Embryological basis of some aspects of cerebral vascular fistulas and malformations

Sean Mullan M.D., D.Sc., Saeid Mojtahedi M.D., Douglas L. Johnson M.D., Ph.D. and R. Loch Macdonald M.D., Ph.D.
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✓ The literature on the formation of cerebral veins is reviewed to obtain a better understanding of some cerebrovascular anomalies. Clinical observations such as the entry of the superior ophthalmic vein into the cavernous sinus through the inferior rather than the superior orbital fissure, the relative infrequency of middle cerebral vein backflow in the presence of an extensive cavernous fistula, and the relative infrequency of hemorrhage in relation to the inferior petrosal fistula all relate to the persistence of an older venous pathway. The frequent occurrence of hemorrhage in association with the superior petrosal sinus fistula and the frequent failure of the superior petrosal sinus to connect to the cavernous sinus similarly have an embryological explanation. The frequent association of the vein of Galen aneurysm and an absent or deformed straight sinus probably relates to the time at which the paired internal cerebral veins fuse into one channel. It is speculated that the origins of cerebral venous malformations (CVMs) and arteriovenous malformations (AVMs) probably relate to sequential formation and absorption of surface veins, which occur in human embryonic development mainly in the 40- to 80-mm length interval, although persistent AVM growth is possible even after birth. The frequent absence or anomaly of the middle cerebral vein and its failure to communicate with the cavernous sinus in the presence of both CVMs and AVMs are linked to the late development of that vein and to its even later connection to the cavernous sinus.

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Contributor Notes

Address reprint requests to: Sean Mullan, M.D., The University of Chicago, Section of Neurosurgery, 5841 South Maryland Avenue, Chicago, Illinois 60637.
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