BACKGROUND: The 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. RESULTS: Data 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). CONCLUSIONS: Changes in the ICP and pulse waveform shape after EEG burst suggest that these signals can be related within the context of neurovascular coupling. SIGNIFICANCE: Existence of a physiological relationship between ICP and EEG may allow the study of neurovascular coupling in acute brain injury patients.
BACKGROUND: The 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. RESULTS: Data 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). CONCLUSIONS: Changes in the ICP and pulse waveform shape after EEG burst suggest that these signals can be related within the context of neurovascular coupling. SIGNIFICANCE: Existence of a physiological relationship between ICP and EEG may allow the study of neurovascular coupling in acute brain injurypatients.
Authors: Anthony J Strong; Peter J Anderson; Helena R Watts; David J Virley; Andrew Lloyd; Elaine A Irving; Toshiaki Nagafuji; Mitsuyoshi Ninomiya; Hajime Nakamura; Andrew K Dunn; Rudolf Graf Journal: Brain Date: 2007-04 Impact factor: 13.501
Authors: P M Vespa; M R Nuwer; V Nenov; E Ronne-Engstrom; D A Hovda; M Bergsneider; D F Kelly; N A Martin; D P Becker Journal: J Neurosurg Date: 1999-11 Impact factor: 5.115
Authors: C Baumgartner; W Serles; F Leutmezer; E Pataraia; S Aull; T Czech; U Pietrzyk; A Relic; I Podreka Journal: J Nucl Med Date: 1998-06 Impact factor: 10.057
Authors: Cesar Reis; Yuechun Wang; Onat Akyol; Wing Mann Ho; Richard Applegate Ii; Gary Stier; Robert Martin; John H Zhang Journal: Int J Mol Sci Date: 2015-05-26 Impact factor: 5.923