EEG Burst Research Articles

Repetitive muscle silent periods in acute post-anoxic brain injury: A novel phenotype of negative myoclonus

ObjectiveTo report a novel phenotype of negative myoclonus in acute post-anoxic brain injury (PABI). MethodsWe performed a retrospective analysis of 18-channel video-EEG and surface-EMG (sEMG) recordings of three patients with PABI. sEMG electrodes were placed on the neck, bulbar and arm muscles. ResultsAll three patients had whole body tonic posturing with intermittent brief relaxation. In patients #1 and #2, a generalized EEG burst-suppression was present. Repetitive silent periods (SPs) were noted in the sEMG channels, time-locked to EEG bursts. The bursts preceded the SPs by 135 ms and 124 ms, respectively. The average SP duration was 910 ms and 852 ms in patients #1 and 2, respectively. Patient #3 had a generalized background suppression pattern and average SP duration of 272.5 ms. The SP recruitment pattern in patient #1 was rostro-caudal whereas patient #3 had a variable recruitment pattern. ConclusionAcute post-anoxic negative myoclonus can be detected in comatose patients with sEMG electrodes. The muscle SPs produce intermittent relaxation of the tonic posturing. The putative generator can be cortical or reticular, similar to Lance-Adams syndrome. SignificanceWe describe a novel phenotype of negative myoclonus in acute PABI. We also describe the EEG and sEMG characteristics and the localization of the putative generator.

Relationships between the qNOX, qCON, burst suppression ratio, and muscle activity index of the CONOX monitor during total intravenous anesthesia: a pilot study

Background: Processed electroencephalographic (EEG) indices can help to navigate general anesthesia. The CONOX (Fresenius Kabi) calculates two indices, the qCON (hypnotic level) and the qNOX (nociception). The CONOX also calculates indices for electromyographic (EMG) activity and EEG burst suppression (BSR). Because all EEG parameters seem to influence each other, our goal was a detailed description of parameter relationships. Methods: We used qCON, qNOX, EMG, and BSR information from 14 patients receiving propofol anesthesia. We described index relationships with linear models, heat maps, and box plot representations. We also evaluated associations between qCON/qNOX and propofol/remifentanil effect site concentrations (ceP/ceR). Results: qNOX and qCON (qCON = 0.79*qNOX + 5.8; p < 0.001; R2 = 0.84) had a strong linear association. We further confirmed the strong relationship between qCON/qNOX and BSR for qCON/qNOX < 25: qCON=-0.19*BSR + 25.6 (p < 0.001; R2 = 0.72); qNOX=-0.20*BSR + 26.2 (p < 0.001; R2 = 0.72). The relationship between qCON and EMG was strong at higher indices: qCON = 0.55*EMG + 33.0 (p < 0.001; R2 = 0.68). There was no qCON > 80 without EMG > 0. The relationship between ceP and qCON was qCON=-3.8*ceP + 70.6 (p < 0.001; R2 = 0.11). The heat maps also suggest that the qCON and qNOX can at least partially separate the hypnotic and analgetic components of anesthesia. Conclusion: We could describe relationships between qCON, qNOX, EMG, BSR, ceP, and ceR, which may help the anaesthesiologist better interpret the information provided. One major finding is the dependence of qCON > 80 on EMG activity. This may limit the possibility of detecting wakefulness in the absence of EMG. Further, qNOX seems generally higher than qCON, but high opioid doses may lead to higher qCON than qNOX indices.

The Influence of Preoperative Physical Activity on Intraoperative Brain Function in Cardiac Surgical patients.

Background Preoperative physical activity and intraoperative brain health are recognized to influence postoperative delirium (POD). Electroencephalogram (EEG) burst suppression and cerebral desaturation are indicators of abnormal intraoperative brain health. Our study aimed to investigate the associations between preoperative physical activity and intraoperative EEG burst suppression and cerebral desaturation. Methods We retrospectively analyzed data from 67 patients from one of the institutions participating in a multisite randomized controlled trial, PANDORA, involving patients undergoing cardiac surgery. The preoperative PCS12 score calculated using the SF12 questionnaire was used as an indicator of preoperative physical activity. Intraoperative EEG and cerebral oximetry data (not the current standard of care in this facility) were collected, and the anesthesiologists were blinded to the information. We analyzed the following associations between the PCS12 score and i) burst suppression duration, ii) the number of cerebral desaturations, and iii) the number of observations with concurrent cerebral desaturation and burst suppression using a generalized linear model. The results are presented as percentage changes in outcomes, and a 95% C.I. p value < 0.05 was considered to indicate statistical significance. Results Each unit increase in the PCS12 score was associated with a 3.3% decrease in the duration of burst suppression (-3.3 [-5.3, -1.2], p value = 0.002). The duration of burst suppression decreased by 29.2% with each successive quartile increase in the PCS-12 score, indicating a dose‒response relationship (-29.2 [-41.6, -16], p < 0.001). Specifically, the patients in the last three quartiles exhibited a 55.4% reduction in BSD compared to those in the first quartile (-55.4 [-74.4, -24.6], p = 0.002) (Fig. 2). We did not observe any significant association between the PCS12 score and cerebral desaturation. Conclusion Decreased preoperative physical activity, as measured by the SF-12 questionnaire, is significantly associated with increased EEG burst suppression duration. Preoperative physical activity did not show any association with cerebral desaturations and concurrent cerebral desaturation and burst suppression. Clinical Trial information ClinicalTrials.gov Identifier- NCT04093219 https://clinicaltrials.gov/ct2/show/NCT04093219 Principal Investigator - Balachundhar Subramaniam Date of registration - September 13, 2019.

Continuity with caveats in anesthesia: state and response entropy of the EEG

The growing use of neuromonitoring in general anesthesia provides detailed insights into the effects of anesthetics on the brain. Our study focuses on the processed EEG indices State Entropy (SE), Response Entropy (RE), and Burst Suppression Ratio (BSR) of the GE EntropyTM Module, which serve as surrogate measures for estimating the level of anesthesia. While retrospectively analyzing SE and RE index values from patient records, we encountered a technical anomaly with a conspicuous distribution of index values. In this single-center, retrospective study, we analyzed processed intraoperative electroencephalographic (EEG) data from 15,608 patients who underwent general anesthesia. We employed various data visualization techniques, including histograms and heat maps, and fitted custom non-Gaussian curves. Individual patients’ anesthetic periods were evaluated in detail. To compare distributions, we utilized the Kolmogorov–Smirnov test and Kullback–Leibler divergence. The analysis also included the influence of the BSR on the distribution of SE and RE values. We identified distinct pillar indices for both SE and RE, i.e., index values with a higher probability of occurrence than others. These pillar index values were not age-dependent and followed a non-equidistant distribution pattern. This phenomenon occurs independently of the BSR distribution. SE and RE index values do not adhere to a continuous distribution, instead displaying prominent pillar indices with a consistent pattern of occurrence across all age groups. The specific features of the underlying algorithm responsible for this pattern remain elusive.

Electroencephalographic guided propofol-remifentanil TCI anesthesia with and without dexmedetomidine in a geriatric population: electroencephalographic signatures and clinical evaluation.

Elderly and multimorbid patients are at high risk for developing unfavorable postoperative neurocognitive outcomes; however, well-adjusted and EEG-guided anesthesia may help titrate anesthesia and improve postoperative outcomes. Over the last decade, dexmedetomidine has been increasingly used as an adjunct in the perioperative setting. Its synergistic effect with propofol decreases the dose of propofol needed to induce and maintain general anesthesia. In this pilot study, we evaluate two highly standardized anesthetic regimens for their potential to prevent burst suppression and postoperative neurocognitive dysfunction in a high-risk population. Prospective, randomized clinical trial with non-blinded intervention. Operating room and post anesthesia care unit at Hospital Base San José, Osorno/Universidad Austral, Valdivia, Chile. 23 patients with scheduled non-neurologic, non-cardiac surgeries with age > 69years and a planned intervention time > 60min. Patients were randomly assigned to receive either a propofol-remifentanil based anesthesia or an anesthetic regimen with dexmedetomidine-propofol-remifentanil. All patients underwent a slow titrated induction, followed by a target controlled infusion (TCI) of propofol and remifentanil (n = 10) or propofol, remifentanil and continuous dexmedetomidine infusion (n = 13). We compared the perioperative EEG signatures, drug-induced changes, and neurocognitive outcomes between two anesthetic regimens in geriatric patients. We conducted a pre- and postoperative Montreal Cognitive Assessment (MoCa) test and measured the level of alertness postoperatively using a sedation agitation scale to assess neurocognitive status. During slow induction, maintenance, and emergence, burst suppression was not observed in either group; however, EEG signatures differed significantly between the two groups. In general, EEG activity in the propofol group was dominated by faster rhythms than in the dexmedetomidine group. Time to responsiveness was not significantly different between the two groups (p = 0.352). Finally, no significant differences were found in postoperative cognitive outcomes evaluated by the MoCa test nor sedation agitation scale up to one hour after extubation. This pilot study demonstrates that the two proposed anesthetic regimens can be safely used to slowly induce anesthesia and avoid EEG burst suppression patterns. Despite the patients being elderly and at high risk, we did not observe postoperative neurocognitive deficits. The reduced alpha power in the dexmedetomidine-treated group was not associated with adverse neurocognitive outcomes.

Utility and limitations of EEG in the diagnosis and management of ALDH7A1-related pyridoxine-dependent epilepsy. A retrospective observational study.

Pyridoxine-dependent epilepsy due to ALDH7A1 variants (PDE-ALDH7A1) is a rare disorder, presenting typically with severe neonatal, epileptic encephalopathy. Early diagnosis is imperative to prevent uncontrolled seizures. We have explored the role of EEG in the diagnosis and management of PDE. A total of 13 Norwegian patients with PDE-ALDH7A1 were identified, of whom five had reached adult age. Altogether 163 EEG recordings were assessed, 101 from the 1st year of life. Median age at seizure onset was 9 h (IQR 41), range 1 h-6 days. Median delay from first seizure to first pyridoxine injection was 2 days (IQR 5.5). An EEG burst suppression pattern was seen in eight patients (62%) during the first 5 days of life. Eleven patients had recordings during pyridoxine injections: in three, immediate EEG improvement correlated with seizure control, whereas in six, no change of epileptiform activity occurred. Of these six, one had prompt clinical effect, one had delayed effect (< 1 day), one had no effect, one had uncertain effect, and another had more seizures. A patient without seizures at time of pyridoxine trial remained seizure free for 6 days. Two patients with prompt clinical effect had increased paroxysmal activity, one as a conversion to burst suppression. Autonomic seizures in the form of apnoea appeared to promote respiratory distress and were documented by EEG in one patient. EEG follow-up in adult age did not show signs of progressing encephalopathy. A neonatal burst suppression EEG pattern should raise the suspicion of PDE-ALDH7A1. Respiratory distress is common; isolated apnoeic seizures may contribute. EEG responses during pyridoxine trials are diverse, often with poor correlation to immediate clinical effect. Reliance on single trials may lead to under-recognition of this treatable condition. Pyridoxine should be continued until results from biomarkers and genetic testing are available.

Cerebellar Purkinje cell firing promotes conscious recovery from anesthesia state through coordinating neuronal communications with motor cortex.

Background: The neurobiological basis of gaining consciousness from unconscious state induced by anesthetics remains unknown. This study was designed to investigate the involvement of the cerebello-thalamus-motor cortical loop mediating consciousness transitions from the loss of consciousness (LOC) induced by an inhalational anesthetic sevoflurane in mice. Methods: The neural tracing and fMRI together with opto-chemogenetic manipulation were used to investigate the potential link among cerebello-thalamus-motor cortical brain regions. The fiber photometry of calcium and neurotransmitters, including glutamate (Glu), γ-aminobutyric acid (GABA) and norepinephrine (NE), were monitored from the motor cortex (M1) and the 5th lobule of the cerebellar vermis (5Cb) during unconsciousness induced by sevoflurane and gaining consciousness after sevoflurane exposure. Cerebellar Purkinje cells were optogenetically manipulated to investigate their influence on consciousness transitions during and after sevoflurane exposure. Results: Activation of 5Cb Purkinje cells increased the Ca2+ flux in the M1 CaMKIIα+ neurons, but this increment was significantly reduced by inactivation of posterior and parafascicular thalamic nucleus. The 5Cb and M1 exhibited concerted calcium flux, and glutamate and GABA release during transitions from wakefulness, loss of consciousness, burst suppression to conscious recovery. Ca2+ flux and Glu release in the M1, but not in the 5Cb, showed a strong synchronization with the EEG burst suppression, particularly, in the gamma-band range. In contrast, the Glu, GABA and NE release and Ca2+ oscillations were coherent with the EEG gamma band activity only in the 5Cb during the pre-recovery of consciousness period. The optogenetic activation of Purkinje cells during burst suppression significantly facilitated emergence from anesthesia while the optogenetic inhibition prolonged the time to gaining consciousness. Conclusions: Our data indicate that cerebellar neuronal communication integrated with motor cortex through thalamus promotes consciousness recovery from anesthesia which may likely serve as arousal regulation.

Effect of remimazolam on electroencephalogram burst suppression in elderly patients undergoing cardiac surgery: Protocol for a randomized controlled noninferiority trial

BackgroundPostoperative delirium (POD) is a common complication following cardiac surgery and increases postoperative morbidity and mortality. Intraoperative electroencephalogram (EEG) burst suppression suggests excessively deep anesthesia and predicts POD. Use of remimazolam provides a stable hemodynamic status and an appropriate depth of anesthesia. We aim to assess remimazolam administered for anesthesia and sedation in elderly patients having cardiac surgery. MethodsThis is a randomized controlled clinical trial with noninferiority design. A total of 260 elderly patients aged equal to or greater than 60 years undergoing cardiac surgery will be randomly allocated to receive remimazolam or propofol (1:1) for general anesthesia and postoperative sedation until extubation. The primary outcome is the cumulative time with EEG burst suppression which is obtained from the SedLine system. The noninferiority margin is 2.0 min. The secondary outcomes include the POD occurrence within the first 5 days postoperatively and the duration of perioperative hypotension. DiscussionThis noninferiority trial is the first to evaluate the effect of perioperative remimazolam administration on EEG burst suppression, POD occurrence, and duration of hypotension in elderly patients who undergo cardiac surgery. Trial registrationChinese Clinical Trial Registry (ChiCTR2200056353).

The dosage of thiopental as pharmacological cerebral protection during non-shunt carotid endarterectomy: A retrospective study.

Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3±10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3±10.1 mg/kg/hr.

Activation of glutamatergic neurones in the pedunculopontine tegmental nucleus promotes cortical activation and behavioural emergence from sevoflurane-induced unconsciousness in mice

BackgroundThe neural mechanisms underlying sevoflurane-induced loss of consciousness and recovery of consciousness after anaesthesia remain unknown. We investigated whether glutamatergic pedunculopontine tegmental nucleus (PPT) neurones are involved in the regulation of states of consciousness under sevoflurane anaesthesia. MethodsIn vivo fibre photometry combined with electroencephalography (EEG)/electromyography recording was used to record changes in the activity of glutamatergic PPT neurones under sevoflurane anaesthesia. Chemogenetic and cortical EEG recordings were used to explore their roles in the induction of and emergence from sevoflurane anaesthesia. Optogenetic methods combined with EEG recordings were used to explore the roles of glutamatergic PPT neurones and of the PPT-ventral tegmental area pathway in maintenance of anaesthesia. ResultsThe population activity of glutamatergic PPT neurones was reduced before sevoflurane-induced loss of righting reflex and gradually recovered after return of righting reflex. Chemogenetic inhibition of glutamatergic PPT neurones accelerated induction of anaesthesia (hM4Di-CNO vs mCherry-CNO, 76 [17] vs 121 [27] s, P<0.0001) and delayed emergence from sevoflurane anaesthesia (278 [98] vs 145 [53] s, P<0.0001) but increased sevoflurane sensitivity. Optogenetic stimulation of glutamatergic PPT neurons or of the PPT-ventral tegmental area pathway promoted cortical activation and behavioural emergence during steady-state sevoflurane anaesthesia, reduced the depth of anaesthesia, and caused cortical arousal during sevoflurane-induced EEG burst suppression. ConclusionsGlutamatergic PPT neurones regulate induction and emergence of sevoflurane anaesthesia.

Mapping sleep's oscillatory events as a biomarker of Alzheimer's disease.

Memory-associated neural circuits produce oscillatory events including theta bursts (TBs), sleep spindles (SPs), and slow waves (SWs) in sleep electroencephalography (EEG). Changes in the"coupling" of these events may indicate early Alzheimer's disease (AD) pathogenesis. We analyzed 205 aging adults using single-channel sleep EEG, cerebrospinal fluid (CSF) AD biomarkers, and Clinical Dementia Rating® (CDR®) scale. We mapped SW-TB and SW-SP neural circuit coupling precision to amyloid positivity, cognitive impairment, and CSF AD biomarkers. Cognitive impairment correlated with lower TB spectral power in SW-TB coupling. Cognitively unimpaired, amyloid positive individuals demonstrated lower precision in SW-TB and SW-SP coupling compared to amyloid negative individuals. Significant biomarker correlations were found in oscillatory event coupling with CSF Aβ42 /Aβ40 , phosphorylated- tau181 , and total-tau. Sleep-dependent memory processing integrityin neural circuits can be measured for both SW-TB and SW-SP coupling. This breakdownassociateswith amyloid positivity, increased AD pathology, and cognitive impairment. At-home sleep EEG is a potential biomarker of neural circuits linked to memory. Circuit precision is associated with amyloid positivity in asymptomatic aging adults. Levels of CSF amyloid and tau also correlate with circuit precision in sleep EEG. Theta burst EEG power is decreased in very early mild cognitive impairment. This technique may enable inexpensive wearable EEGs for monitoring brain health.

Analysis of the relationship between EEG burst suppression and poor prognosis in children under general anaesthesia: study protocol for a prospective, observational, single-centre study

BackgroundEmergence delirium (ED) in children refers to the immediate postoperative period when children experience decreased perception of their surroundings, accompanied by disorientation and altered perception. Burst suppression (BS) is recognised as periods longer than 0.50 s during which the EEG does not exceed approximately + 5.0 mV, which is an electroencephalographic state associated with profound inactivation of the brain. Our primary objective was to determine the association between BS on electroencephalogram (EEG) under general anaesthesia with postoperative wake-up delirium and multiple adverse outcomes, such as prolonged awakening and extubation.MethodsIn this prospective, observational cohort study at Beijing Children’s Hospital, Capital Medical University, Beijing, China, children aged 6 months to 9 years who underwent surgery under general anaesthesia and underwent EEG monitoring between January 2022 and January 2023 were included. Patients’ prefrontal EEGs were recorded intraoperatively as well as analysed for the occurrence and duration of BS and scored postoperatively for delirium by the PAED scale, with a score of no less than 10 considered as having developed wake-up delirium.DiscussionThis study identified a relationship between EEG BS and postoperative awakening delirium under general anaesthesia in children and provides a novel preventive strategy for postoperative awakening delirium and multiple adverse outcomes in paediatric patients.Trial registrationChinese Clinical Trial Registry, ChiCTR2200055256. Registered on January 5, 2022.

Outcome of Absence Epilepsy With Onset at 8-11 Years of Age: Watershed Ages When Syndromes Overlap.

Introduction: Absence seizures occur in various epilepsy syndromes, including childhood and juvenile absence epilepsy and juvenile myoclonic epilepsy. When children present with absence seizures at ages when syndromes overlap, initial syndrome designation is not always possible, making early prognostication challenging. For these children, the study objective is to determine clinical and initial electroencephalograph (EEG) findings to predict the development of generalized tonic-clonic seizures, which is a factor that affects outcome. Methods: Children with new-onset absence seizures between 8 and 11 years of age with at least 5 years of follow-up data were studied through the review of medical records and initial EEG tracings. Results: Ninety-eight patients were included in the study. The median age of absence seizure onset was 9 years (interquartile range [IQR] = 8.00, 10.00) and follow-up was 15 years (IQR = 13.00, 18.00). Forty-six percent developed generalized tonic-clonic seizures and 20% developed myoclonic seizures. On multiple regression analysis, a history of myoclonic seizures, anxiety, as well as bifrontal slowing and mild background slowing on initial EEG (P < .05) were associated with generalized tonic-clonic seizures. Although not statistically significant, a shorter duration of shortest EEG burst on baseline EEG was also associated with generalized tonic-clonic seizures. Conclusion: On initial EEG, bifrontal and background slowing and myoclonic seizures and anxiety are associated with developing generalized tonic-clonic seizures, which is of prognostic significance when early syndrome designation is difficult.

The dosage of thiopental as pharmacological cerebral protection during non-shunt carotid endarterectomy: A retrospective study

Background: Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods: The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results: The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3+10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions: The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3+10.1 mg/kg/hr.

Diversity of electroencephalographic patterns during propofol-induced burst suppression.

Burst suppression is a brain state consisting of high-amplitude electrical activity alternating with periods of quieter suppression that can be brought about by disease or by certain anesthetics. Although burst suppression has been studied for decades, few studies have investigated the diverse manifestations of this state within and between human subjects. As part of a clinical trial examining the antidepressant effects of propofol, we gathered burst suppression electroencephalographic (EEG) data from 114 propofol infusions across 21 human subjects with treatment-resistant depression. This data was examined with the objective of describing and quantifying electrical signal diversity. We observed three types of EEG burst activity: canonical broadband bursts (as frequently described in the literature), spindles (narrow-band oscillations reminiscent of sleep spindles), and a new feature that we call low-frequency bursts (LFBs), which are brief deflections of mainly sub-3-Hz power. These three features were distinct in both the time and frequency domains and their occurrence differed significantly across subjects, with some subjects showing many LFBs or spindles and others showing very few. Spectral-power makeup of each feature was also significantly different across subjects. In a subset of nine participants with high-density EEG recordings, we noted that each feature had a unique spatial pattern of amplitude and polarity when measured across the scalp. Finally, we observed that the Bispectral Index Monitor, a commonly used clinical EEG monitor, does not account for the diversity of EEG features when processing the burst suppression state. Overall, this study describes and quantifies variation in the burst suppression EEG state across subjects and repeated infusions of propofol. These findings have implications for the understanding of brain activity under anesthesia and for individualized dosing of anesthetic drugs.

Increased propensity for infantile spasms and altered neocortical excitation-inhibition balance in a mouse model of down syndrome carrying human chromosome 21

Children with Down syndrome (DS, trisomy of chromosome 21) have an increased risk of infantile spasms (IS). As an epileptic encephalopathy, IS may further impair cognitive function and exacerbate neurodevelopmental delays already present in children with DS. To investigate the pathophysiology of IS in DS, we induced IS-like epileptic spasms in a genetic mouse model of DS that carries human chromosome 21q, TcMAC21, the animal model most closely representing gene dosage imbalance in DS. Repetitive extensor/flexor spasms were induced by the GABAB receptor agonist γ-butyrolactone (GBL) and occurred predominantly in young TcMAC21 mice (85%) but also in some euploid mice (25%). During GBL application, background electroencephalographic (EEG) amplitude was reduced, and rhythmic, sharp-and-slow wave activity or high-amplitude burst (epileptiform) events emerged in both TcMAC21 and euploid mice. Spasms occurred only during EEG bursts, but not every burst was accompanied by a spasm. Electrophysiological experiments revealed that basic membrane properties (resting membrane potential, input resistance, action-potential threshold and amplitude, rheobase, input-output relationship) of layer V pyramidal neurons were not different between TcMAC21 mice and euploid controls. However, excitatory postsynaptic currents (EPSCs) evoked at various intensities were significantly larger in TcMAC21 mice than euploid controls, while inhibitory postsynaptic currents (IPSCs) were similar between the two groups, resulting in an increased excitation-inhibition (E-I) ratio. These data show that behavioral spasms with epileptic EEG activity can be induced in young TcMAC21 DS mice, providing proof-of-concept evidence for increased IS susceptibility in these DS mice. Our findings also show that basic membrane properties are similar in TcMAC21 and euploid mice, while the neocortical E-I balance is altered to favor increased excitation in TcMAC21 mice, which may predispose to IS generation.

The dosage of thiopental as pharmacological cerebral protection during non-shunt carotid endarterectomy: A retrospective study

Background: Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods: The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results: The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3+10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions: The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3+10.1 mg/kg/hr.

Association Between Induced Burst Suppression and Clinical Outcomes in Patients With Refractory Status Epilepticus: A 9-Year Cohort Study.

To investigate the frequency of induced EEG burst suppression pattern during continuous IV anesthesia (IVAD) and associated outcomes in adult patients treated for refractory status epilepticus (RSE). Patients with RSE treated with anesthetics at a Swiss academic care center from 2011 to 2019 were included. Clinical data and semiquantitative EEG analyses were assessed. Burst suppression was categorized as incomplete burst suppression (with ≥20% and <50% suppression proportion) or complete burst suppression (with ≥50% suppression proportion). The frequency of induced burst suppression and association of burst suppression with outcomes (persistent seizure termination, in-hospital survival, and return to premorbid neurologic function) were the endpoints. We identified 147 patients with RSE treated with IVAD. Among 102 patients without cerebral anoxia, incomplete burst suppression was achieved in 14 (14%) with a median of 23 hours (interquartile range [IQR] 1-29) and complete burst suppression was achieved in 21 (21%) with a median of 51 hours (IQR 16-104). Age, Charlson comorbidity index, RSE with motor symptoms, the Status Epilepticus Severity Score and arterial hypotension requiring vasopressors were identified as potential confounders in univariable comparisons between patients with and without any burst suppression. Multivariable analyses revealed no associations between any burst suppression and the predefined endpoints. However, among 45 patients with cerebral anoxia, induced burst suppression was associated with persistent seizure termination (72% without vs 29% with burst suppression, p = 0.004) and survival (50% vs 14% p = 0.005). In adult patients with RSE treated with IVAD, burst suppression with ≥50% suppression proportion was achieved in every fifth patient and not associated with persistent seizure termination, in-hospital survival, or return to premorbid neurologic function.

Telemetric electroencephalography recording in anesthetized mice—A novel system using minimally-invasive needle electrodes with a wireless OpenBCI™ Cyton Biosensing Board

Telemetric electroencephalography (EEG) recording, using subdermal needle electrodes, is a minimally-invasive method to investigate mammalian neurophysiology during anesthesia. These inexpensive systems may streamline experiments examining global brain phenomena during surgical anesthesia or disease. We utilized the OpenBCI™ Cyton board with subdermal needle electrodes to extract EEG features in six C57BL/6J mice undergoing isoflurane anesthesia. Burst suppression ratio (BSR) and spectral features were compared for a verification of our method. Following an increase from 1.5% to 2.0% isoflurane, the BSR increased (Wilcoxon-signed-rank statistic; p = 0.0313). Furthermore, although the absolute EEG spectral power decreased, the relative spectral power remained comparable (Wilcoxon-Mann-Whitney U-Statistic; 95% CI exclusive AUC=0.5; p < 0.05). Compared to tethered systems, this method confers several improvements for anesthesia specific protocols: 1-Avoiding electrode implant surgical procedures, 2-Anatomical non-specificity for needle electrode placement to monitor global cortical activity representative of anesthetic state, 3-Facility to repeat recordings in the same animal, 4-User-friendly for non-experts, 5-Rapid set-up time, and 6-Lower costs.•Minimally-invasive telemetric EEG recording systems ergonomically improve tethered systems for anesthesia protocols.•Using this method, we verified that higher isoflurane concentrations resulted in an increased EEG burst suppression ratio and decreased EEG absolute spectral power, with no change in frequency distribution.

0860 Burst Suppression due to Diffuse Encephalopathy

Abstract Introduction Burst suppression is a finding on electroencephalography (EEG) associated with a severe encephalopathy associated with coma, severe infantile-onset epilepsy syndromes, hypothermia, or may be medically induced by general anesthesia. It presents as a pattern of alternating high-voltage, 75-250µV, activity separated by periods of amplitude dampening, less than 5µV, of electrical brain activity1. The duration of the burst’s activity is 1-20 seconds while the suppression lasts longer than 10 seconds1. When not medically induced, burst suppression is a known marker of poor prognosis. Report of Cases: An 18-year-old male with cerebral palsy, spastic quadriplegia, and static encephalopathy secondary to hypoxemia ischemic injury in the perinatal period presents with excessive sleepiness during therapy sessions. He was empirically placed on non-invasive ventilatory support with BPAP ST 8/4 cm H2O with a rate of 10 breaths per minute for chronic respiratory failure during sleep. While awake he shows no evidence of hypoxemia or hypercapnia on room air. A polysomnogram was ordered showing moderate obstructive sleep apnea (oAHI 9.73) and central sleep apnea (5.84 events per hour) without hypoxemia (SpO2 nadir 90%), or hypercapnia (TcCO2 max 48 mmHg). The study was scored as REM/NREM as specific sleep architecture was not identified. Diffuse burst suppression was observed. No epileptiform abnormalities were recorded. A MRI of the brain shows diffuse encephalomalacia involving the supratentorial brain parenchyma with volume loss of the cerebellum, the pons, and brain stem. Conclusion The abnormal brain activity noted in our patient is due to underlying encephalomalacia and diffuse brain injury secondary to his perinatal hypoxemic ischemic injury. Despite his significant underlying neurological abnormality, he can maintain adequate ventilation and oxygenation while awake. While asleep, he has moderate obstructive and central sleep apnea without hypoxemia or hypercapnia. This is likely due to the activity of control centers of respiration being spared despite the volume loss noted on the brain MRI. Support (If Any)