EEG Spectra Research Articles

Universal theory of brain waves: from linear loops to nonlinear synchronized spiking and collective brain rhythms.

An inhomogeneous anisotropic physical model of the brain cortex is presented that predicts the emergence of non-evanescent (weakly damped) wave-like modes propagating in the thin cortex layers transverse to both the mean neural fiber direction and to the cortex spatial gradient. Although the amplitude of these modes stays below the typically observed axon spiking potential, the lifetime of these modes may significantly exceed the spiking potential inverse decay constant. Full brain numerical simulations based on parameters extracted from diffusion and structural MRI confirm the existence and extended duration of these wave modes. Contrary to the standard paradigm that the neural fibers determine the pathways for signal propagation in the brain, the signal propagation due to the cortex wave modes in highly folded areas will exhibit no apparent correlation with the fiber directions. The results are consistent with numerous recent experimental animal and human brain studies demonstrating the existence of electrostatic field activity in the form of traveling waves (including studies where neuronal connections were severed) and with wave loop induced peaks observed in EEG spectra. In addition, we demonstrate that the resonant and non-resonant terms of the nonlinear coupling between multiple modes produce both synchronous spiking-like high frequency wave activity as well as low frequency wave rhythms as a result of their unique dispersion properties. Numerical simulation of forced multiple mode dynamics shows that as forcing increases there is a transition from damped to oscillatory regime that subsequently decays away as over-excitation is reached. The resonant nonlinear coupling results in the emergence of low frequency rhythms with frequencies that are several orders of magnitude below the linear frequencies of modes taking part in the coupling. The localization and persistence of these cortical wave modes, and this new mechanism for understanding the nature of spiking behavior, have significant implications in particular for neuroimaging methods that detect electromagnetic physiological activity, such as EEG and MEG, and in general for the understanding of brain activity, including mechanisms of memory.

Wake-Promoting and EEG Spectral Effects of Modafinil After Acute or Chronic Administration in the R6/2 Mouse Model of Huntington\u2019s Disease

Huntington’s disease (HD) is characterised by progressive symptoms including cognitive deficits and sleep/wake disturbances reflected in an abnormal electroencephalography (EEG). Modafinil, a wake-promoting and cognitive-enhancing drug, has been considered as a treatment for HD. We used HD (R6/2) mice to investigate the potential for using modafinil to treat sleep-wake disturbance in HD. R6/2 mice show sleep-wake and EEG changes similar to those seen in HD patients, with increased rapid eye movement sleep (REMS), decreased wakefulness/increased non-REMS (NREMS), and pathological changes in EEG spectra, particularly an increase in gamma power. We recorded EEG from R6/2 and wild-type mice treated with modafinil acutely (with single doses between 25 and 100 mg/kg; at 12 and 16 weeks of age), or chronically (64 mg/kg modafinil/day from 6 to 15 weeks). Acutely, modafinil increased wakefulness in R6/2 mice and restored NREMS to wild-type levels at 12 weeks. It also suppressed the pathologically increased REMS. This was accompanied by decreased delta power, increased peak frequency of theta, and increased gamma power. At 16 weeks, acute modafinil also restored wakefulness and NREMS to wild-type levels. However, whilst REMS decreased, it did not return to normal levels. By contrast, in the chronic treatment group, modafinil-induced wakefulness was maintained at 15 weeks (after 9 weeks of treatment). Interestingly, chronic modafinil also caused widespread suppression of power across the EEG spectra, including a reduction in gamma that increases pathologically in R6/2 mice. The complex EEG effects of modafinil in R6/2 mice should provide a baseline for further studies to investigate the translatability of these result to clinical practice.

Preferred EEG brain states at stimulus onset in normal ageing: Explorations in a fixed interstimulus interval Go/NoGo task

Some 40 years ago, Erol Başar began an interesting line of brain dynamics research on the phase of oscillatory EEG activity. Stimuli presented at a fixed interstimulus interval (ISI) were reported to produce a “preferred phase angle” at stimulus onset in the ongoing EEG oscillations, so that cortical negativity occurred more often than expected. Our previous work has confirmed this phenomenon in young adults, and linked it to enhancements in stimulus-elicited ERP components and behaviour. The present study sought evidence for this phenomenon in older adults. Twenty healthy independent-living participants (5 males) aged 59.8 to 74.8 years (M = 68.2) completed a fixed ISI equiprobable auditory oddball task. EEG phases in four traditional bands were computed separately for each artefact-free Go and NoGo trial. These were used to group accepted trials according to the phase quartile at stimulus onset in each band, forming 16 mean ERPs for each participant at each phase quartile/band combination, separately for Go and NoGo. The 32 mean ERPs were decomposed by separate Principal Component Analyses, and the N1 and P3 components were examined as a function of EEG phase at stimulus onset in each band. Differential preferential occurrence of phase states was found in all bands, generally confirming prior results in young adults despite important age differences in both EEG spectra and ERP morphology. Substantial effects on N1 and P3 components, as well as prestimulus CNVs, are discussed. The stability of this phenomenon across age indicates its important role in perception and cognition.

On the Quality, Statistical Efficiency, and Safety of Simultaneously Recorded Multiband fMRI/EEG

The recent development of multiband functional magnetic resonance imaging (MB-fMRI) allows for the reduction of sampling period by simultaneously exciting multiple slices-the number of which is referred to as the multiband factor. Simultaneously recorded electroencephalography (EEG)/MB-fMRI has yet to be validated for data quality against conventional single band (SB)-fMRI. Pilot scans were conducted on phantoms twice and on a healthy volunteer to ensure no heating effects. In the main study, two thermometer probes were attached to 16 healthy individuals (ages 20-39, 9 females) whilst they completed two sets of 16-min resting-state and two sets of 9-min n-back task scans-each set consisting of one MB4 and one SB pulse sequence. No heating effects were reported and thermometer data showed mean increases of < 1.0°C. Minimal differences between the two scan types were found in EEG channel variance and spectra. Expected decreases in MB4-fMRI tSNR were observed. In n-back task scans, little to no differences were detected in both EEG source analyses and fMRI local analyses for mixed effects. Resting-state posterior cingulate cortex seed-based analyses of the default mode network along with EEG-informed fMRI analysis of the occipital alpha anticorrelation effect showed improved statistical and spatial sensitivity at lower scan durations. Using EEG/MB4-fMRI for n-back tasks provided no statistical advantages nor disadvantages. However, for studying the resting-state, MB4-fMRI potentially allows for reduced scanning durations for equivalent statistical significance to be obtained or alternatively, larger effect sizes for the same scanning duration. As such, simultaneous EEG/MB4-fMRI is a viable alternative to EEG/SB-fMRI.

Expanding the clinical and EEG spectrum of CNKSR2-related encephalopathy with status epilepticus during slow sleep (ESES)

ObjectiveTo investigate the clinical and EEG features of Encephalopathy with Status Epilepticus during slow Sleep (ESES) related to CNKSR2 pathogenic variants. MethodsDetailed clinical history, repeated wakefulness/overnight sleep EEGs, brain MRI were collected in five patients, including one female, with CNKSR2-related ESES. ResultsNeurodevelopment in infancy was normal in two patients, delayed in three. Epilepsy onset (age range: 2–6 years) was associated with appearance or aggravation of cognitive impairment, language regression and/or behavioral disorders. Worsening of epilepsy and of cognitive/behavioral disturbances paralleled by enhancement of non-rapid eye movement (NREM) sleep-related, frontally predominant, EEG epileptic discharges [spike-wave-index (SWI): range 60–96%] was consistent with ESES. In three patients, episodes of absence status epilepticus or aggravation of atypical absences occurred, in this latter case associated with striking increment of awake SWI. Speech/oro-motor dyspraxia was diagnosed in four patients. In two patients, long-term follow-up showed epilepsy remission and persistence of mild/moderate cognitive disorders and behavioral disturbances into adulthood. ConclusionsNovel findings of our study are occurrence also in females, normal neurodevelopment before epilepsy onset, epilepsy aggravation associated with enhanced awake SWI, mild/moderate evolution in adulthood and language disorder due to speech/oro-motor dyspraxia. SignificanceOur findings expand the phenotypic spectrum of CNKSR2-related ESES.

Arousal State-Dependent Alterations in VTA-GABAergic Neuronal Activity.

Decades of research have implicated the ventral tegmental area (VTA) in motivation, learning and reward processing. We and others recently demonstrated that it also serves as an important node in sleep/wake regulation. Specifically, VTA-dopaminergic neuron activation is sufficient to drive wakefulness and necessary for the maintenance of wakefulness. However, the role of VTA-GABAergic neurons in arousal regulation is not fully understood. It is still unclear whether VTA-GABAergic neurons predictably alter their activity across arousal states, what is the nature of interactions between VTA-GABAergic activity and cortical oscillations, and how activity in VTA-GABAergic neurons relates to VTA-dopaminergic neurons in the context of sleep/wake regulation. To address these, we simultaneously recorded population activity from VTA subpopulations and electroencephalography/electromyography (EEG/EMG) signals during spontaneous sleep/wake states and in the presence of salient stimuli in freely-behaving mice. We found that VTA-GABAergic neurons exhibit robust arousal-state-dependent alterations in population activity, with high activity and transients during wakefulness and REM sleep. During wakefulness, population activity of VTA-GABAergic neurons, but not VTA-dopaminergic neurons, was positively correlated with EEG γ power and negatively correlated with θ power. During NREM sleep, population activity in both VTA-GABAergic and VTA-dopaminergic neurons negatively correlated with δ, θ, and σ power bands. Salient stimuli, with both positive and negative valence, activated VTA-GABAergic neurons. Together, our data indicate that VTA-GABAergic neurons, like their dopaminergic counterparts, drastically alter their activity across sleep-wake states. Changes in their activity predicts cortical oscillatory patterns reflected in the EEG, which are distinct from EEG spectra associated with dopaminergic neural activity.

Features of the Dynamics of the Human EEG Spectrum at a Constant Level of Acute Hypoxia

Studies of 12 subjects using Fourier analysis addressed the EEG amplitude-frequency spectrum at a constant level of normobaric hypoxia (breathing an oxygen-nitrogen mix containing 8% oxygen for 25 min). Cluster analysis of the 16-channel EEG identified two groups of subjects differing in terms of relative spectral power (SP) in the EEG δ range averaged over the period of hypoxia. Six of the subjects of the group 1 (n = 7), with greater relative SP in the δ range during hypoxia showed dominance o δ activity in all subsequent 1-min segments and all leads starting after 6 min of hypoxia. Subjects of group 2 (n = 5) showed dominant α activity in the occipital leads overall for the 25 min of hypoxia. In sequential 1-min segments, the dominance of α activity in some subjects of this group changed to a dominance of δ and θ activity. These studies showed that the dynamics of the EEG amplitude-frequency spectrum at a constant level of hypoxia do not always correspond to sequential “slowing” of the EEG described in increasing hypoxia.

Altered SWD stopping mechanism in WAG/Rij rats subchronically treated with the cannabinoid agonist R(+)WIN55,212-2

A single injection of the cannabinoid agonist R(+)WIN55,212-2 (WIN) is known to cause an increase of the mean duration of spontaneously occurring spike-and-wave discharges (SWDs) in rats of the WAG/Rij strain, a genetic model for absence epilepsy. The aim of the present study was to establish whether repeated activation of CB1 receptors with WIN leads to tolerance in its effect on SWD parameters, spectral density, and behavior over time.Adult male WAG/Rij rats (n = 16) were treated with WIN (6 mg/kg) or vehicle (olive oil). Injections (s.c.) took place 3 times per week during 2 weeks. Electroencephalogram (EEG) recordings, each lasting 24 h, were made 3 times: immediately before the first injection (baseline), immediately after the first injection (acute treatment), and after 2 weeks of treatment (subchronic treatment). The recordings were analyzed regarding incidence, durations of SWDs, and hazard rates of the durations of SWDs, the latter to describe SWD stopping probabilities. Putative changes in the spectral content of the EEG before and after WIN during active and passive behaviors were additionally investigated.Spike-and-wave discharge incidence was not affected by the acute and subchronic treatments. The mean duration of the SWDs was significantly longer than controls in the acute WIN-treated animals [11.9-s standard error of the mean (SEM): 0.64 compared with 8.4-s SEM: 0.25] as well as in subchronically treated animals (11.5-s SEM: 1.00 compared with 8.4-s SEM: 0.25). Hazard rates were significantly lower for WIN-treated animals at SWD durations in the 5.04–20.16-s range on both occasions. No effects of WIN on the frequency spectrum of the ongoing EEG were found, neither acutely nor after repeated administration.Evidence for tolerance was not found. The results on the mean duration and hazard rates suggest that stimulating the endocannabinoid system affects the SWD stopping mechanism, resulting in more long SWDs. We speculate that this effect is likely to be a direct result of CB1 receptor agonism and a subsequent decrease in the availability of gamma-aminobutyric acid (GABA) in the reticular thalamic nucleus, which further weakens, in WAG/Rij rats already disturbed, the stopping mechanism of the SWDs.

Simultaneous EEG/fMRI recorded during ketamine infusion in patients with major depressive disorder

A single subanaesthetic dose of ketamine rapidly alleviates the symptoms of major depressive disorder (MDD). However, few studies have investigated the acute effects of ketamine on the BOLD pharmacological magnetic resonance imaging (phMRI) response and EEG spectra. In a randomised, double-blind, active placebo-controlled crossover trial, resting-state simultaneous EEG/fMRI was collected during infusion of ketamine or active placebo (remifentanil) in 30 participants with MDD. Montgomery-Asberg depression rating scale scores showed a significant antidepressant effect of ketamine compared to placebo (69% response rate). phMRI analyses showed BOLD signal increases in the anterior cingulate and medial prefrontal cortices and sensitivity of the decrease in subgenual anterior cingulate cortex (sgACC) BOLD signal to noise correction. EEG spectral analysis showed increased theta, high beta, low and high gamma power, and decreased delta, alpha, and low beta power with differing time-courses. Low beta and high gamma power time courses explained significant variance in the BOLD signal. Interestingly, the variance explained by high gamma power was significantly associated with non-response to ketamine, but significant associations were not found for other neurophysiological markers when noise correction was implemented. The results suggest that the decrease in sgACC BOLD signal is potentially noise and unrelated to ketamine's antidepressant effect, highlighting the importance of noise correction and multiple temporal regressors for phMRI analyses. The lack of effects significantly associated with antidepressant response suggests the phMRI methodology employed was unable to detect such effects, the effect sizes are relatively small, or that other processes, e.g. neural plasticity, underlie ketamine's antidepressant effect.

Automated EEG mega-analysis I: Spectral and amplitude characteristics across studies

Significant achievements have been made in the fMRI field by pooling statistical results from multiple studies (meta-analysis). More recently, fMRI standardization efforts have focused on enabling the joint analysis of raw fMRI data across studies (mega-analysis), with the hope of achieving more detailed insights. However, it has not been clear if such analyses in the EEG field are possible or equally fruitful. Here we present the results of a large-scale EEG mega-analysis using 18 studies from six sites representing several different experimental paradigms. We demonstrate that when meta-data are consistent across studies, both channel-level and source-level EEG mega-analysis are possible and can provide insights unavailable in single studies. The analysis uses a fully-automated processing pipeline to reduce line noise, interpolate noisy channels, perform robust referencing, remove eye-activity, and further identify outlier signals. We define several robust measures based on channel amplitude and dispersion to assess the comparability of data across studies and observe the effect of various processing steps on these measures. Using ICA-based dipolar sources, we also observe consistent differences in overall frequency baseline amplitudes across brain areas. For example, we observe higher alpha in posterior vs anterior regions and higher beta in temporal regions. We also detect consistent differences in the slope of the aperiodic portion of the EEG spectrum across brain areas. In a companion paper, we apply mega-analysis to assess commonalities in event-related EEG features across studies. The continuous raw and preprocessed data used in this analysis are available through the DataCatalog at https://cancta.net.

Natural alpha frequency components in resting EEG and their relation to arousal

ObjectiveGlobal EEG alpha activity is negatively correlated with skin conductance level (SCL), supporting alpha as an inverse marker of arousal. Frequency Principal Components Analysis (f-PCA) of resting EEG amplitude spectra has demonstrated natural components in the alpha band of healthy persons. This is a preliminary exploration of whether such components differ with arousal, possibly underpinning the anomalous ADHD hypoarousal link to reduced alpha. MethodTwenty-seven right-handed undergraduate students participated in three 2 minute blocks of resting eyes-open/closed EEG and SCL: EO1, EC, EO2. For each condition, mean EEG spectra were submitted to separate f-PCAs. ResultsThe inverse alpha/SCL relationship was confirmed for band amplitudes. EO had two alpha components; both correlated negatively with SCL. EC alpha contained four components, but only one had a substantial negative correlation with SCL; two had no relationship, suggesting natural alpha components with different non-arousal functionality in EC. ConclusionSome alpha components in both EC and EO reflect arousal, with other non-arousal components in EC. Our f-PCA approach offers insight into previously-noted alpha anomalies in disorders such as ADHD. SignificanceThis proof of concept demonstration in typical participants may provide the basis for a new research effort in clinical disorders involving atypical arousal patterns.

Optogenetic/Chemogenetic Activation of GABAergic Neurons in the Ventral Tegmental Area Facilitates General Anesthesia via Projections to the Lateral Hypothalamus in Mice.

The ventral tegmental area (VTA) reportedly regulates sleep and wakefulness through communication with the lateral hypothalamus (LH). It has also been suggested that adequate anesthesia produced by administration of chloral hydrate, ketamine, or halothane significantly reduces the GABAergic neuronal firing rate within the VTA. However, the exact effects on GABAergic neurons in the VTA and the mechanisms through which these neurons modulate anesthesia through associated neural circuits is still unclear. Here, we used optogenetic and chemogenetic methods to specifically activate or inhibit GABAergic neuronal perikarya in the VTA or their projections to the LH in Vgat-Cre mice. Electroencephalogram (EEG) spectral analyses and burst suppression ratio (BSR) calculations were conducted following administration of 0.8 or 1.0% isoflurane, respectively; and loss of righting reflex (LORR), recovery of righting reflex (RORR), and anesthesia sensitivity were assessed under 1.4% isoflurane anesthesia. The results showed that activation of GABAergic neurons in the VTA increased delta wave power from 40.0 to 46.4% (P = 0.006) and decreased gamma wave power from 15.2 to 11.5% (P = 0.017) during anesthesia maintenance. BSR was increased from 51.8 to 68.3% (P = 0.017). Induction time (LORR) was reduced from 333 to 290 s (P = 0.019), whereas arousal time (RORR) was prolonged from 498 to 661 s (P = 0.007). Conversely, inhibition of VTA GABAergic neurons led to opposite effects. In contrast, optical activation of VTA–LH GABAergic projection neurons increased power of slow delta waves from 44.2 to 48.8% (P = 0.014) and decreased that of gamma oscillations from 10.2 to 8.0%. BSR was increased from 39.9 to 60.2% (P = 0.0002). LORR was reduced from 330 to 232 s (P = 0.002), and RORR increased from 396 to 565 s (P = 0.007). Optical inhibition of the projection neurons caused opposite effects in terms of both the EEG spectrum and the BSR, except that inhibition of this projection did not accelerate arousal time. These results indicate that VTA GABAergic neurons could facilitate the anesthetic effects of isoflurane during induction and maintenance while postponing anesthetic recovery, at least partially, through modulation of their projections to the LH.

Diffuse to fuse EEG spectra – Intrinsic geometry of sleep dynamics for classification

We propose a novel algorithm for sleep dynamics visualization and automatic annotation by applying diffusion geometry based sensor fusion algorithm to fuse spectral information from two electroencephalograms (EEG). The diffusion geometry approach helps organize the nonlinear dynamical structure hidden in the EEG signal. The visualization is achieved by the nonlinear dimension reduction capability of the chosen diffusion geometry algorithms. For the automatic annotation purpose, the support vector machine is trained to predict the sleep stage. The prediction performance is validated on a publicly available benchmark database, Physionet Sleep-EDF [extended] SC* (SC = Sleep Cassette) and ST* (ST = Sleep Telemetry), with the leave-one-subject-out cross validation. When we have a single EEG channel (Fpz-Cz), the overall accuracy, macro F1 and Cohen's kappa achieve 82.72%, 75.91% and 76.1% respectively in Sleep-EDF SC* and 78.63%, 73.58% and 69.48% in Sleep-EDF ST*. This performance is compatible with the state-of-the-art results. When we have two EEG channels (Fpz-Cz and Pz-Oz), the overall accuracy, macro F1 and Cohen's kappa achieve 84.44%, 78.25% and 78.36% respectively in Sleep-EDF SC* and 79.05%, 74.73% and 70.31% in Sleep-EDF ST*. The results suggest the potential of the proposed algorithm in practical applications.

Cognitive Impairment Is Associated with Absolute Intraoperative Frontal α-Band Power but Not with Baseline α-Band Power: A Pilot Study

Background: Cognitive abilities decline with aging, leading to a higher risk for the development of postoperative delirium or postoperative neurocognitive disorders after general anesthesia. Since frontal α-band power is known to be highly correlated with cognitive function in general, we hypothesized that preoperative cognitive impairment is associated with lower baseline and intraoperative frontal α-band power in older adults. Methods: Patients aged ≥65 years undergoing elective surgery were included in this prospective observational study. Cognitive function was assessed on the day before surgery using six age-sensitive cognitive tests. Scores on those tests were entered into a principal component analysis to calculate a composite “g score” of global cognitive ability. Patient groups were dichotomized into a lower cognitive group (LC) reaching the lower 1/3 of “g scores” and a normal cognitive group (NC) consisting of the upper 2/3 of “g scores.” Continuous pre- and intraoperative frontal electroencephalograms (EEGs) were recorded. EEG spectra were analyzed at baseline, before start of anesthesia medication, and during a stable intraoperative period. Significant differences in band power between the NC and LC groups were computed by using a frequency domain (δ 0.5–3 Hz, θ 4–7 Hz, α 8–12 Hz, β 13–30 Hz)-based bootstrapping algorithm. Results: Of 38 included patients (mean age 72 years), 24 patients were in the NC group, and 14 patients had lower cognitive abilities (LC). Intraoperative α-band power was significantly reduced in the LC group compared to the NC group (NC –1.6 [–4.48/1.17] dB vs. LC –6.0 [–9.02/–2.64] dB), and intraoperative α-band power was positively correlated with “g score” (Spearman correlation: r = 0.381; p = 0.018). Baseline EEG power did not show any associations with “g.” Conclusions: Preoperative cognitive impairment in older adults is associated with intraoperative absolute frontal α-band power, but not baseline α-band power.

Theta dominance in the power spectra of eeg in chronic neurogenic pain

To identify the theta over activity in power spectra of EEG in chronic neurogenic pain patients, spectral analysis of resting EEG of the patients (n=15, 41-64 years, median 48 years, 6 men) in the eye closed state was compared with that of healthy controls (n=15, 39-62 years, median 48 years, 6 men). The study was done with the approval of Institute Ethics Committee and after obtaining written informed consent from the study participants. The average power spectral density of all channels revealed higher spectral power (expressed as μV2/Hz) in the theta band (5-7 Hz frequency range) for the patient group (1.901 ± 1.687) when compared with that of the control group (1.559 ± 0.812). Lower spectral power in the alpha band (8-12 Hz frequency range) was also noted in the patient group (3.401±3.624) when compared to the control group (4.864±4.173). The limitation in sample size may have been the reason for not obtaining statistical significance (p value = 0.485 for theta power comparison and p value = 0.314 for alpha power comparison) for the differences noted between the two groups. Although the data obtained from power spectra of EEG is not confirmatory, increased theta activity and decreased alpha activity may underlie the pathophysiological mechanisms involved in chronic neurogenic pain.

Features of postconcussion symptoms recovery after traumatic brain injury among military personnel

Traumatic brain injuries due to hostilities inEastern Ukrainein 2017 accounted for 30.8% of all mechanical combat damage and injuries and are an important problem because of postconcussion syndrome manifestation in the long-term period. Purpose – to study the features of postconcussion symptoms recovery among combatants during their rehabilitation in hospital conditions based on electroencephalography and the dynamics of psychophysiological characteristics assessment. Materials and methods. 42 combatants aged 35–45 years who suffered a closed craniocerebral injury during 2017–2018 (more than 3 months after head injury) and 76 healthy men the same age, constituted group II (control), were involved in the study. The study evaluated and analyzed the results of electroencephalography (EEG), manifestations of postconcussion symptoms using К. Cicerone modified special questionnaire as well as the characteristics of attentiveness and short-term memory using a special computer program. Results. Among individuals with postconcussion syndrome, the functioning of non-specific brain systems was found to be impaired making dysregulation changes in the electrical activity of the brain stable and long-lasting. It was shown that the applied rehabilitation programs had a positive effect on the balance and improvement of the brain bioelectrical activity rhythms and, accordingly, the functional activity of these structures (θ and δ characteristics of EEG spectrum improved after rehabilitation (P < 0.05), which may indicate the inclusion of neuro-emotional stress coping mechanisms during rehabilitation in inpatient conditions). Somatic manifestations which very often occur and impair performance, as well as definite complaints from the cognitive sphere, reliably decreased (P < 0.05), but complaints due to sensory functions impairment remained almost unchanged in 17 % of people after the rehabilitation course. The characteristics of attentiveness and short-term memory had a positive (P < 0.001) dynamics after the rehabilitation course and did not exceed the calculated standard indicators. Conclusions. The features of postconcussion symptoms recovery among combatants during their rehabilitation in hospital conditions in terms of θ and δ characteristics of the EEG spectrum have been revealed. The presence of significant (P < 0.001) differences in objective characteristics of cognitive functions in patients before rehabilitation compared with the control group (below standard values), as well as significant (P < 0.001) positive dynamics of attentiveness and short-term memory after rehabilitation of military personnel with postconcussion symptomatology and approximation of these characteristics to standard values have been found. It has been noted that the diagnosis of cognitive disorders associated with traumatic brain injury should be essentially based on the results of neuropsychological objective testing of attentiveness and short-term memory, since they are more dynamic (P < 0.001) indicators compared with complaints relating to cognitive function changes.

Transcranial focused ultrasound pulsation suppresses pentylenetetrazol induced epilepsy in vivo

BackgroundEpilepsy is a neurological disorder characterized by abnormal neuron discharge, and one-third of epilepsy patients suffer from drug-resistant epilepsy (DRE). The current management for DRE includes epileptogenic lesion resection, disconnection, and neuromodulation. Neuromodulation is achieved through invasive electrical stimulus including deep brain stimulation, vagus nerve stimulation, or responsive neurostimulation (RNS). As an alternative therapy, transcranial focused ultrasound (FUS) can transcranially and non-invasively modulate neuron activity. ObjectiveThis study seeks to verify the use of FUS pulsations to suppress spikes in an acute epileptic small-animal model, and to investigate possible biological mechanisms by which FUS pulsations interfere with epileptic neuronal activity. MethodsThe study used a total of 76 Sprague-Dawley rats. For the epilepsy model, rats were administered pentylenetetrazol (PTZ) to induce acute epileptic-like abnormal neuron discharges, followed by FUS exposure. Various ultrasound parameters were set to test the epilepsy-suppressing effect, while concurrently monitoring and analyzing electroencephalogram (EEG) signals. Animal behavior was monitored and histological examinations were conducted to evaluate the hazard posed by ultrasound exposure and the expression of neuronal activity markers. Western blotting was used to evaluate the correlation between FUS-induced epileptic suppression and the PI3K-mTOR signaling pathway. ResultsWe observed that FUS pulsations effectively suppressed epileptic activity and observed EEG spectrum oscillations; the spike-suppressing effect depended on the selection of ultrasound parameters and highly correlated with FUS exposure level. Expression level changes of c-Fos and GAD65 were confirmed in the cortex and hippocampus, indicating that FUS pulsations deactivated excitatory cells and activated GABAergic terminals. No tissue damage, inflammatory response, or behavioral abnormalities were observed in rats treated with FUS under these exposure parameters. We also found that the FUS pulsations down-regulated the S6 phosphorylation and decreased pAKT expression. ConclusionOur results suggest that pulsed FUS exposure effectively suppresses epileptic spikes in an acute epilepsy animal model, and finds that ultrasound pulsation interferes with neuronal activity and affects the PTZ-induced PI3K-Akt-mTOR pathway, which might help explain the mechanism underlying ultrasound-related epileptic spike control.

Correlation of EEG spectra, connectivity, and information theoretical biomarkers with psychological states in the epilepsy monitoring unit — A pilot study

At the level of individual experience, the relation between electroencephalographic (EEG) phenomena and subjective ratings of psychological states is poorly examined. This study investigated the correlation of quantitative EEG markers with systematic high-frequency monitoring of psychological states in patients admitted to the epilepsy monitoring unit (EMU).We used a digital questionnaire, including eight standardized items about stress, energy level, mood, ward atmosphere, seizure likelihood, hopefulness/frustration, boredom, and self-efficacy. Self-assessments were collected four times per day, in total 15 times during the stay in the EMU. We extracted brainrate, Hjorth parameters, Hurst exponent, Wackermann parameters, and power spectral density from the EEG. We performed correlation between these quantitative EEG measures and responses to the 8 items and evaluated their significance on single subject and on group level.Twenty-one consecutive patients (12 women/9 men, median age: 29 years, range: 18–74 years) were recruited. On group level, no significant correlations were found whereas on single-subject level, we found significant correlations for 6 out of 21 patients. Most significant correlations were found between Hjorth parameters and items that reflect changes in mood or stress.This study supports the feasibility of correlating quantitative EEG measures with psychological states in routine EMU settings and emphasizes the need for single-subject statistics when assessing aspects with high interindividual variance. Future studies should select samples with high within-subject variability of psychological states and examine a subsample with patients encountering a critical number of seizures needed in order to relate the psychological states to the ultimate question: Are psychological states potential indicators for seizure likelihood?

DIAGNOSTICS OF PERIODONTITIS ON THE BASIS OF SPECTRAL ANALYSIS OF THE RHYTHMIC ACTIVITY OF BRAIN

Used a standard electroencephalograph of the brand «Neuron-spectrum-1» and a specialized program of narrow-band spectral analysis in the frequency range 0,1-27 Hz and integration time 160 seconds. A number of characteristic features of EEG spectrum envelope function were revealed in the studied patients, and four decisive Signs were identified. For the present study included was identified diagnostic features 1,2 characterized by the synchronization of the hemispheres and reliable a pronounced decrease in the amplitude spectral estimate in the frequency range 0,91-0,95 Hz, 7,26-8,0 Hz. Sign 3 - was associated with increased synchronization of hemispheres and increased amplitude of spectral estimation in the frequency range 3,72-4,033 Hz. Desynchronization of brain hemispheres is a diagnostic symptom 4 was identified in the frequency range of 0,96 to 1,01 Hz. The amplitude of the asymmetry of the spectrum of sign 4 was specific for the separation of 1,2,3 groups of the present study included in severity. The revealed changes of spectrograms are proposed to be used for refinement of pathogenesis and early diagnosis of periodontitis.

Quantitative EEG reactivity and machine learning for prognostication in hypoxic-ischemic brain injury

ObjectiveElectroencephalogram (EEG) reactivity is a robust predictor of neurological recovery after cardiac arrest, however interrater-agreement among electroencephalographers is limited. We sought to evaluate the performance of machine learning methods using EEG reactivity data to predict good long-term outcomes in hypoxic-ischemic brain injury. MethodsWe retrospectively reviewed clinical and EEG data of comatose cardiac arrest subjects. Electroencephalogram reactivity was tested within 72 h from cardiac arrest using sound and pain stimuli. A Quantitative EEG (QEEG) reactivity method evaluated changes in QEEG features (EEG spectra, entropy, and frequency features) during the 10 s before and after each stimulation. Good outcome was defined as Cerebral Performance Category of 1–2 at six months. Performance of a random forest classifier was compared against a penalized general linear model (GLM) and expert electroencephalographer review. ResultsFifty subjects were included and sixteen (32%) had good outcome. Both QEEG reactivity methods had comparable performance to expert EEG reactivity assessment for good outcome prediction (mean AUC 0.8 for random forest vs. 0.69 for GLM vs. 0.69 for expert review, respectively; p non-significant). ConclusionsMachine-learning models utilizing quantitative EEG reactivity data can predict long-term outcome after cardiac arrest. SignificanceA quantitative approach to EEG reactivity assessment may support prognostication in cardiac arrest.