001_170_Suppl_II_05_JON 31.05.2005 14:55 Uhr Seite 1
`
`J Neurol (2005) 252 [Suppl 2]: II/1–II/51
`DOI 10.1007/s00415-005-2001-7
`
`Fifteenth Meeting of the
`European Neurological Society
`18–22 June 2005, Vienna, Austria
`Symposia and Free Communications
`
`The abstracts have been reviewed by:
`Z. Argov, V. Dietz, M. Donaghy, C. Elger, F. Fazekas, J. M. Ferro,
`C. Krarup, M.-H. Marion, I. Milonas, G. Moonen, E. Nobile-Orazio,
`V. Planté-Bordeneuve, G. Said, R. Soffietti, A. Steck, E. Tolosa,
`J. Valls-Solé, Y. von Cramon
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`II/2
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`Contents
`
`Presidential symposium
`Advances in multiple sclerosis
`
`II/3
`
`Symposia
`Imaging the human mind II/4
`Cell and gene therapy
`II/5
`Controversies in neurology
`
`II/6
`
`FREE COMMUNICATIONS
`Oral Sessions
`
`Session 1: Cerebrovascular disorders 1
`Session 2: Cerebrovascular disorders 2
`Session 3: Clinical neurophysiology 1
`Session 4: Clinical neurophysiology 2
`Session 5: Epilepsy 1
`II/14
`Session 6: Epilepsy 2
`II/15
`II/17
`Session 7: Motor neuron disease 1
`II/18
`Session 8: Motor neuron disease 2
`Session 9: Multiple sclerosis 1
`II/20
`Session 10: Multiple sclerosis 2
`II/22
`Session 11: Muscle and neuromuscular junction disorders
`Session 12: Muscle disorders 2
`II/25
`II/26
`Session 13: Cerebrovascular disease 3
`II/28
`Session 14: Cerebrovascular disease 4
`II/29
`Session 15: Extrapyramidal disorders 1
`II/31
`Session 16: Extrapyramidal disorders 2
`Session 17: Neuro-ophthalmology and vestibular disturbance
`Session 18: Infections of the nervous system II/34
`Session 19: Neurogenetics 1
`II/35
`Session 20: Neurogenetics 2
`II/37
`Session 21: Multiple sclerosis 3
`II/38
`Session 22: Multiple sclerosis 4
`II/40
`Session 23: Higher function disorders 1
`Session 24: Higher function disorders 2
`Session 25: Multiple sclerosis 5
`II/45
`Session 26: Peripheral neuropathy
`II/47
`Session 27: Neuro-oncology
`II/49
`
`II/23
`
`II/32
`
`II/8
`II/10
`II/11
`II/12
`
`II/41
`II/43
`
`II/58
`
`II/55
`Epilepsy
`General neurology
`Genetics
`II/59
`Headache
`II/60
`II/62
`Multiple sclerosis
`Neurobiology
`II/66
`Neuro-oncology
`II/68
`Neuro-ophthalmology
`Rehabilitation II/72
`
`II/70
`
`II/74
`
`Poster session 2
`Cerebrovascular disorders
`Epilepsy
`II/79
`General neurology
`Genetics
`II/85
`Infection II/86
`II/88
`Motor neuron disease
`Multiple sclerosis
`II/90
`
`II/82
`
`Poster session 3
`Cerebrovascular disorders
`Extrapyramidal disorders
`General neurology
`II/101
`Headache
`II/103
`Higher function disorders
`Multiple sclerosis
`II/108
`Neurophysiology
`II/113
`
`II/95
`II/98
`
`II/105
`
`Poster session 4
`Cerebrovascular disorders
`Extrapyramidal disorders
`General neurology
`II/122
`Higher function disorders
`Multiple sclerosis
`II/126
`Muscle disorders
`II/132
`Peripheral neuropathy
`II/134
`
`II/115
`II/119
`
`II/125
`
`II/137
`
`II/144
`
`Poster session 5
`Cerebrovascular disorders
`Neurophysiology
`II/142
`Extrapyramidal disorders
`Multiple sclerosis
`II/146
`Muscle disorders
`II/149
`Pain II/153
`Peripheral neuropathy
`Sleep disorders
`II/158
`
`II/154
`
`Abstracts for Poster Sessions
`
`Poster Session 1
`II/51
`Child neurology
`Cerebrovascular disorders
`
`II/53
`
`Author index
`
`II/160
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`O139
`Long-term follow-up of patients treated with glatiramer acetate: a multi-
`centre, multi-national extension of the European/Canadian double-blind,
`placebo-controlled, MRI-monitored trial
`M. Rovaris, G. Comi, M. Rocca, D. Ladkani, P. Valsasina, E. Pieri, G. Shifroni,
`J. S. Wolinsky, M. Filippi
`Ospedale San Raffaele, TEVA Pharmaceutical Industries, TEVA Italia, The
`University of Texas (Milan, I; Petah Tiqva, IL; Netanya, IL; Houston, USA)
`
`Objective: To investigate the long-term evolution of clinical and MRI find-
`ings in patients with relapsing-remitting (RR) multiple sclerosis (MS) who
`participated in the glatiramer acetate (GA) 9003 trial, in order to explore
`the correlates of long-term GA treatment.
`Background: GA is effective in reducing clinical and MRI activity in
`RRMS. Serial MRI data on a long-term basis were never obtained for large
`samples of GA-treated patients.
`Design/Methods: The 9003 study consisted of two consecutive phases,
`each lasting nine months. The first treatment phase was randomized, dou-
`ble-blind and placebo-controlled. The second was an active treatment
`phase for all patients. Treatment consisted of daily administration of 20 mg
`GA subcutaneously. All patients underwent brain MRI at screening (to be
`included, they had to have one or more enhancing lesions), baseline, every
`month during the double-blind phase and every three months during the
`open-label phase. Clinical assessment included neurological visits with
`Expanded Disability Status Scale (EDSS) score rating. For the long-term
`follow-up (LTFU), dual echo, pre- and post-gadolinium T1-weighted brain
`MRI scans were obtained with the same acquisition scheme as for the orig-
`inal trial and a neurological assessment was performed. Total T2-hyperin-
`tense and T1-hypointense lesion volumes, as well as normalized brain vol-
`umes (NBV) and percentage BV changes (PBVC), were measured.
`Results: One hundred and forty-two of 224 patients who completed the
`9003 study (63.4 %) underwent the LTFU after a mean period of 5.8 years.
`Seventy-three of them had been treated with GA since the study initiation.
`At 9003 baseline, there were no significant differences between patients
`who subsequently came at LTFU and those who did not.Among the former
`ones, MRI measures of disease burden and activity, as well as brain volume
`changes, at LTFU did not significantly differ between patients originally
`assigned to placebo and those who were always treated with GA. The pro-
`portion of patients who did not reach relevant locomotor disability (EDSS
`≥6.0) at LTFU was significantly greater in patients treated with GA during
`the first nine months of the 9003 trial (p = 0.03). PBVC between baseline
`and LTFU was significantly correlated with T2 lesion volume at study en-
`try.
`
`Conclusions: This study indicates that the earlier initiation of GA treat-
`ment in patients with active RRMS might have a favorable impact on the
`long-term disease evolution.
`
`O140
`A phase II randomised, double-blind, placebo-controlled study to evalu-
`ate the preliminary efficacy and safety of abatacept, a selective co-stimu-
`lation modulator, in patients with relapsing-remitting multiple sclerosis
`C. Fieschi, O. Andersen, C. Markowitz, J. Simon, D. Hough, T. McCann, D.
`Hagerty, C. Gruber
`University of Roma ‘La Sapienza’, Sahlgrenska University Hospital, Hospi-
`tal of University of Pennsylvania, University of Colorado Health Sciences
`Center, Bristol-Myers Squibb Company (Rome, I; Göteborg, S; Philadel-
`phia, Denver, Princeton, USA; Braine-L’Alleud, B)
`
`Background: Abatacept selectively modulates the co-stimulatory signal re-
`quired for the full activation of T-cells expressing CD28. Abatacept has
`demonstrated efficacy in experimental autoimmune encephalomyelitis, a
`surrogate animal model thought to be predictive of human multiple scle-
`rosis (MS).
`Objective: To evaluate the efficacy and safety of abatacept in patients
`with relapsing-remitting MS (RRMS).
`Methods: This was a randomized, double-blind, placebo-controlled co-
`hort study in RRMS male and female patients aged 18–58 years. Patients
`had definite MS, an Expanded Disability Status Scale (EDSS) ≤6 (inclu-
`sive), at least 1 relapse in the preceding 2 years (clinically stable for 2
`months prior to treatment) and at least 1 gadolinium T1 (GdT1) enhanc-
`ing lesion on magnetic resonance imaging. Patients were randomized into
`1 of 3 cohorts receiving: abatacept 2 mg/kg, abatacept 10 mg/kg or placebo
`by infusion on Days 1, 15, 29, and then every 4 weeks until Day 197.
`Results: The study terminated early due to an increase in patients with
`≥5 new GdT1 lesions in the abatacept 2 mg/kg group. The cohort design re-
`sulted in excess patients in the abatacept 2 mg/kg group with poor baseline
`prognostic factors; 80 % of patients with > 10 GdT1 enhancing lesions were
`randomized to abatacept 2 mg/kg. A total of 127 of a planned 219 patients
`
`II/41
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`were randomized and received ≥1 infusion of study medication. Com-
`pared with abatacept 2 mg/kg and placebo, abatacept 10 mg/kg-treated pa-
`tients had fewer new (1.5 vs. 8.0 vs. 5.5) and total GdT1 enhancing lesions
`(3.0 vs. 13.0 vs. 8.5), fewer protocol defined exacerbations (20.6 vs. 56.6 vs.
`30 %), a lower mean annualized relapse rate (0.38 vs. 1.49 vs. 0.73), a greater
`proportion free from enhancing activity (12 (36, 4 %) vs. 7 (13, 2 %) vs. 6
`(15 %)) and with improved EDSS (44.1 vs. 17.0 vs. 25 %).
`Conclusions: The cohort design contributed to clinically important
`treatment group imbalances at baseline that precluded conclusive assess-
`ment of the safety and efficacy profile of abatacept in RRMS. However,
`while the abatacept 2 mg/kg group experienced more MS-related symp-
`toms and relapses, data from the abatacept 10 mg/kg cohort were sugges-
`tive of reduced disease activity.
`
`O141
`FTY720 in relapsing MS: results of a double-blind placebo-controlled trial
`with a novel oral immunomodulator
`L. Kappos, E. W. Radü, J. Antel, G. Comi, X. Montalban, P. O’Connor, O.
`Bettoni-Ristic, T. Haas, R. Preiss, A. Korn
`on behalf of the FTY720D2201 Study Group
`
`FTY720 is an oral immunomodulator (sphingosine-1 phosphate receptor
`(S1P) modulator) that reversibly sequesters tissue damaging T and B cells
`away from blood and the central nervous system to peripheral lymph
`nodes. FTY720 has demonstrated both preventive and therapeutic efficacy
`in several animal models of MS.
`Methods: We report the clinical and MRI results of an international,
`multicenter, double-blind study to evaluate efficacy, safety and tolerability
`of two doses of FTY720 and placebo (PL). 281 patients with active relaps-
`ing MS were randomized to receive PL (n = 93), 1.25 mg (n = 94) or 5.0 mg
`FTY720 (n = 94) q. d. for 6 months. Patients had monthly cranial MRI scans
`and 3-monthly neurological assessments by a neurologist otherwise not
`involved in their care.
`Results: Clinical and MRI baseline characteristics were balanced
`amongst groups. The primary outcome, mean (median) total number of
`Gadolinium(Gd)-enhancing lesions in monthly post baseline MRI scans
`was 14.8 (5.0), 8.4 (1.0) and 5.7 (3.0) for PL, FTY 1.25 and 5.0 mg groups
`(p < 0.001 1.25 vs. PL, p = 0.006 5.0 vs. PL). Similar, clearly significant effects
`favoring both FTY720 groups vs. PL were found for Gd-enhancing lesion
`volume, new T2 lesions and change in T2 lesion volume (only 5 mg qd sign.
`better than PL). The proportion of relapse-free patients (70.0, 86.0 and
`86 %; p = 0.007 1.25 mg vs. PL, p = 0.008 5 mg vs. PL), annualized relapse
`rate (0.77, 0.35 and 0.36) and time to first relapse were significantly better
`in both FTY720 groups vs. PL. There was no compelling dose-related dif-
`ference in efficacy on MRI or clinical endpoints. Treatment was generally
`well tolerated with 255 (91 %) of patients completing study and 249 (89 %)
`electing to continue into the extension phase where PL patients were
`rerandomized to one of the active drug dose groups. Adverse events were
`more common in the 5 mg group, with the most frequently reported
`(> 15 % patients) being mild headaches and nasopharyngitis.
`Conclusion: This proof of concept study demonstrated efficacy of
`FTY720 on both MRI and relapse-related endpoints. Both the efficacy and
`safety evaluations strongly suggest that FTY720 has the potential to be an
`efficacious disease modifying treatment for relapsing forms of MS with the
`additional benefit of once daily oral administration.
`Study supported by Novartis Pharma AG Basel.
`
`Session 23
`
`Higher function disorders 1
`
`O142
`Interaction between CYP19-aromatase and butyrylcholinesterase genes
`increases Alzheimer’s disease risk
`J. Infante, J. Riancho, I. Mateo, E. Rodríguez, J. Berciano, O. Combarros
`University Hospital Marques Valdecilla (Santander, E)
`
`Background: Biological evidence suggests that the enzymes aromatase
`(CYP19) and butyrylcholinesterase (BCHE) play a role in disrupting the
`cholinergic neurotransmission observed in Alzheimer’s disease (AD).
`CYP19 is a critical enzyme in the peripheral synthesis of estrogens, which
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