Preterm brain Injury: White matter injury

Abstract

Despite the advances in neonatal intensive care, the preterm brain remains vulnerable to white matter injury (WMI) and disruption of normal brain development (i.e., dysmaturation). Compared to severe cystic WMI encountered in the past decades, contemporary cohorts of preterm neonates experience milder WMIs. More than destructive lesions, disruption of the normal developmental trajectory of cellular elements of the white and the gray matter occurs. In the acute phase, in response to hypoxia-ischemia and/or infection and inflammation, multifocal areas of necrosis within the periventricular white matter involve all cellular elements. Later, chronic WMI is characterized by diffuse WMI with aberrant regeneration of oligodendrocytes, which fail to mature to myelinating oligodendrocytes, leading to myelination disturbances. Complete neuronal degeneration classically accompanies necrotic white matter lesions, while altered neurogenesis, represented by a reduction of the dendritic arbor and synapse formation, is observed in response to diffuse WMI. Neuroimaging studies now provide more insight in assessing both injury and dysmaturation of both gray and white matter. Preterm brain injury remains an important cause of neurodevelopmental disabilities, which are still observed in up to 50% of the preterm survivors and take the form of a complex combination of motor, cognitive, and behavioral concerns.

Keywords: Brain maturation; Dysmaturation; Oligodendrocyte; Periventricular leukomalacia; White matter injury.