Electrocorticography Electrodes Research Articles

Automated electrocorticographic electrode localization on individually rendered brain surfaces

Brain surface electrocorticographic (ECoG) recordings can investigate human brain electrophysiology at the cortical surface with exceptionally high signal to noise ratio and spatio-temporal resolution. To be able to use the high spatial resolution of ECoG for accurate brain function mapping and neurophysiology studies, the exact location of the ECoG electrodes on the brain surface should be known. Several issues complicate robust localization: surgical photographs of the electrode array made after implantation are often incomplete because the grids may be moved underneath the skull, beyond the exposed area. Computed tomography (CT) scans made after implantation will clearly localize electrodes, but the effects of surgical intervention may cause the exposed brain to move away from the skull and assume an unpredictable shape (the so-called brain shift). First, we present a method based on a preoperative magnetic resonance imaging (MRI) coregistered with a post-implantation CT scan to localize the electrodes and that automatically corrects for the brain shift by projecting the electrodes to the surface of the cortex. The calculated electrode positions are visualized on the individual subjects brain surface rendering. Second, the method was validated by comparison with surgical photographs, finding a median difference between photographic and calculated electrode centers-of-mass of only 2.6 mm, across 6 subjects. Third, to illustrate its utility we demonstrate how functional MRI and ECoG findings in the same subject may be directly compared in a simple motor movement experiment even when electrodes are not visible in the craniotomy.

ECoG-based short-range recurrent stimulation techniques to stabilize tissue at risk of progressive damage: Theory based on clinical observations

AbstractWe introduce theoretical concepts based on chaos control to stabilize in acute stroke the tissue at risk of progressive damage by preventing adverse effects of waves of mass neuronal depolarization. Moreover, we present clinical electrocorticography (ECoG) recordings of relevant signals suggested for the feedback control. The recordings are performed in combination with novel subdural opto-electrode technology for simultaneous laser-Doppler flowmetry in patients with aneurysmal subarachnoid haemorrhage (aSAH). In aSAH patients waves of spreading depolarization (SD) have a high incidence and cause hypoxia in tissue at risk, and, importantly, the haemodynamic response is the inverse of that seen in healthy tissue. In previous clinical studies, clusters of prolonged SDs have been measured in aSAH patients in close proximity to structural brain damage as assessed by neuroimaging, and, in theoretical studies, a mechanism was presented, suggesting how a failure of internal feedback could be a putative mechanism of such SD cluster patterns in acute stroke. This failing internal feedback control is now suggested to be replaced by ECoG-based short-range recurrent functional stimulation that initiates the normal hyperperfusion haemodynamic response in a demand-controlled way and stabilizes the tissue at risk during the critical phase of SD passage. The suggested method has three key features: (i) it is short-range, i.e., in the order of the distance of the ECoG electrode strip, (ii) it is demand-controlled, and (iii) it uses no prior knowledge of the target state, in particular, it adapts to conditions in the healthy physiological range. On-demand type stimulation provides minimal invasive feedback as the control force is off when the target state is reached, i.e., the tissue at risk is without SD or it is back to the physiological range (out of risk). These last two features (ii-iii) are shared with classical methods of chaos control, where major progress was made in the last years with respect to extensions for spatio-temporal wave patterns. A detailed bifurcation analysis of the nonlinear model is presented, in particular, the SD cluster forming cortical state is suggested to be caused by a delay-induced saddle-node bifurcation.

Fetal cerebral blood flow, electrocorticographic activity, and oxygenation: responses to acute hypoxia

Arterial blood gases are critical in regulation of cerebral blood flow (CBF) and cerebral metabolic rate for O(2) (CMRO(2)). However, the relation of these variables to cortical tissue (t ), and electrocorticographic (ECoG) activity (high voltage low frequency, HVLF, versus low voltage high frequency, LVHF), are not well defined. In the fetus, we tested the hypothesis that ECoG pattern is associated closely with cerebral oxygenation. In fetal sheep (n = 8) with laser Doppler flowmeter, fluorescent O(2) probe and ECoG electrodes, we measured laser Doppler CBF (LD-CBF), tP(O2), ECoG and spectral edge frequency-90 (SEF(90)) in response to 40 min isocapnic hypoxia. In the normoxic fetus, LD-CBF and CMRO(2) correlated highly with ECoG state. With a shift from HVLF to LVHF, tP(O2) decreased followed by increased LD-CBF (18%) and CMRO(2) (13%). With acute hypoxia (P(aO2)= 12 +/- 1 Torr), tp(O2) decreased toapproximately 3 Torr, LD-CBF increased 48 +/- 10%, ECoG shifted to chiefly the HVLF state, SEF(90) decreased approximately 15%, and CMRO(2) decreased approximately 20% (P < 0.05 for each). For the normoxic fetus, CBF was closely related to ECoG state, but this association was less evident during acute hypoxia. We speculate that, in the otherwise stressed fetus, acute hypoxia may further compromise cerebral oxygenation.

Repetitive cortical spreading depolarizations in a case of severe brain trauma

Objective and importance: Cortical spreading depolarizations (CSD) are waves of mass tissue depolarization that mediate progressive development of cortical infarction in animal models and occur in ∼50% of patients with acute brain injury. Here we performed multi-modal cerebral monitoring to investigate pathologies associated with CSD occurrence in a case of severe traumatic brain injury.Clinical presentation: A 20 years old male suffering severe traumatic brain injury from a fall had extensive frontal subdural and intraparenchymal hemorrhage with mass effect. Craniectomy was performed for hematoma evacuation and decompression.Intervention: During surgery, a subdural electrocorticography (ECoG) electrode strip, along with microdialysis and PtiO2 probes, was placed beside injured cortex for CSD monitoring. Within 13–81 hours post-injury, 34 CSD occurred. CSD incidence increased during spontaneous hyperthermia and decreased during induced normothermia. Periods of CSD activity were also associated with low brain glucose (<0.10 mmol/l), elevated glutamate (>40 mmol/l) and lactate/pyruvate (>40), and PtiO2<10 mmHg. CSD caused progressive deterioration of ECoG activity only in regions with infarction at follow-up on day 27.Conclusion: Repetitive mass tissue depolarizations accompanied a negative course of hemorrhagic lesion progression in the presence of ischemic conditions after traumatic brain injury. Whether as cause or effect, CSD may represent an inherent component of progressive metabolic failure leading to tissue death, and temperature appears to be an important factor influencing their occurrence. Continuous ECoG is a valuable tool for monitoring subclinical events such as CSD and seizures and for translational research in acute brain injury mechanisms and therapeutics.

Detection of temporal lobe spikes: Comparing nasopharyngeal, cheek and anterior temporal electrodes to simultaneous subdural recordings

ObjectiveTo compare nasopharyngeal (NP), cheek and anterior temporal (AT) electrodes for the detection yield and localization of interictal spikes in temporal lobe epilepsy. MethodsIn patients evaluated for epilepsy surgery with subdural electrocorticography electrodes, we simultaneously recorded NP, cheek and AT electrodes. Two observers identified spikes in EEG traces and marked in which channels they occurred. Interobserver agreement was calculated using Cohen’s kappa. For localization, data-sets with high interobserver agreement (κ-value ⩾0.4) were evaluated. The subdural distribution of NP and AT spikes was mapped. ResultsSeven patients were included, six were analyzed for localization. Only 1.5% of spikes recorded by cheek electrodes were not seen on temporal leads, while 25% of NP spikes were not seen on either. Spikes only recorded by NP electrodes had mesiobasal, while AT spikes had lateral temporal distribution. ConclusionsNP electrodes can increase EEG spike detection rate in temporal lobe epilepsy and are more useful than cheek electrodes. Spikes that are seen only on NP electrodes tend to be mesiobasal temporal lobe spikes. SignificanceAdding NP electrodes to scalp EEG can aid interictal spike detection and source localization, especially in short recordings like MEG–EEG.

Functional dynamics of spoken and signed word production: A case study using electrocorticographic spectral analysis

Background: Event-related changes in the EEG power spectrum have recently been used to study functional brain activation in humans. Like traditional event-related potentials, event-related spectral changes provide information about the temporal evolution of cortical activation that is difficult to obtain with fMRI or PET. These spectral changes include event-related suppression of power in the alpha band (8-13 Hz) and even-related augmentation of power in the gamma band (>30 Hz). Most studies of the gamma band have focused on frequencies in and around 40 Hz. Using electrocorticographic (ECoG) signals recorded with subdural electrodes implanted for the surgical management of epilepsy, we have also observed a broadband augmentation of power in higher gamma frequencies (>80 Hz). This index of cortical activation has compared favourably with alpha suppression and with electrical cortical stimulation mapping in studies utilising simple motor and auditory processing, but such a comparison has not been done for tasks requiring more complex language processing. Aims: We used two different spectral indices of cortical activation - alpha power suppression and gamma power augmentation, to study the spatial and temporal patterns of human cortical activation during different word production tasks. Methods: Subdural ECoG electrodes were implanted for clinical purposes in a patient with normal hearing, who had learned sign language as an adult and later developed intractable epilepsy. We measured event-related spectral changes during language tasks with different input and output modalities: Picture naming and word reading (visual inputs), and word repetition (auditory input) were performed with spoken responses (oral-articulatory output) and with signed responses (manual-gestural output). In addition we used a visually guided motor task to map tongue and hand representations independent of language. Results: Speech and signing differentially activated tongue and hand regions of sensorimotor cortex. Although posterior superior temporal gyrus was activated early during auditory word repetition, picture naming and word reading also activated this region, albeit slightly later, consistent with phonological and/or lexical-semantic processing. In contrast, basal temporal-occipital cortex was activated earlier and with greater magnitude during picture naming and word reading than during word repetition, suggesting semantic processing or object and word recognition. In all of the tasks, event-related gamma augmentation occurred in more discrete spatial and temporal patterns than event-related alpha suppression. Conclusions: Event-related alpha suppression and gamma augmentation provide complementary information about task-related cortical activation. This study demonstrates the utility of ECoG spectral analysis for studying the functional anatomy of human language with excellent temporal resolution.

Dipole localization of human induced focal afterdischarge seizure in simultaneous magnetoencephalography and electrocorticography.

Localizations were compared for the same human seizure between simultaneously measured MEG and iEEG, which were both co-registered to MRI. The whole-cortex neuromagnetometer localized a dipole in a sphere phantom, co-registered to the MEG sensor array, with an error of 1.4 mm. A focal afterdischarge seizure was induced in a patient with partial epilepsy, by stimulation at a subdural electrocorticography (ECoG) electrode with a known location, which was co-registered to the MRI and to the MEG sensor array. The simultaneous MEG and ECoG during the 30-second seizure was measured and analyzed using the single, moving dipole model, which is the localization model used clinically. The dipole localizations from simultaneous whole cortex 68-channel MEG and 64-channel ECoG were then compared for the repetitive spiking at six different times during the seizure. There were two main regions of MEG and ECoG activity. The locations of these regions were confirmed by determining the location clusters of 8,000 dipoles on ECoG at consecutive time points during the seizure. The mean distances between the stimulated electrode location versus the dipole location of the MEG and versus the dipole location of the ECoG were each about one (1) centimeter. The mean distance between the dipole locations of the MEG versus the dipole locations of the ECoG was about 2 cm. These errors were compared to errors of MEG and ECoG reported previously for phantoms and for somatosensory evoked responses (SER) in patients. Comparing the findings from the present study to those from prior studies, there appeared to be the expected stepwise increase in mean localization error progressing from the phantom, to the SER, to the seizure.

Organization of Cortical Activities Related to Movement in Humans

The extent and function of synchronization of oscillatory elements in the human sensorimotor cortex during movement remains unclear. Here we determine whether synchronization is distributed in both the spatial and frequency domains and whether it changes according to task. Electrocorticographic (ECoG) signals were recorded from presumed nonpathological areas simultaneously with electromyographic (EMG) signals from upper limb muscles during isometric and phasic movement tasks in humans with subdural electrodes in situ for investigation of epilepsy. Functional mapping of the sensorimotor cortex was performed by previous electrical stimulation through the same ECoG electrodes used for recording. Significant coherence between ECoG and EMG was seen at discrete frequencies in the range of 7-100 Hz. There was no predilection for coherence within a given frequency band to be associated with cortical sites that had been functionally defined as producing contralateral arm motor responses on stimulation. However, coherence with muscle in the 7-14 and 15-30 Hz band tended to be associated with ECoG sites that lay close to or within the central sulcus as determined intraoperatively. The spatial pattern and frequency of coherence changed with different tasks, although similarities in the coherence pattern remained for tasks that shared common features. These findings provide support for the hypothesis that that synchronization at specific frequencies links cortical activities into a functional ensemble during voluntary movement.

Low grade glioma in intractable epilepsy: lesionectomy versus epilepsy surgery.

In approximately 30% of patients with intractable partial epilepsy, an intra-axial cerebral lesion is the aetiology of the seizure disorder. Lesions adjacent to mesiotemporal structures often result in secondary epileptogenicity in the same region. The authors present 22 cases of low-grade gliomas associated with intractable epilepsy. In 15 cases the location was temporal (8 extra-hippocampal and 7 with invasion of the amygdalo-hippocampus), 7 cases were extratemporal in eloquent areas. The eight extra-hippocampal tumours were originally treated with lesionectomy. The seizure outcome was class 1 in only 4 cases, the remaining 4 were class 4 according to Engel's classification. The 4 cases with class 4 outcome required additional temporal lobectomy associated with amygdalo-hippocampectomy for seizure control. The 2 cases with associated hippocampal atrophy at MRI after lobectomy had outcome class 1. The 2 cases without hippocampal atrophy at MRI presented outcome class 2. The 7 cases with invasion of amygdala and hippocampus were treated with selective lesionectomy+amygdalo-hippocampectomy. In all these cases convergence of focal structural abnormality, ictal onset of epileptiform EEG abnormality and interictal epileptiform EEG abnormality provided powerful evidence of focal epileptogenicity. All these patients had a favourable epilepsy outcome (class 1-2). In the seven extratemporal cases the first step was lesionectomy. In 1 case located in the parietal region intraoperative mapping was required. 5 had class 1 outcome, one case had outcome class 2 and one case had an outcome class 4. The last patient required a second step operation with intraoperative strip and deep electrode monitoring that led subsequently to a frontal lobectomy. This patient is seizure free 2 years after surgery. There was no perioperative mortality and post-operative morbidity was 3/22. This study indicates that lesionectomy may be the first step procedure if the structural abnormality is localized to extra-temporal eloquent cortex and concordance is documented. Patients may subsequently be candidates for a cortical resection as a second step procedure if the lesionectomy does not provide an adequate reduction in seizure tendency. Since MRI identified hippocampal atrophy was predictive in this study of an unsatisfactory seizure outcome after lesionectomy, MRI defined dual pathologies consisting of a temporal lesion plus hippocampal atrophy necessitate temporal lobectomy+amygdalo-hippocampectomy. In patients with negative MRI findings of hippocampal atrophy and temporal lobe lesions, intraoperative electrocorticography and deep electrode monitoring are indicated for planning the surgical strategy.

Automatic calculation of epileptogenic focus location within the brain.

The authors propose a hypothesis about the mathematical relationship between the position and intensity of epileptogenic discharge and the potential recorded from an electrocorticographic electrode. A computer program is used to solve the equation and to determine a small area of maximal probability for the focus to be found.

Effects of acute and chronic paleocerebellar stimulation on experimental models of epilepsy in the cat: studies with enflurane, pentylenetetrazol, penicillin, and chloralose.

Effects of acute and chronic paleocerebellar stimulation were evaluated in four experimental models of epilepsy in 24 adult cats chronically implanted with bilaterally symmetric parasagittal electrocorticographic electrodes and anterior lobe cerebellar stimulation electrodes. Pentylenetetrazol was given intraveneously in 50-mg increments or 4% enflurane was inspired until grand mal seizures occurred spontaneously or were triggered by photic or auditory stimuli. Alpha-chloralose, 50 mg/kg, was injected intraperitoneally to produce a model of stimulus-sensitive myoclonus and sodium penicillin G, 350,000 units/kg, was injected intramuscularly to produce a model of petit mal epilepsy. One- to 250-Hz electrical stimulation of paleocerebellar cortical surfaces was performed with constant-voltage or constant-current stimulators at threshold and suprathreshold intensities with average intensities of 8 V and 2.5 mA, respectively. Acute or chronic, threshold or suprathreshold paleocerebellar stimulation did not predictably alter the electrographic or clinical manifestations in any of these four models.