I Ask This Of You!

I have Parkinson's diseases and thought it would be nice to have a place where the contents of updated news is found in one place. That is why I began this blog.

I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible.

I am not responsible for it's contents. I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish.

This is for you to read and to always keep an open mind.

Please discuss this with your doctor, should you have any questions, or concerns.

Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. I will not accept any information about Herbal treatments curing Parkinson's, dementia and etc. It will go into Spam.

This is a free site for all with no advertisements.

Thank you for visiting!

Saturday, March 26, 2016

Deep-brain stimulation helps Erie Parkinson's patients plus video

March 26, 2016

Mark Richardson, M.D., prepares to insert a small electrode into the brain of patient Joyce Dowdy during surgery at UPMC Hamot in Erie on March 24. Dowdy, 66, is being treated for Parkinson's disease and was conscious during the procedure. GREG WOHLFORD/ERIE TIMES-NEWS Powerful medicines that help control the 66-year-old Springfield Township woman's tremors and keep her muscles loose are working for shorter periods of time.

ERIE, Pa. -- Joyce Dowdy is slowly giving ground in her nearly 20-year battle with Parkinson's disease.

Powerful medicines that help control the 66-year-old Springfield Township woman's tremors and keep her muscles loose are working for shorter periods of time.

"Unfortunately it's common with Parkinson's patients to see the medication not last as long," said Dimitrios Nacopoulos, M.D., a UPMC Hamot neurologist who treats Dowdy.

Instead of increasing Dowdy's medications, which could cause serious side effects, Nacopoulos and other UPMC physicians offered Dowdy deep-brain stimulation.

It's a surgery where tiny electrodes are placed deep in the areas of Dowdy's brain responsible for movement. Electrical charges are delivered through the electrodes to block the abnormal nerve signals that cause tremors and related Parkinson's symptoms."Not everyone with Parkinson's is a good candidate," Nacopoulos said. "Patients, like Joyce, who still respond to medication tend to do well, even if they maybe aren't responding to the medication as long."

Parkinson's patients who also have any type of dementia usually do not respond well to deep-brain stimulation.

Deep-brain stimulation is a treatment, but not a cure, for Parkinson's. The goal is to control tremors and other symptoms as well as medication does, only for longer periods of time, allowing doctors in many cases to reduce the amount of medication a patient requires.

Dowdy underwent the first stage of deep-brain stimulation Thursday at Hamot. UPMC neurosurgeon Mark Richardson, M.D., now performs deep-brain stimulation at the Erie hospital in addition to UPMC Presbyterian.

"Before we implant each DBS electrode, we thread three microelectrodes into that area of the brain," Richardson said in a Hamot operating room as his surgical team prepared Dowdy for surgery. "They allow us to monitor and record the neuron activity, which gives us a more precise map of exactly where the DBS electrode should go."

Dowdy was sedated but awake during the surgery because Richardson at times needed to ask her questions and have her raise her hands to test for Parkinson's symptoms.

"Joyce, can you say 'Today is a sunny day in Erie?'" Richardson asked Dowdy.

"Today is a sunny day in Erie," Dowdy said clearly.

It took Richardson and his team about four hours to implant two DBS electrodes in Dowdy's brain through a pair of 14-millimeter holes near the top of her head, then test the electrodes to see if they reduced her Parkinson's symptoms.

Dowdy underwent a second procedure Friday where a wire was threaded down her neck and attached to a pacemaker-like device under her collarbone that generates a pulse to block the abnormal nerve signals.

"We will wait about four weeks to turn on her device," Nacopoulos said. "Her brain needs time to heal from the surgery."

Nacopoulos will tweak Dowdy's device during three postoperative office visits, making small changes in the pulse's voltage, frequency and area.

By the end of the third visit, Dowdy should be able to walk as well as she does during her best moments on medication, but for most of the day instead of just a couple of hours, Nacopoulos said.

Some patients have benefitted from deep-brain stimulation for more than 10 years.

"We can then see about decreasing her medications, which can help because as the disease progresses we can then increase those doses again," Nacopoulos said.

DAVID BRUCE can be reached at 870-1736 or by e-mail. Follow him on Twitter at

Friday, March 25, 2016

Electroencephalographic prodromal markers of dementia across conscious states in Parkinsons disease

March 25, 2016

In Parkinson’s disease, electroencephalographic abnormalities during wakefulness and non-rapid eye movement sleep (spindles) were found to be predictive biomarkers of dementia. Because rapid eye movement sleep is regulated by the cholinergic system, which shows early degeneration in Parkinson’s disease with cognitive impairment, anomalies during this sleep stage might mirror dementia development. 

In this prospective study, we examined baseline electroencephalographic absolute spectral power across three states of consciousness (non-rapid eye movement sleep, rapid eye movement sleep, and wakefulness) in 68 non-demented patients with Parkinson’s disease and 44 healthy controls. All participants underwent baseline polysomnographic recordings and a comprehensive neuropsychological assessment. Power spectral analyses were performed on standard frequency bands. Dominant occipital frequency during wakefulness and ratios of slow-to-fast frequencies during rapid eye movement sleep and wakefulness were also computed. 

At follow-up (an average 4.5 years after baseline), 18 patients with Parkinson’s disease had developed dementia and 50 patients remained dementia-free. In rapid eye movement sleep, patients with Parkinson’s disease who later developed dementia showed, at baseline, higher absolute power in delta and theta bands and a higher slowing ratio, especially in temporal, parietal, and occipital regions, compared to patients who remained dementia-free and controls. In non-rapid eye movement sleep, lower baseline sigma power in parietal cortical regions also predicted development of dementia.

During wakefulness, patients with Parkinson’s disease who later developed dementia showed lower dominant occipital frequency as well as higher delta and slowing ratio compared to patients who remained dementia-free and controls. At baseline, higher slowing ratios in temporo-occipital regions during rapid eye movement sleep were associated with poor performance on visuospatial tests in patients with Parkinson’s disease. Using receiver operating characteristic curves, we found that best predictors of dementia in Parkinson’s disease were rapid eye movement sleep slowing ratios in posterior regions, wakefulness slowing ratios in temporal areas, and lower dominant occipital frequency. 

These results suggest that electroencephalographic slowing during sleep is a new promising predictive biomarker for Parkinson’s disease dementia, perhaps as a marker of cholinergic denervation.

Genetic syndrome may underlie some Parkinson's cases

March 25, 2016 at 5:15 PM
By Eleanor McDermid

Rare deletions at chromosome 22q11.2 are present at an increased rate in patients with Parkinson's disease (PD), researchers report in The Lancet Neurology.

PD has been reported in patients with 22q11.2 deletion syndrome, which is a heterogeneous, multisystem disorder, with features including cleft palate, cardiac and skeletal abnormalities and learning difficulties. This latest study shows the converse to be true, with 22q11.2 deletions present in eight of 9387 PD patients from four independent studies, but none of 13,863 controls.
The eight identified patients all had the 3 Mb deletion, the most common form of 22q11.2 deletion. The deletion was associated with an early age at PD onset, at an average of 42.1 years compared with 60.3 years among patients without the deletion.

Even among patients with early-onset (<45 years) PD, the rate of 22q11.2 deletions was just 0.49% (0.04% for later onset). But researcher Nicholas Wood (UCL Institute of Neurology, London, UK) and colleagues stress that "the presence of a 22q11.2 deletion has direct implications for management, especially the identification and medical management of comorbidities."
None of the patients had a diagnosis of 22q11.2 deletion syndrome, but the team says: "With hindsight, some cases had other features suggestive of 22q11.2 deletion syndrome, such as hypocalcaemia, depression, fatigue, mental retardation, and cleft palate."

They did not, however, have any of the cardiac features that are frequently reported in 22q11.2 deletion syndrome patients.
In a linked commentary, Eng-King Tan (Singapore General Hospital) stresses that, although the findings may focus a search for a novel PD gene, they do not prove that the deletion causes PD. For one thing, it is not clear why only 3% of patients with such deletions develop PD and what might trigger the condition in those who do develop it, he says.

"Despite many missing connections in the pathophysiological link between 22q11.2 deletion syndrome and Parkinson's disease, the present study will certainly raise clinicians' awareness and heighten their vigilance in looking for features of 22q11.2 deletion syndrome in patients with early-onset Parkinson's disease, and carefully considering Parkinson's disease as a differential diagnosis in patients with 22q11.2 deletion syndrome even if these patients are on antipsychotic drugs", he concludes.

Parkinson’s sufferers ‘able to work’, says the new Work and Pensions Secretary Stephen Crabb

March 25, 2016

Minister made comments the day before replacing Iain Duncan Smith - and later admitted they were 'inaccurate

Stephen Crabb has been appointed as the new Work
and Pensions Secretary AFP/Getty

People with brain tumours, motor neurone disease, Parkinson’s disease and a number of other conditions are “able to work”, new work and pensions secretary Stephen Crabb has said.

Mr Crabb made the comments the day before he replaced Iain Duncan Smith, who resigned from his position because he found the planned cuts to disability benefits announced in the latest Budget "not defensible".
The MP for Preseli Pembrokeshire wrote on his Facebook page last Thursday: “A decision was taken by MPs to change the benefit awarded to a specific group of people who receive Employment Support Allowance.”
The 43-year-old - who later backtracked on the statement - added: “These people are in the Work Related Activity Group (WRAG) and they do have a disability or illness but are able to work.”
In response to a freedom of information request, the Department for Work and Pensions confirmed disabilities and illness under the employment and support allowance work-related activity group include: strokes, brain haemorrhages, multiple sclerosis, brain tumours, motor neurone disease, Parkinson’s disease, quadraplegia, polio and cerebral palsy.
Mr Crabbs’ words were not well-received online. 
Brian Davies, a member of the public, wrote on the Facebook post: “Could you explain how people who are admitted are unwell and really shouldn't be put under this kind of pressure, how does lowering money help them?”
Natalie Windsor added: “This would be great if it were true. The government, however, has not adequately responded to either help, correct error, or even apologise for the thousands of people who have wrongly been diagnosed as able to work.”
The controversy follows on from the Government’s u-turn on the Budget, which had previously suggested a saving of £4.4bn by 2020-21 through cuts to the disability budget.
Mr Crabbs has since updated his Facebook post, admitting “it previously contained a factual inaccuracy.”
He added: “Of course we absolutely continue to protect those who are ‘too ill to work’. There is no question about that. Those with the most severe health conditions and disabilities will quite rightly continue to get a higher rate of benefit and support.”

A few days ago:   

Stephen Crabb:
A few days ago my constituency office was vandalised in response to my recent vote to approve changes to the Employment Support Allowance (ESA). This was not an isolated attack as other MPs offices were targeted by individuals involved in a social media campaign.

I’m disappointed that some individuals choose to do this instead of making an appointment to see me to discuss their concerns. Sadly all these individuals achieved on Saturday was to create an inconvenience to my office staff, local residents, and the Police. There are lots of ways to communicate to convey concerns but criminal damage just isn’t an option. 

There has been a lot of miscommunication about this vote which I want to put right. A decision was taken by MPs to change the benefit awarded to a specific group of people who receive Employment Support Allowance. These people are in the Work Related Activity Group (WRAG) and they do have a disability or illness but are considered able to work with support in the future. 
The overwhelming majority of people in this group say they want to work, and so I think it is right that we do all we can to help them get back into work. The changes mean that this group will now access the same level of benefit as those on Job Seekers Allowance, but will be given better tailored support to help them into employment. It doesn’t affect anyone who is already claiming ESA, they will receive the exactly the same amount of benefit as they do now. 

The truth is that not all disabilities prevent people from working. A great many disabled people get enormous fulfilment from being in work. They would be extremely offended not to be considered equal in the job market, and this benefit change means that more people will be able to take these important steps from being benefit-dependent to the workplace.
Of course we absolutely continue to protect those who are ‘too ill to work’. There is no question about that. Those with the most severe health conditions and disabilities will quite rightly continue to get a higher rate of benefit and support. And despite the political banter from Labour, the disability budget is actually going to be rising by more than £1 billion over the next 5 years which means that more money is being spent in real terms on support for disabled people than at any point under the previous Labour government. 

I can see that there have been a few comments on this page and I encourage people to email me directly if you would like a personal response from me. I don’t always have time to reply to every comment on Facebook as I am busy working on constituent casework via the telephone, email, letter and face to face appointments. If you email me, I will always provide a response to people who are living in Preseli Pembrokeshire. I cannot respond to people outside of the area and suggest they contact their own MP directly.

Note: This post has been updated, as it previously contained a factual inaccuracy.


What’s in the PD Pipeline? Gene and Cell Therapies

March 25, 2016

When:      Tuesday, April 5, 2016, 1:00 PM - 2:00 

To sign up go to:

Are there new therapies on the horizon to help treat PD? In the search for more effective treatments, two promising areas of research are gene therapies and cell therapies. Learn more about the potential of these two types of experimental treatments by joining a one-hour online seminar led by PDF and Roger Barker, M.B.B.S, M.R.C.P, Ph.D., Professor of Clinical Neuroscience and Honorary Consultant, Neurology, University of Cambridge and Addenbrooke's Hospital.

Learning Objectives:

  • Learn how cell-based therapies for Parkinson’s are designed to replace dopamine cells lost to the disease.
  • Understand how gene therapies are designed to either rescue dopamine cells or produce dopamine more efficiently in the brain.
  • Understand why neither approach is a cure, but how each might one day offer exciting ways to help people with Parkinson’s live better and reduce their other medications.


Roger Barker, M.B.B.S, M.R.C.P, Ph.D., is Professor of Clinical Neuroscience and Honorary Consultant, Neurology, University of Cambridge and Addenbrooke's Hospital in the United Kingdom.
Since setting up his own research group in 1997, Dr. Barker has run a laboratory investigating basic and clinical aspects of Parkinson’s disease. He has been involved in several clinical trials studying gene and cell-based therapies for people living with PD. Dr. Baker also currently coordinates a European Union funded transplant program for PD. In addition to publishing over 300 papers, he is Co­-Editor in Chief of the Journal of Neurology.
Dr. Barker completed his neurology training and obtained his doctorate in neural grafting at the University of Cambridge. He received additional training at Oxford University and St. Thomas Hospital.

Hope Flies Health Series Webinar— Research Connecting Parkinson’s and Mitochondrial Disease

March 24, 2016 11:58 AM 

The Foundation for Mitochondrial Medicine (FMM) hosts its next Hope Flies Health Series Webinar:

Research Connecting Parkinson’s Disease and Mitochondrial Disease on Wednesday, April 6, 2016 at 1:00 pm EDT.  

The Foundation developed the webinar with partners including the
Michael J. Fox Foundation (MJFF), Wilkins Parkinson’s Foundation and Sharecare to particularly bring greater awareness to mitochondrial disease and its connection to Parkinson’s disease.

The webinar is free; however registration is requested in advance at

Free webinar on Parkinson's and mitochondrial disease
on April 6:

During the webinar, participants can learn more about the scientific connection and interest Parkinson’s researchers have inmitochondria and mitochondrial function. Experts on the call willshare the latest developments from a specific research projectthe FMM and MJFF co-funded exploring this link to activate and
stabilize the Parkin protein, which may allow it to break down damaged mitochondria and thereby prevent cell death in some Parkinson’s patients. Stabilizing Parkin will be a positive strike for Parkinson’s disease and for mitochondrial disease.

Panelists for the webinar include Wolfdieter Springer, PhD, Assistant
Professor of Neuroscience, Mayo Clinic; Laura Stanley, Executive
 Director, FMM; Bill Wilkins, Founder of the Wilkins Parkinson’s
 Foundation, and the moderator will be Darria Gillespie, MD MBA,
FACEP, SVP Clinical Strategy of Shareware. 

Dr. Springer will provide an update on his primary research focus: the molecular and cellular mechanisms underlying the pathogenesis of Parkinson's disease and other related neurodegenerative disorders.

Additional topics include an overview of Parkinson’s and the challenges and progress today surrounding research of Parkinson’s and mitochondrial function; an overview of mitochondrial disease today and progress being made; and how patients and caregivers can manage both diseases.

About the Foundation for Mitochondrial Medicine
The Foundation for Mitochondrial Medicine is a 501(c) (3) non-profit organization dedicated to supporting the development of the most promising research and treatments of the many forms of mitochondrial disease. Visit for more information.
Contacts For The Foundation for Mitochondrial Medicine

Jennifer Grizzle, 770-409-1152