Poster No:
2633
Submission Type:
Abstract Submission
Authors:
Antis George1, Sarah Vinette1, Jospeph Peedicail1, Daniel Pittman1, William Wilson1, Paolo Federico1
Institutions:
1University of Calgary, Calgary, Alberta
First Author:
Co-Author(s):
Introduction:
Recent animal work has demonstrated that seizures can result in vasoconstriction-induced hypoperfusion and hypoxia in brain regions involved in the seizure and is a putative mechanism of postictal impairments (Farrell et al., 2016). We have previously shown that arterial spin labeling MRI and CT- perfusion can be used to detect postictal hypoperfusion localizing to the seizure onset zone (SOZ) in people with medication resistant focal epilepsy (Gaxiola-Valdez et al., 2017; Li et al., 2019). However, postictal hypoxia has yet to be directly measured.
Hypoperfusion and hypoxia are related pathophysiological concepts, however, they are not always correlated. In fact, only approximately 50% of postictal hypoxia is mediated by vasoconstriction and hypoperfusion while dysfunctional metabolism accounts for the remaining 50% (Villa et al., 2023). The extent of postictal symptoms is related to the resultant hypoxia. Therefore, measurement of oxygen levels in the area of brain generating seizures is superior to perfusion measurements. This is the first report of brain tissue hypoxia following seizures in patients with medication resistant focal epilepsy.
Methods:
Eight adult patients with medication resistant focal epilepsy undergoing intracranial video-EEG monitoring were recruited. Patients underwent implantation of an oxygen sensing probe in their presumed SOZ at the same time as depth electrode implantation. Using a continuous oxygen detection system with high temporal resolution, the partial pressure of oxygen (pO2) was measured before, during and importantly, after a seizure. Oxygen dynamics associated with focal aware (FAS), focal impaired awareness (FIAS) and focal to bilateral tonic-clonic seizures (FBTCS) were analyzed. Severe hypoxia was defined as a pO2 of ≤10 mmHg.
Results:
Our data show an enduring severe hypoxia (i.e., ≤10 mmHg) following a FAS, FIAS and FBTCS localized to the SOZ. Patients with FBTCS spent more time hypoxic relative to the other seizure types and had longer mean seizure duration. Although patients that had FBTCS had worse postictal hypoxia this is likely a function of seizure duration which was positively correlated with severity of hypoxia.

·Figure 2 Brief seizures induce severe postictal hypoxia.
Conclusions:
This work provides important proof-of-concept that postictal hypoxia can be measured in people with epilepsy. Following a FAS, FIAS or FBTCS, the area of the brain involved in the seizure becomes severely hypoxic. FBTCS are associated with worse postictal hypoxia compared to other seizure types. While epilepsy has long and correctly been considered an electrical disorder, the vascular system plays an important causal role, highlighting that seizures cause vascular insufficiency leading to brain tissue hypoxia.
Modeling and Analysis Methods:
EEG/MEG Modeling and Analysis
Novel Imaging Acquisition Methods:
EEG
Physiology, Metabolism and Neurotransmission :
Cerebral Metabolism and Hemodynamics 2
Neurophysiology of Imaging Signals
Physiology, Metabolism and Neurotransmission Other 1
Keywords:
Cerebral Blood Flow
Electroencephaolography (EEG)
ELECTROPHYSIOLOGY
Epilepsy
1|2Indicates the priority used for review
Provide references using author date format
Farrell J.S. (2016). 'Postictal behavioural impairments are due to a severe prolonged hypoperfusion/hypoxia event that is COX-2 dependent'. Elife. 22;5:e19352.
Gaxiola-Valdez I. (2017). 'Seizure onset zone localization using postictal hypoperfusion detected by arterial spin labelling MRI'. Brain. 140(11):2895-911
Li E. (2019). 'CT perfusion measurement of postictal hypoperfusion: localization of the seizure onset zone and patterns of spread'. Neuroradiology.1;61:991-1010.
Villa B.R. (2023). 'Postictal hypoxia involves reactive oxygen species and is ameliorated by chronic mitochondrial uncoupling'. Neuropharmacology.238:109653.