J Neurol (2012) 259 (Suppl 1):S1–S236 DOI 10.1007/s00415-012-6524-4 ABSTRACTS Twenty-second Meeting of the European Neurological Society 9–12 June, 2012 Prague, Czech Republic Symposia and Free Communications The abstracts have been reviewed by: O. Abramsky, C. Angelini, P. Annunziata, F. Antonaci, Z. Argov, A. Arzimanoglou, T. Back, O. Bajenaru, E. Bartels, J. Bednarˇik, P.D. Berlit, K. Bhatia, P. Boon, T. Brandt, B. Brochet, M.J. Brodie, C. Caltagirone, P. Canha˜o, H. Cock, C. Colosimo, G. Comi, L. Cunha, M. de Carvalho, J. de Keyser, J.L. De Reuck, M. de Visser, L. Deecke, R. Dengler, S. Di Donato, M. Dieterich, V. Dietz, C. Elger, M. Eraksoy, F. Fazekas, J. Ferro, M. Filippi, D. Galimberti, T. Gasser, A. Grau, W. Grisold, U. Gschwandtner, O. Hardiman, H.P. Hartung, W. Heide, C. Helmchen, G. Ickenstein, R. Jech, P. Kanˇovsky´, P. Kalvach, L. Kappos, A. Keyser, B. Kieseier, T. Klopstock, C. Krarup, G. Lammers, S. Laureys, G. Mayer, S.I. Mellgren, G. Meola, R. Milo, I. Milonas, X. Montalban, O. Nascimento, E. Nobile-Orazio, L. Nobili, W.H. Oertel, M. Onofrj, A. Palla, S.G. Papageorgiou, D. Pareyson, Y. Parman, M. Partinen, H.W. Pfister, W. Poewe, D. Pohl, P. Portegies, H. Reichmann, P.F. Reyes, M.A. Rocca, A. Rossetti, P.M. Rossini, J. Roth, E. Ru˚zˇicˇka, G. Said, M. Sandberg-Wollheim, J. Santamaria, E. Scarpini, N. Schaeren-Wiemers, B. Schalke, P. Schestatsky, E. Schmutzhard, J. Schoenen, A. Sena, V. Silani, A. Siva, P. Soelberg-Sørensen, R. Soffietti, C. Sommer, K. Sˇonka, A. Steck, G. Stoll, A. Sumner, E. Tolosa, A. Toscano, K.V. Toyka, H. Tumani, J. Valls-Sole´, M. Veloso, A. Vendelho, P. Vermersch, M.J. Viana Baptista, R.D. Voltz, J. Vymazal, M. Weller We would like to thank the reviewers for their precious help and assistance. 123 S2 J Neurol (2012) 259 (Suppl 1):S1–S236 Presidential Symposium POSTER SESSIONS Parkinson Syndrome: an everlasting challenge 45–47 Poster session 1 Symposia Multiple sclerosis: disease modifying treatment I P336–P360 Joint ENS-CNS Symposium—Audio & video media in evaluation of Cerebrovascular disorders I P361–P380 movement disorders 100–104 Neuro-imaging P381–P406 Symposium—Stem cells ready for clinical practice 106–109 Movement disorders P407–P424 Symposium—Neuro-imaging and early diagnosis of General neurology P425–P451 neurological diseases 110–113 Preclinical biology P452–P456 Symposium—MS and acquired demyelinating disorders 143–146 Symposium—Neurology and sleep-wake disorders 147–150 Poster session 2 Symposium—Knowledge exchange programme in neurology between European and Indian Clinicians 158–161 Multiple sclerosis: disease modifying treatment II P457–P482 Cerebrovascular disorders II P483–P498 Peripheral neuropathy P499–P524 FREE COMMUNICATIONS Dementia I P525–P541 Motor neuron disease P542–P555 General neurology II P556–P570 Oral sessions Child neurology P571–P578 Session 1: Multiple sclerosis: Poster session 3 Imaging/neurophysiology O192–O197 Session 2: Epilepsy I O198–O203 Multiple sclerosis: variants and symptomatic treatment P579–P602 Session 3: Movement disorders I O204–O209 Cerebrovascular disorders III P603–P619 Session 4: Neuro-ophthalmology O210–O215 Pain and headache P620–P644 Session 5: Multiple sclerosis II O216–O221 Dementia II P645–P661 Session 6: Epilepsy II O222–O227 Epilepsy P662–P677 Session 7: Movement disorders II O228–O233 Neurogenetics P678–P692 Session 8: Imaging O234–O239 Clinical neurophysiology P693–P700 Session 9: Movement disorders III O240–O245 Session 10: Sleep disorders O246–O251 Poster session 4 Session 11: General neurology O252–O256 Session 12: Multiple sclerosis III O258–O263 Multiple sclerosis: miscellaneous P701–P729 Session 13: Cerebrovascular disorders I O264–O269 Cerebrovascular disorders IV P730–P752 Session 14: Neuromuscular disorders O270–O275 Muscle disorders P753–P768 Session 15: Child neurology O276–O281 Neurorehabilitation P769–P780 Session 16: Neuro-oncology O282–O287 Neuro-oncology P781–P790 Session 17: Multiple sclerosis IV O288–O293 Infection P791–P799 Session 18: Cerebrovascular disorders II O294–O299 Neuro-ophthalmology P800–P805 Session 19: Motor neuron disease O300–O305 Session 20: Infection O306–O311 Session 21: Neurorehabilitation O312–O317 Session 22: Clinical neurophysiology O318–O323 Session 23: Dementia O324–O329 Session 24: Pain and headache O330–O335 123 J Neurol (2012) 259 (Suppl 1):S1–S236 S3 Presidential Symposium short half-life drug L-Dopa is now seen as the main factor for the development of motor response oscillations and drug-induced dy- skinesias associated with this type of treatment. Improving the Parkinson Syndrome: an everlasting challenge pharmacokinetics and mode of delivery of dopaminergic agents is therefore a key element of managing motor response oscillations. Standard approaches include adjunct COMT-inhibition and/or MAO- 45 B-inhibition with L-Dopa as well as the use of longer half-life non- Does early diagnosis lead to early treatment ergolinic dopamine agonists and their extended release formulations. of Parkinson’s disease? Continuous drug delivery using subcutaneous apomorphine infusions H. Reichmann or intrajejunal infusions of duodopa not only smooth out motor University of Dresden (Dresden, DE) fluctuations but also lead to reductions in pre-existing dyskinesias. Future developments of novel dopaminergic approaches to PD ther- We don’t know how long it takes from the onset of first clinical apy may also include intrapulmonary delivery with inhaler systems as symptoms of Parkinson’s disease (PD) to medical diagnosis. Until well as gene-therapeutic enhancement of local DA-production in the recently, no major interest has focused in these early stages, because it striatum. Currently amantadine is the only drug with proven efficacy is classically recommended to wait for prescribing treatments until to reduce levodopa dyskinesias, but several non-dopaminergic drugs disability occurs. Such views are changing, with novel concepts in the targeting glutamatergic receptors are being developed to broaden the natural history of early PD and new attempts to diagnose and treat the spectrum of antidyskinetic agents of PD. In addition, drugs targeting patients earlier than previously. glutamatergic, serotonergic, alphaadrenergic as well as adenosine- We know for many years that PD begins years before patients and A2a receptors are being developed and may be a promising approach doctors notice the first motor signs. There is increasing evidence that a to control levodopa-induced dyskinesias or motor fluctuations. variety of non-motor symptoms are common in PD patients before the Deep brain stimulation (DBS) targeting the STN or GPi are an onset of any motor sign. Such non-motor symptoms include hyposmia, established modality for the management of motor complications in REM sleep behaviour disorder, constipation, depression, problems in drug refractory patients. colour discrimination and sensory signs. It is now proposed that these Recent randomized trials have shown similar effects of STN and symptoms may characterize a ‘‘pre-motor’’ phase of PD. GPi stimulation and also that DBS improves quality-of-life of patients There is a growing debate to decide whether we should continue or with advanced PD. not to wait for ‘‘sufficient’’ disability before treating patients. The UK PD-LIFE study showed that immediate anti-Parkinsonian treatment maintained quality of life scores (PDQ-39) stable in early PD patients over 18 months, while scores deteriorated in those remaining 47 untreated. Moreover, the recent ADAGIO placebo-controlled study, Treatment of non-motor symptoms using the delayed-start design, showed that patients with early PD (5 months from diagnosis) randomized to receive rasagiline (1mg/day) P. Barone immediately (early-start group) had less worsening in UPDRS scores University of Salerno (Salerno, IT) after 18 months of follow-up than those receiving the same treatment Non-motor symptoms (NMSs) are common in Parkinson’s disease 9 months later (delayed-start group). Unfortunately, the PROUD (PD) and have recently gained relevance for their impact on prospective placebo-controlled delayed-start study with the dopamine patients’ quality of life (QoL) and their contribution to institution- agonist pramipexole did fail and showed no superiority for patients alization. Despite their impact, NMSs in PD are under-recognized in who were treated immediately after diagnosis. clinical practice and, consequently, undertreated. NMSs can present To avoid dyskinesia it is common practice to start with a dopamine at any stage of disease, including early and pre-motor phase of PD. agonist and due to the results of ADAGIO and previously TEMPO it The pathophysiology of NMSs is still poorly understood, and a may be well taken to add a MAO-B-inhibitor. dysfunction of both dopaminergic and non-dopaminergic systems A practical way would therefore be to start mildly impaired de contributes to their development. Recently the PRIAMO study novo patients with a MAO-B-inhibitor and those who are more described the prevalence of NMSs, their relevance for cognitive impaired with a dopamine agonist to add the other substance later. impairment and their overall impact on QoL in a large cohort of During the course of the disease levo-Dopa will be needed which Italian patients with PD. Most frequently reported NMSs were should be initiated in biologically old patients at the beginning of psychiatric, sleep, gastrointestinal, pain, fatigue and urinary. More- their PD disease. over patients who reported apathy, attention/memory deficit and Professor