VENOUS ARCHITECTURE OF CEREBRAL HEMISPHERIC WHITE-MATTER AND COMMENTSON PATHOGENESIS OF MEDULLARY VENOUS AND OTHER CEREBRAL VASCULAR MALFORMATIONS

Citation
Yp. Huang et al., VENOUS ARCHITECTURE OF CEREBRAL HEMISPHERIC WHITE-MATTER AND COMMENTSON PATHOGENESIS OF MEDULLARY VENOUS AND OTHER CEREBRAL VASCULAR MALFORMATIONS, The Mount Sinai journal of medicine, 64(3), 1997, pp. 197-206
Citations number
11
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00272507
Volume
64
Issue
3
Year of publication
1997
Pages
197 - 206
Database
ISI
SICI code
0027-2507(1997)64:3<197:VAOCHW>2.0.ZU;2-5
Abstract
The parenchymal veins, especially the deep medullary veins, of the cer ebral hemispheres were studied in detail by analyzing the stereoroentg enograms of multiple brain slices of postmortem injected brain specime ns (injected into the internal carotid arteries in 17 cases and into t he jugular veins in 12 cases). The presence of four zones-the first (o r outer), the second (or candelabra), the third (or palmate) and the f ourth (or subependymal) zone-of venous convergence was confirmed withi n the centrum semiovale, particularly in the frontoparietal area. Othe r venous convergences such as those related to the optic radiation in the para-atrial area were also found. Arterial branching zones were al so observed in the areas similar to those of the medullary veins. It a ppears that these converging zones are created by rapidly growing cros sing nerve fiber tracts, i.e., projection, commissural, and associatio n fibers which grow rapidly during intrauterine and postnatal life. Pa thogenesis of medullary venous malformation is also discussed from ana tomical viewpoint, venoarchitecture of the pial, parenchymal, and sube pendymal veins and of the dural venous sinuses. The possibility of a s imilar mechanism (partial, mild, repetitive venoocclusive disease deve loping over a long period with fluctuating venous pressure) leading to formation of most (if not all) cases of medullary venous malformation and in some, if not many, cases of cerebral vascular malformations [a side from gene abnormality (chromosome 7) in familial cavernous angiom atosis, particularly in Hispanic American or other familial hereditary conditions] has been postulated.