Cerebral Venous Malformation as a Cause of Neonatal Intra-Ventricular Haemorrhage and Unexplained Infant Subdural HaemorrhageDavid Talbert*
Imperial College, London, United Kingdom
- *Corresponding Author:
- David Talbert
Imperial College, Institute of Reproductive and Developmental Biology
Imperial College School of Medicine
Queen Charlotte’s Hospital
London W12 ONN, U.K.
E-mail: [email protected]
Received date: February 01, 2016 Accepted date: February 16, 2016 Published date: February 19, 2016
Citation: Talbert D (2016) Cerebral Venous Malformation as a Cause of Neonatal Intra-Ventricular Haemorrhage and Unexplained Infant Subdural Haemorrhage. Anat Physiol 6:202. doi:10.4172/2161-0940.1000202
Copyright: © 2016 Talbert D. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
An Intra-ventricular Haemorrhage (IVH) is a bleeding into the brain’s ventricular system. Most intra-ventricular haemorrhages occur in the first 72 hours after birth. They originate in a layer of tissue (Germinal Matrix), under the lining of the ventricles (Ependymal), while it is in the process of manufacturing neurons and glia. This has normally regressed by term but may still be active in premature infants. Pathological investigations have found accumulations of peri-venous plasma and blood suggesting that excessive cerebral venous pressure has disrupted vessels, initiating the intra-ventricular bleeding observed. This has led to unsuccessful searches for evidence of A-V shunts within the developing cerebrum, or loss of auto regulation in arterioles, producing excessive cerebral venous hypertension.
An alternative mechanism , reported here, is of venous rather than arterial origin; that high venous pressure results from inadequate venous drainage. Forcing increasing cerebral flow through inadequate venous vasculature requires increasing cerebral venous pressure. This is particularly significant at birth when the brain is suddenly stimulated to widespread activity which requires increased blood flow. This would explain why this disorder occurs shortly after birth. However, if rising cerebral pressure is insufficient to cause damage at birth, the infant may survive with a chronically high cerebral venous pressure. Then, minor stresses such as short falls, vomiting in pyloric stenosis, violent coughing, etc., may provide sufficient extra pressure to initiate haemorrhaging.
In the embryo the pattern of arteries is pre-programmed, but veins climb gas gradients and their normal patterns are quite variable. Neonatal intra-ventricular haemorrhage is typically highly asymmetrical, and a typical inappropriate venous pattern is described. Recognition of inadequate venous patterns may not benefit the infant itself, but may protect any siblings from loss of home and parents.