Causes and Terminology in Neonatal Encephalopathy: What is in a Name? Neonatal Encephalopathy, Hypoxic-ischemic Encephalopathy or Perinatal Asphyxia.

Neurologic depression in term/near-term neonates (neonatal encephalopathy, NE) is uncommon with modern obstetric care. Asphyxial birth, with or without co-factors, accounts for a minority of NE, while maldevelopment (congenital malformations, growth aberrations, genetic, metabolic and placental abnormalities) plays an enlarging role in identifying etiologic subgroups of NE. The terms NE and hypoxic-ischemic encephalopathy (HIE) have not been employed uniformly, hampering research and clinical care.

Consensus definition and diagnostic criteria for neonatal encephalopathy-study protocol for a real-time modified delphi study.

Background: 'Neonatal encephalopathy' (NE) describes a group of conditions in term infants presenting in the earliest days after birth with disturbed neurological function of cerebral origin. NE is aetiologically heterogenous; one cause is peripartum hypoxic ischaemia. Lack of uniformity in the terminology used to describe NE and its diagnostic criteria creates difficulty in the design and interpretation of research and complicates communication with families.

Interobserver Reliability for Identifying Specific Patterns of Placental Injury as Defined by the Amsterdam Classification.

Context.—: Placental pathology is an essential tool for understanding neonatal illness. The recent Amsterdam international consensus has standardized criteria and terminology, providing harmonized data for research and clinical care.

Brain arteriolosclerosis.

Brain arteriolosclerosis (B-ASC), characterized by pathologic arteriolar wall thickening, is a common finding at autopsy in aged persons and is associated with cognitive impairment. Hypertension and diabetes are widely recognized as risk factors for B-ASC. Recent research indicates other and more complex risk factors and pathogenetic mechanisms.

The epidemiology of FIRS in term and late preterm births.

The definition of FIRS requires systemic inflammation and elevated levels of IL-6 in fetal plasma. That definition does not specify how systemic inflammation is to be recognized, and perinatal measurement of IL-6 is not a standard procedure. FIRS has not been examined in a population-based study that included post-neonatal outcome so its incidence and natural history are not known.

The Placenta in Neonatal Encephalopathy: A Case-Control Study.

Objective: We assessed whether specific histologic placental lesions were associated with risk for neonatal encephalopathy, a strong predictor of death or cerebral palsy.

Study Design: Case-control study of singletons with gestational ages ≥35 weeks. Data were abstracted from a prospectively collected database of consecutive births at a hospital in which placental samples from specified sites are collected and stored for all inborn infants.

Electronic fetal monitoring, cerebral palsy, and caesarean section: assumptions versus evidence.

Given evidence that cerebral palsy is not reduced by electronic fetal monitoring, , , and ask why routine monitoring and related litigation continue to contribute to high rates of caesarean births

Does aetiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy influence the outcome of treatment?

Neonatal encephalopathy, a clinical syndrome affecting term-born and late preterm newborn infants, increases the risk of perinatal death and long-term neurological morbidity, especially cerebral palsy. With the advent of therapeutic hypothermia, a treatment designed for hypoxic or ischaemic injury, associated mortality and morbidity rates have decreased. Unfortunately, only about one in eight neonates (95% confidence interval) who meet eligibility criteria for therapeutic cooling apparently benefit from the treatment.

Seizures, encephalopathy, and vaccines: experience in the National Vaccine Injury Compensation Program.

Objectives: To describe the demographic and clinical characteristics of children for whom claims were filed with the National Vaccine Injury Compensation Program (VICP) alleging seizure disorder and/or encephalopathy as a vaccine injury.

Study Design: The National VICP within the Department of Health and Human Services compensates individuals who develop medical problems associated with a covered immunization. We retrospectively reviewed medical records of children younger than 2 years of age with seizures and/or encephalopathy allegedly caused by an immunization, where a claim was filed in the VICP between 1995 through 2005.

Fetal growth restriction and risk of cerebral palsy in singletons born after at least 35 weeks' gestation.

Objective: The objective of the study was to improve the understanding of etiological paths to cerebral palsy (CP) that include fetal growth restriction by examining factors associated with growth restriction that modify CP risk.

Study Design: In a total population of singletons born at or after 35 weeks, there were 493 children with CP and 508 matched controls for whom appropriateness of fetal growth could be estimated. Fetal growth was considered markedly restricted if birthweight was more than 2 SD below optimal for gender, gestation, maternal height, and parity.

Neuroimaging in the evaluation of neonatal encephalopathy.

Background And Objective: Computed tomography (CT) is still used for neuroimaging of infants with known or suspected neurologic disorders. Alternative neuroimaging options that do not expose the immature brain to radiation include MRI and cranial ultrasound. We aim to characterize and compare the use and findings of neuroimaging modalities, especially CT, in infants with neonatal encephalopathy.

Biomarkers S100B and neuron-specific enolase predict outcome in hypothermia-treated encephalopathic newborns*.

Objectives: To evaluate if serum S100B protein and neuron-specific enolase measured during therapeutic hypothermia are predictive of neurodevelopmental outcome at 15 months in children with neonatal encephalopathy.

Design: Prospective longitudinal cohort study.

Setting: A level IV neonatal ICU in a freestanding children's hospital.

Antecedents of cerebral palsy and perinatal death in term and late preterm singletons.

Objective: To examine the antecedents of cerebral palsy and of perinatal death in singletons born at or after 35 weeks of gestation.

Methods: From a total population of singletons born at or after 35 weeks of gestation, we identified 494 with cerebral palsy and 508 neonates in a matched control group, 100 neonatal deaths, and 73 intrapartum stillbirths (all deaths in selected birth years). Neonatal death and cerebral palsy were categorized as without encephalopathy, after neonatal encephalopathy, or after neonatal encephalopathy considered hypoxic-ischemic.

The association of cerebral palsy with birth asphyxia: a definitional quagmire.

Aim: The aim of this study was to investigate whether current literature provides a useful body of evidence reflecting the proportion of cerebral palsy (CP) that is attributable to birth asphyxia.

Method: We identified 23 studies conducted between 1986 and 2010 that provided data on intrapartum risks of CP.

Results: The proportion of CP with birth asphyxia as a precursor (case exposure rate) varied from less than 3% to over 50% in the 23 studies reviewed.

Antecedents of neonatal encephalopathy in the Vermont Oxford Network Encephalopathy Registry.

Background: Neonatal encephalopathy (NE) is a major predictor of death and long-term neurologic disability, but there are few studies of antecedents of NE.

Objectives: To identify antecedents in a large registry of infants who had NE.

Methods: This was a maternal and infant record review of 4165 singleton neonates, gestational age of ≥ 36 weeks, meeting criteria for inclusion in the Vermont Oxford Network Neonatal Encephalopathy Registry.

The Vermont Oxford Neonatal Encephalopathy Registry: rationale, methods, and initial results.

Background: In 2006, the Vermont Oxford Network (VON) established the Neonatal Encephalopathy Registry (NER) to characterize infants born with neonatal encephalopathy, describe evaluations and medical treatments, monitor hypothermic therapy (HT) dissemination, define clinical research questions, and identify opportunities for improved care.

Methods: Eligible infants were ≥ 36 weeks with seizures, altered consciousness (stupor, coma) during the first 72 hours of life, a 5 minute Apgar score of ≤ 3, or receiving HT. Infants with central nervous system birth defects were excluded.

Biomarkers of brain injury in neonatal encephalopathy treated with hypothermia.

Objective: To determine if early serum S100B and neuron-specific enolase (NSE) levels are associated with neuroradiographic and clinical evidence of brain injury in newborns with encephalopathy.

Study Design: Patients who received therapeutic whole-body hypothermia were prospectively enrolled in this observational study. Serum specimens were collected at 0, 12, 24, and 72 hours of cooling.