Abnormalities in Electroencephalographic Microstates Among Adolescents With First Episode Major Depressive Disorder

Background: Recent studies have reported changes in the electroencephalograms (EEG) of patients with major depressive disorder (MDD). However, little research has explored EEG differences between adolescents with MDD and healthy controls, particularly EEG microstates differences. The aim of the current study was to characterize EEG microstate activity in adolescents with MDD and healthy controls (HCs).Methods: A total of 35 adolescents with MDD and 35 HCs were recruited in this study. The depressive symptoms were assessed by Hamilton Depression Scale (HAMD) and Children's Depression Inventory (CDI), and the anxiety symptoms were assessed by Chinese version of DSM-5 Level 2-Anxiety-Child scale. A 64-channel EEG was recorded for 5 min (eye closed, resting-state) and analyzed using microstate analysis. Microstate properties were compared between groups and correlated with patients' depression scores.Results: We found increased occurrence and contribution of microstate B in MDD patients compared to HCs, and decreased occurrence and contribution of microstate D in MDD patients compared to HCs. While no significant correlation between depression severity (HAMD score) and the microstate metrics (occurrence and contribution of microstate B and D) differing between MDD adolescents and HCs was found.Conclusions: Adolescents with MDD showed microstate B and microstate D changes. The obtained results may deepen our understanding of dynamic EEG changes among adolescents with MDD and provide some evidence of changes in brain development in adolescents with MDD.

EEG Changes Related to Gut Dysbiosis in Diabetes—Review

Humans are facing a devastating epidemic of metabolic syndrome that is linked to the worldwide dramatic increase in obesity and diabetes. Significant evidence suggests that the intestinal microbiota plays a major role in the pathogenesis of metabolic diseases. Due to the gut–brain axis link, dysbiosis in the gut microbiota have been demonstrated in both metabolic and neurological disease. Increasing evidence suggests that the gut microbiota is very important in maintaining health and changes in its composition may contribute to psychiatric and neurodegenerative disorders. It is also in research that changes in microbiota composition profile due to diabetes are modulated by the vagus nerve. Therefore, it is plausible that disruptions in the gut microbiota may be captured through electroencephalography signaling. Several studies which used standard methods of signal processing have highlighted some changes in electroencephalographic rhythms on patients with diabetes.

An Experimental Model for the Study of Underwater Pressure Waves on the Central Nervous System in Rodents: A Feasibility Study

Underwater blast differs from blast in air. The increased density and viscosity of water relative to air cause injuries to occur almost exclusively as primary blast, and may cause disorientation in a diver, which may lead to inability to protect the airway and cause drowning. However, cognitive impairments from under water blast wave exposure have not been properly investigated, and no experimental model has been described. We established an experimental model (water shock tube) for simulating the effects of underwater blast pressure waves in rodents, and to investigate neurology in relation to organ injury. The model produced standardized pressure waves (duration of the primary peak 3.5 ms, duration of the entire complex waveform including all subsequent reflections 325 ms, mean impulse 141–281 kPa-ms, mean peak pressure 91–194 kPa). 31 rats were randomized to control (n = 6), exposure 90 kPa (n = 8), 152 kPa (n = 8), and 194 kPa (n = 9). There was a linear trend between the drop height of the water shock tube and electroencephalography (EEG) changes (p = 0.014), while no differences in oxygen saturation, heart rate, S100b or macroscopic bleedings were detected. Microscopic bleedings were detected in lung, intestines, and meninges. Underwater pressure waves caused changes in EEG, at pressures when mild hemorrhage occurred in organs, suggesting an impact on brain functions. The consistent injury profile enabled for the addition of future experimental interventions.

Electroencephalography-demonstrated mechanisms of dexmedetomidine-mediated deepening of propofol anesthesia: an observational study

Background Although dexmedetomidine (Dex) is known to reduce bispectral index (BIS) values and propofol dosage, there is little information regarding raw electroencephalography (EEG) changes related to Dex deepening of propofol general anesthesia (GA). This study investigated the Dex effects on propofol GA via analysis of EEG changes. Methods A study cohort of 21 surgical patients (age range, 20–60 years) categorized as American Society of Anesthesiologists (ASA) class I or II was enrolled. We used time-varying spectral and bicoherence methods to compare electroencephalogram signatures 5 min before versus 10 min after intravenous Dex injection under propofol GA. The means and medians are reported with 95% confidence intervals (CIs) and inter-quartile ranges (IQRs), respectively. Results Dex augmented the slow waves power and theta (θ) oscillation bicoherence peak from a mean (95% CI) of 22.1% (19.0, 25.2) to 25.2% (21.8, 28.6). Meanwhile, Dex reduced alpha (α) peak power and bicoherence from 3.5 dB (1.0, 6.0) and 41.5% (34.0, 49.0) to 1.7 dB (− 0.6, 4.0) and 35.4% (29.0, 41.8), respectively, while diminishing the median frequency of α oscillation peak values and the mean frequency of α peaks in bicoherence spectra from 12.0 Hz (IQR 11.2, 12.6) and 11.7 Hz (11.3, 12.2) to 11.1 Hz (IQR 10.3, 11.8) and 11.2 Hz (10.9, 11.6), respectively. Conclusions Profound EEG changes support the supposition that Dex enhances propofol-induced GA from a moderate to a deeper state. The present findings provide a theoretical basis and reference regarding protocols aimed at reducing anesthetic/sedative dosage while maintaining sufficient depth of GA. Clinical trial registration ChiCTR, ChiCTR1900026955. Registered on 27 October 2019

Quantitative Electroencephalography (EEG) Predicting Acute Neurologic Deterioration in the Pediatric Intensive Care Unit: A Case Series

Introduction: Continuous neurologic assessment in the pediatric intensive care unit is challenging. Current electroencephalography (EEG) guidelines support monitoring status epilepticus, vasospasm detection, and cardiac arrest prognostication, but the scope of brain dysfunction in critically ill patients is larger. We explore quantitative EEG in pediatric intensive care unit patients with neurologic emergencies to identify quantitative EEG changes preceding clinical detection. Methods: From 2017 to 2020, we identified pediatric intensive care unit patients at a single quaternary children's hospital with EEG recording near or during acute neurologic deterioration. Quantitative EEG analysis was performed using Persyst P14 (Persyst Development Corporation). Included features were fast Fourier transform, asymmetry, and rhythmicity spectrograms, “from-baseline” patient-specific versions of the above features, and quantitative suppression ratio. Timing of quantitative EEG changes was determined by expert review and prespecified quantitative EEG alert thresholds. Clinical detection of neurologic deterioration was defined pre hoc and determined through electronic medical record documentation of examination change or intervention. Results: Ten patients were identified, age 23 months to 27 years, and 50% were female. Of 10 patients, 6 died, 1 had new morbidity, and 3 had good recovery; the most common cause of death was cerebral edema and herniation. The fastest changes were on “from-baseline” fast Fourier transform spectrograms, whereas persistent changes on asymmetry spectrograms and suppression ratio were most associated with morbidity and mortality. Median time from first quantitative EEG change to clinical detection was 332 minutes (interquartile range: 201-456 minutes). Conclusion: Quantitative EEG is potentially useful in earlier detection of neurologic deterioration in critically ill pediatric intensive care unit patients. Further work is required to quantify the predictive value, measure improvement in outcome, and automate the process.

Influence of Electrochemically Exfoliated Graphite Addition on the Dielectric Properties of Epoxy/Montmorillonite Nanocomposites

The influence of hydrophilic electrochemically exfoliated graphite (EEG) and hydrophobic reduced EEG (rEEG) on the electrical conductivity, dielectric properties, and high-frequency dielectric losses of epoxy-based composites with montmorillonite was described. It was confirmed, that the addition of EEG changes the low-temperature conduction mechanism. The electrical conductivity in composite with EEG and montmorillonite was described by correlated barrier hopping model, whereas for composites with montmorillonite and rEEG two models were used: non-overlapping small polaron tunneling and correlated barrier hopping. The addition of EEG drastically changes the activation energy of charge carriers motions from 2.68 to 0.83 eV, whereas the addition of rEEG only to 2.43 eV. Also composite with EEG was characterized by highest high-frequency dielectric losses.

A Neurochemical and Electrophysiological Study on the Combined Effects of Caffeine and Nicotine in the Cortex of Rats

Objective: Caffeine and nicotine are the most consumed psychostimulants worldwide. Although the effects of each drug alone on the central nervous system (CNS) were studied extensively, the literature on the neurochemical and electrophysiological effects of their combined treatments is scarce. The present study investigates the cortical electrophysiological and neurochemical alterations induced by acute administration of caffeine and nicotine in rats. Methods: Rats received caffeine and nicotine with 1h interval between the two treatments. Results: Caffeine and nicotine administration resulted in a significant decrease in the concentrations of cortical amino acid neurotransmitters namely glutamate, aspartate, glycine and taurine while γ-aminobutyric acid (GABA) was significantly increased. An increased cortical lipid peroxidation and decreased reduced glutathione and nitric oxide levels and acetylcholinesterase and Na+, K+-ATPase activities were also observed. The electroencephalogram (EEG) showed an increase in delta frequency power band while theta, beta-1 and beta-2 were decreased after caffeine and nicotine treatment. These findings suggest that caffeine and nicotine adversely exacerbate their stimulant effects. This was manifested by the EEG changes and mediated by increasing cholinergic transmission, disturbing the balance between the excitatory and inhibitory amino acids leading to oxidative stress.

The meaning of EEG indicators of loss of consciousness during anaesthesia and coma.

Raw EEG changes correlate well with the effects of anaesthetics on arousal. The purpose ofthe present paper is to analyse the significance of the EEG spectrograph. The alpha rhythm isa signature of the unconscious and according to the MAB hypothesis (Monoaminergic-Acetylcholinergic Balance) is an index of increased relative inhibitory muscarinic effects onmonoaminergic modulated conscious networks. The source of alpha rhythms varies, as doesthe type of unconscious information: from classical occipital alpha during resting state witheyes closed where no external visual information is processed, to states of unconsciousanaesthesia where alpha shifts to fronto-parietal networks. These are spontaneous oscillatorynetwork responses and the effects of GABA agonist anaesthetics increase the amplitude ofthese intrinsic rhythms. The hypothesis states that the concurrent presence of sustained deltaoscillations and alpha spindles signifies suppressed unconscious and conscious responsesrespectively, and permit neither implicit nor explicit cognition nor recollections. Further, themodel will be used to interpret EEG changes associated with more atypical anaesthetics andprovide reasons for the related cognitive effects. This will be based on the agents’pharmacological profiles and how they interact with these dual neuromodulatory systems.Evidence will also be drawn from EEG states associated with pathophysiology in coma andepilepsy. The pharmacological interpretation of EEG makes predictions of awareness indisorders of consciousness. The difficult circumstances of behaviourally inadequateindicators refers to situations of minimally conscious and in particular, vegetative stateswhere decision making is fraught with uncertainty.

Clinico-etiological profile of first episode of seizure and its correlation with electroencephalogram in children aged 2 months to 18 years

Background: Seizure is one of the commonest neurological illnesses. About 4-10% of children experience at least one episode in the first 16 years of life. Approximately 30% of children who experience, first afebrile seizure later develop epilepsy. Risk is approximately 20% if neurological examination, electroencephalogram (EEG) and neuroimaging is normal. The objective of the study is to determine the age of onset, etiology of first episode of seizure in children between the age group of 2 months to 18 years and the pattern of EEG changes in the above group of children.Methods: In a prospective single centre observational study at Cheluvamba tertiary care hospital in Mysore, around 80 children who were admitted with first episode of afebrile seizure to our emergency department between October-2020 to July-2021 (10 months) were studied. Seizures defined using international league against epilepsy (ILAE) and EEG was done for all 80 children and their records were analysed.Results: A total of 80 children presenting with first episode of seizure were included in the study. Toddlers represented the major portion of our study with male gender predominance. Idiopathic seizure was the most common etiology identified (81.2%), followed by meningitis (7.5%). EEG abnormality was seen in 58.7% of the children which was statistically significant (p<0.05). MRI was done in 72.5% of the children, of which abnormality was seen in only 8.6% of the children.Conclusions: Seizure is mainly diagnosed clinically and EEG can be normal in many children. First episode of seizure is common in the age group of 1-3 years. Normal EEG at present may not indicate the non-recurrence in future. Though EEG interpretation is useful, treatment can be started based on clinical diagnosis and has to be individualized.

Aperiodic EEG activity masks the dynamics of neural oscillations during loss of consciousness from propofol

EEGs are known to provide biomarkers for consciousness. Although EEG correlates of loss of consciousness (LOC) are often ascribed to changes in neural synchrony, mounting evidence suggests that some changes result from asynchronous neural activity. By combining EEG recordings of humans undergoing propofol administration with biophysical modelling, we present here a principled decomposition of EEG changes during LOC into synchronous and asynchronous sources. Our results reveal that IPSP decay rate and mean spike rate shape aperiodic EEG features, and that propofol's effects on these parameters largely explain the changes in EEG spectra following propofol infusion. We further show that traditional spectral EEG analysis likely conflates these effects with changes in rhythmic activity, thereby masking the true dynamics of neural synchrony. We conclude that the well-documented propofol-induced alpha rhythm in fact appears before LOC, and that the moment of LOC is uniquely correlated with the sudden appearance of a delta rhythm.