JamesEckburg and Multiple Sclerosis Fingolimod

The information in this medication sheet has been adapted from the FDA-approved prescribing information for Gilenya.
Description

Gilenya™ is a new class of medication called a sphingosine 1-phosphate receptor modulator, which is thought to act by retaining certain white blood cells (lymphocytes) 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.

Gilenya was evaluated in two large-scale, phase III clinical trials involving people with relapsing-remitting MS:

In a two-year study (FREEDOMS) comparing two doses of Gilenya to placebo, Gilenya (at the lower, 0.5mg dose) reduced relapses by 54% and reduced the risk of disability progression by 30% compared to placebo. Gilenya also reduced brain lesion activity as measured by MRI. In a one-year study (TRANSFORMS) comparing two doses of Gilenya to interferon beta-1a (Avonex), Gilenya (at the lower, 0.5mg dose) reduced relapses by 52% compared with Avonex; reduced disease activity as measured by the number of new and newly enlarged T2 lesions on MRI scans compared with Avonex (1.6 vs 2.6, respectively at one year); reduced brain lesion activity as measured by MRI.

In August 2011, the FDA approved an update in the prescribing information for Gilenya to include the MRI findings from both the TRANSFORMS and FREEDOMS studies. In both clinical trials, Gilenya showed a reduction in gadolinium-enhancing lesions, which indicate new MS activity. The data from the TRANSFORMS study indicated that at 12 months, the mean number of gadolinium-enhancing T1 lesions was significantly lower for patients treated with Gilenya at the 0.5 mg dose than for patients taking interferon beta-1a (Avonex), 0.2 vs 0.5 respectively. In the FREEDOMS trial, the mean number of gadolinium-enhancing T1 lesions was significantly lower at 24 months for the group treated with Gilenya (0.5 mg dose) than for the placebo group, 0.2 vs 1.1.

Gilenya has not been studied in people under the age of 18.

Approval by the U.S. Food and Drug Administration (FDA)

Gilenya was approved by the U.S. Food and Drug Administration (FDA) in 2010 for adults with relapsing forms of MS to reduce the frequency of clinical relapses and to delay the accumulation of physical disability.

http://www.youtube.com/watch?v=JSJaDWheyGk&feature=colike

In April, 2012, the FDA (along with the European Medicines Agency -- EMA) revised the prescribing information for Gilenya based on independent safety reviews initiated by the agencies after deaths had been reported among patients taking Gilenya. The revised prescribing information defines who should avoid using this MS therapy based on pre-existing medical conditions, and alters the recommended testing and heart monitoring that occurs when the first dose is given:

All those starting treatment with Gilenya should have an electrocardiogram prior to dosing and after the 6-hour observation period. During the observation period, blood pressure and heart rate should be measured hourly.

People whose first-dose monitoring indicates potentially unsafe heart events may require longer monitoring, and any who require treatment for low heart rate during the first-dose monitoring will need to be monitored overnight.

Gilenya is not advisable for people who have had a history or presence of specific heart and vascular conditions, including heart attack, stroke, and heartbeat irregularities, and people taking heart rate-lowering medication.

If anyone with a pre-existing heart condition is started on Gilenya, after the first dose the patient should be monitored overnight with continuous electrocardiogram in a medical facility. The heart function monitoring applies only to people initiating their first dose, and not to people who are already taking daily doses of Gilenya. There are also revised recommendations for people who re-initiate treatment after discontinuing Gilenya. People should not make changes to their Gilenya therapy without consulting their prescriber.

http://www.youtube.com/watch?v=lUS5Tiq5O28&feature=colike

Macular Edema:

Oral MS Drug May Increase Risk for Macular Edema A report from the North American Neuro-Ophthalmology Society (NANOS) and the AAO

ONE Neuro-Ophthalmology Committee

*ONE Neuro-ophthalmology chair: Andrew G. Lee, MD for the ONE Committee Data from recent multinational Phase 2 and 3 clinical trials of fingolimod (Gilenya, Novartis) suggest an association of the agent to a low risk of cystoid macular edema (CME). Fingolimod is the first oral medication approved by the U.S. FDA for relapsing forms of MS and is an immunomodulator that regulates lymphocyte distribution, reducing lymphocyte recirculation from lymphoid tissue to blood and peripheral tissues. A two-year FDA clinical trial compared fingolimod with placebo and another one-year trial compared fingolimod with interferon beta-1a.

Although several clinical trials to date have shown fingolimod to be well tolerated, side effects have included bradycardia, headache, upper respiratory tract infection, shortness of breath, diarrhea and nausea. In the two-year trial, macular edema occurred in 0.4 percent of patients treated with fingolimod and 0.1 percent who received the placebo.

Study patients were monitored with medical histories, visual acuity, contrast sensitivity, dilated ophthalmoscopy, optical coherence tomography (OCT), and had ophthalmic examinations at 1, 3, 6, 12 and 18 months. Compared to placebo, Fingolimod reduced the MS relapse rate and increased the percentage of patients without a MS relapse in both studies. The differences were statistically significant.

http://www.youtube.com/watch?v=i7hG_YS1WiE&feature=colike

Transient bradycardia, HTN

Because of the risk of transient bradycardias and heart block after the first dose, the recommended level of cardiovascular monitoring of all patients after their first dose of fingolimod has now increased as outlined here

Fingolimod (Gilenya▼) is authorised to treat relapsing-remitting multiple sclerosis in patients whose disease has failed to respond to beta-interferon or is severe and getting worse rapidly. It is a sphingosine-1 phosphate receptor modulator.

Fingolimod is known to cause transient bradycardias and might be associated with atrioventricular block after the first dose; these are reflected in existing recommendations to observe patients for signs and symptoms of bradycardia in the 6 hours post administration.

The European Medicines Agency (EMA) has started a review of the benefits and risks of fingolimod after becoming aware of new post-marketing evidence about its possible cardiovascular effects after taking the first dose. This includes a 59-year-old patient from the USA with multiple sclerosis who died within 24 hours of taking the first dose of Gilenya. This patient was being treated with metoprolol and amlodipine for hypertension.

The exact cause of death is currently unknown. In addition to the unexplained death in the USA, six other unexplained deaths (including three cases of sudden death) after starting treatment with fingolimod have also been reported. As at Feb 6, 2012, we have received four UK reports of suspected adverse reactions with fingolimod, including one case of bradycardia and hypotension occurring 4 hours after the first dose with a drop in heart rate experienced again the following day.

While the review of fingolimod is ongoing, the EMA’s Committee for Medicinal Products for Human Use now recommends that the level of cardiovascular monitoring of all patients is increased after their first dose of fingolimod:

Patients that are taking this drug have to be watched and check on redularly with their Doctors. Their care has to be writen down and saved for research.

http://www.youtube.com/watch?v=L7UvhwORTd4&feature=colike
This is just some of the side effects of Fingloimod in the treatment of Multiple Sclerosis.

James Eckburg
Senior Health and Wellness Strategist
www.Jamescornershop.com,
www.eckburgjoe.veretekk.com
114 E. Franklin St.
Lanark, Illinois 61046
skype: jamesoeck1
joeckburg@gmail.com

James Eckburg and MS

The Three Faces of Fatigue with Multiple Sclerosis

I would like to talk about tree facesof Fatigue: One is Physical, Second one is Mental, and the Third one Emotional. The first one is Physical is extremely comon. Fatigue strikes about four out of five people with Multiple Sclerosis and it is so real. "Multiple Sclerosi fatigueis genuine and has a biologial basis", that Lauren Krupp, MD, Professor of Neureology and Diretor of Neuropsychology research center at Stony Brook University Medical Center in New Yourk.

Multiple Sclerosis fatigue can be distinguished from the garden-variety fatigue when it si abnormally severe, but there are markers that a person has with Multiple Sclerosis. Fatigue temds to accur daily and they can aome on suddenly without much worning. You may feel grood in the morning when you get up and than in middle morning you feel very tired and you have had a good nights sleep. Than as the day goes on you get very tired or fatigue. When it gets very hot and humid is the worst time for me.

Why do I get so tired??

The Primary Multiple Sclerosis fatigue is casused by frayed nerve fibers wearing out easily. You see nerve damage to the vast computer system of the brain causes misfires and split-second dekays in impulse transmissions, this was said by George Kraft, MD, MS Alvord Professor of Research at the University of Washington Medical Center in Seattle.

You will see that your walking becomes more difficult, your speach will slurs and your mind clouds and overtaxed nervous system burns through fuel like aragged motor. YOu see that Fatigue is like a fuel gauge telling you the tank is empty.

Your Secondary energy-sappers include not enough sleep or quality sleep, depression, medication, stress, pain, being out of shape, and the sheer increase inengery used to get around and get things done.

Given the nature of MS, it is expected that central fatigue contributes to fatigue perceived by MS patients.22 Central fatigue is commonly measured with the twitch-interpolated technique during a maximal contraction. The underlying principle is relatively simple.23 During an MVC, a stimulus is given to the appropriate nerve or muscle. If participants activate their muscles maximally, no increase in force is evoked by this stimulus. During a submaximal activation, however, an extra force is evoked.

The size of the interpolated twitch gives a measure of the voluntary activation, and an increase over time reflects central fatigue.8 However, during a sustained contraction, the evoked twitch tends to decline as a result of fatigue-related changes in the periphery. Because the amount of peripheral fatigue differs between MS patients and controls,10,14 it is necessary to correct for peripheral fatigue. Studies that investigated the association between perceived fatigue and central fatigue in MS patients did not always correct for peripheral fatigue.

http://www.youtube.com/watch?v=O3iXoh3fh7w&feature=colike

http://www.youtube.com/watch?v=VQFrmW3K9Bk&feature=colike

Though the casuses of fatigue are understood it is not clear why differentpeople exercise fatigueso differently. Luca Roccatagliata, MD, PhD, and his Neuriscience colleagues at the University of Genoa speculate that anatomical changes tothe brain exist in a complex biological network that is different in every person. That is another reson why Multiple Sclerosis isso diffcult to diagnois. Thus so even tiny bit of damage in the front part of your brain called the frontal lobes can causean action to interact badly with the helathier part of your brain in the healthy deeper part of your brain. Thus so it iwll enhance the nature and preception of fatigue in some unique way.

J. Lamar Freed, Psy.D. wrote anarticle on Understanding the Unique Role Of Fatigue In Multiple Sclerosis:

Yet despite this recognition I do not believe fatigue has been taken as seriously nor viewed as profoundly as what the experience of people with MS merits. Fatigue is a symptom of MS. But is so much more than that. Fatigue underlies and influences a great many of the other symptoms experienced by people with MS.

The essential mechanism of MS is that the Brain's Myelin covered nerve cells that communicate the commands and information from one part of the Brain to another or to other parts of the body are impeded or blocked by the destruction of the Myelin sheath which surrounds and insulates the cells.

These communication cells serve as the superhighway that makes these messages travel quickly and easily. This means that for the information to travel properly when the Myelin has been destroyed or damaged it must bully through on less efficient channels, or go around on other channels that may not be ideally constructed for the task.

It's like getting from New York to Washington without driving on I-95. Depending on the locations and number of these Myelin depleting lesions, communication within the Brain can be profoundly disrupted. Like with drives that last too long, fatigue is one of the results.

Fatigue is experienced both physically and mentally. It is sometimes easily evident because of a feeling of general tiredness and it can also be overlooked.

It can show itself immediately and it can be delayed, at times for days. Its primary treatment is rest. And like everything else about MS, it is highly variable from one person to the next.

Physical fatigue is often experienced as a bone numbing tiredness. It is a tiredness that belays description. It can make movement seem impossible and the requirement for movement overwhelming.Yet despite this recognition I do not believe fatigue has been taken as seriously nor viewed as profoundly as what the experience of people with MS merits. Fatigue is a symptom of MS. But is so much more than that. Fatigue underlies and influences a great many of the other symptoms experienced by people with MS.
The essential mechanism of MS is that the Brain's Myelin covered nerve cells that communicate the commands and information from one part of the Brain to another or to other parts of the body are impeded or blocked by the destruction of the Myelin sheath which surrounds and insulates the cells.
These communication cells serve as the superhighway that makes these messages travel quickly and easily. This means that for the information to travel properly when the Myelin has been destroyed or damaged it must bully through on less efficient channels, or go around on other channels that may not be ideally constructed for the task.
It's like getting from New York to Washington without driving on I-95. Depending on the locations and number of these Myelin depleting lesions, communication within the Brain can be profoundly disrupted. Like with drives that last too long, fatigue is one of the results.
Fatigue is experienced both physically and mentally. It is sometimes easily evident because of a feeling of general tiredness and it can also be overlooked.
It can show itself immediately and it can be delayed, at times for days. Its primary treatment is rest. And like everything else about MS, it is highly variable from one person to the next.Yet despite this recognition I do not believe fatigue has been taken as seriously nor viewed as profoundly as what the experience of people with MS merits. Fatigue is a symptom of MS. But is so much more than that. Fatigue underlies and influences a great many of the other symptoms experienced by people with MS.
The essential mechanism of MS is that the Brain's Myelin covered nerve cells that communicate the commands and information from one part of the Brain to another or to other parts of the body are impeded or blocked by the destruction of the Myelin sheath which surrounds and insulates the cells.
These communication cells serve as the superhighway that makes these messages travel quickly and easily. This means that for the information to travel properly when the Myelin has been destroyed or damaged it must bully through on less efficient channels, or go around on other channels that may not be ideally constructed for the task.
It's like getting from New York to Washington without driving on I-95. Depending on the locations and number of these Myelin depleting lesions, communication within the Brain can be profoundly disrupted. Like with drives that last too long, fatigue is one of the results.
Fatigue is experienced both physically and mentally. It is sometimes easily evident because of a feeling of general tiredness and it can also be overlooked.
It can show itself immediately and it can be delayed, at times for days. Its primary treatment is rest. And like everything else about MS, it is highly variable from one person to the next.Yet despite this recognition I do not believe fatigue has been taken as seriously nor viewed as profoundly as what the experience of people with MS merits. Fatigue is a symptom of MS. But is so much more than that. Fatigue underlies and influences a great many of the other symptoms experienced by people with MS.
The essential mechanism of MS is that the Brain's Myelin covered nerve cells that communicate the commands and information from one part of the Brain to another or to other parts of the body are impeded or blocked by the destruction of the Myelin sheath which surrounds and insulates the cells.
These communication cells serve as the superhighway that makes these messages travel quickly and easily. This means that for the information to travel properly when the Myelin has been destroyed or damaged it must bully through on less efficient channels, or go around on other channels that may not be ideally constructed for the task.
It's like getting from New York to Washington without driving on I-95. Depending on the locations and number of these Myelin depleting lesions, communication within the Brain can be profoundly disrupted. Like with drives that last too long, fatigue is one of the results.
Fatigue is experienced both physically and mentally. It is sometimes easily evident because of a feeling of general tiredness and it can also be overlooked.
It can show itself immediately and it can be delayed, at times for days. Its primary treatment is rest. And like everything else about MS, it is highly variable from one person to the next.
Physical fatigue is often experienced as a bone numbing tiredness. It is a tiredness that belays description. It can make movement seem impossible and the requirement for movement overwhelming.

James Eckburg
Senior Health and Wellness Strategist
www.Jamescornershop.com,
www.eckburgjoe.veretekk.com
114 E. Franklin St.
Lanark, Illinois 61046
skype: jamesoeck1
joeckburg@gmail.com

James Eckburg and MS

Treating Multiple Sclerosis Pain

Some people say that they do not have any pain with Multiple Sclerosis. I can tell you that I have had pain all the time with my Multiple Sclerosis. The pain is not in the same place all the time but it is very painfull when it stikes. I have been on the same meds for a long time and the side effects of the medicne is rough. So my new neurologist Dr. is trying me on something new for a month. I can not take any of the new meds that have come on the market to treat MS becasue I can not walk and have been in a wheelchair since 1989. I had very bad tremmors and I gained weight and got up over 300 lbs. So back in April of 2007 I strated a program and have lost over 110 lbs and have kept it off. You might not think that is good but remember I can not walk so the only exercise I can do is ride a stationary bike and I have woren out 12 of them. I try to do at least 30+ miles a day. That is jsut an update of my condition. I have to be watched very close these next few weeks and months to see how this new meds work. Becasuse with MS it strikes a person differently so not all meds work the same.

So now I would like to share some articles I found on the subject of Treating Multiple Sclerosis Pain. Many options are available to treat pain in patients with multiple sclerosis. But the big question is will they help you manage your pain.

Anticonvulsant Drugs Offer Relief

For the most part, however, acute MS pain can't be effectively treated with aspirin, ibuprofen, or other common OTC pain reliever medications or treatments. "Since most MS pain originates in the central nervous system, it makes it a lot more difficult to control than joint or muscle pain," says Kathleen Hawker, MD, an assistant professor of neurology in the multiple sclerosis program at the University of Texas Southwestern Medical Center in Dallas (UTSW).

So what's the alternative? In many cases, the treatment of choice is one of a range of anticonvulsant medications, such as Neurontin and Tegretol. "The main thing that links them all up is that we're not quite sure how they work -- either for seizures or for pain," says Hawker. Since the FDA hasn't officially approved these anticonvulsants for the treatment of pain, they're all being used "off-label," but Neurontin, for example, is prescribed five times more often for pain than for seizures, says Hawker.

Recommended Related to Multiple Sclerosis

Multiple Sclerosis Medications

Ampyra (dalfampridine) Aventyl HCI (nortriptyline) Avonex (interferon beta-1a) Betaseron (interferon beta-1b) Carbatrol (carbamazepine) Copaxone (glatiramer) Dantrium (dantrolene) Decadron (dexamethasone) Duralone (methylprednisolone) Endep (amitriptyline) Epitol (carbamazepine) Extavia (interferon beta-1b) Klonopin (clonazepam) Lioresal (baclofen) Medipred (methylprednisolone) Medralone ...

"In the vast majority of patients, these medications do work," says George Kraft, who directs the Multiple Sclerosis Rehabilitation, Research, and Training Center and the Western Multiple Sclerosis Center at the University of Washington in Seattle. "There's a problem, though, in that most of them can make people sleepy, groggy, or fatigued, and MS patients have a lot of fatigue anyway."

The good news: Most pain in MS can be treated. There are more than half a dozen of these anticonvulsants, and they all have a slightly different mechanism of action and different side effects. The side effects of these drugs can also include low blood pressure, possible seizures, and dry mouth. They can also cause some weight gain.

"Some drugs are so similar to each other that if one drug in the class fails, another is unlikely to work," says Hawker. "That's not the case with these. Which one you use for which patient depends on the side effect profile."

Finding the right anticonvulsant is all about trial and error, says Bethoux. "We'll start them at the lowest possible dose of one medication and increase it until the person feels comfortable or until side effects aren't tolerable. If one medication doesn't work, we'll try another," he says. "It's a process that can take a long time, but it's the only way we have to do this."

New Frontiers in Treatment

Some patients, however, still haven't found the right drug and the right dosage to control their pain. "About 1% to 2% of patients have extremely refractory pain that's very hard to manage," says Kraft. So MS experts are still looking for options to add to their treatment arsenal.

One intriguing possibility: Botox. The anti-wrinkle injections popular with Park Avenue socialites have shown promise in helping to control some types of MS pain. Botox, which acts locally to temporarily paralyze a nerve or muscle, has been used for years at some multiple sclerosis clinics, including Hawker's, to manage spasticity and bladder problems. "Serendipitously, we found that it also seemed to have an effect on pain," she says. "It's far from being a known treatment for pain in MS at this point, but it's an exciting possibility."

http://www.youtube.com/watch?v=mdIUqZ-2p18&feature=colike

http://www.youtube.com/watch?v=SaqbQAVNLTo&feature=colike

UTSW, along with two other centers, will soon be launching a small study involving about 40 patients with MS to assess whether Botox can indeed relieve the stabbing pain of trigeminal neuralgia.

"There are no systemic side effects, only mild local facial weakness. The biggest drawback is that you can only inject it in a limited area, so even if we do find that it's effective against MS pain, Botox will certainly not replace any of the medications we currently have. But it may be used in very specific conditions like trigeminal neuralgia," Hawker says.

Kraft, meanwhile, has recently begun a study looking at a very different approach to MS pain: hypnosis. "It's well known that there is a 'gating' mechanism in the higher cognitive parts of the brain to let signals come through to the consciousness. There can be all kinds of mischief in the pain fibers in the spinal cord, but it has to get through to the cortex before it's painful," he says.

"With hypnosis, we hope to block or at least reduce the interpretation of that stimulus as a painful stimulus. It looks promising so far, and obviously it doesn't have the problem of medication side effects."

James Eckburg
Senior Health and Wellness Strategist
www.Jamescornershop.com,
www.eckburgjoe.veretekk.com
114 E. Franklin St.
Lanark, Illinois 61046
skype: jamesoeck1
joeckburg@gmail.com

James Eckburg and Multiple Sclerosis and Vitamin D

Vitamin D Deficiency and Multiple Sclerosis

(NaturalNews) Researchers from Oxford University and the University of British Columbia have discovered that Vitamin D deficiency affects a section of the human genome already linked with multiple sclerosis (MS) risk, adding further weight to theories that this vitamin deficiency might play a role in development of the disease.

"Here we show that the main environmental risk candidate -- vitamin D -- and the main gene region are directly linked and interact," said co-author George Ebers.

The study was published in the journal PLoS Genetics.

MS is a disease characterized by the loss of the myelin sheath that insulates cells in the central nervous system. The loss of this insulation leads to disordered transmission of nerve signals, causing a cluster of neurological and muscular symptoms.

Scientists do not know what causes MS, but both genetic and environmental factors have been implicated. One study found that rates of the disease were significantly higher among Northern European populations who receive less sunlight than among those who receive more, suggesting a vitamin D link.

Vitamin D is produced by the body upon exposure to sunlight, and deficiencies are common in areas of the world far from the equator. The vitamin is now believed to play a critical role in immune functioning and the prevention of autoimmune diseases.

MS is highly suspected of being an autoimmune disorder.

In the current study, researchers examined a portion of chromosome six known to play a role in MS risk -- the risk is three times higher among those carrying one copy of the DRB1*1501 gene variant on this chromosome, and 10 times higher among those carrying two. They found that proteins activated by vitamin D bind to and alter the functioning of a section of the chromosome right near this gene. This suggests that vitamin D deficiency during pregnancy might alter the function of fetal genes, predisposing children to MS.

"Our study implies that taking vitamin D supplements during pregnancy and the early years may reduce the risk of a child developing MS in later life," lead researcher Sreeram Ramagopalan said.

Sources for this story include: news.bbc.co.uk.

Learn more: http://www.naturalnews.com/025791.html#ixzz1tAadCWkn

Role of Vitamin D Supplementation

The role of vitamin D supplementation in preventing these diseases is also not well understood.

Exposure to sunlight is an efficient way to raise blood levels of vitamin D hormone, and food sources of the nutrient include oily fish like salmon, fortified milk, and other fortified foods.

But most people would have a hard time getting the vitamin D they need from food, and the increased use of sunscreen has reduced sun exposures.

By one recent estimate, as many as half of adults and children in the U.S. were deficient in the vitamin.

Current recommended daily vitamin D intake is 200 IU (international units) for those up to age 50; 400 IU for people 51 to70; and 600 IU for those over 70. Most experts say that these doses are too low.

Many experts, including Ramagopalan, say 2,000 IU of the vitamin may be optimal for preventing disease.

Blood levels of the vitamin are measured as 25-hydroxyvitamin D. Levels below 20 nanograms per milliliter are generally considered deficient.

Harvard School of Public Health nutrition researcher Edward Giovannucci, MD, says blood 25-hydroxyvitamin D levels of between 30 and 40 nanograms per milliliter may be about right for reducing the risk of autoimmune diseases and certain cancers.

While he says some people can reach these levels without supplementation, many others would need to take 1,000 to 2,000 IU of the vitamin a day.

"Based on what we know, I think it is reasonable to recommend that people maintain blood levels of around 30 nanograms per milliliter," he says.

Nutrition Can Save America!

http://www.youtube.com/watch?v=dsWBo2dcdbc&feature=colike

James Eckburg
Senior Health and Wellness Strategist
www.Jamescornershop.com,
www.eckburgjoe.veretekk.com
114 E. Franklin St.
Lanark, Illinois 61046
skype: jamesoeck1
joeckburg@gmail.com