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Saturday, December 31, 2011

An MS Patient's story: Resilient Ann Romney has key role in husband's campaign Read more: Resilient Ann Romney has key role in husband's campaign


By Salena Zito, PITTSBURGH TRIBUNE-REVIEW
Saturday, December 31, 2011

AMES, Iowa -- Ann Romney wasn't always comfortable talking about her husband's prospects for becoming president, whether on stage or engaging people one-on-one.


"I was definitely burned out after the last experience," she said during a ride on the Mitt Romney campaign bus, which sported a banner across the window from a "Keep Michigan on the Move" campaign by her late father-in-law, Gov. George Romney.
Mitt Romney's failed 2008 presidential race left his wife of 42 years emotionally drained, she confessed. "You have expectations. It is crushing; it takes a lot out of your life."
When they considered Romney's run this time, she initially thought, "Well, not doing that one again." He reminded her on stage recently that she said the same thing after the birth of each of their five sons.
Their spirits should be buoyed at this moment, given Romney's rise to the top of polls in Iowa just before the Republican caucuses on Tuesday. An NBC-Marist poll released Friday showed Romney and Texas Rep. Ron Paul virtually tied for the lead among likely caucus-goers.
Wearing white pearls to offset her black pants and sweater, the former first lady of Massachusetts was readying to introduce her husband at Kinzler Construction Co. It's her role at each stop on his Iowa bus tour.
At 62, a grandmother of 16, she has dealt with situations far more devastating than her husband's losing the GOP nomination to Arizona Sen. John McCain three years ago. Diagnosed with multiple sclerosis in 1998, she struggled immediately with how to behave as a sick person. Before that, Ann Romney ran the household -- cooking meals, paying bills, mothering their children.
"I was in a pretty bad hole," she said. "I went from being completely normal to hardly being able to get out of bed. I was really, really sick, completely fatigued." Her medications, she said, made her feel worse. "I kept thinking, 'I am not getting better, and this is now my life?' "
She still gets teary-eyed at the memory of her husband's response, when she knew her role in the family had changed. "He told me, 'Don't worry about it; we will be OK. Those things that you do don't matter. You matter,' " she recalled. "It took this huge burden away, that I could be sick."
Eventually, her goal became not to be sick -- though in 2008, she weathered a second health scare when a mammogram detected early-stage breast cancer. She underwent a lumpectomy. She found that riding horses helps her to manage her MS, and she has become an accomplished amateur competitor in equestrian contests.
Ann Romney's engaging presence is an important aspect to the campaign.

Read more: Resilient Ann Romney has key role in husband's campaign - Pittsburgh Tribune-Review http://www.pittsburghlive.com/x/pittsburghtrib/news/s_774398.html#ixzz1iAHuEkEV




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Multiple Sclerosis May Cause Changes in Thalamus: Study



FRIDAY, Dec. 30 (HealthDay News) -- New research suggests that in addition to the disabling lesions it's known to cause, multiple sclerosis also damages the part of the brain that affects thinking skills, motor function and the senses.
"The thalamus is a central area that relates to the rest of the brain and acts as the 'post office,'" study co-author Khader Hasan, an associate professor at University of Texas Health Science Center at Houston, said in a university news release. "It also is an area that has the least amount of damage from lesions in the brain, but we see volume loss, so it appears other brain damage related to the disease is also occurring."
Hasan and colleagues published their observations in a recent issue of the Journal of Neuroscience.
The study authors noted that aging alone can bring about changes in the size of the thalamus region, resulting in some shrinkage after age 70. However, the research team wanted to see if multiple sclerosis (MS) -- which is often associated with the onset of dementia -- accelerates such structural shifts.
The radiology researchers used cutting-edge MRI scanning equipment to analyze brain structure in 109 MS patients, compared to 255 healthy men and women.
The result: MS patients had greater volume loss in the thalamus region than healthy patients, after accounting for age. And the greater the loss in thalamus volume, the more disabled the patient was, the investigators noted.
"This is looking at multiple sclerosis in a different way," Hasan said in the news release. "The thalami are losing cellular content and we can use this as a marker of what's going on. If we can find a way to detect the disease earlier in a more vulnerable population, we could begin treatment sooner."



Source: Healthday



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an MS Patients' Story: A miraculous life WITH LDN




by Chris Norwood

Dec 31, 2011 

Lucretia Roberts Page, Bill Roberts and Amy Roberts Grimes visiting each other before Bill began treating his MS with LDN, and was confined to a wheelchair. Submitted photo
SYLACAUGA — There is no cure for multiple sclerosis.

Bill Roberts of Sylacauga, who was diagnosed with the disease in 1998, is well aware of this, and yet he has managed to live with the disease and remain highly functional, thanks to an unconventional treatment: Low dose Naltrexone.

Roberts was working as a full-time firefighter for the city of Sylacauga on New Year’s Day 1998 when he said his entire side went numb and stayed that way. “I had symptoms going back to the 1970s, but they always went away,” he said. “And I had a younger sister that had it, but back then they said it wasn’t genetic.”

Roberts said at first he “thought I had just been watching football too long. I was at station two at the time, and I called station one to let them know what was going on. Then I went to the emergency room the next morning. The doctor started sticking me with a safety pin. By the time he was done, there was blood just running out of me but I never felt a thing. So he sent me to a neurologist in Birmingham, they did an MRI, and I was diagnosed with MS.”

After being transferred to University of Alabama Birmingham Hospital, Roberts “spent the next three years going down fast. I took all the treatment I could take, but the more I took, the faster the disease progressed.”

He was able to stay with the Sylacauga Fire Department as an inspector long enough to get 10 years of service in for retirement purposes, but was unable to work after that. He also had worked as a landscaper for many years, another thing he couldn’t do any more.

In August 2002 he underwent a six month chemotherapy treatment as an experiment. “Cytoxin is nasty stuff,” he said. “I’d go in Friday, come back out at 9 a.m. and 10 minutes later I’d be throwing up. It took me about a month to get over each treatment, and by then it was time to do it again. The last time, I actually lost 32 pounds in one day.”

The situation got worse in April 2003. Roberts came down with the flu, and since the chemotherapy had effectively wiped out his immune system, he was unable to fight off the disease on his own.

“Any kind of infection, I ended up in the emergency room,” he said. “They thought I had spinal meningitis, so they took me to do a lumbar puncture and hit an artery. They were going to have to transfer me to a private hospital, so they put me on a room on the fourth floor and then forgot about me for the next 17 hours. My wife finally got me to St. Vincent’s, and she stayed with me the whole time, three or four weeks.”

His temperature peaked at 106 degrees, and even after the fever broke, he would be unable to walk for the next two and a half years.

By June 2005, he was catheterized and, due to steroid treatments, his weight was up to 310 pounds. “My doctor said he didn’t know what to do,” he said. “He told my wife I probably wouldn’t make it another 16 months.”

At this point, Roberts met Emily Riser at Lakeshore, who treats MS cases exclusively. “She ran all the tests and recommended another round of chemo.”_Roberts had other ideas. He said he had begun reading about a treatment called low-dose Naltrexone, which had shown some promising results.

The drug itself is designed to fight withdrawal symptoms of alcohol and opiates, which is what it is marketed for. But in small doses, it had also shown promising results in treating a host of maladies, including MS.

“She didn’t recommend it, but I said give me three months and if I don’t see any results, we’ll go back to chemo. I took one and a half milligrams the first two weeks, then three milligrams after that, which is what I’m still taking today. By the end of the first month, I noticed I had more strength, and that I could stand up for more than a few seconds and take more than a couple of steps on my own. When I went back in three months, I walked in on my own without assistance.”

Unfortunately, his sister’s disease was far too advanced to be arrested by LDN. “She was in a nursing home for 20 years before she passed, and she always had a smile. At the end, her bones were so brittle she couldn’t even hold a spoon.”

Roberts’ twin sister moved in with the younger sister in Tuscaloosa and helped “make sure she kept up with everything. She always active in net support groups, and she asked people to send cards from all over the world. She got cards from Israel, from Turkey, from Australia and from every state in the union. She told me she got one card with a stamp on it that cost $5.”

Read more:The Daily Home - A miraculous life



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..............................

Disability-Benefits System Faces Review




The Social Security Administration has commissioned an independent review of the federal disability system amid concerns it awards benefits to those who don't deserve them and denies benefits to those who do.

A focus of the study is expected to be the work of roughly 1,500 administrative-law judges, who hear appeals by applicants but whose award rates vary widely.

Meanwhile, the Social Security Administration next week plans to stop notifying people applying for benefits of which judge they've been assigned for their case. This is being done, someone briefed on the plan said, to prevent applicants and their lawyers from trying to shop their appeals to the most lenient judges.
The review will be undertaken by the Administrative Conference of the United States, which studies government policy in Washington. The conference said it planned to release recommendations for overhauling the disability-appeals process next year.



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Mists Lift on Laquinimod in MS



By John Gever, Senior Editor, MedPage Today
Published: December 30, 2011


As part of the Year in Review series, MedPage Today reporters are revisiting major news stories and following up with an analysis of the impact of the original report, as well as subsequent news on the topic. Here's what's happened with the investigational multiple sclerosis drug laquinimod since we published the first 2011 piece on its safety and efficacy.

The investigational oral drug laquinimod has stirred interest in the multiple sclerosis community like few other agents have. Not only can it be taken as a daily pill instead of by injection, but clinical trials are suggesting it is better than existing MS drugs at slowing disability progression and that it may be suitable as an add-on to current treatments.

But the enthusiasm has been somewhat dampened by a mystery surrounding its mechanism of action. Studies in animals and humans indicated that laquinimod alters immune cell activity to reduce the destruction of nerve fibers' myelin sheaths. How it does so, though, has been unclear.

And people get nervous when they don't know how a new drug works, if only because it thwarts prediction of potential adverse effects.

However, announcements of results from two major phase III trials earlier this year have now been followed by a report that claims to uncover the key to laquinimod's mechanism of action.

The Backstory
Laquinimod is a derivative of roquinimex, an immunomodulatory drug first developed in the 1980s that drew substantial attention as a potential MS treatment.

Although early clinical studies indicated that roquinimex (also known as linomide) was well-tolerated, serious cardiovascular effects turned up when the drug went into larger trials. Phase III studies were halted in 1997 when two deaths and eight nonfatal myocardial infarctions occurred in two trials involving a total of about 1,200 patients.

But the initially promising results meant that the drug's quinoline-carboxamide structure could perhaps be tweaked to reduce the side effects while preserving the desired immunomodulatory properties.
Laquinimod came along shortly after roquinimex's demise, with a 2002 report that it blocked an animal model of autoimmune neuritis.

Interest in the drug was piqued earlier this year with presentations of results from the phase III ALLEGRO and BRAVO trials.

ALLEGRO was reported in April at the American Academy of Neurology's annual meeting in Honolulu, while results from BRAVO came out at the October joint meeting of the European and Americas Committees for Research and Treatment in MS in Amsterdam.

The overall picture painted by the two studies was consistent -- laquinimod's efficacy was relatively modest by traditional measures of relapse rates, but was very strong in terms of disability progression.
BRAVO was especially convincing in the latter regard, because it tested beta-interferon as well as laquinimod in the placebo-controlled trial.

The study design did not include a direct head-to-head comparison of the two drugs, but reductions in disability progression relative to placebo were substantially larger with laquinimod than with interferon (40.6% versus 28.3% for six-month progression).

In addition, brain atrophy was significantly slowed with laquinimod in BRAVO, whereas loss of brain volume was the same in the interferon and placebo groups.

And unlike the only currently approved oral drug for MS, fingolimod (Gilenya), laquinimod did not appear to have an immunosuppressive effect.

Independent neurologists told MedPage Today that these points made laquinimod look extremely promising, especially since the lack of immunosuppression suggested that the drug could be combined with other disease-modifying agents. The add-on approach is considered far too dangerous with current products.

The Mechanism Unveiled
In presenting the ALLEGRO results in Honololu, Giancarlo Comi, MD, of the University Vita-Salute San Raffaele in Milan, Italy, said the drug alters T-cell populations to emphasize a regulatory Th2 response instead of the attack-focused Th1. It also appears to prompt a neuroprotective response from microglia and astrocytes within the central nervous system, he said.

Still, the account lacked an explanation of how laquinimod exerts these effects. But that apparently was not because Comi didn't know.

A few weeks ago, researchers from Germany and Italy -- including Comi -- and from Teva Pharmaceuticals, which is developing laquinimod, published a paper in the American Journal of Pathology that filled in the details.

The key, according to the researchers, is brain-derived neurotrophic factor (BDNF).
Led by Jan Thöne, MD, of Ruhr-University Bochum in Germany, the group measured BDNF in blood collected from MS patients participating in Teva's clinical trials.

BDNF levels increased dramatically with laquinimod treatment, with respect to baseline and also compared with study participants assigned to placebo, the researchers found.

A similar effect -- also previously unnoticed -- was documented in the standard mouse model of MS called experimental autoimmune encephalitis, in which an immune reaction to myelin is artificially induced.

The researchers noted that previous research had shown that BDNF enhances survival of damaged neurons and can promote a certain degree of neuroregeneration.

Meanwhile, in vitro experiments by the group pointed to monocytes as the laquinimod's specific cellular target, "skew[ing] the phagocyte population toward a regulatory phenotype, which in turn mediates immune modulation in vivo," Thöne and colleagues wrote.

They noted that monocytes do not appear to be targeted by other MS drugs.

"Our data indicate a multifaceted mechanisms of action of laquinimod, including immunomodulatory and neuroprotective mechanisms of action that should be further tested in human specimens," they added.
Whether these twin actions are indeed independent is the next question, Thöne and colleagues suggested. "We hypothesize that the increase of BDNF might also be involved in [laquinimod's] effects on monocytes and subsequent increase of IL-10," they wrote.

The clinical trials and the mechanism study were funded by Teva.





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