What is LSVT LOUD? and What is LSVT BIG?

LSVT LOUD

LSVT LOUD® is an effective speech treatment for individuals with Parkinson disease (PD) and other neurological conditions.  LSVT LOUD, named for Mrs. Lee Silverman (Lee Silverman Voice Treatment – LSVT) was developed in 1987 and has been scientifically studied for nearly 20 years with funding support from the National Institute for Deafness and other Communication Disorders (NIDCD) of the National Institutes of Health. Published research data support improvements in vocal loudness, intonation, and voice quality for individuals with PD who received LSVT LOUD, with improvements maintained up to two years after treatment. Recent research studies have also documented the effectiveness of this therapy in improving the common problems of disordered articulation, diminished facial expression and impaired swallowing. Additionally, two brain imaging studies have documented evidence of positive changes in the brain following administration of the therapy.
LSVT LOUD improves vocal loudness by stimulating the muscles of the voice box (larynx) and speech mechanism through a systematic hierarchy of exercises. Focused on a single goal “speak LOUD!” – the treatment improves respiratory, laryngeal and articulatory function to  maximize speech intelligibility. The treatment does not train people for shouting or yelling; rather, LSVT LOUD uses loudness training to bring the voice to an improved, healthy vocal loudness with no strain.
Treatment is administered in 16 sessions over a single month (four individual 60 minute sessions per week). This intensive mode of administration is consistent with theories of motor leaning and skill acquisition, as well as with principles of neural plasticity (the capacity of the nervous system to change in response to signals), and is critical to attaining optimal results. The treatment not only simulates the motor system but also incorporates sensory awareness training to help individuals with PD recognize that their voice is too soft, convincing them that the louder voice is within normal limits, and making them comfortable with their new louder voice.
Patients are trained to self-generate the adequate amount of loudness to make their speech understood. While LSVT LOUD has been successfully administered to individuals in all stages of PD, the treatment has been most effective among those who are in early or middle stages of the condition. LSVT LOUD has also been applied to individuals with sub-types of PD (Shy-Drager syndrome, multi-system atrophy and progressive supranuclear palsy), however the largest dataset is for individuals with Idiopathic Parkinson disease (IPD). Recently, LSVT LOUD has been applied to select individuals with stroke, multiple sclerosis, Down syndrome, and cerebral palsy with positive outcomes.

http://www.lsvtglobal.com/patient-resources/what-is-lsvt-loud

LSVT BIG

Recently principles of LSVT LOUD® were applied to limb movement in people with Parkinson disease (LSVT BIG®) and have been documented to be effective in the short term. Specifically, training increased amplitude of limb and body movement (Bigness) in people with Parkinson disease has documented improvements in amplitude (trunk rotation/gait) that generalized to improved speed (upper/lower limbs), balance, and quality of life. In addition, people were able to maintain these improvements when challenged with a dual task.
LSVT BIG can be delivered by a physical or occupational therapist. Treatment is administered in 16 sessions over a single month (four individual 60 minute sessions per week). This protocol was developed specifically to address the unique movement impairments for people with Parkinson disease. The protocol is both intensive and complex, with many repetitions of core movements that are used in daily living. This type of practice is necessary to optimize learning and carryover of your better movement into everyday life!
Start exercising NOW – as soon as possible. Physicians rarely refer their patients to health and fitness programs at diagnosis because medications are very effective early on at alleviating most of the symptoms, and patients experience little change in function. Yet, according to a recent survey it is at the time of diagnosis that patients often begin to consider lifestyle changes and seek education about conventional and complementary/alternative treatment options. Thus referrals to exercise, wellness programs and physical/occupational therapy would be best initiated at diagnosis, when it may have the most impact on quality of life.

Locate an LSVT Certified Clinician go to:

http://www.lsvtglobal.com/clinicians

Re-examining the Relationship between Parkinson’s Disease and Smoking

FoxFeed Blog

Posted by  Rachel Dolhun, MD, October 08, 2014

The ability to quit smoking, especially “cold turkey” or on the first attempt, has been heralded as a marker of strong willpower and determination. But could the ease with which one eschews cigarettes also serve as an early sign of Parkinson’s disease (PD)? This is the conclusion drawn by Beate Ritz, MD, PhD, and colleagues from the University of California, Los Angeles in a recent study published in Neurology.

Researchers compared lifelong tobacco use, use of nicotine substitutes, and individual’s rating of their difficulty in trying to quit tobacco among 1,808 Danish people with PD and 1,876 control volunteers. They found that those with PD were less inclined to ever pick up the smoking habit, but, even if they did, they were less likely to need nicotine replacement therapies and able to more effortlessly stop smoking cigarettes.

Therefore, ease of quitting smoking may be a sign of early PD. This joins a short list of other symptoms — smell loss, constipation and REM sleep behavior disorder — that usually predate diagnosis and are strongly associated with PD. Physicians rely heavily on such information to help confirm the diagnosis of Parkinson’s, given that biomarkers, objective measurements of disease, are currently lacking. Research led by The Michael J. Fox Foundation is ongoing to identify biological markers of PD, which could help diagnose and treat people earlier.

In the meantime, doctors must look for symptoms and behaviors to help identify Parkinson’s. Researchers have long known that tobacco use was linked to a lower risk of PD. An ongoing Foundation-funded study is investigating whether nicotine might guard against or slow the progression of PD.

Dr. Ritz and her team’s findings may reverse this concept. Rather than smoking defending against Parkinson’s disease, they argue that PD protects from smoking because of a decreased sensitivity of the brain’s reward system and, as a result, lack of positive reinforcement to substance use.

Regardless of the actual association in the complex correlation between tobacco and Parkinson’s, this type of research provides insight that aids in development of symptomatic and disease-modifying therapies.

2014 Nobel Prize in Chemistry: Super-resolved fluorescence microscopy

Date:

October 8, 2014

Source:

Nobel Foundation

Summary:

The 2014 Nobel Prize in Chemistry has been awarded to Eric Betzig of Janelia Farm Research Campus, Howard Hughes Medical Institute; Stefan W. Hell of Max Planck Institute for Biophysical Chemistry and the German Cancer Research Center; and William E. Moerner of Stanford University "for the development of super-resolved fluorescence microscopy."

The principle of STED microscopy and the principle of single-molecule microscopy.

Credit: Illustration © Johan Jarnestad/The Royal Swedish Academy of Sciences

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Chemistry for 2014 to Eric Betzig of Janelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA; Stefan W. Hell of Max Planck Institute for Biophysical Chemistry, Göttingen, and German Cancer Research Center, Heidelberg, Germany; and William E. Moerner of Stanford University, Stanford, CA, USA, "for the development of super-resolved fluorescence microscopy."

Surpassing the limitations of the light microscope

For a long time optical microscopy was held back by a presumed limitation: that it would never obtain a better resolution than half the wavelength of light. Helped by fluorescent molecules the Nobel Laureates in Chemistry 2014 ingeniously circumvented this limitation. Their ground-breaking work has brought optical microscopy into the nanodimension.

In what has become known as nanoscopy, scientists visualize the pathways of individual molecules inside living cells. They can see how molecules create synapses between nerve cells in the brain; they can track proteins involved in Parkinson's, Alzheimer's and Huntington's diseases as they aggregate; they follow individual proteins in fertilized eggs as these divide into embryos.

It was all but obvious that scientists should ever be able to study living cells in the tiniest molecular detail. In 1873, the microscopist Ernst Abbe stipulated a physical limit for the maximum resolution of traditional optical microscopy: it could never become better than 0.2 micrometres. Eric Betzig, Stefan W. Hell and William E. Moerner are awarded the Nobel Prize in Chemistry 2014 for having bypassed this limit. Due to their achievements the optical microscope can now peer into the nanoworld.

Two separate principles are rewarded. One enables the method stimulated emission depletion (STED) microscopy, developed by Stefan Hell in 2000. Two laser beams are utilized; one stimulates fluorescent molecules to glow, another cancels out all fluorescence except for that in a nanometre-sized volume. Scanning over the sample, nanometre for nanometre, yields an image with a resolution better than Abbe's stipulated limit.

Eric Betzig and William Moerner, working separately, laid the foundation for the second method, single-molecule microscopy. The method relies upon the possibility to turn the fluorescence of individual molecules on and off. Scientists image the same area multiple times, letting just a few interspersed molecules glow each time. Superimposing these images yields a dense super-image resolved at the nanolevel. In 2006 Eric Betzig utilized this method for the first time.

Today, nanoscopy is used world-wide and new knowledge of greatest benefit to humankind is produced on a daily basis.

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Camden firm sued over mishandled Parkinson's disease research material

By Michael Boren, Inquirer Staff Writer

POSTED: October 07, 2014

The Michael J. Fox Foundation for Parkinson's Research is suing a Camden nonprofit, saying it compromised nearly 26,000 research tubes when a freezer door was left open in March.

The tubes of blood and other fluids were stored at the Coriell Institute for Medical Research along Haddon Avenue, and would have been used to study the causes of Parkinson's disease, according to the lawsuit. It was filed Friday in U.S. District Court in New Jersey.

Fox's foundation, according to the suit, signed two contracts - one in 2010, the other 2011 - worth a combined $4.3 million to store the tubes at Coriell.

On March 28, the day of the incident, a Coriell employee allegedly found the door open to the freezer, where the tubes are supposed to be kept at a temperature of -80 degrees Celsius, or -112 degrees Fahrenheit.

It's unknown how long the door was open, but the thaw spoiled or rendered all of the tubes useless, the suit said.

Kenneth Marek, who is on the scientific advisory board of the New York-based Fox foundation, called the loss an "entirely unnecessary compromise of samples."

"We cannot overstate our disappointment that this incident has occurred," Marek said in a statement.

Coriell officials issued a brief statement Monday.

"We have learned of the lawsuit and plan to vigorously defend ourselves against the allegations," it said. "However, we have a policy of not discussing matters that are in litigation."

The Fox foundation, according to the suit, has spent more than $54 million on two five-year studies, through which some of the research tubes were obtained.

The foundation asks in the suit for the amount in damages to be determined at trial, but says the value of lost goods is "well in excess of $75,000."

Fox was diagnosed with Parkinson's in 1991. He rose to fame in the '80s through roles in the "Back to the Future" films and on television as conservative son Alex P. Keaton in the sitcom Family Ties. From 1996-2001 he played deputy New York City mayor Mike Flaherty in Spin City.

Improving Deep Brain Stimulation to Treat Freezing of Gait

FoxFeed Blog

Posted by  Maggie McGuire, October 06, 2014

While deep brain stimulation (DBS) is a powerful treatment for many people living with Parkinson’s, this therapy does not treat all the symptoms of PD and isn’t suitable for all patients. Earlier this year we launched a funding program to support projects that seek to improve DBS or to explore other neuromodulation techniques.

In DBS, a neurosurgeon implants a thin electrode into the brain, targeting motor and potentially other circuits that are not functioning properly. Small electrical pulses from a device similar to a cardiac pacemaker modulate the signals that cause some Parkinson's motor symptoms.

Dr. Michael S. Okun, co-director and professor of the Center for Movement Disorders and Neurorestoration at the University of Florida College of Medicine and national medical director for the National Parkinson Foundation, is the recipient of an MJFF grant to improve upon the current standards and to help more people with DBS therapy.

His project targets freezing of gait and uses an advanced approach, sending electrical impulses only when the brain needs them. Current DBS sends pulses continuously, which may result in side effects, may not adequately address freezing of gait and may burn the device’s battery at a rapid clip.

Dr. Okun spoke with us about his research:

MJFF: Does current DBS treat freezing of gait?

Dr. Michael Okun: People with gait disturbances frequently report inconsistent responses, no response and sometimes even worsening of freezing following DBS. The current technology works for people with Parkinson’s who have a good response to dopaminergic medications; DBS is very good at addressing tremor, “on/off” fluctuations and dyskinesia. Walking and balance dysfunction and freezing can be very disruptive for patients, and can lead to falls and injury, but the response to DBS has been disappointing. Gait can sometimes improve, especially if “on” time is enhanced by DBS; however gait and balance problems and freezing all tend to progress and become resistant to medications and to DBS.

MJFF: What is the aim of your project?

MO: We’re looking at a novel way to detect brain signals responsible for freezing and to modulate them with a technology we believe may be capable of breaking the freezing episodes.

We’re going to place DBS leads into parts of the brain called the globus pallidus interna (GPi) — a frequent target of DBS for Parkinson’s — and the pedunculopontine nucleus (PPN), which is a well-known locomotor center that has important connections relevant to walking.

We’re not putting in regular DBS devices. The technology we will use will allow us to measure something called local field potentials, where we can monitor, in real time, the electrical currents from both the GPi and the PPN, and more importantly sample the conversations going on between these regions. We believe there’s a network of activity that underpins gait dysfunction in Parkinson’s disease. In this project we are going to begin to get a picture of what the “brain freezing” network looks like.

MJFF: How will that help you develop a new kind of DBS?

MO: For the first several months after implantation we’re going to monitor and learn about these brain signals. In a controlled laboratory setting, we can set the device for closed-loop stimulation, meaning it only fires an electric impulse when the device sees the “freezing signal” in the brain. We think the GPi may be the gas pedal and the PPN may be the brake. So if someone freezes, we may need to take our foot off the gas and de-activate the brake. We’re going to explore different DBS stimulation paradigms to understand the signals, and then to modulate them and try to gain control of freezing symptoms.

MJFF: Why is closed-loop stimulation advantageous?

MO: No two people with Parkinson’s disease are alike. We need to understand what network signals change during individual symptoms, and then we need to deliver an efficient therapy “on demand” that will be appropriate for a particular symptom. We are entering the era of personalized medicine for Parkinson’s disease.

Freezing of gait is one disabling symptom of Parkinson’s disease, and we are hoping that the brain signals will reveal that it is a straightforward problem. If we can demonstrate that the application of these technologies works for freezing, perhaps we can take another step toward some of the more complex issues.

MJFF: How has MJFF played a role in your research?

MO: The partnership has been terrific. The Michael J. Fox Foundation understands the innovation that needs to happen to bring us cutting-edge technologies. We believe we have a very good idea and a lot of reason to believe we can make it work in people with PD. This is where MJFF has done a great job in allowing researchers like us to take a step closer to our dream, which in this case is a personalized approach to treating Parkinson’s disease.

Learn more about other research into closed-loop DBS.

Read more from Dr. Okun in his book on Parkinson’s treatment.

University of Michigan gets $11.5M grant to launch five-year Parkinson's disease study

Monday October 06, 2014

Jeremy Allen

MLive.com - Scientists and doctors at the University of Michigan were given an $11.5 million grant to launch a five-year study into better treating and understanding Parkinson's disease – with the main goal of understanding how changes in the brain cells lead to dangerous falls.

With the grant – administered by the National Institute of Neurological Diseases and Stroke, part of the National Institutes of Health – U-M will become one of only nine homes of the Morris K. Udall Centers of Excellence in Parkinson's Disease Research in the country.

The National Parkinson's foundation estimates that upwards of 60,000 people are diagnosed with the disease each year, adding to the nearly 1 million people who currently have it.

The U-M investigators will focus on the cholinergic system – a brain chemical system that is rapidly emerging as a key player in the disease's effect on walking and balance. Researchers say the cholinergic system helps focus one's attention on tasks such as walking, and may be the next key target for Parkinson's treatments.

"Understanding the role of the cholinergic system is a key unexplored frontier in Parkinson's disease, and will allow us to go beyond the limits of current practice, so we can create better therapies to suppress the terrible symptoms of the disease that affect balance, walking and overall independence," William Dauer, who will be the center's director said in a news release.

Dauer directs the UMHS Movement Disorders program and is the Elinor Levine Professor of Neurology, and an associate professor of Cell and Molecular Biology, in the U-M Medical School.

He added that most Parkinson's disease research and treatment focuses on the brain's dopamine system, which normally helps control movement. This control breaks down in Parkinson's patients, as more and more dopamine-producing brain cells called neurons are lost.

The new center will conduct three interrelated projects to better understand the role of the cholinergic system in falls, focusing on the effect of lost cholinergic neurons in brain areas called the basal forebrain, which regulates attention, and the pedunculopontine nucleus, which controls balance.

The team will work to study the effects, in both rats and people, and to determine if it may be possible to increase cholinergic traffic in the brains of patients using an already-approved drug that targets acetylcholine receptors on the surface of brain cells.

That drug, varenicline or Chantix, is currently available by prescription to help people stop smoking.

The U-M Udall Center team includes researchers in the medical school who treat Parkinson's patients at the U-M Health System and the VA Ann Arbor Healthcare System, as well as a neuroscientist in the College of Literature, Science & the Arts, and biostatisticians from the schools of Nursing and Public Health.

The center will also partner with the Michigan Alzheimer's Disease Center in minority outreach efforts, and run a Udall Center Fellows program, co-funded by U-M Medical School and the Department of Neurology.

It will allow physicians and physician-scientists interested in Parkinson's disease to receive two years of intensive training and participate in center research.

http://www.mlive.com/news/ann-arbor/index.ssf/2014/10/u-m_gets_115m_grant_to_launch.html