Reactivity of burst-suppression EEG patterns following transient global cerebral ischemia in rat and a new insight of visual evoked potential amplitude

Alexandru Stoian (1), Bogdan David (1), Aldebarani Gonzalez (1), Alexandru Calin (1), Zahiu Denise (1), Alexandru Paslaru (1), Mihai Radu Ionescu (1), Stancu Mihai (1), Acatrinei Camelia (1), Voinescu Marc (1), Mirica Stefan (1), Lucian Bajenaru Ovidiu (1), Andrei Ilie (2), Ana-Maria Zagrean (1), Leon Zagrean (1) and Mihai Moldovan (1,3) 1) Division of Physiology and Neuroscience, 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 ISSN 2344 – 3952

SNN 2013
17-19 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. 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. During reperfusion following GCI, the visual evoked potential (VEP) amplitude recovered prior to onset of the EEG bursting activity. Following GCIs of 1 and 3 minutes, most of the early EEG bursts started within 500ms after the flash-induced VEPs, although not all flashes were able to trigger bursts. For GCIs longer than 3 minutes, associated with cerebral ischemic damage, the relationship between the flash and the bursts was less apparent, although the VEPs appeared unaffected. This study raises the hope that measures of BS reactivity can be used to derive early prognostic markers for comatose patients following cerebral ischemia.