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.

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Saturday, September 12, 2015

Parkinson's disease slurs my speech. Will police think I'm drunk?

Oregon State Police

Elliot Njus | The Oregonian/OregonLive

I was diagnosed with Parkinson's disease a few years ago. My particular symptoms are controlled for the most part by medications and I can safely drive my car, but sometimes my speech is slightly slurred and I could not pass a balance-based field sobriety test. If I am stopped for any reason, how should I present myself?

This is a question to which many drivers can relate, at least on some level. Most of the people Clackamas County Sgt. Richard Sheldon stopped as a traffic deputy were so nervous they fumbled and stammered to the point they may have worried their behavior would arouse suspicions of driving under the influence, even if they hadn't been drinking.
But impairment looks different from a traffic cop's perspective, Sheldon said.
"A huge portion of our contacts deal with people that are under the influence of alcohol and other substances," Sheldon said. "We start to develop an understanding of what a drunk person looks like, or what a high person looks like."
And it's not all that unusual to encounter drivers with a medical condition that can affect speech or movement.
That said, if a police officer suspects a driver might be impaired, they'll usually start asking questions to gather more information and establish probable cause. If you haven't already, this would be a good time to bring up a medical condition, Sheldon said.
Keeping a doctor's note in the car that outlines specific symptoms might help get you on your way faster, too.
If it does come down to a sobriety test, there are alternatives to the usual walk-and-turn. Sworn police officers have nine field sobriety tests at their disposal under Oregon's administrative rules, and most don't involve balance.
Alternatives include checking eye movement, touching your fingertips to your thumb while counting, or reciting the alphabet. (Not backward, Sheldon said. "I couldn't do that.") Officers also sometimes ask drivers to tilt their head back for 30 seconds to see if their perception of time is warped, suggesting impairment.
The tests are frequently used when drivers have a disability or injury and can't easily get out of a vehicle for a walking or standing test.
Wanting to get another perspective, we contacted Portland criminal defense attorney Mark Cogan. He said the issue comes up frequently, although his examples came from cases that went to trial — probably not the reader's ideal outcome.
He said it's probably a good idea to carry documentation. And in most traffic stops, medical issues should come up anyway.
"Typically they're required to ask the person, 'Do you have any kind of medical issues? Have you seen a doctor recently?'" Cogan said. "Police do anticipate that as a possible cause for appearance of impairment."

Parkinson's propels Brisbane photographer into gallery star

PHOTO: Budding Brisbane artist Mary-Louise Levick uses her Parkinson's disease to capture her signature style photos. This is a photo of the Story Bridge in Brisbane. September 2015. (Supplied: Mary-Louise Levick)
Like all great photographers, Brisbane's Mary-Louise Levick spends most of her time in pursuit of the perfect shot.
But when she was diagnosed with Parkinson's disease at the age of 34, the budding artist was literally forced to shake things up.
Ms Levick had her first symptoms at age 30 when she noticed a tremor in her thumb.
About three years later, when she began to struggle writing, doctors suspected she had Parkinson's disease.
At the same time, Ms Levick was just beginning to explore her passion for photography.
She sought out a mentor in fellow photographer Marcus Bell to learn how to use her camera properly, but from their relationship an idea blossomed.
"We started talking about the Parkinson's side of things and how it would affect my photography, especially into the future," Ms Levick said.
"And that was when he (Marcus) told me; you know 'go with it'.
"He said 'if you want to stand out in the crowd, you've got to come up with something different'."
It was from these discussions that Ms Levick's signature style, the "Parkinson's disease effect", or "PD effect", was born.
Initially, Ms Levick would just let the tremor go and whatever the result. 
Now she focuses and plans the photograph, taking in the tremor component of it.
"Because I'm still initially I can get the still shots," Ms Levick said.
"But then my tremor starts and you're using lights, you know that as soon as you move the camera you get a pattern."
Mr Bell felt compelled to work with Ms Levick, despite rarely agreeing to one-on-one workshops. 
"It really intrigued me," he said.
"I was able to resonate and understand a little because of my own experiences, with my mum having Parkinson's."

'PD effect' exhibition opening most successful in gallery's history

A collection of Ms Levick's "PD effect" images are currently on display at a Maud Creative, a photographic gallery in Newstead.
The exhibition had the most successful opening in the gallery's history.
"It's not about the sharpness or the perfect picture, it's about the essence of the image," gallery owner Irena Prikryl said.
"I just thought her [Mary-Louise's] passion and enthusiasm for life was just something incredible, and something to show to everybody."
She described Ms Levick's photography as unique and inspiring, and said it highlighted the beauty in imperfection.
"I can see the technique but I think the unintentional movement is so unique that I don't think you could reproduce it, I don't think you could recreate it," Ms Prikryl said.

Red wine compound found to stabilize Alzheimer's biomarker

A clinical trial assessing the compound resveratrol in people with mild to moderate Alzheimer's disease has revealed that it stabilizes a biomarker found to decline alongside the progression of the disease.

Participants in the study received either a placebo or a daily dose of resveratrol equivalent to the amount found in 1,000 bottles of red wine. caption

The study, published in Neurology, was a randomized, phase 2, placebo-controlled, double-blind study to establish the effectiveness of the supplement.
"Given safety and positive trends toward effectiveness in this phase 2 study, a larger phase 3 study is warranted to test whether resveratrol is effective for individuals with Alzheimer's - or at risk for Alzheimer's," reports principal investigator Dr. R. Scott Turner, director of the Memory Disorders Program at Georgetown University Medical Center in Washington, D.C.
Resveratrol is a naturally occurring compound that can be found in red grapes, red wine, chocolate, peanuts and other foods. For the study, the researchers utilized a pure synthetic form of resveratrol with a daily dosage equivalent to the amount found in 1,000 bottles of red wine.
This compound was selected for further study due to its capacity to activate a group of proteins known as sirtuins. These proteins are also activated by caloric restriction, which previous animal studies have demonstrated can prevent or delay age-related diseases. Aging is the biggest risk factor the development of Alzheimer's disease.
In the study, a total of 119 participants were recruited to participate in the 1-year trial. Half of the participants received resveratrol and the other half received a placebo.
The researchers noted that the patients treated with resveratrol experienced little or no change to the levels of amyloid-beta40 (Abeta40) in the blood and cerebrospinal fluid. In contrast, the participants who received the placebo experienced a decline in their Abeta40 levels over the 12 months of the trial.

Definitive phase 3 trial to follow

Dr. Turner explains their findings:
"A decrease in Abeta40 is seen as dementia worsens and Alzheimer's disease progresses; still, we can't conclude from this study that the effects of resveratrol treatment are beneficial. It does appear that resveratrol was able to penetrate the blood-brain barrier, which is an important observation."
The researchers also observed that those receiving resveratrol experienced some benefit in the participation of routine activities in the home. Alongside this was a more surprising discovery: those who received resveratrol experienced a decrease in brain volume in comparison with those who received a placebo. 
"We're not sure how to interpret this finding," Dr. Turner admits. "A similar decrease in brain volume was found with some anti-amyloid immunotherapy trials." The researchers suggest that this finding could be explained by the treatment reducing inflammation and swelling in the brain.
While the findings of the study are not enough for the researchers to be able to start advising patients to commence taking the compound, they enable the team to move on to a more definitive phase 3 trial of resveratrol, to see just how effective it is for patients with Alzheimer's disease.
Previously, Medical News Today reported on a study indicating that a chemical called IRL-1620 could represent a novel therapeutic target for Alzheimer's disease after it was used to treat the condition in rats.
Written by 
Copyright: Medical News Today

Friday, September 11, 2015


10th September 2015 - New research

Although it normally has completely different uses, including orthostatic hypotension, the prodrug droxidopa has been found to reduce the symptoms of Parkinson's Disease. Droxidopa is a synthetic amino acid precursor. It can pass the blood brain barrier and form noradrenaline and adrenaline, which are derivatives of L-dopa and dopamine. Droxidopa is marketed as Northera.

 For more information go to :

The use of droxidopa in Parkinson's Disease was compared to the use of a placebo. The two groups were comparable in all respects. After two weeks and also nearly two months Parkinson's Disease symptoms scores were significantly different from the outset. Individual motor symptoms such as stiffness, resting tremor, and alternate hand motion were also significantly improved with the use of droxidopa, suggesting that droxidopa is effective in improving rigidity, tremor and alternate motion of hand.

Droxidopa was effective as symptomatic adjunct therapy, and significantly improved motor function and activities of daily living. On the way to forming noradrenaline and adrenaline, it must therefore have dopaminergic activity.

Reference : Parkinsonism and Related Disorders [2015] Aug 21 [Epub ahead of print] (S. Zhao, R.Cheng, J.Zheng, Q.Li, J.Wang, W.Fan, L.Zhang, Y.Zhang, H.Li, S.Liu)

Complete abstract :
©2015 Viartis 

Vision testing an effective tool for detecting concussion on the sidelines

Sept. 11, 2015

Review article finds a test of rapid number naming detected concussion 86 percent of the time among youth, collegiate and professional athletes
A timed vision test that involves rapidly reading numbers off of cards can be a valuable sideline tool for detecting whether a concussion occurred while playing sports, according to a meta-analysis and systematic review led by NYU Langone Medical Center concussion specialists.
Researchers at the NYU Langone Concussion Center reviewed studies that involved athletes who sustained a concussion during sporting activities and found the vision test, known as the King-Devick test, was 86 percent sensitive in detecting whether a concussion had occurred, as confirmed by clinical diagnosis. When combined with rapid assessments of balance and cognition, the testing battery was able to detect 100 percent of concussions that occurred among athletes in the studies that measured this outcome.
The study was published Thursday, September 10, 2015, in Concussion.
"There is no diagnostic substitute for a medical professional when it comes to evaluating an athlete for concussion, but physicians are not always on the sidelines during practice or a game when an injury might occur," says senior study author Laura Balcer, MD, MSCE, Co-director of the NYU Langone Concussion Center and a professor of neurology, population health and ophthalmology at NYU Langone. "Our study shows that an easy to administer vision test is a simple, effective tool that empowers parents, coaches, trainers - and even physicians - on the sidelines to have a protocol for deciding if an athlete should be removed from play."
For the rapid number naming test, athletes are given a baseline test before the season starts where they are asked to read numbers as quickly as they can off a series of three reading cards while being timed with a stopwatch. People who don't experience a concussion or head injury tend to have faster reading times when tested again during the season; however, those who are tested immediately after they may have sustained a concussion experience slower times.
Vision is important in concussion diagnosis because the visual pathways have extensive connections throughout the brain, and disruptions in these pathways could suggest a brain injury occurred. Previous studies have shown worsening scores on rapid number naming tests correlate with neurological conditions including Parkinson's diseasemultiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS).
Balcer and her colleagues conducted a meta-analysis review of 15 previously-completed studies where a rapid number naming test was utilized. All the studies were conducted on athletes, and all concussions were defined by a witnessed or reported blow to the head with neurological symptoms.
The review included 1,419 athletes, 112 of whom sustained a concussion. Professional hockey players, along with youth, collegiate and amateur players of football, hockey, soccer, lacrosse, basketball, boxing and rugby were among those studied.
Concussed athletes on average completed the King-Devick test 4.8 seconds longer than their baseline score, whereas non-concussed athletes improved their score by an average of 1.9 seconds. The test detected 96 out of 112 concussions (86 percent), and showed 90-percent specificity in distinguishing a concussed athlete versus a non-concussed, healthy control subject. Overall, if an athlete had a worsening in their time score compared to their baseline reading, they were five times more likely to have sustained a concussion.
Some studies included the review utilized other tests including the SCAT3 symptom checklist and timed tandem gait (walking) test, and importantly, a worsening in scores of at least one of the three tests was observed in 100 percent of concussed athletes.
"This tool as part of a simple battery of tests assessing cognition and balance can raise a flag for those athletes that require follow-up with a medical professional," says study co-author Steven Galetta, MD, the Philip K. Moskowitz, MD Professor and Chair of Neurology at NYU Langone Medical Center. Dr. Galetta, himself a former collegiate athlete, added, "In the heat of a game, there is a lot of chaos and confusion on sidelines, so anything that helps eliminate guesswork is needed."
A March study led by Dr. Galetta and Dr. Balcer, published in the Journal of Neuro-Ophthalmology, found the King-Devick test effective at helping to detect a concussion in student athletes as young as 5 years old.
A concussion is caused by a force transmitted to the head as a result of a direct blow to the body that results in new neurological symptoms. An estimated 4 million sports-related concussions occur each year in the United States each year, with long-term consequences on brain function becoming an increasingly prominent concern among those who play contact and collision sports.
Adapted by MNT from original media release


What is concussion? What is mild traumatic brain injury (MTBI)?

Concussion is also known as mild brain injury, mild traumatic brain injury (MTBI), mild head injury and minor head trauma. Some experts define concussion as a head injury with temporary loss of brain function, which can cause cognitive, physical and emotional symptoms. Concussion may also be defined as an injury to the brain generally caused by a jolt or blow to the head - in the majority of cases the individual does not lose consciousness. 

According to Medilexicon's medical dictionary, concussion is "An injury of a soft structure, as the brain, resulting from a blow or violent shaking."

In sports medicine the term concussion is commonly used, while in general medicine MTBI (mild traumatic brain injury) may be used as well. Lay people are more familiar with the term concussion.

According to the Brain Injury Association of America males are twice as likely as females to sustain a brain injury. Those at highest risk of a brain injury are males aged 15 to 24 years. People who have had a brain injury are more likely to experience a subsequent brain injury. In 2008 there were 351,992 sports-related head injuries that were treated in hospital emergency rooms in the USA, according to the U.S. Consumer Product Safety Commission. 

Researchers from Toronto University reported that children take longer to recover from second or third concussions, compared to those with a first concussion. They reported their findings in the journal Pedatrics (June 2013 issue).

Researchers from the Centre de recherche en neuropsychologie et cognition, Université de Montréal, Canada found evidence that athletes who were concussed during their earlier sporting life show a decline in their mental and physical processes more than 30 years later.

On Monday, March 18th, 2013, the American Academy of Neurology launched:

What are the causes of concussion? 

The brain floats in cerebral fluid which protects it from jolts and bumps. A violent jolt or a severe blow to the head can cause the brain to bump hard against the skull. This can result in the tearing of fiber nerves as well as blood vessel rupture under the skull, leading to an accumulation of blood.
  • Automobile accidents - concussions commonly occur from severe jolts to the head; this can happen when a vehicle suddenly loses speed or stops dead, causing the brain to jar (bash, bump hard) against the skull. 

  • Sports injuries - especially contact sports, such as martial arts, boxing, rugby, American football, and hokey. Non-contact sports such as snowboarding and skiing as well. 

  • Falls - any fall that results in a blow to the head or a severe jolt. The majority of concussion cases in very young children and elderly individuals in the USA and UK occur as a result of a fall in the home. 

  • Horseback riding accidents - there were 11,749 cases of head injuries resulting from horseback riding accidents in 2008 in the USA, according to the U.S. Consumer Product Safety Commission. 

  • Playground accidents - especially in playgrounds that do not have proper soft underlays. 

  • Cycling accidents - according to the U.S. Consumer Product Safety Commission there were 70,802 cases of head injuries that resulted from cycling accidents. 

  • Assaults - 11% of traumatic brain injuries in the USA are caused by assaults (people being attacked), according to the CDC (Centers for Disease Control and Prevention)
  • .

Major complication of Parkinson's therapy explained

Sept. 11, 2015
Researchers have discovered why long-term use of L-DOPA (levodopa), the most effective treatment for Parkinson's disease, commonly leads to a movement problem called dyskinesia, a side effect that can be as debilitating as Parkinson's disease itself.
Striatonigral Pathway
In a recent study, Columbia researchers have investigated why dyskinesias occur in Parkinson's disease patients: they identified a major change in the function of striatonigral GABA synapses in the basal ganglia, a brain circuit that controls movement. Pictured here in green is the striatonigral pathway. 
Credit: Columbia University Medical Center/Borgkvist et al./Neuron 2015
Using a new method for manipulating neurons in a mouse model of Parkinson's, a Columbia University Medical Center (CUMC) research team found that dyskinesia arises when striatonigral neurons become less responsive to GABA, an inhibitory neurotransmitter. This suggests that it may be possible to modulate the activity of these neurons to prevent or delay this disabling side effect. The paper was published recently in the online edition of Neuron.
Parkinson's disease, a progressive neurodegenerative disorder, results from the death of cells in various parts of the brain, especially in a region called the substantia nigra. It is in the substantia nigra that a neurotransmitter called dopamine is formed, and when dopamine is lacking neurons fire abnormally, impairing one's ability to control movement.
"While Parkinson's is not curable, it is treatable with L-DOPA, which is converted into dopamine in the brain," said study leader David L. Sulzer, PhD, a professor of neurobiology in the Departments of Neurology, Psychiatry, and Pharmacology at CUMC and a research scientist at the New York State Psychiatric Institute. "However, while taking L-DOPA helps patients move normally, in many individuals it eventually triggers uncontrolled excessive movements." Parkinson's is estimated to affect about one million people in the U.S. and up to 10 million worldwide.
Most studies into the cause of dyskinesia in Parkinson's have focused on the dopamine receptors that remain in the brain, which over time become over-reactive to L-DOPA therapy. However, the CUMC team decided to look at how neurons of the basal ganglia regulates movement in the absence of dopamine.
"Dopamine neurons modulate the basal ganglia," explained lead author Anders Borgkvist, PhD, a postdoctoral fellow in Dr. Sulzer's laboratory. "And because that circuit is still running in patients with Parkinson's, it's long been suspected that other parts of the circuit behave abnormally in this disease."
However, scientists lacked a way to stimulate selective parts of the basal ganglia to evaluate what was happening when dopamine is no longer available. The CUMC team employed a novel form of optogenetics, a technique that uses light to control neurons that have been genetically sensitized to light, and found that after long-term dopamine loss, striatonigral neurons lose their ability to respond to the neurotransmitter GABA (gamma-aminobutyric acid). This effect was not found with short-term dopamine loss.
"When striatonigral neurons are working normally, they act as a brake on the basal ganglia, in effect shutting down unwanted movement," said Dr. Sulzer. "But when there is dopamine loss, as in Parkinson's, striatonigral neurons try to compensate, and eventually lose their responsiveness to GABA. Our hypothesis is that when L-DOPA is added into the system, you lose the ability to filter, or turn off, unwanted movement."
"Our findings suggest that GABA and GABA receptors are still present in the striatonigral neurons," said Dr. Borgkvist. "So then the question becomes, why they aren't functional? I think that we, or another lab, will eventually find the answer. In any case, the implication is that this defect is correctable, and that would mean that we could prevent or at least delay dyskinesia, so that patients could continue to use L-DOPA."
"Patients do not develop dyskinesias in the early stages of Parkinson's, but only after several years of the disease," said Stanley Fahn, MD, the H. Houston Merritt Professor of Neurology and emeritus director of the Parkinson's Disease Foundation Research Center at CUMC. "A major reason why these patients want to delay the initiation of L-DOPA therapy is to avoid these dyskinesias for as long as possible. These new findings open up possible ways to treat or prevent the dyskinesias. If such treatments were found, patients would probably seek to be treated early and improve their quality of life sooner."
Dr. Sulzer believes it is likely that scientists will identify other mechanisms, in addition to striatonigral neurons, that contribute to Parkinson's-related dyskinesia.
Adapted by MNT from original media release

UNC smart cells teach neurons damaged by Parkinson's to heal themselves

Sept. 11, 2015

Scientists at the UNC Eshelman School of Pharmacy are creating white blood cells that teach brain cells to heal the damage caused by degenerative neurological disorders like Parkinson's disease
Self-healing Neurons

These are white blood cells reengineered by scientists at UNC-Chapel Hill deliver exosomes (red) loaded proteins that stimulate the growth of damaged nerve fibers (green and yellow). Researchers at the UNC Eshelman School of Pharmacy this technique can be developing into a potential treatment for Parkinson's disease. 
Credit: Elena Batrakova/UNC Eshelman School Of Pharmacy
As a potential treatment for Parkinson's disease, scientists at the University of North Carolina at Chapel Hill have created smarter immune cells that produce and deliver a healing protein to the brain while also teaching neurons to begin making the protein for themselves.
The researchers, led by Elena Batrakova, an associate professor at the UNC Eshelman School of Pharmacy's Center for Nanotechnology in Drug Delivery, genetically modified white blood cells called macrophages to produce glial cell-derived neurotrophic factor, or GDNF, and deliver it to the brain. Glial cells provide support and protection for nerve cells throughout the brain and body, and GDNF can heal and stimulate the growth of damaged neurons.
"Currently, there are no treatments that can halt or reverse the course of Parkinson's disease. There are only therapies to address quality of life, such as dopamine replacement," Batrakova said. "However, studies have shown that delivering neurotrophic factor to the brain not only promotes the survival of neurons but also reverses the progression of Parkinson's disease."
In addition to delivering GDNF, the engineered macrophages can "teach" neurons to make the protein for themselves by delivering both the tools and the instructions needed: DNA, messenger RNA and transcription factor.
Successfully delivering the treatment to the brain is the key to the success of GDNF therapy, said Batrakova. Using immune cells avoids the body's natural defenses. The repurposed macrophages are also able to penetrate the blood-brain barrier, something most medicines cannot do. The reprogrammed cells travel to the brain and produce tiny bubbles called exosomes that contain GDNF. The cells release the exosomes, which then are able to deliver the proteins to neurons in the brain. The work is described in an article published online by PLOS ONE.
"By teaching immune system cells to make this protective protein, we harness the natural systems of the body to combat degenerative conditions like Parkinson's disease," Batrakova said.
The North Carolina Biotechnology Center awarded a $50,000 Technology Enhancement Grant to the School to help develop the technology into a viable treatment that can be licensed and commercialized.
"This award is an enormously important step towards further successful commercialization of our very exciting cell technologies," said Alexander Kabanov, director of the nanotechnology center. "We will continue our translational efforts at CNDD, and very soon I believe we will see these discoveries on the frontiers of scientific moving into clinical practice." 
Adapted by MNT from original media release

Thursday, September 10, 2015

Using MR-guided focused ultrasound to treat Parkinson's

By Aine Cryts, Contributing Reporter 

Two patients in the U.S. with Parkinson’s disease have been successfully treated using focused ultrasound, Dr. Howard Eisenberg, chair of the neurosurgery department at University of Maryland School of Medicine, told HCB News. Focused ultrasound is being used specifically to treat dyskinesia, the tremors that can result when patients need to take increased doses of Levodopa, a medication used to manage their disease, said Eisenberg. 

“Focused ultrasound is, in a sense, a ‘back to the future’ thing,” said Eisenberg. He treated his first patient at University of Maryland Medicine in late August. The first patient in the U.S. to be successfully treated using this therapy was treated at the University of Virginia, he said. 
According to the Focused Ultrasound Foundation, this treatment involves sending MR-guided focused ultrasound through the skull to destroy a small volume of targeted issue in the globus pallidus, a structure found deep within the brain that serves as the source of these tremors. 

Most Parkinson’s disease patients will develop dyskinesia after five years of Levodopa treatment, but in only a minority of those – about 20 percent – will the dyskinesia interfere in their day-to-day lives, according to Dr. Paul Fishman, professor of neurology, pharmacology, and neurobiology at University of Maryland School of Medicine. The current best practice for treating dyskinesia in Parkinson’s patients is to implant a device in the brain that helps control the tremors by blocking the abnormal nerve signals that cause them, said Eisenberg. One of the challenges with this invasive procedure is that the battery needed to power the device must be replaced surgically every two to three years. 

Prior to the implant approach, surgeons would open the patient’s skull and cut holes in their brain, to cause lesions to alleviate the tremors. Eisenberg noted that this clinical trial is limited to patients who experience the tremors primarily on one side of their body. In the treatment of his patient at University of Maryland Medicine, Eisenberg chose to focus the therapy on the side of the body that had the most pronounced manifestation of the tremors. He said that patients treated using this protocol must be awake. The procedure itself takes about three hours, and that includes the use of local anesthesia, the patient’s entry into the MR gantry and subsequent adjustments to their body, and the time required to focus the ultrasound on the globus pallidus. Throughout this third and final part of the treatment, the heat of the focused ultrasound is adjusted and the patient is observed. During the procedure, the patient wears a bowl-like device that’s fitted to a frame that’s pinned to their head. The bowl-like device, which is immobilized within the MR scanner, contains as many as 1,000 sonicators that provide beams of energy and deliver the focused ultrasound to create a lesion to alleviate the tremor symptoms. Eisenberg’s work with this patient at University of Maryland is part of an international clinical trial that has included seven patients in Korea and one patient in Canada, in addition to the patient at University of Virginia. The studies are being conducted using the ExAblate Neuro system developed by Israel-based InSightec. According to the University of Maryland, funding for these studies has been provided by the Michael J. Fox Foundation for Parkinson’s Research and the Focused Ultrasound Foundation.

Parkinson's support group helping sufferers and carers prepare for what may be

Posted yesterday at 10:40pm
Every fortnight a group of people get together in a small room at the northern integrated care service building in Launceston and they all have one thing in common — Parkinson's disease.
Some people in the support group live with the disease, others have family members or friends living with it, and the support group offers a place to share ideas and thoughts. 
Diana Newell has been going to the fortnightly sessions for about seven years after her husband was diagnosed with the disease 14 years ago.

"I'm just a carer, but I might be able to give them a little hint on what I've tried and it's worked, and what I've tried and it hasn't worked," Ms Newell said.
"The reason I came along originally was because I didn't know enough about Parkinson's.
"You can come along and speak to some of the people who have it and find out some information."
Ms Newell was attending the meeting alone and now feels she can offer more support and advice to others as well as using it for her own knowledge.

Support for those in the early stages of Parkinson's

The group is mostly made up of people who have been living with the disease for a while, with only a small number of young people in the earlier stages of the disease. 
"The [young] people are actually still working and sometimes they think 'oh, there's nothing there for me, I'm still young, I don't really need that support' and they just don't come along," Ms Newell said.

"Sometimes you find the early onset ones maybe find it a little intimidating with older people, sixties and seventies who have the disease, and they are a little nervous and frightened of what they might see and think."
The one exception in the room is 41-year-old Hayley Milne from Launceston.
She was diagnosed five-weeks-ago and she has a lot of questions.
"I think my first thought was family," Ms Milne said.
"How it will impact in the future, on not only my children and my husband and my friends, but sort of your life, you're only 41 and not sure which way your life is going."
Before her diagnosis Ms Milne noticed tremors in her head, at first she was able to ignore them, until they progressively became worse and started to affect her balance.
"At the beginning, before any medication, they were quite light but then they got that bad that every time I walked it was almost like my brain was hitting my skull," Ms Milne said.
In only her second session with the support group Ms Milne seems quite calm and happy to take in as much information as she can.
"I think the first week was the most interesting," Ms Milne said.
"They call it a designer disease because everybody's so different and seeing the group, everybody is so much older and so much more developed into the disease."
In recent weeks the disease has impacted on Ms Milne's ability to work, stopping her from working altogether, which has been one of the biggest challenges yet.
"I've always worked, I've always worked through all my pregnancies, I've worked up until the day I gave birth and then straight after," Ms Milne said.
Now Ms Milne is on medication, which has stopped her head tremors, making life a little easier and she is just simply hoping to take away one key message from the group sessions.
"Just to be prepared for what may come, but I mean it may not come," Ms Milne said.