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Saturday, March 1, 2014

Pathogenesis and Management of Multiple Sclerosis – An Update for the Multiple Sclerosis Nurse

Bernd Kieseier, Dusseldorf, Germany


The Pathogenesis of Multiple Sclerosis 
Since the clinical presentation of multiple sclerosis (MS) with the typical plaques in the brain was first correlated in 1868,1 much has been learned about this immune-mediated disease, which is characterised by chronic inflammation, demyelination, axonal damage, white matter lesions, brain and spinal cord atrophy and astrocytosis.2 Within white matter lesions that are visible on magnetic resonance imaging (MRI) scans from an early stage,3macrophages strip and engulf the myelin sheath leading to nerve conduction block and neurological deficit.2 A relapse is usually followed by a recovery period, in which remyelination can occur,4 but continued inflammation eventually leads to axonal loss and brain atrophy.5 

Nearly all risk genes identified for MS (currently about 100) are associated with immune function5 and therapies that alter lymphocyte function and migration6 are effective in MS, suggesting an immune aetiology. Some variants of the human leucocyte antigen (HLA) complex and the major histocompatibility complex (MHC) have been associated with MS,7,8 but the risk they confer to a carrier for developing MS is too small to be predictive of disease. These genes, however, are likely to be valuable in determining a clearer understanding of MS pathogenesis. 

In the brains of patients with MS there appears to be an imbalance between the competing pro-inflammatory and anti-inflammatory processes.9 Genetic and environmental factors may assist the movement of autoreactive T cells and antibodies through a damaged blood–brain barrier (BBB) and into the central nervous system (CNS). Once inside brain tissue, pro-inflammatory cytokines, such as interferon gamma(IFNγ), tumour necrosis factor alpha (TNF-α) and interleukin (IL)-2, -15, -17 and -23 are released by activated T-cells. These increase the expression of cell-surface molecules on lymphocytes and antigen-presentingcells (astrocytes, microglia and macrophages), triggering an immune response. In addition, the release of certain anti-inflammatory cytokines (IL-1, -4 and -10) from T-cells stimulates production of antibodies by B cells, which damage host tissue (see Figure 1).10,11 

Disease Course 
MS has an unpredictable and variable course (see Figure 2).12 The disease first manifests with a neurological sign or symptom such as loss of vision, bladder and bowel dysfunction, ataxia or sensory disturbances (e.g. clinically isolated syndrome [CIS]). After this, most patients spend years alternating between periods of relapse and remission (relapsingremitting multiple sclerosis [RRMS]), but approximately 50 % will haveprogressed to a chronic advanced stage within 10 years (secondary progressive MS [SPMS]).12 At this stage there is clear cerebral volume reduction with increased lesion load visible in MRI.10 Most patients show impaired walking within 15 years and are wheelchair bound after 25 years. Up to 65 % of patients show cognitive deficits that may significantly impair work and daily activities.13 

Medications in Current Multiple Sclerosis Management 
In MS, disease-modifying therapies (DMTs), although not a cure, helpmodify and slow down this course and delay progression.12 For almost 20 years the beta interferons (IFNβs) and glatiramer acetate (GA) have been administered to achieve some limitation of damage to the CNS, to delay disease progression and to provide a degree of long-term improvement in symptoms and quality of life (QoL). Regrettably, the latter two goals are only partially achieved with these drugs. Antispastic drugs, analgesics and antidepressants are also used for short-term symptomatic relief and temporarily improve QoL, but have no disease-modifying effect.14,15 

In 1993 the first IFNβ therapy for MS was introduced, followed by GA in 2001, mitoxantrone in 2002 and natalizumab in 2006. Fingolimod,a reversible spingosin-1-phosphate (S1P) receptor antagonist and the first oral DMT in MS treatment, was approved for the treatment of RRMS by the US Food and Drug Administration (FDA) and European Medicines Agency (EMEA) in 2010 and 2011, respectively. Teriflunomide wasapproved by the FDA in for RRMS in 2012 and by the EMEA in 2013 and dimethyl fumarate (BG-12) was approved by the FDA for RRMS in 2013; several other agents are in development (e.g. laquinimod, alemtuzumab, daclizumab, ocrelizumab and pegylated IFNβ).16 

The DMTs are associated with various safety and adherence concerns, particularly flu-like symptoms seen with the IFNβs and administrationsite reactions in the treatments given by subcutaneous injection. Therefore, the decision-making process in MS treatment choice should consider two major dimensions: efficacy and burden (see Figure 3).17 The ideal treatment for MS would have a high efficacy and low burden, but the commercially available DMTs fall short of this target. 

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Research showing advances in Axon restoration, cognitive performance, And a hopeful medication for Primary & Secondary-progressive multiple sclerosis

multiple sclerosis experimental drugsFresh from the Multiple Sclerosis Association of America (MSAA) is the 2014 MS Research Update, published each year, MS Research Updatehighlights recent research and approved therapies in the treatment of multiple sclerosis. Although the report, which was compiled mainly by Stephen Krieger, M.D., and Diana Schneider, Ph.D., details a broad range of medications, this article will focus on some of the new therapeutics under investigation, including those for relapse-remitting, primary-progressive, and secondary-progressive multiple sclerosis.
One biologic under evaluation is “anti-LINGO-1” (BIIB033), an agent that may be able to reverse demyelination of axons. Anti-LINGO-1 blocks LINGO-1, a protein in the central nervous system that prevents myelination and survival of neurons. LINGO-1 exists in the body to provide a sort of “checks and balances” to prevent malignancies, but in multiple sclerosis, this negative regulation actually prevents the body from healing itself. Initial Phase I trials using intravenous injections of anti-LINGO-1 showed that the agent was well tolerated in adults with relapsing or secondary-progressive multiple sclerosis. Two Phase II trials were launched in 2013; the first is recruiting patients with newly-diagnosed multiple sclerosis involving the visual pathways, and the second is looking to recruit 400 patients. These Phase II trials will evaluate remyelination and the extent of improvement in disability, respectively.  Anti-LINGO-1 does not reduce relapses or prevent new MRI lesions, so the second trial is co-administering Avonex and using functional assessments of the effects of multiple sclerosis.
A second therapeutic studied in Germany is erythropoietin, a hormone naturally produced by the kidneys to promote erythropoiesis (red blood cell formation in the bone marrow). Animal studies showed neuroprotective effects, and a Phase I/IIa pilot study showed that high-dose erythropoietin improved cognitive performance and motor function. Researchers are still studying erythropoietin, both on its own and as an adjunct treatment for optic neuritis.
Another drug emulating the body’s own protein production is Idebenone (Catena®, Sovrima®), a drug similar to coenzyme Q10, which is produced for use in the electron transport chain as an electron sink. It also acts as an antioxidant, which is why Idebenone is postulated to reduce oxidative stress that damages nerves and the immune system. This postulation will soon be supported or demoted: a double-blind placebo-controlled Phase I/II clinical trial began in July 2009 and is scheduled to end in September 2016. It is still recruiting patients with primary-progressive multiple sclerosis and is sponsored by the National Institute of Neurological Disorders and Stroke.
A sort of “therapeutic vaccine” is also being developed to treat multiple sclerosis. MIS416 is a potent activator of the innate immune system and has been previously tested in cancer and acquired infections in an attempt to enhance the inherent capacity of the immune system to fight disease. It completed Phase I/II trials in 2012, and interim results showed MIS416 to be well-tolerated by patients with primary-progressive and secondary-progressive multiple sclerosis. Eight of ten patients with secondary-progressive multiple sclerosis showed some improvement after 12 weeks of treatment with MIS416.
Another unique development is transdermal peptides. A Polish study evaluated the safety and efficacy of three myelin peptides (MBP 85-99, PLP 139-151, and MOG) in 30 individuals with relapse-remitting multiple sclerosis. The low-dose group, which received 1 mg of each of the three peptides through a transdermal patch, had a relapse-free rate of 56%, whereas the placebo group had a relapse-free rate of only 10% after one year of treatment. Further studies may be pursued.
This list of new therapeutics is by no means comprehensive, but a number of unique treatments have been highlighted. Many of the drugs discussed are being investigated in patients with primary-progressive and/or secondary-progressive multiple sclerosis, which gives hope to these patients, as most approved drugs are indicated for relapse-remitting multiple sclerosis, only. The full report can be found here.
Article Source: BioNews

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Friday, February 28, 2014

Oral contraceptives linked to increased risk of multiple sclerosis


FoxNews.com

  • Birth Control Pills and Menstrual Cycles
    ISTOCK
In a new study, researchers found an increased risk of multiple sclerosis (MS) among women who have taken oral contraceptives. However, the findings do not mean women should stop using birth control, the researchers say.

Utilizing membership data from Kaiser Permanente Southern California, researchers analyzed the health records of 305 women aged 14 to 48 who were diagnosed with MS or its precursor, clinically isolated syndrome (CIS), between 2008 and 2011.  They looked at the women’s birth control use up to three years prior to the onset of MS symptoms

Overall, researchers found a 30 percent increased risk of developing MS amongst women who had at least three months of oral contraceptive use, compared to a control group of 3,050 women who did not have MS. They found that 29.2 percent of women with MS used birth control before their diagnoses, while 23 percent of women in the healthy control group used birth control– showing an increased risk with higher use of the drug, study author Dr. Kerstin Hellwig, a post-doctoral research fellow at Kaiser Permanente Southern California, told FoxNews.com.

Additionally, for women who did not currently use an oral contraceptive but had in some time in the three years prior to being diagnosed, there was also a slightly higher risk.




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Blood Sample Might Predict MS

Blood Sample Might Predict MS

 
An antibody linked to MS may be detectable long before the onset of any symptoms.



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Thursday, February 27, 2014

February was a Whirlwind! How’s Your MS Today?

Published Feb 26, 2014

February is nearly over and we haven’t had our monthly check-in.  Sorry about that.  Back-to-back-to-back storms have helped the shortest month seem even shorter.
Last month we introduced the Life With Multiple Sclerosis Self-evaluation Scale (LWM3S).  It’s a simple 1-10 scale.  1= The best I’ve felt my symptoms since diagnosis with MS.  10= The worst I’ve felt my symptoms since diagnosis with MS.  This is a very personal scale and allows us to gauge our symptoms relative to the whole of our disease rather than some great 1= no MS, 10= dead medical scale.
You responded with great enthusiasm and several MS patient advocacy groups shared the idea.
So, we’ll keep it up!
We want to know the narrative behind your number, but try to put a figure on where you are relative to your whole life with MS.
Last month I was a 3.  Today I’d have to say that I’m closer to a 5.  Some new areas of hypersensitivity on my back are making the simple act of wearing a shirt or lying on the bed painful.  My legs feel a bit heavier than last month and an old foot pain seems to have settled back in.
Still – and this is one reason I like this scale – I can see that it’s not the worst I’ve ever been; not even close.  So, I’ve jumped two points on the LWM3S.  How’s your MS today?
Wishing you and your family the best of health.
Cheers
Trevis
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Gentle yoga an alternative for MS patients

February 26, 2014
RACINE COUNTY — Some people are content to sit back and relax when they retire, maybe traveling or working in their gardens.
Others want to turn their talents toward helping others. That was true of Jana Gasiorkiewicz.
About seven months ago, Gasiorkiewicz became a certified yoga instructor. Several months ago, she launched her Yoga on a Chair classes.
But her practice targets patients with multiple sclerosis and similar medical conditions. The classes are conducted on chairs “because so many people can’t get down on the mat,” she explains.
“You don’t need the stamina (to stand),” she said. “Without overtaxing those already weakened limbs and your heart, you can bring some movement and build some heat without exhausting yourself.”
Gasiorkiewicz retired in 2011 after working for 20 years for the Kenosha Unified School District. The last 11 years were spent teaching French at Bradford High School. She has been teaching one French class at the University of Wisconsin-Parkside since September.
After retiring, she said she had more time and started going to yoga classes at YogaRoots Racine, 518 College Ave., in Downtown Racine.
Gasiorkiewicz’s daughter, Suzanne Selmo, had become a yoga therapist in California. Gasiorkiewicz, 65, received her instructor certification in July. But then the question became whom would she teach?
She said a friend’s husband has Parkinson’s disease, and he benefited from yoga.
“It gave me the idea to target my practice to a particular audience,” Gasiorkiewicz said. “When I looked into it, I found there were many more MS patients than Parkinson’s patients.”
Multiple sclerosis is an often-disabling central nervous system disorder. Symptoms range from abnormal fatigue to memory, attention and vision problems, according to the National Multiple Sclerosis Society. Some patients may suffer some form of paralysis, or need help from a cane or crutches to work, according to the organization.
Because people with MS may have a limited range of motion, or may not be able to lie on the floor on mats, Gasiorkiewicz teaches her classes on chairs.
Source: Journal Times

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A Closer Look at Clinically Isolated Syndrome (CIS) and MS - Presented by Jack Burks, MD




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Tuesday, February 25, 2014

MS education


Dear Stuart:
        
         Your Programs have spread the growth of education about MS to thousands of people!

Thanks for asking about me but I have accepted that I cannot live the employment working and family lifestyle

that I had prior to my progression of my Multiple Sclerosis Development.

But I have accepted that I have to be dependent on to having to have others assist me to get me dressed and

put into a wheelchair so I can continue to move around my community. But I still have chosen to continue

still others that I can still be a Cofacilitator of MS support groups, visit and play games with seniors in rest homes and

be active in my local church.

But I don't think I could ever accomplish the wonderful job that you have developed and are presenting to people

Around the World.

Thank You,



Dave Lane
Support Group Facilitator
Cape Coral, Florida

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Some Antibiotics Linked to Serious Nerve Damage

By 
WebMD Health News

FDA warning sign
Aug. 27, 2013 -- The FDA is strengthening its warning that a popular class of antibiotics, called fluoroquinolones, may cause sudden, serious, and potentially permanent nerve damage called peripheral neuropathy.
Fluoroquinolones are antibiotics that are commonly used to treat a variety of illnesses such as respiratory and urinary tract infections. These medicines include ciprofloxacin (Cipro), gemifloxacin (Factive), levofloxacin (Levaquin),moxifloxacin (Avelox), norfloxacin (Noroxin), and ofloxacin (Floxin). More than 23 million patients received a prescription for one of them in 2011.
Peripheral neuropathy is damage to the nerves that send information to and from the brain and spinal cord and the rest of the body. Damage interrupts this connection, and the symptoms depend on which nerves are affected. In general, the symptoms are in the arms and legs and include numbness, tingling, burning, or shooting pain.
Peripheral neuropathy has been listed as a side effect of fluoroquinolones since 2004. There have been reports of long-lasting nerve damage and disability in patients taking this type of medication.
A recent FDA review revealed that the existing warnings for fluoroquinolones were inadequate. The FDA's newest alert requires that all drug labels and medication guides for fluoroquinolones be updated to better emphasize the risk for serious and potentially irreversible peripheral neuropathy.

Nerve Damage Risk: What You Need to Know

  • Peripheral neuropathy symptoms typically begin rapidly, within a few days of starting the fluoroquinolones.
  • Nerve damage symptoms may last for months or even be permanent, despite stopping the drug.
  • The risk for peripheral neuropathy appears to affect only those who take fluoroquinolones by mouth or by injection. Fluoroquinolones used in the eyes or ears are not linked to the risk.
  • Contact your doctor immediately if you develop numbness, tingling, weakness, burning, shooting pains, or other symptoms while taking a fluoroquinolone.
  • Your doctor may tell you to stop taking the medication and prescribe a different type of drug, unless the benefits of fluoroquinolones outweigh the risks. Never stop taking any medication before first talking to your doctor.

This is not the first serious warning for fluoroquinolones. In 2008, the FDA required a boxed warning, the most serious type of warning, to be added to the medications, alerting patients of the risk of tendon damage and rupture. 
The FDA encourages patients and doctors to report side effects to the FDA's MedWatch Safety Information and Adverse Event Reporting Program or call 800-332-1088.

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Sunday, February 23, 2014

Researchers Discover New Immunosuppressive Cells in MS Patients that inhibit EAE

Posted by: Mike Winters                                    - Feb 21, 2014


hematopoietic stem cell transplantation
Researchers have identified a new type of white blood cell that can suppress T-cell hyperactivity in experimental autoimmune encephalomyelitis (EAE), an animal model used to study multiple sclerosis (MS) and other human diseases that affect the central nervous system. Moreover, the group found that these blood cells were prominent in patients who responded to interferon-beta (IFN-β) treatment for MS. The results were published in the journal Nature Medicine on February 16, 2014.
The defective generation or function of white blood cells called regulatory T-cells (T-reg cells) in autoimmune disease contribute to chronic inflammation found in diseases such as MS, EAE, and various types of tissue injury.  Yawei Liu, and co-workers at BRIC, the University of Copenhagen, have discovered a group of T-cells that after ectopic expression of the FoxA1 gene, confer suppressive properties in a newly identified T-reg cell population named FoxA1+ T-reg cells. Development of these FoxA1+ T-reg cells occurs primarily in the central nervous system in response to autoimmune inflammation.  The group discovered that ectopic FoxA1 expression generates FoxA1+ T-reg cells that suppress T-cells by inducing activated apoptosis, programmed cell death. The FoxA1+ T-reg cells were adoptively transferred in mice and showed to inhibit EAE.  The researchers also found that the development of FoxA1+ T-reg cells is induced by the cytokine, IFN-β, and requires IFN-α/β receptor (Ifnar) signaling. This was concluded because the frequency of FoxA1+ T-reg cells was reduced in mice lacking the receptor.  Lastly, Yawei Liu, and co-workers discovered that patients with relapsing-remitting MS who exhibited a clinical response to treatment with IFN-β were associated with an increased frequency of the newly discovered FoxA1+ T-reg cells in the blood.

Source: BioNews
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Blood Tests May Detect Multiple Sclerosis Before Symptoms

By: CHRISTINE HSU             - February 21, 2014
Blood Test,
(Photo : Flickr/ tyfn)
Blood tests may detect multiple sclerosis years before symptoms appear, according to new research.
Scientists recently discovered an antibody in the blood of people with multiple sclerosis may be present long before the disease and its symptoms manifest.
"If our results can be replicated in larger populations, our findings may help to detect MS earlier in a subgroup of patients," study author Viola Biberacher, MD, with Technical University in Munich, Germany, said in a news release.
"Finding the disease before symptoms appear means we can better prepare to treat and possibly even prevent those symptoms. This finding also demonstrates that the antibody development to the KIR4.1 protein, a protein found in some people with MS, precedes the clinical onset of disease suggesting a role of the autoantibody in how the disease develops," Biberacher added.
The study compared 16 healthy blood donors who were later diagnosed with multiple sclerosis to 16 healthy blood donors who did not develop the disease. The blood samples were collected between two and nine months before the first symptoms of multiple sclerosis appeared.
Researchers focused on a specific antibody called the KIR4.1. They analyzed antibody levels in the blood at various time points up to six years before and after disease onset in those who had the KIR4.1 antibody in their blood.

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