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duminică, 5 august 2012

NIH's PRB Progesterone Therapy To Combat Infant Mortality Adopted By State Of Michigan

The Michigan Department of Community Health (MDCH) has unveiled the state's Infant Mortality Reduction Plan, a strategy that includes significant recommendations developed from medical research conducted by the Perinatology Research Branch (PRB) of the Eunice Kennedy Shriver National Institute for Child Health and Human Development, National Institutes of Health (NICHD/NIH), at the Wayne State University School of Medicine.

Announced Aug. 1, the plan promotes the adoption of universal cervical length screening by ultrasound and the use of progesterone in women identified as high risk for premature birth. The use of progesterone in women with a short cervix can reduce the rate of preterm birth - the leading factor in infant mortality - by as much as 45 percent, according to research findings published by the PRB. The study, released last year, was conducted at more than 40 centers worldwide. Roberto Romero, M.D., branch chief of the PRB, was the principal investigator on behalf of NICHD/NIH. Wayne State was the lead center in the trial, led by Sonia Hassan, M.D., associate dean for maternal, perinatal and child health at WSU.

The ultrasound examination is simple to perform, painless and can be performed between the 19th and 24th weeks of pregnancy. Pregnant women with a cervix less than 20 millimeters are at very high risk for preterm delivery. If a woman is found to have a short cervix, she can be treated with vaginal progesterone. Treatment with vaginal progesterone reduced the rate of preterm birth, neonatal morbidity and respiratory distress syndrome. Women can self-administer a once-daily dose.

The recommendation that the state adopt the progesterone protocol was first introduced by Valerie M. Parisi, M.D., M.P.H., M.B.A., dean of the WSU School of Medicine, during the state's Call to Action to Reduce and Prevent Infant Mortality Summit in October 2011. The summit, convened by Gov. Rick Snyder to address the state's high rate of infant mortality, brought together hundreds of health care providers and stakeholders to develop recommendations to combat the problem.

"The strategies introduced by the state today will go a long way in dramatically reducing the state's infant mortality rate, which remains too high," Parisi said. "The key recommendations were developed through medical research conducted at the Perinatology Research Branch at Wayne State University, which demonstrates the branch's significant importance to the people of Michigan and the Detroit region."

The MDCH, headed by Director Olga Dazzo, said the strategies were selected because they reflect evidence-based practices that will reduce and prevent infant deaths.

While the 2010 state infant mortality rate set a new record low at 7.1 deaths per 1,000 live births, Michigan's rate remains higher than the national average of 6.1 deaths per 1,000 live births, according to the MDCH.

Premature birth is the leading cause of infant mortality in Michigan. The rate of premature birth increased more than 10 percent between 1998 and 2008. One of every eight babies born in Michigan - 295 in an average week - is born prematurely. And Michigan's rate of preterm birth (12.7 percent) exceeds the national average of 12.3 percent.

The new practices call for the state to partner with Wayne State University and the Detroit Medical Center to share progesterone therapy practices and develop protocol and implementation statewide. The state also will coordinate with the Medical Services Administration to assure benefit coverage for universal ultrasound screening of pregnant women and progesterone administration for Medicaid covered pregnancies.

"The implementation of universal cervical ultrasound screening for all pregnant women to identify women at risk for premature birth, and the use of vaginal progesterone, will be critical in the plan to reduce the rate of preterm birth and infant mortality," said Hassan.

Statewide universal ultrasound screening, Parisi said, would be cost effective if the scan costs no more than $186. With Michigan's 110,000 births annually, the potential cost savings would be $19,603,380 (in 2010 dollars) for every 100,000 women screened.

Premature births are costly. Nationally, preterm birth is a $26 billion annual problem. The CDC reports that preterm births topped the list of the most expensive hospitalizations in Michigan in 2007. Each premature birth in the state costs an average of $102,103 at the time of discharge from the hospital. That is 14 times the cost of a normal birth.

The state's other strategies include promoting the adoption of policies to eliminate medically unnecessary deliveries before the 39th week, promoting safe infant sleep practices to prevent suffocation, expanding home-visiting programs to support vulnerable women and infants, programs to reduce unintended pregnancies, and weaving social determinants of health into all its strategies to reduce racial and ethnic disparities in infant mortality.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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joi, 15 decembrie 2011

Prognostic Model Developed For MDS Related To Prior Cancer Therapy

Main Category: Cancer / Oncology
Article Date: 15 Dec 2011 - 2:00 PST

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A large-scale analysis of patients whose myelodysplastic syndrome is related to earlier cancer treatment overturns the notion that all of them have a poor prognosis, researchers from The University of Texas MD Anderson Cancer Center report at the 53rd Annual Meeting of the American Society of Hematology.

"MDS patients whose disease springs from earlier radiation, chemotherapy or both treatments are usually told that they have a poor prognosis. But by analyzing survival risk factors in a large patient population, we've found these patients fall into good, intermediate and poor prognostic groups," said study leader Guillermo Garcia-Manero, M.D., Ph.D., professor in MD Anderson's Department of Leukemia.

Understanding their differing characteristics will better inform treatment decisions for these patients, Garcia-Manero said.

Myelodysplastic syndrome consists of a group of diseases in which the bone marrow progenitor cells that normally morph into red and white blood cells and platelets fail to respond to normal growth controls. That results in too many progenitor cells (also known as blasts) and too few mature blood cells, and in about 30 percent of patients, the disease progresses to acute myeloid leukemia (AML).

Treatment-related MDS is often more resistant to therapy

Therapy-related MDS generally differs from other MDS cases by having more chromosomal abnormalities, a higher rate of conversions to acute myeloid leukemia and high resistance to standard MDS therapy. Even so, Garcia-Manero notes, a one-size-fits-all poor prognosis is not accurate.

The research team analyzed 1,950 MD Anderson patients treated between 1998 and 2007. It found 438 had a history of one or more previous cancers that were treated before their MDS diagnosis. Of these, 279 cases who had received chemotherapy, radiotherapy or both were analyzed.

A first round of analysis identified at least 15 factors associated with overall survival when considered as isolated, single variables.

Next, the researchers conducted a multi-variable analysis that narrowed factors reducing overall survival to seven:

Age 65 or older.

ECOG performance status scores of 2-4. (Eastern Cooperative Oncology Group criteria range from 0, which means fully active, to 4, signifying complete disability).

Cytogenetics. Having at least seven chromosomal alterations and/or complex cytogenetics.

Two MDS subgroups as determined by World Health Organization Criteria. RARS and RAEB-1/2.

Serum hemoglobin levels of less than 11g/dL.

Platelet levels of less than 50.

Dependency on blood transfusions.

Prognostic model sorts patients into three risk groups

Garcia-Manero and colleagues created a novel prognostic model that incorporated these multivariate factors and divided patients into three categories:

Good prognosis - 57 patients fell into this group by having 0-2 of the multivariate risk characteristics. Their median survival was 34 months.

Intermediate prognosis - 154 patients in this category had 3-4 risk factors and a median survival of 12 months.

Poor prognosis - 61 patients had 5-7 risk factors and a median survival of only five months.

The model also predicted one-year leukemia-free survival of 96 percent in the good category, 84 percent for intermediate, and 72 percent for the poor.

Model validated in a test group of patients

The researchers validated the model by applying it to an additional 189 treatment-related cases diagnosed between 2008 and 2010. Median survival rates in the test group were:

Good - 26 months

Intermediate - 13 months

Poor - 7 months.

"We believe this model will facilitate development of risk-adapted treatment strategies for patients with treatment-related myelodysplastic syndromes," Garcia-Manero said.

Article adapted by Medical News Today from original press release. Source: University of Texas M. D. Anderson Cancer Center
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marți, 13 decembrie 2011

Adults With Hemophilia B Benefit From Gene Therapy

Main Category: Blood / Hematology
Also Included In: Genetics; Liver Disease / Hepatitis; Cystic Fibrosis
Article Date: 13 Dec 2011 - 0:00 PST

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Symptoms improved significantly in adults with the bleeding disorder hemophilia B following a single treatment with gene therapy developed by researchers at St. Jude Children's Research Hospital in Memphis and demonstrated to be safe in a clinical trial conducted at the University College London (UCL) in the U.K.

The findings of the six-person study mark the first proof that gene therapy can reduce disabling, painful bleeding episodes in patients with the inherited blood disorder. Results of the Phase I study appear in the online edition of the New England Journal of Medicine. The research was also scheduled to be presented December 11 at the 53rd annual meeting of the American Society of Hematology in San Diego.

Four study participants stopped receiving protein injections to prevent bleeding episodes after undergoing the therapy and have not suffered spontaneous bleeding. Several have also participated in marathons and other activities that would have been difficult prior to gene therapy. The study volunteers were all treated at the Royal Free Hospital in London under the care of Edward G.D. Tuddenham, M.D., Ph.D., a pioneer in the field of blood coagulation and a study co-author.

"This is a potentially life-changing treatment for patients with this disease and an important milestone for the field of gene therapy. It could have ramifications for the treatment of hemophilia A, other protein and liver disorders and chronic diseases such as cystic fibrosis," said first author Amit Nathwani, M.D., Ph.D., a faculty member at the UCL Cancer Institute, Royal Free Hospital and NHS Blood and Transplant (NHSBT).

Hemophilia B is caused by an inherited mistake in the gene for making a protein called Factor IX, which is essential for normal blood clotting. The gene is carried on the X chromosome. As a result, hemophilia B is almost exclusively a disease of men. About 1 in 30,000 individuals inherit the mutation.

Previous efforts to ease hemophilia B symptoms by introducing a correct copy of the gene have been unsuccessful.

The current study used adeno-associated virus (AAV) 8 as the vector to deliver the Factor IX gene along with additional genetic material into the patient's liver. AAV8 was picked because the incidence of natural infection with AAV8 is low. It belongs to a family of viruses that target liver cells but do not cause disease in humans or integrate into human DNA. Participants in the study received no immune suppressing drugs prior to gene therapy.

This approach was jointly pioneered by St. Jude and UCL, initially in the laboratory of study co-author Arthur Nienhuis, M.D, a member of the St. Jude Department of Hematology.

For this study, each patient received a one-time infusion of the vector into a vein in the arm. Two patients each were treated with escalating doses of the vector. Following treatment, Factor IX levels rose in all six patients from less than 1 percent of normal levels prior to the gene therapy to between 2 and 12 percent.

Factor IX levels increased the most in the two study volunteers who received the highest dose of the experimental vector, researchers said. After treatment, levels of the protein ranged from 3 to 12 percent in those men. Even modest increases that raise Factor IX production to more than 1 percent of normal levels have the potential to dramatically affect a patient's quality of life and reduce bleeding episodes, said the study's senior author Andrew Davidoff, M.D., chair of the St. Jude Department of Surgery.

"The first patient has been followed for the longest time, and his levels have remained at 2 percent for more than 18 months. These results are highly encouraging and support continued research. More patients are scheduled to be enrolled in future trials scheduled to begin later this year," Davidoff said.

One of the participants who received the highest dose of the vector underwent successful, short-term steroid treatment after his liver enzymes rose slightly after the vector infusion. The rise signalled mild liver damage. The volunteer remained otherwise healthy, his Factor IX levels remain above pre-infusion levels and his liver enzymes have returned to normal. Liver enzymes also rose slightly, but remained in the normal range, for the other participant who received the highest dose of the vector. That participant also received a short course of steroids.

Researchers believe an immune response targeting the vector triggered the elevated enzyme levels. A similar response was reported in earlier gene therapy trials conducted by other investigators using a different vector.

The vector used in this study was produced at the Good Manufacturing Practices (GMP) facility on the St. Jude campus. The GMP operates under U.S. government-approved manufacturing guidelines and produces highly specialized medicines, vaccines and other products that pharmaceutical companies are reluctant to pursue. The vector can also now be produced in a similar facility at UCL.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our blood / hematology section for the latest news on this subject. Other authors are Savita Rangarajan, Basingstoke and North Hampshire Foundation Trust; Cecilia Rosales, Jenny McIntosh and David Linch, all of UCL Cancer Institute; Pratima Chowdary, Anja Griffioen, Anne Riddel, Jun Pie, Chris Harrington and James O'Beirne, all of Royal Free NHS Trust; Keith Smith, NHSBT; John Pasi, Bertie Glader, Pradip Rustagi and Mark May, all of Stanford University; Catherine Y.C. Ng, Junfang Zhou, Yunyu Zpense, Christopher Morton, all of Queen Mary's School of Medicine, London; James Allay, the late John Coleman, Susan Sleep, John Gray and Ulrike Reiss, all of St. Jude; John Cunningham, University of Chicago; Etiena Basner-Tschakarjan and Federico Mingozzi, both of Children's Hospital of Philadelphia and Katherine High, of the Howard Hughes Medical Institute and Children's Hospital of Philadelphia.
In the U.S., the research was funded by the National Institutes of Health, the Assisi Foundation of Memphis and ALSAC. In the U.K. the research was funded in part by The Katherine Dormandy Trust, Medical Research Council, Wellcome Trust, NHS Blood and Transplant and the UCLH/UCL NIHR Biomedical Research Centre.
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Therapy Improves Stem Cell Engraftment In Umbilical Cord Blood Transplant Recipients

Main Category: Stem Cell Research
Also Included In: Transplants / Organ Donations
Article Date: 13 Dec 2011 - 1:00 PST

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A therapy involving a natural compound may improve the ability of stem cells from umbilical cord blood to engraft in patients receiving a stem cell transplant for cancer or other diseases, a phase I clinical trial led by Dana-Farber Cancer Institute scientists indicates.

Details of the trial (abstract 653), which involved 12 patients who underwent reduced-intensity chemotherapy and then received a transplant of cord blood stem cells treated with the compound FT1050, will be presented at the American Society of Hematology's 2011 annual meeting on Monday, Dec. 12, at 2:45 p.m. PST.

FT1050-treated blood-forming stem cells are being tested as a possible solution to one of the major shortcomings of transplants involving stem cells from umbilical cord blood: the relatively small number of stem cells infused in such procedures often take longer to engraft or take root in patients than do the more numerous stem cells involved in transplants from adult donors. The delay can leave patients susceptible to dangerous infections and other complications.

"There is a significant need to improve the speed and quality of engraftment of cord-derived stem cells," says trial leader Corey Cutler, MD, MPH, of Dana-Farber and Brigham and Women's Hospital. "FT1050 has shown the ability in preclinical research to activate hematopoetic [blood-forming] stem cells so they engraft more quickly and with a higher degree of success."

Umbilical cord stem cell transplants are an option for patients who do not have a closely-matched adult donor. Because the current pool of potential donors is smaller for non-Caucasians than for Caucasians, members of ethnic minorities tend to receive transplants from cord blood at a higher rate than Caucasians do.

The goal of the phase I trial was to assess the safety of FT1050-treated cord blood cells in adult patients receiving umbilical cord blood stem cell transplants, and determine if the treated cells accelerate engraftment. In the 12 patients who participated in the trial, engraftment occurred approximately three to four days faster than happens with standard cord blood cells. Levels of white blood cells known as neutrophils returned to normal in the patients after a median of 17.5 days, similar to the rate in standard stem cell transplants. Side effects of the FT1050-treated cord blood cells were minimal. In none of the study patients did the stem cells fail to engraft.

The phase I trial was sponsored by Fate Therapeutics, Inc., of San Diego, Calif., which is developing ProHema, a biologic product consisting of hematopoietic stem cells treated with FT1050 for patients undergoing stem cell transplantation. FT1050 was identified by Leonard Zon, MD, a hematologist and director of the Stem Cell Program at Children's Hospital Boston, using chemical screens conducted in zebrafish, and is the first potential therapeutic derived from a zebrafish model to make into clinical trials.

"We're encouraged by the results of this study for patients receiving umbilical cord stem cell transplants after reduced-intensity chemotherapy treatment," Cutler says. "Further studies are planned to test FT1050-treated hematopoietic stem cells in a larger group of these patients."

Article adapted by Medical News Today from original press release. Source: Dana-Farber Cancer Institute
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How Patients Will Respond To Immunomodulator Therapy For Multiple Myeloma

Main Category: Lymphoma / Leukemia / Myeloma
Article Date: 13 Dec 2011 - 0:00 PST

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Research on the same protein that was a primary mediator of the birth defects caused by thalidomide now holds hope in the battle against multiple myeloma, says the study's senior investigator, Keith Stewart, M.B., Ch.B. of Mayo Clinic in Arizona. Dr. Stewart presented the results at the 53rd annual meeting of the American Society of Hematology in San Diego.

The drug thalidomide achieved infamy in the early 1960s as the cause of severe birth defects after being given to pregnant mothers for morning sickness. However, this drug, along with the highly related compounds lenalidomide and pomalidomide, also help to treat blood cancers, and are used worldwide as a cornerstone of therapy for the bone marrow cancer multiple myeloma. These drugs modulate the immune system and together are called immunomodulators or IMiDs.

The exact mechanisms and targets through which these therapies work to enhance immune response or kill cancer cells have been largely unknown. As a result, knowing which patients to treat and how to separate out the positive properties of these drugs from side effects has been impossible.

After recent research identified a protein known as cereblon as a primary mediator of the birth defects caused by thalidomide, researchers theorized that cereblon may also orchestrate the anti-tumor properties and be the primary therapeutic target for multiple myeloma.

In this study, researchers tested the theory and found a possible link between resistance to IMiDs and presence of cereblon. The researchers then found that lowering the level of cereblon allows the IMiDs to work properly.

"Interestingly, some resistant patients had normal cereblon levels, suggesting that while cereblon may be an absolute requirement for response, there are likely other mechanisms present that play a role in drug resistance," says Dr. Stewart. "These findings help us understand which patients may be more or less likely to respond to therapy and allow us to focus on other ways we can target cereblon as a possible biomarker to improve treatment and patient outcomes in multiple myeloma. This work also suggests that we can begin to dissect out the cause of birth defects from the anti-cancer properties and develop safer drugs in the future."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our lymphoma / leukemia / myeloma section for the latest news on this subject. Other researchers involved in the study include Yuan Xiao Zhu, Esteban Braggio, Ph.D., Chang-Xin Shi, Jessica Schmidt, Laura Bruins, Steven Schuster, M.D., Rafael Fonseca, M.D. and, Leif Bergsagel,M.D., of Mayo Clinic and Chad Bjorklund, Ph.D. and Robert Orlowski, Ph.D., M.D., of MD Anderson Cancer Center.
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Clues To Development Of The Pancreas Provided By Rare Genetic Disorder Could Lead To Diabetes Therapy

Main Category: Diabetes
Also Included In: Genetics
Article Date: 13 Dec 2011 - 0:00 PST

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A rare genetic disorder has given researchers at the University of Exeter a surprising insight into how the pancreas develops. The finding provides a clue to how it may be possible to 'programme' stem cells - master cells in the body that can develop into specialised cells - to become pancreatic cells.

Pancreatic agenesis is a rare condition in which the body is unable to produce a pancreas. The pancreas plays an essential role in regulating levels of sugar (glucose) in the blood. It does this by the release of the hormone insulin, which is generated and released by cells known as pancreatic beta cells. It also produces enzymes to help digest and absorb food.

Rare mutations in the genes PDX1 and PTF1A have previously been shown to cause pancreatic agenesis, but have only been identified in a handful of families affected by the condition. Until now, the underlying causes of most cases have been unknown.

In a paper published in Nature Genetics, an international team of researchers led by scientists from the Peninsula College of Medicine and Dentistry at the University of Exeter report a mutation in the gene GATA6 found in fifteen out of twenty-seven individuals with pancreatic agenesis. The study, funded by organisations including the Wellcome Trust, Diabetes UK and the National Institute for Health Research, establishes a key role for GATA6 in the development of pancreatic cells.

The finding was particularly surprising as switching off the GATA6 gene in mouse models appeared to make no difference to the development of the pancreas.

Professor Andrew Hattersley from the Peninsula College of Medicine and Dentistry, said: "This rare genetic condition has provided us with a surprising insight into how the pancreas develops. What is it that programmes cells to become pancreatic beta cells? Our study suggests that GATA6 plays a very important role in this process and we hope this will help the crucial work to try and make beta-cells for patients with type 1 diabetes."

Whilst pancreatic agenesis is an extreme form of pancreatic dysfunction, far more common is diabetes. In type 1 diabetes, which generally develops in childhood, the immune system attacks and destroys pancreatic beta cells and the body is unable to regulate glucose levels, whilst in type 2 diabetes, the beta cells gradually decline until, usually during adulthood, they cease to function.

Professor Sian Ellard, also from Peninsula College of Medicine and Dentistry, added: "This discovery was possible because new sequencing approaches meant we could test all the genetic information in one go and because with the help of doctors throughout the world we were able to study 27 patients with a very rare condition."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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luni, 12 decembrie 2011

Treating Latent Tuberculosis - Easier Therapy, Study

Editor's Choice
Main Category: Tuberculosis
Article Date: 12 Dec 2011 - 7:00 PST

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An investigation led by Timothy Sterling, M.D., professor of Medicine at Vanderbilt University Medical Center, has resulted in a vital alteration in CDC recommendations in the plan of prevention for tuberculosis (TB). The study was published December 8 in New England Journal of Medicine (NEJM).

On December 9 in the Morbidity and Mortality Week Report (MMWR), the Centers for Disease Control and Prevention (CDC) announced that the novel method, which takes one-third the time of current treatment, provides several individuals at a high risk of developing TB an effective treatment option. Latent TB infections result from exposure to TB - the infecting bacteria are alive in the body, but inactive.

Until now, the treatment for latent TB infection involved patients taking daily doses of a medication called isoniazid (INH). Over the course of nine months, a total of 270 daily doses were taken in order to destroy the bacteria, which can remain dormant in the body for several years.

The study, which consisted of 8,000 individuals in 4 countries over a 10 year period, demonstrated that just 12 doses of INH combined with another TB medication called rifapentine, taken once-weekly was safe and effective. In addition the novel therapy improved compliance by at least 10%

Sterling explained:

"This is a game changer. Currently less than half of the people who start the current therapy complete it. The new combination would require a direct observation, but more people would complete treatment."

The CDC explained that although cases of active TB are at an all-time low, around 4% of individuals in the U.S., or 11 million people, have latent TB. Active TB cases, which can be potentially fatal to individuals who have a compromised immune system, still occur in Nashville. In order to prevent a return of active and infections disease, the Metro Nashville Public Health Department's Division of TB Elimination works with an average of 700 novel cases of latent TB every year.

One of the locations for the investigation was The Metro Nashville Public Health. The study received funding by the Centers for Disease Control and Prevention (CDC). Other Vanderbilt investigators included Amy Kerrigan, MSN, R.N., and Alicia Wright, among others.?

Sterling says further research is vital. The novel treatment is not an option for all patients, and may not work well in countries with a higher TB incidence. Children under 2 were excluded from the investigation.

Written by: Grace Rattue

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Using Eyebrain Tracker In Parkinson's Therapy Clinical Trial

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Main Category: Parkinson's Disease
Also Included In: Neurology / Neuroscience; Medical Devices / Diagnostics
Article Date: 12 Dec 2011 - 7:00 PST

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After Alzheimer's, Parkinson's disease is the second most common neurodegenerative disease, affecting 0.3% of the general population in western countries, with 100,000 sufferers in France and 8,000 new diagnoses each year. Its prevalence increases with age, reaching 1% in those above the age of 60 years, and as much as 4% in the over-80s.

An announcement made by EyeBrain, a company that develops medical devices for the early diagnosis of neurological diseases, states that the company's EyeBrain Tracker device will be used in a clinical trial that will explore the dyskinesia induced by treating patients suffering from idiopathic Parkinson's disease with levodopa. ?The trials' endpoint is to identify biomarkers for the late-onset complications of a treatment regime using levodopa (BIODYS). This compound, naturally transformed into dopamine in the brain, is the only drug available that can slow down the effects of Parkinson's disease, however, it induces dyskinesia in these patients over time, which is characterized as abnormal movements that primarily affect the face (tongue, lips, jaw) and extends as far as the arms and legs.

Researchers will involve a total of 30 people in the trial, half of these will be Parkinson's sufferers who will received treatment with levodopa and who have developed dyskinesia, while the other half will be the control group consisting of healthy subjects.

The trial, set up by professor Jean-François Tison, a neurologist at the CNRS Physiopathology of Parkinsonian syndromes unit at the University of Bordeaux Two (the Institute of Neurodegenerative Diseases, CNRS UMR 5293E, Bezard) is being sponsored and financed by Bordeaux University Hospital, whilst the EyeBrain Tracker device is being funded under the joint 2007-2013 State-Region Plan (Aquitaine Regional Council and the FEDER fund). ?

?Professor Tison explained:

"Patients suffering from idiopathic Parkinson's disease will undergo an acute test as part of a pre-operational assessment for stimulating the deep recesses of the brain."

The EyeBrain Tracker will evaluate and measure patients' motricity effects through speed of eye movements.

Tison said:

"We will see whether levodopa modifies the parameters of blinking in a way that is correlated with the improvement in motricity. Using the EyeBrain Tracker enables us to measure the motricity effect through eye movements, since the blinking parameters are also linked to the patient's general motricity. The patient's response to this trial is also a predictor of their reaction to the neurosurgery that will follow."?

?The EyeBrain Tracker has already been utilized for early diagnosis of Parkinsonian syndromes, such as progressive supra-nuclear paralysis (PSP), cortico-basal degeneration (CBD) and multiple systems atrophy (MSA). With the new trial, the device is broadening its field of application as a valuable aid in the early diagnosis and follow-up of these diseases, and now plays a significant part in clinical research into other neurological diseases, such as multiple sclerosis. ?

The chairman of EyeBrain, Serge Kinkingnéhun states:

"We are delighted to know that the EyeBrain Tracker is playing a part in a clinical trial targeting idiopathic Parkinson's. This forms part of our goal of making the benefits of eye motricity available to a larger number of people suffering from neurological pathologies." ?

?About EyeBrain? Tracker
eyebraintracker

EyeBrain Tracker allows clinicians for the first time to depend on a simple set of eye movement parameters to differentiate between very similar syndromes, such as progressive supra-nuclear paralysis (PSP) and cortico-basal degeneration (CBD). The tests are easy to perform, non-invasive and low-cost, with results being available in less than 20 minutes. ? ?

The Mobile EyeBrain Tracker (EBT) is a complete unit, including headphones, a computer with two monitors and software for stimulation and analysis and is already routinely utilized in hospitals to assist in the early characterization of Parkinsonian syndromes, with studies also underway for the diagnosis of multiple sclerosis (MS). ? ?

The Mobile EBT is a globally novel device that has obtained CE marking in addition to the company's ISO-9001 and ISO-13485 certification.

?EyeBrain is based in the Paris suburb of Ivry-sur-Seine

Written by: Petra Rattue

Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Additional References Citations Visit our parkinson's disease section for the latest news on this subject. http://www.eyebrainpedia.com
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