Reactivity of burst-suppression EEG patterns following transient global cerebral ischemia in rat

Alexandru Stoian1, Bogdan David1, Aldebarani Gonzalez1, Alexandru Calin1, Ovidiu Lucian Bajenaru1, Alexandru Paslaru1, Andrei Ilie2, Ana-Maria Zagrean1Leon Zagrean1, and Mihai Moldovan1,3 1) Department of Physiology, "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania; 2) Department of Pharmacology, Oxford University, Oxford, United Kingdom; 3) Institute of neuroscience and pharmacology, Faculty of health sciences, University of Copenhagen, Copenhagen, Denmark

Published in: Abstract Book - Conference of the National Neuroscience Society of Romania, "Carol Davila" University Press ISBN 978-973-708-636-5

SNN 2012
18-19 Oct, 2013


After global cerebral ischemia (GCI), electrocortical activity resumes from the isoelectric line through a sequence of “bursts” of activity alternating with periods of electrical “suppression”, the post-ischemic burst-suppression (BS) pattern. BS activity is typically recorded in comatose states, where the presence of a reactive BS has a more favorable outcome than a non-reactive BS. External stimuli are known to be able to trigger bursts and reorganize at least some BS patterns referred to therefore as reactive. We investigated the reactivity of BS patterns following 1, 3, 5, and 10 minutes of transient global cerebral ischemia (GCI) by 4-vessel occlusion in adult male Wistar rats under chloral-hydrate anesthesia. BS patterns were recorded from occipital cortex by implanted epidural electrodes. Super-bright LED flashes were delivered every 2 seconds to one eye. Given the predominantly crossed visual projection in rats, the ipsilateral occipital recording was uncontaminated by the evoked visual responses and could be used to quantify the BS patterns. Time to electrical recovery (TER) and time to first burst (TTB1) were used to compare the BS pattern reactivity after GCI. 1 and 3 minutes ischemia were followed by a BS pattern more reactive at visual stimulation than 5-10 minutes, which means that, at rat, longer ischemia equals bigger neuronal damage. This study raises the hope that measures of BS reactivity can be used to derive early prognostic markers for comatose patients following cerebral ischemia.