TP4.2 Transient global amnesia: p3 findings

TP4.2 Transient global amnesia: p3 findings

Talking Posters / Clinical Neurophysiology 117 (2006) S112–S120 TP4.2 Transient global amnesia: p3 findings A. Ragazzoni, E. Torre, E. Del Sordo, D. B...

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Talking Posters / Clinical Neurophysiology 117 (2006) S112–S120

TP4.2 Transient global amnesia: p3 findings A. Ragazzoni, E. Torre, E. Del Sordo, D. Battista, G. Zaccara Ospedale S. Maria Nuova, Neurology, Italy Background: Transient Global Amnesia (TGA) is characterised by sudden reversible anterograde amnesia. SPECT, PET and fMRI studies have localized changes to temporal lobes and hippocampi during TGA. P3 component of the endogenous event-related potentials (ERPs) has been suggested to originate from a hippocampal generator and has been linked to memory mechanisms: it represents therefore a useful neurophysiological tool to investigate the pathophysiology of TGA. Objectives: To detect possible changes in P3 component during/following an attack of TGA. Methods: Seventeen patients (aged 46–76 years; 7 women) were studied following an episode of TGA. Auditory ERPs (oddball paradigm, count-rare task) were recorded within 48 h following the resolution of ictal symptoms (control 1). In two of the patients, ERP recordings were also obtained during an attack. A second ERP investigation was performed in all patients 1–12 months following the TGA (control 2). Results: the latency and amplitude of the auditory P3 at control 1 were within the normal range at the midline electrodes (Fz, Cz, Pz). However, over the left and right temporal leads, P3 presented with markedly reduced amplitudes and in six patients it was not detectable at all. Detection rate for rare (target) auditory stimuli was unremarkable (99% hits). On control 2, P3 regained a normal voltage over the temporal leads in all patients. P3 latencies were significantly shorter on control 1 than on control 2 (p < 0.05). Conclusions: The peculiar ERP abnormalities recorded at a short interval from TGA (i.e., the marked attenuation or suppression of P3 component over the temporal leads of both hemispheres), suggest that the hippocampal P3 contributes to the scalp P3 only at the corresponding temporal region. The persistence of P3 abnormalities for many hours following TGA demonstrates that functional impairment is still present after the end of the amnestic episode. doi:10.1016/j.clinph.2006.06.172

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St. Vincent’s University Hospital, Clinical Neurophysiology, Ireland

Background: Neonatal seizures and particularly status epilepticus (SE) are associated with an increased risk of epilepsy and long-term neurological deficits. It is therefore important that neonates with SE are identified and treated as soon as possible. Status epilepticus is generally defined as 30 min of continuous seizure activity, or recurrent seizures with persistent unconsciousness between seizures. Difficulties in assessing conscious level in neonates make this definition of SE hard to implement. Objective: To use continuous video-EEG monitoring to quantify seizure burden and identify periods of status epilepticus in neonates with recurrent seizures. Methods: Continuous video-EEG recordings lasting at least 48 h in full term neonates with recurrent seizures were analysed. Total seizure number, duration of each seizure, total duration of recurrent seizures and percentage seizure activity per hour was determined for each recording. Results: EEG data from 10 neonates with 658 electrographic seizures was analysed. Seizure number ranged from 4 to 156 per neonate. Only one seizure in one neonate lasted more than 30 min; all other seizures were well below 30 min in duration (mean 3 min and 40 s). Seizures were more likely to be brief and occur frequently over a prolonged period of time (4–38 h). Mean percentage seizure activity per hour ranged from 0.68% to 57.25%. Three neonates had periods when the percentage seizure activity per hour exceeded 50%. Conclusion: Almost all neonatal seizures are less than 30 min in duration. Recurrent brief seizures over a prolonged period are more common. As periods of SE may be detrimental to the neonatal brain it is important that a clear and concise definition exists to enable accurate identification and treatment. doi:10.1016/j.clinph.2006.06.173

TP4.4 Multiparametric assessment of mild cognitive impairment: First results D. Debatisse 1, S. Joray 1, M. Allaoua 2, E. Pralong 1, P.A. Despland 3, J. Ghika 1 1 2 3

TP4.3 What is neonatal status epilepticus? G. Boylan 1, D. Murray 1, B. Greene 2, A. Ryan 1, B. McNamara 3, S. Connolly 4 1

University College Cork, Paediatrics and Child Health, Ireland 2 University College Dublin, Electrical, Electronic and Mechanical Engineering, Ireland 3 Cork University Hospital, Clinical Neurophysiology, Ireland

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CHUV, NCH-UNN, Switzerland CHUV, Neuroradiology PET scan, Switzerland CHUV, Neurology, Switzerland

Background: Mild cognitive impairment (MCI) is an intermediate state between normal and pathological aging. MCI is characterized by acquired cognitive deficits without decline in the everyday activities. Considerable heterogeneity exists in the definitions and significance of MCI. The sensitivity and specificity of neuropsychological measurements, neuro-imaging, electrophysiology and genetic approach as markers for MCI remain to be defined.