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London, United Kingdom 2013 Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 487 * Figure 1: AF detection strategy based on admission BNP level. * Figure 2: AF detection rate and number of CEM days saved according initial plasma BNP level. 380 Heart and brain Generalized periodic discharges after acute cerebral ischemia: reflection of selective synaptic failure? M.C. Cloostermans1, R. Hindriks2, J. Hofmeijer3, M.J.A.M van Putten4 Department of Clinical Neurophysiology, MIRA-Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, THE NETHERLANDS1, Center for Brain and Cognition, Computational Neuroscience Group, Department of Information and Communica-tion Technologies, Universitat Pompeu Fabra, Barcelona, SPAIN2, Department of Neurology, Rijn-state Hospital, Arnhem, THE NETHERLANDS3, Departments of Neurology and Clinical Neuro-physiology, Medisch Spectrum Twente, Enschede, THE NETHERLANDS4 Background: Generalized periodic discharges (GPDs) can be observed in the EEG of patients af-ter acute cerebral ischemia and reflect pathological neuronal synchronization. It is unclear which pathophysiological processes lead to the generation of GPDs. Whether GPDs represent ictal activity, which can be treated with anti-epileptic drugs, or severe ischemic damage, in which treatment is fu-tile, is also unknown. We hypothesize that GPDs result from selective ischemic damage of glutama-tergic synapses, which are known to be relatively vulnerable to effects of ischemia. Methods: We employed an established macroscopic model (Figure 1) (Liley, Network 2002) of cor-tical dynamics in which we increasingly eliminated glutamatergic synapses. We compared the out-put of the model with clinical EEG registrations showing GPDs of eight patients after acute cerebral ischemia due to cardiac arrest. Results: Selective elimination of glutamatergic synapses from pyramidal cells to inhibitory interneu-rons led to simulated GPDs whose wave shape and frequency matched those of patients after acute cerebral ischemia (Figure 2). Further reducing the number of glutamatergic synapses from pyrami-dal cells to inhibitory interneurons rapidly resulted in complete depression of simulated cortical ac-tivity. Mere reduction of glutamatergic synapses between pyramidal cells themselves did not result in GPDs. Conclusion: Selective ischemic damage of glutamatergic synapses on inhibitory cortical interneu-rons probably leads to the generation of ischemia induced GPDs. Disinhibition of cortical pyramidal neurons is the likely mechanism.


Karger_ESC London_2013
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