The diagnosis of the etiology of audio-vestibular symptoms is a clinical challenge; nevertheless, the use of MRI in diagnosis has increased the recognition of the underlying pathologic conditions. The 3-D CISS sequence provides a more comprehensive analysis of the CPA, IAC, root exit zone, and cisternal and intracanalicular segments of the cranial nerves [17]. Adoption of the role of VCS as a causative pathology for hemifacial spasm and trigeminal neuralgia was widely accepted. Meanwhile, its causal relationship with the neuro-otologic symptoms as tinnitus, deafness, or vertigo has been argued.
The exact pathophysiology of VCS is still to be elucidated. On the basis of the concept suggested by Jannetta et al. [2] which supported the role of neurovascular compression in causing cranial nerve dysfunction, several attempts were conducted to study a relationship between vascular compression and a number of clinical conditions [4, 18]. It was proposed that the arterial pulsatile compression causes mechanical irritation and focal demyelination which results in the development of these audio-vestibular symptoms. The other hypothesis is that the neurovascular compression disturbs the normal blood flow with decreased vascular perfusion of the nerve.
The present study was designed to evaluate the association of audio-vestibular symptoms with the presence of vascular loops and vascular contact in CPA and the IAC using the 3D CISS sequence done by 3 Tesla magnetic resonance imaging machine. Based on the results of the current study, it was concluded that no possible role of the presence of vascular loop in causing tinnitus, SNHL, or vertigo using 3D-CISS sequence as an assessment tool. Therefore, the presence of vascular loops in contact with the 8th cranial nerve is not certainly considered pathological but possibly to be a normal anatomical coincidental finding. Hence, this radiological finding alone should not be used to qualify patient for further invasive microvascular decompression surgery and is not suggested to be applied as a sole stratification criterion for any unnecessary intervention and its relation to cranial nerve should be cautiously considered.
In attempt to address the neurovascular conflict involving the 8th cranial nerve, and in accordance to our findings, several studies corroborated our data. Sirikci et al. reported no relationship between cochleovestibular symptoms and the type of vascular compression [14]. Furtherly, they suggested that MR modalities could be the preferred procedure in studying this anatomical relationship precisely. Similarly, several researches demonstrated the presence of neurovascular contact in both symptomatic and asymptomatic groups with no statistically significant association detected [3, 19, 20]. Additionally, several trials applied microvascular decompression techniques as an attempt to relief VCS of 8th cranial nerve and reported that variable percentages of patients did not improve after the microvascular decompression which raised the doubt about this clinical radiological relationship [21, 22]. Meanwhile, Bae et al. showed that the AICA loop anatomic location in the IAC and CPA in the symptomatic and asymptomatic sides of subjects with tinnitus and controls without tinnitus did not show statistically significant differences. However, the 8th cranial nerve angulation was significantly higher on the symptomatic sides of patients with tinnitus than in the other groups [23]. McDermott et al. reported similar results concerning tinnitus, where they showed no association between tinnitus and the presence of vascular loops, though they showed a relationship between AICA loops and unilateral hearing loss [16].
Nevertheless, other studies were not in accordance with the present study findings [10, 24, 25]. These studies supported the concept of VCS of the 8th CN based on the symptomatic improvement after microvascular decompression surgery of 8th CN. Furtherly, they even recommended early microvascular decompression before permanent damage of the nerve. Moreover, these studies showed a correlation between the presence of vascular loops in the IAC and pulsatile tinnitus and attributed the tinnitus to direct transmission of arterial pulsations to the cochlea via a resonance effect in the petrous bone. However, in a contradictory note, McLaughlin et al. study that assessed the efficacy of microvascular decompression after 4400 surgeries for various cranial nerves reported that variable percentages of patients did not benefit from the intervention [21].
In relative accordance to our study, an interesting multicenter study was proposed by Di Stadio et al. investigating the correlation between specific characteristics of the vascular loop with audio-vestibular symptoms using MRI scanning of CPA of asymptomatic patients [26]. In Di Stadio study, the assessed loop metrics were the depth of loop penetration into IAC, caliber of the vessel, position, number, and length of contacts between vessel and nerve. In accordance with our data, Di Stadio et al. concluded the absence of correlation between the presence of vertigo or tinnitus and a single neurovascular contact, while significantly correlated with an increased number of neurovascular contacts. The results were explained in the context of the multiplicity of mechanisms recruited by the vestibular system to maintain the balance including the visual and motor system which can lessen the incidence of these symptoms [27].
Stratification criteria for patients with cochleovestibular compression syndrome was proposed by De Ridder et al. who developed diagnostic criteria that are now widely adopted [28]. These criteria are (1) unilateral paroxysmal tinnitus; (2) co-existent ipsilateral symptoms including hemifacial spasms, otalgia, vertiginous spells, or hearing losses at tinnitus frequencies; (3) MRI findings evidencing vestibular conflict; and (4) abnormal auditory brainstem responses( ABR) [28]. Thus, clinical evaluation should be considered as more consistent diagnostic evidences than radiologic imaging of neurovascular compression of the cochlear nerve.
The underlying rationale for selection of 3D CISS over the conventional MRI is the high gradient amplitude. High strength magnets are employed to reach the maximum intensity within a short period of time [29]. CISS as a high resolution heavily T2WI 3D sequence with a very high CSF-tissue contrast provides optimal images for evaluation of neurovascular relationships allowing visualization of small vessels and enables the best assessment of an accurate relationship between nerve roots or their branches and adjacent vessels with a minimal signal loss due to CSF pulsations. Any desired imaging plane can be obtained by the multiplanar reconstructive technique [30].
However, CISS sequence is limited by the long image-acquisition times [30]. Furtherly, CISS sequences may be constrained by banding artifact as a result of magnetic field inhomogeneity causing pseudolesions to appear in the IAC assessment [31]. The deficiency of contrast between soft tissues and even between soft tissues and bone can obscure the lesions on CISS images [32]. CISS as a T2W sequence although of high diagnostic accuracy, can miss small CPA lesions which could be the occult cause for the patient’s symptoms and requires contrast-enhanced studies to be detected [33]. A study proposed by Abele et al. suggested an unenhanced MR imaging protocol utilizing axial CISS and coronal T2WI as a screening protocol to identify small IAC lesions ≤ 10 mm with 100% sensitivity [34].
In an attempt to minimize the bias in our study, we designed it to include a control group of healthy persons along with unaffected healthy ears in the patients. The current study was non-invasive and performed with no contrast administration, hence, saving health and financial burden. Using high strength MRI machine in the current study offers increased diagnostic sensitivity and specificity due to its higher SNR which is beneficial in improved visualization of small anatomical structures at higher field strengths. The high-field MR imaging (3 T and higher) has the potential to significantly improve clinical care in various neurologic disorders. Further studies recruiting a larger number of patients and control groups are recommended to confirm our data making it possible to apply our results for the general population.