Friday, December 30, 2005

ABC 7 Medical: New Treatment for Multiple Sclerosis

http://www.wjla.com/news/stories/1205/289778.html


RSS Feeds From ABC 7 UPDATED - Thursday December 29, 2005 7:06pm
IPOD Enabled Story Watch the abc7 e-Video eVideo: ABC 7 Medical:
Multiple Sclerosis

-WJLA Script-
Anchor:
IT'S NOT A CURE, BUT THERE IS NEW HOPE FOR PEOPLE SUFFERING FROM
MULTIPLE SCLEROSIS. IT'S A NEW VACCINE, AND ALTHOUGH IT'S STILL IN
CLINICAL TRAILS DOCTORS SAY PATIENTS ARE SEEING SOME EXCITING RESULTS AS
MEDICAL REPORTER KATHY FOWLER REPORTS.

Kathy Fowler on set:
MULTIPLE SCLEROSIS SHORT CIRCUITS THE WIRING IN THE BRAIN, CAUSING LOSS
OF FEELING, VISION PROBLEMS, FATIGUE AND WEAKNESS. BUT A NEW VACCINE
SEEMS TO BE HELPING.

Story Script:
SUE CARLSON WORKS UP TO 12 HOURS A DAY HELPING OTHERS FEEL BETTER.

Sue Carlson: "Theres' nothing I can't do."

BUT FOUR YEARS AGO, SUE COULD BARELY MUSTER ENOUGH ENERGY TO WORK A HALF
DAY. MULTIPLE SCLEROSIS WEAKENED THE ENTIRE RIGHT SIDE OF HER BODY. Sue
Carlson: "I had to move a body part predominantly with my left side and
prop it on pillows or towels or blankets in order to do the work I
needed to do"

AFTER 6 MONTHS ON AN EXPERIMENTAL VACINE CALLED NEUROVAX, HER STRENGTH
CAME BACK.

Carlson: "And it just kept getting better, and better and better."

NEUROVAX INCREASES THE NUMBER OF DISEASE-FIGHTING-WHITE BLOOD CELLS IN
THE IMMUNE SYSTEM. IT WORKED FOR ALL 40 PATIENTS WHO RECEIVED IT.

UNLIKE STANDARD TREATMENTS, WHICH HAVE TO BE GIVEN DAILY OR WEEKLY, THE
VACCINE ONLY HAS TO BE GIVEN ONCE A MONTH, AND IT DOESN'T CAUSE FLU-LIKE
SIDE EFFECTS.

Dr. Dennis Bourdette Neurologist: "What patients want are treatmetns
that are not only effective, but also aren't impacting their quality of
life because of side effects.

RESEARCHERS SAY THE RESULTS ARE ENCOURAGING BUT LARGER STUDIES ARE
NEEDED BEFORE IT CAN BE APPROVED.

Dr. Arthur Vandenbark, Neurologist: "We still have to have a large
enough trial that goes on for a minimum of 2 years where we see a
difference between the vaccinated patients and the control group, or the
placebo group"

AFTER A YEAR WITHOUT AN INJECTION, SUE IS WAITING FOR A NEW TRIAL TO
BEGIN, HOPING THAT ANOTHER DOSE OF THE VACCINE WILL GIVE HER EVEN MORE
STRENGTH.

FOR MORE INFORMATION ON THIS VACCINE LOG ONTO:
http://www.ohsu.edu/ms/contact.html

The Multiple Sclerosis Center of Oregon

http://www.ohsu.edu/ms/drugtrials.htmlThe Multiple Sclerosis Center of Oregon
Where healing, teaching and discovery come together
Research Studies

To learn more about these research studies please call our research line at (503) 494-7241


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Ginseng for Multiple Sclerosis Related Fatigue
IRB# 1357
Principal Investigator: Ruth Whitam, M.D.

The MS Center of Oregon is currently recruiting study subjects to enroll in a placebo controlled cross-over design trial that will study the effect of an American Ginseng extract on multiple sclerosis related fatigue.

To enroll in the study, subjects must

  • be between the ages of 18 and 65 years,

  • carry a diagnosis of multiple sclerosis and

  • have problems with fatigue for greater than two months.

    Participation in the study requires that subjects undergo clinical assessments at OHSU on seven separate occasions over a 17-week period. There will be two 6-week treatment periods, separated by a 2-week washout period. All subjects take ginseng for one treatment period and placebo for one treatment period. Those participating in the study will be asked to wear activity monitors at the waist and wrist for several weeks over the course of the study. Clinical assessments will be done at the beginning and end of each treatment period and will involve physical exams, questionnaires, blood draws and collection of saliva samples.

    There will be no financial costs to subjects who choose to participate in this study.

    If you would like further information about this study or to refer a subject, please contact:

    The MS Center of Oregon Research Line at (503) 494-7241

    This study will take place in association with the MS Center of Oregon at Oregon Health & Science University in Portland, Oregon.

  • Treatment of Multiple Sclerosis-Specific Fatigue with Traditional Chinese Medicine (TCM): A Randomized, Placebo-controlled Pilot Study.
    IRB# 6788
    Principal Investigator: Richard Hammerschlag, PhD.

    Research participants are needed for a 12-week collaborative study between the OHSU MS Center (IRB#6788) and the Oregon College of Oriental Medicine (OCOM IRB#01-004) to test acupuncture and herbs for treating MS-related fatigue.

    Participants must:

    • Be diagnosed with MS

    • Have MS related fatigue

    • Be age 18-55

    • Have no prior treatments with acupuncture

    To determine if you qualify, please contact Meggan Baumgartner, OCOM Research Coordinator at (503) 253-3443 ext 231.

    Double-blind Placebo Controlled Pilot Trial of Memantine for Cognitive Impairment in Multiple Sclerosis.
    IRB# 8211
    Principal Investigator: Dennis Bourdette, MD

    The MS Center of Oregon is currently recruiting patients to enroll in a clinical trial that will study the cognitive function in patients with multiple sclerosis.

    To enroll in the study:

    • Patients must carry a diagnosis of multiple sclerosis, and be between 18 and 60 years of age.

    • Participation in the study requires that patients undergo clinical assessment at OHSU on five separate occasions over a 21-week period. These clinical assessments involve physical exams, a questionnaire, blood draws, and mental function tests.

    • Enrolled patients will be treated with either Memantine or placebo (sugar pill) for 18 weeks.

    There will be no financial costs to patients who choose to participate in this study.

    Fish Oil as an Adjunct Therapy for Depression in MS

    IRB# 8295

    Principal Investigator: Lynne Shinto, ND

    The MS Center of Oregon at Oregon Health & Science University is looking for people with a confirmed diagnosis of relapsing remitting MS who are suffering from depression. The purpose of the study is to determine if taking omega-3 fatty acids helps with symptoms of depression in people with MS. In addition we will determine if omega-3 fatty acids decrease blood levels of substances that are associated with MS and depression

    You may be eligible to participate in the study if you meet the all of the following criteria:

    • 18-65 years old

    • Have a diagnosis of relapsing remitting MS

    • On a stable dose of Copaxone, Betaseron or Avonex

    • On a stable dose of anti-depressant medication

    • Have not had an MS relapse or received corticosteroid treatment 1 month prior to enrollment

    • Have not eaten more than one 6 oz serving of fish per week 1 month prior to enrollment

    • Have not taken fish oil or omega-3 fatty acid supplementation 1 month prior to enrollment

    • Not pregnant

    • Have no other significant health conditions (like coronary heart disease, uncontrolled diabetes mellitus, liver disease, severe psychiatric disorders)

    • Not participating in any other studies

    This is a three-month pilot study in which 60 participants will be randomly assigned to receive either fish oil capsules (which have high amounts of omega-3 fatty acids) or placebo oil capsules.

    The study requires 8 visits to MS Center at OHSU. The research study will pay for all costs associated with the participation in this study. You will be responsible for any expenses that have to do with other aspects of your participation such as childcare and transportation.

    If you meet the eligibility requirements described above and are interested in participating in this study please call Rachel Frank at (503) 494-7963.




    What is MS? | TCR Peptide Research | Research Studies | Our Team | Neurology Home




    December 28, 2005
    OHSU Multiple Sclerosis Center of Oregon
    www.ohsu.edu/ms/

    Email: MSNews@ohsu.edu

    Thursday, December 29, 2005

    predictions : Tysabri will be brought back onto the market.


    Biomed Rounds: Will Biogen�s Tysabri make a comeback in 2006?

    12/27/2005 08:19 AM
    By Dyke Hendrickson
    Looking ahead to 2006, here is a list of predictions from Your Scribe, who doesn�t always see 20-20, even in hindsight:

    Tysabri will be brought back onto the market.
    The multiple-sclerosis drug is a potential blockbuster for Biogen Idec Inc., but the Cambridge company pulled it from the shelves in early 2005 after three deaths caused by a rare brain disease were linked to the compound.

    The evidence that Tysabri was the direct cause is scant.

    Subsequent tests by Biogen Idec have persuaded the U.S. Food and Drug Administration to re-investigate the data, and at some point in 2006 give it the green light.

    One variable: MS patients want the drug, and they themselves are pressuring regulatory officials to help bring back the medication.

    Vertex Pharmaceuticals will emerge as a biotech titan.
    The Cambridge company, led by chief executive Joshua Boger, has had a roller-coaster ride in its 16-year history.

    Its stock was selling at close to $100 per share in 2001, but fell to about $15 in early 2005. But it is up to $27 per share now, on the strength of good data and strengthened partnerships. It recently reported encouraging test results for its hepatitis C compound.

    And in recent years it has enhanced partnerships with a range of large allies, including Aventis SA; GlaxoSmithKline plc; Novartis Pharma AG; Merck & Co. Inc.; Mitsubishi Pharma Corp.; and Cystic Fibrosis Foundation Therapeutics Inc.

    It also has collaboration agreements with Schering AG and Eli Lilly and Co. It appears that the company, which employs about 725, has reached the tipping point, and is ready to join the select few of �mature� bio techs that are making progress in the lengthy struggle for prosperity.

    Or it could be purchased by one of the giants with whom it has a partnership.

    Cambridge will be recognized as �Institute City.�
    The community has dominant universities, of course, that bring in millions in research funds. Now the cachet of its scientific community is drawing in donations in the multiple millions.

    The Broad Institute recently received word that it would receive another $100 million donation from the Eli Broad family in California, making the Broad contribution $200 million over barely two years.

    Other new institutes that have been created by multimillion-dollar gifts include the McGovern, Picower, Deshpande, and years ago, the Whitehead.

    When economic demographers run their numbers each year to determine which markets have the most vibrant presence in the life sciences, metro Boston will be at the top of the list.

    Hologic Corp. will be purchased by a major corporation desiring to enter the imaging field.
    The company is a leader in digital imaging, which is among the �can�t miss� technologies of the upcoming year.

    And Hologic, headed by Jack Cumming, is coming up to speed.

    Its stock price in late 2004 was hovering near $10 per share. But as 2005 comes to an end, the share price is at $37 per share.

    That is because it has focused on the development, manufacture and supply of diagnostic and medical imaging systems, primarily serving the health care needs of women.

    Its areas of concentration are osteoporosis assessment, breast cancer detection, and direct capture X-ray detectors for digital radiography applications.

    The company has strategic alliances with giants such as Siemens AG.

    Though Hologic has 870 employees, it is still �small enough� to be gobbled up by a market giant seeking to enter this prosperous field.

    Biotech and pharma companies will lobby furiously to oppose the federal government�s intervention in discussion of the price of pharmaceuticals.
    The feds will become more involved in 2006 when the Medicare drug prescription benefit becomes available to about 40 million seniors.

    Some industry analysts say cheap-drug advocates will urge the government to �buy in en masse,� as it does for recipients of benefits from the Veterans Administration. Both patients and advocates complain that many drugs cost too much.

    A recent media report reflected the fact that a drug produced by Genzyme for a rare disease costs close to $600,000 per year � for one patient.

    It�s likely that medication populists will seize on such unusual situations to call for less expensive medications. They have certainly done that in the �buy Canada� campaign that has been popular in Springfield, Cambridge and other communities in recent years.

    But the biotechs and pharmas are already getting ready to hold the line on their belief that the �for profit� produces better life-saving medications.

    http://www.masshightech.com/displayarticledetail.asp?art_id=70622

    tysabri

    Biomed Rounds: Will Biogen's Tysabri make a comeback in 2006?
    Boston Mass High Tech - MA, USA
    ... disease were linked to the compound. The evidence that Tysabri was the direct cause is scant. Subsequent tests by Biogen Idec have ...

    Resources and commodities provided the most cheer
    Unison.ie - Bray,Ireland
    ... have been the biggest of the year's losers but it certainly suffered the sharpest fall back in February when the Multiple Sclerosis drug Tysabri was withdrawn ...

    Wednesday, December 28, 2005

    Ottawa team unravelling brain damage in multiple sclerosis

    Last Updated Wed, 21 Dec 2005 13:47:38 EST

    http://www.cbc.ca/story/science/national/2005/12/21/ms-051221.html
    CBC News

    The puzzle of how nerve coatings are damaged in the brains of people with multiple sclerosis may have been solved by a Canadian-led research team.

    Nerve fibres that send electrical signals in the brain are coated in a fatty sheath called myelin. The myelin acts as an insulator, like a plastic coating covering a copper wire.

    Neurologist Dr. Peter Stys of the Ottawa Health Research Institute and his colleagues proposed a reason why myelin becomes damaged and invented a way to test the idea in the lab.

    The researchers showed myelin contains specialized receptors for glutamate, a neurotransmitter that transmits signals to brain cells.

    They also found chemicals that block the receptor can reduce myelin damage.

    "Such a mechanism may represent a potentially important therapeutic target in disorders in which [myelin damage] is a prominent feature," the researchers write in Thursday's online issue of the journal Nature.

    The laboratory findings need to be confirmed and tested in animals before a potential drug could be tried in humans.

    To make the discovery, Stys's team invented a state-of-the-art laser scanning microscope technique. It allowed the first measurements of changes in calcium levels in the tiny spaces within myelin in a rat model.

    Stys suspects glutamate from inflammatory cells may directly injure myelin in immune disorders such as MS.

    The findings help fill in the details of what molecules are involved and how they interact in MS, agreed Dr. Stephen Waxman, neurology chair at Yale University School of Medicine. He was not involved in the research.

    The research was funded by the the National Institute of Neurological Disorders and Stroke, the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Ontario, the Canadian Institute for Photonic Innovations and private donors.

    Tuesday, December 20, 2005

    Elan Momentum Seen Easing Over Holidays



    Monday, December 19, 2005 8:38:49 AM ET
    Dow Jones Newswires


    1229 GMT [Dow Jones] Elan -4.2% at EUR11.20 in profit-taking after a 30%-plus gain since the start of December, says Goodbody Stockbrokers' Ian Hunter. The FDA Advisory Committee for peripheral and central nervous system drugs will possibly review MS drug Tysabri on March 7 and 8, according to Elan's partner on Tysabri. Hunter says momentum in Elan could ease over the holidays. Maintains buy. (QAF)


    Contact us in London.
    +44-20-7842-9464
    Markettalk.eu@dowjones.com


    Copyright (c) 2005 Dow Jones & Company, Inc.

    Elan Corporation | detailed quote - chart - all headlines previous | next

    12/19/05 Elan "buy" Goodbody Stockbrokers
    12/08/05 Elan +6% As Tysabri Hopes Continue
    11/18/05 NCB Sees Elan's Tysabri Hitting $1B Sales

    http://www.newratings.com/analyst_news/article_1163515.html

    Multiple Sclerosis

    Nutra Pharma Reports Discovery of New Gene Involved in Multiple ...
    Genetic Engineering News - Larchmont,NY,USA
    ... NPHC) a biotechnology holding company that owns rights to intellectual property related to the development of drugs for HIV and Multiple Sclerosis (MS) has ...

    Scientists Demonstrate Investigational MS Drug Down Regulates the ...
    Genetic Engineering News - Larchmont,NY,USA
    Scientists at Bayhill Therapeutics report promising findings for an investigational multiple sclerosis (MS) drug, BHT-3009, which represents a novel DNA plasmid ...

    Wednesday, December 14, 2005

    Multiple Sclerosis

    Multiple Sclerosis

    Super Cities WALK: Over One Million Dollars for Multiple Sclerosis
    Canada NewsWire (press release) - Canada
    14 /CNW Telbec/ - This year's Super Cities WALK, organized by the Quebec Division of the Multiple Sclerosis Society of Canada, finally broke the million dollar ...
    See all stories on this topic

    Cary Mayor Ernie McAlister named to Eastern NC Multiple Sclerosis ...
    dBusinessNews Triangle (press release) - Raleigh,NC,USA
    CARY , NC -- Cary Mayor Ernie McAlister has been named to the Board of Trustees of the National Multiple Sclerosis (MS) Society's Eastern North Carolina ...

    New strides with Multiple Sclerosis research
    WKRN - Nashville,TN,USA
    Researchers in Italy followed 14 patients with the relapsing-remitting form of Multiple Sclerosis for 18 months , monitoring their brains with MRI scans both ...

    Drug May Slow Down Multiple Sclerosis
    WebMD - USA
    Dec. 12, 2005 -- An immune system-suppressing drug may slow progression of multiple sclerosis, new research suggests. Using magnetic ...

    Legendary funnyman had multiple sclerosis for years.
    MTV.com - USA
    ... Fernando Valley, according to The Associated Press. He had long suffered from multiple sclerosis after being diagnosed in the 1990s. ...

    Multiple Sclerosis
    Lahontan Valley News - Fallon,NV,USA
    ... Multiple sclerosis is believed to be an autoimmune disease (a disease in which the body attacks its own tissue) affecting the central nervous system (CNS). ...

    Scientists Push Forward Understanding Of Multiple Sclerosis
    Medical News Today (press release) - UK
    New findings by a research team from the University of Edinburgh may help explain why diseases like multiple sclerosis (MS) which attack the myelin sheath - an ...

    Marijuana derivatives may provide multiple sclerosis treatment
    GG2.net - UK
    MARIJUANA derivatives or "cannabinoids" taken for one year for the treatment of multiple sclerosis (MS) may reduce muscle spasms and other aspects of disability ...

    Experts say nation may have more MS cases than thought
    Taipei Times - Taiwan
    With results of the first nationwide research of multiple sclerosis showing that reported incidences of the disease in Taiwan are much lower than in Japan or ...

    Promising Multiple Sclerosis Vaccine Tested
    abc7news.com - San Francisco,CA,USA
    7 - KGO - Multiple sclerosis short-circuits the wiring in the brain, causing loss of feeling, vision problems, fatigue and weakness for about 400,000 Americans ...

    Promising Multiple Sclerosis Vaccine Tested

    Promising Multiple Sclerosis Vaccine Tested

    Only Side Effect: A Sore Arm

    KGO By Dr. Dean Edell

    - Multiple sclerosis short-circuits the wiring in the brain, causing loss of feeling, vision problems, fatigue and weakness for about 400,000 Americans. Now a new vaccine is showing promise.

    Sue Carlson works up to 12 hours a day helping others feel better.

    Sue Carlson, multiple sclerosis patient: "There's nothing I can't do."

    Four years ago, Sue could barely muster enough energy to work a half-day. Multiple sclerosis weakened the entire right side of her body.

    Sue Carlson, multiple sclerosis patient: "I had to move a body part, predominantly with my left side, and prop it on pillows or towels or blankets in order to do the work I needed to do."

    But after six months on an experimental vaccine called neurovax, her strength came back.

    Sue Carlson, multiple sclerosis patient: "And it just kept getting better and better and better."

    The vaccine works by increasing the number of disease-fighting white blood cells in the immune system. In the first study, it did that for all forty patients who received it - and that's pretty impressive.

    Unlike standard treatments, which have to be given daily or weekly, the vaccine only has to be given once a month, and it doesn't cause flu-like side effects.

    Dennis Bourdette, M.D., neurologist: "What patients want are treatments that are not only effective, but also aren't not impacting their quality of life because of side effects."

    Researchers say the results are encouraging, but larger studies are needed before it can be approved.

    Arthur Vandenbark, Ph.D.: "We still have to have a large enough trial that goes on for a minimum of two years, where we see a difference between the vaccinated patients and the control group, or the placebo group."

    After a year without an injection, Sue is waiting for a new trial to begin, hoping that another dose of the vaccine will give her even more strength.

    Patients say the only side-effect of the vaccine is a sore arm.

    >> Video On Demand: Build Your Own Newscast

    http://abclocal.go.com/kgo/story?section=edell&id=3704652

    AP

    Sidebar:

    For More Information, Contact:

    Multiple Sclerosis Center of Oregon at OHSU
    3181 S.W. Sam Jackson Park Road
    Portland, OR 97239-3098
    (503) 494-5759
    msnews@ohsu.edu
    www.ohsu.edu/ms

    Quick Links

    Quickly find your favorite sections on our Web site by using our Quick Links pull-down menu.


    Scientists push forward understanding of multiple sclerosis

    New findings by a research team from the University of Edinburgh may help explain why diseases like multiple sclerosis (MS) which attack the myelin sheath – an insulator which protects the body’s nervous system - cause such severe symptoms in MS patients. Their discoveries may lead to new ways to help treat patients with MS, it is reported in the journal Neuron today (Thursday, 8 December).

    The scientists have made an important breakthrough in understanding how animals with complex nervous systems, such as humans, achieve rapid signalling between their nerve cells. Communication between nerve cells and other organs such as muscles needs to be extremely fast, so that the body responds quickly to instructions from the brain. Electrical signals can travel rapidly from the brain because they ‘jump’ down nerves using specialised hotspots called nodes.

    Professor Peter Brophy of the Centre for Neuroscience Research at the Unversity and leader of the study explained: “It has been known for some time that the location of the nodes along nerves is determined by specialised cells called glia, which surround nerves with a myelin sheath. The nerves of babies are surrounded by these glial cells in the first few years after birth, which ensures proper development of the human nervous system. If nerves do not get their myelin sheath, or if they lose it later because of diseases like MS, the nodes either don’t form, or are disrupted, leading to a serious loss of nervous system function, which in turn can lead to blindness, paralysis or even death.”

    Professor Brophy’s team has discovered the key molecules- two proteins found in the gene Neurofascin- that link glial ensheathment of the nerve fibres to the formation of nodes. “We hope that the discovery of these proteins will help us to find ways to improve nerve conduction in patients with conditions where the myelin sheath is attacked,” he said.

    External Links:
    University of Edinburgh


    http://www.bionews.in/index.php/archives/599

    Viral Trigger for Multiple Sclerosis

    http://spaces.msn.com/members/bartgrl69/Blog/cns!1pUzN9ZPRuXysBnC-txCl3Ww!899.entry

    December 02
    Viral Trigger for Multiple Sclerosis
    Herpes Virus Strain Identified as a Trigger in Multiple Sclerosis:
    Multiple sclerosis (MS) is a debilitating neuromuscular disorder in which the body attacks its own tissues. It affects approximately 350,000 Americans. To date, the causes of MS have been obscure and the treatment options extremely limited. A new study, published in the December 1997 issue of Nature Medicine, may help change this. The study suggests that infection by a strain of the Herpes virus, called HSV-6, may facilitate development of MS. Researchers found that more than 70 percent of patients who had the most common form of MS showed an immune response to HSV-6, indicating prior exposure to this pathogen. In contrast, only 18 percent of control subjects tested positive for HSV-6 exposure. Also, 15 of 50 individuals with MS had HSV-6 DNA in their serum--indicating an active infection. None of the 47 control subjects had HSV-6 DNA in their blood. Additional testing of larger numbers of MS patients to confirm the results of this study is underway.

    If the apparent viral connection holds up, it may open the door to new treatment options. Currently infections involving other strains of Herpes are treated, although not cured, with acyclovir and other antiviral drugs. Any treatment that ameliorates the symptoms or slows the progression of MS would be a great breakthrough.

    Visit the following sites for more information:

    Herpes Virus Strain Identified as a Trigger in Multiple Sclerosis: A press release from the National Institute of Neurological Disorders and Stroke describing the study.

    Multiple Sclerosis: An extremely thorough tutorial. It includes video of the neurological signs of MS.

    http://www.ninds.nih.gov/news_and_events/press_releases/pressrelease_herpes_virus_strain_112497.htm

    Tuesday, December 13, 2005

    Find Out How Your Brain Sleeps

    Find Out How Your Brain Sleeps

    Obviously, your brain never stops working. So how does it rest?

    When you lose consciousness and enter the deepest part of the sleep cycle, your brain stops communicating with itself, according to a new study from researchers at the University of Wisconsin-Madison. The awake brain functions as chemicals and nerve cells chatter continually, but in the deepest part of sleep, all those cranial pieces and parts break down into little islands that can't communicate with one another, report LiveScience and HealthDay News.

    Led by professor of psychiatry Giulio Tononi, the team used a noninvasive technique called transcranial magnetic stimulation to activate certain parts of volunteer subjects' brains. Electrodes were attached to each person's head to monitor how the stimulation triggered reactions in other parts of the brain and body. When the volunteers were dreaming in the early morning hours, brain signals were almost as active as when they were awake, but during deeper sleep, the brain was quiet. "During deep sleep early in the night the response is short-lived and doesn't propagate at all," Tononi told LiveScience managing editor Robert Roy Britt.



    Research team member Marcello Massimini, a research associate at the Wisconsin university's Psychiatric Institute and Clinics, explains that the brain is compartmentalizing to allow the synapses--those areas in the brain that let us think--to take a break and rest. "This process would allow cortical circuits to eliminate noisy synapses and renormalize in order to be ready for the next day," Massimini told LiveScience. He added that this process may also explain the well-known phenomenon of improved performance and learning after sleep.

    The study findings, which were published in the journal Science, help clarify scientific thought about consciousness. Tononi told HealthDay News that conscious thought depends on the ability of the brain to integrate information, and this research helps verify that belief.

    MS drug withdrawal dashes patients' hopes

    MS drug withdrawal
    dashes patients' hopes

    Medication triggered serious side effects

    http://www.msnbc.msn.com/id/7049364/
    FDA GRANTS ACCELERATED APPROVAL OF TYSABRI, FORMERLY ANTEGREN, FOR THE TREATMENT OF MULTIPLE SCLEROSIS
    Biogen Idec
    Tysabri received a fast-track approval by the FDA for the treatment of relapsing forms of multiple sclerosis.

    Updated: 10:04 a.m. ET March 1, 2005

    BOSTON - When the drug Tysabri was introduced to treat multiple sclerosis just three months ago, there was “a lot of buzz” among people with MS eager to embrace new hope, said Michele Maglione, who was diagnosed with the incurable disease four years ago.

    Now, some of that hope has dissolved with news that the drug given fast-track approval by federal regulators has been pulled from the market, said Maglione, a 36-year-old worker at a New York City nonprofit agency, who takes another MS drug, Betasteron.

    However, the makers of Tysabri say the medication may eventually return to the market even though it appears the drug — in combination with another medication — triggered a serious disease in two patients, killing one of them.

    Massachusetts-based Biogen Idec Inc. and Elan Corp. announced Monday they were voluntarily pulling the drug from the market and advised doctors to suspend prescribing the medication. The companies also have stopped using the drug in clinical trials.

    'We're disappointed'
    Still, even if the drug is never returned to the marketplace, Tysabri has helped advance research in an area that has seen few successes since the central nervous system disorder was first identified in 1868.

    “We’re disappointed,” said Dr. Howard L. Weiner, author of a book on MS and director of the Partners MS Center at Brigham & Women’s Hospital in Boston. “But the results that we saw with this drug moved forward our understanding and treatment of MS, and identified an avenue for treatment that is still very much alive.”

    Multiple sclerosis is a brain disease which can lead to muscle weakness, difficulty concentrating, slurred speech and paralysis. About 400,000 Americans and 2.5 million people worldwide are believed to be affected by MS, which is more common in women than men and often strikes between the ages of 20 and 50, according to the MS Society.

    Q & A Multiple sclerosis
    Multiple sclerosis is a chronic disease that affects the central nervous system by destroying the tissue surrounding nerves in the brain, spinal cord and eyes. This tissue, known as myelin, normally protects nerve fibers and allows them to conduct electrical impulses. MS damages the myelin and replaces it with scars of hardened tissue. The nerves are then unable to send electrical impulses to and from the brain, resulting in various neurological symptoms.
    Source: National Multiple Sclerosis SocietyPrint this

    While no cure has emerged, Tysabri had been considered a promising therapy because of its unique approach in blocking the movement of inflammatory cells from the bloodstream into the brain, Weiner said.

    In patients with multiple sclerosis, their body’s immune system turns rebellious, attacking, inflaming and damaging its own nerve tissue. The most common type of MS involves a worsening, or relapse, of acute symptoms.

    The decision to withdraw Tysabri came after recent reports of two cases of serious effects among patients who used it along with an earlier Biogen Idec MS drug, called Avonex, in clinical trials. In one case, the person died; in another, the person developed a suspected case of a rare and frequently fatal disease of the central nervous system.

    Both patients had taken Tysabri for more than two years in combination with Avonex, the companies said.

    The companies planned to review records from clinical trials, including MRI brain scans, to search for possible further evidence that the drugs — in combination, or Tysabri alone — could put patients at increased risk.

    About 5,000 patients have received intravenous infusions of Tysabri since its November approval, Biogen executives said.

    Dr. Steven Galson, acting director of FDA’s Center for Drug Evaluation and Research, said that the regulatory agency “continues to believe Tysabri offers great hope to MS patients.”


    Friday, December 09, 2005

    Multiple sclerosis

    Multiple sclerosis

    From Wikipedia, the free encyclopedia.

    Jump to: navigation, search
    Multiple sclerosis
    ICD-10 code: G35
    ICD-9 code: 340
    MRI image showing a bright spot where multiple sclerosis has damaged myelin in the brain
    Enlarge
    MRI image showing a bright spot where multiple sclerosis has damaged myelin in the brain

    Multiple sclerosis (MS) is a chronic disease that affects the brain and spinal cord. MS can cause a variety of symptoms, including changes in sensation, visual problems, weakness, depression, and difficulties with coordination and speech. Although many patients lead full and rewarding lives, MS can cause impaired mobility and disability in the more severe cases.

    Multiple sclerosis affects neurons, the cells of the brain and spinal cord that carry information, create thought and perception and allow the brain to control the body. Surrounding and protecting these neurons is a fatty layer known as the myelin sheath, which helps neurons carry electrical signals. MS causes gradual destruction of myelin (demyelination) in patches throughout the brain and spinal cord, causing various symptoms depending upon which signals are interrupted. The name multiple sclerosis refers to the multiple scars (or scleroses) on the myelin sheaths. It is thought that MS results from attacks by an individual's immune system on the nervous system and is therefore categorized as an autoimmune disease.

    Multiple sclerosis may take several different forms, with new symptoms occurring in discrete attacks or slowly accruing over time. Between attacks, symptoms may resolve completely, but permanent neurologic problems often persist. Although much is known about how MS causes damage, its exact cause remains unknown. MS currently does not have a cure, though several treatments are available which may slow the appearance of new symptoms. MS primarily affects adults, with an age of onset typically between 20 and 40 years, and is more common in women than in men.[1][2]

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    Signs and symptoms

    Individuals with multiple sclerosis may experience a wide variety of symptoms. The initial attacks are often transient, mild (or asymptomatic), and self-limited. They often do not prompt a health care visit and sometimes are only identified in retrospect once the diagnosis has been made based on further attacks. The most common initial symptoms reported are: changes in sensation in the arms, legs or face (33%), complete or partial vision loss (optic neuritis) (16%), weakness (13%), double vision (7%), unsteadiness when walking (5%), and balance problems (3%). Fifteen percent of individuals have multiple symptoms when they first seek medical attention.[3] Most people find their initial MS symptoms occur over a period of hours to weeks. For some people the initial MS attack is preceded by infection, trauma or strenuous physical effort.

    Other symptoms and physical findings common in multiple sclerosis are flickering eye movements (nystagmus), speech difficulties, tremor, clumsiness of the hands, abnormal muscle spasms, bladder and bowel difficulties, and sexual dysfunction. Cognitive impairments are also common, such as difficulty performing multiple tasks at once, difficulty following detailed instructions, loss of short term memory, emotional instability, and fatigue. Emotional symptoms are common and can be the normal response to having a debilitating disease or the result of damage to the nerves that generate and control emotions. The most common condition, clinical depression, is a product of both causes. Feelings such as anger, anxiety, frustration, and hopelessness are also common, and suicide is a very real threat.

    Three clinical entities warrant further discussion because affected individuals are often eventually diagnosed with MS. (However, MS is only one of several potential causes for these entities.)

    Individuals typically experience rapid onset of pain in one eye, followed by blurry vision in part or all of the visual field of that eye. This is a result of involvement of the optic nerve by MS. Only 10% to 50% of patients (depending on the population studied) with optic neuritis go on to develop MS . The blurred vision usually resolves within six months, but individuals are often left with less vivid color vision (especially red) in the affected eye.
    Individuals usually notice binocular diplopia (double vision with both eyes open) when looking to one side. Internuclear ophthalmoplegia occurs when MS affects a part of the brain stem called the medial longitudinal fasciculus, which is responsible for communication between the two eyes. This results in the failure of the medial rectus muscle to contract appropriately, so that the eyes do not move equally (called disconjugate gaze).
    Individuals typically develop rapid onset of numbness, weakness, bowel or bladder dysfunction, and/or loss of muscle function, typically in the lower half of the body. This is the result of MS attacking the spinal cord. As many as 80% of individuals with transverse myelitis are left with lasting disabilities, even though there is usually some improvement during the first two years.

    Diagnosis

    Multiple sclerosis is difficult to diagnose in its early stages. In fact, definite diagnosis of MS cannot be made until there is evidence of at least two anatomically separate demyelinating events occurring at least thirty days apart. The McDonald criteria represent international efforts to standardize the diagnosis of MS using clinical data, laboratory data, and radiologic data.[4]

    • Clinical data alone may be sufficient for a diagnosis of MS. If an individual has suffered two separate episodes of neurologic symptoms characteristic of MS, and the individual also has consistent abnormalities on physical examination, a diagnosis of MS can be made with no further testing. Since some people with MS seek medical attention after only one attack, other testing may hasten the diagnosis and allow earlier initiation of therapy.
    • Magnetic resonance imaging (MRI) of the brain is often used to evaluate individuals with suspected MS. MRI shows areas of demyelination as bright lesions on T2 images or when gadolinium contrast is used. Because MRI can reveal lesions which occurred previously but produced no clinical symptoms, it can provide the evidence of chronicity needed for a definite diagnosis of MS.
    • Testing of cerebrospinal fluid (CSF) can provide evidence of chronic inflammation of the central nervous system. The CSF is tested for oligoclonal bands, which are immunoglobulins found in 85% to 95% of people with definite MS (but also found in people with other diseases). [5] Combined with MRI and clinical data, the presence of oligoclonal bands can help make a definite diagnosis of MS. Lumbar puncture is the procedure used to collect a sample of CSF.
    • The brain of a person with MS often responds less actively to stimulation of the optic nerve and sensory nerves. These brain responses can be examined using Visual evoked potentials (VEPs) and somatosensory evoked potentials (SEPs). Decreased activity on either test can reveal demyelination which may be otherwise asymptomatic. Along with other data, these exams can help find the widespread nerve involvement required for a definite diagnosis of MS.[6]

    Another test which may become important in the future is measurement of antibodies against myelin proteins such as myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP). As of 2005, however, there is no established role for these tests in diagnosing MS.

    The signs and symptoms of MS can be similar to other medical problems, such as stroke, brain inflammation, infections, tumors, and other autoimmune problems, such as lupus. Additional testing may be needed to help distinguish MS from these other problems.

    Disease course and clinical subtypes

    Graph representing the different types of multiple sclerosis
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    Graph representing the different types of multiple sclerosis

    The course of MS is difficult to predict, and the disease may at times either lie dormant or progress steadily. Several subtypes, or patterns of progression, have been described. Subtypes use the past course of the disease in an attempt to predict the future course. A person diagnosed with a particular subtype may, for unclear reasons, switch from one subtype to another over time. Subtypes are important not only for prognosis but also for therapeutic decisions. In 1996 the United States National Multiple Sclerosis Society standardized the following four subtype definitions:[7]

    • Relapsing-remitting
    Relapsing-remitting describes the initial course of 85% to 90% of individuals with MS. This subtype is characterized by unpredictable attacks (relapses) followed by periods of months to years of relative quiet (remission) with no new signs of disease activity. Deficits suffered during the attacks may either resolve or may be permanent. When deficits always resolve between attacks, this is referred to as "benign" MS.
    • Secondary progressive
    Secondary progressive describes around 80% of those with initial relapsing-remitting MS, who then begin to have neurologic decline between their acute attacks without any definite periods of remission. This decline may include new neurologic symptoms, worsening cognitive function, or other deficits. Secondary progressive is the most common type of MS and causes the greatest amount of disability.
    • Primary progressive
    Primary progressive describes the approximately 10% of individuals who never have remission after their initial MS symptoms. Decline occurs continuously without clear attacks. The primary progressive subtype tends to affect people who are older at disease onset.
    • Progressive relapsing
    Progressive relapsing describes those individuals who, from the onset of their MS, have a steady neurologic decline but also suffer superimposed attacks.

    Factors triggering a relapse

    Multiple sclerosis relapses are often unpredictable and can occur without warning with no obvious inciting factors. Some attacks, however, are preceded by common triggers. In general, relapses occur more frequently during spring and summer than during autumn and winter. Infections, such as the common cold, influenza, and gastroenteritis, increase the risk for a relapse. Emotional and physical stress may also trigger an attack, as can severe illness of any kind. Statistically, there is no good evidence that either trauma or surgery trigger relapses. People with MS can participate in sports, but they should probably avoid extremely strenuous exertion, such as marathon running. Heat can transiently increase symptoms, which is known as Uhthoff's phenomenon. This is why some people with MS avoid saunas or even hot showers. However, heat is not an established trigger of relapses.

    Pregnancy can directly affect the susceptibility for relapse. The last three months of pregnancy offer a natural protection against relapses. However, during the first few months after delivery, the risk for a relapse is increased 20%–40%. Pregnancy does not seem to influence long-term disability. Children born to mothers with MS are not at increased risk for birth defects or other problems.[8]

    Many potential triggers have been examined and found not to influence relapse rates in MS. Influenza vaccination is safe, does not trigger relapses, and can therefore be recommended for people with MS. There is also no evidence that hepatitis B, varicella, tetanus, or Bacille Calmette-Guerin (immunization for tuberculosis) increases the risk for relapse.[9]

    Pathophysiology

    Although much is known about how multiple sclerosis causes damage, the reasons why multiple sclerosis occurs are not known.

    How multiple sclerosis causes damage

    Multiple sclerosis is a disease in which the body's immune system attacks the myelin surrounding nerve cells. Myelin is a fatty substance which covers the axons of nerve cells and is important for proper nerve conduction. A special subset of white blood cells, called T cells, plays a key role in the development of MS. Under normal circumstances, these lymphocytes can distinguish between self and non-self. However, in a person with MS, these cells recognize healthy parts of the central nervous system as foreign and attack them as if they were an invading virus.

    In MS, certain T cells trigger inflammatory processes when they encounter myelin, stimulating other immune cells and soluble factors like cytokines and antibodies. Normally, there is a tight barrier between the blood and brain, called the blood-brain barrier, built up of endothelial cells lining the blood vessel walls. The inflammatory processes triggered by the T cells create leaks in the blood-brain barrier. These leaks, in turn, cause a number of other damaging effects such as swelling, activation of macrophages, and more activation of cytokines and other destructive proteins such as matrix metalloproteinases. The final result is destruction of myelin, called demyelination.

    Repair processes, called remyelination, also play an important role in MS. Remyelination is one of the reasons why, especially in early phases of the disease, symptoms tend to decrease or disappear temporarily. Nevertheless, nerve damage and irreversible loss of neurons occur early in MS. Often, the brain is able to compensate for some of this damage, due to an ability called plasticity. MS symptoms develop as the cumulative result of multiple lesions in the brain and spinal cord. This is why symptoms can vary greatly between different individuals, depending on where their lesions occur.

    The oligodendrocytes that originally formed a myelin sheath cannot completely rebuild a destroyed myelin sheath. However, the brain can recruit stem cells, which migrate from other unknown regions of the brain, differentiate into mature oligodendrocytes, and rebuild the myelin sheath. These new myelin sheaths are often not as effective as the original ones. Repeated attacks lead to successively less effective remyelinations, until a scar-like plaque is built up around the damaged axons. Under laboratory conditions, stem cells are quite capable of differentiating and remyelinating axons; it is therefore suspected that inflammatory conditions or axonal damage somehow inhibit stem cell differentiation in the body.

    Why multiple sclerosis occurs

    Although many risk factors for multiple sclerosis have been identified, no definitive cause has been found. MS likely occurs as a result of some combination of both environmental and genetic factors. Various theories try to combine the known data into plausible explanations. Although most accept an autoimmune explanation, several theories suggest that MS is an appropriate immune response to an underlying condition.

    • Environmental

    The most popular hypothesis is that a viral infection or retroviral reactivation primes a susceptible immune system for an abnormal reaction later in life. On a molecular level, this might occur if there is a structural similarity between the infectious virus and some component of the central nervous system, leading to eventual confusion in the immune system. Since MS seems to be more common in people who live further from the equator, another theory proposes that decreased sunlight exposure[10] and possibly decreased vitamin D production may help cause MS. Other theories, noting that MS is less common in children with siblings, suggest that less exposure to illness in childhood leads to an immune system which is not primed to fight infection and is thus more likely to attack the body. One explanation for this would be an imbalance between the Th1 type of helper T-cells, which fight infection, and the Th2 type, which are more active in allergy and more likely to attack the body. Another theory describes MS as an immune response to a chronic viral infection. The association of MS with the Epstein-Barr virus suggests a potential viral contribution in at least some individuals.[11]

    • Genetic

    MS is not strictly a hereditary disease. However, increasing scientific evidence suggests that genetics may play a role in determining a person's susceptibility to MS. Some populations, such as Gypsies, Eskimos, and Bantus, never get MS. Native Indians of North and South America, the Japanese, and other Asian peoples have very low incidence rates. It is unclear whether this is due mostly to genetic or environmental factors.

    In the population at large, the chance of developing MS is less than a tenth of one percent. However, if one person in a family has MS, that person's first-degree relatives—parents, children, and siblings—have a one to three percent chance of getting the disease.

    For identical twins, the likelihood that the second twin may develop MS if the first twin does is about 30 percent; for fraternal twins (who do not inherit identical gene pools), the likelihood is closer to that for non-twin siblings, or about 4 percent. The fact that the rate for identical twins both developing MS is significantly less than 100 percent suggests that the disease is not entirely genetically controlled. Some (but definitely not all) of this effect may be due to shared exposure to something in the environment, or to the fact that some people with MS lesions remain essentially asymptomatic throughout their lives.

    Further indications that more than one gene is involved in MS susceptibility comes from studies of families in which more than one member has MS. Several research teams found that people with MS inherit certain regions on individual genes more frequently than people without MS. Of particular interest is the human leukocyte antigen (HLA) or major histocompatibility complex region on chromosome 6. HLAs are genetically determined proteins that influence the immune system.

    The HLA patterns of MS patients tend to be different from those of people without the disease. Investigations in northern Europe and America have detected three HLAs that are more prevalent in people with MS than in the general population. Studies of American MS patients have shown that people with MS also tend to exhibit these HLAs in combination-that is, they have more than one of the three HLAs-more frequently than the rest of the population. Furthermore, there is evidence that different combinations of the HLAs may correspond to variations in disease severity and progression.

    Studies of families with multiple cases of MS and research comparing genetic regions of humans to those of mice with EAE suggest that another area related to MS susceptibility may be located on chromosome 5. Other regions on chromosomes 2, 3, 7, 11, 17, 19, and X have also been identified as possibly containing genes involved in the development of MS.

    These studies strengthen the theory that MS is the result of a number of factors rather than a single gene or other agent. Development of MS is likely to be influenced by the interactions of a number of genes, each of which (individually) has only a modest effect. Additional studies are needed to specifically pinpoint which genes are involved, determine their function, and learn how each gene's interactions with other genes and with the environment make an individual susceptible to MS.

    Treatment

    There is no known definitive cure for multiple sclerosis. However, several types of therapy have proven to be helpful. Different therapies are used for patients experiencing acute attacks, for patients who have the relapsing-remitting subtype, for patients who have the progressive subtypes, for patients without a diagnosis of MS who have a demyelinating event, and for managing the various consequences of MS attacks. Treatment is aimed at returning function after an attack, preventing new attacks, and preventing disability.

    Modern medicine has failed to find an effective treatment for the overall condition although various drugs give short-term relief of different symptoms. Valium or similar tranquilizers are used to treat muscle spasms but can have the associated side effect of addiction, and doses often have to be increased sharply over time. MS patients who use Cannabis report a soothing of the painful muscle spasms and improved muscle coordination. Some are able to walk unaided when they were previously unable to do so. It also helps blurred vision, tremors, loss of bladder control, insomnia and depression.

    Management of acute attacks

    During symptomatic attacks, patients may be hospitalized. Patients in the United States are typically given high doses of intravenous corticosteroids, such as methylprednisolone, to end the attack sooner and leave fewer lasting deficits. When given to treat optic neuritis, although generally effective in the short term for relieving symptoms, corticosteroid treatments do not appear to have a significant impact on long-term recovery. Despite this fact, some neurologists recommend aggressive steroid treatment at the first signs of an exacerbation to reduce the duration in which inflammation persists in order to minimize the opportunity for damage to the nerves. Oral steroids tend to be given more often to patients in European nations, and they are frequently the only treatment offered to patients in countries where it is difficult to obtain the expensive disease-modifying medications. Recent findings suggest that oral steroid pills are just as effective at treating MS symptoms as intravenous treatment; the primary factor in the effectiveness of the treatment appears to be the high dosage over a short period of time, regardless of how the steroid is administered.

    Management of relapsing-remitting MS

    In the United States, as of 2005 there are five FDA-approved treatments for patients with relapsing-remitting MS. Three are interferons: Interferon beta-1a (Avonex and Rebif) or beta-1b (Betaseron [in Europe Betaferon]). The interferons are medications derived from human cytokines which help regulate the immune system. A fourth medication is glatiramer acetate (Copaxone), a mixture of polypeptides which may protect important myelin proteins by substituting itself as the target of immune system attack. The final medication, mitoxantrone is effective but is limited by cardiac toxicity. All five medications have been proven to be modestly effective at decreasing the number of attacks and slowing progression to disability. They differ primarily in ease of use, price, side effects, and the likelihood that extended use will decrease their effects. All of these therapies are expensive and require frequent injections, with Avonex requiring weekly injections and Copaxone daily injections. All of the interferons can lose effectiveness after continued use, with Avonex being the least likely and Betaseron the most likely. This is the result of neutralizing antibodies against the interferons. The interferons all require laboratory monitoring of blood tests. Even with appropriate use of medication, most patients with relapsing-remitting MS still suffer from some attacks and subsequent disability. Side effects are covered below.

    Management of progressive MS

    Treatment of progressive MS is more difficult than relapsing-remitting MS, and many patients do not respond to any therapy. A wide range of medications have been used to try to slow the progression of disease. Many therapies have been shown to have some effect on disease progression and resulting disability, but most therapies have significant side effects which limit their long-term use. Therefore they are often appropriate only for the most rapidly progressive cases. Azathioprine, cladribine, and cyclosporine have all shown small benefits, which in most cases are outweighed by side effects such as an increased cancer risk. Mitoxantrone, a chemotherapy drug, offers a significant reduction in progression to disability, but causes dose-dependant cardiac toxicity which limits its long-term use. Natalizumab (marketed as Tysabri) showed promise in early trials but has been withdrawn from the market in the United States because of an association with progressive multifocal leukoencephalopathy. Bone marrow transplant, plasmapheresis, and total lymphoid irradiation (exposure to high doses of radiation in order to kill parts of the immune system) have been studied and are currently reserved for the most dire cases. Cyclophosphamide and methotrexate are chemotherapy drugs which can slow the progression of MS, but which also have a number of side effects. Frequent courses of high-dose corticosteroids, often given weekly or monthly, are also commonly employed to good effect. Interferons show promise in secondary progressive MS, but more data is needed to support widespread use.

    Management of demyelination without a diagnosis of MS

    Several studies have shown that starting treatment with interferon beta-1a during the initial attack (and prior to the second attack required for a definite diagnosis of MS) can decrease the chance that a patient will develop MS. A separate medication, intravenous immunoglobulin (IVIG) has also shown promise in reducing progression to MS in this set of patients. Therefore, in certain patients, it is important that therapy be started prior to definite diagnosis.[12][13]

    Management of the effects of MS

    Because much of the damage caused by MS is irreversible, management of the resulting deficits is very important. As for any patient with neurologic deficits, a multidisciplinary approach is key to limiting and overcoming disability. Physical therapy, occupational therapy, and speech therapy are all important components of a comprehensive approach to maintaining quality of life. Treatment of emotional distress and depression should involve mental health professionals such as therapists, psychologists, and psychiatrists. Neurocognitive testing is important for determining the extent of cognitive deficits. Management of cognitive defects relies on lifestyle strategies, but also may respond to donepezil. Medications such as baclofen, tizanidine, dantrolene and Sativex have been shown to improve spasticity. Depression can be treated with a variety of antidepressants; selective serotonin reuptake inhibitors (SSRIs) are most commonly employed. The anticonvulsant drugs gabapentin and carbamazepine and the antidepressant amitriptyline can improve pain and tingling sensations in certain cases. Fatigue can often be managed by amantadine, pemoline, methylphenidate, and modafinil. Bladder spasms can be treated by oxybutynin and trospium chloride. Erectile dysfunction may respond to sildenafil, vardenafil, or tadalafil.

    Therapies under investigation

    Scientists continue their extensive efforts to create new and better therapies for MS. One of the most promising MS research areas involves naturally occurring antiviral proteins known as interferons. Beta interferon has been shown to reduce the number of exacerbations and may slow the progression of physical disability. When attacks do occur, they tend to be shorter and less severe. In addition, there are a number of treatments under investigation that may curtail attacks or improve function. Over a dozen clinical trials testing potential therapies are underway, and additional new treatments are being devised and tested in animal models.

    • A family of cholesterol-lowering drugs, the statins, have shown anti-inflammatory effects in animal models of MS. However, as of 2005 there is not sufficient evidence that statins are beneficial in the treatment of human MS patients with normal cholesterol levels.
    • A recent study found that women who took vitamin D supplements were 40% less likely to develop MS than women who did not take supplements. However, this study does not provide enough data to conclude that vitamin D has a beneficial influence on ongoing MS. Furthermore, it could not distinguish between a beneficial effect of vitamin D and that of multivitamin supplements including vitamin E and various B vitamins, which may also exert a protective effect.[14]
    • Low-dose naltrexone has been reported to reduce the progression and relapse rates in MS; however, as of 2005, the evidence is principally based on patient reports, and no formal studies have confirmed its effectiveness.
    • Beginning in the 1960s, a possible role in the etiology of MS for mercury exposure from amalgam used to fill dental caries (cavities) was explored. Although multiple studies[15] have shown no link between mercury amalgam and MS, a recent study [16] suggests an improvement after replacement of mercury amalgam in a small subset of patients identified by a blood test called MELISA.
    • One study [17] has documented that MS patients with a history of head or neck trauma may benefit from upper cervical chiropractic care.

    Side effects of medications for relapsing-remitting MS

    The two most common types of medications used to treat relapsing-remitting MS have significant side effects which warrant further discussion. Both the interferons and glatiramer acetate are available only in injectable forms, and both can cause irritation at the injection site. Interferons are produced in the body during illnesses such as influenza in order to help fight the infection. They are responsible for the fever, muscle aches, fatigue, and headache common during influenza infections. Many patients report influenza-like symptoms when using interferon to fight MS. This reaction often lessens over time and can be treated with over-the-counter fever reducers/pain relievers like paracetamol (acetaminophen), ibuprofen, and naproxen. Many patients choose not to take interferon due to the unpleasant experience of frequent injections and their subsequent side effects, citing a loss in their quality of life, although neurologists strongly discourage going without clinically proven treatment if one has been diagnosed with MS, since the long-term loss of quality of life due to unmodified progression of disability almost always outweighs the short-term discomforts of the treatment. Interferons can cause liver damage, and laboratory blood tests must be monitored to ensure safe use. Patients taking glatiramer acetate often experience a "post-injection" reaction manifested by flushing, chest tightness, heart palpitations, breathlessness, and anxiety.

    Prognosis

    The future course of the disease (or prognosis) for people with multiple sclerosis depends on the subtype of the disease, the individual's sex and race, their age, their initial symptoms, and the degree of disability they experience. The life expectancy of people with MS is now nearly the same as that of unaffected people. This is mainly due to improved methods of limiting disability, such as physical therapy and speech therapy, and more successful treatment of common complications of disability, such as pneumonia and urinary tract infections.[18]

    • Individuals with progressive subtypes of MS, particularly the primary progressive subtype, have a more rapid decline in function. In the primary progressive subtype, a wheelchair is often needed after six to seven years. In contrast, when the initial disease course is the relapsing-remitting subtype, the average time until a wheelchair is needed is twenty years. This means that many individuals with MS will never need a wheelchair.
    • The earlier in life MS occurs, the slower disability progresses. Individuals who are older than fifty when diagnosed are more likely to experience a chronic progressive course, with more rapid progression of disability. Those diagnosed before age 35 have the best prognosis. Females generally have a better prognosis than males. Although black individuals tend to develop MS less frequently, they are often older at the time of onset and may have a worse prognosis.
    • Initial MS symptoms of visual loss or sensory problems, such as numbness or tingling, are markers for a relatively good prognosis, whereas difficulty walking and weakness are markers for a relatively poor prognosis. Better outcomes are also associated with the presence of only a single symptom at onset, the rapid development of initial symptoms, and the rapid regression of initial symptoms.
    • The degree of disability varies among individuals with MS. In general, one of three individuals will still be able to work after 15–20 years. Fifteen percent of people diagnosed with MS never have a second relapse, and these people have minimal or no disability after ten years.[19] The degree of disability after five years correlates well with the degree of disability after fifteen years. This means that two-thirds of people with MS with low disability after five years will not get much worse during the next ten years. It should be noted that most of these outcomes were observed before the use of medications such as interferon, which can delay disease progression for several years.

    Currently there are no clinically established laboratory investigations available that can predict prognosis or response to treatment. However, several promising approaches have been proposed. These include measurement of the two antibodies anti-myelin oligodendrocyte glycoprotein and anti-myelin basic protein, and measurement of TRAIL (TNF-Related Apoptosis Inducing Ligand).[20]


    Epidemiology

    World map showing the that risk for MS increases away from the equator
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    World map showing the that risk for MS increases away from the equator

    In northern Europe, continental North America, and Australasia, about one of every 1000 citizens suffers from multiple sclerosis, whereas in the Arabian peninsula, Asia, and continental South America, the frequency is much lower. In sub-Saharan Africa, MS is extremely rare. With important exceptions, there is a north-to-south gradient in the northern hemisphere and a south-to-north gradient in the southern hemisphere, with MS being much less common in people living near the equator. Climate, diet, geomagnetism, toxins, sunlight exposure, genetic factors, and infectious diseases have all been discussed as possible reasons for these regional differences. Environmental factors during childhood may play an important role in the development of MS later in life. This idea is based on several studies of migrants showing that if migration occurs before the age of fifteen, the migrant acquires the new region's susceptibility to MS. If migration takes place after age fifteen, the migrant keeps the susceptibility of his home country.[21] Additionally, smoking has been shown to be an independent risk factor for developing MS.[22]

    MS occurs mainly in Caucasians. It is twenty-fold lower in the Inuit people of Canada than in other Canadians living in the same region. It is also rare in the Native American tribes of North America, the Australian Aborigines and the Maori of New Zealand. These few examples point out that genetic background plays an important role in the development of MS.

    As observed in many autoimmune disorders, MS is more common in females than males; the mean sex ratio is about two females for every male. In children (who rarely develop MS) the sex ratio may reach three females for each male. In people over age fifty, MS affects males and females equally. Onset of symptoms usually occurs between twenty to forty years of age, rarely before age fifteen or after age sixty.

    As previously discussed, there is a genetic component to MS. On average one of every 25 siblings of individuals with MS will also develop MS. Almost half of the identical twins of MS-affected individuals will develop MS, but only one of twenty fraternal twins. If one parent is affected by MS, each child has a risk of only about one in forty of developing MS later in life.[23]

    History

    A French neurologist named Jean-Martin Charcot (182593) was the first person to recognize multiple sclerosis as a distinct, separate disease in 1868. Summarizing previous reports and adding his own important clinical and pathological observations, Charcot called the disease sclerose en plaques. The three signs of MS now known as Charcot's triad are dysarthria (problems with speech), ataxia (problems with coordination), and tremor.[24] Prior to Charcot, Robert Hooper (17731835), a British pathologist and practicing physician, Robert Carswell (17931857), a British professor of pathology, and Jean Cruveilhier (17911873), a French professor of pathologic anatomy, had described and illustrated many of the disease's clinical details.

    There are several historical accounts of people who probably had MS. Saint Lidwina of Schiedam (13801433), a Dutch nun, may have been the first identifiable MS patient. From the age of sixteen until her death at age 53, she suffered intermittent pain, weakness of the legs, and vision loss—symptoms typical of MS. Augustus Frederick d'Este (17941848), an illegitimate grandson of King George III of Great Britain, almost certainly suffered from MS. D'Este left a detailed diary describing his 22 years living with the disease. His symptoms began at age 28 with a sudden transient visual loss after the funeral of a friend. During the course of his disease he developed weakness of the legs, clumsiness of the hands, numbness, dizziness, bladder disturbances, and erectile dysfunction. In 1844, he was confined to a wheelchair. Despite his illness, he kept an optimistic view of life. Another early account of MS was kept by the British diarist W. N. P. Barbellion, who maintained a detailed log of his diagnosis and struggle with MS. His diary was published in 1919 as The Journal of a Disappointed Man.

    Multiple sclerosis in film and television

    Famed British cellist Jacqueline Du Pre died of MS in 1987 after a long struggle with the disease, which robbed her of her capacity to perform as she progressively lost sensitivity in her fingers, muscle coordination, and her hearing. This decline was portrayed in some detail in the 1998 film, Hillary and Jackie.

    In the American television series The West Wing, the fictional United States President, Josiah "Jed" Bartlet, has the relapsing-remitting subtype of MS. The storylines have educated many viewers about the nature of MS and have helped to dispel some of the myths about the disease.

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