**1. Introduction**

Intracranial aneurysm (IA), a pathological dilation of the vessel wall, is the result of hemodynamic forces on the wall of the intracranial artery. It is characterized by mild to moderate structural changes of the vessel wall, which may result in aneurysm rupture, leading to a severe form of hemorrhagic stroke [1].

In the last 15 years, there has been increasing incidental detection of unruptured intracranial aneurysms (UIA) due to an increasing use of noninvasive radiological examinations, such as computed tomography angiography (CTA) and magnetic resonance angiography (MRA) [2]. The increasing use of these noninvasive techniques for various non-specific complaints results in higher detection and increasing treatment of UIA. While 20% of individuals operated on for an IA in 1998 were carrying a UIA, in more recent years, the number has increased to more than 50% of all patients operated on for IA in the Department of Neurosurgery of

the Jan Evangelista Purkyně, Masaryk Hospital in Ústí nad Labem, Czech Republic. Concurrently, there have been an increasing number of patients that we monitor for UIA who do not receive treatment. Should the aneurysm not rupture, which occurs in the majority of IA cases, very few become symptomatic in other ways. If it does rupture, it results in severe consequences including death, various levels of neurological disabilities, and cognitive or social difficulties.

The decision on whether to treat an individual with a UIA is based on the balance between the risk of treatment and the risk of the natural history of the aneurysm. If the aneurysm does not rupture, the risk of other clinical symptoms is quite low. These symptoms may appear as compression of the nervous structures (the optic nerve may be compressed by an ophthalmic aneurysm, the oculomotor nerve by a posterior communicating artery aneurysm, or the brain stem may be compressed by a large basilar aneurysm). Other symptoms may result from embolization of thrombi from the sac of an aneurysm; this is, however, very rare [3]. The worst outcome is that patients may experience aneurysm rupture. Overall, this risk is low in most patients and therefore does not occur in the vast majority of them in their lifetime [4]. The risk of rupture is associated with many factors; some of them are inherent (higher risk of rupture in females, some nations, such as Japanese); other factors are modifiable (higher risks are associated with hypertension or smoking). The rupture leads to a severe form of hemorrhagic stroke or even death. The risk of death after rupture is somewhere between 26 and 36% of patients [5]. The improved care of patients with SAH in specialized neurovascular centers improves survival rates [6]. Alternatively, about 15% of patients die immediately after rupture or before they are transported to hospital. Approximately 20% of those that survive develop a global cognitive deficit [7].

Contrarily the treatment, even in selected UIA, may carry the risk of severe complications may be as high as 16% of patients; the risk of mortality being 0–3.2% and the chance of not being discharged home almost 20% [8]. All the scoring systems used for analyzing the risk of rupture are based on data from large population studies. These factors include the size of the aneurysm, its location within the circle of Willis, its shape, etc. However, the size or the shape of the aneurysm is a result of forces that themselves lead to aneurysm initiation, its growth, and eventual rupture (or stability with no rupture). This is the result of the balance between hemodynamic forces and the quality of the blood vessel wall at the site of the aneurysm. Immediately when the hemodynamic forces overcome the strength of the aneurysm wall, it will rupture. Consequently an understanding of the hemodynamics within the cerebral blood vessels and the aneurysm itself may help with understanding its initiation, growth, and eventual rupture. The ability to model the hemodynamics within the aneurysm could also possibly assist with predicting their risk element and the direction to preventive treatment. It may also be possible to securely monitor aneurysms with a non-risky hemodynamic profile.

In this chapter we aim to provide current information on aneurysm hemodynamic modeling, using CFD. We will focus on ruptured and unruptured aneurysms, the hemodynamic characteristics at the point of rupture and the difference between ruptured and unruptured IA. We will discuss the issue from the perspective of neurosurgery and its possible contribution to clinical practice. We will summarize our 8 years of experience with CFD modeling in intracranial aneurysms, as well as the current literature.

#### **2. The pathophysiology of the life cycle of intracranial aneurysms**

During physiological conditions, the cerebral blood vessels consist of three layers: (1) tunica intima with a basal membrane, endothelial cells, and the internal

**23**

**Figure 1.**

*Hemodynamics in Ruptured Intracranial Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.88695*

seems that possibly both scenarios could play a role [13].

**3. Computational fluid dynamics (CFD) of intracranial aneurysms**

group, the basic flow characteristics of both groups were identical.

change depending on the shear stress [16–19].

The actual process of modeling hemodynamic parameters consists of several steps. Creating a 3D model is done by manual or semiautomatic segmentation (**Figure 1**). Angiographic examinations (3D angiography, CT angiography, or MR angiography) are used as the source data. Each radiological method has its own limitations (calcifications, flow artifacts, etc.). Several studies have tried to assess the relationship between different imaging examinations [14, 15]. In one such study, the authors compared the results of CFD obtained from CTA or DSA [14]. In conclusion, the authors state that, despite the quantitative differences in the individual hemodynamic parameters between the CTA and the DSA segmented

In the next step, a calculation is performed using the Navier-Stokes equations, which describe the flow of incompressible fluid with constant viscosity. The use of the numerical solution of the Navier-Stokes equations calculates with assumption of blood having laminar flow. Possible influences of phenomena not captured by this model are further investigated, such as the influence of turbulent flow or viscosity

*The process of obtaining patient-specific geometry from the CT or MR scan with high resolution includes accurate voxel segmentation of the vessel, generating surface mesh, and finally smoothing, generating volumetric* 

*mesh, and prescribing inlets and outlets with possible shortening and elongating of the outputs.*

elastic lamina; (2) tunica media, which consists of circumferentially oriented smooth muscle cells inside a dense network of collagen and elastin fibers; and (3) tunica adventitia, which consists mostly of collagen providing strength for the vessel wall. Tunica intima and tunica media are separated by a layer of lamina elastica interna, which is the key structure and has to degrade for the intracranial aneurysm to develop [9]. Cerebral blood vessels differ from extracranial blood vessels in that they have a thicker internal elastic lamina, less elastin, and smooth muscle cells in the media; in addition, they have no lamina elastica externa and a thinner layer of adventitia. There is minimum perivascular tissue in the subarachnoid space. The bifurcations of cerebral blood vessels contain irregularities in the vessel wall. The bifurcations are the typical areas of aneurysm development [10, 11]. Due to the small diameter of intracranial blood vessels, the wall shear stress plays a significant role in the degeneration of blood vessels and development of IA. The small diameter of cerebral blood vessels is also influenced by pathological forces induced, for example, by hypertension, and these lead to the development of IA. On the other hand, it is not quite clear what is the character of hemodynamic forces that lead to the development and rupture of IA. Some hypotheses describe the pathological influence of low wall shear stress leading to blood flow stagnation and the accumulation of blood elements (erythrocytes, leukocytes, thrombocytes), causing degeneration of the vessel wall together with inflammatory changes [12]. Another theory is based on high wall shear stress (WSS) causing damage of the endothelium, remodeling of the blood vessel wall, and its eventual degradation. It

*Hemodynamics in Ruptured Intracranial Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.88695*

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

logical disabilities, and cognitive or social difficulties.

20% of those that survive develop a global cognitive deficit [7].

tor aneurysms with a non-risky hemodynamic profile.

Contrarily the treatment, even in selected UIA, may carry the risk of severe complications may be as high as 16% of patients; the risk of mortality being 0–3.2% and the chance of not being discharged home almost 20% [8]. All the scoring systems used for analyzing the risk of rupture are based on data from large population studies. These factors include the size of the aneurysm, its location within the circle of Willis, its shape, etc. However, the size or the shape of the aneurysm is a result of forces that themselves lead to aneurysm initiation, its growth, and eventual rupture (or stability with no rupture). This is the result of the balance between hemodynamic forces and the quality of the blood vessel wall at the site of the aneurysm. Immediately when the hemodynamic forces overcome the strength of the aneurysm wall, it will rupture. Consequently an understanding of the hemodynamics within the cerebral blood vessels and the aneurysm itself may help with understanding its initiation, growth, and eventual rupture. The ability to model the hemodynamics within the aneurysm could also possibly assist with predicting their risk element and the direction to preventive treatment. It may also be possible to securely moni-

In this chapter we aim to provide current information on aneurysm hemodynamic modeling, using CFD. We will focus on ruptured and unruptured aneurysms, the hemodynamic characteristics at the point of rupture and the difference between ruptured and unruptured IA. We will discuss the issue from the perspective of neurosurgery and its possible contribution to clinical practice. We will summarize our 8 years of experience with CFD modeling in intracranial aneurysms, as well as

**2. The pathophysiology of the life cycle of intracranial aneurysms**

During physiological conditions, the cerebral blood vessels consist of three layers: (1) tunica intima with a basal membrane, endothelial cells, and the internal

the Jan Evangelista Purkyně, Masaryk Hospital in Ústí nad Labem, Czech Republic. Concurrently, there have been an increasing number of patients that we monitor for UIA who do not receive treatment. Should the aneurysm not rupture, which occurs in the majority of IA cases, very few become symptomatic in other ways. If it does rupture, it results in severe consequences including death, various levels of neuro-

The decision on whether to treat an individual with a UIA is based on the balance between the risk of treatment and the risk of the natural history of the aneurysm. If the aneurysm does not rupture, the risk of other clinical symptoms is quite low. These symptoms may appear as compression of the nervous structures (the optic nerve may be compressed by an ophthalmic aneurysm, the oculomotor nerve by a posterior communicating artery aneurysm, or the brain stem may be compressed by a large basilar aneurysm). Other symptoms may result from embolization of thrombi from the sac of an aneurysm; this is, however, very rare [3]. The worst outcome is that patients may experience aneurysm rupture. Overall, this risk is low in most patients and therefore does not occur in the vast majority of them in their lifetime [4]. The risk of rupture is associated with many factors; some of them are inherent (higher risk of rupture in females, some nations, such as Japanese); other factors are modifiable (higher risks are associated with hypertension or smoking). The rupture leads to a severe form of hemorrhagic stroke or even death. The risk of death after rupture is somewhere between 26 and 36% of patients [5]. The improved care of patients with SAH in specialized neurovascular centers improves survival rates [6]. Alternatively, about 15% of patients die immediately after rupture or before they are transported to hospital. Approximately

**22**

the current literature.

elastic lamina; (2) tunica media, which consists of circumferentially oriented smooth muscle cells inside a dense network of collagen and elastin fibers; and (3) tunica adventitia, which consists mostly of collagen providing strength for the vessel wall. Tunica intima and tunica media are separated by a layer of lamina elastica interna, which is the key structure and has to degrade for the intracranial aneurysm to develop [9]. Cerebral blood vessels differ from extracranial blood vessels in that they have a thicker internal elastic lamina, less elastin, and smooth muscle cells in the media; in addition, they have no lamina elastica externa and a thinner layer of adventitia. There is minimum perivascular tissue in the subarachnoid space. The bifurcations of cerebral blood vessels contain irregularities in the vessel wall. The bifurcations are the typical areas of aneurysm development [10, 11]. Due to the small diameter of intracranial blood vessels, the wall shear stress plays a significant role in the degeneration of blood vessels and development of IA. The small diameter of cerebral blood vessels is also influenced by pathological forces induced, for example, by hypertension, and these lead to the development of IA. On the other hand, it is not quite clear what is the character of hemodynamic forces that lead to the development and rupture of IA. Some hypotheses describe the pathological influence of low wall shear stress leading to blood flow stagnation and the accumulation of blood elements (erythrocytes, leukocytes, thrombocytes), causing degeneration of the vessel wall together with inflammatory changes [12]. Another theory is based on high wall shear stress (WSS) causing damage of the endothelium, remodeling of the blood vessel wall, and its eventual degradation. It seems that possibly both scenarios could play a role [13].
