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The Neurovascular Basis of Postictal Amnesia

View ORCID ProfileJordan S. Farrell, Roberto Colangeli, Barna Dudok, Marshal D. Wolff, Sarah L. Nguyen, Clayton T. Dickson, Ivan Soltesz, View ORCID ProfileG. Campbell Teskey
doi: https://doi.org/10.1101/2020.01.30.926717
Jordan S. Farrell
Department of Neurosurgery, Stanford University, Stanford, CA, USAHotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada
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  • For correspondence: jsfarrel@stanford.edu
Roberto Colangeli
Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada
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Barna Dudok
Department of Neurosurgery, Stanford University, Stanford, CA, USA
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Marshal D. Wolff
Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada
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Sarah L. Nguyen
Department of Psychology, University of Alberta, Edmonton, AB, Canada
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Clayton T. Dickson
Department of Psychology, University of Alberta, Edmonton, AB, CanadaDepartment of Physiology, University of Alberta, Edmonton, AB, CanadaNeuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada
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Ivan Soltesz
Department of Neurosurgery, Stanford University, Stanford, CA, USA
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G. Campbell Teskey
Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada
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Abstract

Long-lasting confusion and memory difficulties during the postictal state remain a major unmet problem in epilepsy that lacks pathophysiological explanation and treatment. Previously, we demonstrated that the postictal period is marked by a long-lasting stroke-like event in both animal models and humans with epilepsy (Farrell et al., 2016). Here, we assessed potential mechanisms by which this vascular event leads to memory impairment by studying the hippocampus of rodent seizure models. While neuronal activity and local field oscillations were unchanged during the postictal state, memory and long-term potentiation of the temporoammonic pathway to CA1 were significantly impaired, but only when severe local hypoxia occurred. Prevention of postictal stroke-like events by cyclooxygenase inhibition rescued memory impairment and supports a necessary role of hypoperfusion/hypoxia in postictal amnesia. These results provide an objective pathophysiological criterion for defining the postictal state and identifies a strategy and potential drug candidates for treating it.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted January 31, 2020.
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The Neurovascular Basis of Postictal Amnesia
Jordan S. Farrell, Roberto Colangeli, Barna Dudok, Marshal D. Wolff, Sarah L. Nguyen, Clayton T. Dickson, Ivan Soltesz, G. Campbell Teskey
bioRxiv 2020.01.30.926717; doi: https://doi.org/10.1101/2020.01.30.926717
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The Neurovascular Basis of Postictal Amnesia
Jordan S. Farrell, Roberto Colangeli, Barna Dudok, Marshal D. Wolff, Sarah L. Nguyen, Clayton T. Dickson, Ivan Soltesz, G. Campbell Teskey
bioRxiv 2020.01.30.926717; doi: https://doi.org/10.1101/2020.01.30.926717

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