Brain injury in premature infants: a complex amalgam of destructive and developmental disturbances

Abstract

Brain injury in premature infants is of enormous public health importance because of the large number of such infants who survive with serious neurodevelopmental disability, including major cognitive deficits and motor disability. This type of brain injury is generally thought to consist primarily of periventricular leukomalacia (PVL), a distinctive form of cerebral white matter injury. Important new work shows that PVL is frequently accompanied by neuronal/axonal disease, affecting the cerebral white matter, thalamus, basal ganglia, cerebral cortex, brain stem, and cerebellum. This constellation of PVL and neuronal/axonal disease is sufficiently distinctive to be termed “encephalopathy of prematurity”. The thesis of this Review is that the encephalopathy of prematurity is a complex amalgam of primary destructive disease and secondary maturational and trophic disturbances. This Review integrates the fascinating confluence of new insights into both brain injury and brain development during the human premature period.

The emergence of functional architecture during early brain development

“…During the waiting period, which lasts approximately four weeks, afferents receive instructive input and start projecting onto their cortical targets. Concurrently, the corpus callosum extends in an anterior to posterior fashion (Huang et al, 2009(Huang et al, , 2006, first synapsing on neurons in the transient subplate zone before establishing its definitive connections in the cortical plate (Kostovic and Jovanov-Milosevic, 2006;Volpe, 2009). Once thalamocortical connections are established, which has been noted to occur between 24-32 PCW (Figure 2), sensory stimuli including visual and auditory input can reach the developing cortex (Kostovic and Jovanov-Milosevic, 2006).…”

“…Thalamocortical and corticothalamic fibers form transient circuits with subplate neurons before growing into the developing cortex and thalamus respectively (Kostovic and Jovanov-Milosevic, 2006;Volpe, 2009). The subplate is located below the cortical plate and serves as a 'waiting' compartment for afferent fibers.…”

Cortical folding of the preterm brain: a longitudinal analysis of extremely preterm born neonates using spectral matching

“…Recently, there has been much interest in understanding changes in altered brain development during the preterm period (Volpe 2009). Boardman et al.…”

À propos du développement cérébral des prématurés

“…Trois hypothèses sont actuellement en concurrence pour expliquer ces altérations et, notamment, la réduction du volume cortical observée chez les prématurés par rapport aux témoins du même âge : (1) la dégénérescence neuronale primaire, éventuellement accompagnée d'une dégé-nérescence secondaire rétrograde provoquée par des lésions de la matière blanche [6] ; (2) l'altération du mécanisme de maturation neuronale normal [7] ; et (3) l'altération de la croissance des zones thalamiques du cerveau [8].…”

“…Ainsi, celles-ci sont plus élevées aux premiers stades du développement car la majorité des processus de la matu- Ces dernières années, nombres d'études ont pointé du doigt une association entre syndrome métabolique et processus inflammatoire [4][5][6][7]. En effet, la prise de poids s'accompagne d'une inflammation des tissus et, plus particulièrement, du tissu adipeux blanc [6,[8][9][10]15]. Cette inflammation entraîne une production importante de facteurs pro-inflammatoires comme le TNF-α (tumor necrosis factor-a), le MCP1 (monocyte chemotactic protein 1) et une diminution des adi-…”