Writing Mom’s Story

         I began writing the story in late 2007.  Actually, I began the story in February 1978. Immediately after getting out of bed that February morning, I couldn’t stand. The   room was whirling, my stomach was churning. I sat on the edge of t he bed until my head cleared a little and I could stand. I tried to dress, but wasn’t able to bend down without the room spinning again and the nausea returning. I made a doctor’s appointment. He couldn’t find anything and treated me with Dramamine for a mild middle ear inflammation. It cleared after about a week and I put the occurrence in the back of my mind. In August of the same year, I awoke one morning with a gray spot in the vision of my left eye. It enlarged over the morning. By afternoon, my vision in my left eye was limited to the extreme outer edges. Being Saturday, I went to the Emergency Room, convinced I was going blind. An Ophthalmologist happened to be on duty. He diagnosed the problem immediately as optic neuritis and prescribed prednisone. That cleared in about eight weeks.

         Fast forward to 1989. I had been a “normal volunteer” at the National Institutes of Health for several years. I was asked if I would volunteer for an MRI. They said it’s easy if you’re not claustrophobic, no needles, only some noise. I said I would be glad to do it. They were right, lots of noise but no other discomforts. About a week later, a physician called to tell me that they found something strange on my brain. I went back to the physician and came away with a definite diagnosis of multiple sclerosis (MS). I launched a search for information, this being pre-internet, I went to libraries and contacted the National Multiple Sclerosis Society (www.nmss.org ).

         By June of 2006 I had retired on disability from my position as a Science Librarian and worked from home as an editor and writer. I attended a meeting of the Outdoor Writers Association of America (www.owaa.org ). I was interested in writing for children by this time and I attended a session given by the renowned children’s author, Kathleen Kudlinski (www.kathleenkudlinski.com ). Her one piece of advice (among others) that I took away from her presentation was: “Write what you know.”

         In October 2007, after spending over a year researching and learning about writing for children, I asked myself, “What do I know?” It came to me quickly, I know about MS. I have been interested in health issues and have read quite extensively, especially about plagues and infectious diseases. But also about MS, I have an extensive library about the disease and I have reviewed books on the subject for Library Journal. 

       Now in its second edition.

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Mom's Story

The Second Edition is now available with new treatments available for MS discussed.

Unique type of immune cell contributes to multiple sclerosis (MS

Researchers at the National Institutes of Health have found evidence that a unique type of immune cell contributes to multiple sclerosis (MS). Their discovery helps define the effects of one of the newest drugs under investigation for treating MS — daclizumab — and could lead to a new class of drugs for treating MS and other autoimmune disorders.
In these disorders, the immune system turns against the body's own tissues. Ongoing clinical trials have shown that daclizumab appears to help quiet the autoimmune response in MS patients, but its precise effects on the legions of cells that make up the immune system are not fully understood.
The new study, published in Science Translational Medicine, shows that one effect of daclizumab is to thin the ranks of lymphoid tissue inducer (LTi) cells. These cells are known to promote the development of lymph nodes and related tissues during fetal life, but their role during adulthood has been unclear. The new study marks the first time that LTi cells have been implicated in any human autoimmune disorder.
"While further study is required to confirm the role of LTi cells in autoimmunity, our results point to the cells as a promising target for the development of new drugs to treat autoimmune disorders," said Bibiana Bielekova, M.D., an investigator at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
Dr. Bielekova and her team found that among MS patients participating in clinical trials of daclizumab, the number of LTi cells was elevated in patients not receiving daclizumab compared to those on the drug. Patients receiving daclizumab also had reduced signs of inflammation in the cerebrospinal fluid (CSF) that surrounds the brain. And the researchers found that daclizumab appears to steer the body away from producing LTi cells, in favor of another cell type that counteracts autoimmunity.
In MS, the immune system attacks myelin, a material that insulates nerve fibers running throughout the brain and spinal cord. This typically leads to vision loss, and other sensory changes such as numbness and tingling, weakness, and fatigue. The disorder affects approximately 400,000 people in the United States. In about 85 percent of patients, MS starts as a relapsing-remitting form, in which symptoms come and go. Many patients eventually develop secondary progressive MS, in which symptom flare-ups are followed by worsening disability. Many medications are available to decrease the number of flare-ups, but no medication is effective at slowing the course of progressive MS.
The newer, sophisticated drugs for relapsing-remitting MS target key cells and molecules responsible for triggering and maintaining autoimmunity. Cytotoxic T cells, the immune system's specialized mobile infantry, are known to lead the attack. Antibodies, the immune system's guided missiles, appear to help reinforce it.
Daclizumab is a lab-engineered antibody, or monoclonal antibody, that alters signaling by interleukin-2 (IL-2), a key factor that mobilizes T cells. In a large clinical trial (NCT00109161), it has shown promise as an add-on therapy for patients taking the approved MS drug interferon-beta. Another ongoing trial (NCT00390221) is investigating whether or not daclizumab is effective as a stand-alone therapy for reducing relapses in MS.
The drug was designed to suppress T cell responses to IL-2, and it does so — but Dr. Bielekova had found previously that this suppression is indirect and depends on other immune cells. For example, one effect of daclizumab is to stimulate the non-specialized counterparts of T cells, called natural killer cells. These cells in turn suppress T cell activity.
In their new study, Dr. Bielekova and her team discovered that daclizumab's stimulatory effect on natural killer cells is paired with an inhibitory effect on LTi cells. They found evidence that the drug, via its effects on IL-2 signaling, acts on a type of stem cell. The drug appears to decrease the likelihood that this stem cell will develop into LTi cells, and sway it toward becoming natural killer cells.
"This helps explain why natural killer cells are activated and their numbers are expanded by daclizumab therapy," Dr. Bielekova said. Meanwhile, she said, the drop in LTi cells was "intriguing" in itself, given the cells' role in lymph node development.
Lymph nodes — found conspicuously in the armpits, neck and groin — are patches of tissue where T cells and antibody-producing B cells set up camp. Inside the nodes, T cells and B cells are found in clusters called lymphoid follicles, where they wait for a signal that the body is under siege from infection. In autoimmune disorders, abnormal lymphoid follicles can develop and contribute to the autoimmune response. Secondary progressive MS, in particular, is associated with abnormal lymphoid follicles in the connective tissues (or meninges) surrounding the brain. These are believed to contribute to chronic brain inflammation in MS, eventually leading to shrinkage of the brain.
Dr. Bielekova and her team reasoned that daclizumab, by suppressing LTi cells, should reduce the growth of lymphoid follicles. Since it is not possible to visualize these follicles in the live brain, the researchers measured the effects of daclizumab on markers of inflammation in the CSF. They found that CXCL13, a protein linked to lymphoid growth, and the IgG index, a measure of antibody production, decreased by an average of 50.4 percent and 13.5 percent, respectively, in trial participants who took the drug for six and half months.
"To our knowledge, no other MS therapy reduces IgG index," Dr. Bielekova said.
She cautioned that these data provide only an indirect link between LTi cells and brain inflammation in MS. If further research confirms that the cells play an important role in MS or other autoimmune disorders, "pursuing the development of new drugs to selectively inhibit LTi cells could be a useful therapeutic strategy," she said.
This study was funded by the NIH-NINDS intramural research program. The lead authors were Justin Perry and Sungpil Han. Mr. Perry was a fellow in NIH's Postbaccalaureate Intramural Research Training Award program, and is currently a Ph.D. student in the neuroscience program at Washington University in St. Louis. Mr. Han is an M.D.-Ph.D. student at Pusan National University in South Korea, and is supported in part by a fellowship from the Korea Research Foundation to study at NIH. Patient data were derived from a small completed trial (NCT00071838) which showed that daclizumab may reduce lesions in relapsing-remitting MS, and from an ongoing trial to investigate the drug's mode of action (NCT01143441).
NINDS (http://www.ninds.nih.gov) is the nation’s leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease – a burden borne by every age group, by every segment of society, by people all over the world.

Mom's Story

I am working on a second edition of Mom's Story, A Child Learns About MS. It will be at Amazon this fall.

Mom's Story

I am working on a second edition of Mom's Story, A Child Learns About MS. It will be at Amazon this fall.

Study Identifies Gene Linked to Vitamin D Deficiency

A recent study at Oxford University in England and published in Annals of Neurology, has identified a gene that causes vitamin D deficiency, a condition suspected of having a role in the development of MS.
The study examined the DNA of a group of people with MS who also have a large number of family members with the disease. All the DNA samples showed a distortion of the CYP27B1 gene which controls vitamin D levels in the body. And in a few rare cases where the DNA showed two copies of the distorted gene, the person was found to have a genetic form of rickets caused by vitamin D deficiency as well as MS.
The cause of myelin damage related to MS is still hotly debated: some believe it to be an autoimmune disease while others cite viruses or the environment as the culprit. There is growing evidence however of a correlation between MS and vitamin D deficiency. Epidemiological studies also show that populations closer to the equator and the sun, have far fewer case of MS than populations closer to the north or south poles. Researchers at Oxford University have now taken this premise a step further by showing that vitamin D deficiency and therefore possibly MS could have a genetic cause.
Despite this pivotal link, not all people with vitamin D deficiency develop MS. More research is needed to fully understand why. However, a distortion of the CYP27B1 gene is increasingly apparent in MS cases and it’s possible that the gene generates other, yet undetected, complications that lead to the disease—such as genetically caused rickets.
“Although vitamin D deficiency doesn’t always cause MS, it unveiled a critical genetic source that could be causing other problems that lead to MS,” says Jeffrey Epstein, whose foundation partially supported the study. “Even if we don’t understand all of the implications of that gene’s distortion, research can focus on gene therapy, and that will accelerate a cure.”
The study was partly funded by the National Multiple Sclerosis Society, The Wellcome Trust and the support of science investor, Jeffrey Epstein and The Jeffrey Epstein VI Foundation.

New blog for Mom's Story

Please visit my new Mom's  Story blog at: http://wp.me/P2l34j-l

Study: Woman’s Risk of Having a First Neurologic Event, Which Often Leads to MS, Decreased with Increased Number of Pregnancies

Women’s risk for developing clinically isolated syndrome, which often leads to multiple sclerosis, was shown to decrease with increased number of pregnancies in a comprehensive study undertaken in Australia. Clinically isolated syndrome (CIS) is a first neurologic episode caused by inflammation or damage to nerve fiber-insulating myelin in the brain or spinal cord. Although the results of this Ausimmune Study need to be confirmed, the findings encourage further exploration of potential treatments such as sex hormones, which may mimic pregnancy’s benefits in women with MS. The sex hormone estriol is currently in clinical trials, supported by the National MS Society and the National Institutes of Health, to treat women MS.


Anne-Louise Ponsonby, PhD (Murdoch Childrens Research Institute, Melbourne) and colleagues across Australia report their findings in Neurology (2011;76:540-548). This study was supported by a research grant from the National MS Society to Anthony McMichael, PhD, the National Health and Medical Research Council of Australia, and MS Research Australia.

Background: Before 1950, most women with MS were counseled to avoid pregnancy because of the belief that it might make their MS worse. Over the past 40 years, studies in hundreds of women with MS have almost all reached the opposite conclusion: that pregnancy reduces the number of MS exacerbations, especially in the second and third trimesters.

The Ausimmune Study was undertaken to investigate whether increased exposure to sunlight and vitamin D may be protective against MS in people who had not yet been diagnosed with MS, but who had experienced a CIS. Read more about previously released findings. In the current study, the team used this unique population to study whether the number of pregnancies or offspring affects the risk for developing a CIS.

The Study: Investigators looked at the records of 282 men and women who had developed a CIS, and compared the number of children – and in women, the number of pregnancies – with controls who did not develop CIS.

Women who had one pregnancy were nearly half as likely to develop CIS, and those with three or more pregnancies had more than one fourth the risk of developing CIS compared with controls. Other factors considered – such as sun exposure and immune-system-related genes associated with MS – did not otherwise explain these associations. There was no association between risk of CIS and the number of children in men.

Comment: In an accompanying editorial, Martin Daumer, PhD, Brian G. Weinshenker, MD, and Rhonda Voskuhl, MD, comment that these findings need to be replicated in other countries to be validated, and caution that the study does not address whether pregnancy affects the long-term course of MS or development of disability.

Even with these caveats, the editorial authors say that because of studies such as this one, there is a compelling need for research to develop therapeutic approaches that mimic pregnancy’s benefits in women with MS. Dr. Voskuhl is now leading a team of investigators at seven medical centers to conduct a two-year, controlled clinical trial of estriol – a sex hormone that is increased during pregnancy – added to standard therapy to treat MS in 150 women with relapsing-remitting MS. This study recently completed enrollment.

This study provides additional evidence of a link between gender and autoimmunity. Read more about the Society’s efforts to study this link for clues to stopping MS in its tracks and ending it forever.

Virtual Insight Panel

WEGO Health will be hosting a sponsored virtual Insight Panel for active members of the online Multiple Sclerosis (MS) Community. This panel will focus on the needs of the online community and review of Multiple Sclerosis tools and resources. All participants will receive a $25 Amazon.com gift card for their participation. http://bit.ly/ppYhDf

ABC News highlights treatment advances for MS

ABC News highlights treatment advances for MS. Watch the video (.wmv) and Read the article http://abcnews.go.com/Health/Wellness/multiple-sclerosis-sees-explosion-treatment-advances/story?id=15290688

Positive Results Announced from Second Phase III Study of Alemtuzumab in MS

Genzyme has announced that the experimental intravenous therapy alemtuzumab (with a proposed brand name Lemtrada™) met two primary endpoints by significantly reducing relapse rates and the worsening of disability in a two-year study comparing alemtuzumab to standard subcutaneous dosing of Rebif® (interferon beta-1a, EMD Serono Inc. and Pfizer). The study, called CARE-MS II, involved 840 people with relapsing-remitting MS. The results were announced in a November 14, 2011 press release, which also indicated that the company plans to apply in early 2012 to the U.S. Food and Drug Administration for marketing approval. Data analysis is ongoing and the company expects to provide a full report at an upcoming medical meeting. Alemtuzumab has been designated by the FDA as a “Fast Track Product,” which should expedite its future review.

Mom's Story

Mom's Story, A Child Learns About MS* featured at Barnes and Noble, 90th and Shea, Scottsdale, AZ  on December 6, 6:30-8:00 pm.

Discussion with three authors, including Mary Jo Nickum, about memoir writing. We will sell and sign our books after the talks.

*Ten percent of the net proceeds from the sale of this book will be donated to the National Multiple Sclerosis Society.

Phase 3 trial of BG-12

Biogen Idec announced that the experimental oral therapy BG-12 significantly reduced the average number of annual MS relapses in a two-year, Phase III clinical trial of more than 1400 people with relapsing-remitting MS. Although its exact mode of action is not known, BG-12 is thought to inhibit immune cells and molecules involved in MS attacks on the brain and spinal cord. The results of the CONFIRM study were announced in an October 26 press release. Data analysis is ongoing and the company expects to provide a full report at an upcoming medical meeting. Positive results from another Phase 3 trial of BG-12 were also announced this year, paving the way for a potential application for marketing approval.


Full details and evaluation of this study should help to define further the safety and promise of BG-12 as a potential therapy for relapsing MS. According to the company press release, these positive results set the stage for upcoming filings for marketing approval from drug regulatory agencies.

Book Trailer

I just completed a Savvy Authors' Workshop. View my new book trailer on YouTube: http://www.youtube.com/watch?v=ggw6dnVgYro

Blocking Crucial Molecule Could Help Treat Multiple Sclerosis

Neuroscientists have reported identifying a driving force behind autoimmune diseases such as MS, and suggest that blocking this cell-signaling molecule is the first step in developing new treatments to eradicate these diseases.

Researchers led by Abdolmohamad Rostami, M.D., Ph.D., Professor and Chairman of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University, found that GM-CSF, which stands for Granulocyte-macrophage colony-stimulating factor, appears to be the key culprit in the onset of MS. Without GM-CSF, T helper 17 cells (Th17) cells did not induce the MS-like disease in an experimental animal model.

These findings were recently published in an advanced, online publication of Nature Immunology.

Th17 cells have been shown to play an important pathogenic role in humans and experimental models of autoimmune diseases, but the mechanisms behind this have not been understood until now.

There was no connection between GM-CSF and Th17 cells before," said Dr. Rostami. "What we have shown in this paper is that GM-CSF derived from Th17 cells is important in the cell-signaling process that leads to inflammation in the central nervous system."

"Now we know how the Th17 cells work and a better understanding of this mechanism and biology leads to new therapeutics," he adds.

The results suggest that blocking GM-CSF activity may be a successful therapeutic strategy in MS, one of the most common neurological diseases affecting young adults, and other autoimmune diseases, said Dr. Rostami, who is also the Chair of Neurology at Thomas Jefferson University Hospital.

These findings identify the interleukin-23 (IL-23)/ Th17/GM-CSF axis as the major pathway in pathogenesis of autoimmune central nervous system inflammation and likely other autoimmune diseases. IL-23, a known cytokine that causes autoimmune inflammation of the brain, induces production of more GM-CSF in Th17 cells, the researchers explain.

Dr. Rostami, who is also director of the Neuroimmunology Laboratory in the Department of Neurology at JMC, and his colleagues used an animal model of MS called experimental autoimmune encephalomyelitis (EAE) for the investigation, a common model used to study the pathogenesis of the disease. Mice whose Th17 cells cannot produce GM-CSF did not develop neuroinflammation, thus GM-CSF is responsible for disease manifestation in this experimental model. This scenario suggests feed-forward loop of IL-23 and GM-CSF driving the pathogenic encephalitogenic immune response in the brain and spinal cord.

Another recently published paper in Nature Immunology by Dr. Rostami and his team unraveled a mechanism that may help fight MS. The researchers found that a protein known as interkeukin-27 (IL-27) helped block, not induce, the onset of symptoms in animals with an MS-like disease. While increasing levels of GM-CSF may cause the disease, as shown in the current paper, increasing IL-27 concentrations may help quell an over-active immune system, the researchers reported.

"That was the first time that we had direct evidence that by actively giving IL-27 like a drug, we can suppress EAE in mice," Dr. Rostami said.

If similar findings from this current study of GM-CSF are found in human blood samples, this approach could eventually also be shown to be useful in the clinical setting, Dr. Rostami explains.

Whether GM-CSF drives neuroinflammation in MS remains unknown, but the current findings highlight the potential that IL-23 and GM-CSF might serve a similar role in human disease.

"This is the first step towards finding a new treatment," he said. "If we can try to neutralize GM-CSF by different means, for example, by trying to mimic it or trying to block the receptor for GM-CSF, we can hopefully ameliorate the disease."

Mother's Day

Consider giving a gift of love to Mother on Mother's Day: Mom’s Story, A Child Learns About MS.

Controlling the Muscle Spasms of Multiple Sclerosis

Many people with multiple sclerosis experience spasticity, or muscle stiffness and spasms. It usually affects the muscles of the legs and arms, and may interfere with the ability to move those muscles freely.

Spasticity can occur either as a sustained stiffness caused by increased muscle tone or as spasms that come and go, especially at night. It can feel like a muscle tightening or it can cause severe pain. Spasticity can also produce feelings of pain or tightness in and around joints and can cause low back pain. The intensity may vary depending on your position, posture, and state of relaxation.

What Causes Spasticity in Multiple Sclerosis?

Spasticity is the result of an imbalance in the electrical signals coming from the brain and spinal cord, often caused by damage to these areas from by multiple sclerosis. This imbalance causes hyperactive muscle stretch reflexes, which result in involuntary contractions of the muscle and increased muscle tension.

What Triggers Spasticity Due to Multiple Sclerosis?

For someone who has multiple sclerosis, spasticity may be aggravated by extremes of temperature, humidity, or infections. It can even be triggered by tight clothing.

How Is Spasticity Diagnosed?

To diagnose spasticity your doctor will first evaluate your medical history, including what medications you have taken and whether there is a history of neurological or muscular disorders in your family. To confirm the diagnosis, several tests can be performed to evaluate your arm and leg movements, muscular activity, passive and active range of motion, and ability to perform self-care activities.

How Is Spasticity Treated if I Have Multiple Sclerosis?

If you suffer from multiple sclerosis, spasticity can be treated using physical therapy, medications, surgery, or any combination of these treatments. Your doctors will consider the severity of your condition, your overall health, and the following factors when prescribing an appropriate treatment plan:

• Is the spasticity affecting function or independence?

• Is the spasticity painful?

• What treatment options have already been tried, and how did they work?

• What are the costs of the possible treatments?

• What are the limitations and side effects of the treatment?

• Will the benefits outweigh the risks?

How Does Physical and Occupational Therapy Help Spasticity?

A basic physical therapy stretching program is the first step in treating spasticity linked to MS. A daily regimen of stretching can lengthen muscles to help decrease spasticity.

An occupational therapist may prescribe splinting, casting, and bracing techniques to maintain range of motion and flexibility.

If physical and occupational therapy do not adequately control the spasticity, medications may be added to the treatment plan.

What Drugs Are Used to Treat Spasticity?

Common drugs used to treat spasticity include the muscle relaxants baclofen and Zanaflex.

Another drug that might be used to treat spasticity is Valium, which is often helpful when taken at night to relieve spasms that interfere with sleep.

If medications taken orally are not effective, a pump can be surgically implanted to deliver the medication (such as the baclofen pump). Botulinum toxin (or Botox) can also be injected locally into the affected area to relax the muscles.

What Types of Surgery Are Available for Spasticity?

When other treatments fail, rhizotomy and tendon release are two surgical procedures used to treat spasticity.

Rhizotomy involves surgically cutting away part of the spinal nerve. It is performed to relieve pain or decrease muscle tension.

Tendon release, also called a tenotomy, may be performed to help reduce the frequency or magnitude of the spasticity, depending on the age of the patient. The surgery involves cutting severely contracted tendons away from the muscles to which they're attached.

Tendon release may need to be repeated.

These surgeries are usually only done in extreme cases that do not respond to other treatments.

What Does “Disabled” Mean?

There is really only one criterion for disability: can you do substantial paid work? “Substantial” means earning $800 a month. And it doesn’t have to be work you know, or work that is available in your community. Ability to do any kind of full-time paid work at all can disqualify you. (One major exception: if you work for yourself, the Social Security Administration [SSA] looks at your net income – what you report to the IRS – not at your gross.)

There are five ways people with MS can prove disability. These include substantial limitation of vision, cognitive problems, fatigue, or major disability of two extremities. SSA can also combine these factors, evaluated on what they call a “grid” of over-all disability.

You’ll need evidence to get disability. Rosemarie Johnson says, “You have to be proactive. Keep a journal and write about your symptoms and how they limit your activity. See your doctors regularly. That way, if you do need to apply for disability, you’ll have solid documentation.”

A detailed letter from your doctor testifying to fatigue or cognitive problems is powerful evidence of disability. So your doctors should ask about fatigue and cognition at each appointment, or you should bring it up. It’s helpful to get a neuro-psychological evaluation every couple of years and again before applying for disability. Letters from family, friends or anyone who has observed your daily activities can also document your disability

Mom's Story

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