Increased EEG Power Research Articles

Electrophysiologic Analysis of Antidepressant Drug Effects on the GABAA Receptor Complex Based upon Antagonist-Induced Encephalographic Power Spectrum Changes

To better understand antidepressant drug effects on the GABA_A receptor complex (the GABA_A receptor, chloride ionophore and benzodiazepine receptor), we investigated how antidepressants influenced power spectrum changes induced by pentylenetetrazol (PTZ), a chloride ionophore antagonist, in the rat hippocampal electroencephalogram (EEG). In control recording, PTZ (27.5 mg/kg i.p.) increased EEG power at frequencies under 12 Hz up to five times. After rats were pretreated with imipramine, fluoxetine or trazodone for 7 days (10 mg/kg i.p., twice a day), PTZ could not increase EEG power to more than three times the power before injection; this effect was not observed after pretreatment for 3 days. These three antidepressants inhibit serotonin uptake, while two other antidepressants, desipramine and nortriptyline, that inhibit norepinephrine uptake failed to counter the PTZ effect. We concluded that antidepressants with serotonergic effects enhanced the function of the GABA_A receptor complex.

Effects of electromagnetic field emitted by cellular phones on the EEG during a memory task

The effects of electromagnetic fields (EMF) emitted by cellular phones on the ERD/ERS of the 4-6 Hz, 6-8 Hz, 8-10 Hz and 10-12 Hz EEG frequency bands were studied in 16 normal subjects performing an auditory memory task. All subjects performed the memory task both with and without exposure to a digital 902 MHz EMF in counterbalanced order. The exposure to EMF significantly increased EEG power in the 8-10 Hz frequency band only. Nonetheless, the presence of EMF altered the ERD/ERS responses in all studied frequency bands as a function of time and memory task (encoding vs retrieval). Our results suggest that the exposure to EMF does not alter the resting EEG per se but modifies the brain responses significantly during a memory task.

Changes in EEG spectral power in the prefrontal cortex of conscious rats elicited by drugs interacting with dopaminergic and noradrenergic transmission.

1. The electroencephalographic (EEG) effects of drugs interacting with dopaminergic and noradrenergic systems were studied in conscious rats. Power spectra (0 - 30 Hz) were recorded from electrodes implanted bilaterally in the prefrontal cortex. Drug effects on EEG power were calculated as the spectral power following drug administration divided by the spectral power after vehicle administration. 2. Dopaminergic agonists at low doses, (apomorphine 0. 01 mg kg-1 s.c., quinpirole 0.01 mg kg-1 i.p.) and dopaminergic antagonists (haloperidol 1 mg kg-1 i.p., raclopride 2.5 mg kg-1 s.c. ), which decrease dopaminergic transmission, induced an increase of EEG power. Conversely, dopaminergic agonists at higher doses (apomorphine 0.5 mg kg-1 s.c., quinpirole 0.5 mg kg-1 i.p.) which increase activation of postsynaptic D2 and D3 receptors, induced a decrease of EEG power. 3. The alpha1-adrenoceptor antagonists (phenoxybenzamine 0.64 mg kg-1 s.c., prazosin 0.32 mg kg-1 s.c.) and the alpha2-adrenoceptor agonists (UK 14304 0.05 mg kg-1 s.c., clonidine 0.025 mg kg-1 i.p.), which decrease noradrenergic transmission, induced an increase of EEG power. Conversely, the alpha1-adrenoceptor agonist, cirazoline (0.05 mg kg-1 s.c.), the adrenergic agent modafinil (250, 350 mg kg-1 i.p.) and alpha2-adrenoceptor antagonists (RX 821002 0.01 mg kg-1 s.c., yohimbine 0.5 mg kg-1 i.p.), which increase noradrenergic transmission, induced a decrease of EEG power. The effects of prazosin (0.64 mg kg-1 s.c.) were dose-dependently antagonized by co-administration with modafinil and cirazoline, but not by apomorphine. 4. In conclusion, pharmacological modulation of dopaminergic and noradrenergic transmission may result in consistent EEG changes: decreased dopaminergic or noradrenergic activity induces an increase of EEG spectral power; while increased dopaminergic or noradrenergic activity decreases EEG spectral power.

Effects of cigarette smoking on EEG spectral-band power, dimensional complexity, and nonlinearity during reaction-time task performance.

Electroencephalogram (EEG) and heart rate (HR) were recorded while individuals performed visual and auditory go/no-go reaction time (RT) tasks. Overnight-abstaining smokers smoked two types of cigarettes in a single morning session. The first type was smoked once and had a nicotine yield of 0.05 mg. Two cigarettes of the second type (1.1 mg) were smoked. Four recordings were made: presmoking, postsmoking 0.05 mg, and postsmoking each 1.1 mg. HR was increased only by the first 1.1-mg cigarette. Smoking both the 1.1-mg cigarettes decreased RT. Smoking the first 1.1-mg cigarette increased EEG power in the beta2 band. A flexible effect of smoking the first 1.1-mg cigarette on EEG dimensional complexity (DCx) was obtained at locus Cz. Specifically, DCx was (a) raised when the presmoking level was low, (b) not affected when the presmoking level was intermediate, and (c) lowered when the presmoking level was high. Surrogate-data testing indicated the presence of nonlinearity in the EEG data that was not affected by smoking. Decreased RT was associated with increased DCx in the visual task only.

Effect of Total Sleep Deprivation on Reaction Time and Waking EEG Activity in Man

Nine paid volunteers were sleep deprived over a period of 40 hours. Every 2 hours during total sleep deprivation (TSD) and after recovery sleep, oral temperature (OT), reaction time (RT) in a vigilance task and electroencephalogram (EEG) with eyes open and closed (C3, C4, T3 and T4) were recorded. Ten artifact-free samples from each condition were Fourier transformed. Absolute power was calculated for six bands. Analyses of variance with deprivation and time of day as factors showed the following significant results: 1) TSD induced an increase in RT, of theta power in all derivations, of beta power in both centrals and a decrease of alpha power with eyes closed; OT was not affected. 2) All bands showed a peak of power at 1800 hours, 2 hours in advance of the OT acrophase at 2000 hours. All variables recovered baseline values after 1 night of sleep. Significant linear correlations of hours of wakefulness with EEG and RT, and of EEG power with OT and RT, were observed. The present findings show a linear increase in EEG power and RT with TSD, and a diurnal oscillation of EEG power, which is independent of TSD.

EEG–Korrelate der Schmerzkontrolle

Cerebral responses in anticipation of painful stimulation and while coping with it were investigated in transcultural studies (Greek fire walkers, a fakir and hook hanging ceremony in Sri Lanka). EEG was recorded using a telemetry system. In all subjects a significant increase in EEG power within the ϑ–band occurs in anticipation and during control of pain. More intense pain covaried with less power within the slow ϑ–frequency band (3.5–5.0Hz). Field studies investigating marathon runners analoguous shifts towards slower EEG frequencies covarying with increased endorphin plasma levels could be observed.

Effects of systemic clonidine on auditory event-related potentials in squirrel monkeys

Event-related potential (ERP), electroencephalographic (BEG), and behavioral data were collected from squirrel monkeys ( Saimiri sciureus) in a 90−10 auditory oddball paradigm. Background or target tones were presented once every 2 s, and responses to the targets were rewarded. ERPs were recorded from epidural electrodes following systemic administration of clonidine (0.1 mg/kg) or a saline placebo. EEG power spectra and behavioral performance were assessed simultaneously as indices of behavioral state. Clonidine significantly decreased the area and increased the latency of a P300-like potential. The amplitudes and areas of the earlier P1, N1, and P2 components and a later slow wave-like potential were not reduced, nor were their latencies altered. Clonidine produced increased EEG power in the alpha range (7.5–12 Hz) and decreased power in the upper beta range (20–40 Hz) but did not affect performance in the oddball task. Because two major effects of clonidine are to substantially reduce activity in the noradrenergic nucleus locus coeruleus (LC) and to reduce norepinephrine (NE) release from axons, the present results support the hypothesis that the LC and its efferent projection system are important in modulating the activity of P300-like potentials.

Intérêt de l'EEG quantifié dans la maladie d'Alzheimer. Modifications induites par le piracétam

One study was performed in 12 patients with presenile Alzheimer's disease (group I), the other one in 16 patients with mild senile dementia of Alzheimer type (group II). In each study, patients were divided into two randomized parallel groups, one receiving placebo, the other piracetam (9 g daily in group I piracetam and 2.4 g daily in group II piracetam) during three months, piracetam induced a decrease in EEG power on the 2-6 Hz range (group I piracetam), 3-5 Hz and 7 Hz (group II piracetam) and an increase of EEG power in the 9-11 Hz range (group I piracetam) and in the 10 Hz and 13 Hz frequencies (group II piracetam). There was also a significant improvement in the Trail Making Test part A in group II piracetam. Correlations between decreased EEG low frequency components and improvement in some psychometric tests were found significant in the two groups. It seems that the main effect of piracetam was to induce increased alertness. The same results were found in both studies; the good reproducibility suggests that EEG spectral analysis is a reliable tool in the assessment of psychotropic drug effects.

REM sleep deprivation during 5 hours leads to an immediate REM sleep rebound and to suppression of non-REM sleep intensity

Nine healthy male subjects were deprived of REM sleep during the first 5 h after sleep onset. Afterwards recovery sleep was undisturbed. During the deprivation period the non-REM EEG power spectrum was reduced when compared to baseline for the frequencies up to 7 Hz, despite the fact that non-REM sleep was not experimentally disturbed. During the recovery interval a significant rebound of REM sleep was observed, which was only accompanied by a very slight increase of power in the lower non-REM EEG frequencies. In order to control for intermittent wakefulness, the same subjects were subjected to non-REM sleep interruption during the first 5 h after sleep onset 2 weeks later. Again subsequent recovery sleep was undisturbed. The interventions resulted in a similar amount of wakefulness in both conditions. During the intervention period, the non-REM EEG power spectrum was only marginally reduced in the delta frequency range. REM sleep duration was only slightly reduced. During the recovery interval, however, a substantial increase in EEG power in the delta frequency range was noted, without notable changes in REM time. It is concluded that an increased pressure for REM sleep results in longer REM episodes and a reduced intensity of non-REM sleep.

Comparative effects of almitrine and raubasine, singly and in combination, on electroencephalographic activity in young and old rats

A new method for quantification of electroencephalographic (EEG) signals was used to study the effects of almitrine and raubasine, alone and combination, in two groups of six unanesthetized rats, aged 8 months (young) and 22 months (old). Coadministration of almitrine (7.5 mg/kg −1 i.p.) and rabausine (2.5 mg/kg −1 i.p.) induced an increased EEG power from 7 to 30 Hz; the frequencies concerned were identical in young and old rats, but the degree of their power variations was more marked in old rats. Almitrine induced a 20 to 50% increase in EEG power in young rats on nearly all spectral components. The effects of almitrine were only seen in the low-frequency range in old rats. Rabausine increased the EEG power in the 10 to 20 Hz frequency range; these effects were significantly greater in old rats. In both age groups, the effects on EEG power observed with coadministration of almitrine and raubasine were significantly different from those expected if raubasine and almitrine add their individual effects. These results show that a) almitrine and raubasine modify cortical electrical activity in a different manner as a function of age; b) the modification of the EEG activity induced by the coadministration is suggestive of an interaction between the cortical effects of each drug; and c) the modification of EEG power induced by the coadministration is qualitatively identical in young and old rats but quantitatively more marked in old rats.

Effect of Drugs Acting on Monoaminergic and Cholinergic Systems on the Quantified EEG of Rats

Five different classes of drugs (clonidine: 0, 0.10, 0.30, 0.50 mg/kg; yohimbine: 0, 2, 4, 8 mg/kg; haloperidol: 0, 0.02, 0.04, 0.08 mg/kg; piracetam: 0, 150, 300, 600 mg/kg, and eserine: 0, 0.10, 0.30, 0.50 mg/kg) were studied on two cortical EEG derivations as well as a deep structure, the locus ceruleus in the rats. Each drug affected the EEG in its own particular manner. Clonidine significantly decreased frequency in the theta band (3.7-7.5 Hz) and increased it in the alpha band (7.6-13.5 Hz). A general significant increase in power was observed. Yohimbine's effects on the EEG varied according to the regions studied. There were significant modifications of power and frequency in the theta, alpha and beta bands in the three derivations studied. Notable effects of haloperidol were observed as an increase in power in all frequency bands at all doses administered particularly in the anteroparietal and posteroparietal derivations. In the locus ceruleus derivation, power was significantly increased at all doses only in the alpha and beta frequency bands. Concerning piracetam, while no significant effects were noted on the EEG frequency, this drug significantly increased EEG power in the posteroparietal and anteroparietal derivations. The most important effects are obtained at the lowest dose (150 mg/kg) administered. Finally, it was shown that eserine significantly decreased power in the delta bandwidth shortly after its administration. Afterwards, the power gradually regained its original level.

EEG and CBF in Cerebral Ischemia. Follow-up Studies in Humans and Monkeys

Publisher Summary This chapter discusses a follow-up study of electroencephalogram (EEG) and cerebral blood flow (CBF) in patients with strokes in the territory of the middle cerebral artery (MCA) compared with monkeys studied before and after occlusion of the middle cerebral artery. The experiments described in the chapter are to establish whether the induced ischemia in monkeys could be considered an appropriate model for the spontaneous ischemia occurring in man. The results are compared with six rhesus monkeys studied before and after occlusion of the MCA. The ischemia in humans gave rise to an increase in EEG power in the higher frequencies, as well as in the lower frequencies with a subsequent decrease in power in the recovery period. The same results are obtained from the cortical electrodes in the monkeys. Changes in the power spectrum on the unaffected side are observed in humans as well as in monkeys (EEG diaschisis). The measurements of mean rCBF (xenon inhalation) in humans gave only limited information: the CBF values after the (minor) strokes are low but hardly asymmetrical. From the neurophysiological point of view, the rhesus monkey studied before and after occlusion of the MCA, seems the optimal model available for the studies of human ischemia.

Developmental comparison of sleep EEG power spectral patterns in infants at low and high risk for sudden death

Power spectral density measured from central cortical EEG recordings during sleep was compared in two groups of 20 infants each at intervals between 1 week and 6 months of age. One group consisted of siblings of infants who had previously died of the sudden infant death syndrome, as determined by history and autopsy report (sibling group). The second group was made up of age, sex, and socioeconomically matched infants with no familial history of sudden infant death (control group).

Contamination of scalp EEG spectrum during contraction of cranio-facial muscles

Autospectral and coherence values were determined for three EEG derivations, two craniofacial muscles, and the biceps during separate 90 sec periods of strong contraction. Spectra of contracting frontalis and masseter muscles showed peak power between 30 and 60 c/sec, with peak biceps power during contraction centered around 50 c/sec. Over the course of contraction, all three muscles showed an increase in the proportion of low frequency power (below 40 c/sec) and a decrease in power above that frequency. During contraction of the cranio-facial muscles, there were generalized increases in EEG power at all frequencies from vertex-frontal, vertex-mastoid and vertex-temporal derivations. However, these increases were minimal below about 14c/sec unless one electrode of a derivation was located directly over the contracting muscle. Coherences between EEG derivations showed considerable increases during muscle contraction only at frequencies above 14c/sec. In addition, coherence between EEG and EMG derivations were large only when one EEG electrode was located over the muscle. These results indicate that there is very little direct, linear EMG infiltration of the EEG signal below 14 c/sec during tonic contraction of individual muscles unless the EEG electrode is extremely close to a contracting muscle.