Posters S69

area. Neuronavigation and fiber-tracking might be helpful toprevent damage to these fibers.Ad patient 2: There is increased risk of primary motor cortexof the hand-area damage; invasive recording (fiber-trackingand fMRI) is helpful to clarify the neighbouring relationshipbetween the lesion and primary hand area.Ad patient 3: Because of the involvement of insula withits many arteries, there is increased risk for ischemiccomplications causing hemiparesis, and also for neighboringcortical hand area (cortical face-area can be resected).Conclusion: Reasonable precise judgments on risk-benefit-ratios are possible in patients with focal cortical dysplasiatype II, prior to presurgical work-up and finally surgery.

P157 Mortality following antiepileptic drug use in childrenand adolescents

R. Ackers1,5, F.M.C. Besag1,7 *, E. Hughes6, W. Squier4,I.C.K. Wong1. 1Centre for Paediatric Pharmacy Research, Schoolof Pharmacy, London, United Kingdom; 2Twinwoods HealthResource Centre, Bedfordshire and Luton Partnership NHS Trust;3Paediatrics Department, Kings College Hospital, London, UnitedKingdom; 4Neuropathology Department, John Radcliffe Hospital,Oxford, United Kingdom; 5Evelina Children’s Hospital, Guy’s andSt Thomas’ NHS Foundation Trust, London, United Kingdom;6Paediatrics Department, Kings College Hospital, London, UnitedKingdom; 7Twinwoods Health Resource Centre, Bedfordshire andLuton Partnership NHS Trust, United Kingdom

Objectives:1. To identify cases and causes of death in a UK cohort

of children with epilepsy who have been prescribed anantiepileptic drug (AED).

2. To calculate standardised mortality ratios (SMRs).3. To perform a causality assessment to determine the

likelihood of the AED being responsible.Methods: The general practice research database (GPRD) wasused to identify a cohort of children, 0−18 years, prescribedAEDs 1993 2005. Subjects who had died were identified. GPscompleted questionnaires. Death certificates were obtained.SMRs (95%CI) were calculated using UK Office for NationalStatistics general population mortality rates. A consensuspanel performed causality assessments.Results: A cohort of 6190 subjects (54% male), 26890 person-years was examined. 151 subjects died (57% male); mean ageof death 8.7 years. Crude mortality rate was 5.62 per 1000person-years. The majority who died had severe underlyingdisorders. Cause of death was attributable to epilepsy in18/151 subjects, with 9 SUDEP (3.3 per 10,000 person-years).Overall SMR was 22.36 (18.93, 26.22). Subjects prescribednewer or both newer and conventional AEDs had higher SMRsof 30.21 (15.08, 54.06) and 32.51 (25.09, 41.43) respectivelycompared to conventional AEDs alone 17.33 (13.65, 21.69). TheAEDs were probably (n=2) or possibly (n=3) associated withdeath in only five subjects, suggesting they are not a majorcause of death.Conclusions: In this large cohort study, children prescribedAEDs for epilepsy had an increased risk of mortalitycompared to the general population. Although most of thedeaths were in children with a severe underlying disorder, asmall number of SUDEP cases were also identified. Subjectsprescribed a newer AED or polytherapy appeared to be atgreater risk of death but this may be related to the severityof the epilepsy or underlying disorder.

P158 Changes in slow wave characteristics in children withelectrical status epilepticus during sleep (ESES)

B. Boelsterli1 *, B. Schmitt1, O.G. Jenni1, H. Critelli1, R. Huber1.1University Children’s Hospital Zurich, Zurich, Switzerland

Objective: “Continuous spike-waves during slow-wave sleep”(CSWS) and “Landau Kleffner syndrome” (LKS) are charac-terised by the EEG-pattern of “electrical status epilepticusduring sleep” and cognitive, language and behaviouraldisturbances. Spike-wave activity was suggested to beresponsible for these impairments.The synaptic homeostasis hypothesis predicts that thestrength of cortico-cortical synapses is decreased duringsleep. This “downscaling” is related to the decline of slow-wave sleep across the night. It has been shown that the slopeof slow waves in the non-REM-sleep EEG best reflects suchchanges in synaptic strength.The aim of this study is to elucidate pathophysiologicalmechanisms of spike-waves and cerebral dysfunction inCSWS/LKS. We hypothesise an aberrant downscaling inCSWS/LKS as measured by the slope of slow waves.Methods: All night EEG data of 6 patients with CSWS/LKSand 6 age-matched, healthy controls were analysed in aretrospective study. We automatically detected EEG waves inthe frequency range of 1−4Hz and calculated the ascendingslope. We assessed slope changes across the night bycomparing the first to the last hour of slow-wave sleep inboth groups.Results: In controls, the slope of slow waves declines from thefirst to the last hour of slow-wave sleep (p< 0.05). In contrast,patients show no significant change in slope across the night.There is preliminary evidence for overall differences in theslope of slow waves between patients and controls.Conclusions: The slope of slow waves in patients withCSWS/LKS does not show the physiological decrease asobserved in healthy controls. This may reflect a disruption ofthe downscaling process during sleep and therefore may bethe basis for the developmental regression in these children.Acknowledgements: Supported by the Anna Muller Gro-cholski Foundation.

P159 The role of video-EEG in differential diagnosis ofparoxysmal dystonia and partial seizure

S. Yilmaz1 *, G. Serdaroglu1, S. Gokben1, H. Tekgul1. 1PediatricNeurology, Ege University, Izmir, Turkey

Video-EEG has an important role in differential diagnosis ofnon-epileptic disorders and epileptic seizures.Sixteen-year-old girl was referred for the tonic spasmsinvolving the left side of her body. It was previously consid-ered to be a psychogenic nonepileptic seizure secondary todepression and anxiety disorder. The patient had receivedsome combinations of antidepressant and antipsychoticagents. Tonic spasms had no response to these agents andstarted to awaken her at nights. The video-EEG analysisrevealed no electrophysiological abnormality accompanyingthe defined involuntary movements. The diagnosis ofpsychogenic nonepileptic seizure was ruled out becauseof resistance to therapy and semiologic features of theparoxysmal phenomenon. The tonic spasms were consideredto be a movement disorder, and defined as paroxysmaldystonia. The cranial magnetic resonance imaging revealedactive demyelinating plaques involving the basal gangliasand thalamus. The patient was diagnosed as possiblemultiple sclerosis according to the 2005 revised Mc Donald’scriteria. A rapid response was obtained with carbamazepinetherapy for paroxysmal distonia.Paroxysmal dystonia is an uncommon non-epileptic phe-nomenon in multiple sclerosis. Video-EEG studies shouldbe performed in the differential diagnosis of paroxysmaldistonia and epileptic seizures.