Mechanisms of neuroinflammation in hydrocephalus after intraventricular hemorrhage: a review

Intraventricular hemorrhage (IVH) is a significant cause of morbidity and mortality in both neonatal and adult populations. IVH not only causes immediate damage to surrounding structures by way of mass effect and elevated intracranial pressure; the subsequent inflammation causes additional brain injury and edema. Of those neonates who experience severe IVH, 25-30% will go on to develop post-hemorrhagic hydrocephalus (PHH). PHH places neonates and adults at risk for white matter injury, seizures, and death. Unfortunately, the molecular determinants of PHH are not well understood. Within the past decade an emphasis has been placed on neuroinflammation in IVH and PHH. More information has come to light regarding inflammation-induced fibrosis and cerebrospinal fluid hypersecretion in response to IVH. The aim of this review is to discuss the role of neuroinflammation involving clot-derived neuroinflammatory factors including hemoglobin/iron, peroxiredoxin-2 and thrombin, as well as macrophages/microglia, cytokines and complement in the development of PHH. Understanding the mechanisms of neuroinflammation after IVH may highlight potential novel therapeutic targets for PHH.

Automated summary

Intraventricular hemorrhage (IVH) is a significant cause of morbidity and mortality in both neonatal and adult populations. The subsequent inflammation caused by IVH not only leads to additional brain injury and edema, but also places individuals at risk for white matter injury, seizures, and death. Understanding the mechanisms of neuroinflammation after IVH may highlight potential novel therapeutic targets for post-hemorrhagic hydrocephalus (PHH).