Final Program,Abstract Listing and Meeting Information

Transcription

7th Annual Meeting of the
Americas Committee for
Treatment and Research
in Multiple Sclerosis
18th Congress of the
European Committee for
Wednesday,
September 18
through
Saturday,
September 21
2002
Baltimore Marriott
Waterfront Hotel
700 Aliceanna Street
Baltimore, Maryland, USA
A
Acknowledgement of Sponsors
The ACTRIMS-ECTRIMS 2002 Steering Committee
acknowledges the generous support of our Gold Sponsors:
The Steering Committee also acknowledges
the support of Wyeth Pharmaceuticals
This program is offered in collaboration with
the National Multiple Sclerosis Society.
Welcome Letter
Dear Colleagues and Friends,
We cordially welcome you to Baltimore, Maryland, and ACTRIMS-ECTRIMS 2002, the second joint meeting of the
Americas and European Committees for Research and Treatment in Multiple Sclerosis. This is an exciting time in MS
research and clinical care. Decades of basic investigation have resulted in greatly improved understanding of MS,
which is now being translated into proven therapies. However, we—and the patients we serve—cannot be satisfied
with the current state of our knowledge and treatments. We hope that the information provided during this important meeting will further advance the goal of finally conquering MS and its resulting disability.
Our three key areas of research highlighted at the conference are:
• Inflammation, Demyelination, and Axonal Loss: Pathological and MRI Perspectives
• Neuroprotection
• Methodological Issues in Clinical Trials
In addition to the official program, we are pleased to offer two pre-conference symposia sponsored by groups long
associated with the treatment of MS and five satellite symposia supported by our gold sponsors.
We extend our appreciation to our Program Committee, chaired by Drs. Suhayl Dhib-Jalbut and Paul O’Connor,
for their tireless effort in guiding and shaping the content of this comprehensive meeting.
We hope that you will join us for each of the social activities, planned by our Local Arrangements Committee
chaired by Drs. Chris Bever and Peter Calabresi, and that you will allow some time to explore the harbor city of
Baltimore, with its array of shopping destinations, historical sites, museums and galleries.
We look forward to your active participation in this very interesting program. Thank you for joining us.
Dr. Kenneth Johnson
Chair, ACTRIMS
Dr.Alan Thompson
President, ECTRIMS
1
Committees
Steering Committee
Program Committee
Kenneth Johnson (USA)
Chair, ACTRIMS
Alan Thompson (UK)
President, ECTRIMS
Jack Antel (Canada)
Ludwig Kappos (Switzerland)
Donald Paty (Canada)
Chris Polman (The Netherlands)
Per Soelberg Sorensen (Denmark)
Jerry Wolinsky (USA)
Suhayl Dhib-Jalbut (USA)
Co-Chair
Paul O’Connor (Canada)
Co-Chair
Jeffrey Cohen (USA)
Giancarlo Comi (Italy)
Christian Confavreux (France)
Anne Cross (USA)
Mark Freedman (Canada)
Hans Peter Hartung (Germany)
Reinhard Hohlfeld (Germany)
Ludwig Kappos (Switzerland)
Roland Martin (USA)
Chris Polman (The Netherlands)
John Richert (USA)
Per Soelberg Sorensen (Denmark)
Alan Thompson (UK)
Local Arrangements Committee
Chris Bever, Co-Chair
Peter Calabresi, Co-Chair
Lee Koski
Mary Rose
Peggy Allen
National MS Society Organizing Committee
Debra Entin, Chair
Leslie DiLeo
Abe Eastwood
Nancy Holland
Dinah Martinez
Diann Rohde
Bill Rosen
Kristin Summers
2
Content Index
Abstracts Author Index. . . . . . . . . . . . . . . . . . . . . . 50–55
Acknowledgement of Sponsors . . . . . . . Inside front cover
Ancillary Meetings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
Committees. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Exhibition Information. . . . . . . . . . . . . . . . . . . . . . . 32–35
Floor Diagrams . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
General Information . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Late Breaking News Abstracts . . . . . . . . . . . . . . . . 56–57
Maps of Downtown Baltimore . . . . . . . . . . . . . . . . . . . 58
Next Year’s Meetings . . . . . . . . . . . . . . . . . . . . . . . . . . . 60
Poster Display Schedule . . . . . . . . . . . . . . . . . . . . . 40–48
Program Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
Program Schedule . . . . . . . . . . . . . . . . . . . . . . . . . . 19–27
Social Events . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
Transportation Schedule . . . . . . . . . . . . . . . . . . . . . . . . 13
Travel Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Welcome Letter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
3
Response.
Proven
results for
people
with
relapsing
MS.
MS affects different people in different ways each and
every day. Rebif ® has been proven to provide patients
with the following treatment benefits in the main
measures of disease activity:
• Reduces MRI lesion activity1*
• Reduces frequency of relapse1,2
• Delays progression of disability1,2
*The exact relationship between MRI findings and the clinical
status of patients is unknown.
Rebif is the market leader outside the US.
Rebif is available in more than 70 countries.
Please see brief summary directly following MS LifeLinesTM ad
References:
1. PRISMS (Prevention of Relapses and Disability by Interferon beta-1a Subcutaneously in Multiple Sclerosis) Study Group. Randomized
double-blind placebo-controlled study of interferon beta-1a in relapsing/remitting multiple sclerosis. Lancet. 1998;352:1498-1504.
2. Rebif® (interferon beta-1a) Prescribing Information. Serono, Inc; 2002.
3. Data on File. Amendment to BLA File, Study 21125, Serono, Inc; 2002.
4
®
Results. Rebif.
Patients
• 75% of Rebif patients vs 63% of Avonex® patients were relapse-free2
taking Rebif – 32% relative reduction in risk of relapse (p<0.001)
• Rebif patients experienced a mean of 28% fewer relapses at
were less
24 weeks2,3
likely to
0.40 Avonex vs 0.29 Rebif (p=0.022)
experience • –Treatment
effect was maintained over 48 weeks
a relapse at
24 weeks.2,3
2
®
®
*Primary Endpoint: Proportion Relapse-free
Adverse reactions at 24 weeks were generally similar despite
higher, more frequent, subcutaneous dosing with Rebif 2.
Exceptions included injection-site disorders, hepatic function
disorders, and leukopenia2,3.
Rebif® (interferon beta-1a) is indicated for the treatment
of patients with relapsing multiple sclerosis to decrease
the frequency of clinical exacerbations and delay the
accumulation of physical disability. Rebif should be used
with caution in patients with depression, pre-existing
seizure disorders, and liver problems.
Avonex® is a registered trademark of Biogen, Inc.
5
Convenience
Independence for Patients
• Rebif ® is the first and only interferon available in ready-to-use, prefilled syringes
• Rebif is administered subcutaneously
• Rebiject™ injection device ensures proper injection technique
• Injection training with a licensed nurse
• Travel Kit including prepaid phonecard makes travel easier
• Patients are just one toll-free phone call away from professionals who
can offer immediate assistance
For more information on the benefits of Rebif therapy,
please visit www.rebif.com or call 1-877-44-Rebif (447-3243)
Please see brief summary directly following
MS LifeLinesTM ad
6
Rebif® is a registered trademark of Serono, Inc.
MS LifeLines™ and RebijectTM are trademarks of Serono, Inc.
©2002 Serono 02-19201 06/02 All rights reserved. Printed in the USA.
Prescribe Your
Patients Rebif
and More.
®
Response
• Dedicated team of trained Customer Support Specialists
available Monday through Friday from 8 AM to 8 PM EST
• English and Spanish language support available
Results
• Reimbursement support
• Pharmacy coordination
• Injection training
• Ongoing nurse follow-up
Rebif®
• Complimentary Travel Kit
• Education support materials
• Rebiject™ injection device
Patients with MS are just one toll-free phone call away from
professionals who can offer immediate assistance.
Patients can call today
Phone:1-877-44-Rebif (1-877-447-3243)
Fax:1-866-22-Rebif (1-866-227-3243)
or visit our websites at:
www.MSLifeLines.com
www.rebif.com
MS LifeLines™ and Rebiject™ are trademarks of Serono, Inc.
Program Overview
Wednesday
September 18
Thursday
September 19
Friday
September 20
Saturday
September 21
Registration
6:30 am–7:30 pm
Grand Ballroom Level
Registration
6:30 am–7:00 pm
Registration
7:00 am–1:30 pm
Continental Breakfast
6:30 am–8:00 am
6:30 am–8:15 am
7:00 am–8:15 am
Welcome and
Keynote Address
8:15 am–9:30 am
Grand Ballroom I–X
Welcome and
Keynote Address
8:30 am–9:30 am
Parallel Sessions
10:00 am–12:00 pm
Session I
Grand Ballroom I–V
Session II
Grand Ballroom VI–X
Parallel Session
10:00 am–12:00 pm
Session V
Session VI
Pre-conference Symposia
12:00 pm–1:30 pm
MS Forum
European Charcot Fdn
Grand Ballroom VI
Poster Session I
and Lunch
12:00 pm–2:00 pm
Harborside Level
Poster Session II
and Lunch
12:00 pm–2:00 pm
Harborside Level
Young Scientific
Investigators Session
2:00 pm–4:30 pm
Parallel Sessions
2:00 pm–4:00 pm
Session III
Session IV
Parallel Sessions
2:00 pm–4:00 pm
Session VII
Session VIII
Satellite Symposium II
4:30 pm–5:30 pm
Satellite Symposium IV
4:30 pm–5:30 pm
Satellite Symposium I
5:00 pm–6:00 pm
Grand Ballroom VI
Satellite Symposium III
6:00 pm–7:00 pm
Satellite Symposium V
6:00 pm–7:00 pm
Welcome Reception
7:00 pm–9:00 pm
Harborside Ballroom
Social Event
National Aquarium
in Baltimore
7:30 pm–10:30 pm
Social Event
B&O Railroad
Museum
7:30 pm–10:00 pm
Registration
10:00 am–9:00 pm
Welcome and
Parallel Sessions
8:30 am–10:30 am
Session IX
Session X
ECTRIMS Lecture
11:00 am–11:45 am
Closing Lunch
12:00 pm–1:00 pm
Harborside Ballroom
Committee Reception
(by invitation)
7:00 pm–10:00 pm
Baltimore Museum
of Industry
Exhibits and Poster Displays
Harborside and Grand Ballroom Levels
Wednesday: 1:00 pm–5:00 pm Thursday and Friday: 8:00 am–5:00 pm
9
Biogen and Elan –
pioneers in adhesion molecule biotechnology
®
General Information
Attire
Since meeting room temperature and personal comfort
levels vary, it is recommended that you bring a sweater
or jacket to the conference activities. Attire for meetings
and social events is business casual.
Badges
Attendees will be required to wear their delegate badge
at all times to access the exhibition area, the conference
rooms and the posters area. Colored ribbons denote
the following:
Committee Members WHITE
Exhibitors
ORANGE
Poster Presenters
LIGHT BLUE
Press
PINK
Speakers
BLUE
Staff
RED
Volunteers
GREEN
Baltimore
For information regarding airports, activities, ground transportation, etc., consult the Baltimore Area Convention
and Visitors Association website at www.baltimore.org.
Child Care Information
A variety of child care options are available in Baltimore.
You may wish to check with the concierge at your hotel
upon arrival.
Language
English is the official language of the conference. No
simultaneous translation is available.
Meals
The registration fee for conference participants includes
continental breakfast, coffee breaks, lunches during the
conference, and the evening social events organized by
the Steering Committee.
Mobile Phones
The Steering Committee request that attendees turn
cellular phones and pagers to vibrate upon entering all
exhibit and social functions.
No Smoking
For the health and comfort of everyone, smoking is prohibited at any meeting function. This includes all scientific
activities, exhibits and social functions.
Optional Social Tours
For half-day and whole-day excursions to sites in and
around Baltimore, please consult the conciege at your hotel.
Photography
Flash picture taking is not allowed during the scientific
activities or in the exhibit area.
Contact Information
ACTRIMS-ECTRIMS 2002
c/o NMSS
733 Third Avenue 6th Floor
New York, NY 10017 USA
Phone: 212-476-0465
Fax: 212-661-9735
E-mail: ae2002@nmss.org
www.actrimsectrims2002.nmss.org
Recording of Programs
Audio and videotaping are not allowed in the meeting
rooms, exhibit area, or at social functions.
E-Mail Stations
Complimentary e-mail stations and printers will be available in the Harborside Level Foyer. Please limit your use
to 15 minutes. This service is available to registered participants only. Thank you for your cooperation.
Weather
September temperatures range from 65 F (18 C) to
80 F (27 C).
Special Needs
If you have a special need that requires an accommodation, please stop by the registration desk and speak
with an organizing staff member.
11
Floor Diagrams
Level 4
Level 3
12
Transportation Schedule
Wednesday
September 18
Conference
10:00 am –10:00 pm A
Thursday
September 19
Friday
September 20
Saturday
September 21
Conference
6:00 am–7:30 pm A
Conference
6:30 am–7:30 pm A
Conference
7:00 am–2:00 pm A
Aquarium Party
7:00 pm–7:30 pm B
B&O Party
7:00 pm–8:00 pm D
Committee Reception
(by invitation)
6:30 pm–10:30 pm F
8:30 pm–11:00 pm C
8:30 pm–11:00 pm E
A Continuous shuttle service between auxiliary hotels and Baltimore
Marriott Waterfront Hotel
B
Transportation from Baltimore Marriott Waterfront Hotel to the
National Aquarium in Baltimore for those unable/reluctant to walk
C Transportation from the National Aquarium in Baltimore to auxiliary
hotels and to Baltimore Marriott Waterfront Hotel
D Transportation from Baltimore Marriott Waterfront Hotel to B&O
Railroad Museum
E
Transportation from B&O Railroad Museum to auxiliary hotels and
to Baltimore Marriott Waterfront Hotel
F
Round-trip water taxi service from Baltimore Marriott Waterfront
Hotel to the Baltimore Museum of Industry
13
She works hard
STRONG ALL WEEK LONG
14
So does her treatment
AVONEX® in relapsing forms of MS
• Strong against both disability and relapses
– reduces the progression to sustained disability by 37%
and lowers relapse rates 1
• Strong against inflammation
– 91% reduction in T2 lesion volume and 89% reduction
in gadolinium-enhanced lesions 2,3
• Strong against atrophy
– decreased brain atrophy by 55% in year 2 of a clinical trial 4
• Strong with patients
– AVONEX® is the #1 prescribed MS therapy and delivers 95%
patient satisfaction 5,6
• The difference is in the delivery
– IM administration keeps effective amounts of AVONEX®
in the body longer than the SC route 7
The most common side effects associated with AVONEX® treatment are flu-like symptoms,
muscle ache (myalgia), fever, and chills. Other common side effects seen, but not statistically
different from placebo, were headache (AVONEX®: 67%, placebo: 57%), pain (AVONEX®:
24%, placebo: 20%), and asthenia (AVONEX®: 21%, placebo: 13%).
AVONEX® should be used with caution in patients with depression and in patients with
seizure disorders. AVONEX® should not be used by pregnant women. Patients with cardiac disease should be closely monitored. Routine periodic blood chemistry and hematology tests are
recommended during treatment with AVONEX®.
The exact relationship between MRI findings and the clinical status of patients is unknown.
Changes in lesion area often do not correlate with changes in disability progression.
®
Please see brief summary of full prescribing information.
©2002 Biogen, Inc. All Rights Reserved. 1-5074-01
AVONEX® (Interferon beta-1a)
For more detailed information, consult full prescribing information.
A brief summary follows.
INDICATIONS AND USAGE
AVONEX® ( Interferon beta-1a) is indicated for the treatment of relapsing forms of
multiple sclerosis to slow the accumulation of physical disability and decrease the frequency of clinical exacerbations. Safety and efficacy in patients with chronic progressive
multiple sclerosis have not been evaluated.
CONTRAINDICATIONS
AVONEX® (Interferon beta-1a) is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, human albumin, or any other component
of the formulation.
WARNINGS
AVONEX® (Interferon beta-1a) should be used with caution in patients with depression.
Depression and suicide have been reported to occur in patients receiving other interferon
compounds. Depression and suicidal ideation are known to occur at an increased
frequency in the multiple sclerosis population. A relationship between occurrence of
depression and/or suicidal ideation and the use of AVONEX® has not been established. An
equal incidence of depression was seen in the placebo-treated and AVONEX® -treated
patients in the placebo-controlled multiple sclerosis study. Patients treated with AVONEX®
should be advised to report immediately any symptoms of depression and/or suicidal
ideation to their prescribing physicians. If a patient develops depression,
cessation of AVONEX® therapy should be considered.
PRECAUTIONS
General
Caution should be exercised when administering AVONEX® ( Interferon beta-1a) to
patients with pre-existing seizure disorder. In the placebo-controlled study, 4 patients
receiving AVONEX® experienced seizures, while no seizures occurred in the placebo
group. Three of these 4 patients had no prior history of seizure. It is not known whether
these events were related to the effects of multiple sclerosis alone, to AVONEX®, or to a
combination of both. For patients with no prior history of seizure who develop seizures
during therapy with AVONEX®, an etiologic basis should be established and appropriate
anti-convulsant therapy instituted prior to considering resumption of AVONEX® treatment.
The effect of AVONEX® administration on the medical management of patients with seizure
disorder is unknown.
Patients with cardiac disease, such as angina, congestive heart failure, or arrhythmia,
should be closely monitored for worsening of their clinical condition during initiation and
continued treatment with AVONEX®. While AVONEX® does not have any known directacting cardiac toxicity, during the post-marketing period infrequent cases of congestive
heart failure, cardiomyopathy, and cardiomyopathy with congestive heart failure have
been reported in patients without known predisposition to these events or other known etiologies; in rare cases, these events have been temporally related to the administration of
AVONEX®. In rare cases, these events have recurred upon rechallenge in patients with
known predisposition.
Information to Patients
Patients should be informed of the most common adverse events associated with
AVONEX® administration, including symptoms associated with flu syndrome (see Adverse
Reactions section). Symptoms of flu syndrome are most prominent at the initiation of
therapy and decrease in frequency with continued treatment. In the placebo-controlled
study, patients were instructed to take 650 mg acetaminophen immediately prior to injection and for an additional 24 hours after each injection to modulate acute symptoms associated with AVONEX® administration.
Patients should be cautioned to report depression or suicidal ideation (see Warnings).
Patients should be advised about the abortifacient potential of interferon beta (see
Pregnancy – Teratogenic Effects).
When a physician determines that AVONEX® can be used outside of the physician’s
office, persons who will be administering AVONEX® should receive instruction in reconstitution and injection, including the review of the injection procedures (see full
prescribing information). If a patient is to self-administer, the physical ability of that patient
to self-inject intramuscularly should be assessed. The first injection should be performed
under the supervision of a qualified health care professional. A puncture-resistant container for disposal of needles and syringes should be used. Patients should be instructed
in the technique and importance of proper syringe and needle disposal and be cautioned
against reuse of these items.
Laboratory Tests
In addition to those laboratory tests normally required for monitoring patients with multiple sclerosis, complete blood and differential white blood cell counts, platelet counts,
and blood chemistries, including liver function tests, are recommended during AVONEX®
( Interferon beta-1a) therapy. During the placebo-controlled study, these tests were performed at least every 6 months. There were no significant differences between the placebo
and AVONEX® groups in the incidence of liver enzyme elevation, leukopenia, or thrombocytopenia. However, these are known to be dose-related laboratory abnormalities associated with the use of interferons. Patients with myelosuppression may require more intensive monitoring of complete blood cell counts, with differential and platelet counts.
Drug Interactions
No formal drug interaction studies have been conducted with AVONEX® ( Interferon
beta-1a). In the placebo-controlled study, corticosteroids or ACTH were administered for
treatment of exacerbations in some patients concurrently receiving AVONEX®. In addition, some patients receiving AVONEX® were also treated with anti-depressant therapy and/or
oral contraceptive therapy. No unexpected adverse events were associated with these
concomitant therapies.
Other interferons have been noted to reduce cytochrome P-450 oxidase-mediated drug
metabolism. Formal hepatic drug metabolism studies with AVONEX® in humans have not
been conducted. Hepatic microsomes isolated from AVONEX®-treated rhesus monkeys
showed no influence of AVONEX® on hepatic P-450 enzyme metabolism activity.
As with all interferon products, proper monitoring of patients is required if AVONEX® is
given in combination with myelosuppressive agents.
Carcinogenesis, Mutagenesis, and
Impairment of Fertility
Carcinogenesis: No carcinogenicity data for Interferon beta-1a are available in animals
or humans.
Mutagenesis: Interferon beta-1a was not mutagenic when tested in the Ames bacterial
test and in an in vitro cytogenetic assay in human lymphocytes in the presence and
absence of metabolic activation. These assays are designed to detect agents that interact
directly with and cause damage to cellular DNA. Interferon beta-1a is a glycosylated protein that does not directly bind to DNA.
Impairment of Fertility: No studies were conducted to evaluate the effects of interferon
beta on fertility in normal women or women with multiple sclerosis. It is not known whether
Interferon beta-1a can affect human reproductive capacity.
Menstrual irregularities were observed in monkeys administered interferon beta at a
dose 100 times the recommended weekly human dose (based upon a body surface area
comparison). Anovulation and decreased serum progesterone levels were also noted transiently in some animals. These effects were reversible after discontinuation of drug.
Treatment of monkeys with interferon beta at 2 times the recommended weekly human
dose (based upon a body surface area comparison) had no effects on cycle duration or
ovulation.
The accuracy of extrapolating animal doses to human doses is not known. In the
placebo-controlled study, 6% of patients receiving placebo and 5% of patients receiving
AVONEX® (Interferon beta-1a) experienced menstrual disorder. If menstrual irregularities
occur in humans, it is not known how long they will persist following treatment.
Pregnancy – Teratogenic Effects
Pregnancy Category C: The reproductive toxicity of AVONEX® has not been studied in
animals or humans. In pregnant monkeys given interferon beta at 100 times the recommended weekly human dose (based upon a body surface area comparison), no teratogenic
or other adverse effects on fetal development were observed. Abortifacient activity was
evident following 3 to 5 doses at this level. No abortifacient effects were observed in monkeys treated at 2 times the recommended weekly human dose (based upon a body surface area comparison). Although no teratogenic effects were seen in these studies, it is not
known if teratogenic effects would be observed in humans. There are no adequate and
well-controlled studies with interferons in pregnant women. If a woman becomes pregnant
or plans to become pregnant while taking AVONEX®, she should be informed of the potential hazards to the fetus, and it should be recommended that the woman discontinue
therapy.
Nursing Mothers
It is not known whether Interferon beta-1a is excreted in human milk. Because of the
potential of serious adverse reactions in nursing infants, a decision should be made to
either discontinue nursing or to discontinue AVONEX®.
Pediatric Use
Safety and effectiveness in pediatric patients below the age of 18 years have not been
established.
Geriatric Use
Safety and effectiveness in geriatric patients above the age of 65 years have not been
established.
ADVERSE REACTIONS
The safety data describing the use of AVONEX® ( Interferon beta-1a) in multiple sclerosis patients are based on the placebo-controlled trial in which 158 patients randomized to AVONEX® were treated for up to 2 years (see Clinical Studies).
The 5 most common adverse events associated (at p ≤ 0.075) with AVONEX® treatment
were flu-like symptoms (otherwise unspecified), muscle ache, fever, chills, and asthenia.
The incidence of all 5 adverse events diminished with continued treatment.
One patient in the placebo group attempted suicide; no AVONEX®-treated patients
attempted suicide. The incidence of depression was equal in the 2 treatment groups.
However, since depression and suicide have been reported with other interferon products,
AVONEX® should be used with caution in patients with depression (see Warnings).
In the placebo-controlled study, 4 patients receiving AVONEX® experienced seizures,
while no seizures occurred in the placebo group. Three of these 4 patients had no prior history of seizure. It is not known whether these events were related to the effects of multiple sclerosis alone, to AVONEX®, or to a combination of both (see Precautions).
The following table enumerates adverse events and selected laboratory abnormalities
that occurred at an incidence of 2% or more among the 158 multiple sclerosis patients
treated with 30 mcg of AVONEX® once weekly by IM injection. Reported adverse events
have been classified using standard COSTART terms. Terms so general as to be uninformative and those events that were equal in incidence or more common in the
placebo-treated patients have been excluded.
calculus, kidney pain, leukorrhea, menopause, nocturia, pelvic inflammatory disease,
penis disorder, Peyronies Disease, polyuria, postmenopausal hemorrhage, prostatic
disorder, pyelonephritis, testis disorder, urethral pain, urinary urgency, urinary retention,
urinary incontinence, vaginal hemorrhage.
Serum Neutralizing Activity
Throughout the placebo-controlled multiple sclerosis study, serum samples from patients
were monitored for the development of Interferon beta-1a neutralizing activity. During the
study, 24% of AVONEX®-treated patients were found to have serum neutralizing activity at
one or more time points tested. Fifteen percent of AVONEX®-treated patients tested positive for neutralizing activity at a level at which no placebo patient tested positive. The
significance of the appearance of serum neutralizing activity is unknown.
DRUG ABUSE AND DEPENDENCE
There is no evidence that abuse or dependence occurs with AVONEX® (Interferon beta1a) therapy. However, the risk of dependence has not been systematically evaluated.
DOSAGE AND ADMINISTRATION
The recommended dosage of AVONEX® (Interferon beta-1a) for the treatment of relapsing forms of multiple sclerosis is 30 mcg injected intramuscularly once a week.
AVONEX® is intended for use under the guidance and supervision of a physician.
Patients may self-inject only if their physician determines that it is appropriate and with
medical follow-up, as necessary, after proper training in intramuscular injection technique.
AVONEX® (INTERFERON BETA-1a)
Manufactured by:
BIOGEN, INC.
14 Cambridge Center
Cambridge, MA 02142 USA
©2000 Biogen, Inc. All rights reserved.
1-800-456-2255
U.S. Patent Pending
I63005-2 (4/00)
Rx only.
AVONEX® ( Interferon beta-1a) has also been evaluated in 290 patients with illnesses
other than multiple sclerosis. The majority of these patients were enrolled in studies to
evaluate AVONEX® treatment of chronic viral hepatitis B and C, in which the doses studied
ranged from 15 mcg to 75 mcg, given SC, 3 times a week, for up to 6 months. The incidence of common adverse events in these studies was generally seen at a frequency similar to that seen in the placebo-controlled multiple sclerosis study. In these non-multiple sclerosis studies, inflammation at the site of the SC injection was seen in 52% of
treated patients. In contrast, injection site inflammation was seen in 3% of multiple sclerosis patients receiving 30 mcg AVONEX® by IM injection. Subcutaneous injections were
also associated with the following local reactions: injection site necrosis, injection site
atrophy, injection site edema and injection site hemorrhage. None of the above was
observed in the multiple sclerosis patients participating in the placebo-controlled study.
Other events observed during premarket and postmarket evaluation of AVONEX®,
administered either SC or IM, are listed in the paragraph that follows. Because most of
the events were observed in open and uncontrolled studies, or in marketed use, the
role of AVONEX® ( Interferon beta-1a) in their causation cannot be reliably determined.
Body as a Whole: abscess, ascites, cellulitis, facial edema, hernia, injection site fibrosis, injection site hypersensitivity, injection site pain, lipoma, neoplasm, photosensitivity reaction, rigors, sepsis, sinus headache, toothache; Cardiovascular System:
arrhythmia, arteritis, cardiomyopathy, congestive heart failure, heart arrest, hemorrhage, hypotension, palpitation, pericarditis, peripheral ischemia, peripheral vascular
disorder, postural hypotension, pulmonary embolus, spider angioma, tachycardia,
telangiectasia, vascular disorder; Digestive System: blood in stool, colitis, constipation, diverticulitis, dry mouth, gallbladder disorder, gastritis, gastrointestinal hemorrhage,
gingivitis, gum hemorrhage, hepatitis, hepatoma, hepatomegaly, increased appetite,
intestinal perforation, intestinal obstruction, liver function test abnormalities, periodontal abscess, periodontitis, proctitis, thirst, tongue disorder, vomiting; Endocrine System:
hyperthyroidism, hypothyroidism; Hemic and Lymphatic System: coagulation time
increased, ecchymosis, lymphadenopathy, petechia; Metabolic and Nutritional Disorders: abnormal healing, dehydration, hypoglycemia, hypomagnesemia, hypokalemia;
Musculoskeletal System: arthritis, bone pain, myasthenia, osteonecrosis, synovitis;
Nervous System: abnormal gait, amnesia, anxiety, Bell’s Palsy, clumsiness, confusion, depersonalization, drug dependence, emotional lability, facial paralysis, hyperesthesia, hypertonia, increased libido, neurosis, paresthesia, psychosis, transient
severe weakness; Respiratory System: bronchospasm, emphysema, hemoptysis,
hiccup, hyperventilation, laryngitis, pharyngeal edema, pneumonia; Skin and
Appendages: basal cell carcinoma, blisters, cold clammy skin, contact dermatitis,
erythema, furunculosis, genital pruritus, nevus, pruritus, rash, seborrhea, skin ulcer,
skin discoloration; Special Senses: abnormal vision, conjunctivitis, earache, eye pain,
labyrinthitis, vitreous floaters; Urogenital: breast fibroadenosis, breast mass, dysuria,
epididymitis, fibrocystic change of the breast, fibroids, gynecomastia, hematuria, kidney
References:
1. Jacobs LD, Cookfair DL, Rudick RA, et al, and the Multiple Sclerosis Collaborative Research Group
(MSCRG). Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. Ann
Neurol. 1996;39:285-294. 2. Jacobs LD, Beck RW, Simon JH, et al, and the CHAMPS (Controlled High-Risk
Subjects Avonex Multiple Sclerosis Prevention Study) Study Group. Intramuscular interferon beta-1a
therapy initiated during a first demyelinating event in multiple sclerosis. N Engl J Med. 2000;343:898-904.
3. Data on file: Jacobs LD; Phase III pivotal trial. Biogen, Inc. 4. Rudick RA, Fisher E, Lee J-C, Simon J,
Jacobs L, and the Multiple Sclerosis Collaborative Research Group. Use of the brain parenchymal fraction
to measure whole brain atrophy in relapsing-remitting MS. Neurology. 1999;53:1698-1704. 5. IMS Health,
Inc., through Oct 2001. 6. Taylor-Nelson Sofres Healthcare MS Patient Study 2001. 7. Alam J, McAllister A,
Scaramucci J, Jones W, Rogge M. Pharmacokinetics and pharmacodynamics of interferon beta-1a
(IFNß-1a) in healthy volunteers after intravenous, subcutaneous or intramuscular administration.
Clin Drug Invest. 1997;14:35-43.
1-8321-01
Ancilliary Meetings
18
ACTRIMS Steering Committee
Friday, Sept. 20, Noon–1 pm, Board Room, Level 3
ECTRIMS Council
Friday, Sept. 20, Noon–1 pm, Kent AB, Level 4
EDMUS Users Group
Thursday, Sept. 19, 4–6 pm, Essex C, Level 4
MS Journal Editorial Board
Friday, Sept. 20, 7:30 – 9:30 am, Iron, Level 4
NMSS Pediatric Study Group
Wednesday, Sept. 18, 10:00 am–Noon Board Room, Level 3
NMSS Rescue Therapy
Wednesday, Sept. 18, Noon–4 pm, Heron, Level 4
NMSS Directors of Affiliated
Clinical Facilities
Friday, Sept. 20, 7 – 8:30 am, Atlantic, Level 3
Wednesday, September 18
12:00 pm–1:30 pm PRE-CONFERENCE SYMPOSIA
MS FORUM
EUROPEAN CHARCOT FOUNDATION
Controversies Across Continents
Co-chairs: D Bates (Newcastle, UK)
G Ebers (Oxford, UK)
Does IVIG Have an Effect on Brain Atrophy?
A Second Look at ESIMS Results
12:00 WELCOME and INTRODUCTION D Bates
12:00 INTRODUCTION OR Hommes
12:10 SCENARIO I: DIAGNOSIS M Clanet (Toulouse, France) and
B Arnason (Chicago, USA)
12:05 ESIMS CLINICAL RESULTS IN PERSPECTIVE OF PREVIOUS
TRIALS PS Sørensen (Copenhagen, Denmark)
12:25 ANN GUIDELINES AND THE EUROPEAN PERSPECTIVE
D Goodin (San Francisco, USA) and X Montalban (Barcelona, Spain)
12:25 ESIMS MRI RESULTS (BPF, MT-MRI) C Enzinger (Graz, Austria)
12:40 SCENARIO 2: FAILING SLIGHTLY, NO DISEASE PROGRESSION
L Kappos (Basel, Switzerland) and G Rice (London, Canada)
1:00 SCENARIO 3: RAPID PROGRESSION OF DISEASE R Hohlfeld
(Munich, Germany) and B Arnason (Chicago, USA)
Moderator: OR Hommes (Nijmegen, Netherlands)
Grand Ballroom VI
12:45 MPRAGE BRAIN ATROPHY MEASUREMENTS IN ESIMS
PATIENTS C Constantinescu (Leicester, UK)
1:05 IS BRAIN ATROPHY A NEW PARAMETER TO USE IN CLINICAL
TRIALS? M Freedman (Ottawa, Canada)
1:25 DISCUSSION
1:20 CONCLUDING REMARKS D Bates
Supported by a grant from Bayer Corporation
Sponsored by Center for BioMedical Communications, Inc.
Supported through an unrestricted educational grant from
Schering AG, Germany / Berlex
19
Wednesday, September 18
2:00 pm–4:40 pm
YOUNG SCIENTIFIC
INVESTIGATORS SESSION
5:00 pm–6:00 pm
SATELLITE SYMPOSIUM I
Co-chairs: D Brassat (San Francisco, USA)
A Petzold (London, UK)
S Dhib-Jalbut (Baltimore, USA)
Selective Adhesion Molecule Inhibition:
A Potential Future Treatment
for Multiple Sclerosis
Chair: C Confavreux (Lyon, France)
2:00 WELCOME and ANNOUNCEMENT, 2002 YOUNG NEUROLO-
5:00 WELCOME and OBJECTIVES C Confavreux
GISTS AND TRAINEES (YNT)–SCHERING FELLOWSHIP AWARD
S Hickmann (London, UK)
2:10 1 HLA-DRB5*0101 AND -DRB1*1501 EXPRESSION IN THE
MULTIPLE SCLEROSIS-ASSOCIATED HLA-DR15DW2 HAPLOTYPE
E Prat,WW Kwok, N Kruse, R Pujol-Borrell, MP Bettinotti, HF McFarland, R Martin
(Bethesda, USA)
5:05 CELLULAR ADHESION PATHWAYS: POTENTIAL TARGETS FOR
FUTURE MULTIPLE SCLEROSIS THERAPIES P Calabresi (Baltimore, USA)
5:25 EMERGING CLINICAL DATA FOR SELECTIVE ADHESION
MOLECULE INHIBITION IN THE TREATMENT OF MULTIPLE SCLEROSIS
D Miller (London, UK)
2:25 2 QUALITATIVE AND QUANTITATIVE ANALYSIS OF THE
BLOOD TCR ␤ CHAIN TRANSCRIPTOME AT DIFFERENT TIME POINTS
OF MULTIPLE SCLEROSIS COURSE DA Laplaud, S Wiertlewski, M Guillet,
C Ruiz, B Melchior, G Edan, P Damier, J Soulillou (Nantes, France)
5:40 CLOSING REMARKS C Confavreux
2:40 3 EXPRESSION OF METABOTROPIC GLUTAMATE RECEPTORS
IN MULTIPLE SCLEROSIS BRAIN: UPREGULATION IN AXONS AND
REACTIVE ASTROCYTES JJ Geurts, W Kamphorst, P van der Valk, EM Aronica
(Amsterdam, Netherlands)
Sponsored by the Division of Continuing Medical Education,
Discovery International
2:55 4 GROUP CONNECTIVITY MAPS OF OPTIC RADIATIONS
5:50 PANEL DISCUSSION
Supported through an education grant from Biogen, Inc.
and Elan
AFTER ISOLATED OPTIC NEURITIS O Ciccarelli, SJ Hickman, AT Toosy,
GJ Parker, CA Wheeler-Kingshott, GJ Barker, DH Miller, AJ Thompson (London, UK)
3:10 5 FUNCTIONAL DIVERSITY OF ANTIBODIES AGAINST
MYELIN/OLIGODENDROCYTE GLYCOPROTEIN IN EXPERIMENTAL
AUTOIMMUNE DEMYELINATION H von Büdingen, SL Hauser,A Fuhrmann,
CB Nabavi, CP Genain (San Francisco, USA)
3:25 6 MRI EVIDENCE OF MORE EXTENSIVE TISSUE DAMAGE IN
MS PATIENTS WITH THE ⑀4 ALLELE OF APOLIPOPROTEIN E: HIGHER
PROPORTION OF LESIONS EVOLVING TO BLACK HOLES DURING
TWO-YEAR FOLLOW-UP C Enzinger, S Ropele, S Strasser-Fuchs, P Kapeller,
T Seifert, B Poltrum, H Schmidt, R Schmidt, F Fazekas (Graz,Austria)
3:40 7 EVIDENCE FOR AXONAL PATHOLOGY AND ADAPTIVE
CORTICAL REORGANIZATION IN PATIENTS AT PRESENTATION WITH
CLINICALLY ISOLATED SYNDROMES SUGGESTIVE OF MULTIPLE SCLEROSIS MA Rocca, D Mezzapesa,A Falini,A Ghezzi,V Martinelli, M Rodegher,
G Scotti, G Comi, M Filippi (Milan, Italy)
3:55 8 A 36-MONTH LONGITUDINAL STUDY ON THE EVALUATION OF THE EFFECT OF INTERFERON BETA IN THE DURATION OF
BLACK HOLES IN MULTIPLE SCLEROSIS F Bagnato, N Jeffries, J Ohayon,
R Stone, N Richert, C Bash, HF McFarland, JA Frank (Bethesda, USA)
4:10 9 DOES FUNCTIONAL MRI ALLOW INFERENCES ABOUT
COGNITIVE TRAINING EFFICACY IN MULTIPLE SCLEROSIS? I Penner,
L Kappos, M Rausch, K Opwis, E Radü (Basel, Switzerland)
4:25 10 COMBINATION THERAPY OF MS PATIENTS WITH
INCOMPLETE RESPONSE TO INTERFERON-BETA WITH HUMANIZED
ANTIBODY AGAINST THE INTERLEUKIN-2 RECEPTOR ALPHA CHAIN
B Bielekova, S Reichert-Scrivner, J Wuerfel, J Ohayon, J McCartin, N Richert, J Frank,
T Waldmann, H McFarland, R Martin (Cambridge, UK)
7:00 pm–9:00 pm
Grand Ballroom
20
ACTRIMS-ECTRIMS 2002 WELCOME RECEPTION
Thursday, September 19
8:15 am–9:30 am
OPENING SESSION
8:15 am WELCOME K Johnson (Baltimore, USA) and A Thompson (London, UK)
Opening Remarks Mike Dugan, General, USAF Ret.
President and CEO, National Multiple Sclerosis Society, New York, USA
Victor Rivera, President, LACTRIMS
8:45 am KEYNOTE ADDRESS
11 Inflammation, Demyelination and Axonal Loss: Unraveling the Relationships
SK Ludwin★ (Kingston, Canada)
9:30 am BREAK
10:00 am–12:00 pm
PARALLEL SESSIONS
SESSION I
SESSION II
Inflammation, Demyelination and
Axonal Loss: Insights from Pathology
Co-chairs: C Polman (Amsterdam, Netherlands)
E Radue (Basil, Switzerland)
Impact of Relapses on Disability;
Natural History and Clinical Trials Data
Co-chairs: L Kappos (Basel, Switzerland)
H Panitch (Burlington, USA)
10:00 12 MECHANISMS OF AXONAL LOSS BD Trapp★, C Bjartmar,
J Peterson,A Chang, R Rudick (Cleveland, USA)
10:00 20 THE ROLE OF EXACERBATIONS IN PERSISTENT IMPAIRMENT IN MS F Lublin★, G Cutter, M Baier (New York, USA)
10:25 13 RELATIONSHIP BETWEEN INFLAMMATION AND
AXONAL LOSS W Brueck★ (Berlin, Germany)
10:20 21 RELAPSES ARE NOT AN IMPORTANT CAUSE OF DISABILITY C Confavreux★ (Lyon, France)
10:50 14 DIFFERENTIAL GENE EXPRESSION ANALYSIS OF MULTI-
10:40 PANEL DISCUSSION Moderator: K Kappos
PLE SCLEROSIS TISSUE: COMPARISON OF ACTIVE AND INACTIVE
LESIONS MP Mycko, R Papoian, U Boschert, CS Raine, KW Selmaj (Lodz,
Poland)
11:00 15 MICROARRAY ANALYSIS OF NORMAL APPEARING
WHITE MATTER (NAWM) AND LESIONS IN SECONDARY PROGRESSIVE
MS VERIFIES MS AS A GENERALIZED CNS DISEASE RL Lindberg,
CJ De Groot, U Certa, R Ravid, F Hoffmann, L Kappos, D Leppert (Basel, Switzerland)
11:10 16 MULTIPLE SCLEROSIS: EXPANDED CSF B CELLS ARE ALSO
PRESENT IN THE BRAIN TISSUE N Goebels, H Weber, M Hofbauer,
H Wekerle, R Hohlfeld (Munich, Germany)
11:20 17 HIGH VULNERABILITY OF HUMAN NEURONS TO T CELL
CYTOTOXICITY:A NEW MODEL TO EXPLAIN NEURODEGENERATION
IN MULTIPLE SCLEROSIS F Giuliani,V Yong (Calgary, Canada)
11:30 18 LEUKEMIA INHIBITORY FACTOR LIMITS IMMUNEMEDIATED DEMYELINATION BY ENHANCING OLIGODENDROCYTE
SURVIVAL H Butzkueven, J Zhang, M Soilu-Hanninen, PF Bartlett, TJ Kilpatrick
(Parkville,Australia)
11:00 22 ONSET OF CLINICAL BENEFIT OF GLATIRAMER
(COPAXONE®) ACETATE IN PATIENTS WITH RELAPSING REMITTING
MULTIPLE SCLEROSIS (RRMS) KP Johnson, BR Brooks, CC Ford, A Goodman,
JB Guarnaccia, RP Lisak, LW Myers, HS Panitch, AA Pruitt, N Kachuck, JS Wolinsky,
and the Copolymer 1 MS Study Group (Baltimore, USA)
11:15 23 EFFECT OF EARLY INTERFERON TREATMENT ON CONVERSION TO DEFINITE MULTIPLE SCLEROSIS: THE ETOMS STUDY—
4-YEAR RESULTS G Comi, M Filippi, F Barkhof, L Durelli, G Edan, O Fernandez,
H Hartung, P Seeldrayers, P Soelberg Sorensen, O Hommes (Turin, Italy)
11:30 24 NEUTRALIZING ANTIBODIES AGAINST INTERFERON
(IFN)-BETA REDUCE THE CLINICAL EFFECT IN RELAPSING-REMITTING
MULTIPLE SCLEROSIS PS Sorensen, N Koch-Henriksen, C Ross, KM Clemmesen, M Svenson, K Bendtzen, J Frederiksen, K Jensen, O Kristensen, T Petersen,
E Stenager, (Copenhagen, Denmark)
11:45 25 THE SYLVIA LAWRY CENTRE FOR MULTIPLE SCLEROSIS
RESEARCH (SLCMSR): BACKGROUND AND PROGRESS REPORT
JH Noseworthy and SLCMSR Staff, Scientific Oversight Committee and
Working Groups (Rochester, USA)
11:40 19 CILIARY NEUROTROPHIC FACTOR ENHANCES MYELIN
FORMATION:A NOVEL ROLE FOR CNTF AND CNTF-RELATED MOLECULES S Bruno, N Frederic, A Marie Stephane, Z Bernard, L Catherine (Paris,
France)
11:50 CONCLUSIONS
★ Invited speaker
21
12:00 pm–2:00 pm
LUNCH and POSTER SESSION I
Harborside Level
2:00 pm–4:00 pm
PARALLEL SESSIONS
SESSION III
SESSION IV
Inflammation, Demyelination and
Axonal Loss: Insights from Imaging
Co-chairs: J Simon (Denver, USA)
N Richert (Bethesda, USA)
The Blood-Brain-Barrier as a Target
for Treatment
Co-chairs: S Dhib-Jalbut (Baltimore, USA)
J Oger (Vancouver, Canada)
2:00 26 RELATIONSHIP BETWEEN CONTRAST ENHANCING
2:00 33 ADHESION MOLECULES AND THEIR ROLE IN PATHO-
LESIONS AND AXONAL LOSS JA Frank★ (Bethesda, USA)
GENESIS JP Antel★, K Biernacki, R Seguin, A Prat (Montreal, Canada)
2:20 27 IN VIVO MONITORING OF AXONS AND MYELIN IN
2:20 34 CHEMOKINES AND CHEMOKINE RECEPTORS:WHAT’S
MULTIPLE SCLEROSIS Z Caramanos, DL Arnold★ (Montreal, Canada)
THE ATTACTION RM Ransohoff★ (Cleveland, USA)
2:40 28 CAN WE IMAGE REMYELINATION? F Barkhof★ (Amsterdam, Netherlands)
2:40 35 MATRIX METALLOPROTEINASES IN MS VW Yong★
3:00 29 WHAT IS NORMAL-APPEARING WHITE MATTER?
3:00 36 CLINICAL TRIALS OF AGENTS TARGETING THE BLOOD
R Grossman★ (San Francisco, USA)
BRAIN BARRIER: SUCCESSES AND FAILURES D Miller★ (London, UK)
3:20 30 BRAIN VOLUME CHANGES IN PATIENTS AT PRESENTA-
3:20 P143 RANTES AND CHEMOKINE RECEPTOR 5 POLYMOR-
TION WITH SUSPECTED MULTIPLE SCLEROSIS: RESULTS FROM THE
ETOMS STUDY G Comi, M Inglese, N De Stefano, S Smith, F Barkhof, L Durelli,
G Edan, O Fernandez, HP Hartung, PM Matthews, P Seeldrayers, PS Sorensen,
V Martinelli, OR Hommes, M Filippi (Milan, Italy)
PHISMS: SUSCEPTIBILITY TO AND OUTCOME IN MULTIPLE SCLEROSIS
JM Partridge, A Fryer, W Ollier, M Boggild, R Strange, C Hawkins (Stoke-on-Trent,
UK)
3:30 31 PREDICTIVE VALUE OF INFRATENTORIAL LESIONS IN
PATIENTS WITH CLINICALLY ISOLATED SYNDROMES FOR LONG
TERM DISABILITY A Minneboo, F Barkhof, CH Polman, BM Uitdehaag,
D Knol, J A Castelijns (Amsterdam, Netherlands)
3:40 32 A 48-MONTH LONGITUDINAL STUDY ON THE RELATIONSHIP BETWEEN THE DURATION OF THE ENHANCEMENT IN
AN ACTIVE LESION AND THE DURATION OF A BLACK HOLE IN
MULTIPLE SCLEROSIS F Bagnato, N Jeffries, J Ohayon, R Stone, JA Frank,
HF McFarland (Bethesda, USA)
3:45 P133 THE EFFECT OF INTERFERON B-1B ON QUANTITIES
DERIVED FROM MT MRI IN SECONDARY PROGRESSIVE MS M Inglese,
J vanWaesberghe, M Rovaris, K Beckmann, F Barkhof, D Hahn, L Kappos, D Miller,
C Polman, C Pozzilli, A Thompson,T Yousry, K Wagner, G Comi, M Filippi (Milan,
Italy)
3:50 P40 ISOLATED SPINAL DEMYELINATING EVENTS WITH
NORMAL BRAIN MRI: PROGRESSION TO MS, CLINICAL AND MRI
FOLLOW UP R Milo,T Katz, J Corat-Simon (Ashkelon, Israel)
3:55 CONCLUSIONS
(Calgary, Canada)
3:25 P145 MMP-9 MICROSATELLITE POLYMORPHISM INCREASES
THE RISK OF MULTIPLE SCLEROSIS N Fiotti, R Zivadinov, N Altamura,
D Nasuelli, A Bratina, MA Tommasi, A Bosco, L Locatelli, A Grop, G Cazzato,
C Giansante, M Zorzon (Trieste, Italy)
3:30 P114 IL-12 DEPENDENT/IFN GAMMA INDEPENDENT
EXPRESSION OF CCR5 BY MYELIN-REACTIVE CD4+ T CELLS
CORRELATES WITH ENCEPHALITOGENICITY L Bagaeva, LP Williams, BM
Segal (Rochester, USA)
3:35 P91 LONGITUDINAL ANALYSIS OF CSF EXPANDED CD8+
CLONOTYPES IN THE PERIPHERAL BLOOD OF MULTIPLE SCLEROSIS
PATIENTS S Cepok, D Zhou, F Vogel, N Sommer, B Hemmer (Marburg,
Germany)
3:40 P98 MOLECULAR TRACKING OF MYELIN BASIC PROTEINSPECIFIC T CELL EXPANSION IN MULTIPLE SCLEROSIS PA Muraro,
K Wandinger, B Bielekova, HF McFarland, R Martin (Bethesda, USA)
3:45 P149 IMMUNE REGULATORY EFFECTS OF GLATIRAMER
ACETATE (GA) ON HUMAN MONOCYTES: BYSTANDER SUPPRESSION
REVISITED? H Kim, M Duddy, A Bar-Or (Montreal, Canada)
3:50 CONCLUSIONS
★ Invited speaker
22
SATELLITE SYMPOSIA
4:30 pm–5:30 pm
SATELLITE SYMPOSIUM II
6:00 pm–7:00 pm
SATELLITE SYMPOSIUM III
Exploring the Boundaries of
Multiple Sclerosis Treatment
Chair: D Goodin (San Francisco, USA)
Defining Factors That Impact Efficacy
in the Treatment of Relapsing Remitting
Multiple Sclerosis
Program Chair: HP Hartung (Dusseldorf, Germany)
Panel Discussion Chair: H McFarland (Washington,
DC, USA)
4:30 WELCOME D Goodin
6:00 WELCOMING REMARKS/INTRODUCTIONS HP Hartung
4:35 EXPLORING TREATMENT OPTIONS FOR PRIMARY PROGRESSIVE MULTIPLE SCLEROSIS X Montalban (Barcelona, Spain)
6:05 SELECTING HIGH-RISK PATIENTS FOR EARLY TREATMENT
F Munschauer (Buffalo, USA)
4:50 LONG TERM EXPERIENCE WITH MULTIPLE SCLEROSIS THERA-
6:15 DO DOSE AND DOSE FREQUENCY IMPACT EFFICACY?
PIES G Rice (London, Canada)
A REVIEW OF THE EUROPEAN DOSE COMPARISON STUDY AND
SUPPORTING DATA X Montalban (Barcelona, Spain)
5:05 BEYOND THE STANDARD DOSE OF BETA INTERFERON IN
MULTIPLE SCLEROSIS HP Hartung (Dusseldorf, Germany)
5:20 DISCUSSION AND CLOSING REMARKS D Goodin
6:25 LONG-TERM EFFICACY OF INTERFERON BETA—WHY NABS
MATTER PS Sorensen (Copenhagen, Denmark)
6:40 PANEL DISCUSSION/Q&A H McFarland
Sponsored by Bio-Medical Communications, Inc.
Supported by an unrestricted educational grant from
Schering AG, Germany / Berlex
Sponsored by the Health Science Center for
Continuing Medical Education
Supported by an unrestricted educational grant
from Biogen
7:30 pm–10:30 pm
RECEPTION and DINNER BUFFET
National Aquarium in Baltimore
23
Friday, September 20
8:30 am–9: 30 am
OPENING SESSION
8:30 am WELCOME S Dhib-Jalbut (Baltimore, USA)
PRESENTATION: ACTRIMS LIFE ACHIEVEMENT AWARD Kenneth P. Johnson, Honoree
8:45 am KEYNOTE ADDRESS
37 Neural Stem Cells to Rebuild the Diseased Brain: How Realistic Is This Approach?
E Snyder ★ (Boston, USA)
9:30 am BREAK
10:00 am–12:00 pm
PARALLEL SESSIONS
SESSION V
Neuroprotection
Co-chairs: A Cross (St Louis, USA)
R Lisak (Detroit, USA)
SESSION VI
Hot topics in Neuroimmunology
Co-chairs: M Racke (Dallas, USA)
J Richert (Washington, DC, USA)
10:00 38 MOLECULAR BASIS OF LIMITED REMYELINATION IN
MULTIPLE SCLEROSIS CS Raine★, G John, CF Brosnan (Bronx, USA)
10:25 39 COMPLEMENT: DUAL ROLE IN INJURY AND PROTECTION ML Shin★, H Rus (Baltimore, USA)
10:50 40 IS NEUROPROTECTION A REALISTIC OPTION IN MS?
R Hohlfeld★ (Munich, Germany)
10:00 44 CYTOKINE REGULATION IN MULTIPLE SCLEROSIS
H Weiner★, SJ Khoury (Boston, USA)
10:25 45 ARE SPECIFIC IMMUNOTHERAPIES AN OPTION FOR MS?
R Martin★ (Bethesda, USA)
11:15 41 CNTF IS A MAJOR PROTECTIVE FACTOR IN DEMYELI-
10:50 46 TCR PEPTIDE THERAPY IN AUTOIMMUNE DISEASE
AA Vandenbark★ (Portland, USA)
NATING CNS DISEASE:A NEUROTROPHIC CYTOKINE AS MODULATOR IN NEUROINFLAMMATION RA Linker, M Maurer, S Gaupp, R Martini,
B Holtmann, H Lassmann, KV Toyka, M Sendtner, R Gold (Wurzburg, Germany)
11:15 47 LARGE SCALE TRANSCRIPTIONAL AND PROTEOMIC
ANALYSIS OF MS TISSUE YIELDS NEW TARGETS FOR THERAPY
L Steinman★ (Stanford, USA)
11:30 42 INTERFERON-BETA GENE THERAPY FOR CENTRAL
11:40 48 RE-INDUCTION OF TOLERANCE IN ESTABLISHED
AUTOIMMUNE DISEASE:A STRATEGY FOR THE TREATMENT OF
MULTIPLE SCLEROSIS G Pryce, JK O’Neill, S Amor, D Baker, G Giovannoni
(London, UK)
NERVOUS SYSTEM DISEASE USING BONE MARROW CELLS AS A
DELIVERY SYSTEM S Dhib-Jalbut,TK Makar, S Wilt, Z Dong, P Fishman,
M Mouradian (Baltimore, USA)
11:45 43 HIGH-DOSE IMMUNOABLATIVE THERAPY WITH
AUTOLOGOUS STEM CELL SUPPORT IN PATIENTS WITH MALIGNANT
COURSE OF MULTIPLE SCLEROSIS E Havrdova, T Kozak, J Kobylka, J Pitha,
J Fiedler, V Koza, J Maaloufova, D Horakova, V Ticha, I Novakova, S Vodvarkova,
E Gregora, E Medova (Prague, Czech Republic)
11:50 49 KV1.3 IS A UNIQUE FUNCTIONAL MARKER OF EFFECTOR MEMORY T CELLS IN MULTIPLE SCLEROSIS R Allie, S Yun, PA Calabresi, H Wullf, K Chandy, M Pennington (Baltimore, USA)
★ Invited speaker
24
12:00 pm–2:00 pm
LUNCH and POSTER SESSION II
Harborside Level
2:00 pm–4:00 pm
PARALLEL SESSIONS
SESSION VII
SESSION VIII
Methodological Issues in Clinical Trials
Co-chairs: HP Hartung (Dusseldorf, Germany)
R Rudick (Cleveland, USA)
Genetics and Hormonal Influence
Co-chairs: M Freedman (Ottawa, Canada)
D Hafler (Boston, USA)
2:00 50 THE NEW DIAGNOSTIC CRITERIA AND THEIR IMPLICA-
2:00 55 GENETIC ANALYSIS OF MULTIPLE SCLEROSIS IN EURO-
TIONS FOR CLINICAL TRIALS JS Wolinsky★ (Houston, USA)
PEANS (GAMES) A Compston★, S Sawcer (Cambridge, UK)
2:25 51 APPLICATION OF MCDONALD CRITERIA TO CLINICALLY
ISOLATED SYNDROMES SUGGESTIVE OF MULTIPLE SCLEROSIS
M Tintore,A Rovira, J Rio, C Nos, E Grive, J Sastre-Garriga, I Pericot, E Sanchez,
M Comabella, X Montalban (Barcelona, Spain)
2:20 56 INSIGHTS INTO THE GENETICS OF MS FROM THE CANA-
2:35 52 METHODOLOGICAL ISSUES IN SHORT-TERM CLINICAL
TRIALS JH Noseworthy★ (Rochester, USA)
S Hauser★, LF Barcellos, MA Pericak-Vance, JL Haines, RR Lincoln, S Schmidt,
A Swerdlin, JR Oksenberg (Durham, USA)
3:00 53 THE ROLE OF MRI AS A SURROGATE MARKER IN MS
3:00 58 HORMONAL INFLUENCES IN MS R Voskuhl★ (Los Angeles,
H McFarland★ (Bethesda, USA)
USA)
3:25 54 A STANDARDIZED MRI SCAN IN THE DIAGNOSIS AND
3:20 59 OVARIAN HORMONES DIFFERENTIALLY EFFECT NEURON
FOLLOW-UP OF MS PATIENTS D Paty★, DK Li,A Traboulsee, J Simon, J Frank
(Vancouver, Canada)
DEATH MEDIATED BY TNF␣ VIA EXPRESSION OF ANTI-APOPTOTIC
PROTEINS AND ACTIVATION OF JNK1 PRO-APOPTOTIC SIGNAL
CASCADE CL Koski, S Hila,T Popescue, G Hoffman (Baltimore, USA)
3:50 P227 COURSE AND PROGNOSIS IN EARLY ONSET MULTIPLE SCLEROSIS IL Simone, D Carrara, C Tortorella, M Liguori,V Lepore, F Pelligrini,A Bellacosa,A Ceccarelli, I Pavone, F Girolamo, P Livrea (Bari, Italy)
3:55 P308 PLACEBO-CONTROLLED DOUBLE-BLINDED DOSE
RANGING STUDY OF FAMPRIDINE-SR IN MULTIPLE SCLEROSIS
AD Goodman,A Blight, JA Cohen,AH Cross, M Katz, MA Rizzo,T Vollmer
(Rochester, USA)
DIAN COLLABORATIVE PROJECT GC Ebers★, D Sadovnick, N Risch
(Vancouver, Canada)
2:40 57 THE ROLE OF THE HLA REGION IN MULTIPLE SCLEROSIS
3:30 60 A NEW GENE OVEREXPRESSED IN MULTIPLE SCLEROSIS
AND RHEUMATOID ARTHRITIS C Greene, R Crusio, L Chen, C Rose,
D Connelly, M Grekova, JR Richert (Washington, USA)
3:40 P325 ASSOCIATION OF APOLIPOPROTEIN E AND MYELOPEROXIDASE GENOTYPES WITH THE CLINICAL COURSE OF FAMILIAL
AND SPORADIC MULTIPLE SCLEROSIS B Zakrzewska-Pniewska,
A Podlecka, M Styczynska, R Samocka, B Peplonska, M Barcikowska,
H Kwiecinski (Warsaw, Poland)
3:45 P314 TUMOR NECROSIS FACTOR RECEPTOR II POLYMORPHISM IN PATIENTS WITH MULTIPLE SCLEROSIS R Ehling, C Gassner,
F Fazekas, H Kollegger,W Kristoferitsch, M Reindl, T Berger (Innsbruck,Austria)
3:50 P297 A SYNTHETIC ANDROSTENE DERIVATIVE WITHOUT
GENDER-RELATED SIDE EFFECTS INHIBITS EAE. CANDIDATE FOR
CLINICAL TRIALS IN MS? H Offner,A Zamora,A Matejuk, D Auci, E Morgan,
C Reading (Portland, USA)
3:55 CONCLUSIONS
★ Invited speaker
25
SATELLITE SYMPOSIA
4:30 pm–5:30 pm
SATELLITE SYMPOSIUM IV
6:00 pm–7:00 pm
SATELLITE SYMPOSIUM V
Milestones in Immunomodulatory Therapy:
Decisions in the Treatment of Multiple Sclerosis
Co-chairs: G Comi (Milan, Italy)
J Wolinsky (Houston, USA)
The Modern Management of Multiple Sclerosis:
An Evidence-Based Approach
Chair: D Bates (Newcastle, UK)
4:30 IMMUNE-MEDIATED INJURY AND NEUROPROTECTION IN MS
6:00 A CRITICAL ANALYSIS OF DISEASE-MODIFYING DRUGS IN
CLINICAL STUDIES: IMPLICATIONS AND TREATMENT GUIDELINES
D Goodin (San Francisco, USA)
W Yong (Calgary, Canada)
4:50 LESSONS FROM MRI: EVIDENCE OF EARLY AND PROGRESSIVE
CNS INJURY D Arnold (Montreal, Canada)
5:10 GLATIRAMER ACETATE IN MS:A NEW LOOK AT THE CLINICAL
EFFECTS IN THE LIGHT OF MECHANISMS OF ACTION R Lisak (Detroit,
USA)
Sponsored by Postgraduate Institute for Medicine
Supported by an unrestricted educational grant from
Teva Pharmaceuticals, LTD,Teva Neuroscience, and Aventis
7:30 pm–10:00 pm
B&O Railroad Museum
26
6:15 THE EVIDENCE FOR EFFICACY OF DISEASE-MODIFYING
DRUGS: IMPLICATIONS FOR THE CLINICIAN M Freedman (Ottawa,
Canada)
6:35 THE PATIENT PERSPECTIVE: LIVING WITH MULTIPLE SCLEROSIS
AFTER STARTING A DISEASE-MODIFYING DRUG
6:50 Q&A AND CLOSING REMARKS
Sponsored by Serono
RECEPTION and DINNER BUFFET
Saturday, September 21
8:30 am–10:30 am
PARALLEL SESSIONS
SESSION IX
SESSION X
Long Term Management Issues in Multiple
Sclerosis
Co-chairs: C Bever (Baltimore, USA)
J Cohen (Cleveland, USA)
Late Breaking News
Co-chairs: P O’Connor (Toronto, Canada)
A Thompson (London, UK)
8:30 WELCOME C Bever
8:30 WELCOME P O’Connor
8:45 61 NEUROPSYCHOLOGICAL ASPECTS OF MULTIPLE SCLE-
8:45 LB1 VALIDATION OF DIAGNOSTIC MRI CRITERIA FOR MS
ROSIS A Feinstein★ (Toronto, Canada)
AND RESPONSE TO TREATMENT WITH INTERFERON-BETA-1A F
Barkhof, M Rocca, G Francis, J van Waesberghe, B Uitdehaag, O Hommes, H Hartung, L Durelli, G Edan, O Fernández, P Seeldrayers, P Sorenson, S Margrie, G
Comi, M Filippi (Milan, Italy)
9:05 62 PATHOPHYSIOLOGY OF MS FATIGUE G Comi★, L Leocani,
P Rossi, B Colombo (Milan, Italy)
9:25 63 STEREOTACTIC SURGERY EB Montgomery★ (Cleveland,
USA)
9:45 64 CHILDHOOD ONSET MULTIPLE SCLEROSIS (THE KIDMUS STUDY): NATURAL HISTORY AND PROGNOSTIC FACTORS IN
THE LYON COHORT C Renoux,Y Mikaeloff, S Vukusic, L Gignoux, F DurandDubief, I Achiti, C Confavreux (Lyon, France)
9:55 65 DISEASE-MODIFYING DRUGS FOR MULTIPLE SCLEROSIS.
CAN TREATMENT FAILURES BE PREDICTED? M Johnson, H Ford, S Denton (Leeds, UK)
10:05 66 GADOLINIUM ENHANCING LESIONS AS A SURROGATE
MARKER OF INTERFERON RESPONSE RA Rudick, G Cutter, M Baier, D
Dougherty, B Weinstock-Guttman, M Mass, E Fisher, DM Miller,A Sandrock, J
Simon (Cleveland, USA)
10:15 67 MITOXANTRONE (NOVANTRONE) FOR TREATMENT
OF RECURRENT NEUROMYELITIS OPTICA B Weinstock-Guttman, J
Feichter, R Bakshi, C Brownscheidle, N Lincoff (Buffalo, USA)
10:25 CONCLUSIONS
9:00 LB2 ANTI-MOG ANTIBODIES PREDICT EARLY CONVERSION
TO CLINICALLY DEFINITE MS IN PATIENTS WITH A FIRST DEMYELINATING EVENT. T Berger, P Rubner, F Schautzer, R Egg, H Ulmer, I Mayringer, E
Dilitz, F Deisenhammer, M Reindl (Innsbruck,Austria)
9:15 LB3 NEUROREHABILITATION IN MULTIPLE SCLEROSIS
CONTRIBUTES TO FUNCTIONAL RECOVERY ACCOMPANIED BY
CHANGES OF BRAIN ACTIVITY ON FMRI—PRELIMINARY RESULTS.
K Rasova, J Krasensky, E Havrdova, J Obenberger, M Zalisova, Z Seidl (Prague,
Czech Republic)
9:30 LB4 TIGHT JUNCTION ABNORMALITY IN MS AFFECTS ALL
CALIBRES OF VESSEL AND CORRELATES WITH LESION ACTIVITY. J Kirk,
J Plumb, M Mirakhur, S McQuaid (Belfast, UK)
9:45 LB5 SINGLE CENTRE, DBPC, RANDOMISED TRIAL OF
INTERFERON␤ 1B IN PRIMARY PROGRESSIVE AND TRANSITIONAL
PROGRESSIVE MULTIPLE SCLEROSIS:AN EXPLORATORY PHASE II
STUDY. X Montalban, L Brieva, M Tintore, C Borras, J Rio, C Nos, X Aymerich,
J Alonso, R Horno, M Vicente,A Rovira (Barcelona, Spain)
10:00 LB6 SUCCESSFUL TREATMENT WITH IFN-␤1B IN RR MS
PATIENTS IS ASSOCIATED WITH AN INCREASE IN THE NUMBER OF IL10 PRODUCING (REGULATORY) CD4 +T CELLS. A van Boxel-Dezaire, M
Smits, B Uitdehaag, C Polman, L Nagelkerken (Leiden, Netherlands)
★ Invited speaker
10:15 LB7 MULTIPLE SCLEROSIS DOCUMENTATION SYSTEM—
MSDS 2.0 M Eulitz,T Kugel, PA Muraro, M Pette (Dresden, Germany)
10:30 am COFFEE BREAK
11:00 am–12:00 pm
CLOSING SESSION
11:00 am ECTRIMS LECTURE 68 Quo Vadis? Agenda for European MS Research OR Hommes ★
(Nijmegen, Netherlands)
11:45 am PRESENTATION: 2ND ANNUAL ECTRIMS AWARD OR Hommes, Honoree
PROGRAM AWARDS and CLOSING REMARKS
12:00 pm–1:00 pm CLOSING LUNCHEON
Harborside Ballroom
7:00 pm–10:00 pm
COMMITTEE RECEPTION
Baltimore Museum of Industry (by invitation)
27
COPAXONE® PRE-FILLED SYRINGE
Consistent. Convenient. Complete.
COPAXONE® is indicated for the reduction of relapses in relapsing-remitting multiple sclerosis.
Please see brief summary of prescribing information on next page.
COPAXONE® is a registered trademark of Teva Pharmaceutical Industries Ltd.
250901/0183B2
© 2002 Teva Neuroscience, Inc.
www.copaxone.com
The only MS therapy with
■ A presumed mechanism of action that distinguishes it
from interferons 1,2
■ No evidence of neutralizing antibodies3
■ No recommended monitoring of liver function or complete
blood count 4
■ Pregnancy Category B rating 4
Significant relapse rate reduction
■ Long-term efficacy demonstrated over 2 years 5,6
■ Efficacy confirmed in 4 additional studies 7-10
Reduction in Gd-enhancing lesions
■ 35% reduction in median cumulative number of lesions
vs placebo 11
Safety and tolerability you can count on
■ No increase in incidence of flu-like symptoms,
depression, or fatigue when compared to placebo 4
■ Most common adverse effects in controlled trials were
injection site reactions, vasodilatation, chest pain, asthenia,
infection, pain, nausea, arthralgia, anxiety, and hypertonia
■ About 10% of patients experienced an immediate postinjection
reaction (flushing, chest pain, palpitations, anxiety, dyspnea,
throat constriction, and urticaria). The symptoms were transient
and self-limited, and did not require specific treatment
■ Transient chest pain was noted in 26% of COPAXONE®
patients (vs 10% placebo); no long-term sequelae
NEW!
Benefits you can measure over time
COPAXONE®
(glatiramer acetate injection)
Brief Summary of Prescribing Information
COPAXONE® Injection is indicated for reduction of the frequency of relapses in patients with RelapsingRemitting Multiple Sclerosis.
CONTRAINDICATIONS
COPAXONE® Injection is contraindicated in patients with known hypersensitivity to glatiramer acetate or
mannitol.
WARNINGS
The only recommended route of administration of COPAXONE® Injection is the subcutaneous route.
COPAXONE® Injection should not be administered by the intravenous route.
PRECAUTIONS
General
Patients should be instructed in self-injection techniques to assure the safe administration of COPAXONE®
Injection (see PRECAUTIONS: Information for Patients and the COPAXONE® INJECTION PATIENT
INFORMATION Leaflet). Current data indicate that no special caution is required for patients operating an
automobile or using complex machinery.
Considerations Regarding the Use of a Product Capable of Modifying Immune Responses
Because glatiramer acetate can modify immune response, it could possibly interfere with useful immune
functions. For example, treatment with glatiramer acetate might, in theory, interfere with the recognition of
foreign antigens in a way that would undermine the body’s tumor surveillance and its defenses against
infection. There is no evidence that glatiramer acetate does this, but there has as yet been no systematic
evaluation of this risk. Because glatiramer acetate is an antigenic material, it is possible that its use may lead
to the induction of host responses that are untoward, but systematic surveillance for these effects has not been
undertaken.
Although glatiramer acetate is intended to minimize the autoimmune response to myelin, there is the
possibility that continued alteration of cellular immunity due to chronic treatment with glatiramer acetate
might result in untoward effects.
Glatiramer acetate-reactive antibodies are formed in practically all patients exposed to daily treatment with the
recommended dose. Studies in both the rat and monkey have suggested that immune complexes are deposited
in the renal glomeruli. Furthermore, in a controlled trial of 125 RR MS patients given glatiramer acetate,
20 mg, subcutaneously every day for 2 years, serum IgG levels reached at least 3 times baseline values in 80%
of patients by 3 months of initiation of treatment. By 12 months of treatment, however, 30% of patients still
had IgG levels at least 3 times baseline values, and 90% had levels above baseline by 12 months. The
antibodies are exclusively of the IgG subtype-and predominantly of the IgG-1 subtype. No IgE type antibodies
could be detected in any of the 94 sera tested; nevertheless, anaphylaxis can be associated with the
administration of most any foreign substance, and therefore, this risk cannot be excluded.
Information for Patients
To assure safe and effective use of COPAXONE® Injection, the following information and instructions should
be given to patients:
1. Inform your physician if you are pregnant, if you are planning to have a child, or if you become pregnant
while taking this medication.
2. Inform your physician if you are nursing.
3. Do not change the dose or dosing schedule without consulting your physician.
4. Do not stop taking the drug without consulting your physician.
Patients should be instructed in the use of aseptic techniques when administering COPAXONE® Injection.
Appropriate instructions for the self-injection of COPAXONE® Injection should be given, including a
careful review of the COPAXONE® INJECTION PATIENT INFORMATION Leaflet. The first injection
should be performed under the supervision of an appropriately qualified health care professional. Patient
understanding and use of aseptic self-injection techniques and procedures should be periodically reevaluated.
Patients should be cautioned against the reuse of needles or syringes and instructed in safe disposal
procedures. They should use a puncture-resistant container for disposal of used needles and syringes. Patients
should be instructed on the safe disposal of full containers according to local laws.
Awareness of Adverse Reactions: Physicians are advised to counsel patients about adverse reactions
associated with the use of COPAXONE® Injection (see ADVERSE REACTIONS section). In addition,
patients should be advised to read the COPAXONE® INJECTION PATIENT INFORMATION Leaflet and
resolve any questions regarding it prior to beginning COPAXONE® Injection therapy.
Laboratory Tests
Data collected during premarketing development do not suggest the need for routine laboratory monitoring.
Drug Interactions
Interactions between COPAXONE® Injection and other drugs have not been fully evaluated. Results from
existing clinical trials do not suggest any significant interactions of COPAXONE® Injection with therapies
commonly used in MS patients, including the concurrent use of corticosteroids for up to 28 days.
COPAXONE® Injection has not been formally evaluated in combination with Interferon beta.
Drug/Laboratory Test Interactions
None are known.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Carcinogenesis
In a two-year carcinogenicity study, mice were administered up to 60 mg/kg/day glatiramer acetate by
subcutaneous injection (up to 15 times the human therapeutic dose on a mg/m2 basis). No increase in systemic
neoplasms was observed. In males of the high dose group (60 mg/kg/day), but not in females, there was an
increased incidence of fibrosarcomas at the injection sites. These sarcomas were associated with skin damage
precipitated by repetitive injections of an irritant over a limited skin area.
In a two-year carcinogenicity study, rats were administered up to 30 mg/kg/day glatiramer acetate by
subcutaneous injection (up to 15 times the human therapeutic dose on a mg/m2 basis). No increase in systemic
neoplasms was observed.
Mutagenesis
Glatiramer acetate was not mutagenic in four strains of Salmonella typhimurium and two strains of
Escherichia coli (Ames test) or in the in vitro mouse lymphoma assay in L5178Y cells. Glatiramer acetate was
clastogenic in two separate in vitro chromosomal aberration assays in cultured human lymphocytes; it was not
clastogenic in an in vivo mouse bone marrow micronucleus assay.
Impairment of Fertility
In a multigeneration reproduction and fertility study in rats, glatiramer acetate at subcutaneous doses of up to
36 mg/kg (18 times the human therapeutic dose on a mg/m2 basis) had no adverse effects on reproductive
parameters.
Pregnancy
Pregnancy Category B. No adverse effects on embryofetal development occurred in reproduction studies in
rats and rabbits receiving subcutaneous doses of up to 37.5 mg/kg of glatiramer acetate during the period of
organogenesis (18 and 36 times the therapeutic human dose on a mg/m2 basis, respectively). In a prenatal and
postnatal study in which rats received subcutaneous glatiramer acetate at doses of up to 36 mg/kg from
day 15 of pregnancy throughout lactation, no significant effects on delivery or on offspring growth and
development were observed.
There are no adequate and well-controlled studies in pregnant women. Because animal reproduction studies
are not always predictive of human response, glatiramer acetate should be used during pregnancy only if
clearly needed.
Labor and Delivery
In a prenatal and postnatal study, in which rats received subcutaneous glatiramer acetate at doses of up to
36 mg/kg from day 15 of pregnancy throughout lactation, no significant effects on delivery were observed.
The relevance of these findings to humans is unknown.
Nursing Mothers
It is not known whether glatiramer acetate is excreted in human milk. Because many drugs are excreted in
human milk, caution should be exercised when COPAXONE® is administered to a nursing woman.
Pediatric Use
The safety and efficacy of COPAXONE® Injection have not been established in individuals under 18 years of
age.
Use in the Elderly
COPAXONE® Injection has not been studied specifically in elderly patients.
Use in Patients with Impaired Renal Function
The pharmacokinetics of glatiramer acetate in patients with impaired renal function have not been determined.
ADVERSE REACTIONS
During premarketing clinical trials approximately 900 individuals received at least one dose of glatiramer
acetate.
In controlled clinical trials the most commonly observed adverse experiences associated with the use of
glatiramer acetate and not seen at an equivalent frequency among placebo-treated patients were: injection site
reactions, vasodilatation, chest pain, asthenia, infection, pain, nausea, arthralgia, anxiety, and hypertonia.
Approximately 8% of the 893 subjects receiving glatiramer acetate discontinued treatment because of an
adverse reaction. The adverse reactions most commonly associated with discontinuation were: injection site
reaction (6.5%), vasodilatation, unintended pregnancy, depression, dyspnea, urticaria, tachycardia, dizziness,
and tremor.
Immediate Post-Injection Reaction
Approximately 10% of MS patients exposed to glatiramer acetate in premarketing studies experienced a
constellation of symptoms immediately after injection that included flushing, chest pain, palpitations, anxiety,
dyspnea, constriction of the throat, and urticaria. In clinical trials, the symptoms were generally transient and
self-limited and did not require specific treatment. In general, these symptoms have their onset several months
after the initiation of treatment, although they may occur earlier, and a given patient may experience one or
several episodes of these symptoms. Whether or not any of these symptoms actually represent a specific
syndrome is uncertain. During the postmarketing period, there have been reports of patients with similar
symptoms who received emergency medical care.
Whether an immunologic or non-immunologic mechanism mediates these episodes, or whether several similar
episodes seen in a given patient have identical mechanisms, is unknown.
Chest Pain
Approximately 21% of glatiramer acetate patients in the pre-marketing controlled studies (compared to 11%
of placebo patients) experienced at least one episode of what was described as transient chest pain. While
some of these episodes occurred in the context of the Immediate Post-Injection Reaction described above,
many did not. The temporal relationship of this chest pain to an injection of glatiramer acetate was not always
known. The pain was transient (usually lasting only a few minutes), often unassociated with other symptoms,
and appeared to have no important clinical sequelae. There has been only one episode of chest pain during
which a full EKG was performed; that EKG showed no evidence of ischemia. Some patients experienced more
than one such episode, and episodes usually began at least 1 month after the initiation of treatment. The
pathogenesis of this symptom is unknown.
Incidence in Controlled Clinical Studies: The following table lists treatment-emergent signs and symptoms
that occurred in at least 2% of MS patients treated with glatiramer acetate in the pre-marketing placebocontrolled trials. These signs and symptoms were numerically more common in patients treated with
glatiramer acetate than in patients treated with placebo. These trials include the first two controlled trials in
RR MS patients and a controlled trial in patients with Chronic-Progressive MS. Adverse reactions were
usually mild in intensity.
The prescriber should be aware that these figures cannot be used to predict the frequency of adverse
experiences in the course of usual medical practice where patient characteristics and other factors may differ
from those prevailing during clinical studies. Similarly, the cited frequencies cannot be directly compared with
figures obtained from other clinical investigations involving different treatments, uses, or investigators. An
inspection of these frequencies, however, does provide the prescriber with one basis on which to estimate the
relative contribution of drug and nondrug factors to the adverse reaction incidences in the population studied.
Controlled Trials in Patients with Multiple Sclerosis:
Incidence of Glatiramer Acetate Adverse Reactions 2%
and More Frequent than Placebo
Glatiramer Acetate (N = 201)
Preferred Term
Body as a Whole
Asthenia
Back Pain
Bacterial Infection
Chest Pain
Chills
Cyst
Face Edema
Fever
Flu Syndrome
Infection
Injection Site Erythema
Injection Site Hemorrhage
Injection Site Induration
Injection Site Inflammation
Injection Site Mass
Injection Site Pain
Injection Site Pruritus
Injection Site Urticaria
Injection Site Welt
Neck Pain
Pain
Cardiovascular System
Migraine
Palpitations
Syncope
Tachycardia
Vasodilatation
Digestive System
Anorexia
Diarrhea
Gastroenteritis
Gastrointestinal Disorder
Nausea
Vomiting
Hemic and Lymphatic System
Ecchymosis
Lymphadenopathy
Placebo (N = 206)
N
%
N
%
83
33
11
43
8
5
12
17
38
101
132
11
26
98
54
147
80
10
22
16
56
41
16
5
21
4
2
6
8
19
50
66
5
13
49
27
73
40
5
11
8
28
78
30
9
22
2
1
2
15
35
99
40
6
1
22
21
78
12
0
5
9
52
38
15
4
11
1
0
1
7
17
48
19
3
0
11
10
38
6
0
2
4
25
10
35
10
11
55
5
17
5
5
27
5
16
5
8
21
2
8
2
4
10
17
25
6
10
44
13
8
12
3
5
22
6
15
23
2
8
34
8
7
11
1
4
17
4
16
25
8
12
13
12
6
6
Glatiramer Acetate (N = 201)
Preferred Term (continued)
Metabolic and Nutritional
Edema
Peripheral Edema
Weight Gain
Musculoskeletal System
Arthralgia
Nervous System
Agitation
Anxiety
Confusion
Foot Drop
Hypertonia
Nervousness
Nystagmus
Speech Disorder
Tremor
Vertigo
Respiratory System
Bronchitis
Dyspnea
Laryngismus
Rhinitis
Skin and Appendages
Erythema
Herpes Simplex
Pruritus
Rash
Skin Nodule
Sweating
Urticaria
Special Senses
Ear Pain
Eye Disorder
Urogenital System
Dysmenorrhea
Urinary Urgency
Vaginal Moniliasis
Placebo (N = 206)
N
%
N
%
5
14
7
3
7
3
1
8
0
0
4
0
49
24
39
19
8
46
5
6
44
4
5
5
14
12
4
23
2
3
22
2
2
2
7
6
4
40
1
4
37
2
2
3
7
11
2
19
0
2
18
1
1
1
3
5
18
38
10
29
9
19
5
14
12
15
7
27
6
7
3
13
8
8
36
37
4
31
9
4
4
18
18
2
15
4
4
6
26
30
1
21
5
2
3
13
15
0
10
2
15
8
7
4
12
1
6
0
12
20
16
6
10
8
10
17
9
5
8
4
Other events which occurred in at least 2% of glatiramer acetate patients but were present at equal or greater
rates in the placebo group included:
Body as a Whole: Headache, injection site ecchymosis, accidental injury, abdominal pain, allergic rhinitis,
neck rigidity, and malaise.
Digestive System: Dyspepsia, constipation, dysphagia, fecal incontinence, flatulence, nausea and vomiting,
gastritis, gingivitis, periodontal abscess, and dry mouth.
Musculoskeletal: Myasthenia and myalgia.
Nervous System: Dizziness, hypesthesia, paresthesia, insomnia, depression, dysesthesia, incoordination,
somnolence, abnormal gait, amnesia, emotional lability, Lhermitte’s sign, abnormal thinking, twitching,
euphoria, and sleep disorder.
Respiratory System: Pharyngitis, sinusitis, increased cough, and laryngitis.
Skin and Appendages: Acne, alopecia, and nail disorder.
Special Senses: Abnormal vision, diplopia, amblyopia, eye pain, conjunctivitis, tinnitus, taste perversion, and
deafness.
Urogenital System: Urinary tract infection, urinary frequency, urinary incontinence, urinary retention, dysuria,
cystitis, metrorrhagia, breast pain, and vaginitis.
Data on adverse reactions occurring in the controlled clinical trials were analyzed to evaluate differences based
on sex. No clinically significant differences were identified. Ninety-two percent of patients in these clinical
trials were Caucasian. This percentage reflects the racial composition of the MS population. In addition, the
vast majority of patients treated with COPAXONE® were between the ages of 18 and 45. Consequently, data
are inadequate to perform an analysis of the adverse reaction incidence related to clinically relevant age
subgroups.
Laboratory analyses were performed on all patients participating in the clinical program for glatiramer acetate.
Clinically significant laboratory values for hematology, chemistry, and urinalysis were similar for both
glatiramer acetate and placebo groups in blinded clinical trials. No patient receiving glatiramer acetate
withdrew from any trial because of abnormal laboratory findings.
Other Adverse Events Observed During Clinical Trials
Glatiramer acetate was administered to 979 individuals during premarketing clinical trials, only some of which
were placebo-controlled. During these trials, all adverse events were recorded by the clinical investigators,
using terminology of their own choosing. To provide a meaningful estimate of the proportion of individuals
having adverse events, similar types of events were grouped into standardized categories using COSTART
dictionary terminology. All reported events occurring at least twice and potentially important events occurring
once are listed below, except those already listed in the previous table, those too general to be informative,
trivial events, and other reactions which occurred in at least 2% of treated patients and were present at equal
or greater rates in the placebo group. Additional adverse reactions reported during the post-marketing period
are included.
Events are further classified within body system categories and listed in order of decreasing frequency using
the following definitions: Frequent adverse events are defined as those occurring in at least 1/100 patients;
Infrequent adverse events are those occurring in 1/100 to 1/1000 patients; Rare adverse events are those
occurring in less than 1/1000 patients.
Body as a Whole:
Frequent: Injection site edema, injection site atrophy, abscess, injection site hypersensitivity.
Infrequent: Injection site hematoma, injection site fibrosis, moon face, cellulitis, generalized edema,
hernia, injection site abscess, serum sickness, suicide attempt, injection site hypertrophy, injection
site melanosis, lipoma, and photosensitivity reaction.
Cardiovascular:
Frequent: Hypertension.
Infrequent: Hypotension, midsystolic click, systolic murmur, atrial fibrillation, bradycardia, fourth
heart sound, postural hypotension, and varicose veins.
Digestive:
Infrequent: Dry mouth, stomatitis, burning sensation on tongue, cholecystitis, colitis, esophageal
ulcer, esophagitis, gastrointestinal carcinoma, gum hemorrhage, hepatomegaly, increased appetite,
melena, mouth ulceration, pancreas disorder, pancreatitis, rectal hemorrhage, tenesmus, tongue
discoloration, and duodenal ulcer.
Endocrine:
Infrequent: Goiter, hyperthyroidism, and hypothyroidism.
Gastrointestinal:
Frequent: Bowel urgency, oral moniliasis, salivary gland enlargement, tooth caries, and ulcerative
stomatitis.
Hemic and Lymphatic:
Infrequent: Leukopenia, anemia, cyanosis, eosinophilia, hematemesis, lymphedema, pancytopenia,
and splenomegaly.
Metabolic and Nutritional:
Infrequent: Weight loss, alcohol intolerance, Cushing’s syndrome, gout, abnormal healing, and
xanthoma.
Musculoskeletal:
Infrequent: Arthritis, muscle atrophy, bone pain, bursitis, kidney pain, muscle disorder, myopathy,
osteomyelitis, tendon pain, and tenosynovitis.
Nervous:
Frequent: Abnormal dreams, emotional lability, and stupor.
Infrequent: Aphasia, ataxia, convulsion, circumoral paresthesia, depersonalization, hallucinations,
hostility, hypokinesia, coma, concentration disorder, facial paralysis, decreased libido, manic
reaction, memory impairment, myoclonus, neuralgia, paranoid reaction, paraplegia, psychotic
depression, and transient stupor.
Respiratory:
Frequent: Hyperventilation, hay-fever.
Infrequent: Asthma, pneumonia, epistaxis, hypoventilation, and voice alteration.
Skin and Appendages:
Frequent: Eczema, herpes zoster, pustular rash, skin atrophy, and warts.
Infrequent: Dry skin, skin hypertrophy, dermatitis, furunculosis, psoriasis, angioedema, contact
dermatitis, erythema nodosum, fungal dermatitis, maculopapular rash, pigmentation, benign skin
neoplasm, skin carcinoma, skin striae, and vesiculobullous rash.
Special Senses:
Frequent: Visual field defect.
Infrequent: Dry eyes, otitis externa, ptosis, cataract, corneal ulcer, mydriasis, optic neuritis,
photophobia, and taste loss.
Urogenital:
Frequent: Amenorrhea, hematuria, impotence, menorrhagia, suspicious papanicolaou smear,
urinary frequency and vaginal hemorrhage.
Infrequent: Vaginitis, flank pain (kidney), abortion, breast engorgement, breast enlargement,
carcinoma in situ cervix, fibrocystic breast, kidney calculus, nocturia, ovarian cyst, priapism,
pyelonephritis, abnormal sexual function, and urethritis.
Postmarketing Clinical Experience
Postmarketing experience has shown an adverse event profile similar to that presented above. Reports of
adverse reactions occurring under treatment with COPAXONE® (glatiramer acetate for injection) not
mentioned above that have been received since market introduction and that may have or not have causal
relationship to the drug include the following:
Body as a Whole: sepsis; LE syndrome; hydrocephalus; enlarged abdomen; injection site hypersensitivity;
allergic reaction; anaphylactoid reaction
Cardiovascular System: thrombosis; peripheral vascular disease; pericardial effusion; myocardial infarct; deep
thrombophlebitis; coronary occlusion; congestive heart failure; cardiomyopathy; cardiomegaly; arrhythmia;
angina pectoris
Digestive System: tongue edema; stomach ulcer; hemorrhage; liver function abnormality; liver damage;
hepatitis; eructation; cirrhosis of the liver; cholelithiasis
Hemic and Lymphatic System: thrombocytopenia; lymphoma-like reaction; acute leukemia
Metabolic and Nutritional Disorders: hypercholesterolemia
Musculoskeletal System: rheumatoid arthritis; generalized spasm
Nervous System: myelitis; meningitis; CNS neoplasm; cerebrovascular accident; brain edema; abnormal dreams;
aphasia; convulsion; neuralgia
Respiratory System: pulmonary embolus; pleural effusion; carcinoma of lung; hay fever
Special Senses: glaucoma; blindness; visual field defect
Urogenital System: urogenital neoplasm; urine abnormality; ovarian carcinoma; nephrosis; kidney failure;
breast carcinoma; bladder carcinoma; urinary frequency
only.
®
Manufactured For: TEVA Neuroscience, Inc., Kansas City, MO 64131
Manufactured By: Baxter Pharmaceutical Solutions LLC, Bloomington, IN 47403
Distributed by: Aventis Pharmaceuticals Inc., Kansas City, MO 64137
Copp0102BP
3-467-1338
I20573
Rev # 01/2002
References: 1. Data on file. Teva Neuroscience, Inc. 2. Neuhaus O, Farina C, Wekerle H, et al.
Neurology. 2001;56:702-708. 3. Duda PW, Schmied MC, Cook SL, et al. J Clin Invest.
2000;105(7):967-976. 4. Johnson KP, the U.S. Phase III Copolymer 1 Study Group, Teitelbaum D,
et al. Ann Neurol. 1995;38(6):973. 5. COPAXONE® prescribing information. Teva Neuroscience, Inc.
6. Johnson KP, Brooks BR, Cohen JA, et al. Neurology. 1995;45(7):1268-1276. 7. Bornstein MB,
Miller A, Slagle S, et al. N Engl J Med. 1987;317:408-414. 8. Comi G, Filippi M, Wolinsky JS, et al.
Ann Neurol. 2001;49(3):290-297. 9. Khan OA, Tselis AC, Kamholz JA, et al. Multiple Sclerosis.
2001;7:349-353. 10. Mancardi GL, Sardanelli F, Parodi RC, et al. Neurology. 1998;50:1127-1133.
11. Miller A, Shapiro S, Gershtein R, et al. J Neuroimmunol. 1998;92:113-121.
Exhibition Information
1
13
2
Floor Plan
3
12
4
5
11
6
7
8
9
10
The Steering Committee acknowledges the exhibitors’ participation in ACTRIMS-ECTRIMS 2002. Stop
by and visit exhibitors during the following hours:
Wednesday, September 18 from 1 pm–5 pm
Thursday, September 19 from 8 am–5 pm
Friday, September 20 from 8 am–5 pm
GOLD SPONSOR EXHIBITORS
Biogen Booth 12
Biogen, Inc., winner of the US National Medal of Technology, is the world's oldest independent biotechnology
company and a recognized leader in the field of multiple sclerosis research. Biogen produces and markets
AVONEX® (Interferon beta-1a), the leading treatment for relapsing forms of multiple sclerosis.
Biogen/Elan Booth 13
Biogen, Inc. and Elan Corporation have established a worldwide, collaboration to develop, manufacture, and commercialize Antegren® (natalizumab), the first Selective Adhesion Molecule (SAM) Inhibitor. Natalizumab, a humanized monoclonal antibody binds to the cell surface receptors known as alpha-4-beta-1 (VLA-4) and alpha-4-beta7 integrins, which are believed to play an important role in the trafficking of mononuclear cells, such as
lymphocytes, into sites of inflammation. Natalizumab is currently in Phase III clinical trials for MS and Crohn’s
Disease and further trials could determine its potential in the treatment of a range of autoimmune diseases.
32
Schering AG Germany / Berlex Booth 11
Betaseron® was the first therapy approved in the United States to treat relapsing-remitting multiple sclerosis.
Berlex has filed a supplemental (sBLA) Biologics License Application to expand the indication of Betaseron® to
include secondary progressive MS. A new room-temperature formulation of Betaseron® is now available.
Betaseron® is the first and only therapy available as a room-temperature formulation (25°C/77°F) for relapsingremitting MS, providing a convenient option for MS patients in the United States.
Serono Booth 1
Rebif (interferon beta-1a) was approved for sale in the United States on March 7, 2002, for the treatment of relapsing forms of multiple sclerosis based upon the results of two large multi-center studies. Rebif provides significant
treatment benefits for people with relapsing forms of MS by decreasing the frequency of relapses and delaying the
accumulation of physical disability. Efficacy in chronic progressive MS has not been established. Rebif is available in
ready-to-use, pre-filled syringes and can be administered using Rebiject, an autoinjector developed exclusively for
use with Rebif. For more information on Rebif visit www.Rebif.com or call MS LifeLines at 877-44-REBIF.
Teva Neuroscience Booth 5
Teva Neuroscience invites you to visit our booth to discuss Copaxone (glatiramer acetate for injection).We will
also be discussing MSWatch, the first fully integrated, interactive disease management Web application for people
with Multiple Scleross. MSWatch is available free of charge to all MS patients and their health care providers.
ASSOCIATION AND COMMERCIAL EXHIBITORS
Arnold Publishers Booth 10
Multiple Sclerosis is published by Arnold Publishers and is now in its 9th year. It focuses on the etiology and
pathogenesis of demyelinating and inflammatory diseases of the central nervous system and on the application of
such studies to scientifically based therapy. Multiple Sclerosis is a vital journal for research in the following areas:
clinical neurology; myelin chemistry; neuroimaging; pathobiology of the blood/brain barrier; glial
pathobiology/myelin repair; pathology; epidemiology; therapeutics; genetics; immunology; and virology. Editor-inChief, Donald H Silberberg, Department of Neurology, University of Pennsylvania School of Medicine, USA. For
more information, visit www.multiplesclerosisjournal.com.
Cephalon Booth 2
Cephalon, Inc., headquartered in West Chester, PA., is an international biopharmaceutical company dedicated to
the discovery, development and marketing of products to treat neurological disorders, sleep disorders, cancer and
pain. The Company currently markets three products in the United States: PROVIGIL® (modafinil) Tablets [C-IV]
for the treatment of excessive daytime sleepiness associated with narcolepsy, which is being developed for other
potential uses; GABITRIL® (tiagabine hydrochloride) for the adjunctive treatment of partial seizures associated
with epilepsy; and ACTIQ® (oral transmucosal fentanyl citrate) for the treatment of breakthrough cancer pain.
Consortium of Multiple Sclerosis Centers Booth 7
The Consortium of Multiple Sclerosis Centers (CMSC) is the largest organization of MS healthcare professionals
in the world. Our membership includes MS Centers, Clinics,VA members, and individual healthcare providers. The
CMSC has established standards of care in MS that are being adopted worldwide. CMSC/NARCOMS, the North
American Research Committee on MS, facilitates multi-center studies and clinical trials through its web site and
registry of 23,000 patients. Our journal is The International Journal of MS Care.The Foundation of the CMSC
provides funds to train healthcare professionals in research and care in MS.
33
Art on the
Waterfront
Serono is pleased
to bring you the Living with MS Art and
Music Festival.
This therapeutic happening is an exhibition
of American and international art created
by patients, neurologists, and nurses in the
MS community.
Evening festivities include:
Gallery viewing and reception
Buffet dinner served on Waterside Boulevard
Jazz concert under the Pavilion on Pier Six
Please join us at 7:00 PM on Pier Six
immediately following the Satellite Symposium
on Friday, September 20, 2002.
Please visit us at booth #1 for more information.
Proud sponsor of the Living with MS Art and Music Festival
EDMUS Booth 4
The European Database for Multiple Sclerosis (EDMUS) is a standardised computerised databasing system which
has been conceived within consecutive European Concerted Actions on Multiple Sclerosis (MS) since 1990.
EDMUS is a working tool available for clinical and research purposes. It is the result of joint reflections of clinicians and researchers from the whole European Union, all involved in MS.A specific Steering Committee with at
least one delegate from each country of the European Union has been set up for this purpose.Today the EDMUS
system is established in more than 190 centers over 26 countries. It is used for the clinical follow-up of patients,
independent research projects and collaborative multicenter studies where a “common language” is mandatory.
A new version of the software has been developed in order to come up to all users’ expectations.
European Charcot Foundation Booth 8
The European Charcot Foundation started in 1990 as the legal carrier of a Concerted Action in Multiple
Sclerosis (MS) Research funded by the European Communities. From 1994 on the European Charcot Foundation continued as a non-profit Foundation, supported by private organisations, National MS Societies and
Industries. Its working base in Europe now consists of more than 550 institutions and 1700 investigators.
With their dedication the Foundation wants to realize a European dimension in MS Research and capitalize
on the great resources of European co-operation and co-ordination to overcome this debilitating disease.
Multiple Sclerosis International Federation Booth 6
The Multiple Sclerosis International Federation (MSIF) was established in 1967 and links the work of its 42
national Member Societies worldwide. It is committed to working with these Societies and with the international research community to eliminate MS and its devastating effects. The MSIF also speaks out on a global level
for those affected by MS.
National Multiple Sclerosis Society Booth 9
Through our Professional Resource Center, the NMSS provides timely and expert information to physicians and
other healthcare professionals involved in the care of people with MS and their families. Contact us for information and consultation about the disease and its management; library and literature search services; information
about insurance and long-term care; continuing education opportunities; and consultation on the development of
National MS Society-affiliated clinical facilities. For further information, contact the PRC by phone at 1-866-MSTREAT, by e-mail at MD_info@nmss.org, or visit us online at www.nationalmssociety.PRC/asp.
The Sylvia Lawry Centre for Multiple Sclerosis Research (SLCMSR) Booth 6
The SLCMSR was founded in February 2001 at the Technical University of Munich under the direction of Prof.
Albrecht Neiß and sponsored by the Multiple Sclerosis International Federation (MSIF). Using the combination of
computer science, mathematics and medicine, it aims to make future development of MS therapies faster and less
costly.This will be achieved by identifying clinical and MRI markers, which will be more reliably predictive of the
future course of MS than those so far identified, using mathematical models based on an unequalled collection of
placebo data from clinical trials and natural history data. It is an excellent example of what can be done when
industry and academics work together.
WebMD Booth 3
WebMD Corporation provides a comprehensive suite of information, transaction and technology solutions that
help consumers, physicians, providers and other participants navigate the complexity of the healthcare system.
Our products and services promote informed decision-making, increased efficiency and, ultimately, higher quality
patient care at a lower cost. WebMD Corporation consists of three divisions, each a leader in their respective
field: WebMD Envoy,WebMD Medical Manager and WebMD Health.
35
NEW
ROOM-TEMPERATURE FORMULATION
REFRIGERATION-FREE
BETASERON® (Interferon beta-1b)
For ambulatory patients with
relapsing-remitting multiple sclerosis (MS)
to treat clinical exacerbations...
Carol—
Betaseron user
since 1994.
Serious side effects include depression, suicide,
suicidal ideation, and injection-site necrosis
(skin breakdown, drainage of fluid, and tissue
destruction), which has been reported in 5% of
patients in a controlled MS trial. The necrotic lesions
are typically 3 cm or less in diameter, but larger
areas have been reported, and they may occur at
single or multiple sites. Patients should be advised
of the importance of rotating areas of injection with
each dose, and of consulting with their physician if
they experience any of the above signs or symptoms.
(See WARNINGS, PRECAUTIONS, and ADVERSE
REACTIONS sections of the full prescribing information.)
Common side effects of Betaseron therapy include
flu-like symptoms, shortness of breath, menstrual
disorders, and injection-site reactions; redness, pain,
swelling, and blue-black discoloration have been reported.
Please see full prescribing information on adjacent page.
Betaseron is a registered trademark and the
service marks of Berlex Laboratories, Inc.
design and MS Pathways are
SM
and deliver the full effect of
the only Refrigeration-Free
interferon therapy — Betaseron
• Deliver NEW Convenience that Helps Improve Compliance —
NEW Refrigeration-Free Betaseron is the only therapy that can be stored and transported
at room temperature — and as always, with a neutral pH of approximately 7.4
• Deliver the Full Effect With Frequent Dosing — taken every other day
subcutaneously, Betaseron (250 mcg) is specifically designed to maintain a constant
effect on biological response markers
• Deliver Manageability — common side effects are usually easily managed and
often improve over time
• Deliver the Full Support of MS PathwaysSM — helps you assist your patients in
managing their therapy through a 24/7 toll-free hot line that features MS-specialized
registered nurses
© 2002, Berlex Laboratories, Inc. All rights reserved.
Manufactured by CHIRON Corporation, Emeryville, CA 94608
Distributed by BERLEX Laboratories, Inc., Montville, NJ 07045
02-521-0051
Printed in USA
June 2002
Fight back right from the start
Betaseron
Interferon beta-1b
MRI data were also analyzed for patients in this study. A frequency distribution of the observed percent changes in MRI area at the end of
2 years was obtained by grouping the percentages in successive intervals of equal width. Figure 1 displays a histogram of the proportions of
patients who fell into each of these intervals. The median percent change in MRI area for the 0.25 mg group was –1.1% which was significantly smaller than the 16.5% observed for the placebo group (p=0.0001).
TABLE 1
2 Year Study Results
Primary and Secondary Clinical Endpoints
Efficacy Parameters
Treatment Groups
Placebo
Primary Endpoints
0.05 mg
0.25 mg
Statistical Comparisons
Placebo
vs
0.05 mg
p-value
0.05 mg
vs
0.25 mg
Placebo
vs
0.25 mg
(N=123)
(N=125) (N=124)
Annual exacerbation rate
1.31
1.14
0.90
0.005
0.113
0.0001
Proportion of exacerbation-free patients†
16%
18%
25%
0.609
0.288
0.094
Exacerbation
0†
20
22
29
0.151
0.077
0.001
frequency
1
32
31
39
per patient
2
20
28
17
3
15
15
14
4
15
7
9
≥5
21
16
8
Secondary Endpoints††
Median number of months
5
6
9
0.299
0.097
0.010
to first on-study exacerbation
Rate of moderate or severe
0.47
0.29
0.23
0.020
0.257
0.001
exacerbations per year
Mean number of moderate or severe
44.1
33.2
19.5
0.229
0.064
0.001
exacerbation days per patient
Mean change in EDSS
0.21
0.21
–0.07
0.995
0.108
0.144
score‡ at endpoint
Mean change in Scripps
–0.53
–0.50
0.66
0.641
0.051
0.126
score‡‡ at endpoint
Median duration in days
36
33
35.5
ND
ND
ND
per exacerbation
% change in mean MRI
21.4%
9.8%
–0.9%
0.015
0.019
0.0001
lesion area at endpoint
ND - Not done
† 14 exacerbation-free patients (0 from placebo, 6 from 0.05 mg, and 8 from 0.25 mg) dropped out of the study before completing
6 months of therapy. These patients are excluded from this analysis.
†† Sequelae and Functional Neurologic Status, both required by protocol, were not analyzed individually but are included as a function
of the EDSS.
‡ EDSS scores range from 0–10, with higher scores reflecting greater disability.
‡‡ Scripps neurologic rating scores range from 0–100, with smaller scores reflecting greater disability.
Figure 1
Distribution of Change in MRI Area
Betaseron 0.25 mg
40
Median Change = –1.1%
n=95
30
% of Patients
DESCRIPTION
Betaseron® (Interferon beta-1b) is a purified, sterile, lyophilized protein product produced by recombinant DNA techniques and formulated for
use by injection. Interferon beta-1b is manufactured by bacterial fermentation of a strain of Escherichia coli that bears a genetically engineered
plasmid containing the gene for human interferon betaser17. The native gene was obtained from human fibroblasts and altered in a way that substitutes serine for the cysteine residue found at position 17. Interferon beta-1b is a highly purified protein that has 165 amino acids and an
approximate molecular might of 18,500 daltons. It does not include the carbohydrate side chains found in the natural material.
The specific activity of Betaseron is approximately 32 million international units (IU)/mg Interferon beta-1b. Each vial contains 0.3 mg of
Interferon beta-1b. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO)
reference standard of recombinant human interferon beta. Mannitol USP and Albumin Human USP (15 mg each/vial) are added as stabilizers.
Prior to 1993, a different analytical standard was used to determine potency. It assigned 54 million IU to 0.3 mg Interferon beta-1b.
Lyophilized Betaseron is a sterile, white to off-white powder intended for subcutaneous injection after reconstitution with the diluent supplied
(Sodium Chloride, 0.54% Solution).
CLINICAL PHARMACOLOGY
General: Interferons are a family of naturally occurring proteins, which have molecular weights ranging from 15,000 to 21,000 daltons. Three
major classes of interferons have been identified: alfa, beta, and gamma. Interferon beta-1b, interferon alfa, and interferon gamma have overlapping yet distinct biologic activities.1-5 The activities of Interferon beta-1b are species-restricted and, therefore, the most pertinent pharmacologic information on Betaseron is derived from studies of human cells in culture and in humans.
Biologic Activities: Interferon beta-1b has been shown to possess both antiviral and immunoregulatory activities. The mechanisms by
which Betaseron exerts its actions in multiple sclerosis (MS) are not clearly understood. However, it is known that the biologic responsemodifying properties of Interferon beta-1b are mediated through its interactions with specific cell receptors found on the surface of human
cells. The binding of Interferon beta-1b to these receptors induces the expression of a number of interferon-induced gene products (e.g.,
2’,5’-oligoadenylate synthetase, protein kinase, and indoleamine 2,3-dioxygenase) that are believed to be the mediators of the biological
actions of Interferon beta-1b.1,3,6-10 A number of these interferon-induced products have been readily measured in the serum and cellular fractions of blood collected from patients treated with Interferon beta-1b.11,12
Pharmacokinetics: Because serum concentrations of Interferon beta-1b are low or not detectable following subcutaneous administration of
0.25 mg or less of Betaseron, pharmacokinetic information in patients with MS receiving the recommended dose of Betaseron is not available.
Following single and multiple daily subcutaneous administrations of 0.5 mg Betaseron to healthy volunteers (N=12), serum Interferon beta-1b
concentrations were generally below 100 IU/mL. Peak serum Interferon beta-1b concentrations occurred between 1 to 8 hours, with a mean
peak serum interferon concentration of 40 IU/mL. Bioavailability, based on a total dose of 0.5 mg Betaseron given as two subcutaneous injections at different sites, was approximately 50%.
After intravenous administration of Betaseron (0.006 mg to 2.0 mg), similar pharmacokinetic profiles were obtained from healthy volunteers
(N=12) and from patients with diseases other than MS (N=142). In patients receiving single intravenous doses up to 2.0 mg, increases in serum
concentrations were dose proportional. Mean serum clearance values ranged from 9.4 mL/min·kg-1 to 28.9 mL/min·kg-1 and were independent of
dose. Mean terminal elimination half-life values ranged from 8.0 minutes to 4.3 hours and mean steady-state volume of distribution values
ranged from 0.25 L/kg to 2.88 L/kg. Three-times-a-week intravenous dosing for 2 weeks resulted in no accumulation of Interferon beta-1b in
the serum of patients. Pharmacokinetic parameters after single and multiple intravenous doses of Betaseron were comparable.
Clinical Trials: The effectiveness of Betaseron in relapsing-remitting MS was evaluated in a double-blind, multiclinic (11 sites: 4 Canadian and
7 United States), randomized, parallel, placebo-controlled clinical investigation of 2 years duration. The study enrolled MS patients, aged 18 to
50, who were ambulatory (Kurtzke expanded disability status scale [EDSS] of ≤ 5.5), exhibited a relapsing-remitting clinical course, met Poser’s
criteria13 for clinically definite and/or laboratory supported definite MS and had experienced at least two exacerbations over 2 years preceding
the trial without exacerbation in the preceding month. Patients who had received prior immunosuppressant therapy were excluded.
An exacerbation was defined, per protocol, as the appearance of a new clinical sign/symptom or the clinical worsening of a previous sign/symptom (one that had been stable for at least 30 days) that persisted for a minimum of 24 hours.
Patients selected for study were randomized to treatment with either placebo (N =123), 0.05 mg of Betaseron (N =125), or
0.25 mg of Betaseron (N=124) self-administered subcutaneously every other day. Outcome based on the 372 randomized patients was evaluated after 2 years.
Patients who required more than three 28-day courses of corticosteroids were removed from the study. Minor analgesics (acetaminophen, codeine),
antidepressants, and oral baclofen were allowed ad libitum but chronic nonsteroidal anti-inflammatory drug (NSAID) use was not allowed.
The primary, protocol defined, outcome assessment measures were 1) frequency of exacerbations per patient and 2) proportion of exacerbation
free patients. A number of secondary outcome measures were also employed as described in TABLE 1.
In addition to clinical measures, annual magnetic resonance imaging (MRI) was performed and quantitated for extent of disease as determined
by changes in total area of lesions. In a substudy of patients (N=52) at one site, MRIs were performed every 6 weeks and quantitated for disease activity as determined by changes in size and number of lesions.
Results at the protocol designated endpoint of 2 years (see TABLE 1): In the 2-year analysis, there was a 31% reduction in annual exacerbation
rate, from 1.31 in the placebo group to 0.9 in the 0.25 mg group. The p-value for this difference was 0.0001. The proportion of patients free of
exacerbations was 16% in the placebo group, compared with 25% in the Betaseron® (Interferon beta-1b) 0.25 mg group.
Of the 372 patients randomized, 72 (19%) failed to complete 2 full years on their assigned treatments. The reasons given for withdrawal varied with
treatment assignment. Excessive use of steroids accounted for 11 of the 26 placebo withdrawals, but only 2 of the 21 withdrawals from the 0.05 mg
assigned group and 1 of the 25 withdrawals from the 0.25 mg assigned group. Withdrawals for adverse events attributed to study article, however,
were more common among Betaseron-treated patients: 1, 5, and 10 withdrew from the placebo, 0.05 mg, and 0.25 mg groups, respectively.
Over the 2-year period, there were 25 MS-related hospitalizations in the 0.25 mg Betaseron-treated group compared to 48 hospitalizations in
the placebo group. In comparison, non-MS hospitalizations were evenly distributed among the groups, with 16 in the 0.25 mg Betaseron group
and 15 in the placebo group. The average number of days of MS-related steroid use was 41 days in the 0.25 mg Betaseron group and 55 days in
the placebo group (p=0.004).
20
10
0
Placebo
40
Median Change = +16.5%
n=100
30
% of Patients
®
20
10
0
From
To
–60
<–40
–40
<–20
–20
<0
0
<20
20
40
60
80
<40
<60
<80
<100
Percent Change in MRI Area
100
<120
120
140
140+
In an evaluation of frequent MRI scans (every 6 weeks) on 52 patients at one site, the percent of scans with new or expanding lesions was 29%
in the placebo group and 6% in the 0.25 mg treatment group (p=0.006).
MRI scanning is viewed as a useful means to visualize changes in white matter that are believed to be a reflection of the pathologic changes
that, appropriately located within the central nervous system (CNS), account for some of the signs and symptoms that typify relapsing-remitting
MS. The exact relationship between MRI findings and the clinical status of patients is unknown. Changes in lesion area often do not correlate
with clinical exacerbations probably because many lesions affect so-called “silent” regions of the CNS. Moreover, it is not clear what fraction of
the lesions seen on MRI become foci of irreversible demyelinization (i.e., classic white matter plaques). The prognostic significance of the MRI
findings in this study has not been evaluated. At the end of 2 years on assigned treatment, patients in the study had the option of continuing on
treatment under blinded conditions. Approximately 80% of patients under each treatment accepted. Although there was a trend toward patient
benefit in the Betaseron® (Interferon beta-1b) groups during the third year, particularly in the 0.25 mg group, there was no statistically significant difference between the Betaseron-treated vs. placebo-treated patients in exacerbation rate, or in any of the secondary endpoints described
in Table 1. As noted above, in the 2-year analysis, there was a 31% reduction in exacerbation rate in the 0.25 mg group, compared with placebo.
The p-value for this difference was 0.0001. In the analysis of the third year alone, the difference between treatment groups was 28%. The
p-value was 0.065. The lower number of patients may account for the loss of statistical significance, and lack of direct comparability among the
patient groups in this extension study makes the interpretation of these results difficult. The third year MRI data did not show a trend toward
additional benefit in the Betaseron arm compared with the placebo arm.
Throughout the clinical trial, serum samples from patients were monitored for the development of antibodies to Interferon beta-1b. In patients
receiving 0.25 mg of Betaseron (N=124) every other day in the clinical trial, 45% were found to have serum neutralizing activity at one or more of
the time points tested. The relationship between antibody formation and clinical efficacy is not known.
Betaseron is indicated for use in ambulatory patients with relapsing-remitting multiple sclerosis to reduce the frequency of clinical exacerbations.
(See CLINICAL PHARMACOLOGY, Clinical Trials section.) Relapsing-remitting MS is characterized by recurrent attacks of neurologic dysfunction followed by complete or incomplete recovery. The safety and efficacy of Betaseron in chronic-progressive MS has not been evaluated.
CONTRAINDICATIONS
Betaseron is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin Human USP, or any
other component of the formulation.
WARNINGS
One suicide and 4 attempted suicides were observed among 372 study patients during a 3-year period. All five patients received Betaseron (three in
the 0.05 mg group and two in the 0.25 mg group). There were no attempted suicides in patients on study who did not receive Betaseron. Depression
and suicide have been reported to occur in patients receiving interferon alfa, a related compound. Patients to be treated with Betaseron should be
informed that depression and suicidal ideation may be a side effect of the treatment and should report these symptoms immediately to the prescribing physician. Patients exhibiting depression should be monitored closely and cessation of therapy should be considered.
Injection site necrosis (ISN) has been reported in 5% of patients in controlled clinical trials (see ADVERSE REACTIONS section). Typically,
injection site necrosis occurs within the first 4 months of therapy, although post-marketing reports have been received of ISN occurring over
1 year after initiation of therapy. Necrosis may occur at single or multiple injection sites. The necrotic lesions are typically 3 cm or less in diameter, but larger areas have been reported. While necrosis has commonly extended only to subcutaneous fat, there are also reports of necrosis
extending to and including fascia overlaying muscle. In some lesions where biopsy results are available, vasculitis has been reported. For some
lesions debridement and, infrequently, skin grafting has been required.
As with any open lesion, it is important to avoid infection and, if it occurs, to treat the infection. Time to healing has varied depending on the
severity of the necrosis at the time treatment was begun. In most cases healing was associated with scarring.
Some patients have experienced healing of necrotic skin lesions while Betaseron® (Interferon beta-1b) therapy continued; others have not.
Whether to discontinue therapy following a single site of necrosis is dependent on the extent of necrosis. For patients who continue therapy
with Betaseron after injection site necrosis has occurred, Betaseron should not be administered into the affected area until it is fully healed. If
multiple lesions occur, therapy should be discontinued until healing occurs.
Patient understanding and use of aseptic self-injection techniques and procedures should be periodically reevaluated, particularly if injection
site necrosis has occurred.
PRECAUTIONS
General: Patients should be instructed in injection techniques to assure the safe self-administration of Betaseron. (See PRECAUTIONS,
Information to patients, and Betaseron Patient Information sheet.)
Information to patients:
Instruction on self-injection technique and procedures. Patients should be instructed in the use of aseptic technique when administering Betaseron. Appropriate instruction for reconstitution of Betaseron and self-injection should be given including careful review of the
Betaseron Patient Information sheet. If possible, the first injection should be performed under the supervision of an appropriately qualified health care professional.
Patients should be cautioned against the re-use of needles or syringes and instructed in safe disposal procedures. A puncture resistant container for disposal of used needles and syringes should be supplied to the patient along with instructions for safe disposal of full containers.
Patients should be advised of the importance of rotating areas of injection with each dose, to minimize the likelihood of severe injection site
reactions or necrosis (see Rotating Injection Sites section of Patient Information sheet).
Patients should be cautioned not to change the dosage or the schedule of administration without medical consultation.
Awareness of adverse reactions. Serious adverse reactions associated with the use of Betaseron have been reported including depression and injection site necrosis (see WARNINGS section).
Patients should immediately report symptoms of depression or suicidal ideation to their physician. The symptoms of depression should be
closely monitored by a physician.
Injection site necrosis was reported in 5% of patients in a controlled MS trial. If the patient experiences any break in the skin, which may be
associated with blue-black discoloration, swelling, or drainage of fluid from the injection site, the patient should be advised to promptly contact their physician prior to continuing their Betaseron therapy.
Other injection site reactions occurred in eighty-five percent of patients in the controlled MS trial, at one or more times during therapy. There
was redness, pain, swelling and discoloration. In general, these were transient and did not require discontinuation of therapy, but the nature
and severity of all reported reactions should be carefully assessed (see ADVERSE REACTIONS section).
Flu-like symptoms are common following initiation of therapy with Betaseron. In the controlled MS clinical trial, acetaminophen was permitted for relief of fever or myalgia (see ADVERSE REACTIONS section).
Patients should be cautioned about the abortifacient potential of Betaseron (see PRECAUTIONS, Pregnancy — Teratogenic effects).
Laboratory tests: The following laboratory tests are recommended prior to initiating Betaseron therapy and at periodic intervals thereafter:
hemoglobin, complete and differential white blood cell counts, platelet counts and blood chemistries including liver function tests. In the controlled MS trial, patients were monitored every 3 months. The study protocol stipulated that Betaseron therapy be discontinued in the event the
absolute neutrophil count fell below 750/mm3. When the absolute neutrophil count had returned to a value greater than 750/mm3, therapy could
be restarted at a 50% reduced dose. No patients were withdrawn or dose reduced for neutropenia or lymphopenia.
Similarly, if hepatic transaminase (SGOT/SGPT) levels exceeded 10 times the upper limit of normal, or if the serum bilirubin exceeded 5 times
the upper limit of normal, therapy was discontinued. In each instance during the controlled MS trial, hepatic enzyme abnormalities returned to
normal following discontinuation of therapy. When measurements had decreased to below these levels, therapy could be restarted at a 50%
dose reduction, if clinically appropriate. Two patients were dose reduced for increased liver enzymes; one continued on treatment and one was
ultimately withdrawn.
Drug interactions: Interactions between Betaseronand other drugs have not been fully evaluated. Although studies designed to examine drug
interactions have not been done, it was noted that corticosteroid or ACTH treatment of relapses for periods of up to 28 days has been administered to patients (N=180) receiving Betaseron.
Betaseron administration to three cancer patients over a dose range of 0.025 mg to 2.2 mg led to a dose-dependent inhibition of antipyrine elimination.14 The effect of alternate-day administration of 0.25 mg of Betaseron on drug metabolism in MS patients is unknown.
Carcinogenesis: The carcinogenic potential of Betaseron was evaluated by studying its effect on the morphological transformation of the
mammalian cell line BALBc-3T3. No significant increases in transformation frequency were noted. No carcinogenicity data are available in animals or humans.
Betaseron® (Interferon beta-1b) was not mutagenic when assayed for genotoxicity in the Ames bacterial test in the presence or absence of
metabolic activation.
Impairment of fertility: Studies in rhesus monkeys at doses up to 0.33 mg/kg/day (32 times the recommended human dose based on body surface area comparison*) in normally cycling rhesus female monkeys had no apparent adverse effects on the menstrual cycle or on associated
hormonal profiles (progesterone and estradiol) when administered over 3 consecutive menstrual cycles. The extrapolability of animal doses to
human doses is not known. Effects of Betaseron on normal cycling human females are not known.
*body surface dose based on 70 kg female
Pregnancy — Teratogenic effects: Pregnancy Category C: Betaseron was not teratogenic at doses up to 0.42 mg/kg/day in rhesus monkeys,
but demonstrated a dose-related abortifacient activity when administered at doses ranging from 0.028 mg/kg/day (2.8 times the recommended
human dose based on body surface area comparison) to 0.42 mg/kg/day (40 times the recommended human dose based on body surface area
comparison). The extrapolability of animal doses to human doses is not known. Lower doses were not studied in monkeys. Spontaneous abortions while on treatment were reported in patients (n=4) who participated in the Betaseron MS clinical trial. Betaseron given to rhesus monkeys
on gestation days 20 to 70 did not cause teratogenic effects, however, it is not known if teratogenic effects exist in humans. There are no adequate and well-controlled studies in pregnant women. If the patient becomes pregnant or plans to become pregnant while taking Betaseron, the
patient should be apprised of the potential hazard to the fetus and it should be recommended that the patient discontinues therapy.
Nursing mothers: It is not known whether Betaseron is excreted in human milk. Because many drugs are excreted in human milk and because
of the potential for serious adverse reactions in nursing infants from Betaseron, a decision should be made as to whether either to discontinue
nursing or discontinue the drug, taking into account the importance of drug to the mother.
Pediatric use: Safety and efficacy in children under 18 years of age have not been established.
ADVERSE REACTIONS
Experience with Betaseron in patients with MS is limited to a total of 147 patients at the recommended dose of 0.25 mg every other day or more
(see CLINICAL PHARMACOLOGY, Clinical Trials section). Consequently, adverse events that are associated with the use of Betaseron in
MS patients at a low incidence may not have been observed in premarketing studies. Clinical experience with Betaseron in other populations
(patients with cancer, HIV positive patients, etc.) provides additional data regarding adverse reactions; however, experience in non-MS populations may not be fully applicable to the MS population.
Injection site reactions (85%) and injection site necrosis (5%) occurred after administration of Betaseron. Inflammation, pain, hypersensitivity,
necrosis, and non-specific reactions were significantly associated (p<0.05) with the 0.25 mg Betaseron-treated group. Only inflammation, pain,
and necrosis were reported as severe events (see WARNINGS and PRECAUTIONS sections). The incidence rate for injection site reactions
TABLE 2
Adverse Reactions and Laboratory Abnormalities
Placebo
Adverse Reaction
N=123
Body as a Whole
Injection site reaction*
Headache
Fever*
Flu-like symptom complex*
Pain
Asthenia*
Chills*
Abdominal pain
Malaise*
Generalized edema
Pelvic pain
Injection site necrosis*
Cyst
Necrosis
Suicide attempt
Cardiovascular System
Migraine
Palpitation*
Hypertension
Tachycardia
Peripheral vascular disorder
Hemorrhage
Digestive System
Diarrhea
Constipation
Vomiting
Gastrointestinal disorder
Endocrine System
Goiter
Hemic and Lymphatic System
Lymphocytes less than1500/mm3
ANC < 1500/mm3*
WBC < 3000/mm3*
Lymphadenopathy
Metabolic and Nutritional Disorders
SGPT > 5 times baseline*
Glucose < 55 mg/dL
Total bilirubin > 2.5 times baseline
Urine protein > 1+
SGOT > 5 times baseline*
Weight gain
Weight loss
Musculoskeletal System
Myalgia*
Myasthenia
Nervous System
Dizziness
Hypertonia
Anxiety
Nervousness
Somnolence
Confusion
Speech disorder
Convulsion
Hyperkinesia
Amnesia
Respiratory System
Sinusitis
Dyspnea*
Laryngitis
Skin and Appendages
Sweating*
Alopecia
Special Senses
Conjunctivitis
Abnormal vision
Urogenital System
Dysmenorrhea
Menstrual disorder*
Metrorrhagia
Cystitis
Breast pain
Menorrhagia
Urinary urgency
Fibrocystic breast
Breast neoplasm
*Significantly associated with Betaseron treatment.
0.25 mg
N=124
37%
77%
41%
56%
48%
35%
19%
24%
3%
6%
3%
0%
2%
0%
0%
85%
84%
59%
76%
52%
49%
46%
32%
15%
8%
6%
5%
4%
2%
2%
7%
2%
2%
3%
2%
1%
12%
8%
7%
6%
5%
3%
29%
18%
19%
3%
35%
24%
21%
6%
0%
2%
67%
6%
5%
11%
82%
18%
16%
14%
6%
13%
2%
3%
0%
0%
2%
19%
15%
6%
5%
4%
4%
4%
28%
10%
44%
13%
28%
24%
13%
5%
3%
2%
1%
0%
0%
0%
35%
26%
15%
8%
6%
4%
3%
2%
2%
2%
26%
2%
2%
36%
8%
6%
11%
2%
23%
4%
10%
4%
12%
7%
11%
8%
8%
4%
3%
3%
2%
1%
0%
18%
17%
15%
8%
7%
6%
4%
3%
2%
was calculated over the course of 3 years. This incidence rate decreased over time, with 79% of patients experiencing the event during the first
3 months of treatment compared to 47% during the last 6 months. The median time to the first occurrence of an injection site reaction was 7
days. Patients with injection site reactions reported these events 183.7 days per year. Three patients withdrew from the 0.25 mg Betaserontreated group for injection site pain.
Flu-like symptom complex was reported in 76% of the patients treated with 0.25 mg Betaseron. A patient was defined as having a flu-like
symptom complex if flu-like symptoms or at least two of the following symptoms were concurrently reported: fever, chills, myalgia, malaise, or
sweating. Only myalgia, fever, and chills were reported as severe in more than 5% of the patients. The incidence rate for flu-like symptom complex was also calculated over the course of 3 years. The incidence rate of these events decreased over time, with 60% of patients experiencing
the event during the first 3 months of treatment compared to 10% during the last 6 months. The median time to the first occurrence of flu-like
symptom complex was 3.5 days and the median duration per patient was 7.5 days per year.
Laboratory abnormalities included absolute neutrophil count less than 1500/mm3 (18%) (no patients had absolute neutrophil counts less than
500/mm3), WBC less than 3000/mm3 (16%), SGPT greater than 5 times baseline value (19%), and total bilirubin greater than 2.5 times baseline
value (6%). Three patients were withdrawn from treatment with 0.25 mg Betaseron for abnormal liver enzymes including one following dose
reduction (see PRECAUTIONS, Laboratory Tests).
Twenty-one (28%) of the 76 premenopausal females treated at 0.25 mg Betaseron and 10 (13%) of the 76 premenopausal females treated with
placebo reported menstrual disorders. All of these reports were of mild to moderate severity and included: intermenstrual bleeding and spotting,
early or delayed menses, decreased days of menstrual flow, and clotting and spotting during menstruation.
Mental disorders have been observed in patients in this study. Symptoms included depression, anxiety, emotional lability, depersonalization, suicide attempts, confusion, etc. In the treatment group, two patients withdrew for confusion. One suicide and four attempted suicides were also
reported. It is not known whether these symptoms may be related to the underlying neurological basis of MS, to Betaseron treatment, or to a
combination of both. Some similar symptoms have been noted in patients receiving interferon alfa and both interferons are thought to act
through the same receptor. Patients who experience these symptoms should be closely monitored and cessation of therapy considered.
Additional common adverse clinical and laboratory events associated with the use of Betaseron® (Interferon beta-1b) are listed in the following
paragraphs. These events occurred at an incidence of 5% or more in the 124 MS patients treated with 0.25 mg of Betaseron every other day for
periods of up to 3 years in the controlled trial, and at an incidence that was at least twice that observed in the 123 placebo patients. Common
adverse clinical and laboratory events associated with the use of Betaseron were: injection site reaction (85%), injection site necrosis (5%), palpitation (8%), hypertension (7%), tachycardia (6%), peripheral vascular disorders (5%), gastrointestinal disorders (6%), absolute neutrophil count
<1500/mm3 (18%), WBC <3000/mm3 (16%), SGPT >5 times baseline value (19%), total bilirubin >2.5 times baseline value (6%), somnolence
(6%), dyspnea (8%), laryngitis (6%), menstrual disorder (17%), cystitis (8%), breast pain (7%), pelvic pain (6%), and menorrhagia (6%).
A total of 277 MS patients have been treated with Betaseron® (Interferon beta-1b) in doses ranging from 0.025 mg to 0.5 mg. During the first
3 years of treatment, withdrawals due to clinical adverse events or laboratory abnormalities not mentioned above included: fatigue (2%,
6 patients), cardiac arrhythmia (<1%, 1 patient), allergic urticarial skin reaction to injections (<1%, 1 patient), headache (<1%, 1 patient), unspecified adverse events (<1%, 1 patient), and “felt sick” (<1%, 1 patient).
TABLE 2 enumerates adverse events and laboratory abnormalities that occurred at an incidence of 2% or more among the 124 MS patients
treated with 0.25 mg Betaseron every other day for periods of up to 3 years in the controlled trial and at an incidence that was at least 2% more
than that observed in the 123 placebo patients. Reported adverse events have been reclassified using the standard COSTART glossary to reduce
the total number of terms employed in the table. In TABLE 2, terms so general as to be uninformative, and those events where a drug cause was
remote have been excluded.
It should be noted that the figures cited in the table cannot be used to predict the incidence of side effects in the course of usual medical practice where patient characteristics and other factors differ from those that prevailed in the clinical trials. The cited figures do provide the
prescribing physician with some basis for estimating the relative contribution of drug and nondrug factors to the side effect incidence rate in the
population studied.
Other events observed during premarketing evaluation of various doses of Betaseron in 1440 patients are listed in the paragraph that follows.
Because most of the events were observed in open and uncontrolled studies, the role of Betaseron in their causation cannot be reliably determined.
Body as a Whole: abscess, adenoma, anaphylactoid reaction, ascites, cellulitis, hernia, hydrocephalus, hypothermia, infection, peritonitis, photosensitivity, sarcoma, sepsis, and shock; Cardiovascular System: angina pectoris, arrhythmia, atrial fibrillation, cardiomegaly, cardiac arrest,
cerebral hemorrhage, cerebral ischemia, endocarditis, heart failure, hypotension, myocardial infarct, pericardial effusion, postural hypotension,
pulmonary embolus, spider angioma, subarachnoid hemorrhage, syncope, thrombophlebitis, thrombosis, varicose vein, vasospasm, venous pressure increased, ventricular extrasystoles, and ventricular fibrillation; Digestive System: aphthous stomatitis, cardiospasm, cheilitis, cholecystitis, cholelithiasis, duodenal ulcer, dry mouth, enteritis, esophagitis, fecal impaction, fecal incontinence, flatulence, gastritis, gastrointestinal
hemorrhage, gingivitis, glossitis, hematemesis, hepatic neoplasia, hepatitis, hepatomegaly, ileus, increased salivation, intestinal obstruction,
melena, nausea, oral leukoplakia, oral moniliasis, pancreatitis, periodontal abscess, proctitis, rectal hemorrhage, salivary gland enlargement,
stomach ulcer, and tenesmus; Endocrine System: Cushing’s Syndrome, diabetes insipidus, diabetes mellitus, hypothyroidism, and inappropriate ADH; Hemic and Lymphatic System: chronic lymphocytic leukemia, hemoglobin less than 9.4 g/100 mL, petechia, platelets less than
75,000/mm3, and splenomegaly; Metabolic and Nutritional Disorders: alcohol intolerance, alkaline phosphatase greater than 5 times baseline value, BUN greater than 40 mg/dL, calcium greater than 11.5 mg/dL, cyanosis, edema, glucose greater than 160 mg/dL, glycosuria, hypoglycemic reaction, hypoxia, ketosis, and thirst; Musculoskeletal System: arthritis, arthrosis, bursitis, leg cramps, muscle atrophy, myopathy,
myositis, ptosis, and tenosynovitis; Nervous System: abnormal gait, acute brain syndrome, agitation, apathy, aphasia, ataxia, brain edema,
chronic brain syndrome, coma, delirium, delusions, dementia, depersonalization, diplopia, dystonia, encephalopathy, euphoria, facial paralysis,
foot drop, hallucinations, hemiplegia, hypalgesia, hyperesthesia, incoordination, intracranial hypertension, libido decreased, manic reaction,
meningitis, neuralgia, neuropathy, neurosis, nystagmus, oculogyric crisis, ophthalmoplegia, papilledema, paralysis, paranoid reaction, psychosis,
reflexes decreased, stupor, subdural hematoma, torticollis, tremor, and urinary retention; Respiratory System: apnea, asthma, atelectasis, carcinoma of lung, hemoptysis, hiccup, hyperventilation, hypoventilation, interstitial pneumonia, lung edema, pleural effusion, pneumonia, and
pneumothorax; Skin and Appendages: contact dermatitis, erythema nodosum, exfoliative dermatitis, furunculosis, hirsutism, leukoderma,
lichenoid dermatitis, maculopapular rash, psoriasis, seborrhea, skin benign neoplasm, skin carcinoma, skin hypertrophy, skin necrosis, skin ulcer,
urticaria, and vesiculobullous rash; Special Senses: blepharitis, blindness, deafness, dry eyes, ear pain, iritis, keratoconjunctivitis, mydriasis,
otitis externa, otitis media, parosmia, photophobia, retinitis, taste loss, taste perversion, and visual field defect; Urogenital System: anuria,
balanitis, breast engorgement, cervicitis, epididymitis, gynecomastia, hematuria, impotence, kidney calculus, kidney failure, kidney tubular disorder, leukorrhea, nephritis, nocturia, oliguria, polyuria, salpingitis, urethritis, urinary incontinence, uterine fibroids enlarged, uterine neoplasm, and
vaginal hemorrhage.
DRUG ABUSE AND DEPENDENCE
No evidence or experience suggests that abuse or dependence occurs with Betaseron® (Interferon beta-1b) therapy; however, the risk of dependence has not been systematically evaluated.
DOSAGE AND ADMINISTRATION
The recommended dose of Betaseron for the treatment of ambulatory relapsing-remitting MS is 0.25 mg injected subcutaneously every other
day. Limited data regarding the activity of a lower dose are presented above (see CLINICAL PHARMACOLOGY, Clinical Trials).
Evidence of efficacy beyond 2 years is not known since the primary evidence of efficacy derives from a 2-year, double-blind, placebo-controlled
clinical trial (see CLINICAL PHARMACOLOGY, Clinical Trials). Safety data are not available beyond the third year. Patients were discontinued from this trial due to unremitting disease progression of 6 months or greater.
To reconstitute lyophilized Betaseron for injection, use a sterile syringe and needle to inject 1.2 mL of the diluent supplied, Sodium Chloride,
0.54% Solution, into the Betaseron vial. Gently swirl the vial of Betaseron to dissolve the drug completely; do not shake. Inspect the reconstituted
product visually and discard the product before use if it contains particulate matter or is discolored. After reconstitution with accompanying
diluent, Betaseron vials contain 0.25 mg Interferon beta-1b/mL of solution.
Withdraw 1 mL of reconstituted solution from the vial into a sterile syringe fitted with a 27-gauge needle and inject the solution subcutaneously.
Sites for self-injection include arms, abdomen, hips, and thighs. A vial is suitable for single use only; unused portions should be discarded. (See
BETASERON PATIENT INFORMATION sheet for SELF-INJECTION PROCEDURE.)
Stability: The reconstituted product contains no preservative.
Store at room temperature 25°C (77°F), excursions permitted to 15-30°C (59-86°F). After reconstitution, if not used immediately, the product
should be refrigerated and used within 3 hours. Avoid freezing.
HOW SUPPLIED
Betaseron is supplied as a lyophilized powder containing 0.3 mg of Interferon beta-1b, 15 mg Albumin Human USP, and 15 mg mannitol USP.
Drug is packaged in a clear glass, single-use vial (3 mL capacity); a separate vial containing 2 mL of diluent (Sodium Chloride, 0.54% solution) is
included for each vial of drug. Store at room temperature.
NDC 50419-523-01
0.3 mg/vial
NDC 50419-523-15
15 vials, 0.3 mg/vial
Caution: Federal law prohibits dispensing without prescription.
REFERENCES
1. Ruzicka FJ, et al. J Biol Chem, 1987; 262: 16142-16149. 2. Uze G, et al. Cell, 1990; 60: 225-234. 3. DeMaeyer E, et al. In: Interferons and
other regulatory cytokines, NY, Wiley 1988. 4. Colby CB, et al. J Immunol 1984; 133: 3091-3095. 5. Pestka S, et al. Annu Rev Biochem 1987; 56:
727-777. 6. Lengyel P. Annu Rev Biochem 1982; 51: 251-282. 7. Witt PL, et al. J Interferon Res 1990; 10: 393-402. 8. Schiller JH, et al. J Biol
Resp Mod 1990; 9: 377-386. 9. Rosenblum MG, et al. J Interferon Res 1990; 10:141-151. 10. Carlin JM, et al. J Immuno 1987; 130(7): 24142418. 11. Witt PL, et al. J Immunotherapy 1993; 13: 191-200. 12. Goldstein D, et al. J Natl Cancer Inst 1989; 81: 1061-1068. 13. Poser CM, et
al. Ann Neurol 1983; 13(3): 227-231. 14. Blaschke TF, et al. Clinical Research 1985; 33(1): 19A.
Manufactured by:
CHIRON Corporation
Emeryville, CA 94608
U.S. License No. 1106
Distributed by:
BERLEX Laboratories
Richmond, CA 94804
U.S. Patent No. 4,588,585; 4,959,314; 4,737,462; 4,450,103
© 2002 Berlex Laboratories All rights reserved.
Printed in U.S.A. on recycled paper C
Part Number 6052100 Revision date 1/02
Poster Display Schedule
The Program Committee congratulates authors whose abstracts were selected for
poster display at ACTRIMS-ECTRIMS 2002. Posters are on display from 8 am– 5 pm.
Presenting authors will stand by their posters from Noon – 2 pm.
Further information regarding poster room assignments will be available onsite.
Poster Session I
Thursday
September 19
Poster Session II
Friday
September 20
P1– P16
Surrogate Markers
P168 – P195
Rehabilitation and Quality of Life
Symptomatic Management
Harborside
Ballroom
Level 4
P17– P108
Clinical Aspects of MS (I)
Epidemiology
Imaging (I)
Immunology (I)
P196– P291
Clinical Aspects of MS (II)
Imaging (II)
Immunology (II)
Neuropsychology
Dover
Level 3
P109– P136
Experimental Allergic
Encephalomyelitis (I)
Neurobiology/Neurophysiology
New Clinical Trials (I)
P292– P313
Encephalomyelitis (II)
Healthcare Systems
New Clinical Trials (II)
Grand
Ballroom
Foyer
Level 3
P137– P167
Genetics (I)
Immunotherapy (I)
Pathology
P314– P345
Genetics (II)
Immunotherapy (II)
Essex
Level 4
40
Poster Session I: Thursday, September 19
Surrogate Markers
P1 CEREBROSPINAL FLUID PROTEIN STATUS AND
ITS CLINICAL USE Adam P, Sobek O,Taborsky L,Vesela B,
Prucha M
P15 RELATIVE SENSITIVITY OF TIME TO WALK
25 FEET FOR PROGRESSION OF DISABILITY Schwid SR,
Goodman AD, Scheid EA, McDermott MP
P31 RECURRENT SYNCOPE AS THE PRESENTING
P16 CYTOCHROME P46,A SUITABLE MARKER FOR
NEURODEGENERATION IN EAE-MODELS AND MS?
Teunissen CE, Dijkstra CD
P32 THE ITALIAN DEVIC’S STUDY GROUP (IDESG)—
P2 INTERLEUKIN-10 / INTERLEUKIN-12 COEFFICIENT AS POTENTIAL INDICATOR OF POSITIVE
RESPONSE TO INTERFERON ␤ TREATMENT BartosikPsujek H, Mitosek-Szewczyk K, Belniak E, Stelmasiak Z
Clinical Aspects of MS (Part 1)
P3 LEPTIN AS PREDICTIVE MARKER OF MULTIPLE
P17 SCREENING FOR DEPRESSION IN MULTIPLE
SCLEROSIS ACTIVITY DURING INTERFERON␤ 1A
THERAPY Batocchi A, Rotondi M, Caggiula M, Frisullo G,
Odoardi F, Nociti V, Carella C,Tonali P, Mirabella M
SCLEROSIS:YALE SINGLE QUESTION VS. BECK DEPRESSION INVENTORY SCALE Avasarala JR, Cross A,Trinkaus K
P4 ANTI-NEUROFILAMENT ANTIBODIES ARE ASSO-
P18 MULTIPLE SCLEROSIS AND HASHIMOTO’S THYROIDITIS:TWO CASES Balcý BP,Yayla V, Özer F
CIATED WITH DISEASE PROGRESSION IN MULTIPLE
SCLEROSIS Ehling R, Reindl M, Schanda K,Wanschitz J,
Deisenhammer F, Berger T
P5 RELATIONSHIP BETWEEN THE MS FUNCTIONAL
COMPOSITE AND MRI IN IMPACT Cohen JA, Goodman
AD, Heidenreich FR, Kooijmans MF, Sandrock AW, Simon JH,
Tsao EC
P6 A FOUR-MONTH LONGITUDINAL STUDY ON
THE RELATIONSHIP BETWEEN CLINICAL ACTIVITY
AND SERA CONCENTRATION OF S100 PROTEIN AND
NEURON SPECIFIC ENOLASE IN MULTIPLE SCLEROSIS.
Finamore L, Zivadinov R, Cecchinelli D, Pichi A, Pierallini A, Bastianello S, Nasuelli D, Bratina A, Locatelli L, Grop A, Reale M,
Zorzon M, Millefiorini E
P7 WHOLE BRAIN N-ACETYLASPARTATE ASSESSMENT IN RELAPSING-REMITTING MULTIPLE SCLEROSIS—EVIDENCE FOR DIFFERENT CLINICAL COHORTS
Gonen O, Moriarity DM, Li BS, Babb JS, Markowitz CM, Grossman RI
P8 INTERFERON BETA-1A IN COMBINATION WITH
AZATHIOPRINE AND LOW DOSE STEROIDS FOR
RELAPSING-REMITTING MULTIPLE SCLEROSIS: PILOT
MODEL FOR PREDICTIVE MULTIVARIATE TYPOLOGY
OF RELAPSES BASED ON CLINICAL AND MRI DATA
Havrdova E, Horakova D, Krasensky J, Dusek L,Vaneckova M,
Seidl Z,Ticha V, Novakova I,Tyblova M
P9 PLASMA LEVELS OF BRAIN-SPECIFIC OXYSTEROL
MAY REFLECT PROGRESSION OF MS Masterman T,
Leoni V, Diczfalusy U, Melzi d’Eril G, Hillert J, Björkhem I
P10 MATRIX METALLOPROTEINASE-9 IN MULTIPLE
SCLEROSIS CLINICAL FORMS Sastre-Garriga J, Comabella
M, Rovira À,Aymerich X, López C,Téllez N, Montalban X
P19 EFFECT OF INTERFERON-BETA-1B ON COGNITIVE FUNCTIONS IN MULTIPLE SCLEROSIS BarakY,
Achiron A
P20 COMPUTERIZED ISOMETRIC MUSCLE
STRENGTH—NATURAL HISTORY IN MULTIPLE SCLEROSIS Brooks BR, Sanjak M, Belden D, Dogan S, Konopacki R,
Roelke K, Peper S, Parnell J
P21 MS FUNCTIONAL COMPOSITE.A TRANSVERSAL
POPULATION BASED STUDY Casanova B, Coret F,
Bernat A, García E, Pascual A,Valero C, De Vera A
P22 EFFECT OF TRAINING ON THE MULTIPLE SCLEROSIS FUNCTIONAL COMPOSITE SCALE IN EARLY
RELAPSING AND REMITTING MS.A LONGITUDINAL
ONE YEAR FOLLOW-UP STUDY Casanova B, Coret F,
García E, Bernat A,Valero C, De Vera A, Pascual A
P23 PROBABLE CUTANEOUS SARCOIDOSIS ASSOCIATED WITH INTERFERON-BETA 1B TREATMENT IN
MULTIPLE SCLEROSIS. Clerc C, Chevalier Y, Bataillard M,
Rumbach L, Richard P
P24 BENIGN MULTIPLE SCLEROSIS IN SARDINIA:
A RETROSPECTIVE STUDY Cocco EE, Lai MM, Marchi PP,
Floris GG, Fadda LL, Sanna SS, Marrosu MM
P25 ACUTE PARTIAL TRANSVERSE MYELOPATHY:
A 7-YEAR PROSPECTIVE STUDY Cordonnier C, de Seze J,
Breteau G, Ferriby D, Michelin E, Stojkovic T, Pruvo J,Vermersch P
P26 MS GENDER ISSUES: CLINICAL PRACTICES OF
WOMEN NEUROLOGISTS Coyle PK, Christie S, Fodor P,
Fuchs K, Giesser B, Gutierrez A, Lynn J,Weinstock-Guttman B,
Pardo LG
SYMPTOM IN MULTIPLE SCLEROSIS Fazio MC, Musolino R,
Buccafusca M, Dattola V, Scalfari A, Girlanda P, Messina C
PART 1: CLINICAL CHARACTERISTICS OF DEVIC’S
NEUROMYELITIS OPTICA AT ONSET Ghezzi A, Bergamaschi R, Martinelli V, Filippi M,Tola R,Trojano M, Zaffaroni M,
Comi G
P33 THE ITALIAN DEVIC’S STUDY GROUP (IDESG)—
PART 2: COURSE AND PROGNOSIS OF DEVIC’S NEUROMYELITIS OPTICA Ghezzi A, Bergamaschi R, Filippi M,
Martinelli V,Tola R,Trojano M, Zaffaroni M, Comi G
P34 THERAPY RELATED ACUTE MYELOGENOUS
LEUKEMIA IN A PATIENT WITH MULTIPLE SCLEROSIS
TREATED WITH MITOXANTRONE Heesen C, Bruegmann M, Koch E, Gold SM, Moench A, Gbadamosi J
P35 RETROSPECTIVELY ANALIZING MONOSYMPTOMATIC DEMYELINATING DISEASES,ACCORDING TO
NEW RECOMMENDED DIAGNOSTIC CRITERIA FOR
MULTIPLE SCLEROSIS Guerrero A, Bueno V, Hernández M,
Martín-Serradilla J, Díez S, Calvo A
P36 A PROSPECTIVE STUDY OF MULTIPLE SCLEROSIS PRESENTING WITH LARGE FOCAL TUMOR-LIKE
LESIONS OF THE BRAIN. Jean P, Bertrand A, Laurent S,
Jean Philippe R, Sylviane C, Patrick C,Andre A
P37 A PROSPECTIVE STUDY OF MULTIPLE SCLEROSIS PRESENTING WITH ACUTE MYELOPATHY Jean P,
Bertrand A, Jean Philippe R, Laurent S,Alban D, Sylviane C,
Patrick C,Andre A
P38 CLINICAL PROFILE AND APPLICATION OF
DIAGNOSTIC CRITERIA IN PRIMARY PROGRESSIVE
MULTIPLE SCLEROSIS Khan O, Caon C, Ching W, Sonenvirth E,Tselis A, Zvartau-Hind M
P39 RELIABILITY OF EDSS AND FS-SCORE RATING
CAN BE IMPROVED BY STANDARDISED TRAINING
Lienert C, Lechner-Scott J, Müller U, Kappos L
P40 ISOLATED SPINAL DEMYELINATING EVENTS
WITH NORMAL BRAIN MRI: PROGRESSION TO MS,
CLINICAL AND MRI FOLLOW UP Milo R, Katz T, CoratSimon J
P41 ASSESSMENT OF SIGNS AND SYMPTOMS IN
MULTIPLE SCLEROSIS (MS) AND EVALUATION OF DISABILITY CONDITION IN PATIENTS REFERRED TO MS
RESEARCH CLINICS FROM 1997–2001 (2412 CASES)
Pakdaman H, Pakdaman R
P42 ONE CASE OF VERY LATE ONSET OF MULTIPLE
TIPLE SCLEROSIS Petzold A, Eikelenboom MJ, Keir G, Lazeron RC, Polman CH, Uitdehaag BJ,Thompson EJ, Giovannoni G
P27 IS DEVIC NEUROMYELITIS OPTICA A SEPARATE
DISEASE? A COMPARATIVE STUDY WITH MULTIPLE
SCLEROSIS de seze J, Lebrun C, Stojkovic T, Ferriby D,
Chatel M,Vermersch P
P12 INCREASED SERUM NITRIC OXIDE METABO-
P28 DIFFERENTIAL DIAGNOSIS BETWEEN MULTIPLE
Chopard G,Vidry E, Revenco E, Moulin T, Rumbach L
SCLEROSIS AND SJOGREN SYNDROME: INTEREST OF
ALPHA-FODRIN ANTIBODIES de seze J, Dubucquoi S,
Matthias T, Lefranc D, Dussart P,Vermersch P,Witte T
P44 FACTORS INFLUENCING PATIENTS’ CHOICE
P11 DYNAMICS OF AXONAL PATHOLOGY IN MUL-
LITES ARE RELATED TO DISEASE ACTIVITY IN PATIENTS
WITH MULTIPLE SCLEROSIS Rejdak K, Petzold A,
Chard D, Griffin C, Miszkiel KA, Davis G, Rashid W, Miller DH,
Stelmasiak Z,Thompson EJ, Giovannoni G
P13 IMMUNOLOGICAL MARKERS OF DISEASE
ACTIVITY IN NEWLY-DIAGNOSED MULTIPLE SCLEROSIS:A ONE YEAR FOLLOW-UP STUDY IN MRI MONITORED PATIENTS Rinaldi L, Motta M, Calabrese M,
Guglielmo A, Ranzato F,Tiberio M, Dalle Carbonare M, Leon A,
Gallo P
P14 COGNITIVE FATIGUE DURING A TEST REQUIRING SUSTAINED ATTENTION Schwid SR,Weinstein A,
Goodman AD, Scheid EA,Tyler CM, McDermott MP
P29 QUANTITATIVE COMPUTERIZED TREMOR
ASSESSMENT IN MULTIPLE SCLEROSIS:TREMOR PREVALENCE,TYPE, LONGITUDINAL EVOLUTION IN 321
PATIENTS Dogan S, Konopacki R, Brooks BR
P30 CLINICAL, CEREBROSPINAL FLUID AND NEUROIMAGING FINDINGS IN OPTICOSPINAL INVOLVEMENT IN THE SPECTRUM OF INFLAMMATORY
DEMYELINATING DISEASES Eraksoy M,Turan N, Kurtuncu M,Akman-Demir G,Yapici Z, Deniz E, Ozcan H
SCLEROSIS WITH ACUTE NEUROPSYCHOLOGICAL
IMPAIRMENT Radu TD, Marc D, Rene A, Luc T, Herve V
P43 APHASIA IN MULTIPLE SCLEROSIS Berger E,
OF IMMUNE MODULATING THERAPY Stoian CA,
Metz LM
P45 FACTORS ASSOCIATED WITH DIFFICULTY INITIATING AND MAINTAINING IMMUNE MODULATING
THERAPY Stoian CA, Metz LM
P46 NON-ADHERENCE TO THE BETA-INTERFERONS
FOR MULTIPLE SCLEROSIS IN CLINICAL PRACTICE
Tremlett H, Oger J, Special Therapies Group M
P47 VISUAL FUNCTION IN MULTIPLE SCLEROSIS
PATIENTS: 20 YEARS LATER Vorobeychik G, Anderson D,
Lindley J, Paty DW, UBC MS Clinic t
41
P48 COMPARISON OF DIAGNOSTIC CRITERIA FOR
MULTIPLE SCLEROSIS Balcý BP,Yayla V, Özer F
P66 ACUTE DISSEMINATED ENCEPHALOMYELITIS
(ADEM) IN ADULTS: COMPARISON WITH AN ADEM
PEDIATRIC POPULATION Papayannis CE, Ferreira J,
Caceres F, Fernandez Liguori N, Sandoval G,Tenembaum S,
Garcea O
P49 LOOKING FOR THE DEFINITION OF BENIGN
P67 MULTIPLE SCLEROSIS IN BOTUCATU, BRAZIL—
Epidemiology
MULTIPLE SCLEROSIS Coustans M, Le Page E, Le Duff F,
Leray E, Sartori E, Edan G
A POPULATION STUDY Rocha FC, Herrera LC,
Morales RR, and the Brazilian Committee for Z
P50 INCIDENCE AND PREVALENCE OF MULTIPLE
P68 CLINICAL CHARACTERISTICS OF NON-
SCLEROSIS IN AN HMO IN ARGENTINA Cristiano E,
Patrucco LB, Soriano ER,Videla GC, Figar S, Hares D, Bauso
Toselli PL
P51 DEVIC’S NEUROMYELITIS OPTICA (NMO) AND
MULTIPLE SCLEROSIS (MS): CLINICAL AND EPIDEMIOLOGIC FINDINGS IN AN MS CENTER IN ARGENTINA
Patrucco LB, Cristiano E,Videla GC, Bauso Toselli PL
P52 FIRST LACTRIMS’ (LATIN AMERICAN COMMITTEE FOR TREATMENT AND RESEARCH IN MS)
E-CENSUS: UNDERSTANDING THE PRESENT TO
DEVELOP THE FUTURE Cristiano E, Patrucco L, Rivera V,
Gold L, Correale J,Videla G
P53 OPTIC NEURITIS AS EARLY MANIFESTATION
OF MULTIPLE SCLEROSIS Eleonora K, Jarmila S
P54 MULTIPLE SCLEROSIS PREVALENCE AND HLA
CLASS II ALLELE DISTRIBUTION IN GYPSIES FROM
MALAGA, SOUTHERN SPAIN Fernández V, Mayorga C,
Leyva L, Guerrero R,Arnal C, Hens M, Luque G, Fernández O
P55 COURSE, DISABILITY AND IMMUNOMODULATORY TREATMENT OF PATIENTS WITH MULTIPLE SCLEROSIS BASED ON A POPULATION BASED REGISTRY
Frederiksen J
P56 INCIDENCE OF MULTIPLE SCLEROSIS IN A
NINE-YEAR PERIOD IN THE PROVINCE OF SEVILLE
(SOUTH-WEST SPAIN) Izquierdo G, Navarro G, Garcia
Moreno J, Durán E, Gamero M, Ruiz-Peña J, Dinca L, Páramo D
P57 THE PREVALENCE OF MULTIPLE SCLEROSIS IN
BELO HORIZONTE, BRAZIL Lana-Peixoto MA, Frota E,
Campos GB, Botelho CM,Aragão AL
RESPONDERS TO INTERFERON BETA (IFNB) THERAPY
IN RELAPSING-REMITTING MULTIPLE SCLEROSIS
(RRMS) Waubant EL,Vukusic S, Gignoux L, Durand-Dubief F,
Achiti I, Blanc S, Renoux C, Confavreux C
Imaging (Part 1)
P69 LONGITUDINALLY DIFFUSION TENSOR IMAGING TO MONITOR MULTIPLE SCLEROSIS COURSE
Cassol E, Ibarrola D, Ranjeva J, Manelfe C, Clanet M, Berry I
P70 MACROPHAGE CELLULAR IMAGING TO MONITOR ANTI-VLA4 ANTIBODY TREATMENT Dousset V,
Deloire-Grassin M,Touil T, Petry KG, Brochet B
P71 COMPARATIVE STUDY OF CELLULAR IMAGING
WITH SINEREM® AND USPIO 7228 IN EXPERIMENTAL
AUTOIMMMUNE ENCEPHALOMYELITIS DeloireGrassin M, Dousset V,Touil T, Petry KG, Brochet B
P72 CORRELATION BETWEEN DIFFUSION MAGNETIC RESONANCE IMAGING HISTOGRAM ANALYSIS
AND TOTAL LESION LOAD IN MULTIPLE SCLEROSIS
Callegaro D, Otaduy M, Lacerda M, Costa M, Bacheschi L,
Leite C
P73 DIFFUSE ABNORMALITY OF THE NORMAL
APPEARING WHITE MATTER IN MS MAY PREDATE
SYMPTOM ONSET: LONGITUDINAL HISTOGRAM
ANALYSIS OF T1 RELAXATION TIME Davies G, Hadjiprocopis A,Altmann D, Rashid W, Griffin C, Chard D, Kapoor R,
Thompson A, Miller D
P74 LONGITUDINAL STUDY OF PROGRESSIVE
GRAPHICAL DISTRIBUTION Lana-Peixoto MA, Araujo CR,
Macedo R, Haase VG
P59 THE NATURAL HISTORY OF MULTIPLE SCLEROSIS IN BRAZIL. I. CLINICAL DATA AND DISABILITY
Lana-Peixoto MA, Callegaro D, Moreira MA, Gama PD, Maciel D,
Sá PN
P75 SERIAL MAGNETIZATION TRANSFER IMAGING
IN OPTIC NEURITIS Hickman SJ,Toosy AT, Miszkiel KA,
Jones SJ,Altmann D, MacManus DG, Barker GJ, Plant GT,
Thompson AJ, Miller DH
P60 CLINICAL ASPECT, COURSE AND PROGNOSIS
P76 CORTICOSTEROIDS AND OPTIC NERVE ATRO-
OF MULTIPLE SCLEROSIS IN SOUTH OF FRANCE:
STUDY FROM 500 CONSECUTIVE MS PATIENTS USING
EDMUS Soriani M, Lebrun C, Bourg V, Chatel M
PHY FOLLOWING OPTIC NEURITIS Hickman SJ,
Kapoor R, Jones SJ,Altmann D, Plant GT, Miller DH
P61 SEASON OF BIRTH IN MULTIPLE SCLEROSIS
OPTIC NEURITIS USING TRIPLE DOSE GADOLINIUM
Hickman SJ,Toosy AT, Miszkiel KA, Jones SJ, MacManus DG,
Plant GT,Thompson AJ, Miller DH
Luetic GG
P62 BIRTH WEIGHT IN MULTIPLE SCLEROSIS
Luetic GG
P63 USE OF ALTERNATIVE PROVIDERS IN MULTIPLE
SCLEROSIS Marrie R, Cohen JA, Hadjimichael O, Vollmer T
P64 THE PREVALENCE OF MULTIPLE SCLEROSIS IN
IRELAND McGuigan C, McCarthy A, Hutchinson M
P65 UNCONVENTIONAL THERAPY USE AMONG
MULTIPLE SCLEROSIS PATIENTS Sastre-Garriga J,
Munteis E, Rio J, Pericot I,Tellez N,Tintore M, Montalban X
42
TOCOL FOR THE DIAGNOSIS AND FOLLOW-UP OF
MULTIPLE SCLEROSIS Li D,Traboulsee A, Paty D,Work
Group on Standardized MRI Protocol C
P82 SPONTANEOUS MAGNETOENCEPHALOGRAPHY RECORDINGS IN MS PATIENTS Ramo C,Amo C,
Fernandez S, Carmen M, Maestú F, Fernandez A, Ortiz T
P83 THE HYPOINTENSE LESION (“BLACK HOLE”)
ON T1-WEIGHTED MAGNETIC RESONANCE IMAGING
IN SECONDARY PROGRESSIVE MS: OBSERVATIONS
WITH T1-WEIGHTED SPIN-ECHO, MPRAGE AND MAGNETIZATION TRANSFER IMAGING Redmond IT,
Tench CR, Blumhardt LD
P84 STEREOTAXIC CO-REGISTRATION OF MRI
BRAIN ATROPHY IN MULTIPLE SCLEROSIS. PRELIMINARY DATA Durand Dubief F, Pachai C,Vukusic S,
Gignoux L, Renoux C, Cotton F, Froment J, Confavreux C
P58 STUDIES ON MULTIPLE SCLEROSIS: A GEO-
P81 GUIDELINES FOR A STANDARDIZED MRI PRO-
P77 SERIAL MAGNETIC RESONANCE IMAGING IN
P78 A LONGITUDINAL STUDY OF BRAIN ATROPHY
WITH TRANSCRANIAL ULTRASOUND IN RELAPSING
MULTIPLE SCLEROSIS Kallmann B, Rieckmann P,Toyka KV,
Mäurer M
P79 FUNCTIONAL MRI CHANGES DURING RECOVERY FROM OPTIC NEURITIS Langkilde AR, Rostrup E, Frederiksen J, Olsen D, Jensen J, Lauritzen M, Larsson HB
P80 DEVELOPMENT OF A BRAIN TUMOUR IN MS:
A CASE REPORT Laule C,Traboulsee A, Keogh C, MaGuire J,
Redekop G, MacKay A
AND HISTOPATHOLOGY IN POST-MORTEM MS BRAIN
SLICES Schmierer K, Scaravilli F, Barker GJ, MacManus DG,
Miller DH
P85 QUANTITATIVE ASSESSMENT OF LESION
PATHOLOGY IN POST-MORTEM MS BRAIN:A CORRELATIVE MRI/HISTOLOGY STUDY Schmierer K, Scaravilli F,
Griffin CM, Barker GJ, Miller DH
P86 T2 LESION BURDEN AND T1-HYPOINTENSE
(T1-BLACK HOLE) MRI RESULTS FROM THE IMPACT
TRIAL Simon JH, Cohen JA, Goodman A, Heidenreich F, Kooijmans M, Sandrock A,Tsao EC, IMPACT Investigators
P87 NEURONAL TRACT DEGENERATION PATTERNS
BASED ON DIFFUSION TENSOR VERSUS T2 MRI
CHANGES IN THE CORPUS CALLOSUM IN MS
Coombs B, Corboy J, Simon JH
P88 EFFECT OF GLATIRAMER ACETATE (GA) THERAPY ON REGIONAL CEREBRAL METABOLIC ABNORMALITIES IN MS PATIENTS (PILOT STUDY) Stoliarov I,
Ilves A, Prakhova L, Kataeva G,Totolian N
Immunology (Part 1)
P89 EARLY IMMUNOLOGIC CHANGES IN SEVERELY
PROGRESSIVE MULTIPLE SCLEROSIS PATIENTS RECEIVING MITOXANTRONE Altintas A, Demir G, Siva A
P90 EFFECT OF 24 MONTHS INTERFERON␤ TREATMENT ON CD4, CD8, CD4CD45RO AND CD4CD45RA
CELLS IN MULTIPLE SCLEROSIS Belniak E, BartosikPsujek H, Mitosek-Szewczyk K, Stelmasiak Z
P91 LONGITUDINAL ANALYSIS OF CSF EXPANDED
CD8+ CLONOTYPES IN THE PERIPHERAL BLOOD OF
MULTIPLE SCLEROSIS PATIENTS Cepok S, Zhou D,
Vogel F, Sommer N, Hemmer B
P92 THE PIVOTAL ROLE OF PEROXYNITRITE IN THE
ESTABLISHMENT OF CENTRAL NERVOUS SYSTEM
INFLAMMATION: INDUCTION OF BLOOD-BRAIN
BARRIER PERMEABILITY CHANGES Hooper DC,
Spitsin SV, Scott GS
P93 T-CELL REACTIVITY IN MULTIPLE SCLEROSIS:
PREDICTIVE VALUE FOR EFFICACY OF INTERFERONBETA Killestein J, Hintzen R, Uitdehaag B, van Lier R,
Polman C
P94 INTERFERON-␤ LEADS TO STABILIZATION OF
THE BARRIER FUNCTION IN BOVINE, MURINE AND
HUMAN BRAIN CAPILLARY ENDOTHELIAL CELLS IN
VITRO Kraus J, Ling AK, Hamm S, Kim KS,Voigt K, Oschmann P, Engelhardt B
Immunology (Part 1) (continued)
P95 FINE SPECIFICITY OF ANTIBODY RESPONSES
TO MYELIN SEQUENCES IN ASSOCIATION WITH HLA
CLASS II ALLELES IN THE SERUM OF BRAZILIAN
PATIENTS WITH MULTIPLE SCLEROSIS Carvalho A,
Liem AM, Santos CC, Sant’Anna G, Frugulhetti I, Leon SV,
Quirico-Santos T
Encephalomyelitis (Part 1)
PRESS EAE IN SJL MICE AND INHIBIT MMP-9 ACTIVITY
IN VITRO Marracci G, Jones R, McKeon G,Winter R, Riscoe M,
Bourdette D
P110 NEUROPROTECTIVE EFFECTS OF GLATIRAMER ACETATE IN A MICE MODEL OF CHRONIC
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
Offen DY, Gilgun-sherki Y, Hodengreber V, Panet H, Melamed E
P97 A ROLE FOR CD1C IN MULTIPLE SCLEROSIS
P111 ROLE OF ALPHA(1,3)FUCOSYTRANSPHERASES
P98 MOLECULAR TRACKING OF MYELIN BASIC
PROTEIN-SPECIFIC T CELL EXPANSION IN MULTIPLE
SCLEROSIS Muraro PA,Wandinger K, Bielekova B,
McFarland HF, Martin R
P99 NITRIC OXIDE AS AN ACTIVITY MARKER IN
MULTIPLE SCLEROSIS Demir Acar G,Ýdiman F,Ýdiman E,
K’rkal’ G, Çakmakç’ H, Özakbas S
P100 LONGITUDINAL CYTOKINE RESPONSES TO
MYELIN PEPTIDES IN MS: PERSISTENCE AND SPREADING OF IMMUNE RESPONSES Pelfrey CM, Moldovan IR,
Cotleur AC, Born SE, Karafa M, Lee J, Fisher E, Rudick RA
P101 FATIGUE AND INFLAMMATION IN PATIENTS
WITH OPTIC NEURITIS Roed H, Olsen D, Langkilde A,
Frederiksen J, Sellebjerg F
P102 DISEASE ACTIVITY IN MULTIPLE SCLEROSIS
CORRELATES WITH ALTERED EXPRESSION RATIOS
OF THE BCL-2 FAMILY PROTEINS IN PERIPHERAL
T LYMPHOCYTES Sharief MK, Noori MA
P103 THE EXPRESSION OF APOPTOSIS REGULATORY PROTEINS IN B LYMPHOCYTES FROM PATIENTS
WITH MULTIPLE SCLEROSIS Sharief MK, Seidi OA
IN LYMPHOCYTE RECRUITMENT IN BRAIN VENULES
AND EXPERIMENTAL AUTOIMMUNE
ENCEPHALOMYELITIS Piccio L, Scarpini E, Rossi B,
Ciabini D, D’Ambrosio D, Ottoboni L, Go A, Homeister JW,
Lowe JB, Constantin G
P112 TYPE IV PHOSPHODIESTERASE INHIBITION
REDUCES MATRIX METALLOPROTEINASE 9 EXPRESSION AND IMPAIRS NUCLEAR FACTOR-KAPPA B
TRANSLOCATION IN EXPERIMENTAL ALLERGIC
ENCEPHALOMYELITIS Puerta C, Sánchez A, Baranda P,
Ortiz P, Garcia-Merino A
P113 DISEASE SIGNS IN GENE KNOCKOUT MODELS OF MULTIPLE SCLEROSIS DIRECTLY CORRELATE
WITH BLOOD-BRAIN BARRIER PERMEABILITY
Scott GS, Brimer CM, Kean RB, Hooper D
P114 IL-12 DEPENDENT/IFN GAMMA INDEPENDENT EXPRESSION OF CCR5 BY MYELIN-REACTIVE
CD4+ T CELLS CORRELATES WITH ENCEPHALITOGENICITY Bagaeva L, Williams LP, Segal BM
P115 ENGAGEMENT OF TOLL LIKE RECEPTOR
(TLR) 9 OR CD40 REVERSES TOLERANCE AGAINST
MYELIN ANTIGENS AND PRECIPITATES AUTOIMMUNE
DEMYELINATION Segal BM, Ichikawa HT
P116 DIFFERENTIAL ANTIGEN-SPECIFIC PREVEN-
P104 INTERFERON-BETA THERAPY IN MULTIPLE
SCLEROSIS DOWNREGULATES SURVIVIN EXPRESSION
IN T LYMPHOCYTES Sharief MK, Zoukos Y
TION OF EXPERIMENTAL AUTOIMMUNE
ENCEPHALOMYELITIS WITH NAKED DNA Walczak A,
Szymanska B, Selmaj K
P105 CHEMOKINE RECEPTOR EXPRESSION ON
P117 PROFILES OF MATRIX METALLOPROTEINASES
CEREBROSPINAL FLUID T-CELLS IN PATIENTS WITH
RELAPSING REMITTING MULTIPLE SCLEROSIS
Sindern E, Patzold T, Ossege LM, Gisevius A, Malin JP
P106 DETECTION OF OLIGOCLONAL FREE KAPPA
CHAINS IN ABSENCE OF OLIGOCLONAL IGG IN THE
CSF OF CLINICALLY SUSPECTED MS PATIENTS
Sophie G, Christian S, Myriam S,Thierry D, H. H
(MMPS) IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS:A SIGNIFICANT ELEVATION OF MMP-12
Weaver A, Pennington CJ, Nuttall R, Hogan A, Edwards DR,
Yong VW
Neurobiology/Neurophysiology
P107 FUNCTIONAL CHARACTERIZATION OF THE
CD28-RELATED MOLECULE ICOS IN MULTIPLE SCLEROSIS:A POSSIBLE TARGET FOR SELECTIVE IMMUNE
INTERVENTION? Wiendl H, Neuhaus O, Mehling M,
Wintterle S, Schreiner B,Weissert R,Weller M, Hartung H,
Tolosa E, Melms A
P108 MODULATION OF NEURONAL ACTIVITY
AND MOG-INDUCED EAE BY THE ENDOGENOUS
PENTAPEPTIDE QYNAD,A PUTATIVE MEDIATOR OF
NEUROLOGICAL DYSFUNCTION IN HUMAN
DEMYELINATING DISEASES Wiendl H, Meuth S,
Duyar H, Elbs M, Landgraf P,Weller M,Weissert R, Budde T
PATIENTS. CLINICAL CORRELATIONS de Andres de
Frutos C, Lopez Esteban P, Peraita Adrados R
P123 ELECTRONYSTAGMOGRAPHY FINDINGS IN
P109 ␣-LIPOIC AND DIHYDROPLIPOIC ACID SUP-
P96 INTERFERON GAMMA SECRETION IN MULTIPLE
SCLEROSIS PATIENS TREATED WITH INTERFERON BETA
AND GLATIRAMER ACETATE Lochmanova A, Dolezil D,
Zapletalova O, Hradilek P
Lyons J,Yeager M, Luecking L,Wang Q, Porcelli S,Trotter J
P122 SLEEP DISORDERS IN MULTIPLE SCLEROSIS
P118 CEREBROSPINAL FLUID ISOELECTROFOCUSING IN A LARGE COHORT OF MULTIPLE SCLEROSIS
AND OTHERS NEUROLOGICAL DISEASES Amina B,
J. D, R. G, B. O, B. H,T. S, D. F, P.V
P119 PERIPHERAL SENSORY AND MOTOR ABNORMALITIES IN PATIENTS WITH MULTIPLE SCLEROSIS
Anlar O,Tombul T, Kisli M
P120 ABSTRACT NOT AVAILABLE FOR PUBLICATION
P121 OLIGODENDROGLIAL EXPRESSION OF EDG-2
RECEPTOR: DEVELOPMENTAL ANALYSIS AND PHARMACOLOGICAL RESPONSES TO LYSOPHOSPHATIDIC
ACID Bruno S, Sonia B, Julien A, Celine J, Gilles B, MarieStephane A, Pierre S, Bernard Z, Catherine L
PATIENTS WITH MULTIPLE SCLEROSIS Ḱyĺynç M, Can U,
Benli S, Özlüolu L, Akkuzu B
P124 BRAINSTEM AUDITORY EVOKED RESPONSE
WITH HIGH CLICK STIMULUS REPETITION RATE IN
MULTIPLE SCLEROSIS Lana-Peixoto MA, Santos MA,
Munhoz MS
P125 NEUROPHYSIOLOGICAL EVALUATION OF
EXECUTIVE FUNCTIONS IN MULTIPLE SCLEROSIS:
A FOLLOW-UP STUDY Leocani L, Martinelli V,Annovazzi P,
Tickonova I, Possa F, Comi G
P126 PRESENCE OF HERPES SIMPLEX VIRUS 1 IN
SAMPLES FROM PATIENTS WITH OPTIC NEURITIS AND
MULTIPLE SCLEROSIS Christodoulou C, Constantinou A,
Koptides D, Paschalidou M, Georgiadis N, Chatzisotiriou A,
Milonas I
P127 HHV-6A ACTIVE INFECTION IN MULTIPLE
SCLEROSIS PATIENTS Roberto Á,Virginia D, Eduardo V,
Juan José P, Rafael A
P128 HOW DOES BETA INTERFERON TREATMENT
AFFECT TO HHV-6 VIRAL LOAD IN MULTIPLE SCLEROSIS PATIENTS? Virginia D, Roberto Á, Eduardo V, Juan José P,
Rafael A
P129 DIFFERENT NON-RADIOACTIVE PERMEABILITY ASSAYS IN AN IN VITRO MODEL OF THE BLOODBRAIN-BARRIER Voigt KE, Kraus JR, Oschmann P, Engelhardt B
New Clinical Trials (Part 1)
P130 THE USE OF PHARMACOKINETIC (PK)
MODELING AND EFFICACY DATA TO ESTABLISH
OPTIMAL DOSING OF NATALIZUMAB (ANTEGRENTM)
Bennett D, Ludden T, Shah J, Floren L, Beckman E
P131 SAFETY AND TOLERABILITY DOSE COMPARISON OF INTERFERON BETA-1A IN RELAPSING-REMITTING MULTIPLE SCLEROSIS:THE EVIDENCE STUDY
Bever CT, for the EVIDENCE Study Group
P132 THE REGISTRY TO EVALUATE NOVANTRONE®
(MITOXANTRONE FOR CONCENTRATE INJECTION)
EFFECTS IN WORSENING MS (RENEW): STATUS
REPORT SEPTEMBER 2002 Goodkin DE, Flanders
K, Leung J, Butine M, Stead R
P133 THE EFFECT OF INTERFERON B-1B ON
QUANTITIES DERIVED FROM MT MRI IN SECONDARY
PROGRESSIVE MS Inglese M, vanWaesberghe J, Rovaris M,
Beckmann K, Barkhof F, Hahn D, Kappos L, Miller D, Polman C,
Pozzilli C,Thompson A,Yousry T,Wagner K, Comi G, Filippi M
P134 SINGLE CENTRE, DBPC, RANDOMISED TRIAL
OF INTERFERON BETA 1B IN PRIMARY PROGRESSIVE
AND TRANSITIONAL PROGRESSIVE MULTIPLE SCLEROSIS:AN EXPLORATORY PHASE II STUDY Montalban X,
Brieva L,Tintore M, Borras C, Rio J, Nos C,Aymerich X, Alonso J,
Horno R,Vicente M, Rovira A
P135 IFN BETA CHRONIC TREATMENT: HOW TO
MANAGE THE DOSE AND THE FREQUENCY OF
ADMINISTRATION IN PATIENTS WITH ABSENCE OF
DISEASE ACTIVITY Pipieri A, Barbero P, Bergui M,Verdun E,
Clerico M, Durelli L
43
New Clinical Trials (Part 1)
(continued)
P136 3 TESLA MAGNETIC RESONANCE IMAGING
COMPARISON OF INTERFERON BETA-1B AND GLATIRAMER ACETATE—A RANDOMIZED, SINGLE-BLIND
STUDY IN RELAPSING-REMITTING MULTIPLE SCLEROSIS Wolansky LJ, Cadavid D, Cook SD, Skurnick J, Biswal B,
Pachner A, Hill J
Genetics (Part 1)
P137 A SCANDINAVIAN GENOME-WIDE LINKAGE
DISEQUILIBRIUM SCREEN IN MULTIPLE SCLEROSIS
PATIENTS INDICATES ASSOCIATION AT 1Q (D1S1601)
AND 11Q (D11S1986) Datta P, Harboe H, Spurkland A,
Ryder L, Sawcer S, Åkesson E, Celilus E, Modin H, SandbergWollheim M, Myhr K,Andersen O, Hillert J, Solberg Sorensen P,
Svejgaard A, Compston A,Vartdal F, Oturai A
P138 -384 INTERLEUKIN-2 POLYMORPHISMS IN
MULTIPLE SCLEROSIS Fernández V, Leyva L, Mayorga C,
Matesanz F, Fedetz M,Alcina A, Guerrero M, León A, Luque G,
Fernández O
P139 CTLA-4 GENE POLYMORPHISMS AND THEIR
INFLUENCE ON SUSCEPTIBILITY TO MULTIPLE SCLEROSIS IN N. IRELAND Heggarty SV, Silversides J, Vandenbroeck K, McDonnell G, Hawkins S, Graham C
P140 ASSOCIATION STUDY OFFAS ANDFASL POLYMORPHISMS WITH MULTIPLE SCLEROSIS Kantarci OH,
Hebrink DD, Achenbach SJ, Elizabeth AJ, McMurray CT, Weinshenker BG
P141 ANALYSIS OF A NOVEL INTRAGENIC SINGLENUCLEOTIDE POLYMORPHISM OF THE FAS GENE IN
RELAPSING MULTIPLE SCLEROSIS Lucas M, Zayas MD,
Costa AF, Solano F, Durán E, Izquierdo G
P142 GENOMIC SCREENING IN SPANISH PATIENTS
WITH MULTIPLE SCLEROSIS Goertsches R,Villoslada P,
Comabella M, Montalban X, Gomez-de-la-Concha E,Arroyo R,
Lopez de Munain A, Otaegui D, Palacios R, Spanish M
P143 RANTES AND CHEMOKINE RECEPTOR 5
POLYMORPHISMS: SUSCEPTIBILITY TO AND OUTCOME
IN MULTIPLE SCLEROSIS Partridge JM, Fryer A, Ollier W,
Boggild M, Strange R, Hawkins C
P144 POLYMORPHISM IN THE GLUTATHIONE
S-TRANSFERASES, GSTA1 AND GSTA2, IN MULTIPLE
SCLEROSIS Partridge JM, Fryer A, Boggild M, Strange R,
Hawkins C
P145 MMP-9 MICROSATELLITE POLYMORPHISM
INCREASES THE RISK OF MULTIPLE SCLEROSIS Fiotti N,
Zivadinov R, Altamura N, Nasuelli D, Bratina A,Tommasi MA,
Bosco A, Locatelli L, Grop A, Cazzato G, Giansante C, Zorzon M
P156 IMMUNOMODULATORY THERAPIES IN FAMIL-
P146 HLA TYPING IN MULTIPLE SCLEROSIS. RELA-
PLE SCLEROSIS PATIENTS Le Page E,Amanda Louise C,
Coles A, Denys V, Miller D, Hale G,Waldmann H, Compston A
TION TO MAGNETIC RESONANCE IMAGING FINDINGS Zivadinov R, Uxa L, Zacchi T, Nasuelli D, Ukmar M,
Furlan C, Pozzi-Mucelli RS,Tommasi MA, Locatelli L, Ulivi S,
Bratina A, Bosco A, Grop A, Cazzato G, Zorzon M
P147 APOE GENOTYPE IS NOT ASSOCIATED WITH
CLINICAL DISEASE CHARACTERISTICS AND MRI FINDINGS IN MULTIPLE SCLEROSIS Zwemmer J, van Veen T,
van Winsen L, van Kamp G, Barkhof F, Polman C, Uitdehaag B
P157 CAMPATH-1H IN THE TREATMENT OF MULTI-
P158 INTERFERON BETA INHIBITS MONOCYTEDERIVED DENDRITIC CELL MATURATION McClurg AE,
Fleming EM, Hawkins SA, Duddy ME, McQuaid S, Johnston JA,
Armstrong MA
P159 INTERFERON BETA-1A VERSUS INTERFERON
BETA-1B IN RELAPSING MS: 4-YEAR CLINICAL EFFICACY RESULTS Patti F, Fiorilla T, Florio C,Vivo P, Reggio A
P160 SAFETY AND TOLERABILITY OF CYCLOPHOS-
Immunotherapy (Part 1)
P148 MITOXANTRONE THERAPY IN PROGRESSIVE
MULTIPLE SCLEROSIS A∂⬘a∂⬘lu J, Emir C, Gur M, Morali S,
Tanik O
P149 IMMUNE REGULATORY EFFECTS OF GLATIRAMER ACETATE (GA) ON HUMAN MONOCYTES:
BYSTANDER SUPPRESSION REVISITED? Kim H,
Duddy M, Bar-Or A
P150 BIOAVAILABILITY OF THREE INTERFERON␤
PREPARATIONS: A 96 HOURS TIME-COURSE STUDY
Bertolotto A, Capobianco M, Di Sapio A, Gilli F, Sala A,
Malucchi S, Milano E, Melis F, Bottero R
P151 USE OF INTERFERON BETA 1B IN SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS IN
ARGENTINA Carra AJ, Sinay V, Onaha P,Alvarez F, Ballario C,
Caceres F, Cristiano E, Deri N, F. Liguori N, Luetic G, Garcea O,
Palacio S, Patrucco L, Reich E, R. Escalante R, Sotelo H,Tarulla A,
Vetere S
P152 RELAPSING REMITTING MULTIPLE SCLEROSIS
THERAPY EXPERIENCE IN ARGENTINA Carra AJ,
Onaha P, Sinay V,Alvarez F, Luetic G, Bettinelli R, Sanpedro E,
Rodriguez L
PHAMIDE PULSES IN MULTIPLE SCLEROSIS Portaccio E,
Zipoli V, Siracusa G, Piacentini S, Sorbi S, Ponziani G,Amato M
P161 EXPERIENCES WITH MITOXANTRONE TREATMENT—SIDE EFFECTS IN SECONDARY CHRONIC
PROGRESSIVE MULTIPLE SCLEROSIS PATIENTS Rajda C,
Bencsik K,Török M,Vécsei L
P162 INTERFERON BETA DOSE REDUCTION IN
MULTIPLE SCLEROSIS PATIENTS: IMMUNOLOGICAL
PROFILE Ricci A,Verdun E, Oggero A, Barbero P, Cucci A,
Clerico M, Pipieri A, Bosio A, Durelli L
P163 A PHASE IIB STUDY OF ORAL INTERFERON
BETA-1A AT TWO DOSES IN RELAPSING REMITTING
MULTIPLE SCLEROSIS USING MRI, CLINICAL AND
IMMUNOLOGIC MEASURES Vollmer TL, Preiningerova J,
Markovic-Plese S, Rizzo M, Cutter G
P164 PROLIFERATIVE RESPONSE TO GLATIRAMER
ACETATE MAY PREDICT CLINICAL RESPONSE TO
THERAPY Weder CR, Baltariu G, Gober H, Lienert C,
De Libero G, Kappos L, Duda PW
Pathology
P153 BBR2778,A NEW NON-CARDIOTOXIC DRUG
STRUCTURALLY RELATED TO MITOXANTRONE,
REDUCES THE SEVERITY OF RAT ACUTE AND
CHRONIC EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS Cavaletti G, Frigo M, Rota S, Stanzani L,Tredici G,
Dassi M, Perseghin P, Lolli F, Mazzanti B, Biagioli T, Ballerini C,
Cavalletti E, Pezzoni G, Sala F, Crippa L, Di Luccio E, Sala V,
Oggioni N, Riccio P
P165 SERUM PARAOXONASE ACTIVITY IN
P154 MITOXANTRONE-INDUCED IMMUNOLOGICAL CHANGES IN PERIPHERAL BLOOD LEUKOCYTES
OF MS-PATIENTS Chan A,Weilbach FX,Toyka KV, Gold R
P167 ALPHA-SYNUCLEIN IMMUNOREACTIVE
P155 EPITOPE SPECIFICITY OF NEUTRALIZING
ANTIBODIES AGAINST INTERFERON-BETA Gneiss C,
Reindl M, Berger T, Deisenhammer F
44
IAL MULTIPLE SCLEROSIS Eraksoy M,Turan N, Kurtuncu M,
Kýyat A,Yapici Z,Akman-Demir G
UNTREATED AND IFN-BETA TREATED MS PATIENTS
Danni M,Viti B, Bacchetti T, Ferretti G, Splendiani G, Fiè A,
Angeleri V, Ceravolo M, Provinciali L
P166 METALLOTHIONEIN EXPRESSION IN THE
CENTRAL NERVOUS SYSTEM OF MULTIPLE SCLEROSIS
PATIENTS Espejo C, Martinez-Caceres EM, Penkowa M,
Ortega A, Hidalgo J, Montalban X
DEPOSITS IN MULTIPLE SCLEROSIS LESIONS Paramo D,
Izquierdo G, Seilhean D
Poster Session II: Friday, September 20
Rehabilitation and
Quality of Life
P168 PRESSURE PAIN IN MULTIPLE SCLEROSIS
PATIENTS Armutlu K, Kerem M, Bumin G,Akbayrak T,
Yigiter K, Keser I, Karabudak R
P169 ASSESSMENT OF RELATION BETWEEN HANDICAP STATUS AND QUALITY OF LIFE IN AMBULATORY
MULTIPLE SCLEROSIS PATIENTS IN TURKEY Armutlu K,
Guclu A, Cetisli N, Bosnak M, Karabudak R
P170 QUALITY OF LIFE, DISABILITY AND DEPRESSION IN EARLY MS Deloire-Grassin M, Ouallet J, Salort E,
Barroso B, Brochet B
P171 AEROBIC TRAINING IN MULTIPLE SCLEROSIS—INFLUENCE ON METABOLIC, ENDOCRINE AND
QUALITY OF LIFE PARAMETERS Heesen C, Gold SM,
Mladek M, Bartsch K, Hartmann S, Ludwig A,Witte J, Reer R,
Braumann K, Schulz K
P172 ONE-YEAR CHANGES ON THE MS FUNCTIONAL COMPOSITE AND PATIENT-PERCEIVED DISABILITY Hoogervorst E, Kalkers N, Uitdehaag B, Polman C
P173 HIGH LEVELS OF ANXIETY AND DISTRESS
IN MS PATIENTS AND THEIR PARTNERS IN THE FIRST
YEARS AFTER DIAGNOSIS Janssens C, van Doorn P,
de Boer J, van der Meche F, Passchier J, Hintzen R
P174 THE MULTIPLE SCLEROSIS QUALITY OF LIFE
INVENTORY AND DISABILITY AS MEASURED BY THE
EDSS: EXPERIENCE IN A BRAZILIAN MULTIPLE SCLEROSIS SAMPLE Lana-Peixoto MA,Araujo CR, Haase VG,
Lacerda SS, Lima EP
P175 PREVIOUS HISTORY OF OPTIC NEURITIS AS A
FACTOR FOR DECREASED VISION-SPECIFIC QUALITY
OF LIFE IN MULTIPLE SCLEROSIS Lana-Peixoto MA, Martins R, Haase VG, Lacerda SS
P176 ASSESSING THE VALIDITY OF THE MULTIPLE
SCLEROSIS IMPACT SCALE IN A COMMUNITY BASED
POPULATION McGuigan C, McCarthy A, Hutchinson M
P177 THE RELATION OF HEALTH RELATED QUALITY OF LIFE AND SUBJECT DISCONTINUATION IN A
PHASE 3 CLINICAL TRIAL Miller DM, Cohen JA,Tsao EC,
Kooijmans MF
P183 FRONTAL SYNDROME AND QUALITY OF LIFE
IN MS PATIENTS Pierre C, Didier D, Delphine L, Céline T,
Florence B, Laurent G
P184 PREDICTION OF QUALITY OF LIFE IN
SEVERELY DISABLED MS-PATIENTS Ritter SB, Ladurner G,
Wranek U
P185 QUALITY OF LIFE AND COST OF ILLNESS IN
MITOXANTRONE TREATED MULTIPLE SCLEROSIS
PATIENTS Vollmer TL, Hadjimichael O, Buenconsejo J
P186 EVOLUTION OVER A 3 MONTH PERIOD OF
GLOBAL, PSYCHOLOGICAL,AND SOCIO-PROFESSIONAL FUNCTIONING IN PATIENTS WITH RELAPSING REMITTING MULTIPLE SCLEROSIS, DURING
AVONEX® TREATMENT INITIATION Warter J, Gentin M
P187 SITUATION OF MEDICAL CARE OF PATIENTS
WITH MULTIPLE SCLEROSIS IN NORTH-EASTERN
GERMANY Zettl UU, Krüger T
Symptomatic Management
P188 GLATIRAMER ACETATE [GA] TREATMENTS
HAVE SIGNIFICANT EFFECTS ON CONTROLLING
FATIGUE-INDUCED TREMOR AMPLITUDE IN MULTIPLE
SCLEROSIS PATIENTS Dogan S, Konopacki R, Brooks BR
P189 OSTEOPOROSIS IN MULTIPLE SCLEROSIS
PATIENTS TREATED WITH CORTICOSTEROIDS
Havrdova E,Tyblova M, Stepan J, Zikan V, Horakova D,Ticha V,
Novakova I
DATION OF MULTIPLE SCLEROSIS QUALITY OF LIFE
QUESTIONNAIRE (MSQOL-54) IN TURKISH MULTIPLE
SCLEROSIS POPULATION Idiman E, Uzunel F, Özakbas S,
Yozbatiran N, Oguz M, Callioglu B, Gökce N, Bahar Z
P182 QUALITY OF LIFE FOR MS PATIENTS: REFERENCE STANDARDS FROM A LARGE PANEL OF
PATIENTS Pierre C, DIDIER V, Laurent G, Maryline L,
Dominique A,Aurélien M
P200 CORRELATION BETWEEN VISUAL EVOKED
POTENTIALS ABNORMALITIES AND PHYSICAL HANDICAP PROGRESSION IN MULTIPLE SCLEROSIS: PROSPECTIVE FOLLOW-UP OF 65 PATIENTS Ferriby D,Ardnt C,
de seze j, Stojkovic t, Hache J,Vermersch P
P201 IMPAIRED SYMPATHETIC ACTIVITY IN
PATIENTS WITH MULTIPLE SCLEROSIS AND FATIGUE
Flachenecker PM, Rufer A, Bihler I, v. Hippel C, Reiners K,
Toyka KV, Kesselring J
P202 MEASURING THE OUTCOME OF INTERFERON
THERAPY FROM THE PATIENTS’ PERSPECTIVE Ford HL,
Johnson MH, Denton S
P203 COAGULATION ABNORMALITIES IN MULTIPLE SCLEROSIS AND POSSIBLE MULTIPLE SCLEROSIS
Galgani S, Corsi F, Corpetti M, Pingi A, Manni M, Gasperini C
P204 THE RANGE OF INFLAMMATORY MYELOPATHIES. CLINICAL, MRI,CEREBROSPINAL FLUID AND
IMMUNOLOGICAL FINDINGS IN 35 CONSECUTIVE
CASES Perini P, Calabrese M,Tiberio M,Tzintzeva E,
Ranzato F, Gallo P
P205 FATIGUE AND AXONAL LOSS IN CORPUS
CALLOSUM IN MULTIPLE SCLEROSIS Greg C, Minier D,
Walker P, Brunotte F, Giroud M, Moreau T
P207 ACUTE DISSEMINATED ENCEPHALO-
P192 VARIABILITY IN THE QUALITIES OF CHRONIC
NEUROPATHIC PAIN IN MULTIPLE SCLEROSIS ASSESSED
BY THE NEUROPATHIC PAIN SCALE (NPS) Rog DJ,
Young CA
P193 BURDEN OF NEUROPATHIC PAIN IN MS
P194 FATIGUE ASSESSMENT BY MECHANICAL AND
P181 CROSS-CULTURAL ADAPTATION AND VALI-
THERAPY CHOICE Eyring S,Wood C, Sherman S, Simone M
P191 SPASTICITY IN MS PATIENTS IN THE NARCOMS REGISTRY: PREVALENCE, SEVERITY AND TREATMENT PATTERNS USING ORAL AGENTS AND/OR
INTRATHECAL BACLOFEN Rizzo M, Hadjimichael O,
Buenconsejo J, Preiningerova J,Vollmer T
FUNCTION IN MULTIPLE SCLEROSIS Nisipeanu P,
Hocherman S, Hardan Y, Inzelberg R
SYSTEMS” OF EXPANDED DISABILITY STATUS SCALE
AND HEALTH RELATED QUALITY OF LIFE:ANALYSIS
OF 184 MULTIPLE SCLEROSIS PATIENTS Idiman E, Özakbas S,Yozbatiran N, Uzunel F, Oguz M, Kürsad F
P199 EFFICACY OF MS THERAPY IS KEY DRIVER IN
P206 CLOMIPHENE CITRATE CAN INCREASE
Rog DJ,Young CA
P180 CORRELATION BETWEEN “FUNCTIONAL
CAL RESPONSE TO BETA-INTERFERON IN RELAPSINGREMITTING MULTIPLE SCLEROSIS Etienne R, Iliu-Florin T,
Dominique P, Jean-Christophe O, Claire G, Olivier H
P190 BOTULINUM TOXIN IN THE TREATMENT OF
DETRUSOR HYPERREFLEXIA IN MULTIPLE SCLEROSIS:
CASE REPORT Hradilek P, Krhut J, Zapletalova O, Mainer K
P178 AN OBJECTIVE FOLLOW-UP OF UPPER LIMB
P179 THE RELATION BETWEEN DECONDITION,
RESPIRATORY MUSCLE WEAKNESS AND FATIGUE IN
MULTIPLE SCLEROSIS Øasová K, Havrdová E, Brandejský P,
Rùûièka J
P198 PREDICTIVE VALUE OF THE ONE-YEAR CLINI-
MYOELECTRICAL OUTPUT DURING SUSTAINED MAXIMAL ISOMETRIC VOLUNTARY CONTRACTION IN
MULTIPLE SCLEROSIS Sanjak M, Belden D, Konapacki R,
Waclawik AJ, Brooks BR
P195 GLATIRAMER ACETATE TREATMENT EFFECT
ON MUSCLE STRENGTH IN MULTIPLE SCLEROSIS
PATIENTS.A PROSPECTIVE LONGITUDINAL MS CLINICBASED STUDY Sanjak M, Belden D, Konapacki R, Brooks BR
Clinical Aspects of MS (Part II)
P196 PREDICTIVE FACTORS TO SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS POINT OUT THE
POTENTIAL IMPORTANCE OF THE INFLAMMATORY
PROCESS Coustans M, Le Duff F,Taurin G, Le Page E, Leray E,
Edan G
P197 MULTIPLE SCLEROSIS ASSOCIATED WITH SYSTEMIC MASTOCYTOSIS:A SINGLE CASE REPORT
Cristina Z, Carlo F
RELAPSE RATE IN MULTIPLE SCLEROSIS Moreau T,
Gere J, Greg C,Vernay D, Clavelou P, Giroud M
MYELOPATHY AND PERIPHERAL NEUROPATHY
ASSOCIATED WITH CHRONIC HCV INFECTION
Giannesini C, Schelp C, Heinzlef O, Roullet E
P208 SAPHO SYNDROME ASSOCIATED WITH MULTIPLE SCLEROSIS Giannesini C, Mahfoud A, Heinzlef O,
Aouba A, Roullet E
P209 MITOXANDRONE FOR PROGRESSIVE TYPE OF
MULTIPLE SCLEROSIS TREATMENT Giannoulis C, Sarafianos A, Hatzidaki G, Kargadou A, Stavropoulos D, Karageorgiou KE
P210 ACTIVE HUMAN HERPESVIRUS SIX (HHV-6)
INFECTIONS AND MS Knox K, Carrigan D
P211 CLINICAL, DEMOGRAPHIC,AND COGNITIVE
FEATURES OF CHILDHOOD ONSET MULTIPLE SCLEROSIS Krupp LB, Belman AL, Cianciulli C, Milazzo M, Blitz K,
Morgan T, Melville P
P212 CORRELATION OF THE GUYS NEUROLOGICAL DISABILITY SCALE WITH THE EDSS IN A SAMPLE
OF BRAZILIAN MULTIPLE SCLEROSIS PATIENTS LanaPeixoto MA,Araújo CR, Haase VG, Lacerda S, Lima EP
P213 ACUTE DEAFNESS REVEALING MULTIPLE
SCLEROSIS Lebrun C, de Seze J, Bourg V, Soriani M,
Vermersh P, Chatel M
P214 MULTIPLE SCLEROSIS WITH HYPERSIGNALFREE T2-WEIGHTED MRI Lebrun C, Bourg V, Chanalet S,
Soriani M, Chatel M
P215 PROGNOSIS IN RELAPSING-REMITTING MULTIPLE SCLEROSIS.A HIERARCHICAL MODEL MartínezYélamos S, Casado V, Carmona O, Martínez-Yélamos A,
Ramón JM, Arbizu T
45
Clinical Aspects of MS (Part II)
(continued)
P216 CLINICAL ISOLATED MYELITIS: EARLY PREDICTION OF MULTIPLE SCLEROSIS BASED ON MAGNETIC
RESONANCE IMAGING AND CEREBROSPINAL FLUID
FINDINGS Meluzinova E, Bojar M, Houzvickova E, Glosova L,
Belsan T
P217 COLLABORATIVE STUDY ON CHILDHOOD
ONSET MULTIPLE SCLEROSIS IN FRANCE (KIDMUS):
ABOUT A COHORT OF 495 PATIENTS Mikaeloff Y, Tardieu M, Catherine L, Edan G, Vallee L, Ponsot G, Confavreux C
P218 PATTERNS OF MS TREATMENT WITH DISEASE
MODIFYING THERAPIES BEFORE ENTRY INTO AN
OPEN-LABEL CLINICAL TRIAL OF REBIF® INJECTIONS
Mikol D, Burns T, Bennett S, Lopez-Bresnahan M
P219 FATIGUE IN MULTIPLE SCLEROSIS.A LONGITUDINAL STUDY Tellez N, Rio J,Tintore M, Sastre-Garriga J,
Pericot I, Nos C, Montalban X
P220 RELAPSING MYELITIS:A DEMYELINATING
SYNDROME DISTINCT FROM MULTIPLE SCLEROSIS
Nicholas R, Fletcher N, Boggild M
P221 HAEMATOLOGICAL ABNORMALITIES RELATED
TO INTERFERON BETA-1A THERAPY O’Connor P,
O’Brien F,Alsop J, Chang P, Grumser Y, and Abdalla J
P231 THE RELATION BETWEEN BRAIN MRI
LESIONS AND DEPRESSIVE SYMPTOMS IN MULTIPLE
SCLEROSIS BeneöováY, Niedermayerová I, Mechl M
P246 COMPARISON OF CEREBRAL PERFUSION IN
P232 DISABILITY AND AXONAL LOSS IN EARLY
RELAPSING AND REMITTING MULTIPLE SCLEROSIS.
ASSESSMENT WITH MSFC AND H1-MRS Casanova B,
Martinez C,Valero C, Celda B, Matí-Bonmatí L, Pascual A, Coret F
P247 FUNCTIONAL CORTICAL CHANGES IN
P233 EARLY CORTICAL ATROPHY IN RELAPSING
REMITTING AND PRIMARY PROGRESSIVE MULTIPLE
SCLEROSIS AND ITS RELEVANCE TO OTHER MR AND
CLINICAL MEASURES De Stefano N, Matthews PM,
Filippi M, Iannucci G, De Luca M, Bartolozzi ML, Guidi L,
Ghezzi A, Montanari E, Federico A, Smith S
P234 1H-MAGNETIC RESONANCE SPECTROSCOPY
IN CORTICAL GREY MATTER, HIPPOCAMPUS AND
THALAMUS OF HEALTHY SUBJECTS AT 1.5 T—A REPRODUCIBILITY STUDY Geurts JJ, Barkhof F, Castelijns JA, Polman CH, Pouwels PJ
MULTIPLE SCLEROSIS USING A NOVEL TECHNIQUE
Rashid W, Parkes L, Ingle G, Chard D, Symms M, Miller D
PATIENTS WITH MULTIPLE SCLEROSIS AND NONSPECIFIC CONVENTIONAL MAGNETIC RESONANCE
IMAGING SCANS OF THE BRAIN Rocca MA, Pagani E,
Ghezzi A, Falini A, Zaffaroni M, Colombo B, Scotti G, Comi G,
Filippi M
P248 THE ROLE OF SPINAL CORD DAMAGE ON
BRAIN CORTICAL PLASTICITY:A FUNCTIONAL MAGNETIC RESONANCE IMAGING STUDY Filippi M,
Rocca MA, Mezzapesa DM, Ghezzi A, Falini A, Martinelli V,
Poggi A, Scotti G, Comi G
P249 SHORT-TERM CORRELATIONS BETWEEN
CLINICAL AND MRI FINDINGS IN RELAPSING-REMITTING MULTIPLE SCLEROSIS Filippi M, Rovaris M,
Rocca MA, Ladkani D, Shifroni G,Wolinsky JS, Comi G
P235 INCREASED GLUTAMATE/GLUTAMINE LEVELS
MEASURED BY 1H-MRS IN MULTIPLE SCLEROSIS BRAIN
Greenstein JI, Luo J, Kanamalla US, Smith SA, Niman D, Boyko OB
P250 PROTON MAGNETIC RESONANCE SPEC-
P236 GLOBAL MAGNETIC RESONANCE SPECTROSCOPY METABOLIC VARIATIONS AS INDICATORS
OF DISEASE ACTIVITY IN RELAPSING REMITTING
MULTIPLE SCLEROSIS Inglese M, Rusinek H, Babb JS,
Grossman RI, Gonen O
P251 A COMPARISON OF DIFFERENT QUANTITA-
TROSCOPY IN FAMILIAL AND SPORADIC MS SigerZajdel M, Selmaj K
TIVE MRI TECHNIQUES TO MEASURE WHOLE BRAIN
ATROPHY IN RELAPSING-REMITTING MULTIPLE SCLEROSIS Zivadinov R, Bakshi R, Grop A, Sharma J, Bratina A,
Kuwata JM, Nasuelli D,Tjoa CW, Zorzon M
P222 OPTIC NEURITIS: CORRELATION OF CLINICAL,VISUAL FIELD AND NEUROIMAGING FINDINGS
AND THEIR PROGNOSTIC ROLE Paschalidou M, Georgiadis N, Haritanti A, Doskas T, Parissis D, Poulios G, Halvatzis N,
Xinou E, Drevelegas A, Dimitriadis AS, Milonas I
P237 PROTON MAGNETIC RESONANCE SPECTROSCOPY EVIDENCE FOR EARLY GRAY MATTER
INVOLVEMENT IN RELAPSING REMITTING MS
Inglese M, Ge Y, Filippi M, Falini A, Grossman RI, Gonen O
P252 REGIONAL BRAIN PARENCHYMAL ATROPHY
P238 BRAIN VOLUME CHANGES AFTER SUPPRES-
P223 ASSOCIATION OF UVEITIS AND MULTIPLE
SION OF MRI-VISIBLE INFLAMMATION IN PATIENTS
WITH SECONDARY PROGRESSIVE MS TREATED WITH
AUTOLOGOUS STEM CELL TRANSPLANTATION
Inglese M, Mancardi G, Murialdo A, Marrosu M, Meucci G, Massaccesi L, Lugaresi A, Pagliai F, De Stefano N, Saccardi R, Filippi M
RELAPSING-REMITTING MULTIPLE SCLEROSIS Zivadinov R, Bagnato F, Nasuelli D, Bastianello S, Bratina A, Finamore L,
Locatelli L, Catalan M, Clemenzi A, Grop A, Millefiorini E, Zorzon M
SCLEROSIS COULD INFLUENCE THE CLINICAL
COURSE OF MULTIPLE SCLEROSIS Patrick V, Jean-yves G,
Pierre L, Didier F, Tanya S, Albert V, Jérôme D
P224 THE EFFECT OF CORTICOSTEROID ON CONDUCTION IN THE VISUAL PATHWAYS.A SERIAL STUDY
USING VISUAL PSYCHOPHYSICS Pye EM, Weatherby SJ,
Kesson D, Foster DH, Hawkins CP
P225 A COMPARISON OF BILATERAL SIMULTANEOUS AND BILATERAL SEQUENTIAL OPTIC NEURITIS
USING VISUAL PSYCHOPHYSICS Pye EM, Weatherby SJ,
Kesson D, Foster DH, Hawkins CP
P239 COGNITIVE AND EMOTIONAL STATUS IN A
POPULATION OF PATIENTS PRESENTED WITH CLINICALLY ISOLATED SYNDROMES SUGGESTIVE OF MULTIPLE SCLEROSIS Jean P,Virginie L, Florence R, Bertrand A, Jean
Philippe R, Sylviane C,Andre A, Patrick C
PLE SCLEROSIS PATIENTS INITIATING INTERFERON
BETA-1A THERAPY Riskind P, Brown V, Kevin K
P240 NEURAL SUBSTRATES UNDERLYING PERFORMANCE OF A CONTROLLED MOTOR TASK IN
PATIENTS WITH MULTIPLE SCLEROSIS Kadom N, Morgen K, Sawaki L,Tessitore A, Ohayon J, Frank J, McFarland H,
Martin R, Cohen LG
P227 COURSE AND PROGNOSIS IN EARLY ONSET
P241 INTERCAUDATE NUCLEUS RATIO (ICR) IN MS
MULTIPLE SCLEROSIS Simone IL, Carrara D,Tortorella C,
Liguori M, Lepore V, Pelligrini F, Bellacosa A, Ceccarelli A, Pavone I,
Girolamo F, Livrea P
PATIENTS AS A LINEAR MEASURE OF BRAIN ATROPHY
Khan O, Zvartau-Hind M, Caon C, Ching W, Lisak R,Tselis A
P226 PHYSICAL ACTIVITY AND FATIGUE IN MULTI-
P228 MS PHENOTYPE:AN AGE-DRIVEN DISEASE?
Vukusic S,Adeleine P, Gignoux L, Durand-Dubief F, Renoux C,
Achiti I, Blanc S, Confavreux C
P229 NEUROGENIC SYNCOPE IN MULTIPLE SCLEROSIS PATIENTS Zapletalova O, Dolezil D, Hradilek P, Stipal R
Imaging (Part II)
P230 CORRELATION BETWEEN BRAIN ATROPHY
AND APOLIPOPROTEIN E GENOTYPES IN PATIENTS
WITH EARLY RELAPSING-REMITTING MULTIPLE SCLEROSIS Amato M, Mortilla M, Bartolozzi M, Nacmias B, Zipoli
V, Siracusa G, Cellini E, Bagnoli S, Guidi L, Lambruschini P, Sorbi S,
Federico A, De Stefano N
46
MEASURES IN MULTIPLE SCLEROSIS Locatelli L,
Zivadinov R, Bratina A, Nasuelli D, Grop A, Zorzon M
P253 SHORT-TERM BRAIN ATROPHY CHANGES IN
P254 MRI MEASURES IN RELAPSING-REMITTING
MULTIPLE SCLEROSIS.A SHORT-TERM OBSERVATION
STUDY Nasuelli D, Bagnato F, Zivadinov R, Bratina A, Bastianello S, Finamore L, Locatelli L, Grop A, Di Pofi B, Millefiorini E,
Zorzon M
Immunology (Part II)
P255 NEW CANDIDATES IN MULTIPLE SCLEROSIS
IDENTIFY BY AN ANALYSIS OF IGG REPERTOIRE COUPLED WITH A PROTEOMIC APPROACH ALMERAS L,
Lefranc D, Drobecq H, de Seze J, Dubucquoi S,Vermersch P, Prin L
P256 IMMUNOPATHOGENIC AND CLINICAL RELEVANCE OF ANTIBODIES AGAINST MOG IN MULTIPLE
SCLEROSIS Berger T, Egg R, Rubner P, Hochfilzer A,
Lutterotti A, Schanda K, Deisenhammer F, Reindl M
P242 CEREBRAL ATROPHY IN SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS: EFFECT OF INTRAVENOUS IMMUNOGLOBULINS Lin X,Turner B, Constantinescu C, Blumhardt LD, Fazekas F, Filippi M, Hommes OR
P257 DECRYPTING THE SPECIFICITY OF THE
P243 CORRELATES OF MAGNETIZATION TRANSFER IMAGING METRICS IN PRIMARY PROGRESSIVE
MULTIPLE SCLEROSIS Rovira A, Brieva L,Aymerich X,
Borras C,Tintore M,Alonso J, Montalban X
P258 PREVALENCE OF HERPESVIRUS DNA IN MS
P244 DISSEMINATION IN SPACE IN BRAINSTEM
SYNDROMES Sastre-Garriga J,Tintore M, Rovira A, Nos C,
Pericot I, Rio J,Thompson AJ, Montalban X
P245 COMPUTER ASSISTED VOLUMETRIC ANALYSIS
OF GADOLINIUM ENHANCEMENT IN MULTIPLE SCLEROSIS Preiningerova J, Ding Z, Cannistraci C, Sun H, Vollmer T,
Anderson A
INTRATHECAL IGG RESPONSE IN PATIENTS WITH
MULTIPLE SCLEROSIS BY PROTEIN ARRAY TECHNOLOGY Cepok S, Stei S, Sommer N, Hemmer B
PATIENTS Daskalovska VA, Daskalovski ZV, PetkovaBoskovska T
P259 SEQUENTIAL STUDY OF SERUM SEX HORMONES AND TH1/TH2 CYTOKINE BALANCE DURING
AND AFTER RELAPSE OF MULTIPLE SCLEROSIS Sanchez-Ramon S, Rodriguez-Saiz C, Lozano N, Resino S, Munoz C,
Rodriguez-Mahou M, Muñoz-Fernández M, de Andrés C
P260 CHEMOKINE RECEPTOR EXPRESSION ON T
CELLS IS RELATED TO NEW LESION DEVELOPMENT IN
MULTIPLE SCLEROSIS Eikelenboom MJ, Killestein J, Izeboud T,
Kalkers NF, van Lier RA, Barkhof F, Uitdehaag BM, Polman CH
Immunology (Part II) (continued)
Neuropsychology
P261 SEVERE URTICARIA AS REACTION TO INTERFERON-␤-1A ADMINISTRATION Fazio MC, Mazzeo L,
Buccafusca M, Dattola V, Scalfari A, Ferlazzo E, Girlanda P,
Messina C
P275 SCREENING FOR EARLY COGNITIVE IMPAIRMENT IN MULTIPLE SCLEROSIS PATIENTS USING THE
CLOCK DRAWING TEST BarakY,Achiron A
P262 A 4-MONTH LONGITUDINAL STUDY ON THE
RELATIONSHIP BETWEEN CLINICAL ACTIVITY AND
BETA2-MICROGLOBULIN EXPRESSION IN MULTIPLE
SCLEROSIS Finamore L, Zivadinov R, Cecchinelli D, Pichi A,
Nasuelli D, Pierallini A, Bratina A, Locatelli L, Grop A, Reale M,
Zorzon M, Millefiorini E
LOGICAL ASSESSMENT IN 48 RR-MS PATIENTS Brescia
Morra V, Lanzillo R, Brunetti A, Salvatore E, Schiavone V, Quarantelli M, Coppola G, Orefice G
P263 LONGITUDINAL STUDY OF SPONTANEOUS
AND INDUCED APOPTOSIS IN LYMPHOCYTES OF
PATIENTS WITH RELAPSING-REMITTING AND SECONDARY-PROGRESSIVE MS TREATED WITH INTERFERON BETA-1B Garcia-Merino A, Diaz D, Bacenilla H,
Prieto A,Alvarez-Mon M
P264 SPONTANEOUS EX-VIVO AND MITOGENINDUCED APOPTOSIS ARE INCREASED IN SEVERAL
LYMPHOCYTE SUBSETS OF PATIENTS WITH RELAPSING-REMITTING AND SECONDARY-PROGRESSIVE MS
Garcia-Merino A, Diaz D, Barcenilla H, Prieto A,Alvarez-Mon M
P265 INTERFERON BETA-1A REGULATES G PROTEIN COUPLED RECEPTORS IN MONONUCLEAR
CELLS FROM HEALTHY DONORS AND MULTIPLE SCLEROSIS PATIENTS Giorelli M, Livrea P, Defazio G, Ricchiuti F,
Mola A, Di Monte E,Trojano M
P266 ORAL TERBUTALINE DIFFERENTIALLY
AFFECTS CYTOKINE (IL-10, IL-12,TNF, IFNG) RELEASE
IN MULTIPLE SCLEROSIS PATIENTS AND CONTROLS
Gold SM, Heesen C, Sondermann J,Tessmer W, Schulz K
P276 QUANTITATIVE MRI AND NEUROPSYCHO-
P277 COGNITIVE PERFORMANCES ARE ALTERED IN
EARLY MULTIPLE SCLEROSIS Salort E, Deloire-Grassin M,
Boudineau M, Ouallet J, Barroso B,Arese P,Verley C, Fabrigoule C,
Leteneur L, Brochet B
P278 PACED AUDITORY SERIAL ADDITION TEST
AND MAGNETIC RESONANCE IMAGING FINDINGS
IN MULTIPLE SCLEROSIS PATIENTS. PRELIMINARY
STUDY Callegaro D, Fuso S, Otaduy M, Costa M, Lacerda M,
Bacheschi L, Leite C, Bueno O
P279 COGNITIVE SCREENING OF MS PATIENTS
RECRUITED FOR A CLINICAL TRIAL Christodoulou C,
Krupp LB, Melville P, Scherl W, Morgan T, McIlree C
P280 COGNITIVE FUNCTIONS IN MULTIPLE SCLEROSIS PATIENTS TREATED WITH INTERFERON-BETA:
A CONTROLLED TWO YEAR FOLLOW-UP STUDY
Danni M,Viti B, Splendiani G, Giambartolomei S,Arabi S, Provinciali L, Ceravolo G
P281 COGNITIVE IMPAIRMENT IN ACTIVE MULTIPLE
SCLEROSIS de Seze J, Bouillaguet S, Dubois G, Cabaret M,
Ferriby D, Dujardin K,Vermersch P
P282 EMOTIONAL ADJUSTMENT IN PATIENTS
WITH MULTIPLE SCLEROSIS Pires-Barata S, Henriques I
P267 CROSS-REACTIVE ANTIBODIES AGAINST
MYELIN BASIC PROTEIN, ACINETOBACTER SP. AND
PSEUDOMONAS AERUGINOSA IN MULTIPLE SCLEROSIS Hughes LE, Bonell S,Wilson C, Smith P,Amor S, Ebringer A
P283 SUCCESSFUL ADULT DEVELOPMENT AS A
FRAMEWORK FOR NEUROPSYCHOLOGICAL COUNSELING IN MULTIPLE SCLEROSIS Lana-Peixoto MA,
Haase VG, Lacerda SS, Lima EP
P268 THE PLASMA LEVELS OF ALPHA-2-
P284 DEVELOPMENT OF THE BRAZILIAN VERSION
MACROGLOBULIN AND THE TRANSFORMED FORM
ARE SIGNIFICANTLY DIFFERENT BETWEEN PATIENTS
WITH MULTIPLE SCLEROSIS AND CONTROLS
Jensen PH, Datta P, Jorgensen S, Oturai AB, Sorensen PS
P269 LOW MOLECULAR WEIGHT GLYCOCONJUGATES IN BRAIN HAVE IMMUNOREGULATORY ACTIVITY Lindsey JW,Waxham MN, Stephens NE,Weiser S
P270 LEVELS OF SAPO-1/FAS IN THE SERUM OF
MULTIPLE SCLEROSIS PATIENTS BEFORE AND AFTER
STEROID TREATMENT Mitosek-Szewczyk K, BartosikPsujek H, Belniak E, Dobosz B, Stelmasiak Z
P271 UPREGULATED SURVIVIN EXPRESSION IN
ACTIVATED T LYMPHOCYTES CORRELATES WITH
DISEASE ACTIVITY IN MULTIPLE SCLEROSIS Noori M,
Sharief MK
P272 DYSREGULATION OF PROGAMMED CELL
DEATH ACTIVATION IN MULTIPLE SCLEROSIS PATIENTS
Saresella M, Clerici M,Trabattoni D, Speciale L, Piacentini L,
Caputo D, Ferrante P
P273 THE EXPRESSION OF CD5 ON PERIPHERAL B
LYMPHOCYTES CORRELATES WITH DISEASE ACTIVITY
IN PATIENTS WITH MULTIPLE SCLEROSIS Seidi OA,
Sharief MK
P274 GLUCOCORTICOID SENSITIVITY IN PATIENTS
WITH MULTIPLE SCLEROSIS Winsen Lv, Muris D, Dijkstra C,
Polman C, van den Berg T, Uitdehaag B
OF THE MULTIPLE SCLEROSIS FUNCTIONAL COMPOSITE MEASURE: RESULTS FROM A PILOT STUDY LanaPeixoto MA, Haase VG, Lacerda S, Lima EP
P285 BECK DEPRESSION INVENTORY AND GENERAL HEALTH QUESTIONNAIRE: RESULTS OF A COMPARISON BETWEEN MULTIPLE SCLEROSIS PATIENTS
AND CONTROLS Lana-Peixoto MA, Haase VG, Lacerda SS,
Lima EP
P286 PSYCHOSOCIAL FUNCTIONING IN MS:
Encephalomyelitis (Part II)
P292 DETECTION OF MAGNETICALLY LABELED
ENCEPHALITOGENIC T-CELLS IN EXPERIMENTAL
AUTOIMMUNE ENCEPHALOMYELITIS (EAE) BY CELLULAR MAGNETIC RESONANCE IMAGING Anderson SA,
Shukaliak-Quandt J,Arbab SA, Jordan EK, Martin R, McFarland HF,
Frank JA
P293 EXPRESSION OF THE ACTIVATION MARKER
UROKINASE PLASMINOGEN ACTIVATOR IN CNS
MICROVASCULAR PERICYTES IN EXPERIMENTAL
AUTOIMMUNE ENCEPHALOMYELITIS Dore-Duffy P,
Balabanov R,Wagnerova J,Washington R
P294 TREATMENT OF EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS WITH INTRAVENOUS
IMMUNOGLOBULIN Humle Jørgensen S, Laursen H,
Soelberg Sørensen P
P295 SUSCEPTIBILITY TO T CELL-MEDIATED CENTRAL NERVOUS SYSTEM INFLAMMATION MODULATED BY NON-MYELIN-SPECIFIC T CELLS Jones RE,
Kay T,Wilkins D,Tsaknaridis L, Bourdette D
P296 AXONAL PROTECTION BY FLECAINIDE
THERAPY IN EAE Bechtold DA, Kapoor R, Smith KJ
P297 A SYNTHETIC ANDROSTENE DERIVATIVE
WITHOUT GENDER-RELATED SIDE EFFECTS INHIBITS
EAE. CANDIDATE FOR CLINICAL TRIALS IN MS?
Offner H, Zamora A, Matejuk A,Auci D, Morgan E, Reading C
P298 THE ROLE OF THE MHC CLASS II TRANSACTIVATOR (CIITA) IN CLASS II EXPRESSION AND ANTIGEN
PRESENTATION BY ASTROCYTES AND IN SUSCEPTIBILITY TO CNS AUTOIMMUNE DISEASE Stuve O,Youssef S,
King CL, Patarroyo JC, Brickey JW, Piskurich JF, Chapman HA,
Zamvil SS
P299 TREOSULFAN IN MYELIN-OLIGODENDROCYTE-GLYCOPROTEIN-INDUCED EXPERIMENTAL
AUTOIMMUNE ENCEPHALOMYELITIS: POTENTIAL
NEW TREATMENT FOR MULTIPLE SCLEROSIS Weissert R,
Pfrommer H,Wiendl H, Baumgart J, Melms A, Sass G,Weller M
Healthcare Systems
P300 COST-BENEFIT AND COST-EFFECTIVENESS
PSYCHOMETRIC CHARACTERISTICS OF SELFREPORTED MEASURES EMPLOYED IN BRAZIL
Lana-Peixoto MA, Haase VG, Lacerda SS, Lima EP
ANALYSIS OF INTERFERON BETA-1A 44MCG TIW,VERSUS INTERFERON BETA-1A 30MCG QW, IN RELAPSINGREMITTING MULTIPLE SCLEROSIS (RRMS) Beresniak A,
Martin M
P287 PSYCHOSIS IN MULTIPLE SCLEROSIS Nieder-
P301 A RELAPSE OF MULTIPLE SCLEROSIS: HOW
mayerová I, Beneöová Y, Mechl M
P288 THE EFFECT OF INTERFERON BETA ON
THE COGNITIVE DYSFUNCTION OF 100 IRANIAN
PATIENTS WITH MULTIPLE SCLEROSIS (MS) Pakdaman H, Pakdaman R
P289 HOPELESSNESS IN MULTIPLE SCLEROSIS
MUCH DOES IT COST IN CATALONIA? Casado V, Martinez-Yelamos S, Martinez-Yelamos A, Carmona O, Hernandez JJ,
Arbizu T
P302 AN AUDIT OF HEALTH SCREENING ISSUES IN
MS PATIENTS IN GENERAL PRACTICE Hawkins SA,
Maclurg K,Whittington D, Evason E, Reilly PM
Patten SB, Metz LM
P303 THE ECONOMIC BURDEN OF RELAPSE IN
P290 COGNITIVE DYSFUNCTION IN MULTIPLE
MULTIPLE SCLEROSIS: DIRECT MEDICAL COSTS PER
EPISODE IN THE UNITED STATES O’Brien J, Patrick A,
Duran P, Caro J
SCLEROSIS Petkovska-Boskova T, Daskalovska V, Bojkovski V
P291 A CROSS-SECTIONAL STUDY OF 21 NEWLY
DIAGNOSED, RELAPSE-REMITTING MULTIPLE SCLEROSIS PATIENTS WITH PET, MRI AND TESTS OF COGNITIVE FUNCTIONS Tscherning T, Mathiesen HK, Jonsson A,
Blinkenberg M, Rostrup E, Larsson HB, Paulson OB, Soelberg
Sorensen P
P304 BURDEN OF NURSING CARE FOR HOSPITALIZED PATIENTS WITH MULTIPLE SCLEROSIS Tissot E,
Rumbach L, Limat S, Berger E, Monnin C, Lavier A,WoronoffLemsi M
47
Healthcare Systems (continued)
P305 THE NEW ZEALAND BETA-INTERFERON PROGRAM. AN APPROACH TO EQUITABLE PROVISION OF
TREATMENT FOR MS WHERE FUNDING IS RESTRICTED
Willoughby EW,Abernethy DA,Wright AR,Anderson NE
New Clinical Trials (Part II)
P306 THE INDEPENDENT COMPARISON OF INTERFERON (INCOMIN) TRIAL: MRI ANALYSIS OF THE NEW
PROTON DENSITY/T2 LESIONS Durelli L, Pipieri A,Verdun
E, Barbero P, Incomin G
P307 BETAFERON®/BETASERON® (INTERFERON
BETA-1B) IN EARLY TREATMENT OF MULTIPLE SCLEROSIS:THE BENEFIT STUDY Freedman M, Edan G, Hartung H,
Kappos L, Miller D, Montalban X, Polman C, Bauer L, Ghazi M,
Sandbrink R
P308 PLACEBO-CONTROLLED DOUBLE-BLINDED
DOSE RANGING STUDY OF FAMPRIDINE-SR IN MULTIPLE SCLEROSIS Goodman AD, Blight A, Cohen JA, Cross AH,
Katz M, Rizzo MA,Vollmer T
P309 DISABILITY AND QUALITY OF LIFE (FLAIR
STUDY) AND NEUROPSYCHOLOGY (COBRA STUDY)
IN RELAPSING MS PATIENTS Jongen P, Carton H, Sindic C,
Tinbergen J,Wesnes K, FLAIR S
P316 LACK OF ASSOCIATION BETWEEN CTLA-4
GENE POLYMORPHISMS AND MULTIPLE SCLEROSIS IN
SARDINIAN PATIENTS Cocco EE, Fadda EE, Rolesu MM,
Melis CC, Solla EE, Schirru LL, Costa GG, Murru MM, Murru RR,
Marrosu MM
P331 A RETROSPECTIVE COMPARATIVE ANALYSIS
P317 A49G CTLA-4 GENE POLYMORPHISM IN SAR-
ANTRONE IN 111 SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS PATIENTS Gregory T, Emmanuelle L,
Emmanuelle L, Eric S, Marc C, Gilles E
DINIAN PATIENTS WITH MULTIPLE SCLEROSIS AND
TYPE 1 DIABETES Cocco EE, Fadda EE, Rolesu MM, Melis CC,
Solla EE, Schirru LL, Fadda LL, Sanna S, Marrosu MM
P318 INFLUENCE OF MHC/HLA ALLELES IN MULTIPLE SCLEROSIS CLINICAL VARIABLES Cocco EE, Fadda E,
Rolesu M, Melis C, Solla E, Costa G, Murru M, Murru R, Fadda L,
Marrosu MM
P319 A GENOME-WIDE LINKAGE SCREEN IN TURKISH MULTIPLEX FAMILIES WITH MULTIPLE SCLEROSIS
Eraksoy M, Kurtuncu M, Sawcer SJ,Akesson E,Akman-Demir G,
Compston AD,Turkish Multiple Sclerosis Genetics Study Group
P320 MOLECULAR ANTHROPOLOGICAL VIEW IN A
POPULATION ANALYSIS OF BRAZILIAN INDIVIDUALS
DURING A MULTIPLE SCLEROSIS GENETIC STUDY OF
HLA DRB1-DQB1-DQA1 Leon SV, Alvarenga RP, Caballero A,
Alonso A, Fernandez O
P321 HISTOCOMPATIBILITY CLASS II DR*, DQ*, DP*
ANTIGENS ASSOCIATION WITH MULTIPLE SCLEROSIS
IN A POPULATION OF THE RIO DE JANEIRO CITY,
BRAZIL Santos CC, Emmerick M, Liem AM, Frugulhetti I,
Leon SV, Quirico-Santos T
SERUM URATE LEVELS THROUGH ADMINISTRATION
OF INOSINE Spitsin S, Hooper D, Scott GS, Koprowski H
P322 PRIMARY ASSOCIATION OF A TUMOR
NECROSIS FACTOR GENE POLYMORPHISM WITH MS
SUSCEPTIBILITY Rafael A,Virginia D,Alfonso M,Ana R,
Miguel F, Xavier M, Emilio G
P311 INTERFERON-␤ TREATMENT IN RELAPSING-
P323 MHC GENE MODULATING MS SUSCEPTIBILITY
REMITTING MULTIPLE SCLEROSIS: RESULTS OF AN
OBSERVATIONAL STUDY IN SOUTHERN ITALY Trojano M, Paolicelli D, Liguori M, Zimatore G,Avolio C, Lavolpe V,
Ruggieri M, Livrea P
CONFERRED BY HLA-DRB1*1501 Rafael A, Virginia D,
Alfonso M, Ana R, Xavier M, Emilio G
P310 TREATMENT OF EAE AND MS BY RAISING
P312 A RANDOMIZED, DOUBLE-BLIND, PLACEBOCONTROLLED STUDY OF INTRAVENOUS IMMUNE
GLOBULINS (IVIG) IN COMBINATION WITH INTRAVENOUS METHYLPREDNISOLONE (MP) IN THE TREATMENT OF RELAPSES IN PATIENTS WITH MULTIPLE
SCLEROSIS (MS) Visser LH, Beekman R,Tijssen CC, Uitdehaag BM, Movig C, Lenderink B
P313 EFFECTS OF INTERFERON BETA-1B DOSE
TITRATION ON EFFICACY AND TOLERABILITY
Wroe S
Genetics (Part II)
P314 TUMOR NECROSIS FACTOR RECEPTOR II
P324 IL10 GENE AND RESPONSE TO IFN BETA IN MS
de las Heras V, Rafael A, Martínez A, Rubio A, G de la Concha E
P325 ASSOCIATION OF APOLIPOPROTEIN E AND
MYELOPEROXIDASE GENOTYPES WITH THE CLINICAL
COURSE OF FAMILIAL AND SPORADIC MULTIPLE SCLEROSIS Zakrzewska-Pniewska B, Podlecka A, Styczynska M,
Samocka R, Peplonska B, Barcikowska M, Kwiecinski H
Immunotherapy (Part II)
P326 RAPID ONSET MITOXANTRONE-INDUCED
CARDIO TOXICITY IN SECONDARY PROGRESSIVE
MULTIPLE SCLEROSIS Avasarala JR, Cross AH, Clifford DB,
Siegel B,Abbey EE
P327 ANTI MOG AND ANTI MBP ANTIBODY SUB-
POLYMORPHISM IN PATIENTS WITH MULTIPLE SCLEROSIS Ehling R, Gassner C, Fazekas F, Kollegger H, Kristoferitsch W, Reindl M, Berger T
CLASSES IN MULTIPLE SCLEROSIS PATIENTS DURING
INTERFERON BETA THERAPY Khalil M, Reindl M, Lutterotti A, Egg R, Schanda K, Deisenhammer F, Berger T
P315 ANTIBODY RESPONSE TO MYELIN OLIGODENDROCYTE GLYCOPROTEIN AND MYELIN BASIC
PROTEIN DEPEND ON FAMILIAL BACKGROUND AND
ARE PARTIALLY ASSOCIATED WITH HUMAN LEUKOCYTE ANTIGEN ALLELES IN MULTIPLEX FAMILIES AND
SPORADIC MULTIPLE SCLEROSIS Lutterotti A, Reindl M,
Gassner C, Poustka K, Schanda K, Deisenhammer F, Berger T
P328 GLATIRAMER ACETATE (GA)-REACTIVE TCELLS PRODUCE BRAIN DERIVED NEUROTROPHIC
FACTOR (BDNF) Chen M, Dhib-Jalbut S
P329 IMPORTANCE OF CONTINUOUS IMMUNOMODULATORY TREATMENT IN MULTIPLE SCLEROSIS
Csépány T, Csiba L
P330 EFFECT OF ORAL GLATIRAMER ACETATE
(COPAXONE) IN MULTIPLE SCLEROSIS: REDUCTION
OF INTERFERON GAMMA PRODUCTION de Seze J,
Dubucquoi S, Lefranc D, Almeiras L, Dutoit V, Clavelou P, Edan G,
Hautecoeur P, Prin L, Vermersch P
48
ON THE EFFICACY OF THREE INTERFERON BETA
TREATMENTS IN MULTIPLE SCLEROSIS Giray S, Demirkiran M, Sarica Y
P332 CLINICAL AND MRI IMPACT OF MITOX-
P333 NEUTRALIZING ANTIBODIES TO INTERFERON BETA-1B AND THERAPEUTIC RESPONSE IN
MULTIPLE SCLEROSIS PATIENTS Hernández-Regadera JJ,
Bas-Minguet J,Arbizu-Urdiain T
P334 LONG-TERM TOLERABILITY OF INTERFERON
BETA-1A IN RELAPSING-REMITTING MULTIPLE SCLEROSIS: 6-YEAR SAFETY FOLLOW-UP OF THE PRISMS
STUDY Kappos L, Stam Moraga M
P335 ALGORITHM FOR LONG-TERM TREATMENT
OF EARLY MULTIPLE SCLEROSIS Koehler J,Wicht S,
Hey W, Holger S
P336 THE BRAZILIAN EXPANDED CONSENSUS ON
TREATMENT OF MULTIPLE SCLEROSIS Lana-Peixoto MA,
Callegaro D, Moreira MA, Marchiori PE, Lino A, Gabbai AA,
Souza AM, Campos GB, Rocha FC, Gama PD, tosta E,Ataide L,
Brito L, Bacheschi LA
P337 INDUCTION TREATMENT WITH MITOXANTRONE DURING 6 MONTHS IN WORSENING
RELAPSING REMITTING MULTIPLE SCLEROSIS:A RESCUE THERAPY FOR SUB-OPTIMAL RESPONDERS TO
INTERFERON BETA? A PILOT STUDY Le Page E, Leray E,
Coustans M,Taurin G, Chaperon J, Edan G
P338 IN VIVO EFFECT OF INTERFERON-␤1A ON
INTERLEUKIN-12 AND TRANSFORMING GROWTH
FACTOR-␤1 CYTOKINES IN PATIENTS WITH RELAPSING-REMITTING MULTIPLE SCLEROSIS Losy JJ,
Michalowska-Wender G
P339 INTERLEUKIN 18 IS MODIFIED DURING THERAPY WITH GLATIRAMER ACETATE (COPAXONE) IN
PATIENTS WITH RELAPSING-REMITTING MULTIPLE
SCLEROSIS Losy JJ, Michalowska-Wender G,Wender M
P340 THERAPEUTIC POTENTIAL OF STATINS IN
RELAPSING-REMITTING MULTIPLE SCLEROSIS
Markovic-Plese S, Powell AW, Cortez A,Vollmer TL
P341 EXPRESSION OF CHEMOKINES AND CHEMOKINE RECEPTORS BY GLATIRAMER ACETATE-REACTIVE
T-CELL LINES Neuhaus O, Bartosik-Psujek H, Kieseier BC,
Wiendl H, Hartung H
P342 ACUTE MYELOID LEUKAEMIA (AML) INDUCED
BY MITOXANTRONE Radu TD, Marc D, Herve V
P343 GLATIRAMER ACETATE AS AN IN VITRO TOOL
TO FOLLOW THE LONG-TERM EFFECT OF IMMUNOMODULATORY THERAPIES ON T CELL RESPONSES IN
PATIENTS WITH MULTIPLE SCLEROSIS Schmied M,
Reindl M,Auff E,Vass K
P344 REDUCED EXPRESSION OF THE INHIBITOR
OF APOPTOSIS PROTEINS IN T CELLS FROM PATIENTS
WITH MULTIPLE SCLEROSIS FOLLOWING INTERFERON-BETA THERAPY SemraYK, Sharief MK
P345 THE EFFECT OF LIVER TRANSPLANT COMBINATION IMMUNOSUPPRESSION ON MULTIPLE SCLEROSIS AFTER 18 MONTHS Vorobeychik G,Yoshida E, Prout A
SM
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Abstracts Author Index
Abbey EE, P326
Abdalla J, P221
Abernethy DA, P305
Achenbach SJ, P140
Achiron A, P19, P275
Achiti I, 64, P68, P228
Adam P, P1
A∂⬘ ao∂⬘ lu J, P148
Adeleine P, P228
Akbayrak T, P168
Akesson E, P319
Åkesson E, P137
Akkuzu B, P123
Akman-Demir G, P30, P156, P319
Alban D, P37
Albert V, P223
Alcina A, P138
Alfonso M, P322, P323
Allie R, 49
Almeiras L, P330
Almeras L, P255
Alonso A, P320
Alonso J, P134, P243
Alsop J, P221
Altamura N, P145
Altintas A, P89
Altmann D, P73, P75, P76
Alvarenga RP, P320
Alvarez F, P151, P152
Alvarez-Mon M, P263, P264
Amanda Louise C, P157
Amato M, P160, P230
Amina B, P118
Amo C, P82
Amor S, 48, P267
Ana R, P322, P323
Andersen O, P137
Anderson A, P245
Anderson D, P47
Anderson NE, P305
Anderson SA, P292
Andre A, P36, P37, P239
Angeleri V, P165
Anlar O-, P119
Annovazzi P, P125
Antel JP, 33
Aouba A, P208
Arabi S, P280
Aragão AL, P57
Araújo CR, P58, P174, P212
Arbab SA, P292
Arbizu T, P215, P301
Arbizu-Urdiain T, P333
Ardnt C, P200
Arese P, P277
Armstrong MA, P158
Armutlu K, P168, P169
Arnal C, P54
Arnold DL, 27
Aronica EM, 3
Arroyo R, P142
Ataide L, P336
Auci D, P297
Auff E, P343
Aurélien M, P182
50
Avasarala JR, P17, P326
Avolio C, P311
Aymerich X, P10, P134, P243
Babb JS, P7, P236
Bacchetti T, P165
Bacenilla H, P263
Bacheschi L, P72, P278, P336
Bagaeva L, P114
Bagnato F, 8, 32, P253, P254
Bagnoli S, P230
Bahar Z, P181
Baier M, 20, 66
Baker D, 48
Bakshi R, 67, P251
Balabanov R, P293
Balcý BP, P18, P48
Ballario C, P151
Ballerini C, P153
Baltariu G, P164
Barak Y, P19, P275
Baranda P, P112
Barbero P, P135, P162, P306
Barcellos LF, 57
Barcenilla H, P264
Barcikowska M, P325
Barker GJ, 4, P75, P84, P85
Barkhof F, 23, 28, 30, 31, P133,
P147, P234, P260
Bar-Or A, P149
Barroso B, P170, P277
Bartlett PF, 18
Bartolozzi M, P230, P233
Bartosik-Psujek H, P2, P90, P270,
P341
Bartsch K, P171
Bash C, 8
Bas-Minguet J, P333
Bastianello S, P6, P253, P254
Bataillard M, P23
Batocchi A, P3
Bauer L, P307
Baumgart J, P299
Baus Toselli PL, P50, P51
Bechtold DA, P296
Beckman E, P130
Beckmann K, P133
Beekman R, P312
Belden D, P20, P194, P195
Bellacosa A, P227
Belman AL, P211
Belniak E, P2, P90, P270
Belsan T, P216
Bencsik K, P161
Bendtzen K, 24
Beneöová Y, P231, P287
Benli S, P123
Bennett D, P130
Bennett S, P218
Beresniak A, P300
Bergamaschi R, P32, P33
Berger E, P43, P304
Berger T, P4, P155, P256, P314,
P315, P327
Bergui M, P135
Bernard Z, 19, P121
Bernat A, P21, P22
Berry I, P69
Bertolotto A, P150
Bertrand A, P36, P37, P239
Bettinelli R, P152
Bettinotti MP, 1
Bever CT, P131
Biagioli T, P153
Bielekova B, 10, P98
Biernacki K, 33
Bihler I, P201
Biswal B, P136
Bjartmar C, 12
Björkhem I, P9
Blanc S, P68, P228
Blight A, P308
Blinkenberg M, P291
Blitz K, P211
Blumhardt LD, P83, P242
Boggild M, P143, P144, P220
Bojar M, P216
Bojkovski V, P290
Bonell S, P267
Born SE, P100
Borras C, P134, P243
Boschert U, 14
Bosco A, P145, P146
Bosio A, P162
Bosnak M, P169
Botelho CM, P57
Bottero R, P150
Boudineau M, P277
Bouillaguet S, P281
Bourdette D, P109, P295
Bourg v, P60, P213, P214
Boyko OB, P235
Brandejský P, P179
Bratina A, P6, P145, P146, P251,
P252, P253, P254, P262
Braumann K, P171
Brescia Morra V, P276
Breteau G, P25
Brickey JW, P298
Brieva L, P134, P243
Brimer CM, P113
Brito L, P336
Brochet B, P70, P71, P170, P277
Brooks BR, P20, P29, P188, P194,
P195
Brosnan CF, 38
Brown V, P226
Brownscheidle C, 67
Brueck W, 13
Bruegmann M, P34
Brunetti A, P276
Bruno S, 19, P121
Brunotte F, P205
Buccafusca M, P31, P261
Budde T, P108
Buenconsejo J, P185, P191
Bueno O, P278
Bueno V, P35
Bumin G, P168
Burns T, P218
Butine M, P132
Butzkueven H, 18
Caballero A, P320
Cabaret M, P281
Caceres F, P66, P151
Cadavid D, P136
Caggiula M, P3
Çakmakçý H, P99
Calabrese M, P13, P204
Calabresi PA, 49
Callegaro D, P59, P72, P278, P336
Callioglu B, P181
Calvo A, P35
Campos GB, P57, P336
Can U, P123
Cannistraci C, P245
Caon C, P38, P241
Capobianco M, P150
Caputo D, P272
Caramanos Z, 27
Carella C, P3
Carlo F, P197
Carmen M, P82
Carmona O, P215, P301
Caro J, P303
Carra AJ, P151, P152
Carrara D, P227
Carrigan D, P210
Carton H, P309
Carvalho A, P95
Casado V, P215, P301
Casanova B, P21, P22, P232
Cassol E, P69
Castelijns JA, 31, P234
Catalan M, P253
Catherine L, 19, P217, P121
Cavaletti G, P153
Cavalletti E, P153
Cazzato G, P145, P146
Ceccarelli A, P227
Cecchinelli D, P6, P262
Celda B, P232
Celilus E, P137
Celine J, P121
Céline T, P183
Cellini E, P230
Cepok S, P91, P257
Ceravolo G, P280
Ceravolo M, P165
Certa U, 15
Cetisli N, P169
Chan A, P154
Chanalet S, P214
Chandy K, 49
Chang A, 12
Chang P, P221
Chaperon J, P337
Chapman HA, P298
Chard D, P12, P73, P246
Chatel M, P27, P60, P213, P214
Chatzisotiriou A, P126
Chen L, 60
Chen M, P328
Chevalier Y, P23
Ching W, P38, P241
Chopard G, P43
Christian S, P106
Christie S, P26
Christodoulou C, P126, P279
Ciabini D, P111
Cianciulli C, P211
Ciccarelli O, 4
Claire G, P198
Clanet M, P69
Clavelou P, P206, P330
Clemenzi A, P253
Clemmesen KM, 24
Clerc C, P23
Clerici M, P272
Clerico M, P135, P162
Clifford DB, P326
Cocco EE, P24, P316, P317, P318
Cohen JA, P5, P63, P86, P177,
P308
Cohen LG, P240
Coles A, P157
Colombo B, 62, P247
Comabella M, P10, 51, P142
Comi G, 7, 23, 30, 62, P32, P33,
P125, P133, P247, P248, P249
Compston A, 55, P137, P157, P319
Confavreux C, 21, 64, P68, P74,
P217, P228
Connelly D, 60
Constantin G, P111
Constantinescu C, P242
Constantinou A, P126
Cook SD, P136
Coombs B, P87
Coppola G, P276
Corat-Simon J, P40
Corboy J, P87
Cordonnier C, P25
Coret F, P21, P22, P232
Corpetti M, P203
Correale J, P52
Corsi F, P203
Cortez A, P340
Costa AF, P141
Costa GG, P316, P318
Costa M, P72, P278
Cotleur AC, P100
Cotton F, P74
Coustans M, P49, P196, P337
Coyle PK, P26
Crippa L, P153
Cristiano E, P50, P51, P52, P151
Cristina Z, P197
Cross A, P17, P308, P326
Crusio R, 60
Csépány T, P329
Csiba L, P329
Cucci A, P162
Cutter G, 20, 66, P163
D’Ambrosio D, P111
Dalle Carbonare M, P13
Damier P, 2
Danni M, P165, P280
Daskalovska V, P258, P290
Daskalovski ZV, P258
Dassi M, P153
Datta P, P137, P268
Dattola V, P31, P261
Davies G, P73
Davis G, P12
de Andrés C, P259
de Andres de Frutos C, P122
de Boer J, P173
Defazio G, P265
De Groot CJ, 15
Deisenhammer F, P4, P155, P256,
P315, P327
de la Concha EG, P142, P324
de las Heras V, P324
De Libero G, P164
Deloire-Grassin M, P70, P71,
P170, P277
Delphine L, P183
De Luca M, P233
Demir G, P89
Demir Acar G, P99
Demirkiran M, P331
Deniz E, P30
Denton S, 65, P202
Denys V, P157
Deri N, P151
de Seze J, P25, P27, P28, P200,
P213, P255, P281, P330
De Stefano N, 30, P230, P233,
P238
De Vera A, P21, P22
Dhib-Jalbut S, 42, P328
Diaz D, P263, P264
Diczfalusy U, P9
Didier D, P183
Didier F, P223
Didier V, P182
Díez S, P35
Dijkstra C, P16, P274
Di Luccio E, P153
Dimitriadis AS, P222
Di Monte E, P265
Dinca L, P56
Ding Z, P245
Di Pofi B, P254
Di Sapio A, P150
Dobosz B, P270
Dogan S, P20, P29, P188
Dolezil D, P96, P229
Dominique A, P182
Dominique P, P198
Dong Z, 42
Dore-Duffy P, P293
Doskas T, P222
Dougherty D, 66
Dousset V, P70, P71
Drevelegas A, P222
Drobecq H, P255
Dubois G, P281
Dubucquoi S, P28, P255, P330
Duda PW, P164
Duddy M, P149
Duddy ME, P158
Dujardin K, P281
Durán E, P56, P141
Duran P, P303
Durand-Dubief F, 64, P68, P74,
P228
Durelli L, 23, 30, P135, P162, P306
Dusek L, P8
Dussart P, P28
Dutoit V, P330
Duyar H, P108
Ebers GC, 56
Ebringer A, P267
Edan G, 2, 23, 30, P49, P196, P217,
P307, P330, P337
Eduardo V, P127, P128
Edwards DR, P117
Egg R, P256, P327
Ehling R, P4, P314
Eikelenboom MJ, P11, P260
Elbs M, P108
Eleonora K, P53
Elizabeth AJ, P140
Emilio G, P322, P323
Emir C, P148
Emmanuelle L, P332
Emmerick M, P321
Engelhardt B, P94, P129
Enzinger C, 6
Eraksoy M, P30, P156, P319
Eric S, P332
Escalante RR, P151
Espejo C, P166
Etienne R, P198
Evason E, P302
Eyring S, P199
Fabrigoule C, P277
Fadda EE, P316, P317, P318
Fadda LL, P24, P317, P318
Falini A, 7, P237, P247, P248
Fazekas F, 6, P242, P314
Fazio MC, P31, P261
Federico A, P230, P233
Fedetz M, P138
Feichter J, 67
Feinstein A, 61
Ferlazzo E, P261
Fernandez A, P82
Fernandez Liguori N, P66, P151
Fernandez O, 30
Fernández O, 23, P54, P138, P320
Fernandez S, P82
Fernández V, P54, P138
Ferrante P, P272
Ferreira J, P66
Ferretti G, P165
Ferriby D, P25, P27, P200, P281
Fiè A, P165
Fiedler J, 43
Figar S, P50
Filippi M, 7, 23, 30, P32, P33, P133,
P233, P237, P238, P242, P247,
P248, P249
Finamore L, P6, P253, P254, P262
Fiorilla T, P159
Fiotti N, P145
Fisher E, 66, P100
Fishman P, 42
Flachenecker PM, P201
Flair S, P309
Flanders K, P132
Fleming EM, P158
Fletcher N, P220
Floren L, P130
Florence B, P183
Florence R, P239
Florio C, P159
Floris GG, P24
Fodor P, P26
Ford H, 65, P202
Foster DH, P224, P225
Frank J, 54
Frank JA, 8, 10, 26, 32, P240, P292
Frederic N, 19
Frederiksen J, 24, P55, P79, P101
Freedman M, P307
Frigo M, P153
Frisullo G, P3
Froment J, P74
Frota E, P57
Frugulhetti I, P95, P321
Fryer A, P143, P144
Fuchs K, P26
Fuhrmann A, 5
Furlan C, P146
Fuso S, P278
Gabbai AA, P336
Galgani S, P203
Gallo P, P13, P204
Gama PD, P59, P336
Gamero M, P56
Garcea O, P66, P151
García E, P21, P22
Garcia-Merino A, P112, P263,
P264
Garcia Moreno J, P56
Gasperini C, P203
Gassner C, P314, P315
Gaupp S, 41
Gbadamosi J, P34
Ge Y, P237
Genain CP, 5
Gentin M, P186
Georgiadis N, P126, P222
Gere J, P206
Geurts JJ, 3, P234
Ghazi M, P307
Ghezzi A, 7, P32, P33, P233, P247,
P248
Giambartolomei S, P280
Giannesini C, P207, P208, P209
Giansante C, P145
Giesser B, P26
Gignoux L, 64, P68, P74, P228
Gilgun-sherki Y, P110
Gilles B, P121
Gilles E, P332
Gilli F, P150
51
Giorelli M, P265
Giovannoni G, 48, P11, P12
Giray S, P331
Girlanda P, P31, P261
Girolamo F, P227
Giroud M, P205, P206
Gisevius A, P105
Giuliani F, 17
Glosova L, P216
Gneiss C, P155
Go A, P111
Gober H, P164
Goebels N, 16
Goertsches R, P142
Gökce N, P181
Gold L, P52
Gold R, 41, P154
Gold SM, P34, P171, P266
Gomez-de-la-Concha E, P142,
P324
Gonen O, P7, P236, P237
Goodkin DE, P132
Goodman A, P5, P14, P15, P86,
P308
Graham C, P139
Greene C, 60
Greenstein JI, P235
Greg C, P205, P206
Gregora E, 43
Gregory T, P332
Grekova M, 60
Griffin C, P73, P85, P12
Grive E, 51
Grop A, P6, P145, P146, P251,
P252, P253, P254, P262
Grossman R, 29
Grossman RI, P7, P236, P237
Grumser Y, P221
Guclu A, P169
Guerrero A, P35
Guerrero M, P138
Guerrero R, P54
Guglielmo A, P13
Guidi L, P230, P233
Guillet M, 2
Gur M, P148
Gutierrez A, P26
Haase VG, P58, P174, P175, P212,
P283, P284, P285, P286
Hache J, P200
Hadjimichael O, P63, P185, P191
Hadjiprocopis A, P73
Hahn D, P133
Haines JL, 57
Hale G, P157
Halvatzis N, P222
Hamm S, P94
Harboe H, P137
Hardan Y, P178
Hares D, P50
Haritanti A, P222
Hartmann S, P171
Hartung H, 23, P107, P307, P341
Hartung HP, 30
52
Hatzidaki G, P209
Hauser S, 5, 57
Hautecoeur P, P330
Havrdová E, P8, 43, P179, P189
Hawkins C, P143, P144, P224,
P225
Hawkins S, P139
Hawkins SA, P158, P302
Hebrink DD, P140
Heesen C, P34, P171, P266
Heggarty SV, P139
Heidenreich F, P5, P86
Heinzlef O, P207, P208
Hemmer B, P91, P257
Henriques I, P282
Hens M, P54
Hernandez JJ, P301
Hernández M, P35
Hernández-Regadera JJ, P333
Herrera LC, P67
Herve V, P42, P342
Hey W, P335
Hickman SJ, 4, P75, P76, P77
Hidalgo J, P166
Hila S, 59
Hill J, P136
Hillert J, P9, P137
Hintzen R, P93, P173
Hippel C v, P201
Hocherman S, P178
Hochfilzer A, P256
Hodengreber V, P110
Hofbauer M, 16
Hoffman G, 59
Hoffmann F, 15
Hogan A, P117
Hohlfeld R, 16, 40
Holger S, P335
Holtmann B, 41
Homeister JW, P111
Hommes O, 23, 30, 68, P242
Hoogervorst E, P172
Hooper D, P92, P113, P310
Horakova D, 43, P8, P189
Horno R, P134
Houzvickova E, P216
Hradilek P, P96, P190, P229
Hughes LE, P267
Humle Jørgensen S, P294
Hutchinson M, P64, P176
Iannucci G, P233
Ibarrola D, P69
Ichikawa HT, P115
Idiman E, P180, P181
Iliu-Florin T, P198
Ilves A, P88
Incomin G, P306
Ingle G, P246
Inglese M, 30, P133, P236, P237,
P238
Inzelberg R, P178
Izeboud T, P260
Izquierdo G, P56, P141, P167
Janssens C, P173
Jarmila S, P53
Jean P, P36, P37, P239
Jean-Christophe O, P198
Jean Philippe R, P36, P37, P239
Jean-yves G, P223
Jeffries N, 8, 32
Jensen J, P79
Jensen K, 24
Jensen PH, P268
Jérôme D, P223
John G, 38
Johnson KP, 22
Johnson M, 65, P202
Johnston JA, P158
Jones R, P109, P295
Jones SJ, P75, P76, P77
Jongen P, P309
Jonsson A, P291
Jordan EK, P292
Jorgensen S, P268
Juan José P, P127, P128
Julien A, P121
Kadom N, P240
Kalkers N, P172, P260
Kallmann B, P78
Kamphorst W, 3
Kanamalla US, P235
Kantarci OH, P140
Kapeller P, 6
Kapoor R, P73, P76, P296
Kappos L, 9, 15, P39, P133, P164,
P307, P334
Karabudak R, P168, P169
Karafa M, P100
Karageorgiou KE, P209
Kargadou A, P209
Kataeva G, P88
Katz M, P308
Katz T, P40
Kay T, P295
Kean RB, P113
Keir G, P11
Keogh C, P80
Kerem M, P168
Keser I, P168
Kesselring J, P201
Kesson D, P224, P225
Kevin K, P226
Khalil M, P327
Khan O, P38, P241
Khoury SJ, 44
Kieseier BC, P341
Killestein J, P93, P260
Kilpatrick TJ, 18
Kim H, P149
Kim KS, P94
King CL, P298
Kisli M-, P119
Knol D, 31
Knox K, P210
Kobylka J, 43
Koch E, P34
Koch-Henriksen N, 24
Koehler J, P335
Kollegger H, P314
Konapacki R, P20, P29, P188,
P194, P195
Kooijmans M, P5, P86, P177
Koprowski H, P310
Koptides D, P126
Koski CL, 59
Koza V, 43
Kozak T, 43
Krasensky J, P8
Kraus J, P94, P129
Krhut J, P190
Kristensen O, 24
Kristoferitsch W, P314
Krüger T, P187
Krupp LB, P211, P279
Kruse N, 1
Kürsad F, P180
Kurtuncu M, P30, P156, P319
Kuwata JM, P251
Kwiecinski H, P325
Kwok WW, 1
Kýlýnç M, P123
Kýrkalý G, P99
Kýyat A, P156
Lacerda M, P72, P278
Lacerda S, P174, P175, P212, P283,
P284, P285, P286
Ladkani D, P249
Ladurner G, P184
Lai MM, P24
Lambruschini P, P230
Lana-Peixoto MA, P57, P58, P59,
P124, P174, P175, P212, P283,
P284, P285, P286, P336
Landgraf P, P108
Langkilde A, P79, P101
Lanzillo R, P276
Laplaud DA, 2
Larsson HB, P79, P291
Lassmann H, 41
Laule C, P80
Laurent G, P182, P183
Laurent S, P36, P37
Lauritzen M, P79
Laursen H, P294
Lavier A, P304
Lavolpe V, P311
Lazeron RC, P11
Le Duff F, P49, P196
Le Page E, P49, P157, P196, P337
Lebrun C, P27, P60, P213, P214
Lechner-Scott J, P39
Lee J, P100
Lefranc D, P28, P255, P330
Leite C, P72, P278
Lenderink B, P312
Leocani L, 62, P125
Leon A, P13
León A, P138
Leon SV, P95, P320, P321
Leoni V, P9
Lepore V, P227
Leppert D, 15
Leray E, P49, P196, P337
Leteneur L, P277
Leung J, P132
Leyva L, P54, P138
Li BS, P7
Li D, 54, P81
Liem AM, P95, P321
Lienert C, P39, P164
Liguori M, P227, P311
Liguori NF, P66, P151
Lima EP, P174, P212, P283, P285,
P284, P286
Limat S, P304
Lin X, P242
Lincoff N, 67
Lincoln RR, 57
Lindberg RL, 15
Lindley J, P47
Lindsey JW, P269
Ling AK, P94
Linker RA, 41
Lino A, P336
Lisak R, P241
Livrea P, P227, P265, P311
Locatelli L, P6, P145, P146, P252,
P253, P254, P262
Lochmanova A, P96
Lolli F, P153
López C, P10
Lopez-Bresnahan M, P218
Lopez de Munain A, P142
Lopez Esteban P, P122
Losy JJ, P338, P339
Lowe JB, P111
Lozano N, P259
Lublin F, 20
Luc T, P42
Lucas M, P141
Ludden T, P130
Ludwig A, P171
Ludwin SK, 11
Luecking L, P97
Luetic G, P61, P62, P151, P152
Lugaresi A, P238
Luo J, P235
Luque G, P54, P138
Lutterotti A, P256, P315, P327
Lynn J, P26
Lyons J, P97
Maaloufova J, 43
Macedo R, P58
Maciel D, P59
MacKay A, P80
Maclurg K, P302
MacManus DG, P75, P77, P84
Maestú F, P82
MaGuire J, P80
Mahfoud A, P208
Mainer K, P190
Makar TK, 42
Malin JP, P105
Malucchi S, P150
Mancardi G, P238
Manelfe C, P69
Manni M, P203
Marc C, P332
Marc D, P42, P342
Marchi PP, P24
Marchiori PE, P336
Marie Stephane A, 19, P121,
Markovic-Plese S, P163, P340
Markowitz CM, P7
Marracci G, P109
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Marrosu M, P24, P238, P316,
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Martin R, 1, 10, 45, P98, P240,
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Martín-Serradilla J, P35
Martinelli V, 7, 30, P32, P33, P125,
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Martínez A, P324
Martinez C, P232
Martinez-Caceres EM, P166
Martínez-Yélamos A, P215, P301
Martínez-Yélamos S, P215, P301
Martini R, 41, P175
Maryline L, P182
Mass M, 66
Massaccesi L, P238
Masterman T, P9
Matejuk A, P297
Matesanz F, P138
Mathiesen HK, P291
Matí-Bonmatí L, P232
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Matthias T, P28
Mäurer M, 41, P78
Mayorga C, P54, P138
Mazzanti B, P153
Mazzeo L, P261
McCarthy A, P64, P176
McCartin J, 10
McClurg AE, P158
McDermott MP, P14, P15
McDonnell G, P139
McFarland H, 1, 8, 10, 32, 53, P98,
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McIlree C, P279
McKeon G, P109
McMurray CT, P140
McQuaid S, P158
Mechl M, P231, P287
Medova E, 43
Mehling M, P107
Melamed E, P110
Melchior B, 2
Melis CC, P316, P317, P318
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Meluzinova E, P216
Melville P, P211, P279
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Mezzapesa D, 7, P248
Michalowska-Wender G, P338,
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Miguel F, P322
Mikaeloff Y, 64, P217
Mikol D, P218
Milano E, P150
Milazzo M, P211
Millefiorini E, P6, P253, P254, P262
Miller D, 36, P133, P246, P307
Miller DH, 4, P12, P73, P75, P76,
P77, P84, P85, P157
Miller DM, 66, P177
Milo R, P40
Milonas I, P126, P222
Minier D, P205
Minneboo A, 31
Mirabella M, P3
Miszkiel KA, P12, P75, P77
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Mladek M, P171
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Mola A, P265
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Schmidt H, 6
Schmidt R, 6
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Seeldrayers P, 23, 30
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P271, P273, P344
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Turkish Multiple Sclerosis Genetics Study Group P319
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55
LATE BREAKING NEWS ABSTRACTS
LB1
VALIDATION OF DIAGNOSTIC MRI CRITERIA FOR MS AND RESPONSE
TO TREATMENT WITH INTERFERON-BETA-1A
Barkhof Fb, Rocca Mc, Francis Gd, van Waesberghe Jb, Uitdehaag Bb, Hommes Oe, Hartung Hf,
Durelli Lg, Edan Gh, Fernández Oa, Seeldrayers Pi, Sorenson Pj, Margrie Sk, Comi Gc, Filippi Mc,b
aMS-MRI centre,VU medical centre, Amsterdam, Europe, Netherlands; bIRCCS San Raffaele,
Milan, Italy; cSerono Laboratories, Rockland, Massachusetts, USA; dEuropean Charcot Foundation, Nijmegen, Netherlands; eKarl-Franzens Universität, Graz, Austria; fUniversity of Turin,Turin,
Italy; gUniversité de Rennes, Rennes, France; hHospital Carlos Haya, Malaga, Spain; iC.H.U. de
Charleroi, and Hôpital Erasme, Brussels, Belgium; jRigshospitalet, Copenhagen, Denmark;
kQuintiles Pty Limited, Sydney, Australia
Background: In the recently adopted diagnostic criteria for MS by McDonald, the modified
criteria of Barkhof have been adopted.
Objectives: To prospectively test the validity of the modified Barkhof criteria and their predictive value for IFN-beta-1a treatment response in the ETOMS study
Methods: The ETOMS study was a randomised, double-blind, placebo-controlled study of
IFN-beta-1a (i.m.) once weekly in 309 patients with a first episode consistent with demyelinating disease. Baseline MRI was assessed for the presence of gadolinium-enhancement (or
9 T2 lesions), juxtacortical, infratentorial, and 3 periventricular lesions. Conversion to CDMS
was used as the outcome parameter.
Results: Conversion to CDMS occurred in 41% of patients with gadolinium-enhancement
or 9 T2 lesions versus 11% of those without (p⫽0.017); similar comparisons were 44% vs.
31% for infratentorial (p⫽0.026), 40% vs. 35% for juxtacortical (p⫽0.413), and 41% vs. 17% for
more than 3 periventricular lesions (p⫽0.034). For the cumulative number of modified Barkhof criteria, the rate of conversion to CDMS was 25% for 1 abnormal criterion, rising to 47%
with 4 abnormal criteria. For a cut-off of 3 positive criteria, the hazard ratio for time to CDMS
was 2.3 (95% CI 1.17-4.56, p⫽0.016).While the effect of treatment seemed most evident in
patients with 4 abnormal criteria, statistically significant treatment by variable interaction
could not be detected. However, the number of patients needed to treat decreases from 50
with 2 or less criteria to 5.6 with 4 positive criteria.
Conclusions: This study confirms the validity of the modified Barkhof criteria for conversion
to CDMS, and suggests that treatment with IFN-beta-1a is more cost-effective in patients
with more abnormal criteria.
Disclosure: Most authors were consultants to Serono
Funding: Supported by the European Charcot Foundation and Serono
LB2
ANTI-MOG ANTIBODIES PREDICT EARLY CONVERSION TO CLINICALLY
DEFINITE MS IN PATIENTS WITH A FIRST DEMYELINATING EVENT.
Berger Ta, Rubner Pa, Schautzer Fb, Egg Ra, Ulmer Hc, Mayringer Ia, Dilitz Ea, Deisenhammer
Fa, Reindl Ma
aNeurology, University of Innsbruck, Innsbruck,Austria; bNeurology, County Hospital,Villach,Austria;
cBiostatistics, University of Innsbruck, Innsbruck,Austria
Background: 90% of MS patients present at onset with a clinically isolated syndrome (CIS).
Although up to 80% of these patients will convert to clinically definite MS (CDMS), the further MS disease course is unpredictable at onset for individual patients.
Objectives: New neuropathological findings, e.g. antibody-mediated demyelination, and the
concept of epitope spreading in the early disease phase, prompted us to investigate whether
the presence of serum anti-MOG and anti-MBP antibodies (abs) in patients with CIS predicts
the further disease course.
Methods: 103 consecutive patients with a CIS, confirmed by MRI and positive oligoclonal
bands in CSF, were included and followed for at least 12 months. Anti-MOG and anti-MBP
abs were measured as previously described (Reindl et al, 1999).
Results: 73 females and 30 males (mean age at disease onset: 32.0 years; mean disease duration: 50.9 months, range 12–96 months). 22 patients (21%) had serum abs against MOG and
MBP, 42 (41%) were seropositive for anti-MOG abs only, and 39 (38%) were seronegative.
Relapses occurred in only 9 (23%) seronegative patients, but in 95% of patients with abs
against MOG and MBP. Seronegative patients had their first relapse after a mean relapse free
interval of 45.1 months (range 25–83 months). In contrast, patients with initial seropositivity for anti-MOG and anti-MBP abs developed their first relapse after only 7.5 months (range
1–18 months, P<0.001). Quantitation of MRI showed higher mean numbers of T2 and Gdenhancing T1 lesions in patients with anti-MOG and anti-MBP abs compared to seronegative
patients. However, the number of MRI lesions varied in individual patients, irrespective of their
antibody status, from 2 to >9 T2 lesions and 0 to 4 Gd-enhancing T1 lesions.
Conclusions: Analysis of antibodies against MOG and MBP in patients with CIS represent
a rapid, unexpensive and precise method to identify patients with either a high or low risk
for early conversion to CDMS.This may have implications for counseling and management in
patients with a first demyelinating event suggestive of MS.
Disclosure:T Berger has nothing to disclose.
Funding:This work was supported by a grant of the Austrian Federal Ministry of Science (Nr. GZ
70.059/2-Pr/4/99).
56
LB3
NEUROREHABILITATION IN MULTIPLE SCLEROSIS CONTRIBUTES TO
FUNCTIONAL RECOVERY ACCOMPANIED BY CHANGES OF BRAIN
ACTIVITY ON FMRI—PRELIMINARY RESULTS.
Rasova K, Krasensky J, Havrdova E, Obenberger J, Zalisova M, Seidl Z
Department of Neurology, Charles University
Background: Although MS is an inflammatory demyelinating disease, which can lead to the
axonal injury and loss, neurorehabilitation may contribute to functional recovery accompanied by the changes in brain activity.
Objectives: To show changes in brain activity on fMRI and their correlation with functional
recovery.
Methods: 18 outpatients with MS were evaluated before and after individualized neurorehabilitation treatment (two sessions per week, 30 weeks) for impairment (EDSS), disability
(BI), handicap (ESS), quality of life (MSQoL) and amplitude of signal in the primary sensorimotor cortex (ASPSMC) using serial fMRI during the performance repetitive index-thumb
opposition.
Results: There were 6 men and 12 women, EDSS was 4.19, age 41.11 yrs and illness duration
11.5 yrs. 8 patients had relapsing-remitting, 4 primary progressive and 6 secondary progressive MS.The therapy led to functional recovery and positively influenced the impairment (EDSS
from 4.19 to 3.63: p<0,1), the disability (BI from 94.16 to 98.05: p<0.05), the handicap (ESS
from 7.30 to 4.25: p<0.05) and quality of life (MSQoL from 152.6 to 161.13: trend shown).
The functional recovery was accompanied by changes in ASPSMC.There was a trend towards
decreased ASPSMC after therapy (ASPSMC for right hand from 7.82 to 7.20%, for left hand
from 8.61 to 7.71%).We found two different responses to therapy: in two thirds of patients
the ASPSMC decreased, while in one third of patients it increased.We have found no relationship between functional recovery and changes in the brain activity. It was shown that
when ASPSMC in left hand changed, it changed in right hand as well during the performance
of paradigm (correlation coefficient 0.56).The therapy was not aimed at improving function
of the hands, but control of the whole body. Nevertheless, the function of the hands and
ASPSMC during the performance of the paradigm changed. It seems that neurorehabilitation
influences the function of the whole brain.
Conclusions: There is very little scientific basis for the therapy that is designed to help damaged brain circuits recover.These preliminary results show that neuorehabilitation in MS contributes to functional recovery and can be accompanied by changes of brain activity.
Disclosure: K Rasova has nothing to disclose.
LB4
TIGHT JUNCTION ABNORMALITY IN MS AFFECTS ALL CALIBRES OF
VESSEL AND CORRELATES WITH LESION ACTIVITY.
Kirk Ja, Plumb Jb, Mirakhur Mb, McQuaid Sb
University, Belfast, Northern Ireland, United Kingdom; bNeuropathology, Royal
Victoria Hospital, Belfast, Northern Ireland, United Kingdom
aPathology, Queen’s
Background: Increased blood-brain barrier (BBB) permeability observed in MS has been
linked to pathological change in the tight junctions (TJ) and vesicular transport of vascular
endothelium.
Objectives: This study quantifies the pathological changes in TJs which we have recently
reported in MS, including their uneven distribution and the relation between abnormal TJ and
BBB leakage.
Methods: Frozen sections from plaque and normal appearing white matter (NAWM) in 14
post-mortem(PM) cases of MS were studied together with white matter from 6 neurological
and 5 normal controls. Using single and double immunofluorescence and confocal microscopy
the TJ-associated proteins zonula occludens-1 (ZO-1) and occludin were examined across
lesion types and tissue categories, and in relation to fibrinogen leakage. Confocal image datasets
were analysed for 2198 MS and 1062 control vessels.
Results: Significant differences in the extent of TJ abnormalities (i.e. beading, interruption,
absence or redistribution of fluorescence signal, separation or opening of junctions) were
detected between the different lesional types in MS and between MS and control white matter.They were frequent in oil-red O(ORO) + ‘active’ plaques, affecting 42.5% of vessels, but
less frequent in ORO- ‘inactive’ plaques (22.8%) or NAWM (13.1%) and in both normal (3.9%)
and neurological controls (9.5%).A similar pattern was found irrespective of the size of vessels examined. In both NAWM and inactive lesions, dual-labelling showed that those with the
most TJ abnormality had the greatest fibrinogen leakage.This was most apparent in active
lesions where 41% of vessels showed severe leakage.
Conclusions: TJ abnormality affects vessels of all sizes, suggesting a diffusable chemical
(?cytokine) cause. It occurs in lesional and non-lesional white matter, being most severe where
there is evidence of active demyelination. Disruption of TJs, affecting both paracellular and
transcellular pathways probably contributes to the BBB leakage detected in this study.The
finding of TJ abnormality and BBB leakage in ‘inactive’ lesions points to a failure of effective
and complete TJ repair or to the continuation of a pathological process. In NAWM it suggests either pre-lesional change or white matter damage secondary to remote lesions.
Disclosure: J Kirk has nothing to disclose.
Funding: JP is supported by The Irish Brain Research Foundation. Pilot studies were supported by
the MS Society of GB & NI.
LATE BREAKING NEWS ABSTRACTS (continued)
LB5
SINGLE CENTRE, DBPC, RANDOMISED TRIAL OF INTERFERON␤ 1B IN
PRIMARY PROGRESSIVE AND TRANSITIONAL PROGRESSIVE MULTIPLE
SCLEROSIS:AN EXPLORATORY PHASE II STUDY.
Montalban Xa, Brieva La,Tintore Ma, Borras Ca, Rio Ja, Nos Ca,Aymerich Xb,Alonso Jb,
Horno Ra,Vicente Ma, Rovira Ab
aClinical Neuroimmunology Unit, Hospital Universitari Vall d, Barcelona, Spain; bMagnetic Resonance Unit–IDI, Hospital Universitari Vall d, Barcelona, Spain
Background: Beneficial effects of interferon␤ have been shown only for patients in the
relapsing phase of MS as its role in the treatment of SPMS patients still remains controversial.The single phase II randomized controlled trial on PPMS using IFN␤ 1a(IM) shows no significant treatment effect on EDSS though some effect on T2 lesion load.
Objectives: To investigate safety and efficacy hints of interferon␤ 1b given to patients with
primary and transitionalprogressive multiple sclerosis (PPMS and TPMS).
Methods: 73 patients (49 PPMS, 24 TPMS) with EDSS scores of 3.0 to 7.0, were randomized to receive 8 million IU of IFN␤ 1b or placebo every other day, subcutaneously for 2
years. Safety parameters including the Ashworth spasticity, Krupp fatigue and Depression
Inventory scales and blood tests were performed three monthly. Clinical outcomes (EDSS
and MS Functional Composite—MSFC) were also performed three monthly and the Sickness Impact Profile six monthly. MRI measures (T2 and T1-weighted brain lesion load, brain
parenchymal fraction, active lesions, spinal cord atrophy, MTR and spectroscopy) and neuropsychological assessment (BRNB) were done annually.
Results: Adverse events significantly associated with IFN␤ included injection-site reaction,
flu-like symptoms and lymphopenia. One patient on placebo died of pulmonary infection. In all,
96% of the patients reached study end and 93% completed the treatment period.Treatment
groups were comparable on all baseline variables.The proportion of patients with confirmed
progression measured by EDSS at 3 months was 27.8% in the IFN arm and 37.8% in the
placebo arm (p⫽0.3135). Statistically significant differences were found for MSFC (PASAT 3”,
9-HPT and AI (p⫽0,03),T2 (p⫽0.006) and T1 (p⫽0.001) lesion load and number of active
lesions (p⫽0.005) in favor of the IFN-treated group.
Conclusions: IFN␤ 1b is safe in treating patients with PPMS and TPMS. Our study seems to
be the first indicating a beneficial effect of IFN␤ in these patients.
Disclosure: X Montalban has nothing to disclose.
Funding:Trial supported by Schering España SA (of Schering AG, Germany)
LB7
MULTIPLE SCLEROSIS DOCUMENTATION SYSTEM—MSDS 2.0
Eulitz Ma, Kugel Ta, Muraro PAb, Pette Ma
Universitaet, Dresden, Germany; bNIB/NINDS, NIH, Bethesda, Maryland,
USA
aNeurologie,Technische
Background: The long and variable course of MS, as well as the individual and unpredictable
response to currently available immune-modifying treatments require a detailed and standardized patient record. Furthermore, the systematic collection of data on large cohorts of
consecutive patients may help to correlate clinical information with basic research.Although
the development of database programs to monitor MS patients started almost thirty years
ago, no single application has gained widespread use so far.
Objectives: To develop a modular electronic patient record supporting both the daily care
of patients and the collection of specific information on MS.
Methods: MSDS is a SQL (structured query language) database.A multilingual (German, English; Italian and Spanish in preparation), graphical user interface allows easy data input and
output. Client-server architecture optimizes MSDS for using it in local area networks.
Results: Since its introduction in 12/2001, MSDS has been distributed to 25 hospitals (16
universities).Through MSDS users recorded and managed visiting dates, patient history (complaints, relapses), physical examination findings, and results of blood and CSF chemistry, evoked
potentials and MRI. MS diagnosis can be specified according to criteria by Poser (applied automatically), by McDonald and by Lublin/Reingold. Clinical scores calculated by MSDS comprise
the EDSS, the MSFC, and the Scripps NRS. In general, data input is standardized (pull-down
menus).Whenever required, specific details can be added as free text. Data consistency is
controlled by internal check mechanisms. Multiple reports describe the individual disease
course, as well as the local patient population. In addition to these built-in features, individual queries can be designed to retrieve specific information. Correspondence to practitioners is supported by MSDS.Additional features include a pedigree generator, a bio-sample database and a study-protocol editor.To support the building of a national MS registry, the present
version of MSDS automatically keeps a consensus minimal data set of each patient up-todate. Current users have found MSDS user-friendly and well suited to accurately describe the
clinical aspects of MS.
Conclusions: MSDS may provide an improved platform for clinical documentation of MS
and facilitate international standardization.
Disclosure: M Pette has nothing to disclose.
Funding: Supported by Gemeinnuetzige Hertie-Stiftung
LB6
SUCCESSFUL TREATMENT WITH IFN-␤1B IN RR MS PATIENTS IS ASSOCIATED WITH AN INCREASE IN THE NUMBER OF IL-10 PRODUCING (REGULATORY) CD4 +T CELLS.
van Boxel-Dezaire Aa,b, Smits Ma, Uitdehaag Bb, Polman Cb, Nagelkerken La
aDivision of Immunological and Infectious Diseases,TNO Prevention and Health, Leiden, Netherlands; bDepartment of Neurology,Vrije Universiteit Medical Center,Amsterdam, Netherlands
Background: Although IFN-␤ is now widely used for treatment of MS, its mode of action
still remains unclear; recent studies do not support a shift in the Th1/Th2 balance. In vitro
studies show that type I interferons induce the differentiation of Tregulatory-1 (Tr1) cells and
the survival of CD4+CD25+ T cells, which are both recently described suppressor T cells able
to produce IL-10.
Objectives: The aim of the present study was to investigate whether IFN-␤1b therapy induces
IL-10 in a general fashion or in a specific (regulatory) T-cell subset only. In addition, it was evaluated whether differential effects on IL-10 production by peripheral blood monocytes, CD4+
or CD8+ T cells could be correlated with clinical efficacy of IFN-␤1b treatment.
Methods: Based on EDSS-progression and the number of relapses and steroid interventions
in the 2 years before initiation of IFN-␤1b treatment compared with those in the 2 years
after initiation of treatment, 24 RR MS patients were classified as responders (15) and nonresponders (9). Using intracellular cytokine staining techniques, the effect of IFN-␤1b after
0, 3 and 6 months of treatment was studied on the number of IL-10 producing CD8+ T cells,
CD4+ (CD25+) T cells and monocytes.
Results: Numbers of IL-10 producing CD4+ T cells were significantly decreased prior to
treatment. Remarkably, after 3 and 6 months of treatment a significant increase in the number of such T cells could be found in the clinical responders only. In contrast, treatment
decreased numbers of IL-10 producing monocytes in both responders and nonresponders
and did not affect numbers of CD8+ T cells that produced IL-10. In a subgroup of the responders (7 out of 15), the effect of IFN-␤1b treatment was also studied on CD4+CD25+ T cells.
Notably, a significant increase in the number of IL-10 producing CD4+CD25+ T cells could be
observed after 6 months of treatment.
Conclusions: Enhancement of the number of CD4+CD25+ T cells that produce IL-10 may be
an important mechanism in the therapeutic effect of IFN-␤ in RR MS.
Disclosure:A van Boxel-Dezaire has nothing to disclose.
Funding: Supported by the Dutch Foundation for the support of MS Research, grant 94-175 MS;
The Multiple Sclerosis Center for Research and Care,Amsterdam,The Netherlands
57
Maps of Downtown Baltimore
1. Baltimore Marriott
Waterfront Hotel
700 Aliceanne Street
Baltimore, MD 21202
Phone: 410-385-3000
Fax: 410-895-1900
2. Courtyard by Marriott
Inner Harbor
1000 Aliceanne Street
Baltiomore, MD 21202
Phone: 443-923-4000
Fax: 443-923-9970
3. Baltimore Marriott
Inner Harbor
110 South Eutaw Street
Baltimore, Maryland 21201
Phone: 410-962-0202
Fax: 410-625-7892
4. Radisson Plaza Hotel
Baltimore Inner Harbor
20 West Baltimore Street
Baltimore, MD 21201
Hotel Phone: 410-539-8400
Hotel Fax: 410-332-4229
5. Renaissance
Harborplace Hotel
202 East Pratt Street
Baltimore, MD 21202
Phone: 410-547-1200
Fax: 410-539-5780
6. Sheraton Inner
Harbor Hotel
300 South Charles Street
Baltimore, MD 21201
Phone: 410-962-8300
Fax: 410-962-8211
7. Wyndham
Baltimore Inner Harbor
101 West Fayette Street
Baltimore, MD 21201
Phone: 410-752-1100
Fax: 410-752-0832
58
Social Events
National Aquarium of Baltimore
Pier 3 at 501 E. Pratt Street, Phone: 410-576-3800
Reception and Buffet Dinner
Thursday, September 19th
7:30 pm–10:30 pm
Begin your evening with a leisurely stroll through the aquarium
exhibits, enjoying a glass of wine and selections of hors d’oeuvres
along the way. Dazzling tropical fish, a giant Pacific octopus, electric
eels, graceful stingrays, playful puffins, two-toed sloths, red-bellied
piranhas, poison dart frogs and a giant anaconda are among the more
than 10,000 marine and freshwater animals waiting to say hello. The
self-guided tour ends with a candlelight dinner buffet.
Welcome Reception at the Baltimore
Marriott Waterfront Hotel
700 Aliceanna Street, Phone: 410-385-3000
Wednesday, September 18th
7:00 pm–9:00 pm
On opening day, the Steering Committee invites all
conference delegates to an informal “Welcome
Reception” at the Baltimore Marriott Waterfront
Hotel. Meet new friends, renew acquaintances, and
congratulate the fine young investigators who presented their research that afternoon.
B&O Railroad Museum
901 W. Pratt Street at Poppleton Street, Phone: 410-752-2490
Reception and Buffet Dinner
Friday, September 20th
7:30 pm–10:00 pm
Affiliated with the Smithsonian Institution, the B&O Railroad Museum is
dedicated to the preservation and interpretation of American railroading—
especially the historic Baltimore and Ohio (B&O) line. You’ll enter the
museum through Mt. Clare Station, built in 1851, and proceed to the 1884
Baldwin Roundhouse—a 22-sided room with a 136-foot high ceiling!
Dinner and dancing are the order of the evening with the opportunity to
stroll through some of the locomotive and artifacts exhibits.
Committee Reception and Dinner (by invitation)
Baltimore Museum of Industry
1415 Key Highway at Lawrence Street
Phone: 410-727-4808
Saturday, September 21st
7:00 pm–10:00 pm
Complimentary round-trip transportation
will be available for all social events.
59
Next Year’s Meetings
ACTRIMS 2003
October 19
San Francisco
8th Annual Meeting of the Americas Committee
for Treatment and Research in Multiple Schlerosis
ECTRIMS 2003
September 17–20
Milan
19th Congress of the European Committee
for Treatment and Research in Multiple Schlerosis
The National Multiple Sclerosis Society
proudly introduces the
The National MS Society has long been a resource for health professionals providing care to people
with multiple sclerosis.The new Professional Resource Center, which houses the most comprehensive
library of MS information in the world, offers multidisciplinary expertise on MS disease process and
management, opportunities for clinial affiliation, and a range of educational programs and materials.
Physicians are invited to consult via email with MS specialist colleagues
who serve on our Medical Advisory Board:
MD_info@nmss.org
Allied health professionals are invited to consult via email with MS specialist colleagues:
HealthProf_info@nmss.org
Questions are also welcome at our toll-free number:
1-866-MS-TREAT ( 678-7328 )
Visit our website: nationalmssociety.org/PRC.asp
An expert source of
MS information for
healthcare professionals
60
Travel Information
Reservation Assistance
Targa Tours can offer discounts with American Airlines
and US Airways, and will also search for the lowest available fare on ANY airline serving Baltimore. A US$20
service fee applies.
Call toll-free: 1-800-756-7957 (From outside the USA
or within the Chicago metro area, call 312-541-0780)
Fax: 312-541-0783
E-mail: targatours@aol.com
On-line: targatours.com
Airport/Airlines
Baltimore/Washington
International Airport
Ronald Reagan Washington
National Airport
Washington Dulles International Airport
American Airlines
Frontier Airlines
Southwest Airlines
US Airways
410-859-7111
703-417-8000
703-572-2700
800-433-7300
410-694-6220
410-290-7001
800-428-4322
To the Airport
The Airport Shuttle, Inc.
Baltimore Airport Shuttle
Butler Transportation
BWI Airport Shuttle
410-381-2772
410-821-5387
410-732-5098
800-258-3826
Taxi and Limousine Services
Yellow Transportation
American Limousines, Inc
Carey Limousine/Baltimore
Prime Time Sedan and Limo Service
410-727-7300
410-522-0400
410-880-0999
443-562-0067
Trains
MARC Commuter trains
(Baltimore/Washington)
AMTRAK
410-539-5000
800-872-7245
Visitor Services
Baltimore Tickets
888-225-8849
Emergency Phone Numbers
Police
Fire
Ambulance
911
911
911
61
7th Annual Meeting of the
Americas Committee for
18th Congress of the
European Committee for
September 18 –21, 2002
Baltimore Marriott
Waterfront Hotel
700 Aliceanna Street
Baltimore, Maryland, USA
Tel: 212-476-0465
Fax: 212-661-9735
E-mail: ae2002@nmss.org
www.actrimsectrims2002.nmss.org
This program is offered
in collaboration with the
National Multiple Sclerosis Society

Final Program,Abstract Listing and Meeting Information

Transcription

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