Abstract
Hypoxic-ischemic encephalopathy (HIE) is the most important cause of cerebral damage and long-term neurological sequelae in the perinatal period both in term and preterm infant.Hypoxic-ischemic (H-I) injuries develop in two phases: the ischemic phase, dominated by necrotic processes, and the reperfusion phase, dominated by apoptotic processes extending beyond ischemic areas. Due to selective ischemic vulnerability, cerebral damage affects gray matter in term newborns and white matter in preterm newborns with the typical neuropathological aspects of laminar cortical necrosis in the former and periventricular leukomalacia in the latter.This article summarises the principal physiopathological and biochemical processes leading to necrosis and/or apoptosis of neuronal and glial cells and reports recent insights into some endogenous and exogenous cellular and molecular mechanisms aimed at repairing H-I cerebral damage.
Highlights
Hypoxic-ischemic encephalopathy (HIE) is the most important cause of cerebral damage and long-term neurological sequelae in the perinatal period both in term and preterm infant [1].Until few years ago, the main acquisitions on the physiopathogenetic mechanisms of this affection came from experimental studies on animals
The main acquisitions on the physiopathogenetic mechanisms of this affection came from experimental studies on animals
In presence of impaired autoregulation, cerebral blood flow (CBF) becomes passive to pressure stimuli. In this way, rising pressure increases CBF and can cause haemorrhagic phenomena, while low pressure reduces CBF and can cause ischemic phenomena. It has to be kept in mind that systemic arterial hypotension is frequent in high-degree premature infants who present cardiac contractile function and sympathetic vascular tone immaturity, and in all newborns with perinatal asphyxia, resulting from impaired myocardial contractility induced by hypoxia and acidosis [5]
Summary
Hypoxic-ischemic encephalopathy (HIE) is the most important cause of cerebral damage and long-term neurological sequelae in the perinatal period both in term and preterm infant [1]. In addition to the peculiarity of periventricular arterial vascularisation, PVL is favoured by other factors related to prematurity such as metabolic hyperactivity of periventricular encephalic areas - where intense processes of proliferation, differentiation and migration of glial and neuronal cells occur, raising oxygen and nutrients demand and, above all, the particular vulnerability of immature oligodendrocytes to the oxidative stress due to their poor content of anti-oxidizing enzymes [18,19] Another important role is played by the lack of neuroprotective factors such as neurotrophines and oligotrophines that are trophic substances capable of supporting brain development and inhibiting apoptotic phenomena. If all these observations are confirmed by further systematic studies in the coming years, it is possible to speculate that, intravenous delivery of the milieu of factors secreted by ASC at 24-72 hours after H-I injury may represent a new promising therapeutic strategy for treatment of human neonatal HIE in addition to hypothermia that, currently, represents the most efficacious option for preventing or attenuating cerebral damage [60]
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