Bitzer M, Topka H, Morgalla M, Friese S, Wöckel L, Voigt K
Department of Neuroradiology, University of Tübingen, Germany.
Neurosurgery. 1998 Apr;42(4):730-7. doi: 10.1097/00006123-199804000-00026.
The exact pathogenesis of peritumoral brain edema (PTBE) in meningiomas is still unknown. A number of different pathophysiological hypotheses have been considered. A detrimental effect of tumor-related venous obstruction has been suggested as one pathogenetic mechanism. We sought to characterize the significance of venous stasis in the development of PTBE in meningiomas.
Angiograms for 134 patients with 136 intracranial meningiomas were analyzed. Pathological changes affecting cortical veins, sylvian veins, bridging veins, deep veins, transmedullary veins, and dural sinuses were evaluated. From preoperative computed tomographic scans, the total tumor volume, the tumor/PTBE volume ratio (edema index [EI]), and the location of the edema were determined. For statistical evaluation, meningiomas associated with pathological venous drainage were compared with size-matched controls.
The edema incidence and the mean EI were not different for meningiomas with unselected signs of obstructed venous drainage, compared with controls. In particular, lesions with involvement of cortical veins, bridging veins, and dural sinuses showed no higher edema incidence. However, meningiomas associated with venous changes in sylvian veins (EI = 4.9 versus EI = 2.7; P < 0.004) and with dysplastic transmedullary veins (EI = 3.3 versus EI = 1.7; P < 0.04) showed significantly higher mean EI values, compared with meningiomas without involvement of these vessels.
Our data suggest that tumor-related venous obstruction does not play an essential role in the development of PTBE for the majority of meningiomas. For a small subgroup of meningiomas with involvement of sylvian veins or development of dysplastic transmedullary veins, changes in venous drainage may aggravate preexisting PTBE.
脑膜瘤周围脑水肿(PTBE)的确切发病机制仍不清楚。人们已考虑了许多不同的病理生理假说。肿瘤相关静脉阻塞的有害作用被认为是一种发病机制。我们试图阐明静脉淤滞在脑膜瘤PTBE发生过程中的意义。
分析了134例患有136个颅内脑膜瘤患者的血管造影片。评估了影响皮质静脉、大脑外侧裂静脉、桥静脉、深部静脉、经髓静脉和硬脑膜窦的病理变化。从术前计算机断层扫描中,确定肿瘤总体积、肿瘤/PTBE体积比(水肿指数[EI])以及水肿的位置。为进行统计学评估,将伴有病理性静脉引流的脑膜瘤与大小匹配的对照组进行比较。
与对照组相比,具有未选择的静脉引流受阻征象的脑膜瘤的水肿发生率和平均EI无差异。特别是,累及皮质静脉、桥静脉和硬脑膜窦的病变水肿发生率并未更高。然而,与未累及这些血管的脑膜瘤相比,伴有大脑外侧裂静脉改变的脑膜瘤(EI = 4.9对EI = 2.7;P < 0.004)和伴有发育异常的经髓静脉的脑膜瘤(EI = 3.3对EI = 1.7;P < 0.04)的平均EI值显著更高。
我们的数据表明,对于大多数脑膜瘤而言,肿瘤相关静脉阻塞在PTBE的发生中并不起关键作用。对于一小部分累及大脑外侧裂静脉或出现发育异常的经髓静脉的脑膜瘤,静脉引流的改变可能会加重已有的PTBE。