Intracranial aneurysm (IA) is defined as a localized, abnormal dilation of the intracranial arterial wall, forming a sac-like protrusion. As a common and life-threatening cerebrovascular disorder, its incidence ranks second only to cerebral thrombosis and hypertensive intracerebral hemorrhage among cerebrovascular events [1]. Rupture of an IA can result in spontaneous subarachnoid hemorrhage (SAH), which is associated with high rates of disability and mortality: the combined mortality and disability rate is approximately 30% after the initial rupture and increases to nearly 70% following rebleeding [2]. Currently, ruptured IAs are primarily managed by surgical clipping or endovascular intervention. However, the identification of high-risk unruptured IAs and the optimal timing of intervention remain significant clinical challenges.

At present, commonly used clinical scoring systems, including PHASES and ELAPSS, are applied to assess rupture risk in unruptured IAs. These scoring systems are summarized in Table 1.

Table 1. Clinical risk scoring systems for rupture assessment of unruptured intracranial aneurysms.

These approaches largely rely on limited morphological features and clinical variables, resulting in a narrow assessment scope, insufficient representation of inter-individual variability, and a lack of dynamic temporal resolution, thereby limiting their ability to achieve precise, individualized risk stratification.

In fact, the hemodynamic environment plays a critical role in the initiation and progression of IAs [3]. The predilection of IAs for arterial bifurcations within the Circle of Willis further supports this hemodynamic hypothesis. However, conventional imaging techniques are limited to visualizing static anatomical structures and are incapable of capturing hemodynamic characteristics. In recent years, computational fluid dynamics (CFD) simulation has increasingly emerged as an important tool for evaluating the hemodynamic features of IAs [4]. Based on medical imaging data, CFD enables the simulation of blood flow dynamics and the quantification of hemodynamic parameters, thereby facilitating a comprehensive assessment of the aneurysmal hemodynamic environment.

To provide an overview of the current state of research, this review synthesizes recent domestic and international studies to summarize the advances in CFD-based investigations of IA formation and progression.

In the investigation of IA formation, the role of hemodynamic factors has been recognized as essential. It is well established that IAs preferentially develop at arterial bifurcations or at the apex of arterial curvatures, where vessels are exposed to concentrated hemodynamic impingement. However, research on IA initiation remains relatively limited, largely because the formation process is often difficult to identify and evaluate in vivo, posing significant challenges for early diagnosis.

Initially, hemodynamic studies of IA formation were primarily based on animal experiments. In the late 20th century, particle-tracking techniques applied in rat models demonstrated that marked particle residence and reduced flow velocity were present at sites of early aneurysm formation, with WSS observed to be highest at the distal region of the aneurysm [21]. In 2007, Meng et al. [22] established a canine carotid bifurcation model and, in combination with CFD analysis, demonstrated that IAs tended to develop in regions near the bifurcation apex where high WSS coexisted with high WSSG. It was suggested that the synergistic effect of elevated WSS and WSSG contributed to early aneurysm initiation. A higher WSSG indicates more pronounced spatial variation in flow, which may impose excessive biomechanical stress on localized vessel wall regions, thereby facilitating aneurysm formation. These experimental findings suggested that elevated WSS may serve as a potential biomechanical biomarker for IA initiation.

Clinical studies have further supported these observations. In 2016, Can et al. [23] conducted a systematic review and meta-analysis and reported that elevated WSS and high GON were closely associated with aneurysm formation at arterial bifurcations. In 2022, a case study involving longitudinal imaging follow-up of two patients demonstrated that, prior to aneurysm formation, localized blood flow exhibited concentrated high-velocity inflow and prominent vortex structures. In these regions, WSS and WSSG were significantly higher than those in the parent artery, further supporting the critical role of elevated WSS in IA initiation [24].

More recently, in 2024, Yang et al. [25] combined CFD with fluid-structure interaction (FSI) analysis in a cohort of 58 unilateral internal carotid artery aneurysms. It was demonstrated that aneurysms tended to form in regions characterized by the coexistence of high WSS and high mechanical strain. In contrast, in the contralateral non-aneurysmal arteries, regions with elevated WSS usually lacked high mechanical strain, suggesting that elevated WSS alone may be insufficient to trigger aneurysm formation.

Aneurysm growth is recognized as one of the key risk factors for IA rupture [26]. IA growth is generally defined as the occurrence of one or more morphological changes during follow-up, including an increase in maximum diameter, the development of new blebs, or progressive morphological irregularity. In most studies, growth has been operationally defined as an increase in aneurysm maximum diameter of 0.5 mm or 1 mm on serial imaging follow-up [15][18][19][27]-[30]. It has been proposed that IA growth is determined by the interaction among local hemodynamic forces, biomechanical conditions, and pathophysiological processes, with abnormal hemodynamic alterations—particularly WSS—playing a dominant role [31]. Accordingly, multiple hemodynamic parameters derived from WSS have also been used to characterize intra-aneurysmal flow conditions.

In 2017, Brinjikji et al. [27] analyzed 12 pairs of size- and location-matched unruptured IAs and found that the LSA in unstable aneurysms (those demonstrating growth or rupture) was 2.26 times larger than that in stable aneurysms, suggesting that an expanded low-shear region may reflect aneurysm instability. In 2022, Cornelissen et al. [28] expanded the sample size and conducted follow-up analysis of 31 growing aneurysms. A decrease in NWSS and increases in OSI and LSA were observed after aneurysm growth. It was hypothesized that low WSS may promote aneurysm progression by inducing local vascular inflammation, degenerative wall remodeling, and wall thinning. In 2023, Weiss et al. [18] studied 11 growing aneurysms and 11 size- and location-matched stable aneurysms and found that the MTLSA 70% at the aneurysm dome was significantly higher in growing aneurysms, further suggesting that expansion of low-shear regions is associated with aneurysm growth.

However, contradictory evidence has also been reported, indicating that high WSS may be associated with aneurysm growth. In 2018, Wang et al. [32] reported a longitudinal case of a left middle cerebral artery aneurysm, which demonstrated growth at 7 months and subsequent enlargement with rupture at 11 months. The location of de novo bleb formation corresponded to the initial high WSS region (20.3 Pa), suggesting that aneurysm growth may also occur in high WSS environments. In 2023, Tsuji et al. [19] conducted an observational study of 215 unruptured small aneurysms and found that the HSCR was significantly higher in 33 growing aneurysms compared with stable ones and was identified as a key predictor of growth in small IAs. Elevated HSCR indicates that high WSS is concentrated in a limited area, and IA growth is promoted via the induction of localized vascular wall injury.

Nevertheless, these studies largely treated IA growth as a single global phenomenon without distinguishing distinct growth patterns. In fact, studies have demonstrated that different hemodynamic environments lead to distinct IA growth patterns. In 2017, Machi et al. [29] classified six aneurysms into two growth patterns: a “focal growth group” (localized bleb formation at the dome) and a “global growth group” (overall aneurysm enlargement with neck widening). Focal growth was predominantly observed in dome regions characterized by low WSS and high OSI, whereas global growth was more frequently associated with regions of high WSS and high WSSG.

In 2025, Fukuda et al. [15] further investigated the relationship between hemodynamics and growth patterns by stratifying aneurysms into two size groups (<4 mm and ≥4 mm). It was demonstrated that small aneurysms presented higher TAWSS and TAWSSG, as well as elevated transWSS at the aneurysm neck and parent artery, and predominantly exhibited a global growth pattern. By comparison, larger aneurysms had higher NtransWSS at the aneurysm dome and were more prone to focal dome growth.

In the same year, Karnam et al. [30] further analyzed aneurysm growth patterns based on location, wall segmentation, and flow direction. It was reported that growth in anterior communicating artery aneurysms and sidewall aneurysms predominantly occurred in the aneurysm body and was associated with high-flow impingement, where elevated WSS contributed to wall degeneration and thinning. In contrast, middle cerebral artery aneurysms and bifurcation aneurysms more commonly exhibited growth at both the dome and body, which was attributed to slow and oscillatory flow in the dome and central regions, leading to wall thickening and remodeling. From the perspective of flow-directional segmentation, growth was most frequently concentrated in the central region across all aneurysm types. Anterior communicating artery aneurysms demonstrated growth tendencies in both inflow and central regions, whereas middle cerebral artery aneurysms were more likely to grow in the central region alone.

Overall, these findings suggest that IA growth is not driven by a single hemodynamic mechanism but is instead influenced by a combination of aneurysm size, anatomical location, morphological characteristics, and local hemodynamic environment.

Most CFD studies investigating IA rupture have employed cross-sectional designs, comparing ruptured and unruptured aneurysms from different patients. Although these studies have identified important hemodynamic features associated with rupture, causal interpretation is limited due to potential confounding from inter-patient variability, including demographic characteristics, vascular risk factors, and genetic background. Moreover, post-rupture morphological changes, such as alterations in aneurysm geometry and thrombus formation, may affect CFD-derived parameters and prevent accurate representation of the pre-rupture hemodynamic state.

To overcome these limitations, longitudinal studies have been performed to evaluate hemodynamic changes within the same aneurysm before and after rupture, providing stronger evidence regarding temporal associations and reducing inter-patient variability [11][33]. In addition, mirror aneurysm studies, which utilize bilateral aneurysms within the same patient as a self-controlled model, have gained increasing attention for minimizing patient-related confounding factors [34][35]. CFD parameters for IA rupture assessment are categorized into quantitative and qualitative types, and the following review is organized accordingly.

CFD technology has provided important insights into the hemodynamic mechanisms underlying intracranial aneurysm formation, progression, and rupture by enabling comprehensive evaluation of complex blood flow characteristics, including quantitative hemodynamic parameters and qualitative flow patterns. Although CFD-derived parameters have demonstrated potential for aneurysm risk stratification, their clinical application requires further validation in longitudinal cohorts to determine whether baseline hemodynamic characteristics can predict subsequent aneurysm growth or rupture. Moreover, the incremental predictive value of CFD parameters beyond established clinical and morphological predictors should be systematically evaluated to determine their added contribution to individualized risk assessment. Future studies integrating CFD with advanced imaging modalities, artificial intelligence, and longitudinal clinical data may facilitate the development of more accurate predictive models and promote the translation of CFD-based approaches into personalized aneurysm management.