Angioarchitectural classification of brain AVMs
As outlined above, in non-ruptured AVMs the first step is to evaluate whether the specific symptoms of an individual patient can be related to the AVM; second, one has to evaluate whether the pathomechanism responsible for the symptoms can be treated by endovascular means (as was also described above). The third step consists in evaluating the angioarchitecture of the AVM to determine whether endovascular therapies are suitable for a specific brain AVM and whether there are any focal weak points within the AVM of an asymptomatic patient.

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

Angioarchitecture related to endovascular therapies 
Before contemplating therapy of an AVM, the angiography must be scrutinised for the following points: the nature and number of the feeding arteries, the presence or absence of flow-related aneurysms, the number of separate compartments of the malformation, any arterial or venous ectasias near to or within the malformation, and the nature of the venous drainage. On the arterial side, flow-related aneurysms are typically present at branching points of the major feeding arteries. They classically resolve following treatment of the AVM and are due to vascular remodelling following increased shear stress [27]. Although not a contraindication for endovascular treatment, they present a danger to the neurointerventionalist, because flow-directed catheters are prone to entering the aneurysm rather than the distal vessels. Concerning the arterial side of the AVM, both the number and the nature of the feeding arteries need to be assessed as they determine whether endovascular approaches will make sense. A large number of only slightly dilated feeders will make an endovascular therapy more challenging than those with a single large feeder [28]. Concerning the nature of the feeding artery, there are two basic types of feeding arteries. Direct arterial feeders end in the AVM. Indirect arterial feeders supply the normal cortex and also supply the AVM “en passage” via small vessels that arise from the normal artery. While direct feeders are safe targets for an endovascular therapy (Fig. 6), en passage feeders may carry the risk of inadvertent arterial glue migration to distal healthy vessels (Fig. 7). In this regard, the “security margin” of the catheter position has to be briefly discussed. Liquid embolic agents may cause reflux at the end of the injection. Depending on the agent, the microcatheter, the injection technique and the skills of the operator, this reflux may be as far as 1 cm proximal to the tip of the catheter. A safe deposition of liquid embolic agent is therefore only possible if the catheter tip is distal enough to be beyond any vessel that supplies normal brain tissue. In the case of en passage feeders, this may not be the case, especially if the catheter is only hooked into the feeding artery and will jump backwards because of the jet effect when injecting a liquid embolic agent. Concerning the angioarchitecture of the nidus, intranidal arterial aneurysms and venous varices that indicate weak points need to be recognised as well as the number of compartments and their nature (nidal vs. fistulous). Finally, on the venous side of the AVM, the number of draining veins per compartment (the more the better for endovascular treatment if venous migration should occur), possible drainage into the deep venous system (higher risk of haemorrhage, more difficult surgical treatment) and stenosis, which restrict venous outflow, have to be identified to fully determine the risk of a specific AVM. At the present time, this information can only be obtained by conventional digital subtraction angiography, which in our practice still precedes any treatment decision in AVMs.
Fig. 6 Single-feeder AVMs are easier to embolise with a higher chance of a complete cure compared with multi-feeder AVMs. In this single compartment AVM, the microcatheter is brought to an intranidal position where a histoacryl deposition was able to completely occlude the AVM
Fig. 7 Whereas the feeder type in Fig. 6 was of the terminal or “direct” type, the feeder type of this AVM is of the “indirect” or “en passage” type. These “en passage” feeders may carry the risk of inadvertent arterial glue migration to distal healthy vessels and in our opinion speak strongly to contraindicate an endovascular treatment approach