Electrocorticogram Research Articles

Local spatial correlation analysis of hand flexion/extension using intraoperative high-density ECoG.

We recorded motor cortical activity using highdensity electrocorticogram (ECoG) from three patients during awake craniotomy. Subjects repeatedly executed hand flexion/extension tasks according to auditory instructions. Clear event-related desynchronization (ERD) in beta band (8-32) Hz and event-related synchronization (ERS) in gamma band (60-200) Hz were observed. High frequency band (HFB: 60-200 Hz) activation was found to be more localized compared to low frequency band (LFB: 8-32 Hz) activation in all subjects. Local spatial correlation maps in LFB and HFB were constructed by computing the correlation between channels. Local spatial correlation dropped more in the ERD/ERS areas consistently in two subjects. The results indicate that ERD/ERS patterns are more spatially uncorrelated and denser ECoG electrode is necessary within these areas to map uncorrelated `sources'. High resolution electrodes might improve both clinical functional mapping and brain machine interface outcomes in the near future.

Adaptive shut-down of EEG activity predicts critical acidemia in the near-term ovine fetus.

In fetal sheep, the electrocorticogram (ECOG) recorded directly from the cortex during repetitive heart rate (FHR) decelerations induced by umbilical cord occlusions (UCO) predictably correlates with worsening hypoxic-acidemia. In human fetal monitoring during labor, the equivalent electroencephalogram (EEG) can be recorded noninvasively from the scalp. We tested the hypothesis that combined fetal EEG – FHR monitoring allows for early detection of worsening hypoxic-acidemia similar to that shown for ECOG-FHR monitoring. Near-term fetal sheep (n = 9) were chronically instrumented with arterial and venous catheters, ECG, ECOG, and EEG electrodes and umbilical cord occluder, followed by 4 days of recovery. Repetitive UCOs of 1 min duration and increasing strength (with regard to the degree of reduction in umbilical blood flow) were induced each 2.5 min until pH dropped to <7.00. Repetitive UCOs led to marked acidosis (arterial pH 7.35 ± 0.01 to 7.00 ± 0.03). At pH of 7.22 ± 0.03 (range 7.32–7.07), and 45 ± 9 min (range 1 h 33 min–20 min) prior to attaining pH < 7.00, both ECOG and EEG amplitudes began to decrease ∼fourfold during each FHR deceleration in a synchronized manner. Confirming our hypothesis, these findings support fetal EEG as a useful adjunct to FHR monitoring during human labor for early detection of incipient fetal acidemia.

Relationship between subthalamic nucleus neuronal activity and electrocorticogram is altered in the R6/2 mouse model of Huntington's disease.

Neural synchrony between the subthalamic nucleus (STN) and cortex is critical for proper information processing in basal ganglia circuits. Using in vivo extracellular recordings in urethane-anaesthetized mice, we demonstrate that single units and local field potentials from the STN exhibit oscillatory entrainment to low-frequency (0.5-4Hz) rhythms when the cortex is in a synchronized state. Here we report novel findings in the R6/2 transgenic mouse model of Huntington's disease (HD) by demonstrating that STN activity is reduced and less phase-locked to cortical low-frequency oscillations. The spectral power of low-frequency oscillations in ECoG recordings of R6/2 mice is diminished while the spectral power of higher frequencies is augmented and such altered cortical patterning could lead to decreased synchrony in corticosubthalamic circuits. Our data establish that cortical entrainment of STN neural activity is disrupted in R6/2 mice and may be one of the mechanisms contributing to disordered motor control in HD. Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder in which impairments in the processing of information between the cortex and basal ganglia are fundamental to the onset and progression of the HD phenotype. The corticosubthalamic hyperdirect pathway plays a pivotal role in motor selection and blockade of neuronal activity in the subthalamic nucleus (STN) results in a hyperkinetic movement syndrome, similar to the HD phenotype. The aim of the present study was to examine the relationship between neuronal activity in the STN and cortex in an animal model of HD. We performed in vivo extracellular recordings in the STN to measure single-unit activity and local field potentials in the R6/2 transgenic mouse model of HD. These recordings were obtained during epochs of simultaneously acquired electrocorticogram (ECoG) in discrete brain states representative of global cortical network synchronization or desynchronization. Cortically patterned STN neuronal activity was less phase-locked in R6/2 mice, which is likely to result in less efficient coding of cortical inputs by the basal ganglia. In R6/2 mice, the power of the ECoG in lower frequencies (0.5-4Hz) was diminished while the power expressed in higher frequencies (13-100Hz) was increased. In addition, the spontaneous activity of STN neurons in R6/2 mice was reduced and neurons exhibited a more irregular firing pattern. Glutamatergic STN neurons provide the major excitatory drive to the output nuclei of the basal ganglia and altered discharge patterns could lead to aberrant basal ganglia output and disordered motor control in HD.

Progressive, Seizure-Like, Spike-Wave Discharges Are Common in Both Injured and Uninjured Sprague-Dawley Rats: Implications for the Fluid Percussion Injury Model of Post-Traumatic Epilepsy.

Variable-duration oscillations and repetitive, high-voltage spikes have been recorded in the electrocorticogram (ECoG) of rats weeks and months after fluid percussion injury (FPI), a model of traumatic brain injury. These ECoG events, which have many similarities to spike-wave-discharges (SWDs) and absence seizures, have been proposed to represent nonconvulsive seizures characteristic of post-traumatic epilepsy (PTE). The present study quantified features of SWD episodes in rats at different time points after moderate to severe FPI, and compared them with age-matched control rats. Control and FPI-injured rats at 1 year of age displayed large-amplitude and frequent SWD events at frontal and parietal recording sites. At 3-6 months, SWDs were shorter in duration and less frequent; extremely brief SWDs (i.e., "larval") were detected as early as 1 month. The onset of the SWDs was nearly always synchronous across electrodes and of larger amplitude in frontal regions. A sensory stimulus, such as a click, immediately and consistently stopped the occurrence of the SWDs. SWDs were consistently accompanied by behavioral arrest. All features of SWDs in control and experimental (FPI) rats were indistinguishable. None of the FPI-treated rats developed nonconvulsive or convulsive seizures that could be distinguished electrographically or behaviorally from SWDs. Because SWDs have features similar to genetic absence seizures, these results challenge the hypothesis that SWDs after FPI reflect PTE.

Analysis of electrocorticographic patterns in rats fed standard or hyperlipidic diets in a normal state or during status epilepticus

Objective: The consumption of hyperlipidic diets has grown markedly in recent decades, and several studies have linked this consumption with the development of neurodegenerative diseases. Conversely, hyperlipidic diets have been used as an alternative therapy for refractory epilepsy. The purpose of this study was to evaluate the effects of a hyperlipidic diet on brain electrical activity before and during status epilepticus (SE) using computational and mathematical methods.Methods: Electrocorticogram (ECoG) was recorded in Wistar rats fed with standard and hyperlipidic diets. Each recording was obtained during 30-minute period (baseline), after this time, the SE was induced by pilocarpine, and recording was continued for another 30 minutes. The ECoG signals were analyzed by the following methods: power spectrum, Lempel–Ziv complexity (LZC), and fractal dimension of the phase space.Results: Hyperlipidic diet in normal animals caused a decrease in the theta, alpha, and beta rhythm, and reduced the LZC of the brain electrical activity. However, when the animals were induced to SE, these differences between nutritional groups were not observed. SE caused in both dietary groups increase in theta, alpha, and beta rhythm values, and increase in the complexity of brain electrical activity.Discussion: Hyperlipidic diet consumption attenuated the brain's electrical activity, suggesting that healthy individuals who habitually eat a hyperlipidic diet may develop dysfunctions such as cognitive decline and memory impairment. Furthermore, the antagonistic effect between hyperlipidic diet and SE suggests that this diet could protect against seizures.

Decreased HCN2 expression in STN contributes to abnormal high-voltage spindles in the cortex and globus pallidus of freely moving rats

Abnormal oscillation in the cortical-basal ganglia loop is involved in the pathophysiology of parkinsonism. High-voltage spindles (HVSs), one of the main type abnormal oscillations in Parkinson’s disease, are regulated by dopamine D2-like receptors but not D1-like receptors. However, little is known about how dopamine D2-like receptors regulate HVSs and the role of hyperpolarization-activated cyclic nucleotide-gated2 (HCN2) in HVSs regulation. We simultaneously recorded the local field potential (LFP) in globus pallidus (GP) and electrocorticogram (ECoG) in primary motor cortex (M1) in freely moving 6-hydroxydopamine (6-OHDA) lesioned or control rats. The expression of HCN2 and dopamine D2 receptor in the subthalamic nucleus (STN) was examined by immunochemical staining and Western blotting. We also tested the role of HCN2 in HVSs regulation by using pharmacological and shRNA methodology. We found that dopamine D2-like receptor agonists suppressed the increased HVSs in 6-OHDA lesioned rats. HCN2 was co-expressed with dopamine D2 receptor in the STN, and dopamine depletion decreased the expression of HCN2 as well as dopamine D2 receptor which contribute to the regulation of HVSs. HCN2 was down regulated by HCN2 shRNA, which thereby led to an increase in the HVSs in naïve rats while HCN2 agonist reduced the HVSs in 6-OHDA lesioned rats. These results suggest that HCN2 in the STN is involved in abnormal oscillation regulation between M1 cortex and GP.

Sarin-induced brain damage in rats is attenuated by delayed administration of midazolam

Sarin poisoned rats display a hyper-cholinergic activity including hypersalivation, tremors, seizures and death. Here we studied the time and dose effects of midazolam treatment following nerve agent exposure. Rats were exposed to sarin (1.2 LD50, 108μg/kg, im), and treated 1min later with TMB4 and atropine (TA 7.5 and 5mg/kg, im, respectively). Midazolam was injected either at 1min (1mg/kg, im), or 1h later (1 or 5mg/kg i.m.). Cortical seizures were monitored by electrocorticogram (ECoG). At 5 weeks, rats were assessed in a water maze task, and then their brains were extracted for biochemical analysis and histological evaluation. Results revealed a time and dose dependent effects of midazolam treatment. Rats treated with TA only displayed acute signs of sarin intoxication, 29% died within 24h and the ECoG showed seizures for several hours. Animals that received midazolam within 1min survived with only minor clinical signs but with no biochemical, behavioral, or histological sequel. Animals that lived to receive midazolam at 1h (87%) survived and the effects of the delayed administration were dose dependent. Midazolam 5mg/kg significantly counteracted the acute signs of intoxication and the impaired behavioral performance, attenuated some of the inflammatory response with no effect on morphological damage. Midazolam 1mg/kg showed only a slight tendency to modulate the cognitive function. In addition, the delayed administration of both midazolam doses significantly attenuated ECoG compared to TA treatment only. These results suggest that following prolonged seizure, high dose midazolam is beneficial in counteracting adverse effects of sarin poisoning.

A probabilistic method for determining cortical dynamics during seizures.

This work presents a probabilistic method for inferring the parameter ranges in a biologically relevant mathematical model of the cortex most likely to be producing seizures observed in an electrocorticogram (ECoG) signal from a human subject. Additionally, this method produces a probabilistic pathway of the temporal evolution of physiological state in the cortex over the course of individual seizures, leveraging a model of the cortex that describes cortical physiology. We describe ways in which these methods and results offer insights into seizure etiology and have the potential to suggest new treatment options. To directly account for the stochastic and noisy nature of the mathematical model and the ECoG signal, we use a probabilistic Bayesian framework to map features of ECoG segments onto a distribution of likelihoods over physiologically-relevant parameter states. A Hidden Markov Model (HMM) is then introduced to incorporate the belief that cortical physiology has both temporal continuity and also a degree of reproducibility between individual seizures. By inspecting the ratio of likelihoods between HMMs run under two possible parameter regions, both of which produce seizures in the model, we determine which physiological parameter regions are more likely to be causing the observed seizures. We show that between individual seizures, there is consistency in these likelihood ratios between hypothesized regions, in the temporal pathways calculated, and in the separation of seizure from non-seizure time segment likelihood maps.

High frequency stimulation of the STN restored the abnormal high-voltage spindles in the cortex and the globus pallidus of 6-OHDA lesioned rats

Many studies showed that abnormal oscillations in the cortical-basal ganglia loop is involved in the pathophysiology of Parkinson’s disease (PD). In contrast to the well-studied beta synchronization, high-voltage spindles (HVSs), another type of abnormal oscillation observed in PD, are neglected. To explore the role of subthalamic nucleus-deep brain stimulation (STN-DBS) in HVSs regulation, we simultaneously recorded the local field potential (LFP) in the globus pallidus (GP) and electrocorticogram (ECoG) in the primary motor cortex(M1) in freely moving 6-hydroxydopamine (6-OHDA) lesioned or control rats before, during, and after STN-DBS. Consistent with our previous study, HVSs occurrence, duration, and relative power and coherence between the M1 cortex and GP increased in 6-OHDA lesioned rats. We found that high but not low frequency stimulation restored the abnormal HVSs activity and motor deficit. These results suggest that the STN is involved in the abnormal oscillation between the M1 cortex and GP.

A unifying principle underlying the extracellular field potential spectral responses in the human cortex.

Electrophysiological mass potentials show complex spectral changes upon neuronal activation. However, it is unknown to what extent these complex band-limited changes are interrelated or, alternatively, reflect separate neuronal processes. To address this question, intracranial electrocorticograms (ECoG) responses were recorded in patients engaged in visuomotor tasks. We found that in the 10- to 100-Hz frequency range there was a significant reduction in the exponent χ of the 1/f(χ) component of the spectrum associated with neuronal activation. In a minority of electrodes showing particularly high activations the exponent reduction was associated with specific band-limited power modulations: emergence of a high gamma (80-100 Hz) and a decrease in the alpha (9-12 Hz) peaks. Importantly, the peaks' height was correlated with the 1/f(χ) exponent on activation. Control simulation ruled out the possibility that the change in 1/f(χ) exponent was a consequence of the analysis procedure. These results reveal a new global, cross-frequency (10-100 Hz) neuronal process reflected in a significant reduction of the power spectrum slope of the ECoG signal.

Treatment and outcome of epileptogenic temporal cavernous malformations.

Background:The aim of this study is to explore the treatment and outcome of epileptogenic temporal lobe cavernous malformations (CMs).Methods:We analyzed retrospectively the profiles of 52 patients diagnosed as temporal lobe CMs associated with epilepsy. Among the 52 cases, 11 underwent a direct resection of CM along with the adjacent zone of hemosiderin rim without electrocorticogram (ECoG) monitoring while the other 41 cases had operations under the guidance of ECoG. Forty-six patients were treated by lesionectomy + hemosiderin rim while the other six were treated by lesionectomy + hemosiderin rim along with extended epileptogenic zone resection. The locations of lesions, the duration of illness, the manifestation, the excision ranges and the outcomes of postoperative follow-up were analyzed, respectively.Results:All of the 52 patients were treated by microsurgery. There was no neurological deficit through the long-term follow-up. Outcomes of seizure control are as follows: 42 patients (80.8%) belong to Engel Class I, 5 patients (9.6%) belong to Engel Class II, 3 patients (5.8%) belong to Engel Class III and 2 patients (3.8%) belong to Engel Class IV.Conclusion:Patients with epilepsy caused by temporal CMs should be treated as early as possible. Resection of the lesion and the surrounding hemosiderin zone is necessary. Moreover, an extended excision of epileptogenic cortex or cerebral lobes is needed to achieve a better prognosis if the ECoG indicates the existence of an extra epilepsy onset origin outside the lesion itself.

Examination of Scale-Invariant Characteristics of Multi-channel ECoG Data for Epileptic Seizure Localization

One of the most important tasks for epilepsy surgery is to localize a region of the brain involved with the development of epileptic seizure. This study investigates the scale-invariant behavior of brain activity for evidence of epileptic seizure localization. Multi-channel electrocorticogram (ECoG) data of a subject diagnosed with right mesial temporal lobe epilepsy obtained from various regions of the brain and associated with different states of the brain are examined using the wavelet-based fractal analysis. The spectral exponent computed from such analysis is used as a measure for quantifying scale-invariant behavior. The computational results show that the ECoG data corresponding to various regions of the brain and also different states of the brain exhibit distinguishable characteristics of the spectral exponent. Furthermore, a significant increase in the spectral exponent is observed only in the ECoG channels associated with an epileptic seizure event (inside the epileptogenic zone) during the ictal state. The computational results provide preliminary evidence that an epileptic seizure can be both temporally and spatially localized using scale-invariant characteristics.

Age-dependent alterations in the cortical entrainment of subthalamic nucleus neurons in the YAC128 mouse model of Huntington's disease

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that results in motor, cognitive and psychiatric abnormalities. Dysfunction in neuronal processing between the cortex and the basal ganglia is fundamental to the onset and progression of the HD phenotype. The corticosubthalamic hyperdirect pathway plays a crucial role in motor selection and blockade of neuronal activity in the subthalamic nucleus (STN) results in hyperkinetic movement abnormalities, similar to the motor symptoms associated with HD. The aim of the present study was to examine whether changes in the fidelity of information transmission between the cortex and the STN emerge as a function of phenotypic severity in the YAC128 mouse model of HD. We obtained in vivo extracellular recordings in the STN and concomitant electrocorticogram (ECoG) recordings during discrete brain states that reflected global cortical network synchronization or desynchronization. At early ages in YAC128 mice, both the cortex and the STN exhibited patterns of hyperexcitability. As symptom severity progressed, cortical entrainment of STN activity was disrupted and there was an increase in the proportion of non-oscillating, tonically firing STN neurons that were less phase-locked to cortical activity. Concomitant to the dissipation of STN entrainment, there was a reduction in the evoked response of STN neurons to focal cortical stimulation. The spontaneous discharge of STN neurons in YAC128 mice also decreased with age and symptom severity. These results indicate dysfunction in the flow of information within the corticosubthalamic circuit and demonstrate progressive age-related disconnection of the hyperdirect pathway in a transgenic mouse model of HD.

Power-law spectrum and small-world structure emerge from coupled evolution of neuronal activity and synaptic dynamics

A co-evolutionary neuronal network model based on previous ones is proposed, and both functional and structural properties are numerically calculated. Recent experiments have revealed power-law behavior in electrocorticogram (ECoG) spectrum related with synaptic plasticity and reorganization. In the present neuronal network model, the network starts its evolution from the initial configuration of random network which is the least biased and without special structure, and the interaction rules among neurons are modified from both models by Bornholdt's and Arcangelis' groups to simulate the process of synaptic development and maturation. The system exhibits dynamic small-world structure which is the result of evolution instead of the assumption beforehand. Meanwhile, the power spectrum of electrical signals reproduces the power-law behavior with the exponent 2.0 just as what is experimentally measured in ECoG spectrum. Moreover, the power spectrum of the average degree per neuron over time also exhibits power-law behavior, with the exponent 2.0 again over more than 5 orders of magnitude. Different from previous results, our network exhibits assortative degree-degree correlation which is expected to be checked by experiments.

Real-time BMI using ECoG for paralyzed patients

Event Abstract Back to Event Real-time BMI using ECoG for paralyzed patients Ryohei Fukuma1, 2* 1 Osaka University Graduate School of Medicine, Department of Neurosurgery, Japan 2 ATR Computational Neuroscience Laboratories, Department of Neuroinformatics, Japan A neuroprosthesis using a brain-machine interface (BMI) is a promising therapeutic option for severely paralyzed patients. However, typical high-performance BMIs require microelectrodes, which damage cortex and lack long-term stability of signals. We have developed a neuroprosthesis controlled by real-time electrocorticogram (ECoG), and adapted the neuroprosthesis to paralyzed patients. In this talk, I first demonstrate characteristic features in the ECoG signals of paralyzed patients, and the representation about the movement of paralyzed limb. The spatial pattern of high-γ power coded information about movements, and by using machine-learning approach, the information could be successfully extracted to control the neuroprosthesis. Next, I introduce an experiment, in which ECoG-based BMI was adapted to an amyotrophic lateral sclerosis (ALS) patient. In this experiment, the patient succeeded in controlling the neuroprosthesis and typing words on computer, using motor imagery. This is the first report to show the successful communication using ECoG from the ALS patient. Finally, I discuss new approaches to realize practical ECoG-based BMI. Keywords: ECoG, Brain machine interface (BMI), Amyotrophic lateral sclerosis (ALS), Paralysis, machine learning Conference: German-Japanese Adaptive BCI Workshop, Kyoto, Japan, 28 Oct - 29 Oct, 2015. Presentation Type: Oral presentation (Invited speakers) Topic: Adaptive BCI Citation: Fukuma R (2015). Real-time BMI using ECoG for paralyzed patients. Front. Comput. Neurosci. Conference Abstract: German-Japanese Adaptive BCI Workshop. doi: 10.3389/conf.fncom.2015.56.00005 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 15 Oct 2015; Published Online: 04 Nov 2015. * Correspondence: Dr. Ryohei Fukuma, Osaka University Graduate School of Medicine, Department of Neurosurgery, Suita, Osaka, Japan, r-fukuma@nsurg.med.osaka-u.ac.jp Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ryohei Fukuma Google Ryohei Fukuma Google Scholar Ryohei Fukuma PubMed Ryohei Fukuma Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Brain-Machine Interfaces in the Completely Locked-In and Stroke

Brain-Machine Interfaces in the Completely Locked-In and Stroke

A wireless fully implantable ECoG recording medical device WIMAGINE� for human Brain Computer Interface applications: toward a clinical trial

Event Abstract Back to Event A wireless fully implantable ECoG recording medical device WIMAGINE® for human Brain Computer Interface applications: toward a clinical trial Guillaume Charvet1*, Corinne Mestais1, Fabien Sauter-Starace1, Michael Foerster1, Aurelien Lambert1, Claude Chabrol1, Napoleon R. Torres Martinez1, Thomas Costecalde1, David Ratel1 and Alim L. Benabid1 1 CEA/LETI, MINATEC Campus, France The WIMAGINE® implant was developed to record ECoG (ElectroCorticoGram) signals for long term clinical applications in the context of a Brain Computer Interface project which goal is to allow a tetraplegic subject to control a 4-limb exoskeleton thanks to his brain activity [1]. This active implantable medical device [2] is composed of an array of 64 biocompatible electrodes, a hermetic titanium housing including the electronic boards and biocompatible antennae for wireless transmission of data and remote power supply. This implant is able to record ECoG on 64 electrodes with selectable gain and sampling frequency, with less than 0.7μV RMS input referred noise in the [0.5Hz – 300Hz] band thanks to a dedicated integrated circuit. It is powered remotely through an inductive link at 13.56MHz, communicates wirelessly on the MICS band at 402-405MHz with a custom designed base station connected to a PC and complies with the regulations applicable to class III AIMD. During the surgical procedure, the implant will be inserted into a 50 mm craniotomy so that the electrode array is in contact with the dura mater, and the implant recovered by the skin (Fig. 1). The design of the WIMAGINE® implant takes into account all the constraints of long term implantable medical devices. In particular, WIMAGINE® was designed to satisfy the Essential requirements of the European Medical Device Directives 93/42/CEE and 90/385/EEC. A risk analysis according to ISO 14971 standards has been carried out, and risk management actions were set up. The implant manufacturing was achieved according to a qualified industrial process under ISO certification 13485. In order to increase the reliability, all electronic boards undergo a burn-in procedure to avoid early in-use system failures, and functional tests. The electronic board is encapsulated into a dedicated titanium packaging with hermetic feedthrough. The hermeticity is achieved by laser welding and tested in terms of helium leakage and yield 10-9 bar.cm-3.s-1. Then, each implant is tested, cleaned and sterilized according to a validated process. The mechanical and electrical qualification tests of the implant according to the ISO 45502-1 standards were successfully achieved by certified bodies, such as resistance to mechanical forces, vibrations and shocks, electrodes leakage current less than 1μA, heating at the surface of the implant less than 2°C. Likewise, the electrical security tests and electromagnetic compatibility (EMC) tests according to the EN 60601-1 were performed on the WIMAGINE® platform. Finally, the long-term biocompatibility is evaluating according to the ISO 10993. The submission of the protocol for clinical trial authorization to the French authorities (ANSM and CPP) in the context of Brain Computer Interface for tetraplegia is in progress. Other neurological applications requiring wireless ECoG recording such as presurgical evaluation of epilepsy, or post stroke rehabilitation [3] can be addressed.

Dexmedetomidine anesthesia enhances spike generation during intra-operative electrocorticography: A promising adjunct for epilepsy surgery

Anesthetic-induced suppression of cortical electrical activity is a major concern during epilepsy surgery. Dexmedetomidine (Dex) has been recently evaluated in a few small series for its effect on the electrocorticographic spikes intra-operatively. In this prospective study, electrocorticogram (ECoG) was monitored during dexmedetomidine infusion in 34 patients (M:F=23:11, age=29.2 ± 10.9 years; duration of epilepsy=15.3 ± 8.9 years) undergoing anterior temporal lobe resection with amygdalo-hippocampectomy for drug-resistant mesial temporal lobe epilepsy (Right: 18, Left: 16). Anesthesia was induced with thiopental/propofol and maintained with oxygen-N2O-isoflurane. ECoG was recorded for 5 min after the end tidal MAC of N2O and isoflurane were decreased to zero; anesthesia was maintained with O2:Air=50:50, vecuronium and fentanyl. ECoG was recorded using a 4-contact strip electrode for: (a) 5 min prior to dexmedetomidine (PreDEX), (b) 5 min during dexmedetomidine infusion (DEX; 1 μg/kg) and (c) 5 min after stopping dexmedetomidine (PostDEX). The ECoG spikes were manually counted in all the channels. The mean spike rate in the 2 channels with maximum spikes (MAX CH A and MAX CH B) was normalized to a 3-min duration. RM-ANOVA and post hoc comparison of three phases were used to compare the spike rates. The mean spike rate during Dex phase was higher compared to preDEX (MAX CH B: p=0.007 and MAX CH A: p=0.079) and PostDEX (MAX CH B: p=0.17, MAX CH A: p=0.79) phases. The spike rate increased in 67.6% patients, while 11.8% patients showed ≤ 25% reduction and 20.6% patients showed >25% reduction in spike frequency. Dexmedetomidine is useful during intra-operative ECoG recording in epilepsy surgery as it enhances or does not alter spike rate in most of the cases, without any major adverse effects.

Neonatal dexamethasone accelerates spreading depression in the rat, and antioxidant vitamins counteract this effect

The use of dexamethasone (Dex) to treat chronic lung disease in preterm infants may produce adverse effects in the developing brain. Here, we evaluated the effects of neonatal Dex on the propagation of cortical spreading depression (CSD), and tested the action of vitamins C and E against the effect of Dex. Five groups of Wistar rats received, respectively: [1] no treatment (Naïve); [2] Vehicle (V); [3] tapering doses of Dex (Dex; 0.5mg/kg, 0.3mg/kg, and 0.1mg/kg) on postnatal day (PND) 1–3; [4] Dex plus 200mg/kg vitamin C and 100mg/kg vitamin E (DexCE); [5] only vitamins C and E (CE). Vehicle and vitamins were administered on PND 1–6. CSD was recorded after the pups reached maturity (PND 60–70). The Dex-treated group presented with higher CSD velocities (mean values±SD, in mm/min: 4.14±0.22, n=10) compared with the control groups (Naïve: 3.52±0.13, n=8; V: 3.57±0.18, n=10; CE: 3.51±0.24, n=10; p<0.05 for all). Vitamins C and E antagonized this effect (DexCE group; CSD velocity: 3.43±0.12, n=9). No intergroup difference was observed concerning P-wave amplitude and duration. In all groups, after the cortex underwent CSD, the electrocorticogram (ECoG) amplitude increased approximately 50% compared with the baseline amplitude for the same animal (CSD-induced ECoG potentiation); however, no intergroup difference was observed. Data suggest that coadministration of antioxidant vitamins with Dex may be a helpful therapeutic strategy to reduce brain adverse effects of dexamethasone.

MULTI-MODALITY IMAGE REGISTRATION FOR SUBDURAL ELECTRODE LOCALIZATION

Surgical treatment has been proved to be an effective way to control seizures for some kinds of intractable epilepsy. The electrocorticogram (ECoG) recorded from subdural electrodes has become an important technique for defining epileptogenic zones before surgery in clinical practice. The exact location of subdural electrodes has to be determined to establish the connection between electrodes and epileptogenic zones. Artifacts caused by the electrodes can severely affect the quality of CT imaging and sequentially image registration. In this paper, we discussed the performance of mean squares and the Mattes mutual information metric methods in multimodal image registration for subdural electrode localization. Since the skull can be regarded as a rigid body, rigid registration is sufficient for the purpose of subdural electrode localization. The vital parameter for the rigid registration is rotation. The translation result depends on the result of rotation. Both the methods performed well in the determination of the rotation center. Rotation angles of different image pairs of the same volume pair fluctuated a lot. Based on the image acquisition process, we assume that the images within the same volume pair should have the same transformation parameters for registration. Results show that the mean rotation angles of images within one dataset are approximate to the manual results that are considered to be the actual result for registration despite their fluctuation range.