Mechanisms of hydrocephalus after neonatal and adult intraventricular hemorrhage

Abstract

Intraventricular hemorrhage (IVH) is a cause of significant morbidity and mortality and is an independent predictor of a worse outcome in intracerebral hemorrhage (ICH) and germinal matrix hemorrhage (GMH). IVH may result in both injuries to the brain as well as hydrocephalus. This paper reviews evidence on the mechanisms and potential treatments for IVH-induced hydrocephalus. One frequently cited theory to explain hydrocephalus after IVH involves obliteration of the arachnoid villi by microthrombi with subsequent inflammation and fibrosis causing CSF outflow obstruction. Although there is some evidence to support this theory, there may be other mechanisms involved, which contribute to the development of hydrocephalus. It is also unclear whether the causes of acute and chronic hydrocephalus after hemorrhage occur via different mechanisms; mechanical obstruction by blood in the former, and inflammation and fibrosis in the latter. Management of IVH and strategies for prevention of brain injury and hydrocephalus are areas requiring further study. A better understanding of the pathogenesis of hydrocephalus after IVH, may lead to improved strategies to prevent and treat post-hemorrhagic hydrocephalus.

Figure 1

Cranial ultrasound showing grade IV germinal matrix hemorrhage-intraventricular hemorrhage.

Figure 2

T2 weighted MRI scans (coronal brain sections) at day 1 after saline injection and IVH, and the time-course of lateral ventricular volume changes. Values are mean ±S.D., n=7, #p<0.01 vs. saline group. Figure reprinted with permission from Chen et al., Stroke 2011;42:465–470.

Figure 3

(A) T2* weighted MRI scans (coronal sections) at day 1 and day 28 after IVH, and the time-course of the T2* lesion (hypodensity) after IVH. Values are expressed as the means ± S.D., n=7. (B) Time course of non-heme brain tissue iron in the left and right hemisphere after IVH. Values are mean ± S.D., n=6, *p<0.05 vs. saline control (same time point) and day 1. Figure reprinted with permission from Chen et al., Stroke 2011;42:465–470.

Figure 4

(A) Immunoreactivity of ferritin in the hippocampus and the periventricular area day 28 after IVH or saline control. Scale bar = 20 μm. (B) Time course of ferritin levels in the hippocampus. (C) Time course of ferritin levels in the periventricular area. Values are mean ± SD, n=3~7 in saline group and n=5~7 in IVH group, *p<0.05 and #p<0.01 vs. saline group. Figure reprinted with permission from Chen et al., Stroke 2011;42:465–470.

Figure 5

Outline of some of the injury pathways that may be initiated by an intraventricular hemorrhage. SVZ = subventricular zone