The purpose of this study was to evaluate the contribution of quantitative EEG (qEEG) to an animal model of cerebral air embolism (CAE). In 12 anesthetized pigs, air was injected into the internal carotid artery, and hyperbaric oxygen (HBO) treatment was started either after 3 minutes or after 60 minutes (United States Navy Treatment Table 6). Off-line spectral analysis was used to determine the frequency content of the EEG signal, and factor analysis was performed to determine the frequency ranges that optimally showed the changes in the power spectrum. Factor analysis revealed two factors that represented different and independent spectral changes during embolization: 0.5 to 7.3 Hz (band 1) and 26.4 to 30.3 Hz (band 2). Shortly after embolization, the power in both bands decreased to a minimum, representing an isoelectric EEG in 11 out of the 12 animals. EEG differences between animals were considerable, despite standardized doses of injected air, and qEEG can objectively assess and quantify these differences in immediate impact of air embolism on brain function. Also, qEEG enabled monitoring of the recovery from the initial embolic event and of the response on treatment. The initial recovery was much more protracted in band 2 than in band 1, but even after completing HBO treatment, qEEG values did not return to baseline values in all animals. In addition, two animals did not survive until the end of the HBO treatment, and qEEG proved to be superior to the other measured hemodynamic variables to detect and ensure a deterioration of brain function. This study showed that qEEG monitoring has significant additional value to monitoring HBO treatment.

Animal model, Cerebral air embolism, Global cerebral hypoxia, Hyperbaric oxygen, Quantitative EEG,
Journal of Clinical Neurophysiology
Department of Neurology

Drenthen, J, van Hulst, R.A, Blok, J.H, van Heel, M.D, Haitsma, J.J, Lachmann, B.F, & Visser, G.H. (2003). Quantitative EEG monitoring during cerebral air embolism and hyperbaric oxygen treatment in a pig model. Journal of Clinical Neurophysiology, 20(4), 264–272. doi:10.1097/00004691-200307000-00006