-
Comparative Study
Detection of Spreading Depolarization with Intraparenchymal Electrodes in the Injured Human Brain.
- Toby Jeffcote, Jason M Hinzman, Sharon L Jewell, Robert M Learney, Clemens Pahl, Christos Tolias, Daniel C Walsh, Sara Hocker, Agnieszka Zakrzewska, Martin E Fabricius, Anthony J Strong, Jed A Hartings, and Martyn G Boutelle.
- Department of Neurosurgery, King's College Hospital, London, UK.
- Neurocrit Care. 2014 Feb 1; 20 (1): 21-31.
BackgroundSpreading depolarization events following ischemic and traumatic brain injury are associated with poor patient outcome. Currently, monitoring these events is limited to patients in whom subdural electrodes can be placed at open craniotomy. This study examined whether these events can be detected using intra-cortical electrodes, opening the way for electrode insertion via burr hole.MethodsAnimal work was carried out on adult Sprague-Dawley rats in a laboratory setting to investigate the feasibility of recording depolarization events. Subsequently, 8 human patients requiring craniotomy for traumatic brain injury or aneurysmal subarachnoid hemorrhage were monitored for depolarization events in an intensive care setting with concurrent strip (subdural) and depth (intra-parenchymal) electrode recordings.Results(1) Depolarization events can be reliably detected from intra-cortically placed electrodes. (2) A reproducible slow potential change (SPC) waveform morphology was identified from intra-cortical electrodes on the depth array. (3) The depression of cortical activity known to follow depolarization events was identified consistently from both intra-cortical and sub-cortical electrodes on the depth array.ConclusionsIntra-parenchymally sited electrodes can be used to consistently identify depolarization events in humans. This technique greatly extends the capability of monitoring for spreading depolarization events in injured patients, as electrodes can be sited without the need for craniotomy. The method provides a new investigative tool for the evaluation of the contribution of these events to secondary brain injury in human patients.
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