Hemifacial spasm (HFS) is a neurological disorder of the brain characterized by involuntary, paroxysmal twitching of the facial muscles, mostly confined to one side, usually starting from the orbicularis oculi muscle and gradually progressing downward to affect even the lower facial muscles, which is more common in middle-aged and elderly people [1]. The prevalence of HFS in the population is about 20/100,000, with a slightly higher prevalence in women than in men. Its diagnosis is mainly based on observation of the characteristic clinical manifestations, such as difficulty opening eyes, facial asymmetry, and twitching noises in the ear, etc. Electrophysiological approach, imaging examinations, and carbamazepine tests are required to facilitate diagnosis for individuals lacking these manifestations. Drugs such as carbamazepine and oxcarbazepine, botulinum toxin injections, and microvascular decompression are the primary modes of treatment for HFS. Vascular compression of the pontine segment of the facial nerve is a major etiological factor in the development of HFS [2], with the vertebrobasilar artery (VBA) being a common implicated factor in clinical practice [3]. However, the VBA is bilaterally asymmetrical, with the left vertebral artery (VA) being the dominant vessel [4]; this dominance is more pronounced in patients with HFS [5]. The bilateral asymmetry of the VBA and the presence of the dominant VBA contribute to the differences in hemodynamics of the bilateral VBA, which, in turn, may cause the VBA to shift or twist to the side with lower blood flow [6]. Fluid dynamics-based analysis has also found that bending of the VBA triggers a pressure difference between the two sides of the vessel wall and increases the wall shear stress, which increases with the angle and degree of bending [7]. A clinical anatomical study demonstrated that the pattern of vessel displacement is consistent with biomechanical characteristics [8]. It is suggested that anatomical variations and hemodynamics differences in the VBA system may contribute to the development of HFS, vascular variations or hemodynamic alterations in the VBA may differ between patients with unilateral and bilateral HFS. However, it is not clear whether vascular variations or hemodynamic changes in the VBA of patients with left- and right-sided HFS are associated with the risk of developing HFS or, in fact, with disease severity. In view of this, 60 patients with HFS were retrospectively included in this study to investigate the correlation of VBA characteristics with the risk of developing HFS and disease severity.

Asymmetry between left and right VAs is a common anatomical variation, with the left-sided dominance observed more frequently. This dominance of the VBA is particularly prominent in HFS patients [15], suggesting that the high-risk population for HFS could be identified by analyzing VBA features. The study also found that the left VA is often more dominant. The proportion of left-sided dominance of the VAs in patients with left-sided HFS is as high as 96.2%, whereas the proportion of right-sided dominance of the arteries in patients with right-sided HFS is 52.4% [16]. This indicates that there may be significant differences in VBA characteristics between patients with left-sided and those with right-sided HFS. Based on this hypothesis, the present study assessed the VBA characteristics in patients with HFS and in healthy individuals, in order to analyze the relationship of these characteristics with the risk of HFS occurrence. Further analysis was conducted to identify differences in VBA characteristics between right-sided HFS and left-sided HFS patients, and examine differences in these characteristics according to different HFS severity grades. In addition, to reduce the influence of age, gender and the correlation of blood pressure, blood glucose and lipid levels on the risk of developing HFS in patients and their condition, 59 cases of healthy controls were included in the analysis, with their age, gender, BMI, hyperlipidemia, mean arterial pressure, total cholesterol level, and fasting glucose levels all matched to the corresponding variables in the HFS group.

Our results showed that the diameter of the left and right VA, as well as the diameter of the basilar artery, were all independent influencing factors for HFS occurrence. There were no statistically significant differences in VBA diameter between patients with HFS on different sides or affected by HFS at different severity levels.

The influence of VBA on HFS occurrence is possibly reflected mainly in vascular compression and nerve excitation. Anatomically, asymmetry of the VBA, the presence of a dominant VA and the tortuosity of blood vessels increase the risk of vascular compression at the pontine exit of the facial nerve. It has been found that a larger diameter of blood vessel is associated with a greater risk for compression [17]. From a hemodynamic point of view, pressure differences and changes in wall shear stress caused by blood flow promote vascular displacement and deformation. The arterial diameter may indicate that the greater the vascular deformation, the higher the risk of compressing the pontine exit of the facial nerve and the greater the risk of HFS occurrence [18]. This study also found that blood flow velocity in the left and right vertebral and basilar arteries was lower in the HFS group than in the control group, though this difference was not statistically significant. This indicates that HFS patients experienced reduced blood flow velocities in the left and right vertebral and basilar arteries; however, the lack of significant differences compared to healthy controls may be attributed to the fact that most included patients had only mild to moderate levels of HFS. A study by Li et al. [19] reported that the dominant VA was associated with HFS and was more prevalent on the left. These findings indirectly support the conclusion of this study that the diameter of the left VA, the diameter of the right VA, and the diameter of the basilar artery are independent influencing factors for the occurrence of HFS.

However, some studies suggest that primary HFS is caused by vascular compression, where offending blood vessels increase the excitability of the facial nerve through mechanical irritation. This increased excitability facilitates transmission between nerve branches, thereby exacerbating the patient’s symptoms [20]. An increased VA diameter is associated with greater vascular compression of the facet nerve from the cerebral pontine segments due to mechanical factors. A study by Xia et al. [21] also found that mechanical compression of the offending blood vessels can lead to the overexpression of Nav1.8 in the sodium ion channel. Nav1.8 overexpression affects the resting potential of neurons and increases the excitability of the facial nerve nucleus. Excessive excitation and ‘cross-excitation’ between axons can cause more severe HFS symptoms. Additionally, in unilateral lesions, the contralateral dominant vessel often exhibits anatomical variations with increased diameter. However, our analysis of VBA characteristics in patients with HFS at different sides and severity levels did not reveal significant differences in VBA diameter between the subgroups. Although the specific mechanism remains unclear, we speculate that the lack of significant results may be attributed to the relatively small sample size of patients included in this study. Furthermore, the study did not adequately control for, or perform stratified analysis of, confounding factors such as vascular atherosclerosis. This may have obscured relevant vascular changes in HFS patients, leading to the lack of statistically significant differences between groups.

The limitations of this study are as follows: Firstly, owing to its retrospective nature, this study is subject to the inherent biases commonly associated with retrospective analyses. Secondly, the small sample size used and the variations in VBA characteristics in patients across different regions could limit extrapolation of the research results. Differences in the site of compression in the exit zone of the facial nerve were not thoroughly examined, limiting the study’s generalizability and mechanistic insight. Thirdly, VBA characteristics may vary depending on the site of vascular compression along the facial nerve’s root exit zone and the sides affected; however, this study did not perform a correlation analysis to investigate these differences. Therefore, further research is warranted in the future to explore this aspect in greater depth.

In summary, the diameters of the left and right VA and the basilar artery are independent influencing factors for HFS occurrence, with greater diameters of these vessels linked to improved predictive value for HFS. However, vessel diameter does not appear to correlate with disease severity.

• The relationship of VBA characteristics with the risk of HFS occurrence and disease severity remains unclear.

• The diameter of the left, right VA, and the basilar artery are associated with the risk of HFS occurrence, but not with HFS severity classification.

• Morphological alterations in the VBA may play a key role in the pathogenesis of HFS, but do not directly influence HFS clinical grading.

All data included in this study are available from the corresponding author upon reasonable request.

XH and JS designed the study. XH and JS conducted the study. XH provided assistance and guidance during the experiment. JS analysed the data. JS drafted the manuscript. Both authors contributed to important editorial changes to the manuscript. Both authors read and approved the final manuscript. Both authors participated fully in the work and agreed to take responsibility for all aspects of it.

This study was conducted in adherence to the Declaration of Helsinki, and the research protocol was approved by the Medical Ethics Committee of Sir Run Run Shaw Hospital, Zhejiang University School of Medicine (Ethics Approval No.: 2025-1076). This retrospective study used fully anonymized data and posed no risk to patient confidentiality and safety. Therefore, informed consent was waived in accordance with the “Ethical Review Measures for Biomedical Research Involving Human Subjects”.

We would like to express our sincere gratitude to our supervisor for designing this study, and to the Department of Neurology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, and its doctors for their valuable support and assistance.

This research received no external funding.

The authors declare no conflict of interest.