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 Table of Contents  
Year : 2021  |  Volume : 5  |  Issue : 1  |  Page : 2-7

Is there an association between the anteroinferior cerebellar artery vascular loop and asymmetrical sensorineural hearing loss?

1 Department of ENT, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, Meghalaya, India
2 Department of Radiodiagnosis, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, Meghalaya, India
3 Department of Radiodiagnosis, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, Meghalaya; Department of Radiology, Sikkim Manipal Institute of Health and Medical Sciences, Gangtok, Sikkim, India

Date of Submission20-Dec-2020
Date of Acceptance02-May-2021
Date of Web Publication03-Jul-2021

Correspondence Address:
Dr. Abhijeet Bhatia
Department of ENT, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong - 793 018, Meghalaya
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aiao.aiao_21_20

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Background: Asymmetrical sensorineural hearing loss is usually idiopathic. Vascular loops are commonly implicated in compression disorders involving lower cranial nerves, which can be relieved on surgical decompression. However, the cause–effect relationship between vestibulocochlear symptoms and vascular loops is still controversial. Objective: The objective of this study is to look for an association between the presence of anteroinferior cerebellar artery (AICA) loops and asymmetrical sensorineural hearing loss of unknown etiology. Methods: Twenty-four patients with complaints of asymmetrical hearing loss of no discernible cause underwent a magnetic resonance imaging of the brain between August 2015 and August 2017. The AICA loops were graded using two classifications, namely Chavda classification and a grading system proposed by Adam Gorrie et al. (second classification). The vascular loops were correlated with the presence of hearing loss, tinnitus, and vertigo. Results: Hearing loss did not correlate significantly with the vascular loops on grading with either Chavda or the second classification. The presence of tinnitus or vertigo too did not correlate significantly with the grading of vascular loops. The caliber of AICA too did not correlate significantly with hearing loss. Conclusion: Vascular loops do not appear to be associated with asymmetrical hearing loss and other cochleovestibular symptoms.

Keywords: Anteroinferior cerebellar artery, asymmetrical hearing loss, magnetic resonance imaging, tinnitus

How to cite this article:
Bhatia A, Phukan P, Sharma B, Polley G. Is there an association between the anteroinferior cerebellar artery vascular loop and asymmetrical sensorineural hearing loss?. Ann Indian Acad Otorhinolaryngol Head Neck Surg 2021;5:2-7

How to cite this URL:
Bhatia A, Phukan P, Sharma B, Polley G. Is there an association between the anteroinferior cerebellar artery vascular loop and asymmetrical sensorineural hearing loss?. Ann Indian Acad Otorhinolaryngol Head Neck Surg [serial online] 2021 [cited 2022 Aug 7];5:2-7. Available from: https://www.aiaohns.in/text.asp?2021/5/1/2/320574

  Introduction Top

The cause of asymmetric sensorineural hearing loss in many cases remains undiagnosed. In some cases, it is believed that the etiology involves a loop of the anterior inferior cerebellar artery (AICA), insinuating itself into the internal auditory meatus.

The cerebellopontine angle (CPA) is bordered superiorly by the medial portion of the midbrain. The trigeminal nerve, facial nerve (FN), and vestibulocochlear nerve (VCN) all exit the brain in this region. The AICA is a branch of the basilar artery and supplies the anterior cerebellum. It courses variably in the CPA and gives off the labyrinthine branch that supplies the vestibule and the cochlea.[1] Due to its anatomy, it is commonly implicated in compression syndromes.[2] The term vascular compression syndrome was first introduced by McKenzie in 1936. However, possibly the first case was described in 1875, where a vertebral artery aneurysm was found to be compressing the FN.[3] The concept has since been expanded to explain diseases related to various cranial nerves.

Microvascular compression (MVC) is described as mechanical irritation of a cranial nerve by another tissue, usually blood vessel. They are of concern usually when they are symptomatic. Trigeminal, facial, vestibulocochlear, and glossopharyngeal nerves are known to be the most commonly involved.[4] There are several commonly used terms for MVC of the VCN such as MVC syndrome, vascular compression syndrome, and AICA syndrome. Vascular loops can be identified in many asymptomatic individuals also and hence the debate whether such loops are an incidental finding or responsible for these symptoms continues.[5],[6],[7],[8],[9]

In the 1970s, Jannetta et al. described how symptoms such as hemifacial spasm, trigeminal neuralgia, VCN symptoms, and glossopharyngeal neuralgia could be explained by vascular loops pressing on cranial nerves. They also demonstrated the salutary effect of vascular decompression of the offending cranial nerves at the nerve roots.[10] However, subsequent studies have failed to conclusively demonstrate the cause-and-effect relationship between vascular loops in the vicinity of the VCN and otological symptoms. In fact, the very existence of the condition is still controversial.

Surgical treatment, where attempted, of a microvascular syndrome involves transposition of the offending blood vessel, whereas medical treatment aims to reduce tinnitus through the use of drugs such as carbamazepine.[11],[12],[13] However, in view of the uncertainty of the causation, surgical decompression has been reported only sporadically. An established cause–effect relationship will offer definitive treatment to selected patients.

The objective of the present study, therefore, was to evaluate and analyze, through magnetic resonance imaging (MRI), the presence of vascular loops and their association with asymmetrical hearing loss (AHL) and other vestibulocochlear symptoms.

  Methods Top


This study (Project no. P252/15/035) was conducted in the institute after clearance from the Institutional Ethics Committee. Informed written consent was obtained from all patients participating in the study.

Study design

Selection and description of participants: Patients who came to the ENT outpatient clinic between August 2015 and August 2017 with complaints of hearing loss were evaluated by detailed history and examination. History of associated tinnitus and vertigo was also elicited. This was then followed by a pure-tone audiometry.

Technical information

AHL was present when there was a difference of 20 dB at 1 frequency or 10 dB at two or more frequencies between the two ears. Pure-tone average (PTA) was calculated as an average of 1000, 2000, and 4000 Hz. Ears with PTA ≤20 dB were considered as normal hearing ears. Those with hearing loss between 21 and 40 dB were categorized as mild hearing loss, those with hearing loss between 41 and 70 dB were categorized as moderate hearing loss, and finally, those with hearing loss more than 70 dB were considered as having severe hearing loss. Among the cases diagnosed with AHL, only consenting patients were included in the study. The rest were managed appropriately but were excluded from the study. Furthermore, cases with bilateral symmetrical hearing loss or history of ear surgery or ear discharge were excluded from the study. The laterality of hearing loss and associated symptoms were noted.

Various hematological, serological, and biochemical investigations (hemoglobin, total leukocyte count, differential leukocyte count, erythrocyte sedimentation rate, platelet count, blood sugar, liver function tests, kidney function test, thyroid function tests, HIV, hepatitis B surface antigen, anti-hepatitis C virus, and Venereal Disease Research Laboratory) were then conducted to exclude metabolic causes of sensorineural hearing loss (SNHL). This was followed by contrast-enhanced MRI brain. Constructive interference in steady state three-dimensional and time-of-flight magnetic resonance angiography T2-weighted images were obtained and assessed. Two senior radiologists blinded to the laterality of the hearing loss of the patients studied the axial contiguous sections of the MRI scans. Patients in whom a definite cause was found (like acoustic neuroma) were excluded from the study. However, the management protocol for the diagnosed disorder was followed. None of the patients underwent microvascular decompression.

Radiologic evaluation

The internal auditory canal (IAC) MRI images of the patient with no definite cause were examined. Both sides were graded for the vascular loops using two classifications:[3]

  1. Chavda system:

    1. Grade 1 – When an AICA loop borders the internal auditory meatus
    2. Grade 2 – When the loop insinuates itself into the internal auditory meatus but occupies 50% or less of the canal
    3. Grade 3 – When the loop occupies more than 50% of the canal.

  2. Grading system proposed by Adam Gorrie et al. (second classification):

    1. Class A – No contact
    2. Class B – Vascular loop lying directly adjacent to nerve
    3. Class C – Loop running in between VII and VIII nerves
    4. Class D – Vascular loop displacing the nerve resulting in bowing of the nerve.

The grades of vascular loops of AICA in relation to the internal acoustic meatus and vestibulocochlear and FNs were correlated with the degree of hearing loss.

The ratio of diameter of AICA/FN in the IAC was then correlated to the degree of hearing loss. The ratio, AICA/FN, was classified as >1, =1, and <1.

Statistic analysis

The data were compiled on Excel worksheet and analyzed using GNU PSPP version 3 software, 2007; copyright- Free Software foundation Inc, USA. Statistical significance was evaluated using two-tailed Chi-square test, with P ≤ 0.05 regarded as demonstrating a statistically significant association.

  Results Top

A total of 24 patients were included in the study, resulting in analysis of 48 ears. The patients included 13 (54.2%) men and 11 (45.9%) women between 7–68 years of age, with a mean age of 36 ± 17.7 years. The AICA was identified in all patients bilaterally. A total of 14 (29.2%) ears had normal hearing and 10 (20.1%) had severe hearing loss. Eighteen patients (75%) reported insidious onset of hearing loss and five (20.1%) reported sudden onset. The onset was unknown in one patient. The mean duration of hearing loss was 76.0 ± 91.8 months and ranged between 3 months and 30 years. An equal number (12 each; 50%) of patients had asymmetrical hearing loss in right and left ears, respectively. All patients complained of hearing loss on presentation. Vertigo or tinnitus was not the presenting complaint in any patient. The mean PTA of ears without hearing loss/lesser degree of hearing loss (n = 24) was 20.2 ± 7.9 dB, whereas PTA of ears with asymmetrical hearing loss (n = 24) was 65.6 ± 18.6 dB.

Using the Chavda classification [Table 1], it was observed that out of 33 ears with Grade 1 loops, 22 ears (66.7%) had some degree of hearing loss, out of which eight ears (36.4%) had severe hearing loss. However, out of 15 ears with Grade 2 and 3 loops, it was observed that 12 ears (80%) had some degree of hearing loss. Conversely, out of 14 ears with normal hearing, 11 (78.6%) had Grade 1 loops. Out of 34 ears with hearing loss, 12 (35.3%) had Grade 2 or 3 loops. The relationship between grade of vascular loops and hearing loss, however, was not statistically significant (P = 0.546). The MRI images of Chavda grading are depicted in [Figure 1].
Figure 1: Magnetic resonance imaging brain axial sections showing relationship between AICA and VCN as per Chavda classification. (a) Grade 1; (b) Grade 2; (c) Grade 3. AICA: Anterior inferior cerebellar artery, FN: Facial nerve, VCN: Vestibulocochlear nerve

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Table 1: Correlation between degree of hearing loss and grade of vascular loop (Chavda classification)

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Using the second classification system [Table 2], none of the ears had Class D loops. Out of 14 (31%) ears with no hearing loss, 9 (64.3%) had Class A loops. Out of 10 ears having severe hearing loss, six (60%) had Class A loops. However, out of 22 ears with moderate or severe hearing loss, 11 (50%) had Class A loops. On the other hand, out of 22 ears with Class B or C loops, only 5 (22.7%) had normal hearing. However, the probability of Class B or C having hearing loss was 0.14429 and 0.56868, respectively, hence statistically not significant (P > 0.05). The MRI images of second classification grading are depicted in [Figure 2].
Figure 2: Magnetic resonance imaging brain axial sections showing relationship between AICA and VCN as per second classification. (a) Class A; (b) Class B; (c) Class C. AICA: Anterior inferior cerebellar artery, FN: Facial nerve, VCN: Vestibulocochlear nerve

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Table 2: Correlation between degree of hearing loss and grade of vascular loop (second classification)

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On correlating AICA/FN ratio with normal hearing, out of 14 ears with normal hearing, only five ears (35.7%) had AICA/FN <1, whereas among 34 ears with hearing loss, AICA/FN was equal to or more than one in 18 (52.9%) ears. AICA/FN ratio did not have any significant relationship with hearing loss (P = 0.624).

A total of 20 patients experienced tinnitus along with hearing loss, of which 16 (80%) experienced tinnitus in the same ear as the one with higher degree of hearing loss. Among them, six patients (37.5%) had Chavda Grade 2 or 3 loops and nine (56.3%) had second classification Class B or C loops. Grade of loops and tinnitus, however, had no significant correlation by Chavda classification (P = 0.204) or second classification (P = 0.148) [Table 3] and [Table 4].
Table 3: Correlation between the presence of tinnitus and degree of loops (Chavda classification)

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Table 4: Correlation between the presence of tinnitus and degree of loops (second classification)

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Vertigo was present in nine (37.5%) patients only, among whom only 4 (16.7%) had Chavda Grade 2 or 3 loops or second classification Class B or C loops. The relationship between history of vertigo and grade of loops by Chavda classification or second classification was not statistically significant (P = 0.537). However, the correlation between history of vertigo and grading of loops by the second classification was not statistically significant (P = 0.794).

  Discussion Top

Vascular compression of the VCN was first attempted to be explained by Jannetta in 1975.[10] However, MVC of VCN as a cause of vestibular and auditory symptoms continues to remain unproven.[14] MVC of VCN can have multiple deficits. These include hearing loss, vertigo, and tinnitus in varying degrees, combinations, and characteristics. Hence, the presentation is complex.[12],[15] Furthermore, cadaveric studies have shown that loops of the AICA occur within the internal auditory meatus in 13%–40% of human temporal bones on dissection and 14%–34% on MRI.[1] MVC is a diagnosis of exclusion since there are no definitive diagnostic criteria.[3] The two classification systems for grading of vascular loops in the IAC were developed in order to explain the unexplained vestibulocochlear symptoms.[3],[6] However, the results of various studies attempting to establish the correlation or association using the classification systems have been highly variable.[3],[6],[13],[15] The Chavda classification has traditionally been used for grading the degree of intrusion of the AICA loops into the IAC, whereas the second classification takes into account the contact and also the displacement or indentation of VCN by AICA loops.[3] A comparison of various studies is compiled in [Table 5].
Table 5: Comparison of various studies that analyze the relationship between otological symptoms and vascular loops in internal acoustic canal and cerebellopontine angle

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In the current study, hearing loss, tinnitus, and vertigo were assessed. The relationship between hearing loss and vascular loops graded by Chavda classification or the second classification was not significant. Similarly, the vascular loops did not correlate significantly with the presence of either tinnitus or vertigo on grading with either classification.

The results were similar to those of Gorrie et al., using similar methodology, except that the latter study was retrospective.[3] McDermott et al. also used the Chavda classification with similar methodology. However, they had a much larger sample size and did not comment upon vertigo. Unlike the current study, they found a significant correlation between higher grade of loops and hearing loss. However, like the current study, they too did not find any significant correlation between caliber of the AICA loops and hearing loss as assessed by the AICA/FN ratio. AICA caliber greater than or equal to one implied a large caliber, which in turn implies good hearing outcomes. They also did not find any relationship between AICA loops and tinnitus.[6] In a study by Gultekin et al., vascular loops were not found to cause tinnitus. They graded vascular loops by the Chavda classification and attributed these results to the observation that AICA loops might be normal variations in a significant proportion of asymptomatic population and to the multiple symptoms of VCN disorders.[15] De Ridder et al. reported tinnitus and frequency-specific hearing improvement following microvascular decompression at specific sites of the VCN in their patients. They supported the tonotopical organization of the cisternal segment of the VCN and reported a significant improvement in hearing loss in patients undergoing microvascular decompression of the VCN.[13]

The results of the current study and its variations with previous studies might be attributed to subjectivity in reporting symptoms and vascular loops. The current methods of diagnosis rely overtly on pure-tone audiometry and MRI. Given the multiplicity of symptoms of VCN disorders and the subjectivity in presentation, the diagnosis of the condition might require developing a more objective and elaborate protocol. A scoring system devised by Okamura et al. takes into account the cochleovestibular symptoms of SNHL, tinnitus, and vertigo, along with audiological, MRI, and brainstem-evoked response auditory findings to diagnose cases of MVC with inconclusive results.[17] However, electrophysiological tests might improve the diagnostic protocols, in view of the complexity of the symptoms of MVC of VCN. Initial carbamazepine trial has also been suggested as a diagnostic modality for typewriter tinnitus.[21]

  Conclusion Top

The current study did not reveal any significant correlation between AICA loops and vestibulocochlear symptoms of hearing loss, tinnitus, and vertigo. The two grading systems that assessed the relationship between AICA loops, VCN, and IAC based on MRI findings reported similar results with respect to vestibulocochlear symptoms.


This study was done as an intramural study in the North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences. No specific funding was provided.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Moosa S, Fezeu F, Kesser BW, Ramesh A, Sheehan JP. Sudden unilateral hearing loss and vascular loop in the internal auditory canal: Case report and review of literature. J Radiosurg SBRT 2015;3:247-55.  Back to cited text no. 1
Brackmann D, Crawford J, Green D. Cerebellopontine Angle Tumors. Head and Neck Surgery - Otolaryngology. 4th ed. Philadelphia: Lippincott Williams and Wilkins; 2006. p. 2208-30.  Back to cited text no. 2
Gorrie A, Warren FM 3rd, de la Garza AN, Shelton C, Wiggins RH 3rd. Is there a correlation between vascular loops in the cerebellopontine angle and unexplained unilateral hearing loss? Otol Neurotol 2010;31:48-52.  Back to cited text no. 3
Haller S, Etienne L, Kövari E, Varoquaux AD, Urbach H, Becker M. Imaging of neurovascular compression syndromes: Trigeminal neuralgia, hemifacial spasm, vestibular paroxysmia, and glossopharyngeal neuralgia. AJNR Am J Neuroradiol 2016;37:1384-92.  Back to cited text no. 4
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Nowé V, de Ridder D, van de Heyning PH, Wang XL, Gielen J, van Goethem J, et al. Does the location of a vascular loop in the cerebellopontine angle explain pulsatile and non-pulsatile tinnitus? Eur Radiol 2004;14:2282-9.  Back to cited text no. 7
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Jannetta PJ. Observations on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction and glossopharyngeal neuralgia. Definitive microsurgical treatment and results in 117 patients. Neurochirurgia (Stuttg) 1977;20:145-54.  Back to cited text no. 10
Levine RA. Typewriter tinnitus: A carbamazepine-responsive syndrome related to auditory nerve vascular compression. ORL J Otorhinolaryngol Relat Spec 2006;68:43-6.  Back to cited text no. 11
Okamura T, Kurokawa Y, Ikeda N, Abiko S, Ideguchi M, Watanabe K, et al. Microvascular decompression for cochlear symptoms. J Neurosurg 2000;93:421-6.  Back to cited text no. 12
De Ridder D, Ryu H, Møller AR, Nowé V, van de Heyning P, Verlooy J. Functional anatomy of the human cochlear nerve and its role in microvascular decompressions for tinnitus. Neurosurgery 2004;54:381-8.  Back to cited text no. 13
de Ridder D, de Ridder L, Nowé V, Thierens H, van de Heyning P, Møller A. Pulsatile tinnitus and the intrameatal vascular loop: Why do we not hear our carotids? Neurosurgery 2005;57:1213-7.  Back to cited text no. 14
Gultekin S, Celik H, Akpek S, Oner Y, Gumus T, Tokgoz N. Vascular loops at the cerebellopontine angle: Is there a correlation with tinnitus? AJNR Am J Neuroradiol 2008;29:1746-9.  Back to cited text no. 15
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Okamura T, Nishizaki T, Ikeda N, Nakano S, Sakakura T, Fujii N, et al. Diagnosis of cochleovestibular neurovascular compression syndrome: A scoring system based on five clinical characteristics. No Shinkei Geka 2017;45:117-25.  Back to cited text no. 17
Grocoske FL, Mendes RD, Vosguerau R, Mocellin M, Oliveira MT, Koerner HN. Neurotology findings in patients with diagnosis of vascular loop of cranial nerves VIII in magnetic resonance imaging. Intl Arch Otorhinolaryngol 2011;15:418-25.  Back to cited text no. 18
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Ryu H, Yamamoto S, Sugiyama K, Nozue M. Neurovascular compression syndrome of the eighth cranial nerve. What are the most reliable diagnostic signs? Acta Neurochir (Wien) 1998;140:1279-86.  Back to cited text no. 20
Bae YJ, Jeon YJ, Choi BS, Koo JW, Song JJ. The role of MRI in diagnosing neurovascular compression of the cochlear nerve resulting in typewriter tinnitus. AJNR Am J Neuroradiol 2017;38:1212-7.  Back to cited text no. 21


  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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