Ringing or humming of one or both ears without any stimulus is called "tinnitus." Its prevalence is 7%-32% in the general population. Tinnitus may be classified as "pulsatile-non-pulsatile" or "objective-subjective." Subjective tinnitus is heard by the patient only, whereas objective tinnitus is the ringing or humming sound heard by both the examining physician and the patient. Objective tinnitus usually has a vascular origin (dural arterio-venous malformation, carotid-cavernous fistula, and arteriovenous malformation of the vascular structures of the neck). Subjective tinnitus is observed more frequently (internal auditory canal [IAC] pathology, presbycusis, acoustic trauma, Meniere's disease, otosclerosis, labyrinthitis, effusion, ossicle system deformities, cholesteatoma, tumors, external auditory canal pathology, metabolic, neurologic, and psychological causes) [1].

One of the most frequent causes of non-pulsatile tinnitus is cerebello-pontine junction neoplasms while the most frequent cause is acoustic neurinomas. Non-pulsatile tinnitus is nearly always subjective. The etiology of tinnitus has not been completely understood despite all the developments in the area of modern medicine. Since the etiological causes of subjective tinnitus are extremely variable, much more studies have to be performed to find actual causes and effective treatment methods [2].

Computerized tomography and magnetic resonance imaging (MRI) procedures recommended in evaluating the IAC help identifying pathologies inside the canal rather than the ones in the canal itself. Up to date, no study has been performed to assess the natural form of the structure of the canal and the contents of it [3]. The aim of the present study was to evaluate the internal acoustic canal and the nerves in it to determine possible structural differences in patients presenting to the outpatient clinic of the ear, nose, and throat (ENT) department with the complaint of subjective tinnitus with no known causes.

Ethical approval was obtained from the Ethics Committee of Elazig Training and Research Hospital.

The mean age was 49.78 years (38 years in males and 40 years in females) in the tinnitus group and 46.31 years (36 years in males and 43 years in females) in the control group (Table 1). The ages of the tinnitus group ranged from 23 to 80 years.

There was no statistically significant difference between the tinnitus group and the control groups in terms of age (P=0.724) and gender (P=0.908). The IAC CSA measurements of the tinnitus group were statistically significantly lower than those of the control group (P<0.007). No statistically significant difference was found between the control group and the tinnitus group in terms of the FN CSA (P=0.366), the SVN CSA (P=0.120), IVN CSA (P=0.119), the total vestibular nerve CSA (P=0.140), and the CN CSA (P=0.235). All of these data are shown in Table 1.

Tinnitus, which has been a subject studied increasingly in recent years, is a symptom that might cause many problems in patients. Tinnitus may be classified as pulsatile-non-pulsatile or as objective-subjective. However, the exact etiological mechanism of tinnitus has not been completely understood yet [6]. Tinnitus can be associated with a number of conditions that may occur at any level of the auditory system. However, it is generally linked to lesions associated with the acoustic nerve and the inner ear, and it has been found that there is increased spontaneous activity in the nerve fibers in almost all of the lesions [7].

Tinnitus is a frequently encountered health problem observed especially in individuals over the age of 40. Its prevalence is higher in industrialized countries [8]. In the present study, the mean age of the patients with tinnitus was 49.78 years, as expected. Tinnitus has a roughly equal prevalence in men and women [7]. The male/female ratio was 0.95 in the present study. Many studies advocate that the probability of tinnitus is increased in patients having hearing loss [7]. This study excluded patients with hearing loss of more than 30 dB as such a loss could be a confounding factor in the etiological evaluation of the tinnitus.

MRI has recently been employed to visualize neuronal structures in the IAC and inner-ear morphology [9,10,11,12,13,14,15,16]. Improvements in MRI resolution have allowed identification of the cochlear, facial, and vestibular nerves and differentiation of them from other nerves within the IAC [17]. In the IAC, vestibulocochlear nerve splits into three parts (cochlear, superior vestibular, and inferior vestibular). These three vestibulocochlear nerve branches, along with the FN, have a characteristic appearance on the sagittal oblique steady-state free precession (SSFP) cross-sectional images (Fig. 2). Images in that plane are most frequently used for the detection of CN aplasia [18].

On any single axial SSFP image, only two of the four nerves within the IAC are typically visible. If one of the nerves is seen to enter the modiolus of the cochlea, then the two visible nerves are the cochlear and IVNs. If the central modiolus is not depicted on the image, the visible nerves are the facial and SVNs. At the lateral aspect of the IAC, the FN lies in the anterosuperior portion, the CN lies in the anteroinferior portion, the SVN lies in the posterosuperior portion, and the IVN lies in the posteroinferior portion. A filling defect within the IAC on SSFP images may signal a nerve abnormality in a branch of the facial or vestibulocochlear nerve [9,13,15,18].

To take full advantage of these imaging sequences, radiologists must be aware of the appearances of similar anatomic details of these nerves and the IAC on SSFP MR images [18]. Consistent with the literature, CN was larger than the branches of the vestibular nerve and had similar or larger size compared to the FN and no abnormality was detected in the IAC caliber of any cases. Through this detailed anatomical information and by applying the above mentioned MRI technique, it is possible to determine the IAC and its content such as vestibular or CN anomalies [9].

Clinical symptoms produced by cross-compression of the cranial nerves were first introduced by Dandy in 1934 [19]. In hemifacial spasm, trigeminal neuralgia and glossopharyngeal neuralgia caused by neurovascular decompression, one of the effective treatment options is microvascular decompression (MVD) [19]. The term cochleovestibular neurovascular compression was introduced after a couple of decades. Microvascular decompression in vertigo was first reported by Jannetta [20] in 1975. These developments encouraged CN MVD operation in tinnitus [21]. Decompression of the 8th nerve through MVD surgery has been reported to improve tinnitus complaints in patients having tinnitus [22].

Clinical symptoms of the acoustic neurinomas are related directly to the tumor dimensions. Tinnitus due to the pressure of the enlarging acoustic neurinomas in the IAC on the CN in the IAC has been reported [23]. Having a temporary improvement in patients with acoustic tumor, sudden hearing loss and tinnitus complaints after steroid treatment was interpreted as the outcome of decompression of the 8th nerve by steroid [24]. Cerebellopontine angle or internal acoustic canal lipomas cause many symptoms depending on the structures adjacent to them.

In a study of Korkut et al. [25], the symptoms were improved with dexamethazone administration in patients with tinnitus who were diagnosed with lipoma in the IAC. This improvement was suggested to be due to decreased pressure on the CN upon decompression [25].

Osteomas, as well as exostoses of the IAC, are rare, benign and usually slow-growing lesions. Reported aetiological factors contributing to the formation of these lesions include injury, inflammation, developmental disorders, and genetic defects. These may cause symptoms in the internal acoustic canal due to pressure [26]. In a study of Coakley et al. [27], internal acoustic canal osteoma was found in a 42 years old patient with normal hearing presenting with a long history of tinnitus. It was reported that the symptoms of tinnitus were abolished after retrosigmoid removal of osteoma [27].

In the present study, the diameters of the IAC in the patients group were found to be statistically significantly smaller when compared to those in the control group (P<0.01). It was thought that narrowed IAC caused a pressure on CN inside the canal and thus tinnitus.

Having original images with low resolution is the limitation of the present study. To what extend the images whose resolution were mathematically enhanced by computer reflected the reality is open to interpretation. However, the images of both the control and the tinnitus groups were treated similarly. Evaluations made by others may have the same standards if the viewer having the capacity of processing DICOM uses the same/similar resolution enhancing logarithms. Three-dimensional SSFP sequence applied by a computer program provides superior results in imaging the IAC and its contents. In the present study, there were significant differences observed in the IAC size in the MRI.

In conclusion, the width of the IAC should be evaluated to detect etiological causes and possible treatment strategies, especially in cases having subjective tinnitus with unknown origin.