Many factors play a role in the increased susceptibility of the premature to both IVH and PVL. But to appreciate the fundamental difference between the two, it is critical to understand the vascular supply of the premature brain.
From 24-32 weeks, arteries traverse the brain from the outer pial surface ending in the deep white matter near the ventricular surface. These long penetrators are few in number with only occasional connections to each other. This results in periventricular end zones which are very vulnerable to decreases in cerebral blood flow (CBF) and perfusion pressure. These end zones correlate with the sites of focal cystic PVL.
In addition, these long penetrators have infrequent anastomoses with the short penetrators, also coming from the pial surface. This creates border zones between the short and long arteries that are also susceptible to ischemia. These border zones correspond to areas of DWMI.
PVL, then is an arterial, ischemic lesion. Its distribution follows the distribution of the arterial supply to the premature brain. From 32 weeks to term, both the number of arteries and the anastomoses between them increases, leading to less potentially ischemic areas and as a result less PVL of either type.
Interestingly, parasagittal cerebral injury, the characteristic lesion of fullterms with hypoxia-ischemia almost never occurs in the premature. This lesion of cortical gray matter and subcortical white matter is caused by ischemia in the watershed areas between the main surface arteries of the brain. The premature has extensive anastomoses between the anterior, middle and posterior cerebral arteries which do not regress until near term. Therefore, the premature's area of ischemic vulnerability is much different than that of the term baby.