Cerebral aneurysms are localised increases in diameter of arteries supplying the brain. These are also referred to as intracranial aneurysms. Some 4–6 % of the population aged greater than 30 years have a CA (Wardlaw and White 2000). The main clinical complication is rupture leading to bleeding. The blood accumulates beneath the arachnoid membrane which surrounds the brain, producing a subarachnoid haemorrhage. The risk of rupture of a CA is low at 0.1–1 % per year (Juvela 2004). However the consequences of rupture are severe for the patient. Mortality following aneurysm rupture is 45 %, 30 % of survivors demonstrate moderate to severe disability, and the remainder have increased risk of re-bleeds and stroke (Brisman et al. 2006). Most CAs are asymptomatic so that the first knowledge of the presence of a CA is the symptoms associated with subarachnoid haemorrhage (‘thunderclap headache’, nausea, vomiting, altered consciousness of varying degree from drowsiness to complete loss of consciousness, and disturbance of vision). In some cases larger CAs may themselves produce similar symptoms immediately prior to rupture. Treatment of CAs involves a variety of procedures concerned with sealing off the aneurysm and these are considered further in Sect. 16.5.

CAs are of 2 main types, saccular and fusiform. Saccular aneurysms are round in shape and also referred to as ‘berry aneurysms’; these usually occur at the branching point of arteries of the Circle of Willis and are the most common type of CA (80–90 %). Fusiform aneurysms involve an overall widening of the artery and usually do not rupture. Saccular aneurysms are also classified by size; small (<15 mm diameter), large (15–25 mm), giant (25–50 mm) and super-giant (>50 mm). The remainder of Sect. 16.2 will be concerned with saccular CAs.

Saccular CAs are not conduit vessels; blood flow enters and exits the aneurysm via the neck. The flow pattern within the aneurysm depends on its orientation with respect to the parent artery (Moftakher et al. 2007) (Fig. 16.2). Figure 16.2a shows a sidewall aneurysm. Flow in the aneurysm recirculates, often through the entire cardiac cycle. Blood velocity is very low, wall shear stress is very low and there is low pressure on the dome (far wall) of the aneurysm. In the case of a bifurcation aneurysm 2 flow patterns are seen. The most common is illustrated in Fig. 16.2b. Here flow enters the aneurysm from the parent artery through a channel within the aneurysm neck, circulates around the aneurysm, and exits through a separate channel in the neck. Velocities, wall shear and pressure at the dome are low. The second flow pattern seen in bifurcation aneurysms is illustrated in Fig. 16.2c. Here flow from the parent artery enters the aneurysm as a jet which impacts on the dome, flow then exits in a random manner through the neck. The impact of the jet causes local high wall shear and pressure on the dome. Because of the persistent flow through the cardiac cycle most CAs have no thrombus, as opposed to AAAs where thrombus is common.

The composition of cerebral arteries is different to that of systemic arteries. Cerebral arteries possess much less elastin in the medial layer, the external elastic lamina is absent, and there are structural abnormalities at the apex of bifurcations, all of which are thought to make cerebral arteries prone to saccular aneurysms. Cerebral aneurysms are characterised by loss of elastin and smooth muscle cells with consequent thinning of the medial layer (Frösen et al. 2012). Collagen fibres remodel, probably in an attempt to mechanically stabilise the aneurysm. The result is an increase in wall stiffness, with the main load-bearing performed by the adventitia rather than the media.

Initiation, growth and rupture of the CA are governed by an interplay between the mechanical environment and the local biology. The exact details of this remain the subject of research for CAs, though central to this will be presence of an intact endothelial layer. Unruptured aneurysms lack an endothelial layer (Frösen et al. 2004), and prior to this there is endothelial dysfunction. An intact endothelial layer is essential for an artery to adapt to its mechanical environment. This suggests that as the CA evolves, initially the endothelial layer is intact and the aneurysm will remodel in an attempt to normalise its mechanical environment. Later there is endothelial dysfunction with impairment in the aneurysms ability to maintain the mechanical environment. Finally there is loss of the endothelial layer and the aneurysm’s ability to remodel is largely absent. Reviews of this area are provided by Sforza et al. (2009), Meng et al. (2014), Penn et al. (2011) and Selimovic et al. (2013) from which the analysis below is derived. The latter paper (Selimovic) describes computational models of aneurysm growth.

Traditional visualisation of CAs was undertaken using angiography which involved an arterial puncture. A number of non-invasive techniques have been used to diagnose the presence of CAs including CT angiography (CTA), rotational angiography (RA) and magnetic resonance angiography (MRA). All these techniques provide 3D data from which measurements may be made of aneurysm dimensions. In addition the 3D geometries may be used to derive indices describing shape and as the input to patient specific modelling. Ultrasound systems may also be used for visualisation of CAs. Further reading on the imaging of cerebral aneurysm is provided in Hoskins et al. (2011).

This section presents a very brief description of the treatment of CAs. Further reading on diagnostic and treatment pathways are provided in Wardlaw and White (2000) and Mehrar et al. (2011). Most CAs that rupture are undiagnosed at the time of rupture and present as an emergency. Treatment of the ruptured aneurysm involves exclusion of the aneurysm from the circulation. The decision to treat the unruptured aneurysm is based on aneurysm diameter. Treatment is considered if the diameter is greater than 7 mm, however if there are other risk factors then treatment is considered if the diameter is greater than 3 mm diameter. Historically surgical clipping of the aneurysm was the preferred method for treatment of a cerebral aneurysm. This is highly invasive involving open surgery with placement of a clip across the aneurysm neck to separate the aneurysm from the main arterial flow channel. It is much more common to perform intervention by catheter based techniques under fluoroscopic guidance (White et al. 2015). The most common technique is the insertion of coils in the aneurysm which are thrombogenic, so that the aneurysm is sealed off by the presence of thrombus. Increasingly coiling is combined with the placement of a stent. The stent helps prevent ingress of the coil into the main arterial channel, hence allowing more aggressive coil placement, and provides a mesh on which an endothelium can grow. Other devices and methods which are used in interventional treatment include balloon remodelling, flow diverters and intrasaccular flow disruptors.

As the name implies, AAAs are localised increases in the diameter of the abdominal aorta (see Fig. 16.6), however they can often extend distally beyond the iliac bifurcation, or begin above the abdominal aorta. They are defined as a maximum aortic diameter ≥3.0 cm with the un-diseased diameter being around 2 cm. The incidence rates of AAAs range from 2 to 8 % for men over 65 years and the prevalence is 4 times lower in women. Over recent years, the incidence rates appear to be falling, with this being attributed to the change in smoking habits in developed countries (Lederle 2011).

Most AAAs are asymptomatic so that the first time the patient is aware of an aneurysm is after rupture. The most common symptom is sudden pain in the abdomen; other symptoms include low blood pressure, loss of consciousness and a pulsatile mass in the abdomen. Following rupture there is usually considerable internal bleeding and this is the main cause of death. If an unruptured AAA is detected, usually with medical imaging, the primary criterion determining surgical intervention is the size of the AAA, more specifically, the maximum diameter. If the maximum anterior-posterior diameter of the AAA exceeds 5.5 cm in men or 5.0 cm in women, and the patient is fit for surgery, repair is offered. Risk of rupture increases with maximum AAA diameter. The annual rupture risk increases from 0.5 to 5 % for diameter of 4.0–4.9 cm, 3–5 % for 5.0–5.9 cm, 10–20 % for 6.0–6.9 cm, and 20–40 % for 7.0–7.9 cm (Brewster et al. 2003).

A minority of AAA are symptomatic in that the patient develops a variety of symptoms associated with imminent rupture. These symptoms include abdominal pain, lower back pain and a pulsatile abdominal mass. Generally symptomatic patients are offered urgent repair of their AAA (De Martino et al. 2010).

The healthy aorta is often approximated as a cylinder; however, AAAs can develop into highly irregular shapes with regions of high curvature and highly tortuous centrelines. As such, the mechanics used to determine the stresses and strains cannot be approximated using the Law of Laplace (see Chap. 5.​1.​5). It is these stresses and strains that contribute to the growth, remodelling and eventual rupture of the AAA, hence the large research focus aimed at accurately predicting them (see Chap. 11.​4.​3). A material will fail when the local stress exceeds the local strength, and although there are many biological processes also at play, this general understanding also applies to AAA. Using patient specific modelling (PSM—discussed in detail in Chap. 11), it is possible to estimate the stress acting on the AAA wall in vivo (Fillinger et al. 2002, 2003; Truijers et al. 2007; Doyle et al. 2009; Gasser et al. 2010; Doyle et al. 2014). By coupling this data with knowledge of the AAA wall strength (Thubrikar et al. 2001; Raghavan et al. 2011, 2006), it is possible to determine the likelihood of rupture. However, predicting in vivo wall strength remains a significant challenge (vande Geest et al. 2006; Reeps et al. 2013).