The analytics batch layer leverages Apache Spark (over HBase & HDFS) and includes a set of complex machine learning algorithms, sophisticated event-based rule engine, an automatic change detection engine and a variety of PD-related measurements.

Examples for those are activity recognition, patients’ sleep quality, tremor detection, PD gait recognition, and others. Mr. Karavney’s presentation included an explanation of the way researchers are using Spark for implementing their machine learning algorithms.

“We’ll focus on our challenges using Spark, starting with data extracting from HBase challenges and solutions for our batch and near-real time calculations, [and] we’ll also review our solution evolution and will show what worked and didn’t work for us (i.e. Many small jobs vs. fewer consolidated larger jobs, multiple vs. single Spark contexts),” Mr.Karavney said.

You can view and download the slideshow from Mr. Karavney’s presentation here.

A YouTube video of the presentation also can be viewed here.

Parkinson’s disease (PD) is a chronic, progressive, degenerative neurological disorder of poorly understood cause, in which the nerve cells that produce the natural brain chemical dopamine are damaged and unable to produce enough of the biochemical agent. The resulting diminished dopamine levels cause a variety of problems associated with movement, including tremors (shaking), stiffness, and slowness of movement. There is currently no known cure for Parkinson’s.

“Nearly 200 years after Parkinson’s disease was first described by Dr. James Parkinson in 1817, we are still subjectively measuring Parkinson’s disease largely the same way doctors did then,” Michael J. Fox Foundation CEO Todd Sherer, PhD told Special Guest Correspondent Chrissie Cluney reporting for IoT Evolution News. “Data science and wearable computing hold the potential to transform our ability to capture and objectively measure patients actual experience of disease, with unprecedented implications for Parkinson’s drug development, diagnosis and treatment.”

Diane M. Bryant, Senior Vice President and General Manager of the Intel Data Center Group

The variability in Parkinson’s symptoms creates unique challenges in monitoring progression of the disease,” Diane M. Bryant, Senior Vice President and General Manager of the Intel Data Center Group, told Ms. Cluney. “Emerging technologies can not only create a new paradigm for measurement of Parkinson’s, but as more data is made available to the medical community, it may also point to currently unidentified features of the disease that could lead to new areas of research.”

Ms. Bryant leads the worldwide organization that develops the data center platforms for the digital services economy, generating more than $14 billion in revenue in 2014. In her current role, she is building the foundation for continued growth by driving new products and technologies from high-end co-processors for supercomputers to high-density systems for the cloud, to solutions for big data analytics.

Sources:

Spark Summit Europe

Intel

Michael J. Fox Foundation

http://parkinsonsnewstoday.com/2015/11/16/might-parkinsons-unlocked-via-big-data-internet-things/