SEARCH · PubMed Health

Results for “ECOG”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources

PubMed1989

Bladder contractions and micturition in fetal sheep: their relation to behavioral states.

Fetal bladder contractions, indicative of micturition (voiding), and behavioral states were monitored in unanesthetized fetal sheep in utero during the last third of gestation. Fetal voids began during low-voltage electrocortical activity (LV ECoG) at a greater frequency (91.4 +/- 1.0%) than expected (57.2%) and began during high-voltage electrocortical activity (HV ECoG) with a lower frequency (8.7 +/- 1.0%) than expected (42.8%). Fetal voids began significantly sooner after the onset of LV ECoG (5.84 +/- 0.13 min) than after the onset of HV ECoG (10.88 +/- 0.04 min). Electroocular and nuchal muscle activities were associated with 96.2 and 66.0% of the voids, respectively, but there was no significant association between fetal voiding and swallowing episodes. Abolition of spontaneous voiding, by urine drainage (24 h), caused no significant differences, relative to a 24-h control period, in the duration or number of episodes of LV or HV ECoG or percentage of time spent in these states. Also, induction of voiding by infusing saline into the bladder did not significantly alter the time to the next change of ECoG state. However, the mean time to the next void and the mean volume of saline infused into the bladder to induce voiding tended to be less during LV ECoG than HV ECoG, although not significantly less. Our data show that most spontaneous voids in the fetus begin during LV ECoG, suggesting that voiding is regulated by descending information from the brain. Furthermore, these experiments demonstrate that fetal bladder contractions and voiding, either spontaneous or induced, do not influence the normal cycling of fetal ECoG states.

Animals↗

PubMed1987

Behavioural and electrocortical changes induced by muscimol in rats withdrawn from chronic treatment with diazepam.

In rats withdrawn from a chronic treatment with diazepam, the effects of muscimol, given into the III cerebral ventricle, on behaviour and spectrum power of activity in the electrocorticogram (ECoG) were studied. In comparison to control rats which received only muscimol, in rats pretreated with diazepam (1 mg/kg/day for 30 consecutive days) the behavioural and ECoG effects of muscimol were significantly reduced or abolished. In fact, in rats pretreated with diazepam a small dose (50 ng) of muscimol did not affect behaviour or ECoG activity, in contrast to control animals in which the same dose produced, after a period of locomotor stimulation and ECoG desynchronization, typical and long-lasting behavioural sedation or sleep accompanied by a significant increase in total voltage power and in the lower frequency bands in the ECoG. In addition, larger doses (100 and 200 ng) of muscimol, which in control rats produced a typical biphasic pattern of ECoG and behavioural changes, i.e. an initial period of ECoG desynchronization and behavioural stimulation, followed by a second period of behavioural and ECoG sleep, in animals pretreated with diazepam, produced only an increase in total voltage power and in the lower frequency bands in the ECoG resembling the effects of the smaller (50 ng) dose. The present experiments suggest that, after chronic stimulation of benzodiazepine receptors a decrease in sensitivity of receptors for gamma-aminobutyric acid (GABA) occurs, since the effects of muscimol on behaviour and spectrum power were significantly reduced or abolished.

Animals↗

PubMed1997

Comparative, behavioural and electrocortical effects of tumor necrosis factor-alpha and interleukin-1 microinjected into the locus coeruleus of rat.

The behavioural and electrocortical (ECoG) effects of human recombinant tumor necrosis factor-alpha (hrTNF-alpha) and various forms of interleukin-1 (IL-1) microinjected into the locus coeruleus (LC) of rats were studied. IL-1 induced a typical, dose-dependent, behavioural sedation and/or sleep which was associated with ECoG synchronization. IL-1 beta appeared more potent than IL-1 alpha. During sleep induced by the various forms of IL-1 a dose-dependent increase in total voltage power (0.25-16 Hz) as well as in the 3-6, 6-9 and sometimes 0.25-3 Hz frequency bands was observed. The behavioural and ECoG effects of IL-1 beta were blocked in rats pretreated with anti-IL-1 monoclonal antibodies. The microinjection of hrTNF-alpha into the LC produced a typical pattern characterized by a first short lasting (20-30 min) phase of behavioural arousal and ECoG desynchronization, followed by a longer lasting (45-80 min) phase of behavioural sedation and/or sleep and ECoG synchronization characterized by an increase in total voltage power as well as in the 3-6, 6-9 and sometimes 0.25-3 Hz frequency bands. The behavioural and ECoG effects of hrTNF-alpha were antagonized by a pretreatment (15 min before) with specific anti-TNF-alpha polyclonal antibodies. In addition, a pretreatment with anti-IL-1 receptor monoclonal antibodies was unable to significantly affect the stimulation of behaviour and ECoG desynchronization effects elicited by hrTNF-alpha whilst the same pretreatment completely prevent the sedative and ECoG synchronizing phase elicited by the microinjection of hrTNF-alpha into the LC. These results are consisted with the hypothesis that the sedative and/or soporific behavioural and ECoG changes of hrTNF-alpha are mediated, at LC level, through a local IL-1 release.

Animals↗

PubMed2005

Electrocorticographic high gamma activity versus electrical cortical stimulation mapping of naming.

Subdural electrocorticographic (ECoG) recordings in patients undergoing epilepsy surgery have shown that functional activation is associated with event-related broadband gamma activity in a higher frequency range (>70 Hz) than previously studied in human scalp EEG. To investigate the utility of this high gamma activity (HGA) for mapping language cortex, we compared its neuroanatomical distribution with functional maps derived from electrical cortical stimulation (ECS), which remains the gold standard for predicting functional impairment after surgery for epilepsy, tumours or vascular malformations. Thirteen patients had undergone subdural electrode implantation for the surgical management of intractable epilepsy. Subdural ECoG signals were recorded while each patient verbally named sequentially presented line drawings of objects, and estimates of event-related HGA (80-100 Hz) were made at each recording site. Routine clinical ECS mapping used a subset of the same naming stimuli at each cortical site. If ECS disrupted mouth-related motor function, i.e. if it affected the mouth, lips or tongue, naming could not be tested with ECS at the same cortical site. Because naming during ECoG involved these muscles of articulation, the sensitivity and specificity of ECoG HGA were estimated relative to both ECS-induced impairments of naming and ECS disruption of mouth-related motor function. When these estimates were made separately for 12 electrode sites per patient (the average number with significant HGA), the specificity of ECoG HGA with respect to ECS was 78% for naming and 81% for mouth-related motor function, and equivalent sensitivities were 38% and 46%, respectively. When ECS maps of naming and mouth-related motor function were combined, the specificity and sensitivity of ECoG HGA with respect to ECS were 84% and 43%, respectively. This study indicates that event-related ECoG HGA during confrontation naming predicts ECS interference with naming and mouth-related motor function with good specificity but relatively low sensitivity. Its favourable specificity suggests that ECoG HGA can be used to construct a preliminary functional map that may help identify cortical sites of lower priority for ECS mapping. Passive recordings of ECoG gamma activity may be done simultaneously at all electrode sites without the risk of after-discharges associated with ECS mapping, which must be done sequentially at pairs of electrodes. We discuss the relative merits of these two functional mapping techniques.

Adolescent↗

PubMed1987

Evidence that locus coeruleus is the site where clonidine and drugs acting at alpha 1- and alpha 2-adrenoceptors affect sleep and arousal mechanisms.

The behavioural and electrocortical (ECoG) effects of clonidine were studied after microinjection into the third cerebral ventricle, or microinfusion into some specific areas of the rat brain rich in noradrenaline-containing cell bodies (locus coeruleus) or into areas receiving noradrenergic terminals (dorsal hippocampus, amygdaloid complex, thalamus, frontal and sensimotor cortex). The ECoG effects were continuously analysed and quantified by means of a Berg-Fourier analyser as total power and as power in preselected bands of frequency. Clonidine (9.4 to 75 nmol) given into the third cerebral ventricle produced behavioural sedation and sleep and a dose-dependent increase in ECoG total voltage power as well as in the lower frequency bands. Much lower doses were required to produce similar behavioural and ECoG spectrum power effects after either unilateral or bilateral microinfusion of clonidine into the locus coeruleus. Doses of clonidine equimolar to those given into the third cerebral ventricle, were almost ineffective in inducing behavioural and ECoG sleep after their microinfusion into the dorsal hippocampus. In addition, a dose (0.56 nmol) of clonidine which, given into the locus coeruleus, produced marked behavioural sleep and ECoG synchronization, lacked effects when given into the ventral or anterior thalamus, into the amygdaloid complex or onto the frontal and sensimotor cortex. The behavioural and ECoG spectrum power effects of clonidine given into the third cerebral ventricle or into the locus coeruleus were prevented by antagonists of alpha 2-adrenoceptors but not by alpha 1-adrenoceptor antagonists. Intraventricular microinjection, or microinfusion into the locus coeruleus, of yohimbine, a selective alpha 2-adrenoceptor antagonist, produced behavioural arousal, increase in locomotor and exploratory activity, tachypnoea and ECoG desynchronization with a significant reduction in total voltage power. Similar stimulatory effects were also observed after microinjection of phentolamine into the same sites. No significant effects on behaviour and ECoG activity were evoked after intraventricular injection or microinfusion into the locus coeruleus of prazosin or methoxamine.

Adrenergic alpha-Antagonists↗

PubMed1988

Ventral tegmental area: site through which dopamine D2-receptor agonists evoke behavioural and electrocortical sleep in rats.

1. In freely moving rats the effects on behaviour and electrocortical (ECoG) spectrum power of some dopamine agonists, i.e. apomorphine and (+)-3PPP, given directly into different areas of the rat brain were studied. In particular, dopamine agonists were microinfused in the ventral tegmental area (VTA) and substantia nigra (SN) or into the caudate nucleus, n. accumbens and prefrontal cortex. The ECoG spectrum power effects were continuously analysed by means of a computerized Berg-Fourier analyser as total spectrum power and power in preselected frequency bands. 2. Apomorphine and (+)-3PPP (0.01, 0.1 and 1.0 nmol) given bilaterally into the VTA produced behavioural and ECoG sleep in a dose-dependent fashion. A statistically significant (P less than 0.01) increase in ECoG total spectrum power with a predominant increase in the lower frequency bands (0.25-3, 3-6 and 6-9 Hz) occurred. No behavioural and ECoG changes were evoked by the same doses of apomorphine bilaterally microinfused into the SN or into the caudate nucleus or by (+)-3PPP (1.0 nml) microinjected into the n. accumbens or applied onto the prefrontal cortex. 3. Behavioural and ECoG sleep was also induced in rats after systemic administration of apomorphine (263 nmol kg-1, i.p.). 4. The behavioural and ECoG spectrum power effects of apomorphine (1.0 nmol) bilaterally micro-infused into the VTA were prevented by a previous microinjection into the same site of (-)-sulpiride (9.8 nmol). Similarly, behavioural and ECoG effects evoked by (+)-3PPP (0.1 nmol) given bilaterally into the VTA, were completely antagonized by a previous injection into the same site of haloperidol (16 pmol given 10 min before). In contrast, pretreatment with SCH 23390 (50 pgkg-1, s.c.), a selective antagonist at dopamine Dl-receptors, was unable to antagonize the behavioural and ECoG spectrum power effects of ( +)-3PPP. 5. Soporific effects induced by systemic administration of apomorphine were antagonized by (-)- sulpiride (9.8 nmol) given bilaterally into the VTA 10min before, whereas, yohimbine (1.3 nmol), (an antagonist at alpha 2-adrenoceptors) bilaterally microinfused into the VTA, was ineffective in this respect. 6. The present experiments provide evidence suggesting that stimulation of dopamine D2-receptors located at the cell body level and/or the dendrites of dopaminergic neurones in the VTA may represent the mechanism through which apomorphine or (+)-3PPP exert their soporific effects in rats.

Animals↗

PubMed1995

Investigating the effects of opioid drugs on electrocortical activity using wavelet transform.

Fetal electrocortical activity (ECoG) is characterized by two distinct patterns: HVSA (high voltage, slow activity) and LVFA (low voltage, fast activity). Using the wavelet transform (WT), we recently reported that the frequency characteristics of these two ECoG patterns undergo significant maturational changes prior to birth (Akay et al. 1994a). We now report that fetal ECoG can also be significantly affected by pharmacological agents. In this paper, we compared the effects of two opioid drugs (morphine and [D-Pen2, D-Pen5]-enkephalin, DPDPE) on fetal ECoG, using the chronically instrumented fetal lamb model. Morphine was infused intravenously (i.v.) at 2.5 mg/h, while DPDPE was infused into the lateral cerebroventricle (i.c.v.) at 30 micrograms/h. The ECoG was analyzed using WT. We performed multi-resolution decomposition for four sets of parameters D2j where -1 < j < -4. The four series WTs represent the detail signal bandwidths: (1) 16-32 Hz, (2) 8-16 Hz, (3) 4-8 Hz, (4) 2-4 Hz. The data were subjected to statistical analysis using the Kolmogorov-Smirnov (KS) test. Both morphine and DPDPE resulted in a significant increase in power in the first wavelet band, while power was reduced in the second, third and fourth wavelet bands. In addition, both drugs resulted in a disruption of the normal cyclic pattern between the two ECoG patterns. There was a difference in the time course of action between morphine and DPDPE. This is the first occasion in which continuous ECoG has been subjected to rigorous statistical analysis. The results suggest that the WT-KS method is most suitable for quantitating changes in the ECoG induced by pharmacological agents.

Animals↗

PubMed2003

Neocortical activation by electrical and chemical stimulation of the rat inferior colliculus: intra-collicular mapping and neuropharmacological characterization.

Classic experiments suggested that the midbrain reticular formation plays an important role in the induction and maintenance of high-frequency, low-amplitude activation of the electrocorticogram (ECoG). However, recent studies have shown that generalized activating systems are not restricted to the reticular formation in that non-reticular brain systems (e.g., basal forebrain, amygdala, superior colliculus) can effectively produce ECoG activation. Here, we investigated the role of the inferior colliculus (IC) in regulating ECoG activation in rats. Urethane-anesthetized rats displayed continuous large amplitude ECoG activity with peak power in the delta frequency range (0.5-3.9 Hz). Electrical 100-Hz stimulation (0.1-0.5 mA) of 40/88 (46%) stimulation sites in the IC suppressed low frequency oscillations and induced ECoG activation (>/=50% suppression of peak delta power). Systematic mapping of different IC territories (central nucleus, external and dorsal cortex) revealed that stimulation of all IC parts was equally effective in producing activation. Chemical stimulation of the IC with intra-collicular glutamate infusions (50 mM, 0.5 micro l) produces similar, but more consistent effects, with ECoG activation elicited in eight of nine rats. Pharmacological experiments were carried out in order to identify transmitters that mediate cortical activation in response to IC stimulation. The muscarinic receptor antagonist scopolamine (1 mg/kg, i.p.) reduced, but did not abolish, activation, as did the serotonergic receptor antagonist methiothepin (1 mg/kg, i.p.). A combination of the two drugs produced a complete block of IC-induced ECoG activation. These experiments demonstrate that the IC contains a distributed network, spanning all IC territories, which can participate in regulating the generalized activation state of the rat neocortex. Rather than by some direct cortical projections, IC neurons appear to induce ECoG activation by acting through both cholinergic and serotonergic systems, thought to provide the final effector mechanisms for cortical activation.

Animals↗

PubMedDate not supplied

Developmental changes in the complexity of the electrocortical activity in foetal sheep.

The foetal sheep brain develops organised sleep states from 115-120 d gestational age (dGA, term 150 dGA) alternating between REM and NREM sleep. We aimed to investigate whether maturation of REM or NREM sleep generating structures leads to the development of distinct sleep states. The electrocorticogram (ECoG) was recorded from five unanaesthetised chronically instrumented foetal sheep in utero and was analysed every 5th day between 115-130 dGA by two different non-linear methods. We calculated a non-linear prediction error which quantifies the causality of the ECoG and applied bispectral analysis which quantifies non-linear interrelations of single frequency components within the ECoG signal. The prediction error during REM sleep was significantly higher than during NREM sleep at each investigated age (P<0.0001) coincidental with poor organisation of the rhythmic pattern in the ECoG during REM sleep. At 115 dGA, organised sleep states defined behaviourally were not developed yet. The prediction error, however, showed already different states of electrocortical activity that were not detectable using power spectral analysis. The prediction error of the premature NREM sleep ECoG decreased significantly during emergence of organised sleep states between 115 and 120 dGA and continued to decrease after the emergence of distinct sleep states (P<0.05). The prediction error of the premature REM sleep ECoG did not change until 120 dGA and began to increase at 125 dGA (P<0.05). Using bispectral analysis, we showed couplings between delta waves (1.5-4 Hz) and frequencies in the range of spindle waves (4-8 and 8-12 Hz) during NREM sleep that became closer during development. The results show that maturation of ECoG synchronisation mediating structures is important for the development of organised sleep states. The further divergence of the prediction error of NREM and REM sleep after development of organised sleep states reveals continuous functional development. Thus, complementary application of non-linear ECoG analysis to power spectral analysis provide new insights in the collective behaviour of the neuronal network during the emergence of sleep states.

Algorithms↗

PubMed2001

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.

Adolescent↗

PubMed2006

AC electrocorticographic correlates of peri-infarct depolarizations during transient focal ischemia and reperfusion.

Several studies have highlighted a delayed secondary pathology developing after reperfusion in animals subjected to prolonged cerebral ischemia, and recently we have shown that peri-infarct depolarizations (PIDs) occur not only during ischemia, but also in this delayed period of infarct maturation. Here we study the electrocorticographic (ECoG) manifestations of PIDs as signatures of developing secondary pathology. DC- and traditional AC-ECoG signals were recorded continuously from epidural, nonpolarizable electrodes during 2 h of middle cerebral artery occlusion (MCAo) and 22 h of reperfusion in freely behaving rats. During MCAo, seizures and PIDs recurred frequently and their incidence was significantly correlated. After reperfusion, seizures and PIDs ceased, and for the next several hours delta wave abnormalities dominated the ECoG with progressively increasing amplitude. After a variable period (5 to 15 h), the ECoG amplitude decremented with the onset of a prolonged repetitive series of PIDs. Initial PIDs in this delayed phase produced transient depressions of the high amplitude ECoG signal, but thereafter the ECoG was persistently attenuated, with no transient depressions during subsequent PIDs. The time of onset of postreperfusion PIDs, and hence measures of ECoG attenuation, correlated with 24 h infarct volumes. PIDs could always be detected in baseline shifts of the AC-ECoG signal with a low high-pass cutoff setting. These results suggest that delayed PIDs after reperfusion contribute to a complex secondary pathology involving delayed edema, intracranial hypertension, and hypoperfusion. The manifestation of PIDs in ECoG/electroencephalography recordings may enable continuous real-time monitoring of infarct progression.

Animals↗

PubMed2001

Prognostic value of electrocochleography in patients with unilateral Menière's disease undergoing saccus surgery.

Although a controversial operation, saccus surgery has continued to be used in patients with severe Menière's disease in whom hearing preservation is the objective. The aim of this study was to determine if electrocochleography (ECoG) could predict the patients who would be free of vertigo, 2 and 5 years after surgery. Seventy patients with severe Menière's syndrome underwent ECoG prior to endolymphatic sac surgery. Eighty-four per cent of the patients had an abnormal electrocochleogram. The patients were interviewed 2 and 5 years after surgery. At 2 years, 4/10 (40%) patients with normal ECoG were relieved of dizziness compared to 38/51 (75%) with abnormal ECoG (P < 0.05). At 5 years, 5/8 (63%) patients with normal ECoG were relieved of dizziness compared to 30/30 (100%) with abnormal ECoG (P < 0.001). The patients with a normal ECoG do have less severe measurable hearing impairment (P < 0.05) although they are more likely (P < 0.05) to complain of constant tinnitus. Their history of dizziness is longer and their dizziness more disabling before surgery. In conclusion, patients with a normal ECoG will be less likely to benefit from saccus surgery in the first 5 years. These patients may represent a different nosological entity.

Adult↗

PubMed2001

The effects of remifentanil on epileptiform discharges during intraoperative electrocorticography in patients undergoing epilepsy surgery.

PURPOSE: High-dose i.v. opioids (e.g., alfentanil, 50 microg/kg bolus) are known to increase the intraoperative reading of epileptiform activity during epilepsy surgery (ES), thereby facilitating localization of the epileptogenic zone (i.e., the site of ictal onset and initial seizure propagation). However, this phenomenon has not been studied with remifentanil (i.e., a novel ultra-short acting opioid). The purpose of the present study was to evaluate the effect of remifentanil on electrocorticography (ECoG) during ES. METHODS: After Institutional Review Board approval, 25 adult patients undergoing elective ECoG-guided anterior temporal corticectomy were enrolled. At the time of ECoG, anesthesia consisted of inhaled isoflurane < or =0.1% (end-tidal) in 50% N2O, and i.v. fentanyl, 2 microg/kg/h and vecuronium. Patients were maintained at normocapnia and normoxia during ECoG. After acquisition of baseline ECoG, bolus remifentanil, 2.5 microg/kg i.v., was administered. The number of epileptiform spikes occurring 5 min before and after this bolus were compared by using a one-sided sign test; p values < or =0.05 were considered statistically significant. RESULTS: When compared with baseline ECoG, bolus i.v. remifentanil significantly increased the frequency of single spikes or repetitive spike bursts in the epileptogenic zone while suppressing activity in surrounding normal brain. CONCLUSIONS: During ES, remifentanil enhanced epileptiform activity during intraoperative ECoG. Such observations facilitate localization of the epileptogenic zone while minimizing resection of nonepileptogenic eloquent brain tissue. Although not specifically evaluated in this study, we speculate that remifentanil's short elimination half-life will facilitate neurologic function testing immediately after ES. Should this be the case, we envision remifentanil has the potential to supplant other opioids (e.g., alfentanil) during ECoG-guided ES.

Adult↗

PubMed1982

Cancer patient accessions into clinical trials: a pilot investigation into some patient and physician determinants of entry.

This study investigated the external validity (or generalizability of results) of randomized clinical trials in cancer. Tao ECOG lung cancer chemotherapy protocols active in the early 1970s were studied using a case-control design. All lung cancer patients of the four specified cell types resident in Monroe County during the ECOG study period were identified from the Rochester Regional Tumor Registry. All of the patients entered into either protocol ("ECOG cases") and a random sample of the nonprotocol cases were examined by medical records review. Thirty-seven percent of the nonprotocol cases were determined to have been eligible for either of the two ECOG protocols, but not entered ("eligible controls"). A comparison of the ECOG cases (n = 65) and the eligible controls (n = 109) revealed that (1) ECOG cases were more likely than eligible controls to have been diagnosed at a hospital which participated in the University of Rochester Cancer Center's medical oncology program; (2) ECOG cases were of higher occupational status than eligible controls; (3) duration from diagnosis to protocol entry for ECOG cases was longer than duration from diagnosis to earliest date of eligibility for eligible controls. The implications of these findings for the conduct of cancer clinical trials are discussed.

Aged↗

PubMed1997

Propofol sedation during awake craniotomy for seizures: electrocorticographic and epileptogenic effects.

This prospective study evaluated the effects of propofol sedation on the incidence of intraoperative seizures and the adequacy of electrocorticographic (ECoG) recordings during awake craniotomy performed for the management of refractory epilepsy. Thirty patients scheduled for temporal or frontal lobectomy for epilepsy under bupivacaine scalp block were randomized to receive patient-controlled propofol sedation (PCS) combined with a basal infusion of propofol (n = 15) or neurolept analgesia using an initial bolus dose of fentanyl (0.7 microg/kg) and droperidol (0.04 mg/kg) followed by a fentanyl infusion (n = 15). Propofol administration was suspended 15 min before ECoG recording in the PCS group. The occurrence of inappropriate intraoperative seizures was noted and, based on blind review, the adequacy of ECoG recordings was compared. A higher incidence of intraoperative seizures was noted among the neurolept patients (6 vs 0, P = 0.008). Intraoperatively, ECoG recordings were adequate to proceed with resection in both groups. Evidence of low spike activity on ECoG did not correlate with the type of sedation administered. Higher frequency background ECoG activity was noted among patients who received propofol, but this did not interfere with ECoG interpretation. The use of propofol sedation does not appear to interfere with ECoG during epilepsy surgery, provided administration is suspended at least 15 min before recording.

Adjuvants, Anesthesia↗

PubMed2004

Is intraoperative electrocorticography reliable in children with intractable neocortical epilepsy?

PURPOSE: To study the relation between the spike frequency during intraoperative electrocorticography (ECoG) under general anesthesia with isoflurane and that during extraoperative ECoG monitoring in children with intractable neocortical epilepsy. METHODS: Twenty-one children (age, 1-16 years; 15 boys and six girls) who underwent intraoperative and extraoperative ECoG monitoring with subdural electrode arrays were studied. The spike frequency and the spatial pattern of spike frequency were compared between intraoperative and extraoperative ECoGs for each patient (by using Wilcoxon signed-ranks and Spearman's rank correlation, respectively). RESULTS: In 15 of 21 patients, the spike frequency was significantly lower during intraoperative than during extraoperative ECoG (mean z = -6.3; p < 0.001). In four of 21 patients, no significant difference was found in the spike frequency between intraoperative and extraoperative recordings. In two of 21 patients, spike frequency reached one spike/min neither during intraoperative nor extraoperative recording; therefore appropriate comparison of spike frequency was not possible. A significant positive correlation in the spike-frequency pattern was seen between intraoperative and extraoperative recordings in nine of nine cases who had > or = 10 spikes/min during intraoperative ECoG (mean rho = 0.62; p < 0.01), in five of six cases with one to nine spikes/min (mean rho = 0.50; p < 0.01), and in none of five cases with less than one spike/min (mean rho = 0.13). CONCLUSIONS: General anesthesia often decreases the spike frequency in children with neocortical epilepsy, yet intraoperative ECoG can reliably reflect the awake interictal spiking pattern when spike frequency exceeds one spike/min during intraoperative ECoG recording.

Adolescent↗

PubMed1999

Recruiting minority cancer patients into cancer clinical trials: a pilot project involving the Eastern Cooperative Oncology Group and the National Medical Association.

PURPOSE: Minority accrual onto clinical trials is of significant interest to cooperative oncology study groups. The Eastern Cooperative Oncology Group (ECOG) conducted a study to identify barriers and solutions to African American accrual onto clinical trials. METHODS: We hypothesize that the National Medical Association (NMA) might provide insight into ways to increase minority participation and that ECOG might facilitate that participation. Four sites were selected in which NMA chapters existed and ECOG main institutions with less than half of the corresponding percentage of minorities in their communities entered trials for 1992. Fifteen workshops were conducted using discussions and open-ended, self-administered questionnaires. RESULTS: Seventy percent of NMA physicians cited mistrust of the research centers, fear of losing patients, and a lack of respect from ECOG institutions as the most important barriers to minority cancer patient referrals, compared with 30% for ECOG physicians. Sixty-nine percent of NMA and 43% of ECOG physicians cited a lack of information about specific trials. Nearly half of NMA physicians (47%) cited a lack of minority investigators as a barrier, compared with 4% of ECOG physicians. Solutions by both groups were improved communication (73%) and culturally relevant educational materials (40%). ECOG physicians cited more minority outreach staff as a potential solution (22% v 6%). NMA physicians cited increased involvement of referring physicians (44% v4%). CONCLUSION: NMA physicians who serve a significant sector of the African American population demonstrated a willingness to participate and work with a cooperative group effort to increase participation of minority patients and investigators.

Clinical Trials as Topic↗

PubMed1996

[Electrocochleography by extra- and transtympanic methods: the results in a group of normal subjects].

Electrocochleography (ECoG) is an electrophysiologic approach to the study of hearing. In ECoG, electrical activity that originates within the cochlea or the auditory nerve is recorded. ECoG represents an evoked or stimulus dependent measure. The electrical potentials which can be analyzed in ECoG are: the cochlear microphonic potential (CM), the summating potential (SP) and the acoustic nerve potential (AP). Two major types of electrocochleography electrodes can be used, transtympanic and extratympanic. Transtympanic ECoG is performed by inserting a long needle electrode, placed through the tympanic membrane onto the promontory. Extratympanic ECoG is recorded by using electrodes placed within the external meatus near the tympanic membrane. At the ENT Department of the University of Parma, ECoG was performed in 10 normal hearing subjects (4 males and 6 females. Their ages ranged from 21 to 29 years (mean 26 years). All subjects underwent ECoG recording simultaneously with extratympanic and transtympanic technique.

Adult↗