The term “tinnitus” was introduced by Pliny and means “to ring.” Tinnitus can be defined as an auditory perception due to altered spontaneous activity within the auditory pathway, which arises as a result of aberrant excitation or inhibition. The underlying mechanism for occurrence of tinnitus can be abnormal afferent excitation at cochlear level, efferent dysfunction, and alteration of spontaneous activity with tonotopic reorganization [8].
Vascular compression syndromes are basically a clinical entity involving compression of one of the cranial nerves by a vessel. The pathophysiology of vascular compression syndromes could be impaired blood flow by a neurovascular compression or focal demyelination, reorganization, and axonal hyperactivity due to compression. However, although the pathophysiology of vascular compression syndromes can be applied on various conditions like hemifacial spasm and trigeminal neuralgia, it cannot fully explain audiovestibular symptoms like tinnitus [9].
It has been hypothesized that AICA loop can cause irritation of VIII cranial nerve, leading to gliosis, edema, axonal degeneration, and eventual fibrosis of the auditory nerve, leading to audiovestibular symptoms like tinnitus, vertigo, and hearing loss. These changes in the auditory nerve can also induce changes in the brainstem auditory nuclei. However, various radiological studies have shown nearly same incidence of AICA loops in the CP angle and IAC in symptomatic and asymptomatic cases, thus creating significant discrepancy regarding association of AICA loop and tinnitus [10, 11].
In our study, the mean age of presentation was 48.06 years, which was comparable to study conducted by Gultekin S et al. [12]; however, Bhatia A et al. [1] showed a younger mean age of presentation (35 years). In our study, more female subjects were seen as compared to males [statistically insignificant, p > 0.05)], similar to the study conducted by de Abreu Junior L et al. [13]. However, Kazawa N et al. [14] showed male preponderance in their study.
In our study, out of 131 patients with unexplained tinnitus, 76 patients (58%) had AICA loop on MRI. Out of them, 46 cases had AICA type 2 loop (Fig. 2), 29 cases had AICA type 1 loop, and 1 case had AICA type 3 loop (Fig. 1). Thus, according to our study, AICA type 2 was most commonly involved with tinnitus, followed by type 1 and type 3. Our finding was consistent with the study conducted by McDermott AL et al. [15] and de Abreu Junior L et al. [13]. However, studies conducted by Bhatia A et al. [1] and Kazawa N et al. [14] showed that AICA type 1 was most commonly associated with unexplained tinnitus. In contrast, Kim M et al. [16] suggested in their study that tinnitus was more frequent with AICA type 3.
In our study (Fig. 3), out of 16 patients with right-sided tinnitus, 11 patients had AICA on the same side, while 5 patients had AICA on the opposite (left) side. Out of 26 patients with left-sided tinnitus, 12 patients had AICA on the same side, while 14 patients had AICA on the opposite (right) side; these findings being statistically insignificant (p = 0.153). Similar finding was shown in their studies by Makins et al. [17], Gultekin et al. [12], and Grocoske et al. [18], who also concluded that there was no cause-effect relationship between tinnitus and vascular loops. However, Nowe et al. [19], Mc Dermott et al. [15], and Ryu et al. [20] suggested significant association between vascular loops in the internal auditory canal and tinnitus. Mc Dermott et al. [15] studied not only tinnitus but also the association of all cochleovestibular symptoms (including hearing loss) with AICA, hence concluding a significant association. We in our study did not include hearing loss/vertigo patients. Furthermore, Ryu et al. [20] explored posterior fossa in AICA patients for microvascular decompression and showed there was significant improvement in tinnitus postoperatively. We in our study did not operate to know the association between AICA and tinnitus but only focused on non-invasive methods like MRI and clinical findings. Again, Nowe et al. [20] grouped tinnitus as pulsatile and non-pulsatile to show significant association between vascular compression of the cisternal segment of eighth cranial nerve and non-pulsatile tinnitus, while stating pulsatile tinnitus was due to direct the transmission of pulsations to the cochlea due to a resonance effect in the petrous bone. We believed that grouping of tinnitus would not change our results.
Thus, in our study, the presence of AICA loop in patients with unexplained tinnitus could just be an incidental finding and AICA loops might be a normal anatomical variation, and thus, unnecessary microvascular decompression surgeries may not be performed. From our study, we could also conclude that the presence of vascular loop in IAC (AICA type 2 loop) does not always lead to reduced regional nerve vascular perfusion, and further research needs to be done on the complicated pathophysiology/symptomatology of microvascular syndromes.
