The Stars in Our Brains – Duke Department of Neurology

More than 10 million people worldwideabout 1 percent of people over age 60live with Parkinsons disease. There are treatments that can help control symptoms, but there is no cure.

The hallmark of the disease is the death of certain brain cellsneurons that produce dopamine. Most Parkinsons researchers have focused on studying these cells. But what if the disease starts elsewhere? What if it involves not only neurons but other cells that interact with neurons? In particular, what role is played by astrocytes, star-shaped cells that nurture and help form the connections, or synapses, between the neurons?

(This article by Angela Spivey, with photos by Alex Boerner, originally appeared in Duke Medical Alumni News. Read that story here.)

Thats the question a team of Duke researchers led by Cagla Eroglu, PhD, associate professor of cell biology and neurobiology, is exploring, thanks to a $1 million grant from the Chan Zuckerberg Initiative.

Sitting in her office, Eroglu picks up an orange plastic object that resembles a piece of coral, its tentacles branching this way and that. This is a model of a mouse astrocyte, she says. It can interact with 100,000 synapses at the same time. Astrocytes, she explains, infiltrate the brain, touching everything within their reach. They communicate with its synapses, regulating blood flow and metabolism.

Astrocytes from the Greek astron, meaning "star"have traditionally been thought of as support cells. But that thinking is changing. Since astrocytes are in such close contact and continuously communicating with synapses, we are beginning to appreciate that they are also fundamentally involved in regulating brain function, Eroglu says.

Collaborating with Albert La Spada, MD, PhD, Eroglu found that a certain gene known to be important in Parkinsons is more highly expressed in astrocytes than in neurons. And when the researchers mutated that gene in astrocytes, they saw some intriguing changes. This still-unpublished work laid the foundation for their proposal to the Chan Zuckerberg Initiative, which is bringing together experimental scientists from divergent fields to take a fresh look at the causes of neurodegenerative disorders.

There are vanishingly few papers that have delved into how astrocytes are contributing to the Parkinsons disease process, says La Spada, professor of neurology and vice chair of research for the Department of Neurology. This is an area that's been under-studied, and I think that the results that we're generating are suggesting that it deserves more attention.In addition to his long experience studying neurodegenerative diseases, La Spada brings expertise in growing astrocytes from induced pluripotent stem cells (IPSCs). That process starts by growing skin cells from a skin biopsy from a Parkinsons patient. Then we use what's called a reprogramming protocol to basically revert them to stem cells that are pluripotent. Once you create the IPSCs, you could use them to make any cell you wanta muscle cell or a cardiac cell or a neuron or an astrocyte, La Spada says. The beauty of this is, it comes from the patient who has the disease of interest."

His labs expertise will only grow because of the Chan Zuckerberg Initiative, which has formed focus groups for grantees around various areas, such as stem cell modeling, CRISPR gene-editing technology, bioinformatic analysis of data sets, and more. We're meeting other researchers from around the world who are doing really unique things. It's a chance for us all to compare notes, and I think this will accelerate all of our endeavors, La Spada says.

Rounding out the team is Nicole Calakos, MD, PhD, a scientist and clinician who treats patients with movement disorders, including Parkinsons. Calakos says that when she first met Eroglu, she was intrigued by her idea that since astrocytes are involved in sculpting the language of neurons, perhaps they play a role in the events that can lead to disease.

Everybody has been fixated like a magnet on the idea that the problem is the neuron that's dying, Calakos says. Cagla said, Hey, let's think outside of the box of that dead cell. Lets consider whether astrocytes are like the soil around a plant, providing the nutrition, and allowing it to form roots, and maybe that is whats broken. Why aren't we even thinking about this critical piece of the brain?

Eroglu puts it this way: Maybe the problem is loss of connections between neurons, even before they die.

Calakos says that part of the reason she came to Duke was the close intermingling of physicians and bench scientists. Because of how the community is at Duke, Cagla and I had been exchanging ideas and collaborating over the years, she says. The Chan Zuckerberg grant is an opportunity to get together as a formal team. I think it's really forward-thinking of them to have teams of basic scientists and practicing physicians all talking to each other.

The Chan Zuckerberg Initiative was launched in December 2015 by Mark Zuckerberg, founder and CEO of Facebook, and Priscilla Chan, a pediatrician and founder and CEO of The Primary School in East Palo Alto. In addition to her clinical insight, Calakos brings expertise in electrophysiologyreal-time recording and observation of electrical signals coming from brain cells. We can listen to the language of synapses, she says. They speak in electrical currents,which we can measure. Eroglu believes that by learning all they can about how astrocytes support synaptic development and health in the normal brain, they may find ways to stop neurodegenerative diseases like Parkinsons.

We are seeing aging as a part of development, Eroglu says. If your house is built on a strong base, then it might last longer. Whereas, if you build it in another way, it may be there for a while, but gradually start to break down.

This doesn't mean that we are destined to have neurodegeneration and we can't do anything. We may be more predisposed to get the disease, but we may not get it if we have done something else in our lives that helps strengthen our brain. I strongly believe that there will be ways to stop neurodegeneration.We will find a way to strengthen the brain connections. If we can figure out the weakest link, then we could concentrate on solving that.

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The Stars in Our Brains - Duke Department of Neurology

Brooks Koepka not in the field at the WGC-HSBC Champions, status of his knee injury remains unclear – Yahoo Sports

Its unclear the extent of Brooks Koepkas knee injury, but its severe enough to keep him out of another PGA Tour event he originally had planned to play. The No. 1 ranked golfer in the world was not listed among those who will be competing at the WGC-HSBC Champions in China next week when the initial field was released on Friday.

Granted, it was a longshot that Koepka would make another flight back to Asia for the tournament after aggravating his left knee while slipping on wet concrete during the CJ Cup @ Nine Bridges two weeks ago in South Korea. Doctors advised Koepka to return to the United States for further testing, so he withdrew from the CJ Cup after the second round and flew home to Florida. At that time, he also announced that he would miss this weeks Zozo Championship but left the WGC-HSBC up in the air.

Koepka underwent stem-cell treatment in August to repair a partially torn patella tendon in the left knee after finishing tied for third at the Tour Championship. He returned to compete in the Shriners Hospitals for Children Open, missing the cut after rounds of 70-71, and said prior to the CJ Cup, where he was the defending champion, that the knee felt good, although more stem-cell treatment might be in the offing.

RELATED: Brooks Koepka reveals painful treatment on knee'I was screaming'

Suffice to say, Koepkas status moving forward is a curiosity among many people not just part of the four-time major winners inner circle. None more so, perhaps, then U.S. Presidents Cup team captain Tiger Woods. Koepka was an automatic qualifier for the American team that will compete in December at Royal Melbourne. When asked prior to the Zozo Championship about Koepka, Woods said hed been in contact with him and was hopeful that hed be able to return in time to compete in Australia.

Were just waiting to see what the surgeons say and see what his protocols will be going forward. Thats something hell keep me abreast of going forward, Woods said. Hes getting other opinions about where his knee is and what his options are. I went through the same thing with my knee and my back. You want as many opinions as you can before you decide which road you want to go down.

Earlier in the week, Koepkas management team told multiple media outlets it had no more information about the injury.

Suffice it to say, Woods knows from bad knees after coming off surgery on his own left knee in August as well. Given that there are still more than six weeks until the competition, Woods sounded content to wait to see what might happen with time.

Theres no hurry, you are part of the team, Woods said he told Koepka. Now you have to figure out whats best for your career and your knee. If you decide you can play, great. If you cant, I totally understand and well cross that bridge when it comes.

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Originally Appeared on Golf Digest

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Brooks Koepka not in the field at the WGC-HSBC Champions, status of his knee injury remains unclear - Yahoo Sports

Cynata Therapeutics awarded grant to progress stem cell therapies for coronary artery disease – Proactive Investors Australia

The company is an Australian clinical-stage stem cell and regenerative medicine corporation focused on the development of therapies based on Cymerus a therapeutic stem cell platform technology.

() has been awarded a Federal GovernmentInnovations Connections grant to advance development of therapies based on itsCymerus technology platform for the treatment of coronary artery disease (CAD).

CAD, which is the narrowing or blockage of the arteries in the heart, causes the majority of heart attacks and about one-third of all deaths in people over the age of 35 in developed countries.

The Innovations Connections grant of $50,000 is supported by the Australian Governments Department of Industry Innovation and Science.

These funds will be used to support the continuation of research at the University of NSW in Sydney under the leadership of Associate Professor Kristopher Kilian, ARC future fellow at the UNSW School of Chemistry and School of Materials Science and Engineering.

Cynata's chief operating officer Dr Kilian Kelly said: We are very pleased to receive this non-dilutive funding which enables us to further our research into the development of customised MSCs that address CAD before a heart attack occurs.

Associate Professor Kristopher Kilian and his team have already demonstrated the potential value of this approach and we now look forward to generating further data in support of a future clinical trial.

Thisfurther research leads on from a collaborative project with this group which started in 2018 and identified optimal cell culture matrices to stimulate the growth of new blood vessels.

These positive effects were demonstrated in a well-established in vitro assay and were maintained after the cells were frozen and then thawed, which is important from a commercialisation perspective.

The additional project, which is expected to complete by the end of 2020, seeks to build on the previous findings by profiling the pro-angiogenic factors released from the primed MSCs, establish the ability of primed cells to promote new blood vessel formation in vivo, followed by in vivo safety and efficacy in a preclinical model.

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Cynata Therapeutics awarded grant to progress stem cell therapies for coronary artery disease - Proactive Investors Australia

Cork father of boy with bone disease hopes his book will inspire others to celebrate difference – Irish Examiner

David King is hoping his sons imagination will inspire others, writes Health Correspondent Catherine Shanahan

Pictured at the launch of David King's book ''But Really, Adventures with a Difference' in the Read and Write shop in Youghal were Mum Fiona, Robert, Dad David, Katie, Adam and Danny King from Killeagh. Picture: Howard Crowdy. Picture: Howard Crowdy

WHEN Tom Clonan rang David King and said finally, here is a book for a parent like me, David knew his story had done what he had set out for it to do: it spoke to families dealing living with difference.

I welled up, it was emotional to hear that, because that was why I wrote it. I was imagining parents like me with children like Adam, in and out of hospital, getting treatments, and I wanted them to feel spoken to by our story.

I wanted to say to them: Difference can be an adventure, just as life is an adventure. For me, its about being empowered by that difference.

Five-year-old Adam King is the star of his fathers book, But Really ... Adventures With a Difference.

Adam was born with osteogenesis imperfecta (OI), a brittle bone condition that causes stunted growth and makes him prone to fractures although he has done very well to date, with the exception of fracturing both his left and right femur.

He is generally a wheelchair user, but thanks to the excellent care he receives from consultants in Temple St Childrens Hospital, Cork University Hospital and Enable Ireland, he is also able to crawl and sometimes walk with assistance.

Adam may be short of stature, but what he lacks in height, he makes up for in spirit.

Like any five-year-old, he has a vivid imagination. His fathers book, as well as being a celebration of difference, is a tribute to innocence, to the indomitable human spirit, but most of all, to the powers of the imagination.

So while those who dont know any better might only see Adams wheelchair, in fact Adam knows its a Formula One car winning the Grand Prix. And where some might see a walking frame, Adam can see a horse going into battle.

And those pesky intravenous drips that must sometimes be inserted during hospital visits But Really they supply the superjuice Adam needs to fly high above the rooftops in full superhero mode. The book is an interplay between reality and fantasy.

So you see Adams life is different, our lives are different, but its not bad. Its just different. Its an adventure, said David.

David and his wife Fiona, who live in Killeagh, East Cork, have three other children Danny (10), Katie (8) and Robert (7).

They are also looking forward to the birth of their fifth child in the run-up to Christmas.

The months prior to and after Adams birth were not easy. He was diagnosed in utero and stem cell treatment was delivered. He was injected, while in the womb, with bone-forming stem cells.

David says the first year was fairly traumatic and, in a way, the book has been a form of catharsis for him.

In part, it was an exercise in getting that trauma out, but also about celebrating our life, which is really great. Adam is inspirational, he is the embodiment of life.

I set out to write a story that would capture his spirit and But Really Adventures With a Difference is it. Its the story of Adam and its the story of our family and its the story of the families of children with additional needs.

Children and families who live with additional needs are a hugely important topic in modern society. There are many children in Ireland, and indeed across the world, who require support for different acute and chronic conditions. But rarely are their tales told in such a way that we can see beyond their disability, to their humanity.

Thats why it meant so much to me when Dr Tom Clonan rang.

Tom a security specialist and analyst with at TheJournal.ie, but first and foremost a father and disability advocate, has a son Eoghan who has Pelizaeus-Merzbacher disease (PMD) a rare progressive condition, which affects the central nervous system. A high-profile campaigner for services and supports for children and adults with disability, he has written passionately about his fears for his sons future.

David asked Tom to review his book.

When Tom told him his book spoke to him in a way no other book had every ever done, David was overwhelmed.

He hopes that other parents who have children with additional needs will feel the same way.

David spent a year working on the book along with illustrator Jesse de la Cour who was born in Cork and is a self-taught painter and illustrator.

It was a labour of love for both of us and she captured the energy, life, and spirit of the children so well in her beautiful illustrations, said David.

Adam has already road-tested the book with his schoolmates at Clonpriest NS, Gortore, where he brought it into every class and explained to pupils what the book was about.

I think its a great way to help educate kids about difference so that they can see its part of everyday life and awesome also, said David.

The book, priced at 11.99 with some of the proceeds going to childrens charity Bumbleance, for whom Adam is an ambassador, went on sale on Amazon at the weekend, and is currently making its way into all good bookshops, David says.

So far, all the feedback has been positive and copies are flying out the door.

Among those to endorse it is Vicky Phelan, the woman who blew the lid on the cervical cancer scandal.

In a tweet, Vicky said: This looks like a fabulous book. I have a daughter with a visual impairment and epilepsy and struggled when she was small to find books that she could relate to that werent about ballet or horse riding things she couldnt do.

The very best of luck with this book.

To find out more, visit http://www.adventureswithadifference.com or follow on: Facebook: @AdventuresWAD; Twitter: @AdventuresWADand Instagram: @adventures_wad

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Cork father of boy with bone disease hopes his book will inspire others to celebrate difference - Irish Examiner

How Ruthin mum’s family tragedy became her driving force to save lives – Daily Post

The mother of a teenage drama student who drowned after after jumping into a "freezing" reservoir on a hot summer's day has vowed to make sure his death won't be in vain.

Leeanne Bartley from Ruthin has already fought for 20 emergency water rescue throw lines to be installed since losing her 18-year-old son, Mark Allen in June 2018.

The tragedy has spurred her to raise awareness of water safety after Mark jumped from a platform into Debdale Reservoir in Gorton, Greater Manchester to cool down on one of the hottest days of the year.

But he immediately got into difficulty due to the incredibly cold water despite efforts from friends to save him.

His body was later recovered by police search and rescue teams.

Trying to channel her grief into something positive, Leeanne is now hoping to launch a not-for-profit organisation in Mark's memory in a bid to get water safety included in the national curriculum to teach youngsters about the risks.

Leeanne said: "After Mark died, I felt like I couldn't just sit back and do nothing.

"I wanted to turn our tragedy into something good to help others and make sure Mark's death isn't in vain.

"I contacted United Utilities to ask if there was anything that could be done to prevent other families going through what we've been through, and ended up taking part in a pilot throw line campaign which saw 20 throw lines installed in different locations, including where Mark died.

"Next year, we are hoping to launch a not-for-profit organisation in his memory to spread the water safety message as far as we can."

In the wake of Mark's death, Leeanne turned to the internet looking for support to cope with her loss.

It was then that she came across the story of a little boy called Enis from London, who was left brain damaged after a non fatal drowning accident at a family pool in Turkey when he was 19 months old.

Leeanne said: "Shortly after Mark's death I was searching for drowning support groups on Facebook and came across Enis the Wonderchild.

"I've been following his journey and supporting him and his mum ever since and now I want to hold a fundraising event to help pay for him to have stem cell treatment.

"It would be fantastic if the local community could support us."

Leeanne, who is married to David and is also mum to Lauren, 25, Kelly, 24, Sophie-Lee, 12, Caitlin-Rose, 10, and Megan-Jessica, 8, paid tribute to her only son.

She said: "Mark was a really random and unconventional person.

"He was very loving, positive and would go out of his way to help anyone.

"He had ambitions of becoming a professional actor and even appeared as an extra in the BBC One series, Wanderlust.

"We've recently been sent DVDs of his TV appearances and have also received his double grade distinction certificate in acting which we will treasure."

* The fundraising event for Enis, which includes a raffle and live music from local band, VU, will be held at Ruthin Rugby Club on November 30 at 7pm.

To buy tickets, click here.

Or to make a donation, click here.

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How Ruthin mum's family tragedy became her driving force to save lives - Daily Post

What is aplastic anemia? Symptoms, causes, and treatment – Medical News Today

Aplastic anemia is a medical condition that damages stem cells in a person's bone marrow. These cells are responsible for making red blood cells, white blood cells, and platelets, which are vital to human health.

Doctors believe various conditions can cause aplastic anemia, while the disease itself ranges in severity from mild to life threatening.

Medical advancements mean that aplastic anemia is more treatable than ever. In this article, learn more about this rare medical disorder.

When a person has aplastic anemia, their bone marrow does not create the blood cells it needs. This causes them to feel ill and increases their risk of getting infections.

Doctors also call aplastic anemia bone marrow failure.

Doctors do not know exactly how many people in the United States have aplastic anemia.

According to the National Organization for Rare Disorders (NORD), doctors diagnose approximately 500 to 1,000 cases every year. It is most common in older children, teenagers, and young adults.

Researchers believe that most cases of aplastic anemia are due to the immune system attacking healthy bone marrow cells, according to NORD.

Doctors have also identified some of the possible causes of this immune system response, including:

However, doctors usually cannot pinpoint the underlying cause in most aplastic anemia cases.

When the cause is unknown, doctors refer to the condition as idiopathic aplastic anemia.

Symptoms of aplastic anemia include:

These symptoms may be severe. Some people may have heart-related symptoms, such as chest pain.

A doctor will start by asking about a person's symptoms and their medical history.

They will usually use a blood test known as a complete blood count (CBC) to evaluate a person's red blood cells, white blood cells, and platelets. If all three of these components are low, a person has pancytopenia.

A doctor may also recommend taking a sample of bone marrow, which comes from a person's pelvis or hip.

A laboratory technician will examine the bone marrow. If a person has aplastic anemia, the bone marrow will not have typical stem cells.

Aplastic anemia can also have similar symptoms as other medical conditions, such as myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria. A doctor will want to rule out these conditions.

Sometimes, a person with other medical conditions can develop aplastic anemia. These conditions include:

If a person has these conditions, a doctor will recognize that they are more likely to get aplastic anemia.

Doctors usually have two goals when treating aplastic anemia. The first is to reduce the person's symptoms, and the second is to stimulate the bone marrow to create new blood cells.

People with aplastic anemia can receive blood and platelet transfusions to correct low blood counts.

A doctor may also prescribe antibiotics as a person needs white blood cells to fight infections. Ideally, these drugs will prevent infections until a person can build more new white blood cells.

Doctors usually recommend a bone marrow transplant to stimulate new cell growth in the long term.

For this, a doctor may first prescribe chemotherapy medications to kill off abnormal bone marrow cells that are affecting a person's overall bone marrow function.

Next, a doctor performs a bone marrow transplant by injecting the bone marrow into a patient's body.

Ideally, the individual will receive bone marrow from a close family member. However, even a sibling donor is only a match in 2030% of cases.

People can also receive bone marrow from someone who is not related to them if doctors can find a compatible donor.

Some people cannot tolerate bone marrow transplants, especially older adults, and those having difficulty recovering from chemotherapy. Others may not be able to find a donor that matches their bone marrow. In these instances, a doctor can prescribe immunosuppressive therapy.

Immunosuppressive medicines suppress the immune system, which ideally stops it from attacking healthy bone marrow cells. Examples of these medications include antithymocyte globulin (ATG) and cyclosporine.

According to NORD, an estimated one-third of people with aplastic anemia do not respond to immunosuppressive drugs.

If this is the case, doctors may consider other treatments, such as hematopoietic stem cell transplantation and a medication called eltrombopag (Promacta).

Those with aplastic anemia may face complications due to their disease as well as their treatment.

Sometimes, a person's body rejects a bone marrow transplant. Doctors call this graft-versus-host disease or GVHD.

GVHD can make a person feel extremely ill and can cause symptoms that include:

According to 2015 research, about 15% of aplastic anemia patients who receive immunosuppressive therapy will develop myelodysplastic syndromes or acute myeloid leukemia.

These conditions can develop years after a person's initial diagnosis.

Some people do not respond to aplastic anemia treatments. When this is the case, they are more vulnerable to infections that can be life threatening.

The outlook for a person with aplastic anemia depends on many factors, including:

A doctor will discuss a person's treatment outlook when considering the various therapies.

Aplastic anemia damages stem cells in a person's bone marrow. The bone marrow makes red blood cells, white blood cells, and platelets, which are all essential for the body.

A person with aplastic anemia may experience severe anemia symptoms. Treatment may include chemotherapy, stem cell transplants, and immunotherapy.

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What is aplastic anemia? Symptoms, causes, and treatment - Medical News Today

American Academy of Stem Cell Physicians Announced Today That Their Safety Panel Session is Open and Free to the Public – P&T Community

MIAMI, Oct. 24, 2019 /PRNewswire/ -- The AASCP has recently created guidelines thatare current safety recommendations given to physicians who are using biologics in their medical practice. A highly anticipated and sought after Safety StandardsPanel session, hosted by AASCP on Nov. 2, 2019, will be moderated by The Alliance for Cell Therapy Now,with President Ms. Janet Marchbrody.The sessions normally are closed to the public but this particular SafetyStandard Panel discussion will be open to the public, covering the growing safety concerns of the industry.

Alliance for Cell Therapy Now is a coalition of organizations representing patients, health care providers and the academic and scientific community, who are working together to advance safe and effective regenerative cell therapies. The mission is to advance the development, manufacturing and delivery of safe and effective regenerative cell therapies through policy development, consensus and advocacy. Alliance for Cell Therapy Now is bringing together experts and stakeholders to gain consensus on and advocate for policies that will advance the science and the field, including those focused on promoting clinical research, assuring the adoption of consensus standards to promote safety and quality, building capacity and expertise within the workforce, and establishing a national outcomes database to advance the science, promote improvements in quality and safety, and inform regulatory, paymentand patient decision-making.

Alliance for Cell Therapy Now is guided by an Advisory Board comprised of leaders in the scientific, academicand patient communities; Ms.Janet M. MarchibrodaPresident, Alliance for Cell Therapy Now Fellow, Bipartisan Policy Center Senior Vice President, Health Policy, Bockorny Group, has agreed to join theAASCP as a moderator for their SafetyPanelat The Hyatt Regency in Miami. This particular coveted safetypanel session will be open to the public and broadcast live on YouTube at 3:00 p.m. on Nov. 2, 2019.

According to AASCP, if you are using biologics in your practice, whether you are using SVF, PRP, bone marrow, UCB, amniotic products,exosomes,xenografts, or peptides, there are key considerations to take into account to achieve the best safety for your patients. The AASCP also recommends communication with the Chief Scientific Officer from the laboratory you work with.AASCP advises that just talking to a sales agent is not sufficient enough when determining the quality of products for your patients. Sales agents typically do not have a medical or scientific background.

The spokesman for the AASCP, Dr. AJFarshchian,said earlier: "The American Academy of Stem Cell Physicians is a group of physicians, scientists and researchers who collectively represent the most authoritativenon-federal group advocating for guidelines and education on stem cell therapy and regenerative medicine. AASCP members are experts within all fields of stem cell therapy from: SVF, BM, UCB, Exosomes, Peptides, Xenografts, Allografts and Amniotic Fluids and are considered the most experienced leaders for proper advocacy in the field. The AASCP is involved directly with other authorities within the field and seeks only to bring knowledge and awareness for the ever growing regenerative medicine industry.My hope is that the SafetyPanel discussion on Nov.2, 2019, is to help get rid of the bad actors that are damaging the field for everyone."

AASCP is hosting their medical conference in Miami on Nov. 1-3 , 2019. Sessions are normally closed to the public and, therefore, require registration. The conference is taking place at the downtown MiamiHyatt Regency, located at 400 SE 2nd Ave, Miami, FL 33131.Becauseof limited seating, we encourage everyone to please RSVP ataascp.net andto register.

The American Academy of Stem Cell Physicians (AASCP) is an organization created to advance research and the development of therapeutics in regenerative medicine, including diagnosis, treatmentand prevention of disease related to or occurring within the human body. Secondarily, the AASCP aims to serve as an educational resource for physicians, scientistsand the public in diseases that can be caused by physiological dysfunction that areameliorableto medical treatment.

For further information, please contact Marie Barbaat AASCP 305-891-4686 and you can also visit us at http://www.aascp.net.

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dr-farshchian-teaching-at-aaoscp.jpeg Dr. Farshchian teaching at AAOSCP workshop Dr. Alimorad Farshchian speaking at AASCP

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AASCP Safety guidelines

AASCP website / registration

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Anthony Harries: In the absence of a true test for latent TB we need shorter, safer preventive treatments – The BMJ – The BMJ

Treating latent tuberculosis infection (LTBI) is a key component of the World Health Organizations End TB strategy, which aims to end the epidemic of TB by 2030. This neglected but vital intervention was given further emphasis in September 2018 at the United Nations high level meeting on TB, where world leaders committed to treating at least 30 million people for LTBI by 2022, including 4 million children under 5 years of age, 20 million household contacts of people affected by TB, and 6 million people with HIV.

In this context, Marcel Behr and colleagues continue their thought provoking journey of questioning established dogma. In August 2018, they provided robust evidence to support the assertion that people infected with M tuberculosis tend to progress to disease over an incubation period of two months to two years rather than over their lifetime. In a new Analysis, they go on to question the widely held assumption that M tuberculosis infection is for life.

As the authors point out, there is no perfect way to directly diagnose LTBI. The diagnosis of LTBI is made in people with no evidence of active TB by measuring the immunological response to M tuberculosis antigens using the tuberculin skin test or interferon gamma release assay. Infection is inferred rather than proven.

Behr and colleagues test the assumption that TB immunoreactivity is the same as lifelong infection in two ways: by analysing studies of the natural history of TB immunoreactivity in people given treatment and by assessing the risk of active TB in immunoreactive people who develop severe immunosuppression.

Data from longitudinal studies and clinical trials show that immunoreactivity persists after successful treatment of either LTBI or active TB, with persistence being most prolonged in those with the longest duration of immunoreactivity before starting treatment. Epidemiological studies also show that most people with TB immunoreactivity who become severely immunosuppressed owing to HIV, solid organ transplantation, haematopoietic stem cell transplantation, or tumour necrosis factor inhibition remain free of active TB.

What should we take from this new analysis? In terms of understanding LTBI, Behr and colleagues argument is persuasive that TB immunoreactivity is a sign of having been infected with M tuberculosis and not a marker of continued infection. Their analysis suggests that about 10% of people with TB immunoreactivity harbour viable organisms capable of causing disease in the right circumstances, such as immunosuppression; in the remainder, M tuberculosis bacteria are likely to be permanently dormant or dead.

This perspective reinforces the urgent need for clinically useful and affordable biomarkers that can clearly distinguish between persistent infection and immunological memory of a past infection. The journey of discovery, development, and deployment of a biomarker that can guide clinical decisions is not likely to be quick or easy. But it is a journey that must be taken, and if successful would enable precise identification of those who are truly infected and at most risk of developing active TB.

In the meantime, we have no choice but to continue providing treatment to those with LTBI if we want to honour our promises to end TB. The current preventive policy is to treat those at the highest risk of TB, such as people with HIV or young household contacts of a person with TB, without testing for LTBI. For other high risk groups, including patients with silicosis, patients in renal failure, and certain vulnerable groups, the preventive policy is to systematically test for LTBI before treatment. We need to recognise, however, that we might be treating many people who do not require this intervention because they do not have latent infection. This would be acceptable if the treatment was short and entirely safe. Unfortunately, this is not the case.

Isoniazid is the current drug of choice for treating LTBI, often for six months, but it can cause peripheral neuropathy or drug induced hepatitis, which if unrecognised or identified too late can be fatal. Shorter and safer alternative regimens are now available, the most attractive being a three month course of weekly rifapentine and isoniazid (12 doses). Two important hurdles in making this regimen widely available are country specific regulatory approval and the huge cost of rifapentine. TB programmes need to embrace new shorter treatment durations, and global advocacy and activism are needed to make the drugs affordable in the countries where they are most needed. At the same time, TB programmes need to agitate for an easy to use and inexpensive biomarker that truly identifies LTBI.

Anthony Harries is senior adviser at the International Union Against Tuberculosis and Lung Disease in Paris, France, and honorary professor at the London School of Hygiene and Tropical Medicine, UK.

Competing interests: None declared

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Rocket Pharmaceuticals Presents First Evidence of Long-Term Improvement and Stabilization in Blood Counts and Durable Mosaicism in RP-L102 Process A…

NEW YORK--(BUSINESS WIRE)--Rocket Pharmaceuticals, Inc. (NASDAQ: RCKT) (Rocket), a leading U.S.-based multi-platform clinical-stage gene therapy company, today presents updated long-term follow-up from the Phase 1/2 clinical trial of RP-L102 at the European Society of Cell and Gene Therapy (ESGCT) 27th Annual Congress in Barcelona, Spain. RP-L102 is the Companys lentiviral vector (LVV)-based gene therapy for the treatment of Fanconi Anemia (FA). The data are included in an oral presentation by Dr. Juan Bueren, Scientific Director of the FA gene therapy program and Head of the Hematopoietic Innovative Therapies Division at CIEMAT in Spain / CIBERER / IIS-FJD, entitled, Gene Therapy for Patients with Fanconi Anaemia.

Two critical validations for an FA gene therapy product are: 1) stem cell engraftment in the absence of cytotoxic conditioning and 2) evidence of sustained clinical improvement. We are proud to report that the maturing long-term data from the patients treated with RP-L102 meet both of these requirements, said Gaurav Shah, M.D., Chief Executive Officer and President of Rocket. In all four patients, bone marrow MMC-resistance, a key measure of phenotypic reversal and engraftment, meets or exceeds the 10% threshold agreed to by the FDA and EMA for the upcoming registration-enabling Phase 2 trial, and all four patients now resemble FA mosaic patients as evaluated by peripheral T-cell chromosomal fragility assay. Remarkably, patients 02002 and 02006, who received what we consider adequate drug product similar to the upcoming Phase 2 trial, now demonstrate durable robust bone marrow MMC-resistance levels of approximately 60% and 32%, respectively, confirming phenotypic correction in long-term bone marrow stem and progenitor cells. Of note, each of the four initial patients continue to show evidence of a proliferative advantage, with ongoing increases in peripheral mononuclear cell VCNs. In addition, improvement or stabilization of peripheral blood counts, which had declined substantially prior to gene therapy, suggests a halt in bone marrow failure progression. In patient 02002, hemoglobin levels are now similar to those in the first year after birth, and all lineages in patients 02002 and 02006 are now stable or improving.

Dr. Shah continued, Preliminary VCN data from three additional patients who were treated with a viable drug product also show engraftment in a dose-dependent manner, consistent with the first four patients. With this progress to date, we look forward to the upcoming results from the first two patients receiving Process B of RP-L102, designed to enable consistent results with commercial-grade product.

The presentation described nine pediatric patients (ages 3-7 years) who received RP-L102 utilizing fresh or cryopreserved mobilized peripheral blood CD34+ cells that were transduced with the therapeutic vector. Four of these patients have been followed for more than 2 years (24-39 months for patients 02002, 02004, 02005, and 02006). The Phase 1/2 study of RP-L102 is an ongoing, open-label, single-center study designed to evaluate the safety and efficacy of Process A RP-L102 without the use of any conditioning regimen conventionally used in allogenic transplant.

Dr. Bueren noted, These results indicate the feasibility of engraftment in FA patients using autologous, gene corrected HSCs in the absence of any conditioning regimen. This indicates the potential of this therapeutic approach as a definitive hematologic treatment, while avoiding the burdensome side effects associated with allogeneic transplant, including the risk of post-transplant mortality and a substantially higher risk of head and neck cancer. The ability to treat patients without the use of genotoxic conditioning and to restore blood cell counts is a life-altering advancement for patients and their families, as well as the scientific community which has dedicated over two decades to finding a minimally toxic alternative for FA patients.

Rocket expects initial data from the Phase 1 Process B trial of RP-L102 by year-end. The registration-enabling Phase 2 study in Spain is now enrolling, and additional global sites will follow.

Full results from the ESGCT presentation will be available online at the conclusion of the oral presentation: https://www.rocketpharma.com/esgct-presentations/.

About Fanconi Anemia

Fanconi Anemia (FA) is a rare pediatric disease characterized by bone marrow failure, malformations and cancer predisposition. The primary cause of death among patients with FA is bone marrow failure, which typically occurs during the first decade of life. Allogeneic hematopoietic stem cell transplantation (HSCT), when available, corrects the hematologic component of FA, but requires myeloablative conditioning. Graft-versus-host disease, a known complication of allogeneic HSCT, is associated with an increased risk of solid tumors, mainly squamous cell carcinomas of the head and neck region. Approximately 60-70% of patients with FA have a FANC-A gene mutation, which encodes for a protein essential for DNA repair. Mutation in the FANC-A gene leads to chromosomal breakage and increased sensitivity to oxidative and environmental stress. Chromosome fragility induced by DNA-alkylating agents such as mitomycin-C (MMC) or diepoxybutane (DEB) is the gold standard test for FA diagnosis. Somatic mosaicism occurs when there is a spontaneous correction of the mutated gene that can lead to stabilization or correction of a FA patients blood counts in the absence of any administered therapy. Somatic mosaicism, often referred to as natures gene therapy provides a strong rationale for the development of FA gene therapy because of the selective growth advantage of gene-corrected hematopoietic stem cells over FA cells1.

1Soulier, J.,et al. (2005) Detection of somatic mosaicism and classification of Fanconi anemia patients by analysis of the FA/BRCA pathway. Blood 105: 1329-1336

About Rocket Pharmaceuticals, Inc.

Rocket Pharmaceuticals, Inc. (NASDAQ: RCKT) (Rocket) is an emerging, clinical-stage biotechnology company focused on developing first-in-class gene therapy treatment options for rare, devastating diseases. Rockets multi-platform development approach applies the well-established lentiviral vector (LVV) and adeno-associated viral vector (AAV) gene therapy platforms. Rocket's clinical programs using LVV-based gene therapy are for the treatment of Fanconi Anemia (FA), a difficult to treat genetic disease that leads to bone marrow failure and potentially cancer, Leukocyte Adhesion Deficiency-I (LAD-I), a severe pediatric genetic disorder that causes recurrent and life-threatening infections which are frequently fatal, and Pyruvate Kinase Deficiency (PKD) a rare, monogenic red blood cell disorder resulting in increased red cell destruction and mild to life-threatening anemia. Rockets first clinical program using AAV-based gene therapy is for Danon disease, a devastating, pediatric heart failure condition. Rockets pre-clinical pipeline program is for Infantile Malignant Osteopetrosis (IMO), a bone marrow-derived disorder. For more information about Rocket, please visit http://www.rocketpharma.com.

Rocket Cautionary Statement Regarding Forward-Looking Statements

Various statements in this release concerning Rocket's future expectations, plans and prospects, including without limitation, Rocket's expectations regarding the safety, effectiveness and timing of product candidates that Rocket may develop, to treat Fanconi Anemia (FA), Leukocyte Adhesion Deficiency-I (LAD-I), Pyruvate Kinase Deficiency (PKD), Infantile Malignant Osteopetrosis (IMO) and Danon disease, and the safety, effectiveness and timing of related pre-clinical studies and clinical trials, may constitute forward-looking statements for the purposes of the safe harbor provisions under the Private Securities Litigation Reform Act of 1995 and other federal securities laws and are subject to substantial risks, uncertainties and assumptions. You should not place reliance on these forward-looking statements, which often include words such as "believe," "expect," "anticipate," "intend," "plan," "will give," "estimate," "seek," "will," "may," "suggest" or similar terms, variations of such terms or the negative of those terms. Although Rocket believes that the expectations reflected in the forward-looking statements are reasonable, Rocket cannot guarantee such outcomes. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including, without limitation, Rocket's ability to successfully demonstrate the efficacy and safety of such products and pre-clinical studies and clinical trials, its gene therapy programs, the pre-clinical and clinical results for its product candidates, which may not support further development and marketing approval, the potential advantages of Rocket's product candidates, actions of regulatory agencies, which may affect the initiation, timing and progress of pre-clinical studies and clinical trials of its product candidates, Rocket's and its licensors ability to obtain, maintain and protect its and their respective intellectual property, the timing, cost or other aspects of a potential commercial launch of Rocket's product candidates, Rocket's ability to manage operating expenses, Rocket's ability to obtain additional funding to support its business activities and establish and maintain strategic business alliances and new business initiatives, Rocket's dependence on third parties for development, manufacture, marketing, sales and distribution of product candidates, the outcome of litigation, and unexpected expenditures, as well as those risks more fully discussed in the section entitled "Risk Factors" in Rocket's Annual Report on Form 10-K for the year ended December 31, 2018. Accordingly, you should not place undue reliance on these forward-looking statements. All such statements speak only as of the date made, and Rocket undertakes no obligation to update or revise publicly any forward-looking statements, whether as a result of new information, future events or otherwise.

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Rocket Pharmaceuticals Presents First Evidence of Long-Term Improvement and Stabilization in Blood Counts and Durable Mosaicism in RP-L102 Process A...

Speaking Multiple Sclerosis: A Glossary of Common Terms – Everyday Health

Whether youve been recently diagnosed with multiple sclerosis (MS) or have been living with the condition for a while, chances are youll sometimes hear terms from your healthcare team that are new to you.

The following is a quick, alphabetical guide to the terminology you may need to know as you manage your condition:

Ankle-Foot Orthosis (AFO) A brace designed to support the position of the foot and motion of the ankle to compensate for nerve damage and muscle weakness in the area caused by MS and other movement disorders. An AFO is typically used to stabilize weak limbs or to reposition a limb with contracted muscles into a more normal position.

Autoimmune Disease Your immune system plays a major part of your bodys defense against bacteria and viruses by sending out cells to attack them once they enter your body. However, if you have an autoimmune disease, your immune system mistakenly attacks healthy cells in your body, causing them to weaken or break down. MS is thought to be just one example of an autoimmune disease. It has been suggested that in MS, your immune system may mistakenly attack the cells in your central nervous system.

Axon Long threadlike structures of nerve cells that send impulses to other cells in your body. Research suggests that damage to or loss of these fibers in progressive MS may be linked to worsening disability and more severe progression.

Central Nervous System (CNS) The group of organs in your body that includes the brain, spinal cord, and optic nerves. If you have MS, your bodys immune system may be working against the CNS, producing neurological symptoms such as muscle weakness and vision problems.

Cerebrospinal Fluid (CSF) A clear, colorless liquid that surrounds the brain and spinal cord to protect the CNS and assist in the circulation of nutrients and removal of waste products. In MS, damage to the myelin sheath of nerve cells causes certain types of proteins to be released into the spinal fluid. The presence of these proteins in the CSF, but not in the blood, may point to a diagnosis of MS.

Clinically Isolated Syndrome (CIS) A first episode of neurologic symptoms that lasts at least 24 hours and is caused by inflammation or demyelination (loss of the myelin that covers the nerve cells) in the CNS. People who experience CIS may or may not go on to develop MS. However, when CIS is accompanied by magnetic resonance imaging (MRI)detected brain lesions similar to those found in MS, you have a 60 to 80 percent chance of a second neurologic event and diagnosis of MS within several years, according to the National MS Society.

Cog Fog A commonly used term that refers to the cognitive changes experienced by many people with MS. According to MS Australia, approximately 50 percent of people with the condition will develop some degree of cog fog, or inhibited ability to think, reason, concentrate, or remember. For some, cognitive problems will become severe enough to interfere in a significant way with daily activities.

Corticosteroids (or Steroids) Prescription medication used to treat relapses in relapsing-remitting MS. Your doctor may prescribe intravenous (IV) corticosteroids if the symptoms of your relapse are causing significant problems, like poor vision or difficulty walking. These drugs work by suppressing the immune system and reducing inflammation in the CNS, and they may help relapse symptoms resolve more quickly. But they wont affect your ultimate level of recovery from a relapse or the long-term course of your MS. Methylprednisolone is a commonly used corticosteroid in MS.

Diplopia (or Double Vision) An eye problem in which you see two images of a single object. It may be present when only one eye is open (monocular) or disappear when either eye is closed (binocular). Diplopia is a common symptom of MS, and it occurs because of damage to the optic nerve.

Disease-Modifying Therapies (DMTs) Drugs designed to reduce new relapses, delay progression of disability, and limit new CNS inflammation in people with MS. Although there are multiple DMTs that have been approved by the U.S. Food and Drug Administration (FDA) for use in MS, these drugs generally work by reducing inflammation in nerve cells in theCNS.

Dysarthria A speech disorder caused by neuromuscular impairment and resulting in disturbances in motor control of the muscles used in speech. Its believed the demyelinating lesions in MS may result in spasticity, weakness, slowness, or ataxic incoordination of the lips, tongue, mandible, soft palate, vocal cords, and diaphragm, causing this speech impairment.

Dysphagia (Difficulty Swallowing) A condition that may occur in people with MS, leading to difficulty in eating solid foods or liquids, frequent throat clearing during eating or drinking, a feeling that food is stuck in the throat, or coughing or a choking sensation when eating or drinking. Its the result of nerve damage within the muscles that control swallowing.

Epstein-Barr Virus (EBV) A virus believed to be a possible cause or trigger for MS. Although the exact cause of MS remains unknown, researchers suggest an infectious agent may be involved in its development. Studies have found that antibodies (immune proteins that indicate a person has been exposed to a given virus) to EBV are significantly higher in people who eventually develop MS than in those who dont. Other research has noted that people with a specific immune-related gene and high levels of antibodies to EBV in their blood are 9 times more likely to develop MS than others.

Evoked Potentials A test that measures the speed of nerve messages along sensory nerves to the brain, which can be detected on your scalp using electrodes attached with sticky pads. Its sometimes used in the diagnosis of MS, because nerve damage can slow down the transmission of nerve signals. Evoked potential tests can indicate nerve pathways that are damaged prior to the onset of MS symptoms.

Exacerbation An occurrence of new symptoms or the worsening of old symptoms that may also be referred to as a relapse, attack, or flare-up. Exacerbations can be very mild, or severe enough to interfere with a person's ability to perform day-to-day activities.

Expanded Disability Status Scale (EDSS) A scale used for measuring MS disability and monitoring changes in the level of disability over time. Developed by neurologist John Kurtzke, MD, in 1983, the EDSS scale ranges from 0 to 10 in 0.5-unit increments (scoring is based on a neurological exam) and relies on walking as its main measure of disability. People with an EDSS of 1 have no disability and minimal loss of function, while those with an EDSS of 9.5 are confined to bed and totally dependent on others for functions of daily living.

Foot Drop (or Drop Foot) A symptom of MS caused by weakness in the ankle or disruption in the nerve pathway between the legs and the brain, making it difficult to lift the front of the foot to the correct angle during walking. If you have foot drop, your foot hangs down and may catch or drag along the ground, resulting in trips and falls. Foot drop can be managed with an AFO or other treatments.

Hematopoietic Stem Cell Transplantation (HSCT) A procedure designed to reboot the immune system, the National MS Society says, using hematopoietic (blood cellproducing) stem cells derived from a persons own bone marrow or blood. If your doctor recommends HSCT, youll undergo a chemotherapy regimen before these cells are reintroduced to the body via IV injection, where they will migrate to your bone marrow to rebuild the immune system.

John Cunningham (JC) Virus A common infection completely unrelated to MS that is found in as many as 90 percent of people, according to the UK's MS Trust. JC virus has no symptoms and is normally controlled by the immune system. However, if your immune system is weakened, the JC virus can reactivate, causing potentially fatal inflammation and damage to the brain known as progressive multifocal leukoencephalopathy (PML). Certain MS disease-modifying therapies have been linked with increased risk for PML.

Lhermittes Sign An electric shock-like sensation experienced by some with MS when the neck is moved in a particular way. The sensation can travel down to the spine, arms, and legs.

Lesion (or Plaque) Refers to an area of damage or scarring (sclerosis) in the CNS caused by inflammation in MS. These lesions can be spotted on an MRI scan, with active lesions appearing as white patches. With regular MRIs, a neurologist can tell how active your MS is.

Lumbar Puncture (or Spinal Tap) A procedure used for the collection of cerebrospinal fluid (CSF), sometimes done to help diagnose MS. For this procedure, your doctor will ask you to lie on your side or bend forward while seated, before cleansing an area of your lower back and injecting a local anesthetic. He will then insert a hollow needle and extract a small amount of spinal fluid using a syringe.

Magnetic Resonance Imaging (MRI) The diagnostic tool that currently offers the most sensitive noninvasive way of imaging the brain, spinal cord, or other areas of the body, according to the National MS Society. Its the preferred imaging method for diagnosis of MS and to monitor the course of the disease. MRI uses magnetic fields and radio waves to measure the relative water content in tissues, which is notable in MS because the layer of myelin that protects nerve cell fibers is fatty and repels water. In areas where myelin has been damaged by MS, fat is stripped away and the tissue holds more water. This shows up on an MRI as a bright white spot or darkened area, depending on how the images are made.

McDonald Criteria A guidance used in the diagnosis of MS, authored by an international panel of experts on the condition, originally in 2010. The guidance was updated in 2017. Among the key changes: advising for the use of brain MRI as part of the diagnostic process.

MS Hug A common symptom of MS. If you experience the MS hug, you may feel like you have a tight band around your chest or ribs, or pressure on one side of your torso. Some people find that it is painful to breathe. The MS hug can last for seconds, minutes, hours, or even longer.

Myelin A substance rich in lipids (fatty substances) and proteins that helps form the myelin sheath. In MS, particularly relapsing-remitting MS, an abnormal immune response produces inflammation in the CNS, effectively attacking the myelin in the cells.

Myelin Sheath An insulating layer of fatty substances and proteins that forms around the nerves in body, including those in the CNS. It allows electrical impulses to transmit quickly and efficiently along the nerve cells, but these impulses can be slowed if the sheath is damaged, causing MS.

Neurodegeneration Refers to the process by which the myelin sheath of cells in the CNS is damaged in MS. Its believed to be a major contributor to neurological disability in the condition, and may be the reason immune modulation treatments (disease-modifying therapy) are generally less effective in the progressive MS than in the relapsing-remitting MS.

Neurologist The point person for monitoring your MS treatment and managing MS symptoms. This specialist typically focuses on conditions affecting the CNS.

Neuropathic Pain A type of pain common in MS that results from changes or damage to the myelin sheath and the axons, or nerve fibers, it normally covers. MS-caused neuropathic pain may be chronic, intermittent, or occur only in response to a stimulus.

Neuropsychologist A specialist you may be referred to who helps you manage the cognitive effects of MS. Neuropsychological testing (or testing of the functioning of your brain) involves identifying memory or learning difficulties associated with MS. Cognitive rehabilitation may improve functioning.

Nociceptive Pain Caused by damage to muscles and joints, it can be either acute or chronic, and may not result from MS itself, but be caused by changes in posture or walking or the overuse of assistive devices in those with the condition.

Nystagmus A common eye abnormality in MS, its characterized by involuntary, rhythmic, back-and-forth motion of the eyeball, either horizontally or vertically. For those with nystagmus, the perception of the rhythmic movement of the surrounding stationary world (oscillopsia) can be disorienting and disabling.

Oligoclonal Bands (OCBs) Immunoglobulins, or proteins, that collect in blood plasma or cerebrospinal fluid (CSF). Although not every person with MS has OCBs, their presence can support a diagnosis of MS. Having OCBs is generally associated with a younger age of MS onset and a poorer prognosis.

Optic Neuritis An inflammatory condition that damages the optic nerve, a bundle of nerve fibers that transmits visual information from your eye to your brain, causing pain and temporary vision loss in one eye. Its been linked with nerve damage resulting from MS, and may be among the first symptoms a person with the condition experiences.

Pseudobulbar Affect (PBA) A neurologic effect experienced by roughly 10 percent of people with MS as well as some with Parkinsons disease or amyotrophic lateral sclerosis (ALS), according to the Multiple Sclerosis Association of America (MSAA). Its characterized by sudden, uncontrollable expressions of laughter or crying without an obvious cause, which can be distressing as well as embarrassing to those who experience it. PBA is believed to be a mood disorder related to the disruption of nerve impulses in the CNS, but its different from depression, which is also common in MS.

Pseudoexacerbation A temporary worsening of symptoms without actual myelin inflammation or damage. It is often triggered by other illnesses or infection, exercise, a warm environment, depression, exhaustion, and stress. Urinary tract infection (UTI) is the most common type of infection to cause a pseudoexacerbation.

Sclerosis A general hardening of the body tissue. The term multiple sclerosis refers to the multiple areas of scar tissue often called lesions that develop along affected nerve fibers and that are visible in MRI scans.

Spasticity A symptom of MS that causes your muscles to feel stiff, heavy, or difficult to move. When a muscle spasms, youll experience a sudden stiffening that may cause a limb to jerk. This may be painful.

Trigeminal Neuralgia (or Tic Douloureux) A type of neuropathic pain that occurs on the face (usually on one side only). Its a known symptom of MS, and you may experience it in your cheek; upper or lower jaw; inside the mouth; or in the area around your eyes, ears, or forehead. In MS, its typically caused by damage to the myelin sheath around the trigeminal nerve, which among other functions controls the muscles used in chewing. The condition is triggered by everyday activities, like tensing facial muscles while shaving or when chewing.

Vertigo An intense sensation of the surrounding environment spinning around one. In MS, vertigo is typically caused by growth of an existing lesion or development of a new lesion on the brain stem or cerebellum, the area in the brain that controls balance. It can also be a symptom of a problem with the inner ear, or it can be side effect of medication used to treat MS or other health conditions you may have.

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Speaking Multiple Sclerosis: A Glossary of Common Terms - Everyday Health