Neonatal brain hemorrhage (NBH) of prematurity: translational mechanisms of the vascular-neural network

Abstract

Neonatal brain hemorrhage (NBH) of prematurity is an unfortunate consequence of preterm birth. Complications result in shunt dependence and long-term structural changes such as posthemorrhagic hydrocephalus, periventricular leukomalacia, gliosis, and neurological dysfunction. Several animal models are available to study this condition, and many basic mechanisms, etiological factors, and outcome consequences, are becoming understood. NBH is an important clinical condition, of which treatment may potentially circumvent shunt complication, and improve functional recovery (cerebral palsy, and cognitive impairments). This review highlights key pathophysiological findings of the neonatal vascular-neural network in the context of molecular mechanisms targeting the posthemorrhagic hydrocephalus affecting this vulnerable infant population.

Fig. (1). CSF accumulation and ventriculomegaly 7 days after neonatal brain hemorrhage induction depicted by imaging

Magnetic resonance imaging (MRI) was used to evaluate injury progression in sham and vehicle P14 rat pups 7 days after NBH induction. These images suggest hydrocephalus development commences as early as 1 week following NBH induction. (A) T2-weighted MRI (top row) depicts CSF accumulation (hyperintense T2-signal marked with an asterisk) and ventriculomegaly. Susceptibility weighted imaging SWI (bottom row) depicts clots within the periventricular region (hypointense signal marked with arrows). Sham animals did not have any visible brain injury. T2-weighted MRI depicting (B) coronal, (C) axial and (D) sagittal cross-sections of NBH animal depicting CSF accumulation, ventriculomegaly, and minor midline shift.