van Overbeeke J J, Hillen B, Vermeij-Keers C
Department of Neurosurgery, Academic Medical Centre, Amsterdam, The Netherlands.
J Anat. 1994 Aug;185 ( Pt 1)(Pt 1):51-63.
The mechanisms by which the anatomical variations of the circle of Willis develop is considered to be related to haemodynamic factors, i.e. the differential growth of the various parts of the brain will continuously change the haemodynamic demands and consequently the flow patterns in the cerebral arteries. It is therefore to be expected that, if a selected part of the brain does not develop, the change in the haemodynamic demand will affect the development of some cerebral arteries. Consequently the arteries at the base of 2 arhinencephalic and 8 holoprosencephalic brains were studied in conjunction with the brain malformations. The defects of holoprosencephaly are believed to arise from a failure of the prosencephalon to separate fully into the telencephalon and diencephalon and become manifest at the time that the prosencephalon normally starts to separate into the hemispheres, i.e. 28-34 d p.c. Arhinencephalic brains are fully diverticulated. There is only a partial or complete agenesis of the olfactory tracts and bulbs. The defect causing arhinencephaly starts at 43 d p.c. In the arhinencephalic brains no particular vascular abnormalities were found. However, at the base of the holoprosencephalic brains no complete circle of Willis was present; the anterior part was lacking and was replaced by anterior branches which emerged unilaterally or bilaterally from the internal carotid artery. The choroidal arteries were of very large calibre and ran to the highly vascularised wall of the dorsal cyst which is usually present in holoprosencephalic brains. In contrast to the anterior part, the posterior arterial pattern was almost identical to the posterior part of the circle of Willis of normal brains. The basic vascular patterns found in the holoprosencephalic brains displayed the features of Padget's developmental stages 2 and 3 of the cerebral vasculature, i.e. the pattern that has normally developed within 28-40 d p.c. The further modification of this pattern could largely be understood from the functional demand imposed on the circulation by the enlarged anterior choroidal arteries. Because the development of the anterior part of the circle of Willis precedes the developmental derangement causing arhinencephaly, a complete circle was found in these brains.
大脑 Willis 环解剖变异的发生机制被认为与血流动力学因素有关，即大脑各部分的差异生长会不断改变血流动力学需求，进而改变脑动脉的血流模式。因此可以预期，如果大脑的某个特定部分未发育，血流动力学需求的变化将影响一些脑动脉的发育。因此，结合脑畸形对 2 例无脑回畸形和 8 例前脑无裂畸形大脑底部的动脉进行了研究。前脑无裂畸形的缺陷被认为是由于前脑未能完全分离为端脑和间脑，并在正常情况下前脑开始分离为半球时显现出来，即妊娠 28 - 34 天。无脑回畸形大脑是完全分开的。仅存在嗅束和嗅球的部分或完全发育不全。导致无脑回畸形的缺陷始于妊娠 43 天。在无脑回畸形大脑中未发现特殊的血管异常。然而，在前脑无裂畸形大脑底部不存在完整的 Willis 环；前部缺失，由单侧或双侧从颈内动脉发出的前分支替代。脉络膜动脉管径非常大，通向通常存在于前脑无裂畸形大脑中的背侧囊肿的高度血管化壁。与前部不同，后部动脉模式几乎与正常大脑 Willis 环的后部相同。在前脑无裂畸形大脑中发现的基本血管模式显示出帕吉特脑脉管系统发育阶段 2 和 3 的特征，即通常在妊娠 28 - 40 天内发育的模式。这种模式的进一步改变在很大程度上可以从扩大的脉络膜前动脉对循环施加的功能需求来理解。由于 Willis 环前部的发育先于导致无脑回畸形的发育紊乱，因此在这些大脑中发现了完整的环。
