MS Types

Being a woman and being young at diagnosis of multiple sclerosis were key hallmarks that allowed for "benign" disease over two decades or more, researchers said here.

Among MS patients who achieved benign status after 10 years, female sex (OR=1.68, P=0.032) was associated with a higher probability of remaining benign, with not more than moderate disability, at 20 years, said Antonio Scalfari, MD, from Imperial College in London, and colleagues at the American Academy of Neurology meeting.

This higher chance for maintaining a benign status was also seen for younger age at disease onset (ages 21 to 30 versus >30, OR=1.77, P=0.02; age ≤20 versus >30, OR=3.36, P<0.001), the authors reported.

Males and those older at disease onset had higher risk to become "no longer benign," Scalfari's group concluded.

"There are patients -- if we can identify them at an early age -- who may not require treatment," Scalfari told MedPage Today at his poster presentation. All of the benign patients in this study are untreated, he said.

He and colleagues reviewed data on 722 patients in the London Ontario Database. They noted that 270 of these patients converted to secondary progressive MS within 10 years of diagnosis, leaving 452 patients, classified by the researchers as experiencing "benign" MS. Of that group, 113 were lost to follow-up, leaving 339 patients for evaluation at 20 years.

Scalfari said that in the 10- to 20-year period, 166 of the subjects converted to secondary progressive disease, leaving 173 of these patients free from progression. However, he did note that lack of progression did not mean the patients were free of MS episodes; only that their condition did no deteriorate beyond an Expanded Disability Status Scale score of 3.

The majority of patients were female (71%) with a mean age of 26.8 at disease onset. Most of patients had monosymptomatic onset characterized by sensory disturbances (52.2%).

"This is a very controversial issue," he said. He noted that many clinicians believe that if MS is identified, patients should undergo early treatment because "there is a narrow opportunity for possibly modifying the disease and preventing progression." However, he added that treatments tend to attack the inflammatory component of the disease, so it remains unclear whether that treatment strategy actually changes the course of disability associated with the disease.

He pointed out that the number of MS episodes did not appear to influence whether a person lost their benign status. For example, the odds ratio of remaining in benign status was 30% greater if the patients had one attack in the first 2 years after diagnosis versus patients who had 3 or more attacks, but the difference was not statistically significant (P=0.50).

There was a 7% increased chance of remaining in benign status if a person had two attack in the first 2 years versus patients who had 3 or more attacks, but that result also did not reach statistical significant (P=0.87).

Abdullatif Al Khedr, MD, from the University Hospital Amiens in France, told MedPage Today, that he did not designate MS patients as "benign" in his practice. "These patients are mostly going to progress, but we think we can slow that progression if we take these patients and begin them on disease modifying treatments as early as possible."

Scalfari and Al Khedr had no disclosures.

Primary source: American Academy of Neurology
Source reference:
Scalfari A, et al "Long-term evolution of 'benign' multiple sclerosis patients in the London Ontario Database" AAN 2012; P01.138.

Source: Medpage Today © 2012 Everyday Health, Inc. (27/04/12)

Patients with relapsing onset Multiple Sclerosis (MS) who consumed alcohol, wine, coffee and fish on a regular basis took four to seven years longer to reach the point where they needed a walking aid than people who never consumed them. However the study, published in the April issue of the European Journal of Neurology, did not observe the same patterns in patients with progressive onset MS.

The authors say that the findings suggest that different mechanisms might be involved in how disability progresses in relapsing and progressive onset MS.

Researchers asked patients registered with the Flemish MS Society to take part in a survey, which included questions on themselves, their MS and their current consumption of alcohol, wine, coffee, tea, fish and cigarettes.

The 1,372 patients who agreed to take part were also asked to indicate whether they had reached stage six on the zero to ten stage Expanded Disability Status Scale (EDSS) and, if so, when this had happened.

"MS is a chronic, often disabling disease that attacks the central nervous system" explains lead author Dr Marie D'hooghe from the National MS Center at Melsbroek, Belgium. "The clinical symptoms, progression of disability and severity of MS are unpredictable and vary from one person to another.

"Two major MS onset types can be distinguished. Progressive onset MS is characterised by a gradual worsening of neurological function from the beginning, whereas patients with relapsing onset MS patients experience clearly defined attacks of worsening neurologic function with partial or full remission.

"EDSS 6 is an important milestone in the development of MS as it is the point at which patients need support to walk a reasonable distance."

The patients who took part were aged between 17 and 89 years-of-age:

- 65% (893) had relapsing onset MS. 76% were female, with an average age of 50 years. Age at MS onset averaged 31.5 years and disease duration averaged 19 years.

- 35% (479) had progressive onset MS. 62% were female, with an average age of 59 years. Age at MS onset averaged 37 years and disease duration averaged 21 years.

The researchers analysed how long it had taken people to reach EDSS 6 and compared those who reported moderate consumption of fish, alcoholic and non-alcoholic drinks and cigarettes with those who reported occasional or no consumption. This showed that:

Just over half (51%) had reached EDSS 6 after an average disease duration of 20 years. The percentage was much higher for people with progressive onset MS (80%) than relapsing onset (36%).
Patients with relapsing onset MS who consumed moderate amounts of alcohol (one drink a week or more) reached EDSS 6 seven years later than people who did not drink at all and wine drinkers reached it four years later than those who did not drink wine. The time differences were insignificant in people with progressive onset MS.
Daily coffee consumption delayed reaching EDSS 6 by five years in people with relapsing onset MS, but there were no significant differences in people with progressive onset MS. Drinking tea daily produced insignificant results in both groups.

People with relapsing onset MS who ate fish two or more times a week reached EDSS 6 seven years later than those who ate it less than once a month. It made no difference whether the fish was lean or fatty.

The time differences quoted above did not take into account gender, age at onset and treatment, which are known to affect disability progression in MS. But even after adjusting for these factors, the hazard risk analysis for time to sustained EDSS 6 (where 1.0 was the reference number for zero consumption) showed that:

The hazard risks for relapsing onset MS were significantly lower for a number of factors: moderate alcohol (0.61), moderate wine (0.67), daily coffee (0.60), occasional coffee (0.60), fish at least twice a week (0.60) and fish at least once a month (0.63).

- Daily cigarette smoking raised the risk to 1.35 in relapsing onset MS.

- The only hazard risk of any statistical significance for progressive onset MS was 1.56 for patients who preferred fatty fish, compared with those who preferred lean fish.

The paper contains full details of the suggested mechanisms that may be involved in the links between consumption and disease progression.

"Although our findings show a number of associations between consumption and disease progression, it is important that patients recognise that this does not imply that certain food and drinks provide a protective effect as other factors may be involved" stresses Dr D'hooghe.

"Our study does, however, provide valuable pointers for future research as it reinforces the theory that different mechanisms may be involved in the progression of disability in relapsing and progressive onset MS."

Full Article

Source: News-Medical.Net (19/03/12)

The Multiple Sclerosis Society of Canada and the Multiple Sclerosis Scientific Research Foundation announced a $3.8 million grant to investigate the complex interplay between degeneration and inflammation in multiple sclerosis (MS).

The grant will fund a study led by Dr. Peter Stys from the University of Calgary's Hotchkiss Brain Institute, which would investigate damage that occurs in MS prior to inflammation. This research may have special relevance for those with progressive forms of MS.

Collaborative grants funded by the MS Scientific Research Foundation support large, innovative, multi-centre studies that will lead to major advances in the field of multiple sclerosis. Key collaborators of the study include colleagues from the University of Calgary, the University of British Columbia, and Laval University and the VU University in Amsterdam. The MS Scientific Research Foundation receives the majority of its funding from the MS Society of Canada.

To date, researchers have largely attributed central nervous system (CNS) damage in MS to an autoimmune attack in which inflammation causes the hallmark patches of demyelination (also called plaques or lesions).

"This study hypothesizes that the inflammatory response in MS is the result of an underlying degenerative process rather than the primary cause of injury," says Dr. Peter Stys, lead researcher, Department of Clinical Neurosciences, University of Calgary. "In other words, an underlying mechanism causes degeneration that prompts the inflammatory process, which in turn causes more degeneration."

In general, progressive disease is characterized by a non-inflammatory neurodegenerative process. Approximately 10 per cent of people with MS are diagnosed with primary progressive MS. A more common type of progressive MS is secondary progressive MS - which begins as relapsing remitting MS, but then transitions to a progressive course. Fifty per cent of those with an initial diagnosis of relapsing MS eventually develop secondary progressive MS within ten years of diagnosis.

"The important roles of autoimmunity and the damage of inflammation are undeniable. But this doesn't mean that this is the starting point. If we can understand more about the earliest triggers in the disease processes in MS, we might learn how to intervene and prevent the damage that occurs prior to an inflammatory response," Dr. Stys says. "This research could provide information that benefits both relapsing remitting and progressive forms of MS."

Currently in Canada, there are seven disease-modifying treatments approved for relapsing forms of MS. However, despite best efforts, little progress has been made to date in the disease management of primary progressive MS or secondary progressive MS without relapses.

"We urgently need research that tackles the challenges unique to the progressive forms of MS," says Karen Lee, vice-president of research, MS Society of Canada. "Our hope is that Dr. Stys and his team of research collaborators will help us find answers. Can we identify the mechanisms that cause damage associated with progressive MS? Will the results lead to the development of new therapies that prevent, delay or slow progressive MS? This research may help answer these questions."

"There are often good news stories about treatments for relapsing-remitting MS and little to hope for with respect to progressive MS," says Michelle Amerie, who was diagnosed with MS over thirty years ago. "It's a relief to know that researchers from across the country are working together to try and understand the progressive form of MS. It makes me feel supported, gives me some hope."

While there are currently no effective medical treatments for progressive MS without relapses, it is possible to alleviate many symptoms, to improve some functions, and compensate for disabilities and thus improve quality of life.

About multiple sclerosis and the Multiple Sclerosis Society of Canada

Multiple sclerosis is a chronic, often disabling disease of the brain and spinal cord. It is the most common neurological disease of young adults in Canada. Most people with MS are diagnosed between the ages of 15 and 40, and the unpredictable effects of MS last for the rest of their lives. The MS Society provides services to people with MS and their families and funds research to find the cause and cure for this disease.

About the Multiple Sclerosis Scientific Research Foundation

The Foundation is related to the MS Society of Canada, which is its main funding source. The foundation funds large, innovative, multi-centre collaborative studies that will lead to major advances in the field of multiple sclerosis. It is a unique Canadian resource.

About the Faculty of Medicine at the University of Calgary

UCalgary's Faculty of Medicine is a national leader in health research with an international reputation for excellence and innovation in health care research, education and delivery. The Faculty of Medicine trains the next generation of health practitioners and move new treatments and diagnostic techniques from the laboratory bench to the hospital bedside, improving patient care. For more information, visit medicine.ucalgary.ca or follow them on twitter.com.

About the Hotchkiss Brain Institute

The Hotchkiss Brain Institute at UCalgary, consists of more than 100 physicians and scientists who are dedicated to advancing neurological and mental health research and education. The Institute's research strengths in foundational neuroscience (axon biology and regeneration, cerebral circulation, neural systems and behaviour) are leading to new treatments for neurological and psychiatric disorders, aimed at improving quality of life and patient care.

Source: Multiple Sclerosis Society of Canada (29/11/11)

Researchers from Mount Sinai School of Medicine presented several key studies at the American Academy of Neurology (AAN) annual meeting, including research providing critical insight into the prognosis and clinical treatment course of people with a certain subtype of Multiple Sclerosis (MS). The meeting is taking place April 9-16 in Honolulu.

In a study titled "Evaluation of Progressive Relapsing MS Patients in the PROMISE Trial," Fred Lublin, MD, Saunders Family Professor of Neurology and the Director of the Corinne Goldsmith Dickinson Center for Multiple Sclerosis at The Mount Sinai Medical Center and Michelle Fabian, MD, Neurology Fellow at Mount Sinai School of Medicine, conducted a subanalysis of the PROMISE trial. The clinical trial is a multinational, multicenter, double-blind, placebo-controlled trial evaluating the effects of glatiramer acetate treatment over three years in patients with primary progressive multiple sclerosis (PPMS). PPMS is characterized by steady disease progression, rather than attacks or exacerbations followed by remissions, which people with relapsing-remitting MS experience.

"We were able to analyze data from a well-controlled clinical trial to determine the frequency and clinical consequences of the occurrence of relapses in MS patients who initially have a progressive course," said Dr. Lublin. "Our data indicate that baseline characteristics and disease progression in PRMS differ from those in PPMS. As such, clinicians should consider evaluating the PRMS subgroup differently from those with PPMS in assessing prognosis and clinical course."

The research team evaluated differences in baseline characteristics and disease progression between patients with PPMS and patients with another subtype called progressive relapsing multiple sclerosis (PRMS) to help determine whether disease prognosis and treatment course should be evaluated differently in these subgroups. People with PRMS have steady disease progression, but also experience exacerbations, or relapses.

Using the data from the PROMISE trial, researchers found that 42 of the 943 PPMS patients in the PROMISE trial had documented relapses over the 53 months of the study, which indicates they could be categorized as PRMS. At the end of the study, the PRMS patients had a larger change in the Expanded Disability Status Scale, a method of quantifying disability in multiple sclerosis (0.92 vs. 0.59) than the PPMS patients, and increased risk for sustained disability progression. These results indicate that there is a definable subgroup that will inevitably convert to PRMS, and that disease progression is more rapid in this group. The data was presented Thursday, April 14, 2011.

Source: Medical News Today (c) MediLexicon International Ltd 2004-2011 (15/04/11)

STANFORD, Calif. — There may be two distinct versions of multiple sclerosis, a study in both animal models and human blood samples suggests. What’s more, a patient’s responsiveness to the most popular first-line drug for this episodic and all-too-often recurring autoimmune condition seems to depend on which version that patient has.

If these findings are confirmed in larger human studies and by other laboratories, people with multiple sclerosis might someday be able to take a simple blood test to see whether they are likely to respond to treatment with the standard multiple-sclerosis therapy, said senior study author Lawrence Steinman, MD, the George A. Zimmerman Professor of Neurology and Neurological Sciences at the Stanford University School of Medicine.

Public health may benefit, too, Steinman said, as the cost savings from being able to predict in advance which patients will benefit from beta-interferon, a costly bioengineered drug whose global sales come to some $4 billion a year, could be considerable.

Beta-interferon’s overall efficacy is only fair, he said, with perhaps half of all multiple-sclerosis patients experiencing an average one-third reduction in recurrences. Plus, its discomfiting side effects — flulike symptoms — can make compliance an issue for patients, especially given the drug’s iffy efficacy.

In a study to be published online March 28 in Nature Medicine, Steinman and his colleagues used an established animal model of multiple sclerosis called experimental autoimmune encephalitis, or EAE, which they induced by injecting the animals with myelin in a way that caused the immune system to inappropriately attack the animals’ own myelin nerve-cell coatings.

Many nerve cells in mammalian brains and peripheral tissues must convey electrochemical impulses over great distances, and quickly. Long, wirelike projections that transmit these cells’ signals to other nerve or muscle cells are coated by myelin, a natural substance whose insulating properties sustain the impulses’ strength and increase their speed.

Multiple sclerosis is triggered when, for reasons that are not yet clear, immune cells called T cells attack the myelin sheathing, causing symptoms including paralysis and blindness. The condition affects 400,000 people in the United States, according to the National Multiple Sclerosis Society.

A few years ago while still a PhD student at the University of Alabama, the study’s first author, Robert Axtell, had shown that, as in people with multiple sclerosis, beta-interferon can reverse paralysis in mice with EAE. But it turns out that EAE can be induced by two different autoimmune pathways, characterized by different patterns of secretion by T cells.

Like nerve cells, immune cells also communicate with one another across long distances, but they accomplish this through various chemicals called cytokines that they secrete into the blood. Immune cells on the receiving end of a cytokine “signal” may respond quite differently, depending on the particular type of cytokine to which they are exposed. Two cytokines called gamma-interferon and IL-17, for example, tend to induce the kinds of inflammatory immune-system arousal that can trigger multiple sclerosis.

Axtell (now a postdoctoral scholar in Steinman’s lab), Steinman and their colleagues were able to induce two superficially similar forms of EAE in mice by directing the myelin-attacking T cells to predominantly secrete either gamma-interferon or IL-17, respectively. The researchers found that beta-interferon improved the condition of animals whose EAE had been induced by gamma-interferon-secreting T cells, but exacerbated symptoms in those whose EAE had been induced by IL-17-secreting T cells.

Intrigued, the investigators turned to humans. Another postdoctoral scholar in the Steinman lab, Brigit deJong, MD, the study’s second author, had previously been involved in research in Amsterdam in which multiple-sclerosis patients were treated with beta-interferon and meticulously followed up. The Stanford group obtained blood samples taken from 26 of these patients both before and about two years after the initiation of treatment. Without knowing which samples came from patients who had responded well or poorly to beta-interferon treatment, they went about measuring IL-17 levels in those samples.

Eventually, patients’ follow-up histories were revealed to the researchers and their measured IL-17 levels were paired with their post-treatment progress. A clear pattern emerged. Measurements of a particular variety of IL-17, called IL-17F, clustered at either very high or very low levels in individual patients’ blood. Those with very low detectable blood levels of IL-17F responded well to beta-interferon treatment, experiencing no relapses or instances of required steroids (to quickly shut down a malfunctioning immune system). But patients with very high IL-17F levels — about one out of three subjects — responded poorly by the same criteria. In fact, said Steinman, there is some evidence that beta-interferon actually worsened these patients’ conditions.

Steinman cautioned that the results need to be confirmed in larger patient groups, in his lab as well as in others. But, he said, “I think this has the potential to transform the way we take care of people with multiple sclerosis.” He said a simple, already available blood test could spare many patients the inconvenience and side effects — and spare the health-care system the expense — of a drug that most likely won’t do any good. “The other side of the coin is that beta-interferon, if it’s given only to those who are predisposed to respond to it, could turn out to be a far better drug than we ever imagined.”

Although Steinman and his colleagues do not stand to benefit in any direct way from this work, Stanford University’s Office of Technology Licensing has filed a patent application on the use of the blood test. Earlier work by Steinman, proceeding from animal models to clinical trials, led to the development of another blockbuster multiple-sclerosis drug, natalizumab, marketed under the trade name Tysabri.

Helen Yates, Chief Executive, MSRC said, “This piece of research potentially offers a very new light on MS particularly in relation to the use of the Beta Interferon drugs.  It has long been a problem understanding why some people with MS seem to do quite well on these drugs whilst others fair badly.  Some people have such a dreadful experience on the Beta Interferon group that they come off the drug but with no explanation as to why this is. 

To be able to test, pre-treatment, for the likelihood of the drug having a positive impact will not only save money on drug prescriptions but more importantly, will mean that the person with MS will know, from the outset if there is any value in starting this particular course of treatment.

MSRC welcomes further study into this very interesting area.”

Several other scientists from Stanford and elsewhere co-authored the Nature Medicine study, which was funded by the National Multiple Sclerosis Society. Axtell’s former PhD advisor, Chander Raman, PhD, of the University of Alabama-Birmingham’s Department of Medicine, shares senior authorship with Steinman. More information about Stanford’s Department of Neurology and Neurological Sciences, which supported the work, is available at http://neurology.stanford.edu/.

Nature Medicine Article - T helper type 1 and 17 cells determine efficacy of interferon-β in multiple sclerosis and experimental encephalomyelitis 

Source: The Stanford University School of Medicine & MSRC (28/03/10)

Regular neurocognitive screening and MRI scans may be able to spot patients with so-called benign multiple sclerosis who will soon develop significant disabilities, researchers said.  

They found that T1-weighted brain lesion volume detected on MRI scans, the number of neurocognitive tests failed at baseline, and male gender, were each significantly predictive of disease progression.

A model combining all three predictors distinguished those who progressed with an accuracy of 82%, the researchers reported.

Some individuals show certain signs of multiple sclerosis but then go 10 years or more without showing any disability. The term "benign multiple sclerosis" has been applied to those signs, but neurologists have debated whether the term is appropriate, although many of these patients do eventually lose peripheral motor function and show other MS-related disabilities.

"Correct and early identification of these patients is crucial as it may provide valuable information in the therapeutic decision-making process," the researchers said.

So they enrolled 63 patients diagnosed with MS at least 15 years previously but who had Expanded Disability Status Scale scores of 3.0 or less, indicating minimal or no functional disability.

They were evaluated with the Stroop Test and the Brief Repeatable Neuropsychological Battery. The latter consists of five subtests that assess verbal and visual memory, attention and speed of information processing, and verbal fluency.

Participants were considered to have failed a test if scores were at least two standard deviations below the mean. Cognitive impairment was defined as failing three or more tests.

MRI scans were performed in 46 participants to evaluate T1- and T2-weighted brain lesions.

At the end of the follow-up period, disability scores were calculated. Disease was considered no longer benign in those with scores of at least 4.0 or who qualified for a diagnosis of secondary progressive MS.

At follow-up, 43 patients still had benign disease, whereas 18 had developed significant disabilities or secondary progression.

Half of those who progressed were men, compared with about 20% of those whose illness remained benign.

Participants whose illness was designated as no longer benign at follow-up had failed a mean of 3.6 neurocognitive tests at baseline (SD 2.3) compared with 1.3 (SD 1.5) among those still classified as benign (P=0.009).

Both T1- and T2-weighted lesion volumes at baseline were significantly higher in those with disability or symptom progression at follow-up, and normalised cortical volume at baseline was significantly smaller:

• Mean T1 lesion volume: 4.9 still benign, 13.4 no longer benign (P=0.001)
• Mean T2 lesion volume: 12.0 still benign, 26.0 no longer benign (P=0.002)
• Normalized cortical volume: 627.1 still benign, 561.1 no longer benign (P<0.001)

Although mean T2 lesion volume and normalized cortical volume seemed to be powerful risk factors in univariate analysis, only T1-weighted volume was an independent predictor of disability in multivariate analysis.

Magnetisation transfer ratios in the normal-appearing white matter or T1 or T2 lesions did not appear to correlate with disease progression.

The researchers developed a statistical model that scored participants on a four-point scale for their risk of showing progression, based on age, T1-weighted volume, and cognitive test failures.

They found a hazard ratio for designation as no longer benign of 9.2 (95% CI 2.7 to 30.8) for participants with scores of 3 or 4, compared with those scoring at 2 or less.

The model correctly classified 82% of participants on the basis of their baseline profile.

In an accompanying editorial, Ralph H.B. Benedict, PhD, of the State University of New York at Buffalo, and Franz Fazekas, MD, of the Medical University of Graz, Austria, called the findings important.

"If some patients with so-called benign disease course have cognitive impairment, and if cognitive impairment is a significant risk of disease progression, much more attention should be devoted to detecting and preventing such pathology in these otherwise healthy-appearing patients," they wrote.

The editorialists said the study supports routine screening of MS patients for cognitive impairment, but they pointed out that the available instruments all have limitations.

"The point at which patients with clinically isolated syndrome or benign MS should be entered into such a neuropsychological screening and monitoring program of medical care is debatable," wrote Drs. Benedict and Fazekas.

Nevertheless, they added, the study highlights "the importance of a more comprehensive evaluation of patients with MS with a seemingly benign course."

Dr. Amato and colleagues said their study was limited by the selection criteria for participants -- they were participants in previous studies and were seen at three Italian specialty clinics -- and the study did not account for disease modifying drugs given during follow-up. Also, not all participants underwent MRI scans.

Source: Medpage Today © 2004-2009 MedPage Today, LLC. (30/07/09)

The findings suggest that doctors should be cautious about using the term "benign multiple sclerosis" or "benign MS."

"We need to be careful what we tell people, and not give them false hope that their symptoms may never get worse," says Ana-Luiza Sayao, MD, in a news release.

Sayao works in Vancouver at the University of British Columbia.

She and her colleagues studied 169 patients with "benign MS," which the researchers defined as having a low level of disability 10 years after diagnosis.

Multiple sclerosis is a disease of the brain and spinal cord. Its symptoms may include vision problems, muscle weakness, and difficulty with walking, coordination, and balance.

Some patients experience relatively mild MS; other cases are severe.

Changes in 'Benign' MS

Sayao and colleagues checked the patients' medical records 20 years after MS diagnosis.

Just more than half the patients — 52 percent — still had "benign MS," meaning their disability was still relatively mild 20 years after MS diagnosis.

But disability had worsened in the other patients.

Of all the patients studied, roughly one in five needed a cane to walk 20 years after their MS diagnosis.

Sayao's team found no factors — such as patients' sex or age at MS onset — that predicted which cases would worsen.

Benign Really?

The study questions the use of the term "benign multiple sclerosis."

"Although there is certainly a unique subgroup of patients with MS who remain mild in disability over the long term, a lack of consensus in the criteria that define 'benign' MS continues to exist," the researchers note.

Journal editorialist Scott Pittock, MD, agrees.

"Whether there is a benign form of multiple sclerosis continues to be a controversial issue," writes Pittock, who works at the Mayo Clinic in Rochester, Minn.

Pittock says "a 'watchful waiting approach,' with regular clinical and MRI monitoring" may be preferable for some patients with benign MS before starting MS drug treatment."

He also sees reason for optimism for such patients.

"The MS prognostic glass is half full for a high proportion of these most benign cases," Pittock writes.

SOURCES: Sayao, A. Neurology, Feb. 13, 2007; vol 68: pp 496-500. Pittock, S. Neurology, Feb. 13, 2007; vol 68: pp 480-481. News release, American Academy of Neurology.

Copyright 2007, WebMD Inc. All rights reserved.(12/02/07)

The crippling degenerative disorder multiple sclerosis may actually be four different diseases, say researchers.

An international team of scientists carried out tests on more than 80 MS patients.

They found that although the patients had similar symptoms they were the result of four different causes.

Lead researcher Dr Hans Lassmann, from the University of Vienna, said the team had still to identify exactly what the causes were.  

They speculate they may include viruses or disorders of the immune system.

Dr Lassmann said the research indicated that treatments that might aid one patient could potentially be harmful to another.

He said: "Therapies must be tailored towards the needs of specific patient subgroups."

Multiple sclerosis is caused when myelin, the fatty substance that protects the nerves, is damaged or destroyed and replaced with scar tissue.

This scarring, called sclerosis, slows the electrical signals in the nerves.

Depending on which nerve fibres are affected, patients have symptoms ranging from weakness and clumsiness to numbness, visual disturbances, and even emotional and intellectual changes.

Some patients experience cycles of relapse and remission while others have a steady progression to severe debilitation and death.

Tissue samples

Dr Lassmann and collaborators from the Mayo Clinic in Rochester, Minnesota and the University of Gottingen in Germany gathered tissue samples from 51 patients who had brain biopsies performed during acute flare-ups of MS and 32 who died during acute episodes.

The researchers were able to identity four distinctly different patterns of nerve demyelination among the patients.

This, they believe, indicates profound differences in the way the disease was caused.

Some researchers believe that MS may be caused by a virus.

A virus resembling polio easily causes MS in laboratory mice.

But the condition also resembles an autoimmune disease, in which the immune system mistakenly attacks healthy tissue.

Dr Lassmann's research suggests both theories may be correct.

A spokesman for the UK MS Society said: "It is known that there are different types of MS and that there could be variations in the cause of the disease.

"This latest research is welcome in helping to increase our understanding of MS and potentially more effective ways of treating it.

"Until then we must continue to rely on clinical judgement based on properly conducted trials to decide which disease-modifying therapies and symptomatic treatments are appropriate in individual cases."

Dr Lorna Layward, head of research at the society, said clinical trials had shown that some patients responded to current drugs in use such as beta interferon and copaxone, while others did not.

She said it appeared that these drugs were more effective for patients suffering from acute attacks of multiple sclerosis, rather than those whose condition was growing gradually worse.

The research is published in the Annals of Neurology.

Source: BBC News © BBC 2000 (08/06/00)

© Multiple Sclerosis Resource Centre