Current Treatments
BETASERON® (interferon beta-1b) is indicated for the treatment of relapsing forms of multiple sclerosis to reduce the frequency of clinical exacerbations. Patients with multiple sclerosis in whom efficacy has been demonstrated include patients who have experienced a first clinical episode and have MRI features consistent with multiple sclerosis

AVONEX® (Interferon beta-1a) is a 166 amino acid glycoprotein with a predicted molecular weight of approximately 22,500 daltons. It is produced by recombinant DNA technology using genetically engineered Chinese Hamster Ovary cells into which the human interferon beta gene has been introduced. The amino acid sequence of AVONEX® is identical to that of natural human interferon beta.

COPAXONE is the brand name for glatiramer acetate (formerly known as copolymer-1). Glatiramer acetate, the active ingredient of COPAXONE, consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000 – 9,000 daltons. Glatiramer acetate is identified by specific antibodies.

Rebif® (interferon beta-1a) is a purified 166 amino acid glycoprotein with a molecular weight of approximately 22,500 daltons. It is produced by recombinant DNA technology using genetically engineered Chinese Hamster Ovary cells into which the human interferon beta gene has been introduced. The amino acid sequence of Rebif® is identical to that of natural fibroblast derived human interferon beta. Natural interferon beta and interferon beta-1a (Rebif®) are glycosylated with each containing a single N-linked complex carbohydrate moiety.

Tysabri is a monoclonal antibody that affects the actions of the body's immune system. Monoclonal antibodies are made to target and destroy only certain cells in the body. This may help to protect healthy cells from damage. Tysabri is used to treat relapsing forms of multiple sclerosis.
Gilenya™ is a new class of medication called a phingosine 1-phosphate receptormodulator, which is thought to act by retaining certain white blood cells (lympohcytes) in the lymph nodes, thereby preventing those cells from crossing the blood-brain barrier into the central nervous system (CNS). Preventing the entry of these cells into the CNS reduces inflammatory damage to nerve cells.


Early Symptoms
The most common early symptoms of MS include:
* Tingling * Numbness
* Loss of balance
* Weakness in one or more limbs
* Blurred or double vision

Less common symptoms of MS may include
* Slurred speech
* Sudden onset of paralysis
* Lack of coordination
* Cognitive difficulties
Listed above, the early symptoms. I tend to be a poster child for these. The symptoms that occur later on are too numerous just to list. There will be a link included that will get you to a site where these symptoms are listed and explained. Keep in mind that someone may have some of these or many of these, there is no way to tell.
Multiple sclerosis statistics show that approximately 250,000 to 350,000 people in the United States have been diagnosed with this disease. The life expectancy for people with multiple sclerosis is nearly the same as for those without MS. Because of this, multiple sclerosis statistics place the annual cost of MS in the United States in the billions of dollars. MS is five times more prevalent in temperate climates -- such as those found in the northern United States, Canada, and Europe -- than in tropical regions. Furthermore, the age of 15 seems to be significant in terms of risk for developing the disease. Some studies indicate that a person moving from a high-risk (temperate) to a low-risk (tropical) area before the age of 15 tends to adopt the risk (in this case, low) of the new area and vice versa. Other studies suggest that people moving after age 15 maintain the risk of the area where they grew up.

Friday, January 22, 2010

Study: Multiple Sclerosis Pills Show Promise and Risk

MIKE STOBBE
AP Medical Writer

ATLANTA (AP) — Tests of the first two oral drugs developed for treating multiple sclerosis show that both cut the frequency of relapses and may slow progression of the disease, but with side effects that could pose a tough decision for patients.

Two experts not involved in the studies said the drugs appear effective but with potentially dangerous side effects. It's too soon to know if the pills will be approved by the government or widely adopted by physicians, they said.

About 2.5 million people around the world have multiple sclerosis, a neurological disease that can cause muscle tremors, paralysis and problems with speech, memory and concentration. The studies involve the most common form of the disease, in which people are well for a while and then suffer periodic relapses.

Current treatments can reduce the duration and severity of symptoms but require daily or regular shots or infusions.

The new studies tested two types of pills. Cladribine, made by Merck Serono, is already sold to treat a rare blood cancer. For MS, it would be taken eight to 10 days a year. Fingolimod is a daily MS pill being developed by Novartis.
The research found that patients on the pills were about half as likely to suffer relapses of symptoms as those who took dummy pills or a commonly prescribed shot for MS.

But they also found both drugs significantly lowered immune defenses that allowed latent herpes viruses to rage in some patients — in one study, two people died of unchecked herpes infections.

The side effects detailed in the new studies are giving some physicians pause.

"There is a price tag attached" to the new medications, said Dr. Silva Markovic-Plese, an MS researcher at the University of North Carolina.

The studies were being published in Thursday's New England Journal of Medicine.

There is no cure for MS, but steroids can reduce the duration and severity of symptoms in the short term, and seven treatments on the market have had success in reducing recurrence of symptoms.

All involve daily or regular injections. So a pill is appealing: Even healthy people can have trouble giving themselves shots, so it can be a nightmare for patients with faltering coordination and concentration.

"Right now I have to think very hard when I make coffee," said Ivana Vuletic, a 49-year-old Chapel Hill, N.C. woman with MS. "I would be greatly relieved if I didn't have to prick myself or be pricked" with needles, she said.

Still, she said she wouldn't take the new pills if their side effects were too dangerous.

Vuletic is on her third MS drug in about four years, and her illness has gotten worse. The MS injections have led to pocked skin and other problems so she is leery of new treatments' side effects.

The new studies reveal the trade-offs:

—A two-year study gave 1,300 MS patients cladribine or dummy pills. Patients on the drug were only half as likely to suffer relapse as those on placebo, and were 30 percent less likely to have worsening disability. However, 20 percent to 30 percent of the cladribine patients developed low counts of infection-fighting white blood cells, compared to just 2 percent of the others. And 20 cladribine patients suffered herpes infections versus none in the dummy pill group.

—A two-year study gave about 1,000 patients fingolimod or dummy pills. Only 17 percent of fingolimod patients had worsening disabilities from MS after three months, compared to 24 percent in those on placebo. Herpes infections were about the same in the pill and placebo groups, but respiratory infections like bronchitis and pneumonia were nearly twice as common in the fingolimod patients.

—A one-year study of 1,200 patients tested fingolimod against shots of Avonex, a form of interferon. Those taking the pills had less brain shrinkage — a measure of progression of the disease. About 20 percent of patients on the pill had relapses versus 30 percent on the dummy pills.

In that study, 9 percent of those on fingolimod had serious side effects, compared to 6 percent of those on Avonex. Two people on fingolimod died of herpes infections; six had eye swelling and eight had skin cancers.

All three studies were funded by Novartis or Merck Serono, the pill manufacturers.

Doctors are likely to turn first to current options until the pills' side effects are better understood, said Dr. Neil Lava, the director of Emory University's multiple sclerosis clinic.

Physicians are mindful of what happened with Tysabri, an MS drug that was approved in November 2004 and pulled from the market the next year after cases of a rare but lethal brain inflammation in some patients. It was reintroduced in 2006, but doctors are still monitoring for side effects, Lava said.

Thursday, January 14, 2010

MS Awareness Week

MS Awareness Week 2010 LogoMove It During MS Awareness Week.

Mark your calendars and get ready to move it closer to a world free of MS. March 8-14, 2010 is MS Awareness Week and is a great opportunity to spread the word and raise awareness for MS.

So many ways to move it.
Step one: awareness.
Step two: action.
Step three: a world free of multiple sclerosis.


Activities in and around
MS Awareness Week:

March 5 Women on the Move Luncheon - Plymouth
March 6 Puzzle-a-thon
March 18 Savor the Flavors
March 26 Women on the Move Luncheon - Nashua

Chapter Calendar at a Glance
You can move it too.
Multiple sclerosis can stop people from moving forward in their lives. Join us and let's make sure it doesn't. No matter what you do, no matter how you do it, you'll keep all of us moving forward.

To find out ways to be a part of MS Awareness Week and to encourage others to move it too, check out the activities listed below, or contact the Central New England Chapter office, and ask for Steve Sookikian at 1-800-344-4867 or steve.sookikian@mam.nmss.org.

Here are just a few ways to be a part of MS Awareness Week, and encourage others to move it too:

* Download web banners and widgets for your social network pages
* Post your videos on YouTube from MS Awareness Week showing how you are moving it and encourage people to post there too! http://www.youtube.com/group/MSmoveit
* Share your story about how you are “moving it?
* Sign up to volunteer at an upcoming chapter event
* Form a team for a Bike MS, Walk MS, or Challenge Walk
* Email a legislator about an issue important to people with MS
* Tell five people it’s MS Awareness Week and ask them to tell five more people
* Support the Society — every donation moves us closer to a world free of MS
* Raise MS aWEARness by wearing orange; need something new? Visit http://www.msstoreipp.org/index.php.
* Visit http://www.nationalmssociety.org/msawarenessweek every day during MS Awareness Week for new tips and ideas

Remember, Move it...
Move it, during MS Awareness Week.
It is the perfect time to join and help build the MS Movement.

Start Date: Monday, March 8, 2010
End Date: Monday, March 15, 2010

Tuesday, January 12, 2010

The psychometric properties of clinical rating scales used in multiple sclerosis.

Sharrack B, Hughes RA, Soudain S, Dunn G.

Department of Neurology, UMDS, Guy's Hospital, London, UK.

OullII;l y Many clinical rating scales have been proposed to assess the impact of multiple sclerosis on patients, but only few have been evaluated formally for reliability, validity and responsiveness. We assessed the psychometric properties of five commonly used scales in multiple sclerosis, the Expanded Disability Status Scale (EDSS), the Scripps Neurological Rating Scale (SNRS), the Functional Independence Measure (FIM), the Ambulation Index (AI) and the Cambridge Multiple Sclerosis Basic Score (CAMBS). The score frequency distributions of all five scales were either bimodal (EDSS and AI) or severely skewed (SNRS, FIM and CAMBS). The reliability of each scale depended on the definition of 'agreement'. Inter-and intra-rater reliabilities were high when 'agreement' was considered to exist despite a difference of up to 1.0 EDSS point (two 0.5 steps), 13 SNRS points, 9 FIM points, 1 AI point and 1 point on the various CAMBS domains. The FIM, AI, and the relapse and progression domains of the CAMBS were sensitive to clinical change, but the EDSS and the SNRS were unresponsive. The validity of these scales as impairment (SNRS and EDSS) and disability (EDSS, FIM, AI and the disability domain of the CAMBS) measures was established. All scales correlated closely with other measures of handicap and quality of life. None of these scales satisfied the psychometric requirements of outcome measures completely, but each had some desirable properties. The SNRS and the EDSS were reliable and valid measures of impairment and disability, but they were unresponsive. The FIM was a reliable, valid and responsive measure of disability, but it is cumbersome to administer and has a limited content validity. The AI was a reliable and valid ambulation-related disability scale, but it was weakly responsive. The CAMBS was a reliable (all four domains) and responsive (relapse and progression domains) outcome measure, but had a limited validity (handicap domain). These psychometric properties should be considered when designing further clinical trials in multiple sclerosis.

PMID: 10050902 [PubMed - indexed for MEDLINE]

Wednesday, January 6, 2010

Multiple Sclerosis: Antibodies Gone Awry

Multiple sclerosis is an autoimmune disease thought to be caused by T cells that attack and destroy myelin, the insulating sheath that surrounds neurons in the central nervous system and nerve cells throughout the body. If myelin is damaged, neuronal transmission can be disrupted, and communications between the brain and other parts of the body may fail.

A few years ago, researchers in California and New York suggested that T cells may not be the only culprit in multiple sclerosis. Within multiple sclerosis lesions, they identified antibodies that target myelin-associated proteins. They hypothesized that these autoreactive antibodies may contribute to the disease by binding to these proteins and attracting immune cells that destroy the myelin.

Recently, a group of scientists added another wrinkle to the story. As described in the Proceedings of the National Academy of Sciences, a team led by Alexander Gabibov, D.Sc., of the Russian Academy of Sciences and including Herbert Morse III, M.D., chief of the Laboratory of Immunopathology at NIAID and a French group from Technological University of Compiegne, examined blood samples of 24 people with multiple sclerosis and found autoreactive antibodies in 20 of them. Blood samples of 20 healthy volunteers were used as controls.

Some of these autoreactive antibodies could degrade myelin proteins. The same reaction was shown by autoantibodies isolated from mice that develop experimental allergic encephalomyelitis (EAE), a disease mirroring human multiple sclerosis.

In their paper, Drs. Gabibov and Morse and their colleagues describe how these antibodies may contribute to the symptoms of multiple sclerosis directly by catalyzing site-specific destruction of myelin basic protein (MBP) and thereby degrading the myelin sheaths. The investigation of such reaction on recombinant proteins designed to model different epitopes or pieces of MBP revealed that the antibodies have a highly pronounced catalytic specificity toward these proteins. The authors suggest that measuring the levels of these catalytic antibodies in the sera of people with multiple sclerosis may be a useful clinical marker for disease progression.

The research team also showed that copaxone—an injectable drug the U.S. Food and Drug Administration approved in 1996 for treating multiple sclerosis—effectively blocks the catalytic activity of the antibodies. This raises the possibility that new drugs for multiple sclerosis might be targeted to these destructive catalytic antibodies. One thing that should aid in the development of such drugs, says Morse, is that similar catalytic antibodies have been found in the mice with a disease mirroring human multiple sclerosis. This may provide a valuable pre-clinical model for testing the effect of potential new inhibitors.

Reference
Ponomarenko, N. et al. Autoantibodies to myelin basic protein catalyze site-specific degradation of their antigen. PNAS DOI: 10.1073/pnas.0509849103 (2006).

About Me

My photo
North Grafton, Massachusetts, United States
Well-educated, disabled at this point with Multiple Sclerosis. I am very glad that I was able to do the things that I have been able to do over the years. had to change the picture, this one's more realistic.