Abstracts

Rationale: EEG is frequently used for monitoring brain function in patients with acute brain injury (ABI). Scalp EEG is often limited or complex in this setting, due to loss of signal amplitude from intervening tissue, poor spatial resolution, scalp edema, artifact-related signal degradation and surgical wounds preventing coverage at the site of interest. We report our early experience with intracranial recording using a small transcortical multicontact depth electrode in patients having other invasive brain monitoring devices in order to bypass many of these limitations.Methods: A depth electrode was placed in 9 patients with ABI (7 subarachnoid hemorrhages – 5 aneurysmal, 2 traumatic; 1 intracerebral hemorrhage and 1 infarct). All patients underwent continuous scalp EEG. 7/9 patients also had multimodal monitoring, including intracranial pressure (ICP), brain tissue oxygen (PbrO2) and microdialysis. Findings on depth EEG were compared to findings on scalp EEG, and to time-locked physiological data from multimodal monitoring, that included lactate-pyruvate ratio (LPR), brain glucose, PbrO2 and ICP.Results: The depth EEG documented cortical physiological changes that were delayed or not detected by other monitoring devices in 5 of 9 patients. 6 patients had potentially epileptiform activity on depth EEG: 1 with seizures, 3 with periodic epileptiform discharges (PEDs) and 2 with isolated discharges. The patient with seizures had corresponding rise in LPR. Of the 3 patients with PEDs, 2 had corresponding decrease in brain glucose and 1 had a increase in LPR from baseline. The 2 patients with isolated discharges had no scalp correlate. 2 patients had SIRPIDs (stimulus-induced rhythmic periodic or ictal discharges) on depth EEG; one had no scalp correlate and no microdialysis catheter; the other showed a substantial increase in LPR. The depth electrode showed markedly decreased artifact when compared to scalp EEG. In one case, change related to hemorrhagic transformation of an infarct was first detected by new-onset suppression burst in the depth electrode with no change in scalp EEG, followed by elevation in LPR, noted about 2 hours later. No definite adverse effects occurred related to the depth electrode placement, though one delayed hemorrhage into a large infarct occurred near the electrode.Conclusions: We demonstrate that data obtained from a small cortical depth electrode can 1) demonstrate abnormal electrophysiological findings that can not be noted on scalp EEG, and 2) in some patients document neurophysiological changes at an earlier time point compared to brain tissue microdialysis. It can also help assess the explanation for abnormalities seen on microdialysis or other devices, and shows less artifact than scalp recordings. Continuous scalp EEG monitoring (for broad coverage) plus cortical depth recording may be valuable for improving real-time neurophysiological monitoring in select patients with acute brain injury.