ABOUT this BLOG and How to use it
WELCOME to Stu's Views & MS News, a product of MS Views and News, a Not-for-Profit 501(c3) organization. Founded in 2008. Providing Educational, Information and Resources to those affected by Multiple Sclerosis via live seminars and via the internet.
Key-Note: Our live MS educational seminars average approx 65 people per educational program and SINCE our first program in February 2010, we have hosted more than 80 educational programs in Florida. In 2013 we expanded to Georgia and in 2014 we will begin expansion into other States as well.
Be Empowered with MS News and Information
Saturday, March 8, 2014
Stairs posed a major barrier for disabled people in wheelchairs. A new Israeli technology is changing the rules of the game. bomber survives his attempted terrorist attack and arrives at a hospital next to his victims. In any other country, this script may seem to be totally fictional, however, in Israel; this cinematic concept is based on reality.
Mar 08, 2014, | Linda Lovitch
Until now, stairs posed a major barrier for disabled people in wheelchairs. A new Israeli technology is changing the rules of the game. Daniel Barel, the CEO explains, “Softwheel gives the freedom to get off the pavement , road, or staircase without using a ramp." The technology absorbs the shock when the wheelchair is lowered from one level to another.
Watch a video of this new technology and read more by clicking here: http://www.jerusalemonline.com/culture-and-lifestyle/new-invention-gives-disabled-a-smooth-ride-down-stairs-4125
Friday, March 7, 2014
ENDECE Neural to Present Updated Data at ASN Annual Meeting Showing NDC-1308 Induces Remyelination in Multiple Sclerosis (MS)
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Monday, March 3, 2014
President and Founder
And AN MS Patient
Sunday, March 2, 2014
Feeling the MS blues? Banish that bad mood with these treatment tactics.
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Lemtrada Update: First-of-Its-Kind Treatment for Relapsing-Remitting Multiple Sclerosis Now Available in Canada
LEMTRADA 12 mg has a dosing and administration schedule of two annual treatment courses. The first treatment course of LEMTRADA is administered via intravenous infusion on five consecutive days, and the second course is administered on three consecutive days, 12 months later. LEMTRADA patients require monitoring at regular intervals between treatment courses and for 48 months following the final infusion.
During an extensive, ongoing clinical development program, 80 per cent of RRMS patients who received two treatment courses of LEMTRADA required no further therapy1 and 55 per cent remained relapse-free through the first year of the extension study. Unlike other current disease modifying therapies (DMTs) in which stopping treatment usually results in resumed disease activity, LEMTRADA continues to have a durable effect far beyond the two annual treatment courses. In fact, in more than 70 per cent of clinical trial patients, disability scores improved or remained stable over three years.1
"The approval of LEMTRADA represents an important new treatment option for Canadians living with MS. In clinical trials, LEMTRADA demonstrated impressive effectiveness following two treatment courses for patients with active relapsing MS," said Dr. Anthony Traboulsee, Associate Professor of Neurology and Medical Director of the UBC Hospital MS Clinic of Vancouver Coastal Health. "Our own experience in treating 35 patients through clinical trials with LEMTRADA has been extremely positive."
LEMTRADA was approved by Health Canada in December 2013. The approval was based on data from the LEMTRADA clinical development program comparing treatment of LEMTRADA to high-dose subcutaneous interferon beta-1a (Rebif®) - which is dosed three times per week - in patients with RRMS who had active disease. In a controlled Phase 3 clinical study, LEMTRADA was more effective compared to Rebif at reducing both the annualized relapse rates (ARR) and the accumulation of disability was significantly slowed in patients given LEMTRADA vs. Rebif.2
In clinical trials, LEMTRADA demonstrated an ARR reduction of 49.4 per cent when compared with Rebif (p<0.0001), and the proportion of relapse-free patients was significantly (p<0.0001) higher in LEMTRADA patients than Rebif (65.4 per cent and 46.7 per cent, respectively). In addition, the risk of sustained accumulation of disability (SAD) over six months was reduced by 42 per cent in patients who received LEMTRADA versus Rebif (p=0.0084).2
"The approval and availability of LEMTRADA represents an important advancement for the MS community," said Dr. Karen Lee, Vice-President, Research, Multiple Sclerosis Society of Canada. "The more treatment options that are available, the more choices Canadians living with MS have to potentially improve their overall quality of life."
In November 2013, Genzyme's AUBAGIO® (teriflunomide) 14 mg was approved by Health Canada as monotherapy for the treatment of patients with RRMS to reduce the frequency of clinical exacerbations and to delay the accumulation of physical disability. The approval was based on efficacy data from two Phase III clinical trials - TEMSO (TEriflunomide Multiple Sclerosis Oral) and TOWER (Teriflunomide Oral in people With relapsing remitting multiplE scleRosis). In the TEMSO trial, AUBAGIO 14 mg significantly reduced the annualized relapse rate (p=0.0005) and the time to disability progression (p=0.0279) at two years versus placebo in patients with RRMS. In the TOWER trial, AUBAGIO 14 mg significantly reduced the annualized relapse rate (p=0.0001) and the time to disability progression sustained for 12 weeks (p=0.0442) was statistically significantly reduced versus placebo in patients with RRMS.
"The Canadian approval and availability of LEMTRADA and AUBAGIO represent an important milestone for Genzyme and demonstrate our focus on scientific innovation and commitment to MS patients," said Peter Brenders, General Manager, Genzyme Canada. "We are proud of our commitment to long-term leadership and partnership with the MS community."
LEMTRADA is supported by a comprehensive and extensive clinical development program that involved 1,188 patients, resulting in 2,363 patient-years of safety follow-up.
A New Standard in Patient Support
Complete story found here: http://www.digitaljournal.com/pr/1762094#ixzz2upmX4zaY
Saturday, March 1, 2014
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
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.
Research showing advances in Axon restoration, cognitive performance, And a hopeful medication for Primary & Secondary-progressive multiple sclerosis
Friday, February 28, 2014
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