A new method of inducing selective brain hypothermia with saline perfusion into the subdural space: effects on transient cerebral ischemia in cats. (9/76)

In this study, we tested brain surface cooling as a new method of inducing selective brain hypothermia, and evaluated its effects on focal cerebral ischemia using a cat model of transient middle cerebral artery (MCA) occlusion. Cats underwent 1 h of MCA occlusion followed by 5 h of reperfusion. Brain surface cooling was induced for 4 h during and after MCA occlusion in the hypothermia group, but not in the normothermia group. Brain surface cooling was performed using saline perfusion into the subdural space. Rectal temperature, brain surface temperature, and deep brain temperature were monitored, and regional cerebral blood flow (rCBF) and somatosensory evoked potential (SEP) were serially measured. After 5 h of reperfusion, water content was also measured. Although the rectal temperature was maintained at about 37 degrees C, the brain surface temperature decreased rapidly to 33 degrees C and was maintained at that temperature. For 3 h following reperfusion, the rCBF was lower in the hypothermia group than in the normothermia group. At 4 and 5 h after reperfusion, the recovery of SEP amplitude was significantly more enhanced in the hypothermia group than in the normothermia group. In the gray matter, the water content was significantly more diminished in the hypothermia group than in the normothermia group. These results demonstrate that our method is useful for protecting the ischemic brain from a transient MCA occlusion. This method may be adapted for neurological surgery.  (+info)

Dipole source analysis of laser-evoked subdural potentials recorded from parasylvian cortex in humans. (10/76)

The location of the human nociceptive area(s) near the Sylvian fissure is still controversial in spite of evidence from imaging and evoked potential studies that noxious heat stimuli activate somatosensory areas in that region. Some studies have suggested the secondary somatosensory cortex (SII) on the upper bank of the Sylvian fissure posterior to the central sulcus, others the anterior insula or parietal area 7b. In this study, we applied dipole source analysis techniques to laser-evoked potentials (LEPs) that were recorded from subdural grid electrodes in three patients. As a functional marker, auditory-evoked potentials (AEPs) with a generator on the opposite bank of the Sylvian fissure were recorded from the same electrodes. The LEP global field power (GFP), a measure of spatial variance, showed a first peak at about 150 ms latency, corresponding to the latency of the N1 recorded from the scalp. In contrast to scalp recordings, the amplitude of the first GFP peak recorded from the grid was larger than the second peak (P2). This finding suggests that the generator of N1, but not that of later LEP components, was close to the subdural grids. When a regional source was fitted to the first GFP peak, its location was within the frontoparietal operculum in all patients. On average, the LEP source was 13 mm anterior, 6 mm superior, and 2 mm medial of the AEP source. This relative location also suggests a source within the frontoparietal operculum overlying the insula. At the latency of the first GFP peak, source orientation pointed inward, suggesting a generator within the inner vertical surface of the operculum. Somatotopy was assessed in one patient and was consistent with that of the projection area of the presumed nociceptive thalamic nucleus posterior part of the ventromedial nucleus, but differed from that of SII. These findings suggest that the nociceptive area in human parasylvian cortex that is activated most rapidly by noxious heat pulses may be separate from the tactile SII area.  (+info)

Epileptogenic foci on subdural recording in intractable epilepsy patients with temporal dysembryoplastic neuroepithelial tumor. (11/76)

To investigate the epileptogenic foci in dysembryoplastic neuroepithelial tumor (DNT) in the temporal lobe, we studied extraoperative electrocorticography (ECoG) with subdural electrode arrays from nine patients with intractable epilepsy due to temporal DNT. Ictal onset zones and irritative zones were decided by the ECoG. The locations of these zones were compared to the location of the tumor. The number of ictal onset zone and irritative zone was 2.1+/-0.93 and 2.9+/-1.45 in a patient with a DNT. They were detected more frequently in the adjacent tissues of the tumor (88.9%) rather than within the tumor or in mesial temporal area (66.7%). Mesial temporal involvement was found in 6 patients (66.7%) as an ictal onset zone, and in 5 (55.6%) as an irritative zone. The 7 patients (77.8%) had ictal onset zone in areas different from active irritative zone. The surgical outcome was better, when ictal onset zone was completely resected rather than partially removed. Temporal DNT can make multiple ictal onset zones and irritative zones in different regions including the mesial temporal area. Deliberate resection of epileptogenic foci, including all ictal onset zones and irritative zones, ensures excellent seizure control.  (+info)

A computer-generated stereotactic "Virtual Subdural Grid" to guide resective epilepsy surgery. (12/76)

BACKGROUND AND PURPOSE: In selected patients undergoing epilepsy surgery, subdural electrode grids play an important role in localizing the epileptogenic zone and identifying eloquent cortex. Determining the relationship of the electrodes to underlying brain architecture traditionally has been difficult. This report describes and validates the use of an original computer-aided method that displays a representation of the electrode positions, based on postimplantation CT or MR findings, coregistered with a 3D-rendered image of the brain, on an image-guided surgery system. METHODS: Seventeen patients underwent the procedure with visual verification of the actual and virtual grids undertaken during the second (postimplantation) surgery. The accuracy of the Virtual Grid electrode positions was further studied in a subgroup of five patients during surgery by plotting the distance from the actual electrode positions by using an infrared stereotactic probe. RESULTS: The accuracy of the Virtual Grid electrode positions by visual inspection was satisfactory in all 17 cases. In the five cases in which quantitative measurements were performed, the mean error for the CT derived electrode positions was 3.4 mm (range 0.5-5.4) compared with the mean error for the MR-derived electrode positions of 2.5 mm (range 0.5-5.2). CONCLUSION: The Virtual Grid electrode positions were highly accurate in localizing the actual position of the subdural electrodes with both CT- and MR-derived images. The MR-derived electrodes demonstrated a trend toward better accuracy, but the CT images were quicker and easier to process. This technology has the potential to minimize both human and technical errors, allowing for a more precise tailoring of the cortical resection in epilepsy surgery.  (+info)

Evidence of basal temporo-occipital cortex involvement in stereoscopic vision in humans: a study with subdural electrode recordings. (13/76)

Stereoscopic vision is based on small differences in both retinal images known as retinal disparities. We investigated the cortical responses to retinal disparities in a patient suffering from occipital epilepsy by recording evoked potentials to random dot stereograms (RDS) from subdural electrodes placed in the parieto-occipito-temporal junction, medial surface of the occipital lobe (pericalcarine cortex) and basal surface of the occipital and temporal lobes (fusiform gyrus). Clear responses to disparity present in RDS were found in the fusiform cortex. We observed that the fusiform responses discriminate the onset from the offset of the stimulus, correlation from uncorrelation, and they show a longer latency than responses found in the pericalcarine cortex. Our findings indicate that the fusiform area is involved in the processing of the stereoscopic information and shows responses that suggest a high level of stereoscopic processing.  (+info)

Quantitative visualization of ictal subdural EEG changes in children with neocortical focal seizures. (14/76)

OBJECTIVE: To quantify the ictal subdural electroencephalogram (EEG) changes using spectral analysis, and to delineate the quantitatively defined ictal onset zones on high-resolution 3D MR images in children with intractable neocortical epilepsy. METHODS: Fourteen children with intractable neocortical epilepsy (age: 1-16 years) who had subsequent resective surgery were retrospectively studied. The subjects underwent a high-resolution MRI and prolonged subdural EEG recording. Spectral analysis was applied to 3 habitual focal seizures. After fast Fourier transformation of the EEG epoch at ictal onset, an amplitude spectral curve (square root of the power spectral curve) was created for each electrode. The EEG magnitude of ictal rhythmic discharges was defined as the area under the amplitude spectral curve within a preset frequency band including the ictal discharge frequency, and calculated for each electrode. The topography mapping of ictal EEG magnitude was subsequently displayed on a surface-rendered MRI. Finally, receiver operating characteristic (ROC) analysis was performed to evaluate the consistency between quantitatively and visually defined ictal onset zones. RESULTS: The electrode showing the maximum of the averaged ictal EEG magnitude was part of the visually defined ictal onset zone in all cases. ROC analyses demonstrated that electrodes showing >30% of the maximum of the averaged ictal EEG magnitude had a specificity of 0.90 and a sensitivity of 0.74 for the concordance with visually defined ictal onset zones. SIGNIFICANCE: Quantitative ictal subdural EEG analysis using spectral analysis may supplement conventional visual inspection in children with neocortical epilepsy by providing an objective definition of the onset zone and its simple visualization on the patient's MRI.  (+info)

Rapid and fully automated visualization of subdural electrodes in the presurgical evaluation of epilepsy patients. (15/76)

For rapid visualization of subdural electrodes with respect to cortical and subcortical structures, we describe a novel and fully automated method based on coregistration, normalization, optional cerebellum masking, and volume rendering of 3D MR imaging data taken before and after implantation. The key step employs the skull-stripped preimplantation image as a mask to also remove the skull in the postimplantation image. The extracted brain is presented in 3D with the electrodes directly visible by their susceptibility artifacts. Compared with alternative methods, ours is based on freely available software and does not require manual intervention.  (+info)

Origin and propagation of epileptic spasms delineated on electrocorticography. (16/76)

PURPOSE: Ictal electrographic changes were analyzed on intracranial electrocorticography (ECoG) in children with medically refractory epileptic spasms to assess the dynamic changes of ictal discharges associated with spasms and their relation to interictal epileptiform activity and neuroimaging findings. METHODS: We studied a consecutive series of 15 children (age 0.4 to 13 years; nine girls) with clusters of epileptic spasms recorded on prolonged intracranial subdural ECoG recordings, which were being performed for subsequent cortical resection, and in total, 62 spasms were analyzed by using quantitative methods. RESULTS: Spasms were associated with either a "leading" spike followed by fast-wave bursts (type I: 42 events analyzed quantitatively) or fast-wave bursts without a "leading" spike (type II: 20 events analyzed quantitatively). Twenty-three of the 42 type I spasms but none of the 20 type II spasms were preceded by a focal seizure. A "leading" spike had a focal origin in all 42 type I spasms and involved the pre- or postcentral gyrus within 0.1 s in 37 of these spasms. A leading spike was associated with interictal spike activity >1/min in 40 of 42 type I spasms and originated within 2 cm from a positron emission tomography glucose hypometabolic region in all but two type I spasms. Failure to resect the cortex showing a leading spike was associated with poor surgical outcome (p = 0.01; Fisher's exact probability test). Fast-wave bursts associated with spasms involved neocortical regions extensively at least in two lobes within 1.28 s in all 62 spasms and involved the pre- or postcentral gyrus in 53 of 62 spasms. CONCLUSIONS: Epileptic spasms may be triggered by a focal neocortical impulse in a subset of patients, and a leading spike, if present, might be used as a marker of the trigger zone for epileptic spasms. Rapidly emerging widespread fast-wave bursts might explain the clinical semiology of epileptic spasms.  (+info)