Burst-Suppression EEG Reactivity to Photic Stimulation—A Translational Biomarker in Hypoxic–Ischemic Brain Injury

Author:

Pâslaru Alexandru-Cătălin1ORCID,Călin Alexandru2ORCID,Morozan Vlad-Petru1,Stancu Mihai13,Tofan Laurențiu1,Panaitescu Anca Maria145ORCID,Zăgrean Ana-Maria1ORCID,Zăgrean Leon1,Moldovan Mihai1678ORCID

Affiliation:

1. Division of Physiology—Neuroscience, Department of Functional Sciences, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania

2. Department of Clinical Neurophysiology, King’s College Hospital NHS Foundation Trust, London SE59RS, UK

3. Division of Neurobiology, Ludwig-Maximilian University, 80539 Munich, Germany

4. Clinical Hospital of Obstetrics and Gynaecology Filantropia, 011132 Bucharest, Romania

5. Obstetrics and Gynaecology Department, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania

6. Department of Neuroscience, University of Copenhagen, 2200 Copenhagen, Denmark

7. Department of Neurology, Rigshospitalet, 2600 Glostrup, Denmark

8. Department of Clinical Neurophysiology, Rigshospitalet, 2100 Copenhagen, Denmark

Abstract

The reactivity of an electroencephalogram (EEG) to external stimuli is impaired in comatose patients showing burst-suppression (BS) patterns following hypoxic–ischemic brain injury (HIBI). We explored the reactivity of BS induced by isoflurane in rat models of HIBI and controls using intermittent photic stimulation (IPS) delivered to one eye. The relative time spent in suppression referred to as the suppression ratio (SR) was measured on the contralateral fronto-occipital cortical EEG channel. The BS reactivity (BSR) was defined as the decrease in the SR during IPS from the baseline before stimulation (SRPRE). We found that BSR increased with SRPRE. To standardize by anesthetic depth, we derived the BSR index (BSRi) as BSR divided by SRPRE. We found that the BSRi was decreased at 3 days after transient global cerebral ischemia in rats, which is a model of brain injury after cardiac arrest. The BSRi was also reduced 2 months after experimental perinatal asphyxia in rats, a model of birth asphyxia, which is a frequent neonatal complication in humans. Furthermore, Oxytocin attenuated BSRi impairment, consistent with a neuroprotective effect in this model. Our data suggest that the BSRi is a promising translational marker in HIBI which should be considered in future neuroprotection studies.

Funder

Romanian National Authority for Scientific Research

Publisher

MDPI AG

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