The anatomy of collateral venous flow from the brain and its value in aetiological interpretation of intracranial pathology
- PMID: 8912316
- DOI: 10.1007/s002340050321
The anatomy of collateral venous flow from the brain and its value in aetiological interpretation of intracranial pathology
Abstract
For more than a century, available data concerning collateral venous outflow from the brain have received insufficient attention, as existing theories did not assign practical importance to them. Ideas concerning arterial blood supply and circulation of cerebrospinal fluid were considered more relevant. But available data afford a schematic model of cerebral venous outflow that does have important pathophysiological consequences. Principal outflow through the internal jugular veins can be substituted completely by the large vertebral plexuses, through communications at the cranial base. Emissary veins of the skull vault are small and few in number. Outflow from the deep venous system through the great vein of Galen can be substituted by choroidal, thalamic and striate anastomoses toward the basal vein. So-called intracerebral venous anastomoses through the centrum semiovale towards the convexity are nonexistent or negligible. Instead, a venous watershed exists separating paraventricular white matter from a layer of subcortical white matter. In most infants, the cavernous sinus is not yet connected to the cerebral veins. Once such communications have been formed, important collateral pathways exist through basal and Sylvian veins via the cavernous sinus to the pterygoid plexuses. Simultaneous hindrance of principal and collateral venous outflow will lead to elevated venous pressure and eventual insufficiency of cerebral blood flow (CBF). This will cause increased intracranial pressure, and ventricular enlargement due to periventricular atrophy. The slow phase of the two-compartment model of CBF coincides with the paraventricular white matter area of the deep venous system. In the neonate CBF was found to be still very low, and in the two compartments CBF increases at a different rate to a maximum in childhood. In hydrocephalus, measurement of CBF in the slow deep compartment, rather than the fast cortical one, will be most informative.
Similar articles
-
Consequences of the anatomy of deep venous outflow from the brain.Neuroradiology. 1999 Apr;41(4):233-41. doi: 10.1007/s002340050739. Neuroradiology. 1999. PMID: 10344506 Review.
-
Intracranial venous pressures, hydrocephalus and effects of cerebrospinal fluid shunts.Childs Nerv Syst. 1989 Oct;5(5):318-23. doi: 10.1007/BF00274522. Childs Nerv Syst. 1989. PMID: 2805004
-
Hyperemic hydrocephalus: a new form of childhood hydrocephalus analogous to hyperemic intracranial hypertension in adults.J Neurosurg Pediatr. 2010 Jan;5(1):20-6. doi: 10.3171/2009.8.PEDS09204. J Neurosurg Pediatr. 2010. PMID: 20043733
-
Spring-assisted cranial vault expansion in the setting of multisutural craniosynostosis and anomalous venous drainage: case report.J Neurosurg Pediatr. 2015 Jul;16(1):80-5. doi: 10.3171/2014.12.PEDS14604. Epub 2015 Apr 10. J Neurosurg Pediatr. 2015. PMID: 25860985
-
The relationship of intracranial venous pressure to hydrocephalus.Childs Nerv Syst. 1994 Jan;10(1):29-35. doi: 10.1007/BF00313582. Childs Nerv Syst. 1994. PMID: 8194060 Review.
Cited by
-
Predicting factors for the follow-up outcome and management decisions in vein of Galen aneurysmal malformations.Childs Nerv Syst. 2010 Jan;26(1):35-46. doi: 10.1007/s00381-009-0959-7. Epub 2009 Aug 7. Childs Nerv Syst. 2010. PMID: 19662427
-
Anatomic variations of the deep cerebral veins,tributaries of Basal vein of rosenthal: embryologic aspects of the regressed embryonic tentorial sinus.Interv Neuroradiol. 2005 Jun 30;11(2):123-30. doi: 10.1177/159101990501100202. Epub 2005 Oct 25. Interv Neuroradiol. 2005. PMID: 20584491 Free PMC article.
-
Multimodality imaging of cortical and white matter abnormalities in Sturge-Weber syndrome.AJNR Am J Neuroradiol. 2007 May;28(5):900-6. AJNR Am J Neuroradiol. 2007. PMID: 17494666 Free PMC article.
-
Focal venous hypertension as a pathophysiologic mechanism for tissue hypertrophy, port-wine stains, the Sturge-Weber syndrome, and related disorders: proof of concept with novel hypothesis for underlying etiological cause (an American Ophthalmological Society thesis).Trans Am Ophthalmol Soc. 2013 Sep;111:180-215. Trans Am Ophthalmol Soc. 2013. PMID: 24385674 Free PMC article.
-
Diagnostic pitfall: atypical cerebral venous drainage via the vertebral venous system.AJNR Am J Neuroradiol. 2002 Mar;23(3):408-11. AJNR Am J Neuroradiol. 2002. PMID: 11901009 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Medical