MS Update

An Overview of the MS Update at the American Academy of Neurology's 57th Annual Meeting

Written by Susan Wells Courtney Edited by Dr. Jack Burks

Introduction

The American Academy of Neurology (AAN) held its annual meeting from April 9th to 16th in Miami Beach, Florida. This is an important event attended by thousands of neurologists from around the world.

Multiple sclerosis is just one of the many neurological conditions that are discussed at the conference, and this is where neurologists receive the latest information in terms of diagnosis, treatment, experimental drugs, and MRI techniques. New findings are also presented in the etiology, pathogenesis, and pathology of MS – identifying the possible causes, development, and cellular processes involved with this disorder.

This article gives an overview of the full-day seminar, which was presented by top MS experts. The week-long meeting also featured several shorter classes to update physicians on the latest findings in MS. Additionally, poster sessions were held throughout the week. At these sessions, attendees view the posters, which are set up on easels and typically give the status or results of a research study. Often one or more of the researchers conducting the study will be present to discuss the findings with those who stop by their poster. Information from these shorter sessions and posters will be included in

In addition to the classes and poster sessions, the annual meeting features an exhibitors' area, where many organizations and vendors set up booths to promote their cause, product, or service. MSAA participates in this exhibit area to increase awareness of the organization and its mission, as well as to expose neurologists to the programs and services MSAA provides. By doing so, physicians may return to their offices and inform their patients of MSAA programs and services that may be helpful to them.

MS Update

On the second day of the conference, a full-day update on MS was given. To follow is an overview of the information presented.

Pathogenic and Clinical Implications of the MS Lesion

The MS Update began with a session on MS pathology, which looks at the disease processes in an effort to better understand what is occurring and why. This first segment was presented by Dr. Claudia Lucchinetti from the Mayo Clinic College of Medicine in Rochester, Minnesota.

The differences in the chronic MS lesion and active MS lesion were presented. Lesions are areas of inflammation and myelin damage within the central nervous system (CNS) as seen through magnetic resonance imaging (MRI) or under a microscope. Generally speaking, the CNS consists of the brain and spinal cord. Myelin is the protective covering or insulation to the nerves within the CNS, allowing nerve impulses to travel quickly and without interruption to their destinations. In MS, damage to the myelin occurs in these areas of inflammation (known as "demyelination"), and damage may occur to the nerves (or "axons") as well – often referred to as "axonal degeneration."

When new myelin is produced to replace damaged myelin, this is called "remyelination." Oligodendrocytes are the cells that make new myelin. While remyelination occurs more often in the early stages of MS, new myelin may also be produced during the chronic stages of MS, but this is more limited. Inflammation, more prevalent in active lesions (typical of earlier stages of MS), was also observed in lesser amounts in chronic, inactive lesions (typical of chronic stages of MS). The reduction of oligodendroctyes is just one possible explanation for the nerve's inability to regenerate myelin; a recent study suggests that the damaged nerve may not be receptive to the message of repairing damaged myelin.

Under normal conditions, the blood-brain barrier (BBB) keeps certain disease-fighting cells that exist in the blood system from passing through the walls of the blood vessels and entering into the CNS. With MS, these immune-system cells are able to cross this important barrier and make their way to the brain and spinal cord – where they cause inflammation and damage to the myelin and nerves. "Adhesion molecules" attach to the vessel walls and work like a key to open the BBB, allowing immune-system cells to cross the barrier. This was noted as an important step in the MS process.

When a body's immune system causes damage to the body's own tissue, this type of disorder is referred to as an "autoimmune" response. MS has traditionally been classified as this type of a disorder. Recent findings, however, indicate that MS may be a much more complicated process than previously recognized.

The role of inflammation in MS is still being defined through research. Most evidence supports that inflammation is a prerequisite for demyelination. It could also occur without demyelination, and may even play a role in the repair of MS lesions.

The author points out that MS differs between patients in terms of clinical, genetic, radiographic, and pathological features. Additionally, studies of MS lesions have shown that four distinct demyelination patterns occur, each with a different mechanism for causing damage to myelin or oligodendrocytes. Of the patients studied, each exhibited only one of the four types of active-lesion patterns. This supports the concept that different therapeutic strategies may be required for subgroups of individuals with MS.

Dr. Lucchinetti concluded by noting that both inflammatory and non-inflammatory factors contribute to the injury caused by MS. At this time, the MS lesion (associated with inflammation and demyelination) remains the target for therapy. Further research is needed to confirm the observations of the four subgroups of patients experiencing different patterns of demyelination, along with finding ways to readily identify markers which distinguish these lesion features. Such research may ultimately lead to more individual and effective therapies. Future approaches will be aimed at inhibiting demyelination, preventing nerve damage, and promoting repair.

Immune Intervention

The next session on immune intervention was presented by Dr. Samia J. Khoury from Harvard Medical School, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts. Dr. Khoury began by noting that MS is an autoimmune disease affecting the myelin within the CNS. As mentioned in the previous session, certain immune-system cells become activated and migrate (across the BBB) into the CNS, where they initiate an inflammatory response.

During the inflammatory response, several proteins (including myelin) may be recognized and targeted by these activated immune cells. These same cells exist in the circulation of healthy individuals, but in individuals with MS, these particular cells are in an activated state. Two theories, both relating to immune responses from a bacteria or virus, were presented as possible mechanisms for these cells to become activated in individuals with MS.

Experimental autoimmune enceph-alomyelitis (EAE) is an inflammatory CNS disease that is given to animals. This is done to observe how an MS-like disorder behaves in terms of symptoms as well as the cellular changes during active disease and recovery (generally the animals recover from this experimental disorder). Through such studies, researchers have been able to understand a great deal about the immune response in MS. This has also led to the therapies presently available to treat the disease.

During the past 10 years, much interaction has taken place between neurology and immunology to improve science's understanding of MS. This has resulted in the development of new therapies that target specific actions within the immune system.

The five approved therapeutic agents for MS affect the immune system in different ways. Interferon beta (which includes Avonex®, Betaseron®, and Rebif®) is a chemical that is normally produced by the body's immune cells during viral infections, explaining why individuals taking this drug may experience flu-like symptoms as a side effect. This chemical works by counteracting the effects of interferon gamma, another naturally-occurring chemical that promotes inflammation. Other potential mechanisms for beneficial effects have been proposed as well.

Glatiramer acetate (Copaxone®) binds to certain molecules through various mechanisms and induces an immune response that also reduces inflammation. Mitoxantrone (Novantrone®) is a chemotherapeutic agent, which works by killing proliferating (rapidly reproducing) cells. The mechanism of action is most likely related to general suppression of the immune system.

Since the approval of these current treatments for MS, other potential therapeutic targets for MS have been proposed and experimental treatments trials are being tested. To follow are some of these targets along with a few of the associated treatments.

• Blocking immune signals that would otherwise activate potentially damaging cells within the immune system; a phase I clinical trial of CTLA4Ig is presently being conducted for MS.
• Reducing the production of chemicals (such as interferon gamma) that may promote inflammation; oral salbutamol (albuterol) is presently in a phase II study (as an add-on therapy to glatiramer acetate); Rolipram® (previously prescribed as an antidepressant) is in a clinical trial for MS; and humanized monoclonal antibodies to IL-12 are also being studied in the treatment of MS.
• Targeting adhesion molecules to stop immune-system cells from migrating through the BBB into the CNS; natalizumab (Tysabri®) was in phase III trials but was voluntarily suspended from the market due to adverse events.
• Blocking other damaging processes involved with MS pathology; Matrix-metalloproteinase inhibitors (MMPI) are being tested in other autoimmune diseases and cancers; MMPs may be involved in the BBB breakdown.
• Reducing inflammation with statins (statins are a group of drugs currently approved as cardiac and cholesterol-lowering treatments); a recent trial suggests that simvastatin may be beneficial for MS patients.
• Promoting neuroprotection (protecting the nerves from damage); "Glu receptor antagonists" may be considered for MS studies in the future; such antagonists would interfere with L-Glutamate's ("Glu") ability to excite the immune system and possibly contribute to neuronal toxicity.

Dr. Khoury concluded with the concept that modern biotechnology and an improved understanding of the immunopathology of MS have led to the development of new therapeutic targets. While animal studies do not always translate directly to humans, EAE and other animal models have made effective treatments possible, bringing new hope to individuals with MS.

Magnetic Resonance Imaging in MS

This portion of the program was presented by Dr. Rohit Bakshi of Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Dr. Bakshi points out that as a result of ongoing technological advances, magnetic resonance imaging (MRI) continues to reveal new information about brain anatomy, chemistry, physiology, and pathology.

The MRI of the brain enables the neurologist to get an "inside view" of the changes that are taking place. MRI scans are vital to the initial evaluation of someone who is suspected of having MS. These are often ordered when a patient experiences an initial sign of the disease, also know as a "presenting symptom(s);" when only one symptom is experienced, this may also be referred to as a "clinically isolated syndrome" or "CIS."

An MRI is far more sensitive than clinical data when assessing disease activity. For this reason, MRI technology has also become an important tool (when needed) for measuring a patient's response to an established treatment. In addition, the worsening of MRI findings – even when a patient is not experiencing worsening symptoms (known as "clinically silent" disease activity) – may indicate long-term clinical deterioration.

Dr. Bakshi noted that MRI has an essential place in the initial evaluation of patients with suspected MS as well as in providing outcome measures in clinical trials. Through the use of a powerful magnet, the MRI is sensitive to processes that alter the water content of people's tissues, and is also sensitive to processes that constrain the motion of the hydrogen molecule. As a result, MRI images are able to show changes and abnormalities in tissues – including those which occur in the brain and spinal cord.

T2-weighted MRI images may reveal hyperintense lesions (those showing increased intensity) and are sensitive to lesion changes over time. This type of imaging is particularly helpful when evaluating patients at the earliest stage of the disease (such as individuals who present with a clinically isolated syndrome) as well as helping physicians to assess the effectiveness of a treatment. T2-weighted hyperintense lesions, however, cannot specifically identify underlying inflammation, edema, demyelination, axonal damage, nerve degeneration, or gliosis (scarring). Additionally, as someone's MS progresses, some hyperintense lesions tend to run together when viewed on this type of imaging. For these reasons, T2-weighted images of hyperintense lesions are less useful as one's MS advances.

Gadolinium (GAD) is a "paramagnetic" contrast agent that may be given to an individual via intravenous (IV) injection prior to an MRI. The gadolinium adheres to areas of acute inflammation which occur around the blood vessels (known as "perivascular inflammation"). These areas of acute perivascular inflammation indicate where the BBB has been compromised and immune cells may be entering the CNS.

When an MRI is performed, these areas of inflammation stand out since they have been enhanced by the contrast agent (GAD). While GAD-enhanced lesions are a weak predictor for short-term change in terms of disability, they do provide a measure of long-term disease activity as well as therapeutic efficacy in clinical trials.

T1-weighted images showing hypointense lesions (those of lower intensity) have been used recently as an outcome measure in clinical trials. Newly formed T1-hypointense lesions likely reflect inflammation, edema, demyelination, early remyelination, axonal changes, and glial activation (which forms scars). Approximately half of these lesions will resolve within six months. Permanent lesions may help to predict accumulating clinical symptoms.

Magnetic resonance spectroscopy (MRS) is used primarily as an investigational tool to examine lesions as well as normal-appearing brain tissue. This technology is able to detect various compounds within the tissue, which may potentially include products that result from the breakdown of myelin. MRS may be more sensitive than MRI in identifying abnormal tissue in MS, but MRS is still being validated as a measure in terms of clinical correlation and sensitivity to therapeutic effects.

Magnetization transfer imaging (MTI) is another technique that may detect demyelination, gliosis, and inflammation that may not be identified through a conventional MRI. The magnetization transfer ratio (MTR) is reduced when tissue damage (demyelination, axonal loss, etc.) occurs in MS. MTR actually declines a few months before GAD-enhancing lesions may be observed, and declines further as the lesion begins to enhance. While still exploratory at this time, MTI has the potential as a measure of long-term disease progression and treatment monitoring in MS.

The involvement of the spinal cord was also included in the presentation. According to Dr. Bakshi, hyperintense lesions on T2-weighted images may be observed in the spinal cord in many individuals with MS. Spinal cord lesions may relate more specifically with one's physical disability. For individuals with a "clinical picture suggestive of MS," but who have a normal brain MRI, lesions in the spinal cord may be visible in roughly five to 15 percent of these individuals. Spinal cord lesions may also be visible in some individuals presenting with a clinically isolated syndrome.

Article reprints on the role of MRI in MS, written by Robert Zivadinov and Rohit Bakshi, were included in this presentation on MRI. The presentation also included extensive information on MRI techniques as well as countless MRI images to assist neurologists with more precise analysis of disease activity.

Diagnostic Criteria for MS

The MS community is aware of the challenges involved with determining whether or not someone has MS. Individuals experiencing symptoms often must go through a long period of uncertainty before this diagnosis may be confirmed.

Dr. Brian G. Weinshenker of the Mayo Clinic College of Medicine in Rochester, Minnesota, outlined the criteria needed to diagnose MS, along with some of the pitfalls that may occur. Specific diagnostic criteria for MS were first proposed more than 50 years ago and since then have been updated many times. The majority of these updates resulted from advances in technology, particularly in regards to cerebrospinal fluid (CSF) analysis and MRI. Although many revisions have introduced new features, several basic principals were retained.

According to Dr. Weinshenker, a diagnosis of MS requires:

• lesions (such as those on an MRI) must be disseminated in time and space – meaning that at least two lesions must occur at different times as well as in different locations
• upon examination, the physician must observe "abnormalities" (in terms of a patient exhibiting one or more symptoms)
• the patient must also experience either relapses lasting at least one day and separated by at least one month, or a progressive disability worsening over at least six months
• no other diagnosis to explain symptoms (in earlier versions of the criteria, the diagnosis was limited to individuals between the ages of 18 and 50, but the medical community has since discovered that individuals with MS may be younger or older at onset)

MRI results, evoked potentials, and spinal fluid analysis were first integrated into diagnostic criteria for MS in 1983, through the work of Poser and others. This was the most widely used criteria until recently. The McDonald criteria are the newest version of diagnostic criteria for MS. Created by a committee in London and published in 2001, these criteria are based on lesions disseminated in time and space. It also removed arbitrary criteria (such as age), enabling some to be diagnosed sooner and possibly benefit from early intervention. The Barkhof criteria have also been adopted, adding MRI specificity to the McDonald criteria, with the intent of minimizing the possibility that inconsequential MRI changes would be misinterpreted.

Dr. Weinshenker notes that a better understanding of the role of MRI, along with enhancements in CSF analysis, have resulted in an improved diagnosis of MS, allowing physicians to better differentiate this disorder from other demyelinating diseases. While the present diagnostic criteria are of great value, they lack specificity. As the understanding of MS evolves, further modifications to the criteria may be appropriate.

Current Therapeutic Strategies

Dr. Dean M. Wingerchuk of the Mayo Clinic College of Medicine in Scottsdale, Arizona, summarized the recent advances in several aspects of therapy for demyelinating disease. He included the treatment of exacerbations, clinically isolated syndromes, and the different types of MS, using specific study results to support his conclusions.

Individuals experiencing an acute exacerbation, which is one that causes moderate or severe symptoms, are usually treated with corticosteroids. Dr. Wingerchuk points out that a short course of parenteral (administered non-orally) corticosteroids, will speed recovery from attacks. A meta-analysis of trials has shown that intravenous administration (IV) of methylprednisolone at 1,000 mg/day for five consecutive days may be the optimal treatment at this time. The value of oral prednisone for treating relapses is not known.

Individuals with very severe exacerbations who do not respond to corticosteroids may respond to plasmapheresis. Plasma-pheresis, also know as plasma exchange or "PE," is a procedure where the blood is circulated through a cleansing machine and returned to the body. A study showed that 42 percent of individuals receiving this therapy experienced significant clinical improvement. Individuals with severe optic neuritis who do not respond to corticosteroids may also benefit from this procedure. [Editor's note: while some individuals respond to plasmapheresis, the treatment effect may be temporary, the procedure is expensive, and plasmapheresis has side effects that should be taken into consideration.]

Dr. Wingerchuk notes that while such treatments are important for patients in order to speed recovery from a severe exacerbation, no treatment approach has been shown to improve long-term recovery. In other words, regardless of whether or not a patient received treatment for a relapse, studies show that his or her long-term outcome may not be altered.

Individuals diagnosed with relapsing-remitting MS (RRMS) often begin with a clinically isolated syndrome as their first episode, such as optic neuritis. Two studies ("CHAMPS" and "ETOMS") have shown that early treatment with interferon beta-1a may delay conversion to clinically definite MS and reduce disease activity in the brain as measured by MRI. Since the study was short term, researchers do not know if this early treatment has any beneficial effects on future disability and disease progression.

The three interferon drugs and glatiramer acetate are the main therapies in the treatment of RRMS. Dr. Wingerchuk's interpretation of the pivotal trials is that all three interferon (IFN) drugs reduce relapse rate by approximately one-third, and both of the IFN beta-1a drugs have at least one study that demonstrates an effect to slow the progression of disability. A pivotal IFN beta-1b study did not show a statistically significant change in EDSS measures (for progression of disability). Glatiramer acetate also shows a reduced exacerbation rate by approximately one-third, but studies did not show a significant impact on the progression of disability. [Editor's note: differences in trial design may prevent these trials from being directly compared.]

Scientific trials (the "INCOMIN" and "EVIDENCE" studies specifically) show some evidence for a dose effect with the interferon drugs, i.e., an increased dose resulting in an increased effect. Any change in dose, however, should only be determined by one's physician. An additional small study demonstrated that patients who remained on a standard dose of IFN beta-1b had a lower relapse rate than those who switched to a weekly dose of IFN beta-1a.

Studies have demonstrated that IFN beta-1b and IFN beta-1a are effective in slowing the rate of progression in SPMS patients over a two-to-three-year period. Critics, however, note that this improvement was very limited. Other studies with the interferons did not show an effect on disability progression in SPMS, but did show a treatment effect on multiple secondary outcomes, including relapse rate, relapse severity, and MRI measures of disease activity and total burden of disease.

With the use of interferon drugs comes the long-standing controversy over the possible impact of neutralizing antibodies (NAbs) on treatment efficacy. Formed by the body as a response to these types of drugs, some studies have indicated that persistent NAbs may have a negative effect on some clinical benefits of IFN treatment. Relapse rates have been higher during NAb-positive periods, but this did not affect progression as measured by EDSS. While brain MRI T2 volume changed during this time as well, MRI results were still better than for those on placebo. The clinical importance of NAbs has not been determined.

Natalizumab (Tysabri®, formerly known as Antegren®) was anticipated to be a strong line of treatment for individuals with RRMS. The drug was approved for treatment of MS in the United States in November 2004. Due to the diagnosis of an often-fatal brain disorder in two MS trial participants, however, the drug was voluntarily suspended from the marketplace in February 2005.

Phase II studies of this drug showed a 90-percent reduction in the number of GAD-enhancing lesions and more than a 50-percent reduction in clinical relapses. These led to the phase III "AFFIRM" study (Tysabri versus placebo) and "SENTINEL" study (Avonex plus Tysabri combination versus Avonex plus placebo). One-year data from the AFFIRM trial showed that the treated group experienced 66 percent fewer relapses and 92 percent fewer GAD-enhancing lesions. Determined by clinical and MRI measures, 46 percent of the treated group versus 14 percent of the placebo group were without disease activity during this first year.

Mitoxantrone (Novantrone®) was noted as a treatment option for worsening RRMS and secondary-progressive MS (SPMS). A small trial demonstrated that some individuals with worsening RRMS and SPMS may be stabilized when given this treatment, which is administered intravenously (IV). Individuals with SPMS are most likely to respond if they are: (1) in transition between RRMS and SPMS or (2) are still experiencing relapses or inflammatory disease activity. The study had a high dropout rate (along with other study-design issues), which may have affected the outcome. Numerous combination studies with mitoxantrone are either being planned or are ongoing. [Editor's note: this drug also has a two-to-three year, lifetime limit for treatment, given the potential for heart damage.]

Dr. Wingerchuk concluded his session with a discussion of unresolved issues. He covered topics such as: what evidence should be used to make treatment decisions; what long-term benefits are gained through reducing inflammation; how are treatment responders and nonresponders identified within trials; and how should treatment failure be defined.

Symptom Management

This session of the MS Update addressed symptom management, presented by Dr. Elliot M. Frohman, University of Texas Southwestern Medical Center at Dallas, in Dallas, Texas. Given space limitations for this article, information from this section will be included in upcoming "Symptom Awareness" columns in The Motivator, as well as other articles as they relate to the treatment of different MS symptoms.

New Directions in MS Therapeutics

This session of the MS Update discusses the many challenges involved with finding treatments for a disease where the cause and mechanisms of action are still not fully known. The information was presented by Robert J. Fox and Richard M. Ransohoff, both from The Mellen Center for Multiple Sclerosis Treatment and Research in Cleveland, Ohio.

Basic immunological research has enabled scientists to have a much better understanding of what they suspect may be happening within the central nervous system (CNS). This knowledge has led to the development and assessment of dozens of immune-based therapies for the treatment of MS.

The different types of MS pose one of the many challenges which arise in its study and successful treatment. Relapsing-remitting MS (RRMS) involves periods of demyelination, inflammation, scarring, edema, and nerve loss. In contrast, progressive forms of MS, including secondary-progressive MS (SPMS), appear to be largely degenerative (deterioration and loss of nerve cells), with little immunological or inflammatory involvement.

The distinct periods of relapses and remissions, characteristic of RRMS, allow for much easier detection of disease activity in terms of observable symptoms and active lesions (as shown on an MRI). This type of immune-system activity allows researchers to conduct studies with various agents and determine short-term results rather quickly. For this reason, most approaches to MS have been focused on the early stages of MS, with the hopes that early treatment will slow or stop the development of disability.

With progressive types of MS and their neurodegenerative component, changes are much harder to detect. Treatment trials for progressive MS require longer periods of time and outcomes are often difficult to determine. The presenters of this update explain that future research into treatments for progressive types of MS will be greatly assisted by (1) appropriate animal models to study the process that occurs in post-inflammatory demyelinating disease, and (2) more advanced clinical imaging techniques to observe this process.

The question still exists as to whether or not MS is an immunopathological disease (resulting from an immune response) or a neurodegenerative disease (resulting from some other cause of nerve damage). A third possibility is that MS evolves over time, changing from an abnormal immune response to a neurodegenerative process. The bottom line, however, is that therapies under development must be precisely targeted to those specific processes found to be involved with MS, whether inflammatory, neurodegenerative, or some other process.

An important aspect of MS research involves the animal models used to (1) evaluate the MS-like behavior of the immune system and inflammatory response, as well as (2) test the efficacy (effectiveness) of various treatments to interfere with the disease process. The most commonly used model is experimental autoimmune encephalomyelitis (EAE), a lab-induced disorder showing that autoimmunity to myelin can produce inflammatory damage to the CNS in animals along with resultant episodic paralysis.

While EAE has been extremely productive in terms of clarifying the different mechanisms that lead to CNS damage similar to MS, treatments do not always carry over well to human studies. Several therapies that have been successful in slowing or stopping the effects of EAE, were later found to have no effect or even a damaging effect on MS. Additionally, the two main lines of treatment for MS today were both found in round-about ways. Interferon beta therapies were originally tested to treat a chronic viral process. After being approved for MS, they were later found to be mildly effective in EAE. Glatiramer acetate was tested on EAE with the idea that it would exacerbate the disorder, but when found that animals with EAE improved, it led to trials in MS.

A wide range of drug therapies are currently under consideration for the treatment of MS. Many different types of therapies are being studied because of the numerous potential targets. Some of these treatments are in early development, while others are in later stages of clinical testing. The fact that some potential treatments may result in an increase of disease activity stresses two points: (1) the complexity of the immune dysfunction and (2) the importance of small studies for safety.

In addition to testing treatments that are injected or administered intravenously (IV), several studies with oral agents are in the planning or trial stages of development. Among others, these include cholesterol-lowering drugs (statins) and a drug named "SAIK-MS" (laquinimod). Oral treatments have obvious advantages, including patient comfort and convenience.

In conclusion, researchers and physicians continue to meet the challenges presented by the complexity of processes involved with MS. At this point in time, treatment has been largely focused on early, active MS versus later or progressive forms of MS. With the latter, including late SPMS, no therapy has been proven effective, although many studies are in progress. For example, intermittent (or "pulsed") corticosteroids may potentially help later-stage MS, but more studies are needed to confirm this finding as well as the long-term safety of this treatment. Protecting neural tissue from secondary degeneration following inflammatory injury is another vital area of research.

Given the vast number of therapies currently being studied for the treatment of MS, the presenters note that better therapies will surely be available in the years ahead. The research gives individuals with MS much hope for the future.

In the Next Issue of The Motivator...

This article on information presented at the AAN's annual meeting will be continued in a special Research News section in the Fall 2005 issue of The Motivator. At that time, highlights of the educational seminars and poster sessions will be listed (often giving specific study findings not yet published). The next issue of The Motivator will also feature an article on the Consortium of MS Centers' Annual Meeting. This will include an overview of the information presented, with topics such as: a full approach to managing symptoms; exercise and rehab; nursing perspectives; ethno-cultural issues; coping with illness and nurturing children; and using assistive technology devices.

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