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Epileptic Disord. 2014 Oct;16 Spec No 1:S23-36. doi: 10.1684/epd.2014.0692.

Prolonged seizures: what are the mechanisms that predispose or cease to be protective? A review of animal data.

Author information

1
Oscar-Langendorff-Institute of Physiology, Rostock University Medical School, Rostock, Germany.

Abstract

There is no doubt that seizures change processes in neuronal networks which themselves impact on seizure susceptibility, and reports on such changes probably account for the majority of studies in experimental epileptology. As much as there is no doubt about this general fact, there is, to date, quite some disagreement on whether such changes are pro-epileptic, anti-epileptic, or both, and which are crucial and which are less so. While it is not possible to provide a general answer to this, this review attempts to categorise and highlight some of these findings, and relate them to specific ontogenetic or pathophysiological conditions. Data from studies of animal models (nearly exclusively) is presented, with a focus on two main aspects: ontogenetic particularities and pathophysiological conditions, supporting evidence of susceptibility and seizure termination mechanisms in adult animal models.

KEYWORDS:

GABA; adenosine; ion channels; ionic currents; metabolism; modeling; neuromodulators; ontogenesis; predisposition; prolonged seizures; seizure termination

PMID:
25323573
DOI:
10.1684/epd.2014.0692
[Indexed for MEDLINE]

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