• Soojin Park, Alexander Roederer, Ram Mani, Sarah Schmitt, Peter D LeRoux, Lyle H Ungar, Insup Lee, and Scott E Kasner.
• Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA. soojin.park@uphs.upenn.edu
• Neurocrit Care. 2011 Dec 1; 15 (3): 469-76.

BackgroundBrain tissue oxygen (PbtO(2)) monitors are utilized in a threshold-based fashion, triggering actions based on the presumption of tissue compromise when PbtO(2) is less than 20 mmHg. Some early published practice guidelines suggest that seizure is a potential culprit when PbtO(2) crosses this threshold; evidence for this is not well defined.MethodsData were collected manually as part of a prospective observational database. PbtO(2) monitors and continuous electroencephalogram (cEEG) were placed by clinical protocol in aneurysmal subarachnoid hemorrhage (aSAH) or traumatic brain injury (TBI) patients with a Glasgow Coma Scale (GCS) ≤ 8. Eight patients with discrete seizures during an overlapping monitored period were identified. Probability of seizure when PbtO(2) value was <20 mmHg (and the inverse) were calculated.ResultsThere were 343 distinct seizure episodes and 1797 PbtO(2) measurements. 8.9% of seizures were followed by a PbtO(2) value below 20 mmHg. Of all observed low PbtO(2) values, 3.8% were associated with seizure. Seizure length did not influence PbtO(2). Two patients with the highest number of seizures developed low PbtO(2) values post-seizure.ConclusionsSeizures were neither associated with a PbtO(2) value of <20 mmHg nor associated with a drop in PbtO(2) value across a clinically significant threshold. However, we cannot rule out the existence of any relationship between PbtO(2) and seizure with this limited data set. Prospective research using electronically recorded data is required to more effectively examine the relationship between PbtO(2) and seizure.

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