gms | German Medical Science

73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

29.05. - 01.06.2022, Köln

Electrocorticographic signature of infarct penumbra in MCA infarction – translational animal model

Elektrokortikographische Signatur von Infarkt Penumbra beim MCA-Infarkt: translationales Tiermodell

Meeting Abstract

  • presenting/speaker Roberto Díaz Peregrino - Universitätsklinikum Heidelberg, Neurochirurgische Klinik, Heidelberg, Deutschland
  • Modar Kentar - Universitätsklinikum Heidelberg, Neurochirurgische Klinik, Heidelberg, Deutschland
  • Carlos Trenado Colín - Heinrich-Heine-Universität Düsseldorf, Institute of Clinical Neuroscience and Medical Psychology, Düsseldorf, Deutschland
  • Renán Sánchez Porras - Evangelisches Krankenhaus Oldenburg, Universitätsklinik für Neurochirurgie, Oldenburg, Deutschland
  • Johannes Woitzik - Evangelisches Krankenhaus Oldenburg, Universitätsklinik für Neurochirurgie, Oldenburg, Deutschland
  • Edgar Santos - Evangelisches Krankenhaus Oldenburg, Universitätsklinik für Neurochirurgie, Oldenburg, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie. Köln, 29.05.-01.06.2022. Düsseldorf: German Medical Science GMS Publishing House; 2022. DocV210

doi: 10.3205/22dgnc203, urn:nbn:de:0183-22dgnc2039

Published: May 25, 2022

© 2022 Díaz Peregrino et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Objective: Subarachnoid hemorrhage (SAH) is a serious condition with a complex evolution, being the delayed cerebral ischemia a possible fate with a bad prognosis. Invasive monitors provide continuous physiological data at the bedside and could be integrated into the surveillance of the neurocritical unwell as a prognosis tool. Therefore, the aim of this work was to characterize the electrocorticographic changes temporally and anatomically occurring after a Middle Cerebral Artery occlusion (MCAo), including those caused by Spreading Depolarizations (SDs) in the swine brain.

Methods: Through a left transorbital approach, the MCAs were surgically clipped and occluded in ten 30-35 Kg swine. Extensive craniotomy and dura mater excision were performed to place bilaterally 5 electrodes over the parietal and frontal cortex corresponding to the irrigation territory of the MCA and the Anterior Cerebral Artery (ACA). After surgical training in 4 animals, six animals were used for electrocorticography (ECoG) recording. Five-minute signal segments were obtained before, 0, 4, 8, and 12 hours after the artery occlusion, and before, during, and after the negative DC shift of the SDs. Sixteen SDs from the ACA channel and 45 SDs from the MCA channels were analyzed, having a frequency of 2 and 5 SDs per hour, respectively. The power spectrum of signals was decomposed into the delta, theta, alpha, beta, and gamma bands.

Results: After artery clipping, channels located near to the MCAo (nMCAo) registered immediate and permanent power drop in all the frequencies. Channels far from the MCAo (fMCAo), coinciding with the penumbra, exhibited instantaneous and constant shrinkage of fast waves mainly alpha, and progressive decline in delta and theta within 12 hours. After 8 hours, the ACA channel recorded power decay in all the frequencies except gamma. During SDs, all brain oscillations were abated at both MCA and ACA channels. Brain waves from the right hemisphere did not experience alterations.

Conclusion: The ECoG is useful to identify the penumbra zone and to monitor infarct progression. A secondary brain injury was observed in the irrigation territory of ACA after 8 hours of blood constraints at MCA. SDs generate drastic frequency disturbances regardless of the cortical location, causing sequelae at the presumable salvable brain tissue. ECoG might be a useful clinical tool to monitor the ischemia progression in patients with SAH, and to evaluate the effectiveness of surgical interventions.

Figure 1 [Fig. 1]