Changes In EEG Power Spectra Research Articles

Changes in EEG power spectra in chronic mild stress depressed rats

目的 探讨应用功率谱方法分析慢性不可预见性应激抑郁模型大鼠大脑脑电信号特征.方法 25只 Sprague-Dewley雄性大鼠随机分为抑郁模型组15只,正常对照组10只.采用慢性轻度不可预见性应激方法及单笼饲养21 d建立抑郁模型,应激前以及应激21 d末对各组大鼠进行敞箱实验及液体消耗实验,21d后通过慢性埋植电极,采集不可预见性应激抑郁大鼠皮层脑电.结果 慢性应激抑郁大鼠在ch1 Theta(4～8Hz)相对谱[5.23±2.08]、ch2 Theta(4～8Hz)相对谱[6.22±1.54]、ch13 Theta(4～8Hz)相对谱[7.70±2.71],ch9 Delta(0～4Hz)绝对谱[192.14±0.45],ch2第四阶距[203.44 ±17.84]、ch7 Delta(0～4Hz)峰值[129.20±9.05]较正常组有显著减少(P＜0.05),但是在ch2 Delta(0～4Hz)[5.23±2.08]、ch13 Beta(13～30)相对谱[26.81 4±2.47]较正常组显著增加(P＜0.05).大部分EEG改变主要发生在左半球.结论 功能谱数据的变化,揭示了抑郁大鼠脑电信息活动特征性及其差异,表明了抑郁大鼠脑电信号复杂度的变化规律及验证了大脑两半球功能不对称性与情绪之间的关系。

Reduced Sleep Spindle Activity in Schizophrenia Patients

High-density EEG during sleep represents a powerful new tool to reveal potential abnormalities in rhythm-generating mechanisms while avoiding confounding factors associated with waking activities. As a first step in this direction, the authors employed high-density EEG to explore whether sleep rhythms differ between schizophrenia subjects, healthy individuals, and a psychiatric control group with a history of depression. Healthy comparison subjects (N=17), medicated schizophrenia patients (N=18), and subjects with a history of depression (N=15) were recruited. Subjects were recorded during the first sleep episode of the night with a 256-electrode high-density EEG. Recordings were analyzed for changes in EEG power spectra, power topography, and sleep-specific cortical oscillations. The authors found that the schizophrenia group had a significant reduction in centroparietal EEG power, from 13.75 to 15.00 Hz, in relation to both the comparison and depression groups. No significant difference in EEG power between the comparison and depression groups was identified. The authors also found a decrease in sleep spindle number, amplitude, duration, and integrated spindle activity in schizophrenia patients. Furthermore, integrated spindle activity had an effect size corresponding to 93.0% or 90.2% separation of the schizophrenia from the comparison or depression group. Sleep spindles are generated by the thalamic reticular nucleus in conjunction with specific thalamic nuclei and are modulated by corticothalamic and thalamocortical connections. The deficit in sleep spindles in schizophrenia subjects may reflect dysfunction in thalamic-reticular and thalamocortical mechanisms and could represent a biological marker of illness.

The glycine transporter-1 inhibitors NFPS and Org 24461: a pharmacological study

The in vitro and in vivo pharmacology of two glycine transporter-1 (GlyT1) inhibitors, N[3-(4′-fluorophenyl)-3-(4′-phenylphenoxy)-propyl]sarcosine (NFPS) and R, S-(+/−) N-methyl- N-[(4-trifluoromethyl)phenoxy]-3-phenyl-propylglycine (Org 24461), was studied. NFPS and Org 24461 inhibited the uptake of [ 3H]glycine in hippocampal synaptosomal preparation with IC 50 values of 0.022 and 2.5 μM. Neither NFPS nor Org 24461 (0.1 μM) showed significant binding to α-1, α-2, and β-adrenoceptors, D 1 and D 2 dopamine receptors, and 5-HT 1A and 5-HT 2A serotonin receptors in membranes prepared from rat brain or to cloned 5-HT 6 and 5-HT 7 receptors. At 10 μM concentrations, binding affinity was measured for NFPS to 5-HT 2A and 5-HT 2C serotonin receptors and α-2 adrenoceptors and for NFPS and Org 24461 to 5-HT 7 serotonin receptors. Glycine (0.1 mM) and sarcosine (5 mM) increased [ 3H]glycine efflux from superfused rat hippocampal slices preloaded with [ 3H]glycine. NFPS and Org 24461 (0.1 mM) did not influence [ 3H]glycine efflux, however, they inhibited glycine-induced [ 3H]glycine release. These findings indicate that NFPS and Org 24461 selectively inhibit glycine uptake without being substrates of the transporter protein. Several antipsychotic tests were used to characterize antipsychotic effects of NFPS and Org 24461 in vivo. These compounds did not alter apomorphine-induced climbing and stereotypy in a dose of 10 mg/kg po in mice and did not induce catalepsy in a dose of 10 mg/kg ip in rats. The ID 50 values of NFPS were 21.4 mg/kg and higher than 30 mg/kg ip for inhibition of phencyclidine (PCP)- and d-amphetamine-induced hypermotility in mice and these values were 2.5 and 8.6 mg/kg ip for Org 24461. NFPS and Org 24461 did not exhibit anxiolytic effects in light–dark test in mice, in the meta-chlorophenylpiperazine (mCPP)-induced anxiety test (minimal effective dose or MED was higher than 3 mg/kg ip) and in the Vogel conflict drinking test in rats (MED was higher than 10 mg/kg ip). Both NFPS and Org 24461 (1–10 mg/kg ip) reversed PCP-induced changes in EEG power spectra in conscious rats. These data support the view that GlyT1 inhibitors may have potential importance in treatment of negative symptoms of schizophrenia.

EEG-NeuroBioFeedback Treatment of Patients with Brain Injury Part 3: Cardiac Parameters and Finger Temperature Changes Associated with Rehabilitation

ABSTRACT Background. Twenty-seven patients with brain injury were treated by computer-assisted electroencephalographic NeuroBioFeedback (EEG-NBF). All patients were medication-free during treatment. Methods. Parallel to targeted changes in EEG power spectra, secondary effects were monitored for heart rate, systolic and diastolic pressures, pulse rate and fingertip temperature. Results. Extreme blood pressure values generally responded by up-and down-regulation toward normal values. Fingertip temperature (FT°) increased in both kinetic movement and amplitude from the beginning to the end of treatment and correlated directly with the rate of the patient's rehabilitation, reflecting an improvement of blood circulation. Blood pressure, pulse and FT° ranks in numerical values were compared by rank correlations. Conclusions. NBF in patients with brain injury results in beneficial physiological regulation in addition to initially targeted improvements in brain functions. Symptom associations versus the success o...

Changes in EEG power spectra and behavioral states in rats exposed to the acetylcholinesterase inhibitor chlorpyrifos and muscarinic agonist oxotremorine

Organophosphates (OPs) inhibit acetylcholinesterase (AChE) activity causing cholinergic stimulation in the central nervous system (CNS). Cholinergic systems are crucial in electroencephalogram (EEG) generation and regulation of behavior; however, little is known about how OP exposure affects the EEG and behavioral states. We recorded EEG, core temperature and motor activity before and after exposure to the OP pesticide chlorpyrifos (CHP) in adult female rats implanted with telemetric transmitters. The recording and reference electrodes were placed in the occipital and frontal bones, respectively. The animals received CHP, 25 mg/kg, p.o., or oxotremorine (OX), 0.2 mg/kg, s.c. CHP led to a significant increase in delta (0.1–3.5 Hz), slow theta (4–6.5 Hz), gamma 2 (35.5–50 Hz), reduction in fast theta (7–8.5 Hz), alpha/sigma (9–14 Hz), beta 1 (14.5–24 Hz), beta 2 (24.5–30 Hz) and gamma 1 (30.5–35 Hz) powers, slowing of peak frequencies in 1–9 Hz range, hypothermia and decrease in motor activity. The drop in 7–14 Hz was associated with cholinergic suppression of sleep spindles. Changes in behavioral state were characterized by dramatic diminution of sleep postures and exploring activity and prolongation of quiet waking. There was recovery in all bands in spite of continued inhibition of AChE activity [44,45] in rats exposed to CHP. OX-induced EEG and behavioral alterations were similar to CHP except there was no increase in delta and the onset and recovery were more rapid. We did not find a correlation between the EEG and core temperature alterations. Overall, changes in EEG (except in delta band) and behavior following CHP were attributable to muscarinic stimulation. Cortical arousal together with increased quiet waking and decreased sleep after CHP occurred independently from inhibition of motor activity and lowering of core temperature.

FFT analysis of EEG during stage 2-to-REM transitions in narcoleptic patients and normal sleepers

The EEG in REM sleep is markedly different from the EEG in non-REM sleep; however, very little research has been conducted analyzing the transition from NREM to REM sleep. The purpose of this study was to describe the changes in EEG power spectra that coincide with significant physiological events throughout the transition from stage 2 to REM sleep. Furthermore, a comparison of the stage 2 to REM transition between narcoleptic patients and normal sleepers was conducted. Five female and five male patients diagnosed with narcolepsy-cataplexy and 10 normal sleepers matched for age and gender participated. Analyses were based on the consecutive appearance of 3 common physiological indicators of REM sleep: First, a decrease in tonic submental EMG activity; second, the appearance of saw tooth waves; and third, the appearance of rapid eye movements. Systematic changes in EEG power density were evident for delta, theta, alpha and sigma frequencies, across the stage 2-REM transition. These changes appeared to be relatively continuous throughout this transition rather than changing dramatically following the onset of any one of the 3 primary physiological indicators of REM sleep. Furthermore, the transition from stage 2 to stage REM appeared to be similar for narcoleptic patients and normal sleepers.

Growth spurts in brain maturation during middle childhood as indexed by EEG power spectra

Developmental changes in background EEG power spectra were examined in 5–12-year-old children. The results confirmed older and more recent studies that reported continuous maturation and more sudden growth spurts in power spectral amplitude. EEG power in the Delta and Theta frequency bands decreased gradually with age, while power in the Alpha and Beta bands changed very little. Changes in spectral power were relatively increased between 6 and 7 years and between 9, 10 and 11 years. Some methodological problems concerning the assessment of cross-sectional age changes in EEG power spectra were addressed. Peak frequency increased with age; between 5 and 12 years the peak in the power spectrum shifted from fast Theta via slow Alpha to fast Alpha. Transformation of absolute power into relative power produced a high degree of interdependency between the broad bands. This interdependency affected the change with age of relative Alpha. Absolute power Alpha only changed in the eldest children, but because of a substantial decrease in Delta and Theta with increasing age, the proportion of Alpha relative to the other three bands increased. Hence, relative Alpha provided a good indication of the general maturational trend.

EEG power spectrum changes due to listening to pleasant music and their relation to relaxation effects.

Electroencephalogram (EEG) power spectrum changes induced by pleasant music (2-min. fractions of 6 samples of music [famous classical and commercially available "alpha music" at 10-sec. intervals]) were investigated in relation to changes in 16 kinds of psychosomatic feelings. Subjects were 42 healthy young people aged 18-25 yrs. Two major components, "pleasant & relaxed" and "calm", were extracted through principal component analysis of the feeling changes, both of which were related to the "relaxation effects" of the music. These component scores were not related to the changes of EEG powers in the delta, theta, alpha and beta frequency components in 6 regions (frontal, parietal and occipital regions of the left and right hemispheres), when examined separately. However, the change of the total delta power for all the regions was significantly associated with both the "pleasant & relaxed" and "calm" component scores. The association between the total theta power change and "calm" score was found to be insignificant if the type-A personality variable was added to their regression model. On the other hand, the alpha-peak frequency was inversely related to the decrease of the "calm" score in the left occipital region (LO). The reduction of the alpha-peak power in the LO was also significant, and was associated not with the alpha-peak frequency changes but inversely with the "calm" score, although these alpha-component changes were not shown to be modified by the personality. Thus, the present study suggests, as a preliminary finding, that the "relaxation effects" of pleasant music can be associated with the EEG power spectrum component changes, especially with the change in the total theta power and possibly with that in the alpha power in the occipital, and the frequency shift of the peak in the alpha-range. Some of the associations were also shown to vary for the type-A personality, suggesting a clue to relating the personality to a differential stress-related psychosomatic trait, although the physiological significance of the changes in the low-frequency component range as well as those in the alpha-frequency component, which are obtained through FFT, should be further clarified.

Inhibitory effect of peony root extract on pentylenetetrazol-induced EEG power spectrum changes and extracellular calcium concentration changes in rat cerebral cortex

To elucidate the mechanism of anticonvulsant action of peony root and to determine the relative contributions of pure component substances, the water, water/acetone and methanol extracts of peony roots, paeoniflorin, albiflorin and pentagalloylglucose were studied in rats using the EEG power spectrum changes induced by pentylenetetrazol administration and the extracellular calcium and potassium concentration changes related to seizure activity. The water extract of peony roots, albiflorin and pentagalloylglucose given orally completely inhibited the EEG power spectrum changes as well as the extracellular calcium, and potassium concentration changes related to seizure activity. The water/acetone and methanol extracts and paeoniflorin were relatively less potent. These findings suggested that the anticonvulsant action of peony roots is due primarily to albiflorin and the gallotannin fraction. Albiflorin and pentagalloylglucose appear to manifest their anticonvulsant action due to inhibition of the seizure-related decrease of extracellular calcium and consequent intracellular calcium increase.

Relationship between regulation of morphine-induced EEG effects and changes in naloxone sensitivity

The present data indicate that pretreatment with i.c.v. injection of dynorphin, morphine and dynorphin/morphine resulted in quantitative and qualitative changes in EEG power spectra in rats given i.c.v. morphine 24 h later. Correlated changes in sensitivity to antagonism of these EEG effects by naloxone were also found. Rats were implanted with cortical EEG electrodes and i.c.v. and i.v. cannulas. I.c.v. injections of morphine (20 μg/rat) produced high-voltage, slow-wave EEG bursts (1–10 Hz) associated with behavioral stupor which lasted about 2 h. Injections of i.c.v. morphine in rats pretreated with i.c.v. dynorphin (20 μg/rat), morphine (20 μg/rat) or dynorphin/morphine 24 h earlier, produced quantitative increases in absolute EEG spectral power. Injections of i.c.v. morphine in rats pretreated with i.c.v. dynorphin/morphine 24 h earlier, also produced qualitatively different EEG power spectra with a predominant peak in the 4–6 Hz band, similar to the EEG power spectra seen after acute administration of κ opioids. After 20 min of morphine-induced high voltage EEG bursts, i.v. naloxone was given in sequential doses (0.0025, 0.0125, 0.025, 0.050 mg/kg) every 3 min until the EEG bursts were suppressed for 20 min. Relatively low doses of naloxone suppressed morphine-induced EEG bursts in rats that received i.c.v. H 2O/H 2O pretreatment. Slightly higher, but significant, doses of naloxone suppressed morphine-induced EEG bursts in rats that received i.c.v. H 2O/morphine or dynorphin/H 2O pretreatment. Moreover, a 10-fold increase in naloxone dose was needed to suppress EEG bursts in rats that received dynorphin/morphine pretreatment. Finally, significant correlations were found between amounts of morphine-induced absolute spectral power and doses of naloxone needed to suppress morphine-induced EEG bursts Thus, dynorphin may act as a possible regulator of certain μ-opioid receptor-associated phenomena, such as morphine-induced EEG bursts and affinity of opioid binding sites

Changes in eeg power, acoustic evoked potentials and heart rate after mildly arousing non-acoustic priming stimuli in carp ( CYPRINUS CARPIO)

1. 1. Changes in EEG power spectrum of carp to a priming non-acoustic stimulus followed by acoustic clicks were compared to those due to acoustic clicks delivered alone. Recordings were made from the telencephalon, midbrain and medulla. Acoustic evoked potentials (AEPs) to the clicks were also recorded. 2. 2. EEG power changes to non-acoustic stimuli occurred over the whole 1–40 Hz frequency range and were regionally specific and consistent. 3. 3. The changes in the EEG midfrequency 12–24 Hz power spectrum to non-acoustic stimuli were significantly correlated with changes in the AEP to subsequent clicks. An elevated medullary AEP amplitude and reduced duration were correlated with increased medullary EEG power and increased midbrain AEP duration. 4. 4. Telencephalic EEG power changes were inversely related to changes in medullary and midbrain AEP amplitude.

All night spectral analysis of EEG sleep in young adult and middle-aged male subjects

The sleep EEGs of 9 young adult males (age 20–28 years) and 8 middle-aged males (42–56 years) were analyzed by visual scoring and spectral analysis. In the middle-aged subjects power density in the delta, theta and sigma frequencies were attenuated as compared to the young subjects. In both age groups power density in the delta and theta frequencies declined from NREM period 1 to 3. In the sigma frequencies, however, no systematic changes in power density were observed over the sleep episode. In both age groups the decay of EEG power (0.75–7.0 Hz) over successive NREM-REM cycles and the time course of EEG power during NREM sleep was analyzed. The decay rate of both EEG power density over successive NREM-REM cycles and EEG power density during NREM sleep was smaller in the middle-aged subjects than in the young subjects. It is concluded that the age-related differences in human sleep EEG power spectra are not identical to the changes in EEG power spectra observed in the course of the sleep episode. Therefore age-related differences in EEG power spectra cannot be completely explained by assuming a reduced need for sleep in older subjects. The smaller decay rate of EEG power during NREM sleep in the middle-aged subjects is interpreted as a reduced sleep efficiency. The results are discussed in the frame work of the two-process model of sleep regulation.

Correlation between the anxiolytic effect of diazepam and changes in EEG power spectra in rats

Correlation between the anxiolytic effect of diazepam and changes in EEG power spectra in rats

EEG power spectrum changes associated with the increase in the blood pressure

EEG power spectrum changes associated with the increase in the blood pressure

Inhibitory effect of TJ-960 (SK) on pentylenetetrazol-induced EEG power spectrum changes

Effects of the Japanese Kampo medicine ‘Shosaiko-to-go-keishika-shyakuyaku-to’ (TJ-960), which is a mixture of 9 herbal drugs and is practically equivalent to ‘Saiko-keishi-to’ (SK), on the pentylenetetrazol (PTZ)-induced EEG power spectrum changes were examined. The EEG power spectrum change with 2 PTZ administrations at an 80 min interval was clearly inhibited by oral administration of 1.0 mg/kg of TJ-960. By separate single administrations of the main component herbal drugs, Bupleuri radix, Cinnamomi cortex, Paeoniae radix and Zingiberis rhizoma, only Paeoniae radix showed statistically significant inhibition of PTZ-induced EEG power spectrum changes at a proportional dose of 1.0 mg/kg of TJ-960. The other main component herbal drugs showed no statistically significant inhibitory effect although they had a tendency to inhibit. These findings suggest that the Japanese Kampo medicine, TJ-960 (SK), has an inhibitory effect on PTZ-induced power spectrum changes and one of the component herbal drugs, Paeoniae radix, is the important component drug.

Effect of anticonvulsants on pentylenetetrazol-induced power spectrum changes in electroencephalograms in rats

The effect of anticonvulsants on pentylenetetrazol (PTZ)-induced EEG power spectrum changes was examined. When the minimum dose of PTZ (15 mg/kg) was administered intravenously twice, with an interval of 80 min, a clear EEG power spectrum change was observed after the second PTZ administration, irrespective of whether or not the first PTZ administration evoked marked EEG changes. We defined the values F N , S N and S F . The value F N , obtained by dividing the power spectrum area after the first PTZ administration by the normal power spectrum area, was 1.06 ± 0.05 ( mean ± S. E.). The value S N , obtained by dividing the power spectrum area after the second PTZ administration by the normal power spectrum area, was 2.00 ± 0.21. The value S F , obtained by dividing S N by F N , was 1.86 ± 0.16. The S F value was almost constant regardless of whether or not the first PTZ administration could evoke marked EEG changes. The effect of anticonvulsants was examined by S F value changes, and 100 mg/kg of PHT completely inhibited the double PTZ effect. Phenobarbital, ethosuximide and sodium valproate also inhibited the double PTZ effect. Using the S F value of the EEG power spectrum with minimum dose double PTZ administration, quantitative evaluation is possible for anticonvulsant drugs.

Statistical characterization of the EEG: The use of the power spectrum as a measure of ergodicity

In order to interpret statistical summaries of treatment-related changes in EEG power spectra, the internal consistency of the set of data from each condition must first be known. A technique for the assessment of such across-record homogeneity (ergodicity) is derived from the defining characteristics of the power-spectrum. A simplified graphic approximation is also detailed. Computer simulations and practical validation confirm it as a useful means of evaluating the erogodicity of sets of EEG data.

Cerebral infarction in rats using homologous blood emboli: development of a new experimental model.

A reproducible model of thromboembolism in the rat was developed and the temporal relationship between hydrogen clearance, regional cerebral blood flow (rCBF) and power spectral-analyzed electroencephalographic (EEG) activity explored for up to four hours postinsult. Sixteen rats were subjected to right internal carotid artery homologous blood embolization after electrocautery of the pterygopalatine artery. Four rats were subjected to sham operation. Cerebral angiography before and for up to four hours postinsult was used to verify the distal migration and fragmentation of the emboli. Preembolic mean rCBF was 62 +/- 9 ml . 100g-1 . min-1 and 65 +/- 12 ml . 100g-1 . min-1 in the embolized and contralateral sides, respectively. Based upon the distribution of the emboli at sacrifice, the experimental group of 12 rats fell into three subgroups: unilateral proximal embolism, n = 8; unilateral peripheral embolism, n = 3; and bilateral proximal embolism, n = 1. In unilateral proximal embolism the mean rCBF in the embolized hemisphere ranged between 10 and 20 ml . 100g-1 . min-1 and correlated well with changes in EEG power spectra. In unilateral peripheral embolism, the mean rCBF in the embolized hemisphere fell significantly 30 min postembolism. It returned progressively towards preembolic values as the embolic clots migrated distally and fragmented. Despite the restoration of rCBF, recovery of EEG activity appeared to be delayed. Our results did not show luxury perfusion after embolic insults. The time course for the reopening of the embolized artery and the delay in recovery of neuronal function (i.e., EEG activity) relative to the restoration of rCBF are discussed.

Electrophysiological measures (CNV — EEG) and Nitrous Oxide at low doses in man

Nitrous oxide (N2O) is a widely used inhalational anesthetic gas, but its exact mode of action and its distribution in the CNS are not yet well known. The aim of this research was to study the effects of N2O at low doses (10 percent) in the CNS of humans. Five healthy volunteers were tested. Contingent Negative Variation (CNV), Reaction time (RT) and quantified EEG recordings were taken while subjects were breathing air and then N2O. A significant reduction of the post-imperative positive CNV components during N2O inhalation was observed; no changes in EEG power spectrum and RT values were seen. These results could be consistent with an early N2O interference with processes underlying CNV resolution, while vigilance and attention were still maintained.