Electroencephalogram Activation Research Articles

Changes in Electroencephalography by Modulation of Interferential Current Stimulation

Interferential current (IFC) stimulation can alter pain perception. This study aimed to investigate the effects of IFC stimulation on motor cortex signals and observe how electroencephalography changes depend on IFC stimulation parameters. Forty-five healthy adults were divided into high frequency (HF)–low intensity (LI), HF–high intensity (HI), and low frequency (LF)–HI groups to compare their electroencephalography before, immediately after, and 30 min after current stimulation. The changes in relative beta power according to the intervention time showed significant differences between the HF–LI and HF–HI, as well as the LF–HI and HF–HI, groups in the C3 and P3 regions immediately after IFC stimulation. Similarly, the gamma band showed significant differences according to the intervention time between the LF–HI and HF–HI groups in the P3 region immediately following IFC intervention. For relative theta power, the interaction between group and time was significantly different in the Fp2, F3, F4, C3, C4, and P4 regions. Based on these results, we were able to map the activation in cerebral cortex regions according to the stimulation level, confirming changes in electroencephalogram activation through peripheral nerve stimulation. This study provides a foundation for future applications for selectively controlling feedback at a proper stimulation level in young adults.

Insufficient Sleep, Electroencephalogram Activation, and Seizure Risk: Re-Evaluating the Evidence.

Insufficient sleep has been considered a seizure trigger in people with epilepsy for thousands of years. Here, we reviewed the evidence upon which this axiomatic association might be predicated. After evaluating evidence suggesting insufficient sleep as an EEG activator, we systematically reviewed the literature for longitudinal studies measuring the effect of insufficient sleep on seizure risk. Ultimately, published works designed to prove a causal relationship were of low level of evidence and disagreed with one another. Despite the idea's deep-seated nature, when considering causal evidence only, no conclusion can be made regarding the relationship between insufficient sleep and seizure risk. This article is protected by copyright. All rights reserved.

Features of the Operation of the Mirror Neuron System in Patients with Affective Disorders

Objectives. To identify the characteristics of changes in the electroencephalogram (EEG) pattern and activation of neural networks on perception and performance of a motor act in healthy people and patients with affective disorders. Materials and methods. The study group consisted of 15 patients with affective disorders and the control group comprised 11 healthy subjects. The task was to first observe a hand movement performed by the experimenter (clenching of the fist), then to imagine this movement, and then to perform it themselves. EEG recordings were made and analyzed; areas of activation were identified by solving the reverse EEG problem using LORETA. Results and conclusions. Activation of the mirror system of the brain in patients with affective disorders was seen in the left temporal hemisphere, while healthy subjects showed activation in the temporal lobes of both hemispheres and the frontal superior, middle, and inferior gyri.

The effects of whole body vibration exercise intervention on electroencephalogram activation and cognitive function in women with senile dementia.

This study conducted the Korean version of Mini-Mental State Examination (MMSE-K) to women aged 65 or older residing in Gangwon-do Province and screened those who were suspicious to have mild dementia for receiving 23 points or lower in it. For eight weeks, this author tried to verify the effects of whole body vibration exercise intervention on electroencephalogram (EEG) activation and cognitive function in women with senile dementia. According to the results, both EEG activation and cognitive function indicated statistically significant difference in terms of the interactive effect between the measuring times and groups, and there was statistically significant improvement found after the whole body vibration exercise intervention. The results of this study are meaningful because they present the possibility of whole body vibration exercise intervention to be integrated into the plan to improve life quality in patients with senile dementia by stimulating their muscle spindles and sensory organs only with the amplitude and the number of vibrations with no burden of physical activity and enhancing their EEG activation and cognitive function through the responses of the neuromuscular system.

Hyperventilation in Patients With Focal Epilepsy: Electromagnetic Tomography, Functional Connectivity and Graph Theory - A Possible Tool in Epilepsy Diagnosis?

Hyperventilation (HV) is a commonly used electroencephalogram activation method. We analyzed EEG recordings in 22 normal subjects and 22 patients with focal epilepsy of unknown cause. We selected segments before (PRE), during (HYPER), and 5 minutes after (POST) HV. To analyze the neural generators of EEG signal, we used standard low-resolution electromagnetic tomography (sLORETA software). We then computed EEG lagged coherence, an index of functional connectivity, between 19 regions of interest. A weighted graph was built for each band in every subject, and characteristic path length (L) and clustering coefficient (C) have been computed. Statistical comparisons were performed by means of analysis of variance (Group X Condition X Band) for mean lagged coherence, L and C. Hyperventilation significantly increases EEG neural generators (P < 0.001); the effect is particularly evident in cingulate cortex. Functional connectivity was increased by HV in delta, theta, alpha, and beta bands in the Epileptic group (P < 0.01) and only in theta band in Control group. Intergroup analysis of mean lagged coherence, C and L, showed significant differences for Group (P < 0.001), Condition (P < 0.001), and Band (P < 0.001). Analysis of variance for L also showed significant interactions: Group X Condition (P = 0.003) and Group X Band (P < 0.001). In our relatively small group of epileptic patients, HV is associated with activation of cingulate cortex; moreover, it modifies brain connectivity. The significant differences in mean lagged coherence, path length, and clustering coefficient permit to hypothesize that this activation method leads to different brain connectivity patterns in patients with epilepsy when compared with normal subjects. If confirmed by other studies involving larger populations, this analysis could become a diagnostic tool in epilepsy.

Electroencephalogram Activation of Meditators During Attention Training Techniques

Electroencephalogram Activation of Meditators During Attention Training Techniques

Comparison of electroencephalogram activation during attention training and meditation

Comparison of electroencephalogram activation during attention training and meditation

Comparison of Relative α-Power Spectral Electroencephalogram Activity Analysis According to Electrical Stimulation Levels in Normal Adults

Objective: To investigate the effect of interferential current (IFC) stimulation level on electroencephalogram (EEG) activation. Method: An adhesive 2-pole electrode pad was placed at the T1~T4 spinal cord segment level and electrical stimulation was applied for 20 minutes to 45 healthy male and female adults recruited from N University located in Gwangju Metropolitan City. Changes in EEG activation were analyzed before stimulation, immediately after stimulation and at 30 minutes after stimulation. This study was performed in three groups: sensory level stimulus group (100 bps, 10~12 mA), exercise level stimulus group (5 bps, 45~50 mA), and noxious level stimulus group (100 bps, 80~90 mA). Results: After IFC stimulation, subjects in each group showed significant differences in terms of the retention time of relative alpha power from each brain region and between-group interaction effects. Changes in EEG activation were different depending on the type of IFC stimulation (p<0.05). Conclusion: Electrical stimulation parameters in clinical practice should be selectively applied based on diverse changes and conditions.

Should We Use Psychostimulant Drugs to Boost the Emergence from General Anesthesia?

Recently, Chemali et al. 1showed that psychostimulants can accelerate the emergence from propofol anesthesia as evidenced by a faster recovery of the righting reflex and by signs of electroencephalogram activation after the injection of methylphenidate during propofol infusion. The authors believe that methylphenidate can be safely used in a clinical setting to facilitate the awakening from prolonged propofol anesthesia or in patients overly sedated by propofol. In our view, the use of psychostimulants such as methylphenidate as emergence drugs may lead to undesirable consequences, especially in the abovementioned subsets of patients.It has been recently suggested that sequential activation of consciousness, connectedness to the environment, and responsiveness may be prerequisites for the smooth and uneventful emergence from anesthesia.2Switching on the connectedness or responsiveness before the consciousness is fully recovered from the effect of GABAergic drugs may be a cause of cognitive dysfunction or even delirium on emergence.2,3Although connectedness to external stimuli is likely to rely on norepinephrinergic signaling,4responsiveness probably requires the engagement of the basal ganglia and is subject to dopaminergic modulation in the striatum.5Methylphenidate can increase extracellular levels of both norepinephrine and dopamine in cortical and subcortical areas.6–9We believe that administering methylphenidate during propofol infusion or immediately after its termination and before the anesthetic is eliminated and consciousness sufficiently restored would interrupt the natural sequential switching-on of consciousness–connectedness–responsiveness and may result in postoperative cognitive dysfunction.We also suspect that accelerated emergence in otherwise uncomplicated anesthesia cases may be unpleasant, similar to sudden and forced awakening from sleep.10The authors themselves noticed that the electroencephalogram pattern after methylphenidate injection during propofol infusion was not exactly a return to a normal awake state: rather, the electroencephalogram showed signs of overactivation.1Administration of methylphenidate at doses comparable to those used in this study causes an increase in locomotion in rats.11,12If the authors had examined the behavior of rats awakened from anesthesia by methylphenidate and compared it with that of animals allowed to naturally awaken from propofol, they would probably have found increased locomotor activity in the former group. The human equivalent of rat hyperlocomotion may be restlessness and agitation, both of which are undesirable and can complicate the postoperative period.Finally, many stimulant drugs with a dopaminergic mechanism of action, including methylphenidate, lead to the so-called rebound hypersomnolence, evidenced by a period of enhanced compensatory sleep after drug-induced waking.13,14For methylphenidate, rebound hypersomnolence occurs at about 3 h after its intraperitoneal administration in rats.14It is unclear whether this phenomenon could be potentiated by residual sedation after propofol anesthesia. However, such potentiation is likely to occur and may have detrimental effects in overly sedated patients and, therefore, should be examined before the drug is used in humans.In conclusion, the results of the study by Chemali et al . certainly enrich our knowledge about the mechanisms of anesthesia and prepare us for possible drug interactions in patients on methylphenidate scheduled for surgery. However, before proceeding to examine the ability of methylphenidate to accelerate the emergence from propofol anesthesia in patients, especially in those with increased drug-induced GABAergic tone, it seems prudent to investigate the effects of methylphenidate on postanesthetic cognitive function in animals. Meanwhile, we can still rely on the natural emergence from anesthesia caused by physiologic elimination of the anesthetic drug. Fortunately, with the ever-improving pharmacokinetic profiles of modern anesthetic drugs, we do not have to wait too long.*Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. abpetr@med.niigata-u.ac.jp

The prevalence and significance of periodic leg movements during sleep in patients with congestive heart failure

The aim of this study was to evaluate (1) the prevalence of periodic leg movements during sleep (PLMs) in a consecutive sample of congestive heart failure (CHF) outpatients; (2) the presence of correlation between PLMs, subjective daytime sleepiness, and sleep architecture; and (3) the heart rate response to PLMs in CHF. Seventy-nine [50 men, age 59 +/- 11 years, body mass index (BMI) 26 +/- 5 kg/m(2)] consecutive adult stable outpatients with CHF [left ventricular ejection fraction (LVEF) 36 +/- 6%] were prospectively evaluated. The patients underwent assessment of echocardiography, sleepiness (Epworth Scale), and overnight in-lab polysomnography. Fifteen patients (19%) had PLM index >5. These subjects were similar in sex distribution, BMI, subjective somnolence, LVEF, and apnea-hypopnea index (AHI), but were significantly older than subjects without PLMs. Sleep architecture was similar in subjects with and without PLMs. There was a small but significant elevation of heart rate after PLMs (80.1 +/- 9.4 vs. 81.5 +/- 9.2; p < 0.001). The cardiac acceleration was also present in absence of electroencephalogram activation. The prevalence of PLMs in consecutive sample of adult CHF outpatients was 19%. There were no differences in subjective daytime sleepiness, sleep architecture, AHI, and severity of CHF in subjects with and without PLMs. PLMs caused a small but statistically significant cardiac acceleration.

Frontal Electroencephalogram Activation Asymmetry, Emotional Intelligence, and Externalizing Behaviors in 10-Year-Old Children

The purpose of the present study was to examine the relations among resting frontal brain electrical activity (EEG) (hypothesized to reflect a predisposition to positive versusnegative affect and ability to regulate emotions), emotional intelligence, and externalizing behaviors in a sample of non-clinical 10-year-old children. We found that boys had significantly lower emotional intelligence than girls, and low emotional intelligence was associated with significantly more externalizing behaviors (i.e., aggression and delinquency), replicating previous work. We also found that children with higher reported externalizing behaviors exhibited significantly greater relative right frontal EEG activity at rest compared with children with little to no externalizing behavioral problems. There was, however, no relation between emotional intelligence and the pattern of resting frontal EEG activity. Thus, emotional intelligence and the pattern of frontal EEG activation at rest are independent predictors of externalizing behaviors in children. Findings also suggest that individual differences in emotional intelligence may not be based on differences in levels of emotional regulation or the generation of positive affect as reflected in frontal EEG asymmetries, but rather other social and cognitive competencies required for adaptive behavior.

Cortical acetylcholine release and electroencephalogram activation evoked by ionotropic glutamate receptor agonists in the rat basal forebrain

To determine the sensitivity of basal forebrain cholinergic neurons to ionotropic glutamate receptor activation, acetylcholine was collected from the cerebral cortex of urethane-anesthetized rats using microdialysis while monitoring cortical electroencephalographic (EEG) activity. α-Amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA; 1, 10, or 100 μM), N-methyl- d-aspartate (NMDA; 100 or 1000 μM) or a combination of AMPA (10 μM) and NMDA (100 μM) was administered to the basal forebrain using reverse microdialysis. Both glutamate receptor agonists produced concentration-dependent, several-fold increases in acetylcholine release indicating that they activated basal forebrain cholinergic neurons; AMPA was more potent, increasing acetylcholine release at a lower concentration than NMDA. The combination of AMPA and NMDA did not produce any greater release than each drug alone, indicating that the effects of these two drugs on cholinergic neurons are not additive. EEG was analyzed by fast Fourier transforms to determine the extent of physiological activation of the cortex. The highest concentrations of AMPA and NMDA tested produced small (25%) but significant increases in high frequency activity. There was a positive correlation across animals between the increases in power in the β (14–30 Hz) and γ (30–58 Hz) ranges and increases in acetylcholine release. These results indicate that glutamate can activate cholinergic basal forebrain neurons via both AMPA and NMDA ionotropic receptors but has a more modest effect on EEG activation.

Slowing of electroencephalogram in rapid eye movement sleep behavior disorder.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by a loss of atonia and an increase in phasic muscle activity during REM sleep, leading to complex nocturnal motor behaviors. Brainstem structures responsible for the pathogenesis of RBD are also implicated in cortical activation. To verify the hypothesis that electroencephalogram (EEG) activation will be impaired in RBD, we performed quantitative analyses of waking and REM sleep EEG in 15 idiopathic RBD patients and 15 age- and gender-matched healthy subjects. During wakefulness, RBD patients showed a considerably higher theta power in frontal, temporal, and occipital regions with a lower beta power in the occipital region. The dominant occipital frequency was significantly lower in RBD. During REM sleep, beta power in the occipital region was lower in RBD. This study shows for the first time an impaired cortical activation during both wakefulness and REM sleep in idiopathic RBD, despite an absence of changes on sleep architecture compared with controls. EEG slowing in these patients may represent an early sign of central nervous system dysfunction, perhaps paralleled by subclinical cognitive deficits. The topographical distribution of EEG slowing and possible pathophysiological mechanisms are discussed in light of the known association between RBD and neurodegenerative disorders.

The neuropathologic effects in rats and neurometabolic effects in humans of large-dose remifentanil.

Given in clinically relevant large doses to rats, mu-opioids produce limbic system hypermetabolism and histopathology. This investigation extends these observations, in both rats and humans, for the short-acting drug remifentanil, which allows more precise control and assessment of the effects of duration of opioid exposure. We performed two series of experiments: one in rats for neuropathologic effects and the second in humans for neurometabolic effects. Fifty mechanically ventilated rats received saline solution or remifentanil 20-160 microg x kg(-1) x min(-1) for 3 h, followed by neuropathologic evaluation 7 days later. Four volunteers underwent induction of anesthesia and endotracheal intubation with propofol and rocuronium administration followed by remifentanil infusion at 1-3 microg x kg(-1) x min(-1) with positron emission tomography evaluation of cerebral metabolic rate for glucose. In rats, dose-related electroencephalogram activation was evident and 19 of 40 remifentanil-treated rats showed brain damage, primarily in the limbic system (P < 0.01). In humans, cerebral metabolic rate for glucose in the temporal lobe increased from 6.29 +/- 0.32 to 7.68 +/- 1.05 mg x 100 g(-1) x min(-1) (P < 0.05). These data indicate that prolonged large-dose remifentanil infusion is neurotoxic in rats with congruent metabolic effects with brief infusion in humans and suggest that some adverse effects reported in rats may be clinically relevant. This study demonstrates dose-related remifentanil neurotoxicity in physiologically controlled rats with congruent brain metabolic effects in four humans undergoing positron emission tomography evaluation during brief large-dose remifentanil anesthesia. These data suggest that some adverse effects reported in rats may be clinically relevant.

Different EEG topographic effects of painful and non-painful intramuscular stimulation in man.

To clarify the specific effects of muscle pain on electroencephalogram (EEG) activation in man, painful and non-painful sensations were produced by intramuscular injections of capsaicin and vehicle solution in the left brachioradialis muscle, with identical procedures in 15 male volunteers. Thirty-one channel EEG data acquired before, during and after the two injections were analysed and compared in respect of topography and power spectrum. Although the painful and non-painful muscular stimulations evoked similar EEG topographic patterns, statistics demonstrated that distinct EEG activation over different areas of the head were induced by the painful and non-painful stimulation compared with the baselines. The decreases in theta and alpha-1 (8-10.5 Hz) activity in central and posterior parietal parts were evoked by non-painful stimulation, but the decreases in alpha-1 and alpha-2 (11-13.5 Hz) activities in the posterior part of the head were induced by painful stimulation. The alpha-2 activity augmented during the waning pain following a decrease in the overt pain. Comparing the EEG changes between baseline, non-painful and painful stimulations as well as waning pain, we found that the increase in beta-2 activity during muscle pain was significant over the extensive areas of the head, whereas a significant increase in alpha-2 activity took place at the posterior part of the head during waning pain following a marked decrease in overt pain. These results may imply that the painful and non-painful muscular stimulations evoke distinct EEG activation in different neural networks of the human brain and the intensity of nociceptive input from muscle may encode the variety of topographic EEG changes.

Stroop color—word interference and electroencephalogram activation: Evidence for age-related decline of the anterior attention system.

Stroop color—word interference and electroencephalogram activation: Evidence for age-related decline of the anterior attention system.

Life events, frontal electroencephalogram laterality, and functional immune status after acute psychological stressors in adolescents.

Past studies have found that environmental stress affects cellular immune function and that extensive variability exists in the magnitude and direction of stress-induced immune changes. Past research also suggests that individuals with greater right, relative to left, resting frontal electroencephalogram (EEG) activation perceive environmental stress as more aversive and have lower baseline cellular immune function. In this study, we examined environmental stressors, resting frontal EEG laterality, and immune responses to short-term psychological stressors in adolescent boys. A sample of twenty-four 14-16 year old right-handed boys underwent a recording of resting EEG and collections of blood taken before and after a laboratory protocol designed to induce psychological stress. Blood samples were used to measure changes in mitogen lymphoproliferative responses, natural killer (NK) cell activity, and T-cell phenotypic subsets. Life events were measured using self-report questionnaires. Life events and frontal laterality showed a first order interaction in predicting changes in lymphocyte proliferation to tetanus toxoid (R2 increment = .26, p < .01) and pokeweed mitogen (R2 increment = .25, p < .02). The interaction also predicted changes in NK activity (R2 increment = .24, p < .02). Changes in lymphocyte proliferation and NK activity were associated with negative life events only among individuals with greater left frontal cortical activation. Our results suggest that recent psychosocial stress and individual differences in resting frontal cortical activation are together linked to immunologic responses to acute psychological stressors.

Intravenous amitriptyline in pediatrics

Oral amitriptyline has been used as an analgesic in a wide range of pain settings. Despite long-term availability of a parenteral form, the few reports about this formulation have been limited to pharmacokinetic studies in normal volunteers, trials in depressed patients, and analyses of electroencephalogram (EEG) activation. We restrospectively reviewed our experience using intravenous (IV) amitriptyline at Children's Hospital, Boston and at Children's Hospital at Stanford. Eight children (aged 5–16.6 years), who were unable to tolerate medications by the oral route, received IV amitriptyline for a variety of indications, including neuropathic pain, depression, sleep disturbance, and as an adjuvant agent for opioid analgesia. One patient experienced an extrapyramidal reaction temporally related to the administration of IV amitriptyline, which was successfully managed with diphenkydramine. Further prospective, controlled studies are needed to further assess the safety, efficacy and tolerability of this novel use of amitriptyline.

The cerebral and systemic effects of movement in response to a noxious stimulus in lightly anesthetized dogs. Possible modulation of cerebral function by muscle afferents.

Afferentation theory predicts that agents or maneuvers that stimulate muscle stretch receptors (i.e., muscle afferents) will produce cerebral stimulation. From this theory it follows that, regardless of the source (e.g., drug effect, active muscle movement), increases in stretch receptor activity should result in a similar effect on the brain. The present study tested the hypothesis that active muscle movement in lightly anesthetized subjects would result in cerebral stimulation. Studies were conducted in six dogs who were lightly anesthetized with halothane (0.70% end-expired). The following physiologic variables were quantified before and for 6 min after the initiation of a standardized (1-min duration) noxious stimulus to the trachea and the skin overlying the hind limb: cerebral blood flow, cerebral metabolic rate for oxygen (CMRO2), cerebral perfusion pressure, cerebral vascular resistance, electroencephalogram activity, electromyogram activity, arterial carbon dioxide partial pressure (PaCO2), central venous pressure, and serum epinephrine and norepinephrine concentrations. Response to stimulation was evaluated initially in unparalyzed dogs and later was evaluated in the same dogs after they were paralyzed with intravenous pancuronium (0.2 mg/kg). In unparalyzed dogs, stimulation produced episodes of coughing plus head and limb movement during the 6-min study period. Accompanying the movement was activation of the electromyogram, an increase in electroencephalogram frequency, and a reduction in electroencephalogram amplitude. There also was a 35% increase in cerebral blood flow, a 25% decrease in cerebral vascular resistance, and a 7% increase in CMRO2 versus the baseline values for each variable. There were no significant increases in either cerebral perfusion pressure, central venous pressure, PaCO2, or serum norepinephrine concentration to account for the cerebral effects; however, serum epinephrine concentrations increased by 61%. In pancuronium-paralyzed dogs, noxious stimulation resulted in a 5% increase in cerebral blood flow, a 7% decrease in cerebral vascular resistance, and an 5% increase in CMRO2 versus baseline levels. Electroencephalogram frequency was increased, but amplitude was unchanged. Central venous pressure, electromyogram activity, and serum norepinephrine concentration were unaffected. The serum epinephrine response was similar to that observed when the dogs were not paralyzed. These data support the hypothesis that active muscle movement in lightly anesthetized subjects has an effect on the brain that is mediated in part by muscle afferent receptors. This cerebral response was manifested as electroencephalogram activation, cerebral vasodilation unrelated to central venous pressure changes, and an increase in cerebral blood flow greater than that required to meet metabolic demands. Paralysis with pancuronium abolished movement induced by stimulation (and, thus, the muscle afferent response) and also attenuated the cerebral blood flow, cerebral vascular resistance, and electroencephalogram responses.

Role of Cholinergic Mechanisms in States of Wakefulness and Sleep

Publisher Summary Pharmacological data on the importance of cholinergic mechanisms in electroencephalogram (EEG) activation and behavioral arousal as well as sleep are impressive. The gross behavioral consequence of the initial EEG activation is clearly a wake-up or arousal state. This chapter summarizes some research on the hypothesis that cholinergic mechanisms are involved in states of wakefulness and sleep. It has previously been reported by Wikler, Bradley and Elkes, Bradley and Nicholson, and others, that cholinergic agonists and antagonists produce EEG dissociation from gross behavior. Similar findings have been made by us using large doses of atropine and physostigmine. However, it should be pointed out that effective doses of physostigmine and other cholinergic agonists produce initial behavioral arousal that is associated with neocortical and limbic activation. The emphasis in the literature on EEG dissociation from gross behavior may have been overstated, particularly in relationship to the awake–sleep cycle of the chronic cat. The findings of Bradley and Elkes and others with cholinergic agonists were made at a time when the stage of fast wave sleep as described by Dement and Jouvet was not generally known. It would appear that in some instances investigators may have been observing fast wave sleep and did not recognize it as such.