BackgroundPast studies found that cerebral developmental venous anomaly (DVA) is often concurrent with cavernous malformation (CM). But the reason of the concurrency remains unknown. The purpose of this study was to confirm whether angioarchitectural factors relate to the concurrence and which angioarchitectural factors can induce the concurrency.MethodsDVA cases were selected from the records of the same 3.0 T MR. The DVA cases was divided into two group which are DVA group and DVA concurrent with CM group. 8 angioarchitectural factors of the DVAs were selected and measured. Statistical analysis was performed by the Pearson chi-square statistic,analysis of variance (ANOVA) and multi-factor logistic regression analysis.ResultsFive hundred three DVA lesions were found and 76 CM lesions coexisting with DVA. In the single factor analysis, all the 8 angioarchitectural factors of DVA were related to the concurrency. In the multivariate analysis, 6 angioarchitectural factors. Result of multi-factor logistic regression analysis is Logit(P) = -4.858-0.932(Location) + 1.616(Direction) + 1.757(Torsion) + 0.237(Number) + 2.119(Stenosis rate of medullary vein)-0.015(Angle), goodness of fit is 90.1 %.ConclusionsThe angioarchitectural factors of DVA are related to the concurrency of DVA and CM. 6 angioarchitectural factors may induce the concurrency.

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BACKGROUND: Subarachnoid hemorrhage (SAH) is characterized by acute and delayed reductions of cerebral blood flow (CBF) caused, among others, by spasms of cerebral arteries and arterioles. Recently, the inactivation of perivascular macrophages (PVM) has been demonstrated to improve neurological outcomes after experimental SAH, but the underlying mechanisms of protection remain unclear. The aim of our exploratory study was, therefore, to investigate the role of PVM in the formation of acute microvasospasms after experimental SAH. METHODS: PVMs were depleted in 8- to 10-week-old male C57BL/6 mice (n=8/group) by intracerebroventricular application of clodronate-loaded liposomes and compared with mice with vehicle liposome injections. Seven days later, SAH was induced by filament perforation under continuous monitoring of CBF and intracranial pressure. Results were compared with sham-operated animals and animals who underwent SAH induction but no liposome injection (n=4/group each). Six hours after SAH induction or sham surgery, numbers of microvasospasms per volume of interest and % of affected pial and penetrating arterioles were examined in 9 standardized regions of interest per animal by in vivo 2-photon microscopy. Depletion of PVMs was proven by quantification of PVMs/mm 3 identified by immunohistochemical staining for CD206 and Collagen IV. Statistical significance was tested with t tests for parametric data and Mann-Whitney U test for nonparametric data. RESULTS: PVMs were located around pial and intraparenchymal arterioles and were effectively depleted by clodronate from 671±28 to 46±14 PVMs/mm 3 ( P <0.001). After SAH, microvasospasms was observed in pial arteries and penetrating and precapillary arterioles and were accompanied by an increase to 1405±142 PVMs/mm 3 . PVM depletion significantly reduced the number of microvasospasms from 9 IQR 5 to 3 IQR 3 ( P <0.001). CONCLUSIONS: Our results suggest that PVMs contribute to the formation of microvasospasms after experimental SAH.