Problems with definitions and classifications of newborn encephalopathy

doi:10.1016/0887-8994(92)90026-U

Pediatric Neurology

Volume 8, Issue 2, March–April 1992, Pages 85-90

https://doi.org/10.1016/0887-8994(92)90026-U Get rights and content

Abstract

Encephalopathy in the newborn has been classified in a manner suggesting that the etiology is known, such as hypoxic-ischemic and post-asphyxial encephalopathy. In the absence of evidence that most cases of newborn encephalopathy reflect these phenomena, we prefer the simple, descriptive terms, neonatal or newborn encephalopathy. Qualitative and quantitative grading schemes are described in this review and some of their potentially correctable limitations are discussed. The ideal grading scheme continues to be an unattained goal.

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Cited by (84)

The Placenta in Neonatal Encephalopathy: A Case–Control Study
2018, Journal of Pediatrics
We assessed whether specific histologic placental lesions were associated with risk for neonatal encephalopathy, a strong predictor of death or cerebral palsy.
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. Placentas of infants with neonatal encephalopathy were compared with randomly selected control infants (ratio of 1:3). Placental histologic slides were read by a single experienced perinatal pathologist unaware of case status, using internationally recommended definitions and terminology. Findings were grouped into inflammatory, maternal, or fetal vascular malperfusion (FVM) and other lesions.
Placental samples were available for 73 of 87 (84%) cases and 253 of 261 (97%) controls. Delivery complications and gross placental abnormalities were more common in cases, of whom 4 died. Inflammation and maternal vascular malperfusion did not differ, and findings consistent with global FVM were more frequent in case (20%) than control (7%) placentas (P = .001). There was a trend toward more segmental FVM and high-grade FVM (fetal thrombotic vasculopathy) among cases. Some type of FVM was observed in 24% of placentas with neonatal encephalopathy. In infants with both neonatal encephalopathy and placental FVM, more often than in infants with neonatal encephalopathy without FVM, electronic fetal monitoring tracings were considered possibly or definitely abnormal (P = .028).
Vascular malperfusion of subacute or chronic origin on the fetal side of the placenta was associated with increased risk of neonatal encephalopathy.
Ischemic brain injury: New insights on the protective role of melatonin
2017, Free Radical Biology and Medicine
Stroke represents one of the most common causes of brain's vulnerability for many millions of people worldwide. The plethora of physiopathological events associated with brain ischemia are regulate through multiple signaling pathways leading to the activation of oxidative stress process, Ca²⁺ dyshomeostasis, mitochondrial dysfunction, proinflammatory mediators, excitotoxicity and/or programmed neuronal cell death. Understanding this cascade of molecular events is mandatory in order to develop new therapeutic strategies for stroke. In this review article, we have highlighted the pleiotropic effects of melatonin to counteract the multiple processes of the ischemic cascade. Additionally, experimental evidence supports its actions to ameliorate ischemic long-term behavioural and neuronal deficits, preserving the functional integrity of the blood-brain barrier, inducing neurogenesis and cell proliferation through receptor-dependent mechanism, as well as improving synaptic transmission. Consequently, the synthesis of melatonin derivatives designed as new multitarget-directed products has focused a great interest in this area. This latter has been reinforced by the low cost of melatonin and its reduced toxicity. Furthermore, its spectrum of usages seems to be wide and with the potential for improving human health. Nevertheless, the molecular and cellular mechanisms underlying melatonin´s actions need to be further exploration and accordingly, new clinical studies should be conducted in human patients with ischemic brain pathologies.
Why the term neonatal encephalopathy should be preferred over neonatal hypoxic-ischemic encephalopathy
2013, American Journal of Obstetrics and Gynecology
The unresponsiveness of the full-term newborn is sometimes attributed to asphyxia, even when no severe physiologic disturbance occurred during labor and delivery. The controversy about whether to use the name “hypoxic-ischemic encephalopathy” or “newborn encephalopathy” has recently flared in publications directed toward pediatricians and neurologists. In this clinic opinion piece, I discuss the importance to obstetricians of this decision and explain why “newborn encephalopathy” should be the default term.
White matter and cortical injury in hypoxic-ischemic encephalopathy: Antecedent factors and 2-year outcome
2012, Journal of Pediatrics
To examine the spectrum of isolated white matter (WM)/cortical injury and its relation to outcomes in infants with hypoxic-ischemic encephalopathy (HIE) and normal appearing basal ganglia and thalami.
From 1992-2007, 84 term infants with HIE and normal basal ganglia and thalami on neonatal magnetic resonance imaging were studied; WM/cortical lesions were classified by site and severity. Neurodevelopmental outcomes and head growth were documented at a median age of 2 years.
The WM was normal or mildly abnormal in 33.5%, moderate in 40.5%, and severely abnormal in 26% of infants. Cortical involvement was not seen or was only mild in 75.5%, moderate in 13%, and severe in 12% of infants. WM and cortical injury severity were highly correlated (Spearman ρ = 0.74; P < .001). Infants with severe WM injury had more severe neonatal courses and a higher incidence of hypoglycemia. No infant died. Five infants (6%) developed cerebral palsy but all could walk independently. Cognitive, visual, language, behavioral, and seizure problems were highly prevalent and correlated significantly with the severity of WM injury and poor postnatal head growth.
Infants with HIE and selective WM/cortical injury have a low prevalence of cerebral palsy but have a wide range of other problems, which occur more often with severe WM/cortical lesions.
Feeding and communication impairments in infants with central grey matter lesions following perinatal hypoxic-ischaemic injury
2012, European Journal of Paediatric Neurology
Basal ganglia and thalamic (BGT) injury is common after acute perinatal hypoxia–ischaemia. Cerebral palsy is the most obvious consequence of BGT injury affecting 70–75% of survivors and is predictable from neonatal magnetic resonance imaging (MRI). However there is no equivalent predictive data for other specific outcomes. Feeding and communication impairments are also common in children following hypoxic–ischaemic encephalopathy (HIE) and BGT injury.
To describe, in infants with HIE and BGT injury, the prevalence of feeding and communication impairments; and to evaluate the accuracy of early MRI for predicting these outcomes.
175 term infants with HIE and BGT injury were studied. Brain lesions were classified by site and severity from the MRI scans. Motor, feeding and communication impairments were documented at 2 years.
Feeding and communication impairments occurred in 65% and 82% of 126 survivors respectively and related strongly to the severity of motor impairment. Forty-one children had a gastrostomy or long-term nasogastric tube. Injury severity in all brain regions was significantly associated with feeding and communication impairment on univariate analysis. On logistic regression analysis BGT (OR 10.9) and mesencephalic lesions (OR 3.7) were independently associated with feeding impairment; BGT (OR 10.5) and pontine lesions (OR 3.8) were associated with gastrostomy; the severity of BGT lesions (OR 20.1) was related to the severity of communication impairment.
Feeding and communication impairment are very common in children with BGT and brainstem injury of neonatal origin and can be well predicted from early MRI scans.
Lasting mesothalamic dopamine imbalance and altered exploratory behavior in rats after a mild neonatal hypoxic event
2023, Frontiers in Integrative Neuroscience

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^☆: Supported in part by a grant from the National Institute of Neurological and Communicative Disorders and Stroke (NS 20658) and a Mental Retardation Center Grant from the National Institute of Child Health and Human Development (HD 06276).

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Review articleProblems with definitions and classifications of newborn encephalopathy☆

Abstract

Am J Obstet Gynecol

Early Hum Dev

Pediatr Neurol

Pediatr Neurol

J Pediatr

J Pediatr

Pediatr Clin North Am

J Pediatr

Lancet

Lancet

Early Hum Dev

Early Hum Dev

Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study

Arch Neurol

Birth asphyxia in the fullterm newborn: Early assessment and outcome

Dev Med Child Neurol

Hypoxic-ischaemic encephalopathy in the newborn

Arch Neurol

Use of calcium-channel blocker after severe asphyxia

Dev Med Child Neurol

Current and potentially new management strategies for perinatal hypoxic-ischemic encephalopathy

Pediatrics

Neurological aspects of perinatal asphyxia

Dev Med Child Neurol

Jitteriness in full-term neonates: Prevalence and correlaries

Pediatrics

The asymptomatic newborn and risk of cerebral palsy

Am J Dis Child

Bias in treatment assignment in controlled clinical trials

N Engl J Med

Review article
Problems with definitions and classifications of newborn encephalopathy☆