Induced EEG Changes Research Articles

GABAergic neurons in the dorsomedial hypothalamus regulate states of consciousness in sevoflurane anesthesia

The neural inhibitory gamma-aminobutyric acid (GABA) system in the regulation of anesthetic consciousness is heterogeneous, and the medial hypothalamus (MH), consisting of ventromedial hypothalamus (VMH) and dorsomedial hypothalamus (DMH), plays an important role in sleep and circadian rhythm. However, the role of MH GABAergic neurons (MHGABA) in anesthesia remains unclear. In this study, we used righting reflex, electroencephalogram (EEG), and arousal behavioral score to evaluate the sevoflurane anesthesia. Activation of MHGABA or DMHGABA neurons prolonged the anesthesia induction time, shortened the anesthesia emergence time, and induced EEG arousal and body movement during anesthesia; meanwhile, VMHGABA neurons activated only induced EEG changes during 1.5% sevoflurane anesthesia. Furthermore, inhibition of DMHGABA neurons significantly deepened sevoflurane anesthesia. Therefore, DMHGABA neurons exert a strong emergence-promoting effect on induction, maintenance, and arousal during sevoflurane general anesthesia, which helps to reveal the mechanism of anesthesia.

The effect of Perampanel on EEG spectral power and connectivity in patients with focal epilepsy

ObjectiveQuantitative Encephalography (qEEG) depicts synthetically the features of EEG signal and represents a promising tool in the assessment of neurophysiological changes brought about by Anti-Seizure Medications (ASMs). In this study we characterized qEEG alterations related to add-on therapy with Perampanel (PER). PER is the only ASM presenting a direct glutamatergic antagonism, hence the characterization of PER induced EEG changes could help to better understand its large spectrum of efficacy. MethodsWe analysed standard-19 channel-EEG from 25 People with Epilepsy (PwE) both before (T0) and after (T1) the introduction of PER as add-on treatment. Normal values were obtained in 30 healthy controls (HC) matched for sex and age. EEGs were analysed using Matlab™ and the EEGlab and Brainstorm toolkits. We extracted spectral power and connectivity (Phase locking Value) of EEG signal and then compared these features between T0 and T1 and across groups (PwE, HC), we also evaluated the correlations with clinical features. ResultsPwE showed increased theta power (p = 0.036) after the introduction of PER but no significant change of EEG connectivity. We also found that PwE have reduced beta power (p = 0.012) and increased connectivity in delta (p = 0.013) and theta (p = 0.007) range as compared to HC, but no significant change was observed between T0 and T1 in PwE. Finally, we found that PwE classified as drug responders to PER have greater alpha power both at T0 and at T1 (p = 0.024) suggesting that this parameter may predict response to treatment. ConclusionsPER causes slight increase of theta activity and does not alter connectivity as assessed by standard EEG. Moreover, greater alpha power could be a good marker of response to PER therapy, and potentially ASM therapy in general. SignificanceOur results corroborate the hypothesis that pharmaco-EEG is a viable tool to study neurophysiological changes induced by ASM. Additionally, our work highlights the role of alpha power as a marker of ASM therapeutic response.

Brain Topography of Emf-Induced Eeg-Changes in Restful Wakefulness: Tracing Current Effects, Targeting Future Prospects.

Covering a handful of decades but spanning across two centuries, mobile phones announced the dawn of the technological revolution, standing at the forefront as its' most prominent symbol. Over the course of their sovereign dominance, human generations born with the birth of the mobile phone reached the age of maturity, while scientific community started reaching for experience-based perceptivity. The following review serves as a short-cut across a half-decade old research gap, and a clear-cut analysis on the cutting-edge knowledge of the EMF induced EEG changes. The selection covers 28 articles about mobile phone effects on resting wakeful EEG in humans conducted over the last two decades, across three continents and 12 countries, of which 75% had positive findings. At present, the general protocol of a typical study includes investigations on adults (20-60 yrs) grouped in smaller samples and exposed to shorter intervals of GSM-like pulse-modulated signal (10-30 subjects/minutes). The assessment usually involves linear methods for quantitative analysis, while the results mostly revolve around posterior increase in alpha and beta frequency range. The qualitative variations, however, remain open to interpretation. Future research may benefit from multiplication of sub-specific studies leading to replication of more consistent results. The long-term and large-size epidemiologic studies, stratified by age and gender, may also improve the expected outcomes. Regarding the interpretation, non-linear methods could be employed for assessment of individual variations. The emphasis should be placed on theories/measures for better understanding of the subtle interplay between the spectral individualities and mobile phone radiation specifics.

Is gamma band EEG synchronization reduced during auditory driving in schizophrenia patients with auditory verbal hallucinations?

Auditory verbal hallucinations (AVH) in schizophrenia patients assumingly result from a state inadequate activation of the primary auditory system. We tested brain responsiveness to auditory stimulation in healthy controls (n=26), and in schizophrenia patients that frequently (n=18) or never (n=11) experienced AVH. Responsiveness was assessed by driving the EEG with click-tones at 20, 30 and 40Hz. We compared stimulus induced EEG changes between groups using spectral amplitude maps and a global measure of phase-locking (GFS). As expected, the 40Hz stimulation elicited the strongest changes. However, while controls and non-hallucinators increased 40Hz EEG activity during stimulation, a left-lateralized decrease was observed in the hallucinators. These differences were significant (p=.02). As expected, GFS increased during stimulation in controls (p=.08) and non-hallucinating patients (p=.06), which was significant when combining the two groups (p=.01). In contrast, GFS decreased with stimulation in hallucinating patients (p=0.13), resulting in a significantly different GFS response when comparing subjects with and without AVH (p<.01). Our data suggests that normally, 40Hz stimulation leads to the activation of a synchronized network representing the sensory input, but in hallucinating patients, the same stimulation partly disrupts ongoing activity in this network.

The effect of prefrontal stimulation on the firing of basal forebrain neurons in urethane anesthetized rat

The basal forebrain (BF) contains a heterogeneous population of cholinergic and non-cholinergic corticopetal neurons and interneurons. Neurons firing at a higher rate during fast cortical EEG activity ( f > 16 Hz) were called F cells, while neurons that increase their firing rate during high-amplitude slow-cortical waves ( f < 4 Hz) were categorized as S-cells. The prefrontal cortex (PFC) projects heavily to the BF, although little is known how it affects the firing of BF units. In this study, we investigated the effect of stimulation of the medial PFC on the firing rate of BF neurons ( n = 57) that were subsequently labeled by biocytin using juxtacellular filling ( n = 22). BF units were categorized in relation to tail-pinch induced EEG changes. Electrical stimulation of the medial PFC led to responses in 28 out of 41 F cells and in 8 out of 9 S cells. Within the sample of responsive F cells, 57% showed excitation ( n = 8) or excitation followed by inhibitory period ( n = 8). The remaining F cells expressed a short ( n = 6) or long inhibitory ( n = 6) response. In contrast, 6 out of the 8 responsive S cells reduced their firing after prefrontal stimulation. Among the F cells, we recovered one cholinergic neuron and one parvalbumin-containing (PV) neuron using juxtacellular filling and subsequent immunocytochemistry. While the PV cell displayed short latency facilitation, the cholinergic cell showed significant inhibition with much longer latency in response to the prefrontal stimulus. This is in agreement with previous anatomical data showing that prefrontal projections directly target mostly non-cholinergic cells, including GABAergic neurons.

The Anterior and Posterior Selective Temporal Lobe Amobarbital Tests: Angiographic, Clinical, Electroencephalographic, PET, SPECT Findings, and Memory Performance

The techniques, results, and problems of three types of selective temporal lobe (TL) amobarbital procedures (balloon technique with temporary occlusion of the internal carotid artery distal to the origin of the anterior choroidal artery (acha) [n= 19]; selective anterior catheterization of the acha [n= 20]; and selective catheterization of the peduncular P2-segment of the posterior cerebral artery [n= 5]) are described in a group of 40 patients with medically refractory complex partial seizures of mesial TL origin. Selective amobarbital tests were carried out before surgery to predict the memory deficit after an intended selective amygdalohippocampectomy. The effects of selective anaesthetization of TL were correlated with clinical data, pattern and duration of amobarbital induced EEG changes, and performance on verbal and nonverbal memory tasks measured during the test. In 4 patients the effect of selective amobarbital injection on regional and global metabolism was studied with18F-FDG-PET, with the PET tracer being injected intravenously immediately after amobarbital. More recently in 2 patients the vascular territory perfused by amobarbital in the acha test was studied with SPECT using99mTc ECD injected immediately prior to the amobarbital into the acha. Whereas the PET studies showed a rather widespread and bilateral amobarbital-induced decrease of metabolism, the SPECT studies confirmed the selective distribution of the tracer in the vascular territory of the acha, i.e., in amygdala and hippocampus. The comparison of selective TL amobarbital test performance with postoperative neuropsychological performance showed that the predictive value of this test is rather good for the postoperative verbal memory but underestimates postoperative nonverbal (“figural”) memory performance.

EEG profile of litoxetine after single and repeated administration in healthy volunteers.

1. Litoxetine is a selective serotonin reuptake inhibitor with antidepressant activity in animal models and in depressed patients. 2. This double-blind, cross-over, placebo-controlled study was carried out in 12 healthy young male volunteers. The aim was to assess the EEG profile of litoxetine in parallel with its pharmacokinetics after a single dose or multiple administrations for 4 days (6 doses) of two dosages (10 mg and 25 mg). Spectral analysis of four EEG leads (F4-T4, F3-T3, T4-02 and T3-01) was done up to 12 h post-dose. 3. In single or multiple doses, litoxetine induced EEG changes characterised by a dose-related increase in fast beta energies, mainly beta 2, without any changes in slow waves (delta and theta). A slight reduction in alpha activity occurred only after repeated doses. 4. EEG changes occurred after a single oral administration and lasted at least 12 h with litoxetine blood concentrations ranging from 4 to 10 ng ml-1. With repeated administrations, the pharmacodynamic steady-state was achieved as the increase in beta 2 energies was the same before and 12 h post-dose. These effects occurred with litoxetine blood concentrations ranging from 3 to 7 ng ml-1 with the 10 mg dosage and from 8 to 18 ng ml-1 with the 25 mg dosage. The EEG profile did not change after 4 days of repeated administration, indicating that tolerance did not develop. 5. Cmax and AUC showed proportionality between the administered dosages of 10 and 25 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

EEG changes, recorded with subdural electrodes, after thiopental injections in patients with temporal lobe seizures

Nineteen patients with temporal lobe epilepsy, examined with intracranial subdural electrodes for seizure monitoring, were subjected to intravenous thiopental injections to the level of deep narcosis. The induced EEG changes were recorded, analyzed, and correlated to the localization of the seizure-generating focus. In 14 patients with unilateral seizure onset, the thiopental injections evoked a focal spike activation on the focus side. The first suppression period in the EEG with a duration exceeding 1 s was recorded from the strip electrode overlying the focus. Only in six patients did asymmetries in the barbiturate-induced beta activity in the background EEG show lateralizing signs in concordance with the side of seizure onset. In five patients with bilateral seizure-generating foci, no significant lateralization in induced beta activity, focal spike activation, or focal suppression pattern could be found. The results are discussed, comparing similar studies performed with surface, sphenoidal, and depth electrodes.

Multivariate EEG power spectral analysis in acute schizophrenics

The electroencephalogram (EEG) during information processing is influenced by specific changes in brain electrical activity. Based on the theory of disturbed information processing in schizophrenics, we analysed auditory stimulus induced EEG changes by Fast Fourier Transformation. The most important of the significant stimulation-dependent EEG power changes were measured in the 0.5–3.5 Hz and 10–13.5 Hz frequency bands in the left frontoparietal lead. In a multivariate analysis the separation of the subjects examined into acute schizophrenics and normals was incorrect in only 21% of the cases (resubstitution rate); using π-method an error of 31% was estimated.

Effects of nonsedating histamine H 1-antagonists on EEG activity and behavior in the cat

The central effects of the newly-developed antihistamines (H 1-receptor antagonists) loratadine, astemizole, mequitazine and terfenadine were evaluated by studying brain electrical activity (EEG), sleep-walking patterns and behavior in the cat. The different stages of the sleep-walking cycle, i.e., wakefulness (W), spindle sleep (SS), slow wave sleep (SWS) and REM sleep (REM) were evaluated. The power spectrum analysis of the EEG was obtained by a computerized technique. For comparison, the sedating agent diphenhydramine was examined. Given at 3 mg/kg orally, a dose slightly above that effective therapeutically, diphenhydramine markedly affected behavior and all sleep stages. In particular, it depressed REM and increased SS (drowsiness). The EEG showed occasional spikes typical of subconvulsive states. Loratadine did not modify either sleep patterns or behavior over the 3–30 mg/kg dose range orally, which is far above that used clinically. The EEG, evaluated either visually or by spectral power analysis, was unaffected. Astemizole at 10 and 30 mg/kg PO reduced REM, markedly altered behavior at 30 mg/kg, but did not modify EEG activity. Mequitazine, at low doses (1–10 mg/kg PO), enhanced SS and decreased SWS and REM. Like diphenhydramine, mequitazine induced EEG changes typical of subconvulsive states and affected EEG power over the frequency range of 0.1–15.0 Hz. Terfenadine did not change sleep patterns and slightly affected behavior only at the high dose of 30 mg/kg orally; EEG activity was not influenced. These data show that: a) diphenhydramine and mequitazine appear to produce CNS effects by altering basic processes within the brain; b) astemizole and terfenadine seem to cross the blood-brain barrier at high doses only; c) loratadine has the lowest liability to produce central side effects. Of the sleep features examined, REM appeared to be the most sensitive stage to blockade of central H 1-receptor pathways.

Vagal afferents and EEG rhythms in the SI area in anesthetized cats : similarities between responses to electrical and chemical (phenyldiguanide) stimulations

In anesthetized, artificially ventilated cats with open chest, bilateral stimulation of all afferent vagal fibres (pulse duration: 800 microseconds, 30 Hz, train duration 30 to 40 s) produced marked changes in the spontaneous EEG activities in the primary somatosensory cortex (Sl area). They were characterized by depressed background rhythms, with a tendency to desynchronization, decreased amplitude and number of spindles, with altered pattern, and/or evoked sustained fast rhythmic activities. These effects occurred within 1 to 5 sec during vagal stimulation. On the contrary, the EEG response was weaker or absent when only myelinated vagal afferents were stimulated (100 microseconds). I.v. injection of phenyldiguanide (PDG), used for stimulation of unmyelinated vagal sensory fibres and mainly of pulmonary afferents, induced EEG changes within the first 30 s, similar to those observed during electrical vagal stimulation. These EEG responses were unrelated to the induced hypotension. Cervical bivagotomy produced persistent changes in EEG activity, with enhancement of the magnitude, duration and number of spindles, which resembled the delayed effects induced by PDG. The present results obtained with three test agents (electrical or chemical vagal stimulation and bivagotomy) demonstrated that, in cats, vagal afferent information interacted with the spontaneous EEG rhythms in the Sl area.

Mental Activation of the Electroencephalogram

ABSTRACT.Mental activation is a simple test consisting of two standardized questions and two commands. This test is given in order to raise the level of vigilance and to differentiate physiological drowsiness from states of mild to moderate impairment of consciousness (obtundation, morbid lethargy). In addition to the induced EEG changes, the patient's mental (behavioral) response is also observed.

Differential effects of dopamine D-1 and D-2 receptor agonists on eeg activity and behaviour in the rabbit

SKF 38393, a selective agonist for dopamine D-1 receptors, LY 171555, a selective agonist for D-2 receptors and apomorphine, an agonist for both receptor sites, all induced activation of the electrical activity of the brain (EEG) in the rabbit. While SKF 38393 induced EEG changes without concomitant signs of stereotyped behaviour, the injection of both LY 171555 and apomorphine also elicited marked behavioural effects, mostly stereotyped mouth and head movements. The EEG effects of SKF 38393 were prevented by SCH 23390 (0.003 mg/kg i.V.), but not by (−)-sulpiride (6.2–25 mg/kg i.V.). Haloperidol attenuated the effects induced by SKF 38393 only at a dose (1 mg/kg) that induced EEG changes of its own. Similarly, effects of apomorphine on both EEG and behaviour were prevented by SCH 23390 and to a lesser extent by haloperidol, but not influenced by (−)-sulpiride. Different patterns of interactions were observed when D-2 receptors were selectively stimulated by LY 171555. Behavioural effects induced by LY 171555 were fully inhibited by both (−)-sulpiride (6.2–12.5 mg/kg i.v.) and haloperidol (0.1–0.3 mg/kg i.v.). The drug SCH 23390 attenuated some behavioural components at 0.3 mg/kg (i.v.), a dose at least 100-fold that effective on the EEG effects induced by SKF 38393. However, all these antagonists exerted weak or no effects on EEG activation induced by LY 171555 and did not restore the control patterns at any doses examined. These data indicate that the population of D-1 receptors is strongly involved in the regulation of EEG and behavioural arousal, while D-2 receptors appear to be mostly involved in mediating stereotyped movements. Based on the findings with apomorphine, it is also suggested that D-1 and D-2 receptors are functionally inter-related, with D-1 receptors playing a prominent role in the modulation of the EEG and in behavioural arousal.

Electrocortical activity patterns during chloral hydrate induced sleep in developing rats

The neocortical EEG was quantified during sleep, while under light chloral hydrate anaesthesia, in rats ranging from 9 to 20 days of postnatal age. Continuous amplitude modulation at 0.5–1.0 min per cycle, synchronously over all frequency bands, was observed in 9- and in 10-day-old pups. By day 13, the mean amplitude had risen considerably in each of the frequency bands, and a slow fluctuation in delta-wave activity began to be discernible. Sodium glutamate injections induced EEG changes at 10 days which mimicked certain aspects of normal maturation (viz., large stereotyped potentials at irregular intervals, along with a selective increase in delta-wave activity). Natural as well as experimentally induced EEG changes were paralleled by a rise in neocortical amino acid concentrations, including glutamic acid and GABA. Delta wave amplitudes during quiet sleep increased still further between 13 and 14 days, while beta activity remained at a constant level. Between days 14 and 15 a precipitous decline in delta-wave activity was found, attributable to greater inhibition of slow waves during active sleep. No further developmental changes were noted, except for a gradual rise in the time spent in quiet sleep relative to active sleep.

抗てんかん薬の定量脳波学的研究

For the purpose of investigating EEG changes provoked by antiepileptic drugs, six different compound, namely phenytoin, valproate sodium, phenobarbital, primidone, carbamazepine and ethosuximide, were orally given to healthy male volunteers and EEGs recorded post-one, three and six hours were quantitatively analyzed. Periodegram program using zero-crossing and power spectra program using FFT algorism were employed for the routine analysis, but the results obtained from the former method were appropriate in the present study and they have been mainly used for the discussion as follows.1. Phenytoin and phenobarbital which are anti-convulsive agents used for controlling generalized motor convulsion and valproate sodium which is essentially anti-petit-mal agent with potent anti-convulsant action produce an increase of fast activity in EEG.2. EEG changes induced by ethosuximide that is anti-petit-mal substance is summarized as an increase of slow activity.3. EEG changes due to carbamazepine which is remedy for psychomotor seizures showed a mood elevator type responce consisting of slow and fast activities.4. Primidone is known as having a wide therapeutic spectrum which may be resulted from its metabolite such as phenobarbital but it is impossible to expect the appearance of phenobarbita l within six hours after the oral administration of primidone. The induced EEG changes are an increase of slow activity in contrast to the phenobarbital induced increase of fast activit y.5. The present auther have presented several different theories on action mechanism of these antiepileptic drugs and discussed their relationship to the EEG changes produced by each drugs.6. The mean values of maximal serum concetration were 3.8μg/ml for PHT 200mg group, 5.9μg/ml for PHT 400mg group, 54.2μg/ml for VPA 400mg group, 70.8, ug/ml for VPA 600mg group, 1.2μg/ml for 60mg PB group, 3.7μg/ml (PB 0.0μg/ml) for PRM200mg group, 14.0μg/ml for ESM 500mg group, 2.0μg/ml for CBZ 100mg group, 2.9μg/ml for CBZ 200mg group.

Effect of passive transfer of anti-brain antibodies to a normal recipient

The intraventricular or suboccipital inoculation of normal recipient rabbits with serum from donor rabbits immunized with brain homogenate induced transient neurological symptomatology and reversible EEG changes. The immunofluorescence technique revealed irregular diffusion of inoculated serum into the neuropil with subsequent antigenic changes of myelin sheaths. Perivascular edema, foci of swelling and, in some animals, mild perivascular and meningeal inflammatory reaction were seen. One of three normal control sera induced EEG changes and discrete foci of swelling. The results give further evidence that brain antibodies can provoke in vivo both disturbances of electrical brain activity and damage to myelin. Slight changes induced by “normal” serum could be explained by the biphasic serum action. The first phase, consisting of nonspecific membrane changes, might facilitate the second phase in which the specific interaction between antibodies and target structures ccurs with subsequent functional or structural changes, or both.