20 research outputs found

    New onset left frontal lobe seizure presenting with ictal asystole

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    AbstractIctal asystole is a presumably rare but potentially fatal complication of seizures, most often of temporal lobe origin. It is believed that at least some cases of sudden unexplained death in epilepsy (SUDEP) might be triggered by ictal bradycardia or asystole. Current standard practice is to implant a permanent pacemaker in these patients to prevent syncope and/or death. However, emerging data suggests that effective medical or surgical treatment of epilepsy might be enough to prevent cardiac asystole, eliminating the need for permanent pacemaker placement. We describe a case of new onset left frontal lobe epilepsy in a young athletic patient who presented with near-syncopal episodes but whose comprehensive work-up revealed frequent events of ictal bradycardia and asystole. He responded well to monotherapy using oxcarbazepine, avoiding a permanent pacemaker

    Diagnosis and Surgical Treatment of Drug-Resistant Epilepsy

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    Despite appropriate trials of at least two antiepileptic drugs, about a third of patients with epilepsy remain drug resistant (intractable; refractory). Epilepsy surgery offers a potential cure or significant improvement to those with focal onset drug-resistant seizures. Unfortunately, epilepsy surgery is still underutilized which might be in part because of the complexity of presurgical evaluation. This process includes classifying the seizure type, lateralizing and localizing the seizure onset focus (epileptogenic zone), confirming the safety of the prospective brain surgery in terms of potential neurocognitive deficits (language and memory functions), before devising a surgical plan. Each one of the above steps requires special tests. In this paper, we have reviewed the process of presurgical evaluation in patients with drug-resistant focal onset epilepsy

    The 4-aminopyridine in vitro epilepsy model analyzed with a perforated multi-electrode array

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    Epileptiform discharges recorded in the 4-aminopyridine (4-AP) in vitro epilepsy model are mediated by glutamatergic and GABAergic signaling. Using a 60-channel perforated multi-electrode array (pMEA) on corticohippocampal slices from 2 to 3 week old mice we recorded interictal- and ictal-like events. When glutamatergic transmission was blocked, interictal-like events no longer initiated in the hilus or CA3/CA1 pyramidal layers but originated from the dentate gyrus granule and molecular layers. Furthermore, frequencies of interictal-like events were reduced and durations were increased in these regions while cortical discharges were completely blocked. Following GABA A receptor blockade interictal-like events no longer propagated to the dentate gyrus while their frequency in CA3 increased; in addition, ictal-like cortical events became shorter while increasing in frequency. Lastly, drugs that affect tonic and synaptic GABAergic conductance modulated the frequency, duration, initiation and propagation of interictal-like events. These findings confirm and expand on previous studies indicating that multiple synaptic mechanisms contribute to synchronize neuronal network activity in forebrain structures. This article is part of a Special Issue entitled 'Trends in Neuropharmacology: In Memory of Erminio Costa'. © 2011 Elsevier Ltd. All rights reserved

    Emergence of dominant initiation sites for interictal spikes in rat neocortex

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    Neuronal populations with unbalanced inhibition can generate interictal spikes (ISs), where each IS starts from a small initiation site and then spreads activation across a larger area. We used in vivo voltage-sensitive dye imaging to map the initiation site of ISs in rat visual cortex disinhibited by epidural application of bicuculline methiodide. Immediately after the application of bicuculline, the IS initiation sites were widely distributed over the entire disinhibited area. After ∼10 min, a small number of sites became “dominant” and initiated the majority of the ISs throughout the course of imaging. Such domination also occurred in cortical slices, which lack long-range connections between the cortex and subcortical structures. This domination of IS initiation sites may allow timing-related plasticity mechanisms to provide a spatial organization where connections projecting outward from the dominant initiation site become strengthened. Understanding the spatiotemporal organization of IS initiation sites may contribute to our understanding of epileptogenesis in its very early stages, because a dominant IS initiation site with strengthened outward connectivity may ultimately develop into a seizure focus
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