Focal weak points 
The basic principle of the concept of “partially targeted embolisation” of brain AVMs is the hypothesis that specific angioarchitectural features of a pial brain AVM can be regarded as “weak points” that may predispose a patient to haemorrhage [20–22]. While not proven by randomised prospective trials, this principle has been used in our practice for more than 20 years, and we were able to show an improved outcome on follow-up when compared with the natural history [23]. These angioarchitectural weak points are (1) intranidal aneurysms and venous ectasias [24], and (2) venous stenosis [21]. The first to state that a specific angioarchitecture present in brain arteriovenous malformations makes them more prone to future haemorrhage were Brown et al. in 1988, who found that the annual risk of future haemorrhage was 3% in brain AVMs alone and 7%/year in brain AVMs with associated aneurysms [12]. Meisel et al. found that among 662 patients with AVMs, there were 305 patients with associated aneurysms, and there was a significant increase in rebleed episodes in AVMs harbouring intranidal aneurysms (p < 0.002) [24]. In the Toronto series of 759 brain AVMs, associated aneurysms were statistically significantly (p = 0.015) associated with future bleeding [25]. It may be difficult to discern intranidal arterial aneurysms from intranidal venous ectasias (Fig. 4), which is why these two angioarchitectural specificities are grouped as one entity in most series. Venous stenoses, on the other hand, are a separate angiographic weak point and are often seen in ruptured AVMs (Fig. 5). The nature of the venous stenosis is not completely understood; most likely, high-flow vessel wall changes or failure of remodelling (for example, an increased vessel wall response to the shear stress induced by the arterialisations) may be put forward as potential reasons. A stenotic venous outlet will lead to an imbalance of pressure in various compartments of the AVM, which may induce subsequent rupture of the AVM. The compartment that is drained by the stenotic vessel should be scrutinised for contrast material stagnation and, if endovascular therapy is contemplated, extreme caution has to be undertaken not to push the liquid embolic agent towards the already stenosed vein as this may have catastrophic results. In addition to these two angioarchitectural risk factors, there are also other factors that may lead to an increased risk of haemorrhage. These are: deep venous drainage only, advanced age and male gender [26].
Fig. 4 In this patient with an acutely ruptured AVM, CTA demonstrates an aneurysm pointing into the haemorrhagic cavity as the most likely source of the bleeding. These focal points of weakness can be targeted by embolisation to secure the AVM in the acute phase
Fig. 5 The pathomechansim of this ruptured AVM is presumably due to the stenosis of the major venous outlet (arrow), which led to increased pressure within the nidus proper. If endovascular therapy is contemplated in cases like these, extreme caution has to be taken that no embolic material penetrates too far into the venous side which would lead to further obstruction of the venous outflow