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PubMedDate not supplied

[The spatial synchronization of the potentials in the background and evoked ECoG of a neuronally isolated strip of rabbit cortex].

Conditions of formation of potentials' spatial synchronization in the neuronally isolated cortical slab were studied in anaesthetized rabbits in acute experiments. Cortical potentials in all recording points of the slab were similar to each other. Seizure potentials induced by electrical stimulation spread over the slab and became synchronous in all points of recording. The neuronal division of the slab in two parts did not lead to a disturbance of initial synchronization of the background potentials in the isolated parts of the slab, while seizure potentials after electrical stimulation spread only over one part of the slab. These results suggest that the spatial synchronization of the EEG activity is a result of activity physically spreading from subcortical structures.

Animals↗
PubMed1993

[Intracranial ECoG electrodes. Location determination using three-dimensional reconstruction of MR data of the brain as a component of the presurgical diagnosis of epilepsy].

Subdural strip electrodes or intracerebral electrodes are required in order to precisely localize epileptic foci, which is mandatory for epilepsy surgery. The subdural electrodes are inserted via a borehole and thus precise positioning cannot be directly monitored. Therefore, the location of the electrodes in relation to the gyri and sulci has to be determined by imaging techniques. In this study, a three-dimensional magnetic resonance imaging (3D MRI) technique was used for visualization of intracranial EEG electrodes. A 3D gradient echo sequence with thin slices of 1 mm is required for the assessment of the gyral anatomy of the brain surface. Using a short repetition time of 30 ms good image quality within an acceptable acquisition time of about 15 min was possible. Post-processing with 3D surface reconstruction was performed using a Sun workstation. Three-dimensional reconstruction allows a more precise delineation of the localization of the EEG electrodes and the simultaneous display of the adjacent brain structures. Misplacement of intracranial electrodes is readily detected. 3D MRI with 3D surface reconstruction proved superior to 2D imaging and CT for the assessment of EEG electrode localization.

Electrodes↗
PubMed1979

Feasibility and efficacy of 5-azacytidine used early in the therapy of adult acute nonlymphocytic leukemia: an ECOG pilot study.

Ten of 19 adult patients (53%) with acute non-lymphocytic leukemia achieved a complete remission (CR) after receiving combination therapy with daunorubicin and cytosine arabinoside. The early administration of 5-azacytidine to treatment failures did not enhance the CR rate. Patients gaining CR received six monthly cycles of single-agent chemotherapy (5-azacytidine, daunorubicin, and cytosine arabinoside) sequentially as consolidation therapy over the next 7 months and no subsequent maintenance therapy. The median duration of CR is 10 months which is similar to previous studies. The early administration of 4-azacytidine did not increase the duration of remission, but was not associated with significant toxicity.

Adult↗
PubMed1998

Recent advances with chemotherapy for NSCLC: the ECOG experience. Eastern Cooperative Oncology Group.

Management of disseminated non-small-cell lung cancer has changed over the past 10 years. Newer agents, such as vinorelbine (Navelbine) and paclitaxel (Taxol), have been shown to modestly improve survival in patients with advanced disease when administered in conjunction with cisplatin (Platinol). Compared with older regimens consisting of cisplatin and a Vinca alkaloid or a podophyllotoxin, the newer regimens yield a 10- to 15-week improvement in median survival and an additional 10% to 15% in 1-year survival. Based on these results derived from randomized trials, it appears that metastatic non-small-cell lung cancer patients with good performance status should be treated with regimens containing either vinorelbine or paclitaxel in conjunction with cisplatin.

Antineoplastic Agents, Phytogenic↗
PubMed1990

Different profile of electrocortical power spectrum changes after micro-infusion into the locus coeruleus of selective agonists at various opioid receptor subtypes in rats.

1. The effects of various opioid receptor agonists given directly by means of a chronically implanted cannula into the locus coeruleus (LC) on behaviour and ECoG activity, continuously analysed, and quantified as total power spectrum (0-16 Hz) and in preselected frequency bands (0-3; 3-6; 6-9; 9-12 and 12-16 Hz), were studied in rats. 2. Dermorphin (0.05, 0.5, 1, 2 and 5 pmol) and Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol (DAMGO; 1, 10, 30, 100 pmol and 1 nmol), two typical mu-receptor agonists, applied unilaterally or bilaterally directly into the LC, produced a typical dose-dependent ECoG synchronization with a significant increase in total power spectrum as well as in the lower frequency bands. Dermorphin was found to be approximately 30 times more powerful than DAMGO in producing similar quantitative ECoG changes. 3. D-Ala-D-Leu-Thr-Gly-Gly-Phe-Leu (DADLE; 1, 10, 50 and 100 pmol), a selective delta-receptor agonist, micro-infused into the LC produced dose-dependent behavioural soporific effects and ECoG increase in total power spectrum as well as in 3-6, 6-9, 9-12 Hz frequency bands. In comparison to dermorphin, the ECoG power spectrum effects of DADLE were 10 fold less potent, whereas in comparison to DAMGO it was approximately 3 times more potent. A lower dose (0.1 pmol) was ineffective in changing behaviour and ECoG power spectrum. 4. The microinfusion into the LC of U 50, 488H, a selective Kappa-opioid receptor agonist, (0.25, 1, 2.5, 5 and lOpmol) produced a typical pattern characterized by a first short-lasting (3-25 min) phase of behavioural arousal and ECoG desynchronization, followed by a longer lasting (20-130min according to the dose) phase of behavioural sleep and ECoG synchronization. A lower dose (0.1 pmol) was ineffective in changing behaviour and ECoG power spectrum. 5. Dextromethorphan and ketamine, two selective agonists at sigma-receptors given into the LC (1, 5 and 1Opmol) induce behavioural arousal, increase in locomotor activity and an intense pattern of stereotypedm movements. However, by increasing the dose of ketamine (50 and lOOpmol), marked sedation, postural changes and an increase in low frequency ECoG bands, sometimes associated with high amplitude fast frequency potentials, were observed. 6. Naloxone applied directly into the LC (1 and 2 pmol 15min before) was able to prevent the behavioural and ECoG effects induced by dermorphin, DAMGO and DADLE. Higher doses of naloxone (1Opmol into the LC) were however, required to antagonize the behavioural and ECoG soporific effects induced by the Kappa-receptor agonist U 50,488H. In contrast, naloxone (1Opmol into the LC) was unable to prevent or reduce the behavioural and ECoG effects induced by subsequent administration into the same site of dextromethorphan and ketamine. 7. In conclusion, the present experiments confirm that behavioural and ECoG effects elicited following stimulation of mu-, delta-, Kappa- and sigma-opioid receptors located in the LC are quite different. Activation of ,mu-, band Kappa-receptors induced sedative effects whereas dextromethorphan and ketamine, two sigma-receptor agonists, induced behavioural arousal and ECoG desynchronization. In addition, the present results strongly support the crucial role played by opioid mechanisms, in the locus coeruleus, in the mediation of the soporific effects of drugs acting as agonists at opioid receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1998

Electrocortical activity in fetal sheep in the last seven days of gestation.

1. Electrocorticogram (ECoG) and myometrial electromyogram (EMG) were recorded continuously in chronically instrumented late gestation sheep fetuses (n = 9) to analyse: (1) 24 h ECoG patterns, (2) relationships between ECoG and myometrial contractility, and (3) 24 h ECoG patterns at the spontaneous onset of labour. 2. Spontaneous onset of labour was determined from the myometrial EMG. ECoG signals were purified by a denoising procedure of wavelet decomposition. High-voltage slow ECoG activity (HV) and low-voltage fast ECoG activity (LV) were determined mathematically, and HV-LV cycle periodicity was calculated by periodogram analysis. 3. Twenty-four hour rhythms were present in fetal ECoG HV-LV cycles in the 3-5 days prior to spontaneous onset of labour (P < 0.01). Cycle frequency was lower at 08.00-12.00 h and higher at 16.00-20.00 h (lights on at 07.00 h, lights off at 21.00 h). LV duration was longer at 20.00-24.00 h, and HV was shorter at 16.00-20.00 h. No relationship was found between ECoG cycles and myometrial contracture cycles. Twenty-four hour ECoG rhythms disappeared 1 day before the spontaneous onset of labour. 4. ECoG patterns changed 7 to 4 h prior to spontaneous onset of labour, percentage of time spent and duration of HV ECoG increased, and percentage of time spent in LV decreased significantly. ECoG HV-LV cyclicity was reduced 4-5 h prior to spontaneous onset of labour, indicating that the altered fetal hormonal and blood gas environment around the spontaneous onset of labour alter fetal neural function.

Animals↗
PubMed1995

Quantitative analysis of the electrocorticogram after forebrain ischemia in the rat.

The purpose of the study was to test the hypothesis that the postischemic neuronal damage is accompanied by changes of the electrocorticogram (ECoG) of freely moving rats during long-term recovery after forebrain ischemia. Ten minutes forebrain ischemia was induced in male Wistar rats. ECoG was recorded 1 day before as well as 1 h, 1 day and 7 days after ischemia. The ECoG power was calculated and for characterizing postischemic ECoG development the percentage of preischemic ECoG power was evaluated. The awake state of the rats was considered for analysis only. Furthermore, the neuroprotective effect of phencyclidine (PCP, 5 mg/kg i.v., 15 min prior to ischemia) was demonstrated in the ECoG changes. One hour after ischemia the ECoG power of the theta (4.75-6.75 Hz), alpha (7.00-12.50 Hz) and beta (12.75-18.50 Hz) band was decreased compared with sham-operated controls and PCP did not influence these changes. However, 1 day after ischemia ECoG power of the saline-treated ischemic rats was completely restored and no longer different from that of the sham-operated group. PCP-treated ischemic animals showed significantly elevated ECoG power in comparison with saline-treated animals. Seven days after ischemia ECoG power of the saline-treated ischemic rats again decreased. In comparison with the ischemic controls, the ECoG activity of the PCP-treated ischemic rats was significantly higher. PCP maintained postischemic ECoG power at the non-ischemic control level. It is suggested that the decrease in the ECoG activity several days after ischemia is related to the delayed neuronal damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Cortical spreading depression and peri-infarct depolarization in acutely injured human cerebral cortex.

Electrocorticographic (ECoG) activity was recorded for up to 129 h from 12 acutely brain-injured human patients using six platinum electrodes placed near foci of damaged cortical tissue. The method probes ECoG activity in the immediate vicinity of the injured cortex and in adjacent supposedly healthy tissue. Six out of twelve patients displayed a total of 73 spontaneous episodes of spreading depression of the ECoG. Of the remaining 6 patients 1 displayed an episode of synchronous depression of ECoG during surgery. Using the same electrodes we also measured the slow potential changes (SPC) (0.005-0.05 Hz) to test the hypothesis that the ECoG depressions were identical to Leao's cortical spreading depression (CSD), and to be able to record peri-infarct depolarisations (PIDs) in electrically 'silent' cortical tissue. Changes in the SPC indicate depolarization of brain tissue. For the analysis, the SPCs were enhanced by calculating the time integral of the ECoG signal. Spreading ECoG depressions were accompanied at every single recording site by stereotyped SPCs, which spread across the cortical mantle at 3.3 (0.41-10) mm/min (median, range), i.e. at the same speed of spread as the depression of the ECoG activity. The amplitude of the SPCs was 0.06-3 mV. In 4 out of 6 patients the ECoG recovered spontaneously. In 2 patients we subsequently recorded recurrent SPCs, but without recovery of the initial ECoG background activity until 2-5 h later. This represents the first direct recording of PIDs in acutely injured human brain. Evidence from this and our previous study of 14 brain-injured patients suggests that CSDs in acute brain disorders occur at higher incidence in patients <30 years (83%) than above (33%). CSD was recorded in 4 out of 5 traumatic brain injury patients, and in 2 out of 7 patients with spontaneous haemorrhages. We conclude that the spreading ECoG depressions recorded in patients are identical to CSDs recorded in animal experiments. We furthermore provide direct electrophysiological evidence for the existence of PIDs and hence a penumbra in the human brain. We hypothesize that the depolarization events might contribute to tissue damage in acute disorders in the human brain.

Adult↗
PubMed2003

Histaminergic facilitation of electrocorticographic activation: role of basal forebrain, thalamus, and neocortex.

The neuromodulator histamine plays an important role in the regulation of behavioural state and the neocortical electrocorticogram (ECoG). With the present experiments, we characterized the anatomical targets that mediate the cortical-activating effects of histamine. Urethane-anaesthetized rats displayed continuous large-amplitude, low-frequency oscillations with a maximal spectral power in the delta (0.5-3.9 Hz) frequency band. Electrical (100 Hz) stimulation of the pontine-tegmentum suppressed slow, large-amplitude oscillations and induced ECoG activation. Application of histamine (1 mm) into the basal forebrain cholinergic complex by reverse microdialysis enhanced ECoG activation elicited by tegmental stimulation without changing resting ECoG activity. Ventrolateral or central thalamic application of histamine had no effect on resting ECoG activity, and ventrolateral thalamic application produced only a slight enhancement of brainstem-induced activation. Neocortical application of histamine in close proximity (< 500 micro m) to the recording electrode reduced low-frequency delta power in the resting ECoG without affecting stimulation-induced ECoG activation. These data suggest that, under the present experimental conditions, histamine facilitates ECoG activation primarily by potentiating the excitatory influence of brainstem fibers at the level of the basal forebrain. Histamine release in some parts of the thalamus results in a minor enhancement of ECoG activation, and cortical histamine release produces a small but consistent suppression of slow delta oscillations in the resting ECoG. These concurrent subcortical and cortical actions probably permit histamine to effectively modulate cortical activation and excitability across different behavioural states.

Animals↗
PubMed1999

Generation of scalp discharges in temporal lobe epilepsy as suggested by intraoperative electrocorticographic recordings.

OBJECTIVES: To study the variability, topography, polarity, duration, and incidence of interictal epileptiform discharges (EDs) in the scalp EEG and electrocorticogram (ECoG) from 16 patients with temporal lobe epilepsy who underwent surgical treatment. METHODS: Preoperative scalp EEGs during quinalbarbitone induced sleep were compared with preresection ECoGs obtained under general anaesthesia. The analysis was based on the initial ECoG record obtained before activation by intravenous thiopentone, and the EEG during stages I and II of sleep. RESULTS: On the scalp, 15 patients had a single discharge pattern, spikes were predominantly negative, EDs were of largest amplitude at the anterior temporal electrode in 13 patients and mean discharge incidence was 4.0 (SD 4.2) discharges/min. In ECoG recordings, nine patients had two independent ECoG patterns, the polarity of spikes was negative, positive-negative, or positive, the site of maximal amplitude varied greatly between subjects, discharge incidence was 7.3 (SD 3.9) discharges/min. There was no relation between the topography of the largest spikes on the scalp and in the ECoG. In 14 patients, scalp spikes showed statistically significant longer duration on the scalp than in the ECoG. In seven patients who had frequent widespread ECoG discharges, averaging spikes across ECoG channels generated spiky patterns of duration similar to that of scalp spikes. CONCLUSION: It seems that, in temporal lobe epilepsy, scalp discharges originate from widespread ECoG discharges and tend to produce a stereotyped pattern on the scalp with largest amplitudes at the anterior temporal electrodes. This is probably due to local anatomical peculiarities in the brain coverings, such as skull discontinuities, rather than to the location of neuronal generators within the temporal lobe. Due to spatiotemporal averaging, widespread cortical discharges which become asynchronous during propagation appear with increased duration and blunted waveform in the EEG, whereas sharply localised phenomena such as positive focal spikes are not recorded from the scalp.

Adolescent↗