Reactivity Of Burst-Suppression EEG Patterns Following Transient Global Cerebral Ischemia In Rat

Author: Zagrean L. (1), Stoian A. (1), David B. (1), Gonzalez A. (1), Calin A. (1), Bajenaru O.L. (1), Loghin M. (1), Ilie A. (2), Zagrean A.-M. (1) & Moldovan M. (1,3) Affiliation: (1) Dept. of Physiology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania; (2) Department of Pharmacology, Oxford University, Oxford, UK; (3) Institute of Neuroscience and Pharmacology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

8th FENS Forum of Neuroscience, Barcelona
Presentation Code: p142.26 - Abstract Number: 3302 - Poster Board Number: B85 Abstract, Volume 6, p142.26, 2012
Session: P142: Oscillations and Synchrony IV
Session Code: 142 Poster boards: B60-85
Date: Wednesday - July 18, 2012 11:15 - 13:15 (attendance: 11:15)
Theme/subtheme/subtopic: B. Excitability, synaptic transmission, network functions/ B.8 Network interactions/ B.8.b Oscillations and synchrony

Severe cerebral ischemia leads to a coma with discontinuous EEG consisting of bursts of activity on a suppressed background. This burst-suppression (BS) pattern is, however, not in itself an indication of brain injury since a BS coma can be safely induced by general anesthetics. 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. The BS ratio (BSR) was calculated as the fraction of time spent in suppression over 30-second epochs. The post-ischemic BSR recovery had an exponential time-course with a time constant increasing with GCI duration. Stimulation reduced the BS recovery time constant for all GCI durations. To quantify the extent of reactivity we measured the stimulation-induced reduction in BSR from a target level of 80% which was attained in all experimental conditions within 30 minutes after GCI. In contrast to shorter GCIs, the reactivity of BS following 10-minute GCIs was lower than the reactivity of the equivalent BS induced by an anesthetic overdose. Our preliminary data suggest that measures of reactivity can differentiate between anesthetic and post-ischemic BS depending on the severity of the ischemic insult. This raises the hope that measures of BS reactivity can be used to derive early prognostic markers of neuronal damage following cerebral ischemia.