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May 2012 articles from Editor-in-Chief Phil Schwartzkroin
The system epilepsies: A pathophysiological hypothesis
Giuliano Avanzini, Paolo Manganotti, Stefano Meletti, Solomon L. Moshé, Ferruccio Panzica, Peter Wolf, Giuseppe Capovilla
Volume 53, Issue 5, pp 771-778, May 2012.
DOI: 10.1111/j.1528-1167.2012.03462.x published online April 25, 2012
The authors propose that some types of epilepsies - “system epilepsies” (SystE) - reflect the pathological expression of an identifiable neural system, made up of brain areas the integrated activities of which subserve normal physiological functions. As such, SystE lead to functional results that cannot be obtained by pathological activity within the individual elements alone.
The phenomenology associated with a given SystE is determined by a contextual involvement of the contributing structures, and therefore predictable according to the functional specialization of the involved system. The SystE hypothesis further postulates that the “enduring propensity to generate seizures” of some epilepsies is due to the specific susceptibility of a system as a whole, although it may be possible to identify some trigger areas within the system. The persistent susceptibility of the seizure-generating system is assumed to exist also in the interictal period.
The authors offer a number of examples of this provocative hypothesis, with absence epilepsy and juvenile myoclonic epilepsy providing the prototypes, and such developmental phenomena as West syndrome (with infantile spasms and hypsarrhythmia) described as potentially system epilepsies. It remains to be seen whether this hypothesis actually provides a productive new way of thinking about and investigating seizure types (and epilepsy syndromes), and whether this approach will result in new therapeutic perspectives.
Abstract | Full Text | PDF
Spatiotemporal neuronal correlates of seizure generation in focal epilepsy
Mark R. Bower, Matt Stead, Fredric B. Meyer, W. Richard Marsh, Gregory A. Worrell
Volume 53, Issue 5, pp 807–816, May 2012.
doi: 10.1111/j.1528-1167.2012.03417.x; published online February 21, 2012
Focal seizures are thought to reflect simultaneous activation of a large population of neurons within a discrete region of pathological brain. Despite a number studies focusing on single-neuron activity in patients with epilepsy, no study has examined long–term firing rates leading into seizures and the spatial relationship of unit activity with respect to the seizure onset zone. In this study, microelectrode arrays were used to record action potentials from neurons in mesial temporal structures (often including contralateral mesial temporal structures) in seven patients with mesial temporal lobe epilepsy.
Surprisingly, only about 8% of microelectrode sites showed increased neuronal firing rates prior to seizure onset, and only about a third of microelectrodes showed any seizure-related activity changes; the majority of microelectrodes (including some located within the seizure onset zone) showed no change throughout the seizure. Furthermore, changes in firing rate prior to and at seizure onset were observed on microelectrodes located outside the seizure onset zone and even in contralateral mesial temporal lobe.
These early changes varied from seizure to seizure, demonstrating the heterogeneity of ensemble activity underlying the generation of focal seizures. Increased neuronal synchrony was primarily observed only following seizure onset. These results challenge our current thinking about neuronal contributions to seizures. The data indicate that cellular contributions to seizure initiation and sustained ictal discharge in mesial temporal lobe epilepsy involve a small subset of the neurons within and outside the seizure onset zone. Further, the “epileptic ensemble” or “network” responsible for seizure generation appears to be quite complex and heterogeneous. This study indicates the need for a new conceptual understanding of seizure mechanisms, and perhaps for new therapeutic approaches that target neuronal activities outside the clinical seizure onset zone.
Abstract | Full Text | PDF
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