• Mark Connolly, Paul Vespa, Nader Pouratian, Nestor R Gonzalez, and Xiao Hu.
• Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
• Neurocrit Care. 2015 Apr 1; 22 (2): 212220212-20.

BackgroundThe objective of this study is to characterize the relationship between ICP and EEG METHODS: Simultaneous ICP and EEG data were obtained from burst-suppressed patients and segmented by EEG bursts. Segments were categorized as increasing/decreasing and peak/valley to investigate relationship between ICP changes and EEG burst duration. A generalized ICP response was obtained by averaging all segments time-aligned at burst onsets. A vasodilatation index (VDI) was derived from the ICP pulse waveform and calculated on a sliding interval to investigate cerebrovascular changes post-burst.ResultsData from two patients contained 309 bursts. 246 ICP segments initially increased, of which 154 peaked. 63 ICP segments decreased, and zero reached a valley. The change in ICP (0.54 ± 0.85 mmHg) was significantly correlated with the burst duration (p < 0.001). Characterization of the ICP segments showed a peak at 8.1 s and a return to baseline at 14.7 s. The VDI for increasing segments was significantly elevated (median 0.56, IQR 0.31, p < 0.001) and correlated with burst duration (p < 0.001).ConclusionsChanges in the ICP and pulse waveform shape after EEG burst suggest that these signals can be related within the context of neurovascular coupling.SignificanceExistence of a physiological relationship between ICP and EEG may allow the study of neurovascular coupling in acute brain injury patients.

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