Mom's Story, A Child Learns About MS

Mom's Story, A Child Learns About MS
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Wednesday, April 27, 2011

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."

Wednesday, April 20, 2011

Mother's Day

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

Tuesday, April 19, 2011

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.

Friday, April 15, 2011

Study shoots hole in 'liberation' theory for multiple sclerosis

By Carmen Chai, Postmedia News

American researchers have cast fresh doubts on the theory underpinning so-called 'liberation therapy' for multiple sclerosis sufferers.

A new University of Buffalo study suggests that chronic cerebral venous insufficiency (CCSVI), which is a blocking or narrowing of extracranial veins that some researchers claim causes MS symptoms, may be a result of MS and not a cause.

"Given the intense interest in the hypothesis that CCSVI is a possible cause of MS, independent evaluation of CCSVI was identified an urgent need," said lead researcher Robert Zivadinov, a University of Buffalo neurology professor and president of the International Society for Neurovascular Disease.

Zivadinov's study, published Wednesday in the journal Neurology, examined 449 patients — 289 people who had MS, 163 who were healthy, 26 who had other neurological diseases and 21 who had experienced a clinically isolated syndrome (CIS), an individual's first neurological episode.

According to Zivadinov, results showed that only 56.1 per cent of MS patients and 38.1 per cent of CIS patients had CCSVI.

"While this may suggest an association between the MS and CCSVI, association does not imply causality," Zivadinov said in a statement.

Meanwhile, 42.3 per cent of participants who had other neurological diseases and 22.7 per cent of healthy people in the story also had CCSVI.

"These findings indicate that CCSVI does not have a primary role in causing MS. Our findings are consistent with increased prevalence of CCSVI in MS, but substantially lower than the sensitivity and specificity rates in MS reported originally by the Italian investigators," Zivadinov said in the press release.

Paolo Zamboni, a doctor at the University of Ferrara in Italy, had argued that CCSVI increased the risk of having MS by 43 times. The vascular condition restricts blood flow to the brain, which could cause muscle weakness and loss of sensitivity, he concluded.

Canadians suffering from MS have travelled abroad to Bulgaria, Poland, Mexico and other countries for the controversial liberation therapy procedure, which involves opening blocked veins in the neck. The procedure, developed by Zamboni, is banned in Canada because it is not scientifically supported.

Last November, a Niagara Falls, Ont., man died after he received liberation therapy at a hospital in Costa Rica.

Canada has one of the highest MS rates in the world.

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Friday, April 8, 2011

Scientists Reverse Multiple Sclerosis in Mice

Experimental treatment suppresses immune cells, forcing remission, study says

By Robert Preidt

.WEDNESDAY, Aug. 12 (HealthDay News) -- An experimental treatment that suppresses the immune system to put multiple sclerosis into remission completely reversed the disease in mice, Canadian scientists say.

In MS, the immune system attacks the central nervous system. The new treatment, called GIFT15, is composed of two proteins, GSM-CSF and interleukin-15, that are fused in the lab. Normally, the individual proteins act to stimulate the immune system, but when they're stuck together, the proteins suppress immune response, the researchers explained.

They do this by converting B-cells -- a type of white blood cell normally involved in immune response -- into immune suppressive cells.

"GIFT15 can take your normal, run-of-the-mill B-cells and convert them ... into these super-powerful B-regulatory cells," study team leader Dr. Jacques Galipeau, of the Jewish General Hospital Lady Davis Institute for Medical Research and McGill University in Montreal, said in a university news release.

He and his colleagues took normal B-cells from mice and sprinkled GIFT15 on the B-cells. "And when we gave them back intravenously to mice ill with multiple sclerosis, the disease went away," Galipeau said.

The treatment was fully effective with a single dose, and no significant side effects were seen in the mice, the researchers reported.

Their findings were published online Aug. 9 in Nature Medicine.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about multiple sclerosis.

Read more: - Connect to Better Health

Friday, April 1, 2011

Book sale and signing

Visit me and pickup a copy of Mom's Story at the Second Annual Disability Empowerment Center (DEC) Health and Wellness Fair, April 9, 9:00-4:00.