Volpe's Neurology of the Newborn 2018
DOI: 10.1016/b978-0-323-42876-7.00015-6
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Encephalopathy of Prematurity

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Cited by 13 publications
(13 citation statements)
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“…Infections cause a systemic inflammatory response that disrupts cerebral blood flow via cardiovascular insufficiency and secondary hypoperfusion manifesting as white matter injury. 10 Perinatal encephalitis secondary to viral infections such as human parechovirus, cytomegalovirus, enterovirus, rotavirus, influenza A and B, chikungunya, and herpes simplex virus may demonstrate extensive white matter injury, predominantly in the periventricular regions and often extending into the subcortical white matter. Deep white matter structures such as the internal capsule and the corpus callosum are commonly involved.…”
Section: Children With Stable/nonprogressive Underlying Neurological Disorder Perinatal Infectionsmentioning
confidence: 99%
“…Infections cause a systemic inflammatory response that disrupts cerebral blood flow via cardiovascular insufficiency and secondary hypoperfusion manifesting as white matter injury. 10 Perinatal encephalitis secondary to viral infections such as human parechovirus, cytomegalovirus, enterovirus, rotavirus, influenza A and B, chikungunya, and herpes simplex virus may demonstrate extensive white matter injury, predominantly in the periventricular regions and often extending into the subcortical white matter. Deep white matter structures such as the internal capsule and the corpus callosum are commonly involved.…”
Section: Children With Stable/nonprogressive Underlying Neurological Disorder Perinatal Infectionsmentioning
confidence: 99%
“…Thus, overt focal periventricular necroses are now uncommon, and WMI consists predominately of few or no focal necroses and principally a diffuse lesion in cerebral white matter [9]. The latter includes, initially, death of pre-myelinating oligodendrocytes (pre-OLs) followed by replenishment of the pre-OL pool, but a subsequent impairment of pre-OL maturation (and ultimately, hypomyelination) [3,10]. The pre-OL dysmaturation is considered to lead to (1) axonal dysmaturation, via impaired trophic interactions with pre-OLs, and (2) impaired development of cerebral cortex and thalamus, via anterograde and retrograde trans-synaptic effects caused by the axonal disturbances [3,10].…”
Section: Microglia In Cerebral White Matter Injury and Subsequent Dysmentioning
confidence: 99%
“…The latter includes, initially, death of pre-myelinating oligodendrocytes (pre-OLs) followed by replenishment of the pre-OL pool, but a subsequent impairment of pre-OL maturation (and ultimately, hypomyelination) [3,10]. The pre-OL dysmaturation is considered to lead to (1) axonal dysmaturation, via impaired trophic interactions with pre-OLs, and (2) impaired development of cerebral cortex and thalamus, via anterograde and retrograde trans-synaptic effects caused by the axonal disturbances [3,10]. The key mediators of the critical pre-OL dysmaturation is the marked gliosis that is the hallmark of the diffuse lesion.…”
Section: Microglia In Cerebral White Matter Injury and Subsequent Dysmentioning
confidence: 99%
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“…Looking at the immune system, preterm birth entails a development deficit in all its parts (innate, specific and passively acquired immunity) and that means they have a greater predisposition for the development of infections which can be vertically transmitted from mothers during pregnancy or delivery or horizontally transmitted in NICU for invasive procedures [5]. Sepsis can represent a further risk factor for the development of central nervous system injury [6,7], because the systemic inflammatory state due to infection increases the oxidative stress in cells and in particular in the white matter, where the maturation of neurons and the myelination process interrupt [8].…”
Section: Introductionmentioning
confidence: 99%