Endovascular Treatment of Symptomatic Vestibular Aqueduct Dehiscence as a Result of Jugular Bulb Abnormalities

A new endovascular treatment consisting of stent-assisted coil implantation is described for jugular bulb abnormalities causing symptomatic vestibular aqueduct dehiscence. Three patients presenting with vertigo associated with pulsatile tinnitus or hearing loss were treated. This technique cured the vertigo and pulsatile tinnitus in all patients and preserved normal cerebral venous drainage with no side effects.     

Tinnitus: imaging algorithms.

The causes of tinnitus can be grouped according to whether the noise is continuous or pulsatile, whether it is subjective or objective and whether there is a retrotympanic mass. Imaging algorithms can be based on these symptoms and signs. For patients with nonpulsatile tinnitus and a normal drum, magnetic resonance imaging is preferred if a retrocochlear lesion is suspected, whereas high-resolution computed tomography (HRCT) is recommended if a cochlear abnormality is likely. If a chronic inflammation in the middle ear is suspected, HRCT is the study of choice to differentiate cholesteatoma from chronic otitis media. If the bruit is objective and the tympanic membrane normal, selective cerebral angiography should be the initial investigation, because most such patients have an acquired vascular abnormality, usually a dural arteriovenous fistula. If there is pulsatile tinnitus and a retrotympanic mass, HRCT should be the first examination because this technique allows differentiation of a vascular variation, such as an aberrant carotid artery or jugular dehiscence, from a paraganglioma.     

MR imaging and MR angiography in the evaluation of pulsatile tinnitus.

PURPOSE1) To evaluate the scope of imaging findings seen with spin-echo MR and MR angiography (MRA) in patients with pulsatile tinnitus; 2) to determine whether MRA adds additional imaging information (to that provided by spin-echo MR) necessary for determining the cause of pulsatile tinnitus; and 3) to suggest MR and MRA imaging techniques for evaluation of patients with pulsatile tinnitus.METHODSForty-nine patients with pulsatile tinnitus were evaluated with MR and MRA. Seventeen of these patients had conventional angiography.RESULTSVascular lesions or paraganglioma were demonstrated in 28 patients. Of these 28 lesions, the majority were seen best (46%) or only (36%) on MRA. The spectrum of lesions detected included dural arteriovenous fistula (nine), extracranial arteriovenous fistula (three), paraganglioma (five), jugular bulb variants (three), aberrant internal carotid artery (one), internal carotid artery stenosis (one), tortuous internal carotid artery (one), carotid dissection with pseudoaneurysm (one), stenosis of the transverse sinus (two), and arteriovenous malformation (two).CONCLUSIONSMRA, in conjunction with spin-echo imaging, markedly enhances the ability of MR to diagnose the lesions responsible for pulsatile tinnitus.     

Imaging of pulsatile tinnitus: a review of 74 patients

OBJECTIVE: Our aim was to assess the effectiveness of imaging modalities in detecting the underlying pathologies in patients with pulsatile tinnitus. MATERIALS AND METHODS: Seventy-four patients with pulsatile tinnitus were radiologically evaluated. All patients except two are evaluated on a thin-section bone algorithm computed tomography scan covering the temporal bone and skull base, 14 patients with or without contrast-enhanced brain computed tomography, 7 patients with magnetic resonance imaging and magnetic resonance angiography, 5 patients with digital subtraction angiography, and 12 patients with Doppler ultrasonography. RESULTS: The underlying pathology of tinnitus was detected in 50 patients (67.6%), and 24 patients were normal with radiologic studies. The most common cause was high jugular bulbus (21%) followed by atherosclerosis, dehiscent jugular bulbus, aneurysm of internal carotid artery, dural arteriovenous fistula, aberrant internal carotid artery, jugular diverticulum, and glomus tumor. CONCLUSION: It was concluded that radiologic imaging methods are effective in detecting the underlying pathology of pulsatile tinnitus.     

Dehiscence of the jugular bulb and vestibular aqueduct: findings on 200 consecutive temporal bone computed tomography scans

OBJECTIVE: To determine the incidence of dehiscence between the vestibular aqueduct and the jugular bulb on computed tomography (CT) scans and assess its implication as a cause of dizziness or hearing loss. METHODS: Two hundred temporal bone CT scans were evaluated for the prevalence of dehiscence between the jugular bulb and vestibular aqueduct. Correlation of the imaging findings and clinical data was performed. RESULTS: A total of 11.5% of patients had dehiscence of the jugular bulb with the vestibular aqueduct; 75% of these cases occurred on the right side and in the setting of a high jugular bulb. Nine (39.1%) of 23 patients with dehiscence had dizziness, and 11 (47.8%) had hearing loss. The correlation between the incidence of dizziness, hearing loss, and dehiscence was not significant. CONCLUSION: The incidence of a dehiscent jugular bulb with a vestibular aqueduct is 11.5%. The prevalences of vertigo and hearing loss associated with this finding are 39.1% and 47.8%, respectively. The depiction of dehiscent jugular bulb-vestibular aqueduct should be considered with caution as the sole cause of symptoms.     

Effects of a high jugular fossa and jugular bulb diverticulum on the inner ear. A clinical and radiologic investigation

From a series of patients undergoing routine radiographic examination, 112 temporal bones with a high jugular fossa were selected. Among these, 43 jugular bulb diverticula were found. The structures affected by a high fossa or diverticulum were recorded and correlated to the clinical symptoms of the patient. The vestibule was suspected to be affected in five patients. Two of these patients had tinnitus and vertigo, and three had hearing loss. In one of the latter the hearing loss was most marked in the supine position. The cochlea was close to the fossa in three patients, all of whom had tinnitus. Four patients had a defect of the posterior semicircular canal. One of them lost his hearing after a severe fit of coughing, became unsteady and showed signs of a fistula. The internal acoustic meatus and the mastoid portion of the facial canal were affected in two and four patients, respectively, who had no recorded symptoms. Twelve of 34 patients with Menière's disease and a high jugular fossa on the side of the diseased ear had a dehiscence of the vestibular aqueduct caused by the fossa or diverticulum, compared with nine of 58 patients in the unselected material. For comparison and demonstration of topographic relationships, 58 casts of unselected radiographed temporal bone specimens with high jugular fossae or diverticula were investigated. In patients with a high jugular fossa or jugular bulb diverticulum, tomographic assessment may be of value.     

Aberrant jugular bulb presenting as a middle ear mass.

Case reports of 3 patients seen with a bluish mass behind the tympanic membrane are presented. The initial diagnosis was probable glomus tumor. In 1 patient, middle ear exploration confirmed the presence of a high-lying jugular bulb. In the other 2, venography demonstrated that the jugular bulb projected superiorly into the middle ear cavity. In all 3, polytomography demonstrated a dehiscence of the bony septum which normally separates the jugular bulb from the hypotympanum. When a bony dehiscence is seen in the absence of destructive changes, a diagnosis of aberrant jugular bulb is strongly suggested.     

Sigmoid Sinus Diverticulum,Dehiscence, and Venous Sinus Stenosis: Potential Causes of Pulsatile Tinnitus in Patients with Idiopathic Intracranial Hypertension?

BACKGROUND AND PURPOSE:Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence was increased in patients with idiopathic intracranial hypertension and pulsatile tinnitus relative to those without pulsatile tinnitus and a control group.MATERIALS AND METHODS:CT vascular studies of patients with idiopathic intracranial hypertension with pulsatile tinnitus (n = 42), without pulsatile tinnitus (n = 37), and controls (n = 75) were independently reviewed for the presence of severe transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence according to published criteria. The prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence in patients with idiopathic intracranial hypertension with pulsatile tinnitus was compared with that in the nonpulsatile tinnitus idiopathic intracranial hypertension group and the control group. Further comparisons included differing degrees of transverse sinus stenosis (50% and 75%), laterality of transverse sinus stenosis/sigmoid sinus diverticulum/dehiscence, and ipsilateral transverse sinus stenosis combined with sigmoid sinus diverticulum/dehiscence.RESULTS:Severe bilateral transverse sinus stenoses were more frequent in patients with idiopathic intracranial hypertension than in controls (P < .001), but there was no significant association between transverse sinus stenosis and pulsatile tinnitus within the idiopathic intracranial hypertension group. Sigmoid sinus dehiscence (right- or left-sided) was also more common in patients with idiopathic intracranial hypertension compared with controls (P = .01), but there was no significant association with pulsatile tinnitus within the idiopathic intracranial hypertension group.CONCLUSIONS:While our data corroborate previous studies demonstrating increased prevalence of sigmoid sinus diverticulum/dehiscence and transverse sinus stenosis in idiopathic intracranial hypertension, we did not establish an increased prevalence in patients with idiopathic intracranial hypertension with pulsatile tinnitus compared with those without. It is therefore unlikely that these entities represent a direct structural correlate of pulsatile tinnitus in patients with idiopathic intracranial hypertension.

Pulsatile tinnitus (PT) is the perception of an abnormal sound that is synchronous with the heartbeat. The phenomenon may result from abnormal mechanical somatosound production (due to abnormal turbulence or location of vascular flow) or enhanced perception (due to increased transmission of the somatosound or reduced conduction of normal sound).¹ PT is a well-recognized feature of idiopathic intracranial hypertension (IIH), being present in approximately 60% of patients.^2–4 The pathophysiology of PT in these patients is unknown; however, observed variations in transverse and sigmoid sinus anatomy seen in IIH have been proposed as a possible underlying cause.Transverse sinus stenosis (TSS) is well-described as a cause of PT, and resolution of symptoms has been reported following successful venous sinus stent placement.^5–8 Venous sinus stent placement performed as a treatment for IIH has also resulted in resolution of PT in affected patients,^7,8 which lends support to the proposal that the resulting turbulent venous flow may be the somatosound responsible for PT in IIH.^9,10 However, PT is not seen in all patients with IIH with TSS, and other factors may be required for the symptom to manifest.More recently, sigmoid sinus diverticulum and/or dehiscence (SSDD) has been shown to be associated with PT.^1,11–16 This association has been noted to be particularly frequent in patients with elevated body mass indices and those with imaging features of IIH,^1,14,15 leading some authors to suggest that SSDD may reflect a manifestation of subclinical IIH.^2,14Interventional studies have revealed that endovascular stenting of TSS or surgical correction of SSDD may resolve PT^{5,7,8,13,17–19}; however, these procedures are not without complications.¹² Understanding the underlying mechanism is therefore essential to enable appropriate targeting of therapy.We aimed to determine whether the prevalence of TSS and SSDD was increased in patients with IIH with PT relative to patients with IIH without PT and a control group without IIH.     

Pulsatile tinnitus and the vascular tympanic membrane: CT, MR, and angiographic findings

The radiologic studies of 107 patients with pulsatile tinnitus or a vascular retrotympanic mass were retrospectively reviewed. Of the 100 patients with pulsatile tinnitus, 25 had objective tinnitus. A vascular tympanic membrane was present in 37 cases (35%). Normal vascular variants were present in 23 patients (21%). Twenty-seven patients (25%) had acquired vascular lesions. Temporal bone tumors were found in 33 patients (31%). No abnormality was identified in 21 cases (20%). To ensure optimal radiologic examination, it is imperative to know the nature of the tinnitus (objective vs subjective) and the appearance of the tympanic membrane. All patients with subjective pulsatile tinnitus or a vascular retrotympanic mass should undergo high-resolution computed tomography of the temporal bone as the initial imaging study. Angiography is recommended for patients with objective tinnitus and a normal tympanic membrane. The role of MR imaging, even with the addition of gradient-echo techniques, remains limited and secondary.     

Imaging of tinnitus: a review

Tinnitus, a buzzing or ringing in the ear, may be pulsatile or continuous (nonpulsatile). The distinction, with a detailed clinical evaluation, determines the most appropriate imaging study. Pulsatile tinnitus suggests a vascular neoplasm, vascular anomaly, or vascular malformation. Most of the neoplasms are glomus tympanicum and glomus jugulare tumors. Vascular anomalies may cause pulsatile tinnitus, but the mechanism is unknown, and another (treatable) cause should be sought. Most neoplasms and anomalies are best seen on bone algorithm computed tomographic (CT) studies. Dural vascular malformations are often elusive on all cross-sectional imaging studies; conventional angiography may be necessary to make this diagnosis. Flow-sensitive magnetic resonance (MR) images show vascular loops compressing the eighth cranial nerve. Carotid dissections, aneurysms, atherosclerosis, and fibromuscular dysplasia can be identified on both MR imaging or MR angiographic studies and CT or CT angiographic studies. Otosclerosis and Paget disease are CT diagnoses. Benign intracranial hypertension often has no abnormal imaging findings. For patients with nonpulsatile tinnitus, MR imaging is the study of choice to exclude a vestibular schwannoma or other neoplasm of the cerebellopontine angle cistern. Multiple sclerosis and a Chiari I malformation are rare causes of pulsatile tinnitus, also best seen on MR studies. Many patients with tinnitus have no abnormal imaging findings.     

耳鸣患者颞骨异常的CT及MRI研究

目的 采用HRCT和MRI对耳鸣患者颞骨进行检查,探讨其异常发生率及最佳扫描方案.方法 回顾性分析1015例耳鸣患者的HRCT和MRI资料.搏动性耳鸣145例,142例行HRCT,7例行MRI,其中4例同时行HRCT和MRI,仅行平扫HRCT者67例,仅行增强HRCT者71例.非搏动性耳鸣870例,650例行HRCT,267例行MRI,其中47例同时行HRCT和MRI,仅行平扫HRCT者598例,仅行增强HRCT者5例.分析颞骨异常阳性率及构成比,比较不同影像学检查方法和序列对颞骨异常的显示效果.采用χ2检验对数据进行组间分析.结果 1015例中显示病变者767例(75.57%).常见颞骨异常发生率分别为:颈静脉窝高位414例(40.79%);乙状窦异常387例(38.13%);中耳乳突炎148例(14.58%);中颅窝低位70例(6.90%).平扫HRCT对颈静脉窝高位显示阳性率最高(365/665,54.89%);增强HRCT对乙状窦异常显示的阳性率最高(56/76,73.68%).在搏动性耳鸣患者中,乙状窦异常发生率最高(96/145,66.21%),且其发生率明显高于非搏动性耳鸣患者(291/870,33.45%;χ2=56.537,P＜0.01).真稳态进动快速成像(FIESTA)序列显示内耳道内血管袢影最佳(42/42,100%).结论 颈静脉窝高位和乙状窦异常是耳鸣患者最常见的颢骨影像异常.搏动性耳鸣首选增强HRCT,非搏动性耳鸣首选平扫HRCT,内耳道内血管显示首选MR FIESTA序列.

Abstract：

Objective To study high resolution CT (HRCT) and MRI findings of temporal bone anomaly in patients with tinnitus and identify the optimal examination method in the detection of the anomaly. Methods The HRCT and MRI data were analyzed retrospectively in 1015 patients including 145 patients with pulsatile tinnitus (PT) and 870 patients with nonpulsatile tinnitus (NPT). The positive rates of HRCT and MRI in the identification of temporal bone anomaly were analyzed and the efficiency of various examination methods was compared in revealing the anomaly. Data were tested by Chi-square test analysis. Results Among 1015 patients, anomaly was seen in 767 cases (75.57%). High jugular bulb was found in 414 patients, accounting for 40. 79%. Sigmoid sinus anomaly was detected in 387 patients (38. 13%), while otitis media was found in 148 cases (14. 58%), and low middle cranial fossa in 70 cases (6. 90%). The positive rate of HRCT in the detection of high jugular bulb was 54. 89% (365/665), which was significantly higher than those of other methods (P ＜ 0. 05). The positive rate of enhanced HRCT in showing sigmoid sinus anomaly was 73.68% (56/76), which was significantly higher than those of other methods(P ＜0. 05). Sigmoid sinus anomaly was the most frequent finding in patients with PT, accounting for 66. 21% (96/145). The incidence of sigmoid sinus anomaly was higher in PT than in NPT (291/870,33.45% ;χ2 =56. 537 ,P ＜0. 01). The fast imaging employing steady-state acquisition (FIESTA) sequence was the best examination method in displaying the vessel within the internal auditory canal (42/42,100%).Conclusions High jugular bulb and sigmoid sinus anomaly were the most frequent abnormal findings of temporal bone in patients with tinnitus. Enhanced HRCT was the choice of modality in patients with PT.Plain HRCT was recommended for NPT. FIESTA sequence was the best in the evaluation of the vessel within the internal auditory canal.     

Twig-like middle cerebral arteries: Clinical and radiological findings

Background and purposeAplastic or twig-like middle cerebral artery (MCA) is a rare vascular anomaly characterized by replacement of the M1 segment by a plexiform network of small vessels. Though rare, familiarity with this entity and ability to differentiate it from radiological mimics such as moyamoya changes and steno-occlusive diseases are important. We review the clinical and radiological manifestations of patients diagnosed with twig-like MCA on cerebral angiograms over a five-year period.Materials and methodsRetrospective review of all patients diagnosed with twig-like MCA on cerebral angiograms was performed from January 2015 to January 2020. This was the inclusion criterion for this retrospective study. For each patient, demographic data, clinical presentation, imaging findings and management strategies were reviewed.Results and conclusionsBetween January 2015 and January 2020, three patients with twig-like MCA were identified from 657 patients who underwent four-vessel diagnostic cerebral angiograms (0.45%). In all three cases, the involvement was unilateral (two left-sided and one right- sided). Two patients were male, and one was female. Patients ages were 25, 26 and 46 years. Two of the three patients presented with headache and the third patient with pulsatile tinnitus. There were otherwise no ischemic or hemorrhagic changes. No other vascular anomaly was identified. Twig-like MCA is a rare anatomical variant in which a plexiform network of small vessels replaces the M1 segment of the MCA. Accurate diagnosis and distinguishing this entity from radiological mimics such as moyamoya and steno-occlusive diseases are important for appropriate management and to prevent unnecessary investigations.     

Does the location of a vascular loop in the cerebellopontine angle explain pulsatile and non-pulsatile tinnitus?

The purpose was to investigate patients with unexplained pulsatile and non-pulsatile tinnitus by means of MR imaging of the cerebellopontine angle (CPA) and to correlate the clinical subtype of tinnitus with the location of a blood vessel (in the internal auditory canal or at the cisternal part of the VIIIth cranial nerve). Clinical presentation of tinnitus and perceptive hearing loss were correlated. In 47 patients with unexplained tinnitus, an MR examination of the CPA was performed. Virtual endoscopy reconstructions were obtained using a 3D axial thin-section high-resolution heavily T2-weighted gradient echo constructive interference in steady state (CISS) data-set. High-resolution T2-weighted CISS images showed a significantly higher number of vascular loops in the internal auditory canal in patients with arterial pulsatile tinnitus compared to patients with non-pulsatile tinnitus (P<0.00001). Virtual endoscopy images were used to investigate vascular contacts at the cisternal part of the VIIIth cranial nerve in patients with low pitch and high pitch non-pulsatile tinnitus. A significantly different distribution of the vascular contacts (P=0.0320) was found. Furthermore, a correlation between the clinical presentation of non-pulsatile tinnitus (high pitch and low pitch) and the perceptive hearing loss was found (P=0.0235). High-resolution heavily T2-weighted CISS images and virtual endoscopy of the CPA can be used to evaluate whether a vascular contact is present in the internal auditory canal or at the cisternal part of the VIIIth cranial nerve and whether the location of the vascular contact correlates with the clinical subtype of tinnitus. Our findings suggest that there is a tonotopical structure of the cisternal part of the VIIIth cranial nerve. A correlation between the clinical presentation of tinnitus and hearing loss was found.     

Computed tomographic evaluation of surgically significant vascular variations related with the temporal bone

Variations of the vascular structures related with the temporal bone may cause important problems in diagnosis, treatment planning and surgery. High resolution computed tomography (CT) scans of 700 temporal bones of 350 patients were retrospectively examined for the incidence of dehiscent jugular bulb, high jugular bulb, diverticulum of jugular bulb, anteriorly located sigmoid sinus and dehiscent internal carotid artery. Dehiscent jugular bulb was seen in 27 (3.9%), high jugular bulb was seen in 142 (20.3%), jugular bulb diverticulum was seen in 55 cases (7.9%). The average distance between external acoustic canal and sigmoid sinus was found to be 13.3 mm and in 12.4% of the cases this distance was < 10 mm. Of 700 temporal bones, 10 (1.4%) showed dehiscent carotid canal. To aid diagnosis, treatment planning and surgery, CT scanning is currently a very reliable tool in determining these conditions. Special attention should be paid to the position of the vascular structures in the preoperative temporal bone CT scans.     

Vascular masses in the middle ear

High resolution computed tomography (CT) is of great value in demonstrating soft tissue masses in the middle ear cavity. However, tissue characterisation even for vascular masses after contrast enhancement has proved disappointing. Differentiation therefore depends upon the site and anatomical configuration of the mass, and in many cases angiography is mandatory for diagnosis. Examples of high ectopic jugular bulb, glomus jugulare and glomus tympanicum tumours and aberrant internal carotid artery are presented and their differential diagnosis considered. The value of CT and more traditional techniques, particularly lateral tomograms to show the spur of bone between the jugular bulb and internal carotid artery, are discussed.     

Imaging of carotid artery-cochlear dehiscence. A cause of pulsatile tinnitus

The petrous bone is a strategic area within the skull base. The cochlea and the carotid artery canal are extremely close to each other within that area. Pulsatile tinnitus requires intact hearing and usually source of sound. It can be arterial or venous in origin, or originating in-between. The aim of this study was to use the MDCT in measurement of the thickness of the bony plate between the internal carotid artery and cochlea within the skull base in patients with pulsatile tinnitus showing no other detectable etiology on MDCT basis as well as for detection of any bony dehiscence involving this bony plate.

Ascending pharyngeal artery-internal jugular vein fistula complicating radical neck dissection

Summary Arteriovenous fistulae of the ascending pharyngeal artery (AP) and internal jugular vein (IJ) are rare. Only two spontaneous AP-IJ fistulae have been described previously, both of which presented with pulsatile tinnitus. A unique case of an AP-IJ fistula developing after radical neck dissection is described in which the clinical presentation was identical to that of a carotid-cavernous fistula.     

Characteristics, diagnosis and treatment of hypoglossal canal dural arteriovenous fistula: report of nine cases

INTRODUCTION: We report the characteristics, diagnosis and treatment of dural arteriovenous fistula (DAVF) of the hypoglossal canal in nine patients with this relatively rare vascular disorder. METHODS: Of 248 patients with intracranial DAVFs managed at our institution, nine patients (3.6%; four men, five women; mean age 62 years) were diagnosed with hypoglossal canal DAVF. We investigated patient characteristics with respect to clinical symptoms, neuroradiological findings, efficacy and complications related to endovascular treatment. RESULTS: Seven patients had experienced head injury. All patients presented with pulsatile tinnitus. One patient displayed ipsilateral hypoglossal nerve palsy before treatment. MR angiography showed a "magic wand" appearance between the affected hypoglossal canal and the internal jugular vein in four patients. Angiography demonstrated an AV fistula on the medial aspect of the superior jugular bulb, mostly arising from the bilateral occipital, ascending pharyngeal and vertebral arteries with drainage to the internal jugular vein via the anterior condylar vein. Contralateral carotid injection accurately clarified the shunting point. Five patients underwent endovascular treatment: transarterial embolization (TAE; n = 2), transvenous embolization (TVE; n = 2), and TAE/TVE (n = 1). Complete shunt obliteration was achieved in four patients and shunt reduction in one. The remaining four patients were treated conservatively and the shunt had disappeared at follow-up. Postoperative hypoglossal nerve palsy occurred in one patient after TVE, possibly due to coil overpacking. CONCLUSION: The incidence of hypoglossal canal DAVF was not very low in our series. Contralateral carotid injection is an essential examination to provide an accurate diagnosis. TVE should be considered when access is available, although TAE is also appropriate for shunt reduction.     

Posterior semicircular canal dehiscence: a morphologic cause of vertigo similar to superior semicircular canal dehiscence

The aim of this study was to assess imaging findings of posterior semicircular dehiscence on computed tomography and to evaluate incidence of posterior and superior semicircular canal dehiscence in patients presenting with vertigo, sensorineuronal hearing loss or in a control group without symptoms related to the inner ear. Computed tomography was performed in 507 patients presenting either with vertigo (n=128; 23 of these patients suffered also from sensorineuronal hearing loss), other symptoms related to the inner ear, such as hearing loss or tinnitus (n=183) or symptoms unrelated to the labyrinth (n=196). All images were reviewed for presence of dehiscence of the bone, overlying the semicircular canals. Twenty-nine patients had superior semicircular canal dehiscence. Of these patients, 83% presented with vertigo, 10% with hearing loss or tinnitus and the remaining 7% with symptoms unrelated to the inner ear. In 23 patients dehiscence of the posterior semicircular canal was encountered. Of these patients, 86% presented with vertigo, 9% with hearing loss or tinnitus and 5% with symptoms unrelated to the inner ear. Defects of the bony overly are found at the posterior semicircular canal, in addition to the recently introduced superior canal dehiscence syndrome. Significant prevalence of vertigo in these patients suggests that posterior semicircular canal dehiscence can cause vertigo, similar to superior semicircular canal dehiscence. Electronic Publication     

Vascular Loops at the Cerebellopontine Angle: Is There a Correlation with Tinnitus?

BACKGROUND AND PURPOSE: Tinnitus is a common disorder, and the etiology remains mostly unclear. The purpose of this study was to investigate the causative effect of the vascular loop and compression of the vestibulocochlear nerve at the cerebellopontine angle in patients with unexplained tinnitus.MATERIALS AND METHODS: This study was approved by our institutional review board. Written informed consent was obtained from all participants. Fifty-eight patients with unexplained tinnitus and 44 age- and sex-matched asymptomatic controls were examined with temporal MR imaging. Besides the tinnitus and control groups, a third group was formed by asymptomatic sides of patients with unilateral tinnitus. A 3D fast imaging employing steady-state acquisition (3D-FIESTA) sequence was performed in addition to the regular pre- and postcontrast axial and coronal sequences. The anatomic type of vascular loop, the vascular contact, and the angulation of the vestibulocochlear nerve at the cerebellopontine angle (CPA) were evaluated by 2 experienced neuroradiologists. The χ² test was used for statistical analysis.RESULTS: No statistically significant differences were found between the patient and control groups for the anatomic type of vascular loop, the vascular contact, and the angulation of the vestibulocochlear nerve at the CPA (P > .05).CONCLUSION: Although 3D-FIESTA MR imaging correctly shows the anatomic relationships of the vestibulocochlear nerve, its vascular compression cannot be attributed as an etiological factor for tinnitus.

Tinnitus is a sound in the ear, occurring without an external stimulus. It is a common complaint with a lifetime incidence of 7%–12% in the general population.^1-3 Tinnitus may be classified as either an arterial pulse synchronous type (pulsatile) or a continuous (nonpulsatile) type. Some investigators also have subdivided the tinnitus into subjective (perceived only by the patient) and objective (perceptible to another person) types. Nonpulsatile tinnitus and subjective tinnitus are more common than pulsatile tinnitus, and nonpulsatile tinnitus is usually subjective. Medical history, neuro-otologic physical examination, and neuroradiologic imaging may identify a treatable cause. Pulsatile tinnitus is most frequently the result of a vascular abnormality or a vascular tumor. However, in some cases, the etiology of tinnitus remains uncertain, and most of these patients have no imaging abnormalities.^4,5Compression of the eighth cranial nerve (eighth CN) by vascular structures has been proposed as a cause of tinnitus.^6-10 However, controversial results have been reported in the medical literature about the relationship between neurovascular compression of the eighth CN and neuro-otologic symptoms.^11-14The purpose of our study was to assess the correlation between the presence of a vascular loop and its contact with the eighth CN in the cerebellopontine angle (CPA) and ipsilateral symptoms of unexplained tinnitus by using a 3D fast imaging employing steady-state acquisition (3D-FIESTA) sequence, which is an MR imaging technique that provides good contrast between CSF, nerves, and vessels.¹⁵