The search for human telencephalic ventriculofugal arteries

Nelson, M.D.Jr; Gonzalez Gomez, I.; Gilles, F.H.

Ajnr 12(2): 215-222

1991


Accession: 007934450

Download citation:  
Text
  |  
BibTeX
  |  
RIS

Article/Abstract emailed within 1 workday
Payments are secure & encrypted
Powered by Stripe
Powered by PayPal

Abstract
Our study traced the vascular development of the fetal telencephalon in the last two trimesters of gestation and the first 15 years of life in 60 fetal and childhood brains. We filled the macro- and microvascular beds with Microfil and made stereoscopic observations of cleared 0.5- to 1.0-cm-thick sections. Separately, we identified developing vascular structures histologically. In our youngest specimen (16-weeks gestation), transcerebral channels with walls consisting of a single layer of endothelium and varying in diameter from 10 to 50 .mu.m originated from leptomeningeal arteries and veins at right angles to the surface and passed through the cortical plate (future cortex). They branched at varying depths within the mantle and germinal matrix surrounding the lateral ventricles. At deeper levels the channels freely anastomosed with each other. A cortical microvascular network did not appear until 22 to 24 weeks. The new endothelial channels were derived from leptomeningeal vessels and from larger transcerebral channels. Most regions of isocortex developed a microvascular plexus simultaneously, regardless of degree of maturation. Striatal channels matured earlier than extrastriatal channels, having developed a muscularis to within 100 .mu.m of the ganglionic eminence by 22- to 24-weeks gestation. Maturation of the vascular walls of extrastriatal channels into proper arteries and veins occurred during the first postnatal year. Anastomotic channels were present throughout the leptomeningeal, striatal, and extrastriatal regions in all of our specimens from 16 weeks gestation to 15 years old. Our study does not support the existence of ventriculofugal arteries and deep white matter arterial border zones in the human fetus and neonate, which have been postulated to be the basis of "periventricular" leukomalacia.