In Cure For Multiple Sclerosis the immune system attacks the myelin sheaths which protect nerve fibers. These nerves carry messages to and from the brain, and if they are disrupted, it leads to a host of problems such as loss of mobility, vision impairment and fatigue.By synthesizing proteins from the sheaths in a lab and then injecting them into the blood stream at increasing doses, the body begins to learn that they are safe and Cure For Multiple Sclerosis no longer attacks them.
This type of therapy has already been used in treating some allergies, a treatment that is called allgergic desensitisation, but it’s only recently that scientists have thought it had potential to be used elsewhere.Cure For Multiple Sclerosis Researchers at the University of Bristol said that this “important breakthrough” could improve the lives of millions of people who suffer from a range of diseases.
The study’s author Dr. Bronwen Burton said that “Cure For Multiple SclerosisThe immune system works by recognizing antigens which could cause infection. In allergies the immune system mounts a response to something like pollen or nuts because it wrongly believes they will harm the body.
Cure For Multiple Sclerosis”But in autoimmune diseases the immune systems sees little protein fragments in your own tissue as foreign invaders and starts attacking them. What we have found is that by synthesizing those proteins in a soluble form we can desensitize the immune system by giving an escalating dose.”
immuno therapies for individual conditions, based on the proteins or antigens that the body is responding too.Cure For Multiple Sclerosis Professor David Wraith, of the university’s School of Cellular and Molecular Medicine, said the research has opened up “exciting new opportunities” These findings have important implications for the many patients suffering from Cure For Multiple Sclerosis autoimmune conditions that are currently difficult to treat,” he added.
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system that affects nearly 2.3 million people worldwide. MS is triggered when the immune system attacks the protective covering around nerve fibers, called the myelin sheath. The “demyelination” that follows damages nerve cells and causes impaired exchange of information between the brain and body as well as within the brain itself.
As the protective sheath — best imagined as the insulating material around an electrical wire — wears off, nerve signals slow down or stop. The result is impairment to a patient’s vision, sensation, and use of limbs depending where the damage takes place. Permanent paralysis occurs when nerve fibers are destroyed by the disease.
As though this were not enough, MS patients are three to six times more likely to develop seizures — abnormal hyperactivity of nerve cells — compared to the rest of the population. However, despite increased occurrence of seizures among MS patients, little research has been done to probe why they happen.
Using a mouse model, a team of scientists at the University of California, Riverside has found for the first time that chronic demyelination is closely linked to, and is likely the cause of, these seizures. Reporting in the journal Neuroscience, the researchers also note that certain neurons in the brain, called “parvalbumin interneurons,” which are important for keeping hyperactivity down, are modified and lost when extensive demyelination occurs in the brain’s cortex and hippocampus.
An image from their research is featured on the cover of volume 346 (pages 409-422) of the journal.
“Demyelination causes damage to axons and neuronal loss, specifically parvalbumin interneurons are lost in mice, hyperactivity is no longer down but up, and this could be a cause of seizures,” said Seema Tiwari-Woodruff, an associate professor of biomedical sciences in the UC Riverside School of Medicine, whose laboratory authored the research. “It’s very likely this is what is occurring in those patients with MS who are experiencing seizures.”
In the lab, Tiwari-Woodruff and her team induced demyelination in mice by feeding them a diet that contained cuprizone, a copper-binding substance that causes damage to oligodendrocytes -the brain cells that produce myelin. After nine weeks of feeding them cuprizone, the majority of mice started having seizures.
“Without myelin, axons are vulnerable,” Tiwari-Woodruff said. “They develop blebs — ball-like structures that hinder transport of important proteins and conduction of electrical signals. In some instances, significant axon damage can lead to neuronal loss. In both MS and our mouse model, parvalbumin interneurons are more vulnerable and likely to die. This causes the inhibition to be removed and induce seizures. Thus axonal and neuronal survival may be directly tied to the trophic support provided by myelin.”
In another study, after nine or twelve weeks, the researchers stopped feeding the mice the cuprizone diet. Oligodendrocytes began to repopulate the demyelinated areas and remyelinate the intact but myelin-stripped axons. Future studies will assess seizure activity with remyelination.
“Does remyelination affect seizure activity? Could we accelerate the remyelination with drugs? Can we thus provide some relief for MS patients? We are interested in addressing these questions,” Tiwari-Woodruff said.
Her team was recently awarded a pilot grant from the National Multiple Sclerosis Society to compare postmortem brain tissue from MS patients with seizures to those without to understand the cellular basis of seizures in MS. Their findings will also be used to check how well the cuprizone mouse model reproduces the changes seen in humans.
“We want to know if these tissues show what we are seeing in our mouse model,” Tiwari-Woodruff said. “Our preliminary data in postmortem tissue show considerable similarity between the two. We now have a mouse model with which we can work to test and suggest some therapeutic cures. When developed, such drugs, which would be aimed at reducing hyperactivity to reduce the incidence of seizures, could also be extended to epilepsy patients.”
Multiple sclerosis (MS) is a chronic disease that affects the nervous system. Nerves are coated in a protective covering called myelin, which also speeds up the transmission of nerve signals. People with MS experience progressive deterioration of myelin.
Nerves may function abnormally when the myelin is damaged. There can be a number of unpredictable symptoms as a result. These include:
pain, tingling, or burning sensations throughout the body
muscle spasms or stiffness
difficulty with balance
impaired memory and cognitive function
Years of dedicated research have led to new treatments for MS. There is still no cure for the disease, but drug regimens and behavioral therapy allow people with MS to lead better-quality lives.
Purpose of Treatments
Many treatment options can help manage the course and symptoms of this chronic disease. Treatment can help:
slow the progression of MS
minimize symptoms during MS exacerbations or flare-ups
improve physical and mental function
Treatment in the form of support groups or talk therapy can also provide much needed emotional support.
A main goal of MS treatment is to slow down the progression of the disease. Drugs that do this are called disease-modifying medications. One such medication is the oral drug teriflunomide (Aubagio). It was approved for use in people with MS in 2012.
A study published in The New England Journal of Medicine found that people with relapsing MS who took teriflunomide once a day showed significantly slower disease progression rates and fewer relapses than those who took a placebo. People given the higher dose of teriflunomide (14 mg vs. 7 mg) experienced decreased disease progression. Teriflunomide was only the second oral disease-modifying medication approved for MS treatment.
Dimethyl Fumarate (Tecfidera)
A third oral disease-modifying drug became available to people with MS in March of 2013. Dimethyl fumarate (Tecfidera) was formerly known as BG-12. It stops the immune system from attacking itself and destroying myelin. It may also have a protective effect on the body, similar to the effect that antioxidants have. The medication is available in capsule form.
Dimethyl fumarate is designed for people who have relapsing-remitting MS (RRMS). RRMS is a form of the disease in which a person typically goes into remission for a period of time before their symptoms worsen. People with this type of MS can benefit from twice-daily doses.
MS-induced myelin destruction affects the way nerves send and receive signals. This can affect movement and mobility. Potassium channels are like pores on the surface of nerve fibers. Blocking the channels can improve the nerve conduction in affected nerves.
Dalfampridine (Ampyra) is a potassium channel blocker. Studies published in The Lancet found that dalfampridine (formerly called fampridine) increased walking speed in people with MS. The original study tested walking speed during a 25-foot walk. It didn’t show dalfampridine to be beneficial. However, post-study analysis revealed that participants showed increased walking speed during a six-minute test when taking 10 mg of the medication daily. Participants who experienced increased walking speed also demonstrated improved leg muscle strength.
Alemtuzumab (Lemtrada) is a humanized monoclonal antibody (lab produced protein that destroys cancer cells). It’s another disease-modifying agent approved to treat relapsing forms of MS. It targets a protein found on the surface of the immune cells called CD52. Though it’s not known exactly how alemtuzumab works, it’s believed to bind to CD52 on T and B lymphocytes (white blood cells) and cause lysis (break down of the cell). The drug was first approved to treat leukemia at a much higher dosage.
Lemtrada had a hard time getting approval for MS in the United States. The Food and Drug Administration (FDA) rejected the application for Lemtrada’s approval in early 2014. They cited the need for more clinical trials showing that it does not cause serious side effects. Lemtrada was later approved by the FDA in November 2014, but it comes with a warning about serious autoimmune conditions, infusion reactions, and increased risk of malignancies like melanoma and other cancers. It was compared to EMD Serono’s MS drug, Rebif, in two phase III trials. The trial found that it was better at reducing the relapse rate and the worsening of disability over two years.
Due to its safety profile, the FDA recommends that it only be prescribed to patients who have had an inadequate response to two or more other MS treatments.
Modified Story Memory Technique
MS affects cognitive function as well. It can negatively affect memory, concentration, and executive functions like organization and planning.
Researchers from the Kessler Foundation Research Center found that a modified story memory technique (mSMT) can be effective for people who experience cognitive effects from MS. Learning and memory areas of the brain showed more activation in MRI scans after mSMT sessions. This promising treatment method helps you retain new memories. It also helps you recall older information by using a story-based association between imagery and context. Modified story memory technique might help someone with MS remember various items on a shopping list, for example.
What Are Myelin Peptides?
Myelin becomes irreversibly damaged in people with MS. Preliminary testing reported in JAMA Neurology suggests that a possible new therapy holds promise. One small group of subjects received myelin peptides (protein fragments) through a patch worn on their skin over a period of a year. Another small group received a placebo. People who received the myelin peptides experienced significantly fewer lesions and relapses than people who received the placebo. The treatment was well tolerated and there were no serious adverse events.
The Future of MS Treatments
Effective MS treatments vary from person to person. What works well for one person won’t necessarily work for another. The medical community continues to learn more about the disease and how to best treat it. Research combined with trial and error are key to finding a cure.
Back pain is a top medical complaint. It’s also a leading cause of missed work. According to theNational Institute of Neurological Disorders and Stroke, virtually all adults will seek attention for back pain at some point in their lives. The American Chiropractic Association reports that Americans spend about $50 billion a year on treating back pain.
There are many possible causes of low back pain. Usually it’s caused by trauma from a sudden strain on the spine. But you should be aware that back pain can also signal a more serious condition called ankylosing spondylitis.
Part 2 of 5
What is ankylosing spondylitis?
Unlike ordinary back pain, ankylosing spondylitis (AS) is not caused by physical trauma to the spine. Rather, it’s a chronic condition caused by inflammation in the vertebrae (the bones of the spine). AS is a form of spinal arthritis.
The most common symptoms are intermittent flare-ups of spinal pain and stiffness. However, the disease can also affect other joints, as well as the eyes and the intestines. In advanced AS, abnormal bone growth in the vertebrae may cause joints to fuse. This can severely reduce mobility. People with AS may also experience vision problems, or inflammation in other joints, such as the knees and ankles.
Part 3 of 5
What are the warning signs?
Sign #1: You have unexplained pain in the lower back.
Typical back pain often feels better after rest. AS is the opposite. Pain and stiffness are usually worse upon waking. While exercise may make ordinary back pain worse, AS symptoms may actually feel better after exercise.
Lower back pain for no apparent reason is not typical in young people. Teens and young adults who complain of stiffness or pain in the lower back or hips should be evaluated for AS by a doctor. Pain is often located in the sacroiliac joints, where the pelvis and spine meet.
Sign #2: You have a family history of AS.
People with certain genetic markers are susceptible to AS. But not all people who have the genes develop the disease, for reasons that remain unclear. If you have a relative with either AS, psoriatic arthritis, or arthritis related to inflammatory bowel disease, you may have inherited genes that put you at greater risk for AS.
Sign #3: You’re young, and you have unexplained pain in the heel(s), joints, or chest.
Instead of back pain, some AS patients first experience pain in the heel, or pain and stiffness in the joints of the wrists, ankles, or other joints. Some patient’s rib bones are affected, at the point where they meet the spine. This can cause tightness in the chest that makes it hard to breathe. Talk to your doctor if any of these conditions occur or persist.
Sign #4: Your pain may come and go, but it’s gradually moving up your spine. And it’s getting worse.
AS is a chronic, progressive disease. Although exercise or pain medications may help temporarily, the disease may gradually worsen. Symptoms may come and go, but they won’t stop completely. Often the pain and inflammation spread from the low back up the spine. If left untreated, vertebrae may fuse together, causing a forward curvature of the spine, or humpbacked appearance (kyphosis).
Sign #5: You get relief from your symptoms by taking NSAIDs.
At first, people with AS will get symptomatic relief from common over-the-counter anti-inflammatory drugs, such as ibuprofen or naproxen. These drugs, called NSAIDs, do not alter the course of the disease, though.
If your doctors think you have AS, they may prescribe more advanced medications. These drugs target specific parts of the immune system. Immune system components called cytokines play a central role in inflammation. Two in particular — tumor necrosis factor alpha and interleukin 10 — are targeted by modern biological therapies. These drugs may actually slow the progression of the disease.
Part 4 of 5
Who is typically affected by AS?
AS is more likely to affect young men, but it can affect both males and females. Initial symptoms usually appear in the late teen to early adult years. AS can develop at any age, however. The tendency to develop the disease is inherited, but not everyone with these marker genes will develop the disease. It’s unclear why some people get AS and others don’t. Amajority of Caucasian people with the disease carry a particular gene called HLA-B27, but not all people with the gene develop AS. Up to 30 genes have been identified that may play a role.
Part 5 of 5
How is AS diagnosed?
There is no single test for AS. Diagnosis involves a detailed patient history and physical exam. Your doctor may also order imaging tests, such as computed tomography (CT), magnetic resonance imaging (MRI), or X-ray. Some experts believe MRI should be used to diagnose AS in the early stages of the disease, before it shows up on X-ray.
More than 100 people danced their hearts out to help raise awareness and money for Multiple Sclerosis.
Sunday was the sixth annual “Zumbathon to benefit the National National Multiple Sclerosis Society of Upstate New York.”
Zumba is a workout that involves fun music and dancing.
Organizer Denise Herkey-Jarosch says this event hits close to home. She has been living with MS for 17 years.
“I found in my time living with ms that being active as you can be helps. And Zumba has helped me, I’ve been doing Zumba for six years. And thanks to the Zumba community and these amazing instructors that volunteer their time, we’re here for the sixth time holding this great event,” said Herkey-Jarosch.
Over the last five years the Zumbathon has raised more than $10,000.
There are more than 12,000 Upstate New Yorkers living with MS. If you would like to get involved and help raise awareness, click here.
A terminally ill, 51-year-old ex-nun living in County Wexford believes she should be allowed to choose when she dies.
Kate Tobin spoke to the Irish Times about living with multiple sclerosis, how the Irish government has failed her and her belief that God will welcome her into to heaven even if she chooses when her life ends. Formerly a nun with the Augustinian Sisters, a nursing order, Tobin worked in the United Kingdom as a palliative care nurse for 10 years and is now suffering through the latter stages of multiple sclerosis.
Tobin, who now lives in Clonroche, in County Wexford, told the Irish Times, “When the disease gets worse I want to choose.
“I want to be able to say when to stop my medical care and say, ‘just let me die, I have suffered enough’.”
She said her futures is “a slow paralysis, needing more help and ultimately my death”.
In January 2015 Tobin told the Irish Independent, “When my MS gets too bad like Marie Fleming I’m going to need somebody to help me commit suicide. I don’t want my death cert to say suicide and I don’t want the person that helps me to end up with six or eight years in prison.”
Marie Fleming, a former University College Dublin law lecturer, brought her fight to overturn the ban on assisted suicide to Ireland’s High Court. She wanted her partner, Tom Curran, to be permitted to assist her death without fear of prosecution. Her campaign was unsuccessful and Fleming passed away after a long illness in December 2013.
Tobin added that she knows her physical condition will not improve.
“It won’t change. I’ll be on my own and have time to think about it. I want to make a plan. I’m adamant that I want to die. I don’t want to become a 24-hour patient in hospital, being fed and having a catheter emptied, and being fed on fluids, I know what it’s like to do that to patients.”
“I’m too ill to travel to Switzerland. I’d have to bring somebody with me, and then there’s the possibility of them being charged when they come back.”
“I feel like if I live to 60 it’d be a miracle. The consultant told me if I celebrated my 50th I wouldn’t celebrate many more. I celebrated it last September, the family put on a big do for my 50th.”
She added that when she loses the use of her hands that would signify a loss of dignity for her.
“My dignity is everything to me. My love of reading – if that was taken from me, the use of my hands, if I couldn’t hold up a book, they’re my life – it’s another part of my independence gone.
“People are saying to suffer with it til the end, but the end could be 20 years.”
The former nurse explained that she spoke to a local priest about her wish to choose when she dies and he “sort of said” he agreed.
Tobin told the Irish Times, “I am of the belief that when I die, God won’t say, ‘Hey Kate, you’re a bit too early for heaven.’ Instead he will say, ‘Welcome home my child. You have suffered enough.’ That’s how I see my life.”
She continued, “I’m suffering my purgatory here on Earth so I believe I have the right to choose when I go to heaven. I have done enough good deeds and suffered enough while I’ve been on Earth to deserve to go to heaven.”
Although she believes that she should have the right to die she also does not believe the decision should be taken lightly.
She said, “I would expect to be tested by two doctors and a psychiatrist to make sure I’m mentally capable of making that decision. I believe in a process involving two doctors, and a psychiatrist, and an oncologist.”
The former nurse and nun has already planned her funeral.
“Originally, the family wanted me to be buried with my parents, but I have chosen to be buried in a plot on my own because when they come to visit mum and dad’s grave I don’t want them to think of how much I suffered or anything,” said Tobin.
“If they want to come to my grave, they’re coming to my grave and not mum and dad’s.”
As a healthcare professional Tobin is used to dealing with death and says that she does not fear it.
“I worked in England in a hospice for 10 years, from staff nurse up to sister, so death was an every day or night occurrence.
“I know I’m going to die. I’m probably luckier than people that have sudden deaths. I’m now facing the reality that I am going to die. How fast I die is another story and when I was so ill last year I couldn’t wait to die.”
She continued, “I know the things I don’t want. I don’t want to end up in hospital having to be fed with a peg feed through my stomach and I don’t want a drip. Just so long as they inject me with painkillers to keep me comfortable that’s it. I don’t want anything to prolong my life.”
Tobin joined the French order the Daughter of Providence when she was 20.
“I left that order when I was 26 and worked for the Church of England and became a Catholic chaplain for her majesty’s prison service.”
She went on to join the Augustinian Sisters, a nursing order, in Liverpool.
“I worked in their nursing home for the three years until I had taken my vows and they thought it would be a nice idea if I trained as a nurse.
“After two years of training they thought I was having such a good time as a student nurse – I don’t quite know how they worked that because it was hard work – and so deciding between the convent, nursing won out. At 33, I qualified as a nurse and it became such a loving career I’m glad I made the decision I did. Beginning as a staff nurse she ended up as a sister but ended up having to return to Ireland to look after her late mother, who was ill.”
Originally from Lismore, County Waterford, Tobin first showed signs of multiple sclerosis when she was 46. She moved to Clonroche in 2016 when her condition worsened. In December last year, her condition was diagnosed as progressive.
Tobin’s financial circumstances are difficult. Last August her laptop, which allowed her to stay in touch with her former colleagues in the UK, Australia and New Zealand, was destroyed and she has been unable to replace it.
Before the Irish general election in 2016 Tobin was promised appropriate furniture by Ireland’s national Health Service Executive along with 14 hours of care per week. Following the election, she was told there were insufficient funds.
She got the furniture at a cost of $4,056. She is currently paying this fee back, at $37 per week from her $206.50 disability benefit. She told the Irish Times that after her rent is paid she has very little left.
Despite her own situation, Tobin is determined to use her remaining time for good. In order to, raise funds for MS Ireland and the Dyslexia Association of Ireland she’s asking people to sponsor her to read books. She plans on reading up to 500 per year.
Anyone wishing to donate to Tobin’s charity efforts can do so via the Dyslexia Association of Ireland and MS Ireland or through the following bank account – Ulster Bank in Enniscorthy, County Wexford, account number 1060856; sort code 98-56-90.
MS researchers are focusing on the content of the gut’s microbiome as a possible contributor to the body’s autoimmune attack on its nervous system
Multiple sclerosis (MS) is an electrical disorder, or rather one of impaired myelin, a fatty, insulating substance that better allows electric current to bolt down our neurons and release the neurotransmitters that help run our bodies and brains. Researchers have speculated for some time that the myelin degradation seen in MS is due, at least in part, to autoimmune activity against the nervous system. Recent work presented at the MS Boston 2014 Meeting suggests that this aberrant immune response begins in the gut.
Eighty percent of the human immune system resides in the gastrointestinal tract. Alongside it are the trillions of symbiotic bacteria, fungi and other single-celled organisms that make up our guts’ microbiomes. Normally everyone wins: The microorganisms benefit from a home and a steady food supply; we enjoy the essential assistance they provide in various metabolic and digestive functions. Our microbiomes also help calibrate our immune systems, so our bodies recognize which co-inhabitants should be there and which should not. Yet mounting evidence suggests that when our resident biota are out of balance, they contribute to numerous diseases, including diabetes, rheumatoid arthritis, autismand, it appears, MS by inciting rogue immune activity that can spread throughout the body and brain.
One studypresented at the conference, out of Brigham and Women’s Hospital (BWH), reported a single-celled organism called methanobrevibacteriaceae that activates the immune system is enriched in the gastrointestinal tracts of MS patients whereas bacteria that suppress immune activity are depleted. Other work, which resulted from a collaboration among 10 academic researcher centers across the U.S. and Canada, reported significantly altered gut flora in pediatric MS patients while a group of Japanese researchers found that yeast consumption reduced the chances of mice developing an MS-like disease by altering gut flora.
Sushrut Jangi, a staff physician at Beth Israel Deaconess Medical Center in Boston who co-authored the BWH study, thinks that regional dietary influences might even be at play. “The biomes of people living in different areas and who consume Western versus non-Western diets are demonstratively different,” he says. “People who emigrate from non-Western countries, including India, where MS rates are low, consequently develop a high risk of disease in the U.S. One idea to explain this is that the biome may shift from an Indian biome to an American biome,” although there is not yet data to support this theory.
The microbiome theory is gaining so much steam in academia that a coalition of four U.S. research centers called the MS Microbiome Consortium recently formed to investigate the role of gut microorganisms in the disease. The group presented data in Boston showing significantly different gastrointestinal bacterial populations in patients treated with the MS drug glatiramer acetate compared with untreated subjects. How exactly the drug suppresses MS activity is unknown but the findings suggest that perhaps it works in part by altering gut flora and, as a result, suppressing abnormal immune activity. “The gut is well-positioned for an important role in the development of autoimmune disease, including MS.,” says Ilana Katz Sand, an assistant professor of neurology at Mount Sinai Medical Center in New York City and member of the MS Microbiome Consortium. “But important questions remain, such as how MS medications affect the microbiome, how an individual’s microbiome may affect treatment responses, whether particular bacterial species are associated with more severe disease and ultimately whether we can manipulate the microbiome to benefit our patients.”
Katz Sand says that dietary and probiotic approaches to treating MS are worth pursuing, as is a less palatable approach: fecal transplantation. Yet answers in science and medicine are rarely simple, she added, pointing out that in all likelihood MS arises from a complicated confluence of genetic and environmental influences that might ultimately trigger autoimmune activity. Beyond just our gut flora well over 100 genetic variants—many related to immune function—are now known to contribute to the disease as are external factors including vitamin D deficiency (MS is more common at higher latitudes), smoking andincreased salt intake.
Further confounding our ability to pinpoint root causes is that our genetic code influences how our bodies and brains respond to these external factors. It could be that both genes and environmental stimuli lead to pathologic microbiomes or that some unfortunate combination of these factors leads to a common autoimmunologic pathway that ravages myelin. “We know the microbiome shapes our immune system and that MS is an immune-mediated disease. We also know that genes influence our microbiomes and immune systems,” says David Hafler, professor of neurology and immunobiology at Yale University School of Medicine who was at the conference but not involved in the microbiome work presented. But there must be nongenetic factors contributing to the disease, too, given that the incidences of MS and other autoimmune disorders are increasing.
“Maybe it’s a lot of little factors like low vitamin D, increased body mass index and increased salt intake,” Hafler says, “but I wouldn’t be surprised if it was one big thing, much like how H. pylori was found to cause ulcers. No one’s identified a clear bug that’s driving MS but I think it’s important we keep looking.”
Multiple Sclerosis is close to being cured after a pioneering treatment was found to stop and even reverse the disease, scientists have said.
Results of a trial were hailed as remarkable, with the progression of the debilitating disease halted in almost all patients who had the treatment. A quarter of the MS sufferers had their condition effectively suppressed.
In the trial at the University of Ottawa in Canada, patients had aggressive chemotherapy combined with a transplant of their own cells. The chemotherapy destroyed the immune system instead of suppressing it as in standard treatment. It was then “reset” using blood stem cells.
The new technique is not without risk. Of the 24 patients treated, one died as a consequence, and the study was too small to assess the true dangers. Even so, the treatment was described as a breakthrough therapy which was “close to being curative”.
MS is a chronic inflammatory disease of the central nervous system. It is caused when the immune system attacks the body and can result in vision problems, memory loss, dizziness, fatigue and spasms. In severe cases it can lead to paralysis.
The condition has very few treatment options and often patients live for many years with the debilitating symptoms.
One of those treated in the Ottawa trial was Jennifer Molson, who was diagnosed with MS in 1996 when she was 21. She had an aggressive form of the condition and limited mobility when she began the trial, and received her transplant in 2002.
“Before my transplant I was unable to walk or work and was living in assisted care at the Ottawa hospital rehabilitation centre,” she said. “Now I am able to walk independently, live in my own home and work full time. I was also able to get married, walk down the aisle with my dad and dance with my husband. I’ve even gone downhill skiing. Thanks to this research I have been given a second chance at life.”
Researchers enrolled 24 people aged 18 to 50 with aggressive MS who had not responded to immunosuppressive therapy. They were followed for an average of six-and-a-half years to test the long-term effects of chemotherapy followed by the treatment, called autologous haematopoietic stem cell transplantation (aHSCT).
After treatment 70 per cent of patients experienced a complete stop in disease progression and 40 per cent saw lasting reversal of symptoms. Several were able to return to work or school and have children. None needed medication.
“[This shows with] unprecedented clarity a near-complete suppression of MS disease for several years following aHSCT,” Paolo Muraro, of Imperial College London, said. “None of the drugs that are currently approved or in late-phase clinical trials has been reported to achieve a similarly profound control of the disease.”
Stephen Minger, a stem cell biologist and independent consultant, said: “The clinical results are truly impressive, in some cases close to being curative, though we need longer-term follow-up to know for certain whether the patients continue to do well or if there is a chance of relapse. For a lifelong progressive disease like MS with few treatment options this is really exciting data.”
During treatment one of the patients died from hepatic necrosis and sepsis caused by the chemotherapy, which is one reason clinicians are approaching the results with caution.
Harold Atkins, a stem cell transplant physician at the Ottawa hospital and author of the study, said: “Our trial is the first to show the complete, long-term suppression of all inflammatory activity in people with MS. However, it is important to note that this therapy can have serious side effects and risks, and would only be appropriate for a small proportion of people with very active MS.”
In Britain MS sufferers can receive aHSCT treatment only if they are chosen for a clinical trial. Emma Gray, a clinical lead at the MS Society, said that more research was needed. “This treatment does offer hope, but it’s also an aggressive procedure that comes with substantial risks and requires specialist after-care. If anyone is considering aHSCT we would recommend they speak to their neurologist,” she said.
I had my first Multiple Sclerosis (MS) episode in 2005 (the formal diagnosis would come later). Naturally, I remember it well: we had just come off the most active hurricane season in history. It was the year of Hurricanes Dennis, Emily, Katrina, Rita and Wilma. We had so many storms, the National Hurricane Center went to the Greek alphabet because we had run out of names.
I was working long hours that fall and was feeling overwhelmingly tired, stressed and depressed from all the devastation we were seeing on television. Little did I know that as I was warning people of the next hurricane, my body was dealing with its own neurological storm, one that had been forming for years.
I took time off and decided to go back to Canada for a week with my boyfriend Sean. The first day of my vacation I woke up to numbness in my feet and parts of my legs. I felt like I couldn’t get out of bed. I had no idea what was wrong.
I went to a doctor in my hometown to see if she could figure it out. She was blunt and honest. “This could be anything from a slipped disc to multiple sclerosis. You should get back to the U.S. to see a neurologist.”
I thought she was crazy. MS? Isn’t that the wheelchair disease? I took her advice, though. When I got back to New York I went to a neurologist who gave me MRIs and a most unpleasant spinal tap.
I remember calling Sean in tears and telling him that he needed to pick me up at the doctor’s office; the news was not good.
I had lesions on both my brain and spine. The spinal tap fluid had also shown the protein they look for in MS patients.
He gave me steroids to help with the numbness and tingling and told me I more than likely had multiple sclerosis: an unpredictable, chronic, incurable and possibly disabling disease of the central nervous system that interrupts the flow of information within the brain and between the brain and the body.
I was at an age when most women who have the disease have already been diagnosed. How I got it was a mystery, and still is – though having lived in Canada (northern countries show a higher frequency of MS, likely due to less sunlight) and the fact that my father had suffered with acute rheumatoid arthritis may have both been factors.
After days of feeling sorry for myself, I decided I had to find people to talk to. Luckily, I knew someone at work who also had MS: Neil Cavuto. The Fox News and Fox Business senior vice president, anchor and managing editor had gone public with his illness (along with having suffered from cancer).
He told me to come talk with him right away.
I remember he kept a stream of tissues in motion, consoling me while I just cried and told him all my fears. What would happen to my career? My personal life? My self-esteem?
Neil calmed me down, promised me I was going to be OK and reminded me that I was working at a great company that would support us, even if that support included building wheelchair ramps.
I’ll never forget that day, and what Neil did for me.
Afterward, I tried to find more people to talk to who were living with MS. It was the one thing that kept me going – seeing others who were not just functioning, thriving.
In 2007, now formally diagnosed after a few relatively mild exacerbations, I decided that I would talk about my diagnosis in order to help others like me who had the disease. It’s never been my goal to be the poster girl for MS, but I do feel called to be someone who can help others identify, and live with, the disease.
Fast forward to now. I’m happily married (to the same boyfriend who was with me during my first flare-up and diagnosis) and have two beautiful boys. I’ve been working full-time at the same company for over a decade and I’m the author of a children’s book series about a frog who is a weather forecaster.
I’m not lying to you when I say I’m the happiest I’ve ever been. I believe part of the reason I am so happy is that I learned almost 10 years ago that your life can change in an instant.
Yes, I live with MS. And yes, I’ve been very lucky to have very few flare-ups since that diagnosis. There are ongoing reminders that my immune system isn’t the greatest, and I do know that this illness remains unpredictable (much like the weather I forecast) and can strike when you least expect it.
I don’t want people to feel sorry for me – this is bigger than me. If I can put a face on an illness that can help others who are diagnosed, then my openness to discuss this is all worthwhile.
But there is also bigger hope on the horizon for the 2 million of us who live with this disease. The medications are getting better and less intrusive. The fact that there are now oral treatments available is a huge step forward. For many of us, the painful injections are a constant reminder that there is something wrong with us.
I think we’re getting closer to stopping the disease in its tracks. I do believe there will be a day soon when having MS will no longer be associated with wheelchairs.
This weekend I will be the emcee for this year’s “MS Climb to the Top” event for The New York City – Southern New York Chapter of the National Multiple Sclerosis Society. Over a thousand people will participate, climbing 66 flights of stairs to from the ground floor the Rockefeller Center observation deck.
It’s a fitting event where people from all walks of life will take part to raise funds and awareness for those of us who live with MS. The climbing can be tough at times, but with support from others, we’ll get there. And when we do, we’ll be stronger in ways that we never imagined.
Donald Trump campaign CEO Stephen Bannon has long been a controversial figure, and a newly revealed lawsuit only figures to give his critics even more ammunition.The New York Post reports that American Vantage Companies was sued back in 2005 by a former employee who alleges that Bannon, her supervisor at the time, fired her while she was on maternity leave.
“Julia Panely-Pacetti, a new mother who suffers from multiple sclerosis, was terminated by defendants from her position as head of public relations and corporate marketing because of her sex and her disability,” the lawsuit alleges.Panley-Pacetti, who reported directly to Bannon during her time at American Vantage, alleged that she was fired even though she was “forced to continue performing her job responsibilities from home throughout her maternity leave.
The lawsuit was settled in 2006 for an undisclosed sum, although a Bannon spokesperson claims that the suit never had any merits.“Ms. Panely-Pacetti was not fired but laid off with all the personnel in her entire division during a corporate restructuring where the parent company exited its international sales and marketing business, and shutdown its communications department,” the spokesperson told the Post.
The defendant claimed that she was fired while on-leave and protected by the Family Medical Leave Act, and that even while at home she continued to do work for the newly-minted campaign CEO. She was, allegedly, urged to respond to work-related requests more quickly, when she shouldn’t have been working at all.She says in the lawsuit that Bannon spoke “disparagingly” about her pregnancy, and that she was treated with frequent disrespect from Bannon and his associates. Her termination came, the suit says, the day she informed her superiors that she had applied for short-term disability in relation to her MS.
“In a statement, a spokesperson for Bannon said that Panely-Pacetti ‘was not fired but laid off with all the personnel in her entire division during a corporate restructuring where the parent company exited its international sales and marketing business, and shutdown its communications department,’”