Novel features of early burst suppression predict outcome after birth asphyxia.
Ontology highlight
ABSTRACT:
SUBMITTER: Iyer KK
PROVIDER: S-EPMC4184550 | biostudies-literature | 2014 Mar
REPOSITORIES: biostudies-literature
Publications
Novel features of early burst suppression predict outcome after birth asphyxia.
Iyer Kartik K KK Roberts James A JA Metsäranta Marjo M Finnigan Simon S Breakspear Michael M Vanhatalo Sampsa S
Annals of clinical and translational neurology 20140218 3
Burst suppression patterns in the electroencephalogram are a reliable marker of recent severe brain insult. Here we analyze statistical properties of bursts occurring in 20 electroencephalographic recordings acquired from hypothermic asphyxic newborns in the hours immediately following birth. We show that the distributions of burst area and duration in these acute data predict later clinical outcome in both structural neuroimaging and neurodevelopment. Our findings indicate the first early elect ...[more]
Similar Datasets
Project description:While electroencephalogram (EEG) burst-suppression is often induced therapeutically using sedatives in the intensive care unit (ICU), there is hitherto no evidence with respect to its association to outcome in moderate-to-severe neurological patients. We examined the relationship between sedation-induced burst-suppression (SIBS) and outcome at hospital discharge and at 6-month follow up in patients surviving moderate-to-severe traumatic brain injury (TBI). For each of 32 patients recovering from coma after moderate-to-severe TBI, we measured the EEG burst suppression ratio (BSR) during periods of low responsiveness as assessed with the Glasgow Coma Scale (GCS). The maximum BSR was then used to predict the Glasgow Outcome Scale extended (GOSe) at discharge and at 6 months post-injury. A multi-model inference approach was used to assess the combination of predictors that best fit the outcome data. We found that BSR was positively associated with outcomes at 6 months (P = 0.022) but did not predict outcomes at discharge. A mediation analysis found no evidence that BSR mediates the effects of barbiturates or propofol on outcomes. Our results provide initial observational evidence that burst suppression may be neuroprotective in acute patients with TBI etiologies. SIBS may thus be useful in the ICU as a prognostic biomarker.
| S-EPMC8727767 | biostudies-literature
Project description:Electroencephalographic (EEG) Burst Suppression (BSUPP) is a discontinuous pattern characterized by episodes of low voltage disrupted by bursts of cortical synaptic activity. It can occur while delivering high-dose anesthesia. Current research suggests an association between BSUPP and the occurrence of postoperative delirium in the post-anesthesia care unit (PACU) and beyond. We investigated burst micro-architecture to further understand how age influences the neurophysiology of this pharmacologically-induced state. We analyzed a subset of EEG recordings (n = 102) taken from a larger data set previously published. We selected the initial burst that followed a visually identified "silent second," i.e., at least 1 s of iso-electricity of the EEG during propofol induction. We derived the (normalized) power spectral density [(n)PSD], the alpha band power, the maximum amplitude, the maximum slope of the EEG as well as the permutation entropy (PeEn) for the first 1.5 s of the initial burst of each patient. In the old patients >65 years, we observed significantly lower (p < 0.001) EEG power in the 1-15 Hz range. In general, their EEG contained a significantly higher amount of faster oscillations (>15 Hz). Alpha band power (p < 0.001), EEG amplitude (p = 0.001), and maximum EEG slope (p = 0.045) all significantly decreased with age, whereas PeEn increased (p = 0.008). Hence, we can describe an age-related change in features during EEG burst suppression. Sub-group analysis revealed no change in results based on pre-medication. These EEG changes add knowledge to the impact of age on cortical synaptic activity. In addition to a reduction in EEG amplitude, age-associated burst features can complicate the identification of excessive anesthetic administration in patients under general anesthesia. Knowledge of these neurophysiologic changes may not only improve anesthesia care through improved detection of burst suppression but might also provide insight into changes in neuronal network organization in patients at risk for age-related neurocognitive problems.
| S-EPMC7744408 | biostudies-literature
Project description:BackgroundIllness severity scores are commonly employed in critically ill patients to predict outcome. To date, prior scores for post-cardiac arrest patients rely on some event-related data. We developed an early, novel post-arrest illness severity score to predict survival, good outcome and development of multiple organ failure (MOF) after cardiac arrest.MethodsRetrospective review of data from adults treated after in-hospital or out-of-hospital cardiac arrest in a single tertiary care facility between 1/1/2005 and 12/31/2009. In addition to clinical data, initial illness severity was measured using serial organ function assessment (SOFA) scores and full outline of unresponsiveness (FOUR) scores at hospital or intensive care unit arrival. Outcomes were hospital mortality, good outcome (discharge to home or rehabilitation) and development of multiple organ failure (MOF). Single-variable logistic regression followed by Chi-squared automatic interaction detector (CHAID) was used to determine predictors of outcome. Stepwise multivariate logistic regression was used to determine the independent association between predictors and each outcome. The Hosmer-Lemeshow test was used to evaluate goodness of fit. The n-fold method was used to cross-validate each CHAID analysis and the difference between the misclassification risk estimates was used to determine model fit.ResultsComplete data from 457/495 (92%) subjects identified distinct categories of illness severity using combined FOUR motor and brainstem subscales, and combined SOFA cardiovascular and respiratory subscales: I. Awake; II. Moderate coma without cardiorespiratory failure; III. Moderate coma with cardiorespiratory failure; and IV. Severe coma. Survival was independently associated with category (I: OR 58.65; 95% CI 27.78, 123.82; II: OR 14.60; 95% CI 7.34, 29.02; III: OR 10.58; 95% CI 4.86, 23.00). Category was also similarly associated with good outcome and development of MOF. The proportion of subjects in each category changed over time.ConclusionsInitial illness severity explains much of the variation in cardiac arrest outcome. This model provides prognostic information at hospital arrival and may be used to stratify patients in future studies.
| S-EPMC3196030 | biostudies-literature
Project description:ObjectiveTo determine if early developmental intervention (EDI) improves developmental abilities in resuscitated children.Study designThis was a parallel group, randomized controlled trial of infants unresponsive to stimulation who received bag and mask ventilation as part of their resuscitation at birth and infants who did not require any resuscitation born in rural communities in India, Pakistan, and Zambia. Intervention infants received a parent-implemented EDI delivered with home visits by parent trainers every other week for 3 years starting the first month after birth. Parents in both intervention and control groups received health and safety counseling during home visits on the same schedule. The main outcome measure was the Mental Development Index (MDI) of the Bayley Scales of Infant Development, 2nd edition, assessed at 36 months by evaluators unaware of treatment group and resuscitation history.ResultsMDI was higher in the EDI (102.6 ± 9.8) compared with the control resuscitated children (98.0 ± 14.6, 1-sided P = .0202), but there was no difference between groups in the nonresuscitated children (100.1 ± 10.7 vs 97.7 ± 10.4, P = .1392). The Psychomotor Development Index was higher in the EDI group for both the resuscitated (P = .0430) and nonresuscitated children (P = .0164).ConclusionsThis trial of home-based, parent provided EDI in children resuscitated at birth provides evidence of treatment benefits on cognitive and psychomotor outcomes. MDI and Psychomotor Development Index scores of both nonresuscitated and resuscitated infants were within normal range, independent of early intervention.
| S-EPMC3582821 | biostudies-literature
Project description:OBJECTIVE:We sought to identify genetic causes of early onset epileptic encephalopathies with burst suppression (Ohtahara syndrome and early myoclonic encephalopathy) and evaluate genotype-phenotype correlations. METHODS:We enrolled 33 patients with a referral diagnosis of Ohtahara syndrome or early myoclonic encephalopathy without malformations of cortical development. We performed detailed phenotypic assessment including seizure presentation, electroencephalography, and magnetic resonance imaging. We confirmed burst suppression in 28 of 33 patients. Research-based exome sequencing was performed for patients without a previously identified molecular diagnosis from clinical evaluation or a research-based epilepsy gene panel. RESULTS:In 17 of 28 (61%) patients with confirmed early burst suppression, we identified variants predicted to be pathogenic in KCNQ2 (n?=?10), STXBP1 (n?=?2), SCN2A (n?=?2), PNPO (n?=?1), PIGA (n?=?1), and SEPSECS (n?=?1). In 3 of 5 (60%) patients without confirmed early burst suppression, we identified variants predicted to be pathogenic in STXBP1 (n?=?2) and SCN2A (n?=?1). The patient with the homozygous PNPO variant had a low cerebrospinal fluid pyridoxal-5-phosphate level. Otherwise, no early laboratory or clinical features distinguished the cases associated with pathogenic variants in specific genes from each other or from those with no prior genetic cause identified. INTERPRETATION:We characterize the genetic landscape of epileptic encephalopathy with burst suppression, without brain malformations, and demonstrate feasibility of genetic diagnosis with clinically available testing in >60% of our cohort, with KCNQ2 implicated in one-third. This electroclinical syndrome is associated with pathogenic variation in SEPSECS. Ann Neurol 2017;81:419-429.
| S-EPMC5366084 | biostudies-literature
Project description:Despite major advances in monitoring technology and knowledge of fetal and neonatal pathophysiology, neonatal hypoxic-ischemic encephalopathy (HIE) remains one of the main causes of severe adverse neurological outcome in children. Until recently, there were no therapies other than supportive measures. Over the past several years, mild hypothermia has been proven to be safe to treat HIE. Unfortunately, this neuroprotective strategy seems efficient in preventing brain injury in some asphyxiated newborns, but not in all of them. Thus, there is increasing interest to rapidly understand how to refine hypothermia therapy and add neuroprotective or neurorestorative strategies. Several promising newer treatments to treat birth asphyxia and prevent its devastating neurological consequences are currently being tested. In this paper, the physiopathology behind HIE, the currently available treatment, the potential alternatives, and the next steps before implementation of these other treatments are reviewed.
| S-EPMC3228371 | biostudies-literature
Project description: Not available
| S-EPMC7810348 | biostudies-literature
Project description:Burst suppression is an electroencepholagram (EEG) pattern in which high-voltage activity alternates with isoelectric quiescence. It is characteristic of an inactivated brain and is commonly observed at deep levels of general anesthesia, hypothermia, and in pathological conditions such as coma and early infantile encephalopathy. We propose a unifying mechanism for burst suppression that accounts for all of these conditions. By constructing a biophysical computational model, we show how the prevailing features of burst suppression may arise through the interaction between neuronal dynamics and brain metabolism. In each condition, the model suggests that a decrease in cerebral metabolic rate, coupled with the stabilizing properties of ATP-gated potassium channels, leads to the characteristic epochs of suppression. Consequently, the model makes a number of specific predictions of experimental and clinical relevance.
| S-EPMC3286963 | biostudies-literature
Project description:Perinatal asphyxia occurs still with great incidence whenever delivery is prolonged, despite improvements in perinatal care. After asphyxia, infants can suffer from short- to long-term neurological sequelae, their severity depend upon the extent of the insult, the metabolic imbalance during the re-oxygenation period and the developmental state of the affected regions. Significant progresses in understanding of perinatal asphyxia pathophysiology have achieved. However, predictive diagnostics and personalised therapeutic interventions are still under initial development. Now the emphasis is on early non-invasive diagnosis approach, as well as, in identifying new therapeutic targets to improve individual outcomes. In this review we discuss (i) specific biomarkers for early prediction of perinatal asphyxia outcome; (ii) short and long term sequelae; (iii) neurocircuitries involved; (iv) molecular pathways; (v) neuroinflammation systems; (vi) endogenous brain rescue systems, including activation of sentinel proteins and neurogenesis; and (vii) therapeutic targets for preventing or mitigating the effects produced by asphyxia.
| S-EPMC3405380 | biostudies-other
Project description:Patients with acute myeloid leukemia (AML) suffer dismal prognosis and the most adverse subpopulation within each tumor determines patient’s prognosis. To better understand challenging features in AML, we studied individual stem cells from a single AML sample, complementing genomic with in vivo functional studies. Primary tumor cells from an AML patient’s first and second relapse were transplanted into NSG mice to establish serially transplantable patient derived xenografts (PDX). In an innovative approach, twelve derivative PDX clones were generated thereof, each derived from a single AML stem cell as proven by molecular barcoding, and were color-marked to facilitate multiplex competitive in vivo assays. PDX clones consisted of four different genomic clusters; one cluster displayed resistance against Cytarabine treatment, while two other clusters harbored increased stem cell potential, indicating that stemness and treatment resistance had evolved independently in the sample. In vivo functional data correlated closely with the phylogenetic tree calculated from exome data. The Cytarabine-resistant cluster was characterized by a distinct gene expression profile, and a score thereof predicted outcome in large clinical patient data cohorts. Taken together, we provide proof of concept that intra-sample heterogeneity mimics inter-sample heterogeneity in AML. Stem cell disparities within a single sample allow insights into adverse characteristics of general importance for AML.
2022-04-04 | PXD026296 | Pride