Mechanisms of neuroinflammation in hydrocephalus after intraventricular hemorrhage: a review

Abstract

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.

Hydrocephalus As Possible Prodromal Manifestation of COVID-19: A Report of Two Cases

“…Despite NPH has been first described in the 1960s [4], its pathophysiology has been only partly explained. In particular, in recent years several studies have highlighted the role of neuro-inflammation in the genesis of NPH, both in the idiopathic [5][6][7][8] and in post-hemorrhagic secondary forms [9,10].…”

The mechanism of microglia-mediated immune inflammation in ischemic stroke and the role of natural botanical components in regulating microglia: A review

“…Cerebral ischemia results in dramatic changes in the morphology, density, and function of branched microglia, including processes such as cell body enlargement, debranching, and cell wall thickening. It eventually becomes "amebic", produces inflammatory proteins, and undergoes changes in proliferation, migration, and phagocytosis (88). Because m i c r o g l i a a n d b l o o d -m i g r a t i n g m a c r o p h a g e s a r e morphologically indistinguishable and perform similar functions, they are represented as microglia/macrophages in many studies.…”

A year in review: brain barriers and brain fluids research in 2022

“…Blood products in the ventricles are suspected to be responsible for the dilatation and Miller et al [ 129 ] have shown that hemoglobin injected into the ventricles of neonatal rats can induce hydrocephalus. Neuroinflammation is also involved in IVH-induced hydrocephalus (reviewed in [ 130 ]). Inflammatory markers in the CSF are associated with hypersecretion of CSF via hyperactivity of choroid plexus transporters, raising the potential for future pharmaceutical treatment [ 43 ].…”