Evaluating the Neurovascular Compression in Virus-associated Peripheral Vestibulopathies: A Comparative Study of Vestibular Neuritis and Ramsay Hunt Syndrome With Dizziness

Abstract

Background: : This study aimed to investigate whether neurovascular compression (NVC) between the anterior inferior cerebellar artery (AICA) and the vestibulocochlear nerve (CVN) in the cerebellopontine angle (CPA) contributes to the pathophysiological differences between vestibular neuritis (VN) and Ramsay Hunt syndrome with dizziness (RHSD), both of which are recognized as vestibular disorders potentially resulting from viral reactivation.

Methods: : Twenty-two VN patients and 10 RHSD patients were included. The AICAs of these patients were assessed using Chavda, Gorrie, and Kazawa classification systems based on magnetic resonance imaging (MRI) findings of the CPA. All patients also underwent pure-tone audiometry (PTA), caloric test, and video head impulse test (vHIT).

Results: : (1) In VN patients, AICA types classified by Kazawa system showed a significant difference between the affected and non-affected sides (p = 0.011). (2) There was no significant difference in AICA types classified by all three systems on the affected side between VN and RHSD patients. (3) In RHSD patients, the AICA types classified by Gorrie system on the affected side were significantly associated with PTA (p = 0.016).

Conclusions: : While NVC appears to play a limited role in the differential pathophysiologic mechanisms of VN and RHSD, its contribution to peripheral vestibulopathy warrants further investigation.

Keywords

vestibular neuritis / Ramsay Hunt syndrome / cerebellopontine angle / anterior inferior cerebellar artery / viral reactivation

1 Introduction

Vestibular neuritis (VN) is an acute peripheral vestibular disease characterized by the sudden onset of persistent vertigo, often accompanied by nausea, vomiting, and postural imbalance, but without hearing loss or central nervous system symptoms. Although its exact etiology remains uncertain, it is generally believed to be related to the reactivation of herpes simplex virus type 1 (HSV-1)^[1]. Ramsay Hunt syndrome is marked by a triad of periauricular herpes, otalgia, and facial palsy, caused by the reactivation of varicella-zoster virus (VZV) latent in the geniculate ganglion^[2]. When vestibular symptoms are present, it is referred to as Ramsay Hunt syndrome with dizziness (RHSD)^[3]. Depending on the extent of nerve involvement, other symptoms such as hearing loss, tinnitus, hyperacusis, and dysgeusia may also occur.

The cerebellopontine angle (CPA) is a triangular space between the pons and cerebellum. The internal auditory canal (IAC) extends from the CPA to the cochlea and vestibular organs, through which the vestibulocochlear nerve (CVN) passes to regulate hearing and balance. The CPA also contains the anterior inferior cerebellar artery (AICA), located near the CVN, which supplies blood to the labyrinth, cochlea, and vestibular organs through its labyrinthine branch. Given the close anatomical relationship between AICA and CVN within CPA, this region may be susceptible to neurovascular compression (NVC). NVC syndromes refer to a group of complex disorders caused by compression of cranial nerves at the root entry/exit zone, including trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, and others. NVC may cause symptoms by altering hemodynamics or neural structure^[2]. Previous studies have explored the connection between the NVC of CVN and AICA and audiological outcomes in patients with asymmetric auditory-vestibular symptoms^[3–^7]. However, the effect of neurovascular compression in causing sensorineural hearing loss, vertigo, tinnitus, and other neurological symptoms is still debated. So far, no research has compared the pathophysiological mechanisms of VN and RHSD from the perspective of NVC. Although both VN and RHSD are considered to be caused by viral reactivation, considering the hematogenous and neural transmission of the viruses, whether the presence of NVC may lead to increased susceptibility to the viruses and contribute to the distinct pathophysiological mechanisms of the diseases remain unknown. Based on the distinct viral transmission characteristics, where HSV-1 may preferentially spread along neural pathways while VZV can also disseminate systemically via the bloodstream, we hypothesize that NVC might play a more pronounced role in VN compared to RHSD.

Advances in magnetic resonance imaging (MRI) techniques have enabled clear visualization of neurovascular structures in IAC and CPA. Based on the structure, position, and proximity of AICA to CVN, three main AICA classification systems—the Chavda, Gorrie, and Kazawa systems—have been used to categorize the neurovascular relationships within CPA-IAC^[8–^10]. This study applies these three AICA classification systems to investigate: (1) differences in AICA types on affected side between VN and RHSD patients; (2) differences in AICA types between affected and non-affected sides in VN and RHSD patients; (3) the correlation between AICA types on the affected side and abnormal hearing and vestibular function test results in VN and RHSD patients, in order to explore whether NVC contributes to the pathophysiological mechanisms underlying these two virus-associated peripheral vestibulopathies.

2 Materials and Methods

2.1 Study population

This single-center retrospective study was conducted at Union Hospital affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Twenty-two patients with VN and 10 patients with RHSD were enrolled.

Patients diagnosed with RHSD met the following criteria^[11]: (1) a sudden onset of peripheral facial nerve paresis; (2) presence of herpetic vesicles on the ipsilesional external auditory canal or auricle and (3) concurrent complaints of acute vertigo or dizziness.

Patients with VN were included based on following criteria^[12]: (1) a single episode of persistent vertigo lasting at least 24 hours; (2) unambiguous evidence of reduced unilateral impaired vestibulo-ocular response (VOR) function, demonstrated by either an impaired VOR gain on video head impulse test (vHIT) or a reduced caloric response and (3) absence of central neurological signs, otologic or audiologic findings.

Exclusion criteria were: (1) co-existing vestibular disorders such as Ménière’s disease, vestibular migraine, benign paroxysmal positional vertigo, and others; (2) history of ear surgeries or intratympanic injections; (3) recurrent episodes of sensorineural hearing loss; (4) structural abnormalities of middle or inner ear; (5) middle ear infections, including otitis media, mastoiditis, etc.; (6) presence of retrocochlear pathologies; (7) central nervous system disorders such as cerebellar infarction, multiple sclerosis, and others. Due to the lack of systematic recording of the total number of patients initially assessed, this study is subject to potential selection bias, which may limit the generalizability of the findings.

This research was carried out in compliance with the tenets of the Declaration of Helsinki. Ethical approval was granted by the Ethical Committee of Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

2.2 Methods

A comprehensive clinical evaluation was conducted for all patients at the initial visit, which included a detailed history inquiry, otoscopy, audiometric testing, tympanometry, videonystagmography, caloric testing, video head impulse test (vHIT) and MRI of the CPA and IAC using 3D sampling perfection with application optimized contrasts using different flip angle evolutions (3D-SPACE) sequence.

2.2.1 Pure tone audiometry

After excluding middle ear impairment through otological examination and tympanometry, pure-tone audiometry was conducted in a soundproof cabin, covering frequencies from 0.25 to 8 kHz. The pure tone average (PTA) was calculated as the simple arithmetic mean at 6 frequencies: 0.25, 0.5, 1, 2, 4 and 8 kHz^[7].

2.2.2 Caloric test

The caloric test was performed using Infrared videonystagmography (Visual Eyes VNG, Micromedical Technologies, Chatham, IL). The patient was positioned supine with the upper body raised by 30°. Cold (24 °C) and warm (50 °C) air stimuli were alternately delivered to each external auditory canal, and the maximum slow phase velocity (SPV_max) of caloric nystagmus was recorded. Canal paresis (CP) values were calculated by Jongkees' formula. Unilateral vestibular hypofunction was diagnosed when interaural asymmetry in caloric nystagmus exceeded 25%. Bilateral vestibular hypofunction was identified if the SPVmax was less than 6°/s in each ear after stimulation or if the total SPVmax for all four stimulation conditions was less than 20°/s.

2.2.3 vHIT

The vHIT test was conducted using the ICS Impulse system (GN Otometrics, Denmark). Patients wore lightweight goggles to track and analyze their eye movements. During the test, they were instructed to focus on a fixed visual target positioned 1.0 meter away. The technician stood behind the patient and manually delivered 20 to 25 passive, random head impulses, each lasting 150 to 200 ms with an amplitude of 5–15° and a peak velocity of 150–250°/s. Corrective saccades with a velocity greater than 50°/s were considered significant. In this study, pathological vHIT was defined as a reduced VOR gain below the canal-specific cutoffs (< 0.8 for horizontal canal and < 0.7 for vertical canals), accompanied by overt and/or covert corrective saccades.

2.2.4 Radiological evaluations

All imaging tests for enrolled patients were conducted within one week of the initial visit. MRI scans were performed on a Verio or Magnetom Trio 3T scanner (Siemens, Erlangen, Germany) using a 12-element phased array coil. T1- and T2-weighted spin-echo sequences were utilized to exclude retrocochlear lesions and pathology in the CPA. For detailed assessment, a 3D-SPACE was applied to (1) examine the course of the AICA and its relationship with adjacent structures, and (2) rule out inner ear malformations. MRI data were transferred to a workstation, and analysis was performed using a picture archiving and communication system (PACS) workstation (Carestream Client, Carestream Health). The data from all patients were randomly mixed and reviewed by two senior neuroradiologists (L.P. with over ten years and C.C. with over five years of experience), who were blinded to the clinical information. The disagreement was jointly re-evaluated to reach a final consensus, ensuring the reliability of the imaging assessments. The study used the Chavda, Gorrie, and Kazawa classification systems for analysis (Table 1 and Figure 1-3)^[8–^10].

2.3 Statistical analysis

Statistical analysis was conducted using SPSS software (version 26.0.0.2). Continuous variables are presented as means ± standard deviations or as medians with interquartile ranges (IQR, 25th to 75th percentiles). Categorical variables are reported as frequencies and percentages. The chi-square test was used to compare nominal categorical data distributions, and the Wilcoxon rank-sum test was used to compare ordinal categorical variables between the two groups. The Wilcoxon signed-rank test assessed differences in imaging classification between the affected and non-affected sides. The association between continuous variables and ordinal categorical variables was analyzed using Spearman rank correlation. Statistical analyses were performed only for subtypes with non-zero sample sizes. Subtypes with zero patients were excluded from the analyses and treated as missing data. A p-value of less than 0.05 was considered statistically significant. Given the small number of RHSD patients, the analyses in this study are exploratory, and the results should be interpreted with caution and validated in future studies with larger sample sizes.

3 Results

3.1 Demographic characteristics

A total of 22 VN patients and 10 RHSD patients were included in this study. Table 2 shows the detailed demographic characteristics of both groups. No significant difference was found between VN and RHSD patients in terms of gender, age, course duration, and the distribution of affected sides.

3.2 Comparison of AICA types between and within VN and RHSD groups

We compared the AICA types on the affected side between the VN and RHSD groups and found no significant differences (Table 3 and Figure 4). We also compared the AICA types on the affected and non-affected sides within each group (Table 4,5 and Figure 5). In VN patients, AICA types classified by the Kazawa system showed a significant difference between the affected and non-affected sides (p = 0.011). While the Wilcoxon signed-rank test does not allow direct identification of which specific subtypes differ between two sides, the descriptive analysis showed that the affected side had a higher proportion of loop-type configurations (Kazawa type IIA and IIB) compared with the non-affected side. The most common AICA type on the affected side was Kazawa IIA type (13/22, 59.09%), followed by IIB (5/22, 22.73%) and IB types (4/22, 18.18%). On the non-affected side, the most common AICA types were IIA and IB types (both occurring in 8/22, 36.36%), followed by IA and IIB types (both occurring in 3/22, 13.64%). RHSD patients exhibited no significant differences in the Chavda, Gorrie, or Kazawa types between the two sides.

3.3 Correlation between AICA types on the affected side and the results of hearing and vestibular tests in patients with VN and RHSD

In VN patients, no significant associations were found between the Chavda, Gorrie, or Kazawa types and the vHIT results [including anterior semicircular canal (ASCC), horizontal semicircular canal (HSCC), and posterior semicircular canal (PSCC)], caloric test results, or PTA (Table 6).

In contrast, in RHSD patients, the AICA types classified by the Gorrie system on the affected side were significantly associated with PTA (ρ = 0.847, p = 0.016), while no significant associations were observed between other types and audiological or vestibular test results (Table 7).

4 Discussion

4.1 The contribution of NVC to the pathogenesis of VN and RHSD

In this study, we found a significant difference in the AICA types classified by the Kazawa system between the affected and non-affected sides in VN patients. While the Wilcoxon signed-rank test does not allow direct identification of which specific subtypes differ between two sides, the descriptive analysis showed that the affected side had higher proportions of Kazawa types IIA and IIB compared with the non-affected side. The predominance of loop-type courses on the affected side raises the possibility that certain AICA trajectories, particularly those involving vascular loops in CPA-IAC, might provide a microanatomical environment conducive to subtle, chronic neural irritation. Such an environment could theoretically facilitate HSV-1 reactivation, although this remains speculative and requires further validation. In contrast, no significant differences in AICA types were observed between the affected and non-affected sides in RHSD patients, suggesting that the development of RHSD is less likely to be influenced by neurovascular configuration. Taken together, these findings support the interpretation that neither VN nor RHSD is directly caused by NVC, although anatomical variations may contribute to side-specific susceptibility in VN.

Furthermore, no significant differences in the AICA types were found on the affected side between VN and RHSD patients in our study. Despite this, previous studies have shown that RHSD patients tended to experience more severe vestibular dysfunction and have a poorer prognosis compared with VN patients^[11, ¹³, ^14]. It is widely believed that VN and RHSD are mainly associated with HSV-1 and VZV infections, respectively. These two viruses differ in their infection routes, reactivation mechanisms, and host immune interactions. HSV-1 primarily spreads via an intercellular pathway and exhibits relatively limited tissue tropism in humans^[15]. In contrast, owing to its resistance to nonspecific antiviral factors in serum, VZV is able to enter neurons via retrograde axonal transport and disseminate hematogenously, resulting in broader tissue tropism in humans^[16, ^17]. Once reactivated, HSV-1 can evade the immune response through various effective strategies, weakening the inflammatory response. In this process, CD8+ T cells play a central role by degrading viral proteins through non-cytolytic mechanisms, controlling HSV-1 infection without inducing neuronal death^[18]. However, the control of VZV reactivation may rely more heavily on CD4+ T cells^[19]. The host will stimulate a strong adaptive immune response to resist the virus. Cytokines and free radicals released by immune cells can directly damage neurons. Moreover, these inflammatory mediators may trigger neuroinflammation, leading to edema and compression of nerves. Furthermore, excessive activation of immune cells can initiate autoimmune responses, mistakenly attacking nerves and resulting in demyelination and axonal degeneration^[20]. At the central level, VZV may also spread retrogradely along the vestibular nerve, affecting the function of the cerebellum and vestibular nuclei. A recent study found that in 5 out of 10 patients with RHS, focal lesions were observed in the ipsilateral vestibular nuclear complex, whereas no such imaging abnormalities were found in VN group^[21]. These factors account for the more extensive and severe neurological damage exhibited by RHSD patients. Given that no significant differences were found in anatomical classifications of AICA between VN and RHSD patients, the role of NVC in the pathophysiological mechanisms of VN and RHSD may be limited.

4.2 Association between NVC and audio-vestibular findings in VN and RHSD patients

Another major finding of this study was that the AICA types classified by the Gorrie system were significantly associated with audiological outcomes in patients with RHSD. In this classification system, the increased contact between vascular loops and nerves correlates with more severe hearing loss in RHSD patients. No significant association with audio-vestibular outcomes was observed in other AICA types in either RHSD or VN.

Until now, few studies have focused on the NVC in VN patients. Loader et al. found that in VN patients with normal caloric test results, the incidence of neurovascular contact was significantly higher than in VN patients with abnormal caloric test results and in asymptomatic control groups^[22]. The differences in sample size, imaging techniques, and NVC classification systems may explain the discrepancies between their findings and ours. Regarding the correlation between audiological and vestibular function test outcomes and vascular loop classifications, previous studies have shown controversial results. Di Stadio et al. evaluated 2,622 patients with asymmetric auditory-vestibular symptoms and found that vascular loops directly contacting the nerve were associated with dizziness and tinnitus, while hearing loss correlated with both the frequency and length of neurovascular contact^[23]. Li et al. analyzed the association between the Chavda classification of vascular loops within CPA-IAC and the audio-vestibular symptoms, but no statistically significant results were found^[24]. A review including 15 related studies (with a total of 11,788 patients) found that in nearly 70% of cases, no association was observed between auditory-vestibular symptoms and vascular loops. This suggests that vascular loops may represent anatomical variations in most cases, with only a minority of cases showing a relationship to auditory-vestibular symptoms^[3].

Possible mechanisms by which neurovascular contact leads to auditory-vestibular dysfunction include focal demyelination of the nerve, disturbed blood flow causing localized hypoperfusion, or mechanical stimulation of the cochlea via arterial pulsations transmitted through the petrous bone. Additionally, in RHSD patients, the characteristic hematogenous spread of VZV might exacerbate this dysfunction. Vascular loop contact or compression may lead to microvascular dysfunction of the internal auditory artery or its branches, particularly under the inflammatory condition associated with VZV reactivation. This could result in more severe hearing loss in RHSD patients. Although advances in imaging technology have improved the detection of vascular loops in CPA, given the lack of a unified and effective classification system and the insufficient validation of hemodynamic and neural structural changes, the underlying mechanisms by which NVC causes audio-vestibular symptoms remain to be further investigated.

4.3 Strengths and Limitations

To the best of our knowledge, this is the first study to comparatively analyze the neurovascular relationships within CPA-IAC in two virus-associated disorders, VN and RHSD. Our findings demonstrated no significant differences between the groups, indicating that NVC may not underlie their clinical distinctions. Only one previous study has examined the relationship between vestibular function and NVC in VN patients^[22]. They found that VN patients with normal caloric test results had a significantly higher incidence of NVC in CPA, which is inconsistent with our findings, indicating the need for further validation with larger samples. Moreover, the association between audio-vestibular dysfunction and NVC in RHSD has not been previously explored and also requires further investigations.

Several limitations should be acknowledged in this study. First, the number of RHSD patients included in this retrospective analysis was relatively small, and no formal sample size calculation was performed, as the study included all eligible patients seen during the study period. This may limit the statistical power and generalizability of the findings. Future studies with larger cohorts are needed to provide more robust conclusions regarding the association between neurovascular relationships and clinical symptoms in RHSD patients. Second, the Kazawa classification system evaluates only the presence of vascular loops in the CPA-IAC region and cannot determine whether there is mere contact or compression between vascular loops and nerves. Therefore, the Kazawa classification system can only suggest potential NVC, and its relationship with CVN dysfunction remains to be further established. Third, this study assessed and compared the AICA classifications in CPA of VN and RHSD patients using routine MRI, focusing solely on anatomical features. However, other studies have shown that high signal intensity detected by delayed gadolinium-enhanced imaging may indicate pathological changes such as disruption of the blood-labyrinth barrier, hemorrhage, or neuritis^[25]. Future research may need to incorporate such imaging techniques to further explore the pathophysiological differences between VN and RHSD.

5 Conclusions

In this exploratory study, no significant differences were found in CPA-IAC AICA types on the affected side between VN and RHSD patients. However, asymmetry in AICA course was observed between affected and non-affected sides in VN patients, and the Gorrie classification was associated with the degree of hearing loss in RHSD patients. These findings suggest that NVC might exert influence differently in these disorders, but its precise role and value in differentiating them require further investigation with larger sample sizes and incorporation of advanced imaging techniques.

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