Spreading depression in continuous electroencephalography of brain trauma
Article first published online: 17 SEP 2014
© 2014 American Neurological Association
Annals of Neurology
Volume 76, Issue 5, pages 681–694, November 2014
How to Cite
Hartings, J. A., Wilson, J. A., Hinzman, J. M., Pollandt, S., Dreier, J. P., DiNapoli, V., Ficker, D. M., Shutter, L. A. and Andaluz, N. (2014), Spreading depression in continuous electroencephalography of brain trauma. Ann Neurol., 76: 681–694. doi: 10.1002/ana.24256
- Issue published online: 29 OCT 2014
- Article first published online: 17 SEP 2014
- Accepted manuscript online: 25 AUG 2014 08:58AM EST
- Manuscript Accepted: 19 AUG 2014
- Manuscript Revised: 15 AUG 2014
- Manuscript Received: 5 JUN 2014
Cortical spreading depolarizations are a pathophysiological mechanism and candidate target for advanced monitoring in acute brain injury. Here we investigated manifestations of spreading depolarization in continuous electroencephalography (EEG) as a broadly applicable, noninvasive method for neuromonitoring.
Eighteen patients requiring surgical treatment of traumatic brain injury were monitored by invasive electrocorticography (ECoG; subdural electrodes) and noninvasive scalp EEG during intensive care. Spreading depolarizations were first identified in subdural recordings, and EEG was then examined visually and quantitatively to identify correlates.
A total of 455 spreading depolarizations occurred during 65.9 days of simultaneous ECoG/EEG monitoring. For 179 of 455 events (39%), depolarizations caused temporally isolated, transient depressions of spontaneous EEG amplitudes to 57% (median) of baseline power. Depressions lasted 21 minutes (median) and occurred as suppressions of high-amplitude delta activity present as a baseline pattern in the injured hemisphere. For 62 of 179 (35%) events, isolated depressions showed a clear spread of depression between EEG channels with delays of 17 minutes (median), sometimes spanning the entire hemisphere. A further 188 of 455 (41%) depolarizations were associated with continuous EEG depression that lasted hours to days due to ongoing depolarizations. Depolarizations were also evidenced in EEG as shifts in direct current potentials.
Leão's spreading depression can be observed in clinically standard, continuous scalp EEG, and underlying depolarizations can spread widely across the injured cerebral hemisphere. These results open the possibility of monitoring noninvasively a neuronal pathophysiological mechanism in a wide range of disorders including ischemic stroke, subarachnoid hemorrhage, and brain trauma, and suggest a novel application for continuous EEG. Ann Neurol 2014;76:681–694