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Glomus jugulare are benign tumors arising from neural crest progenitor crest cells (glomus bodies) located in and around the jugular foramen. Paragangliomas can present as multifocal lesions in up to 3-10% of sporadic cases and in 25-50% of familiar cases (a rarer form with autosomal dominant inheritance). Meningiomas located at the cerebellopontine angle cistern can be a cause of pulsatile tinnitus. Endolymphatic sac tumors are often initially confused with the much more common paragangliomas as their imaging characteristics are similar. The key to diagnosis is recognition of the epicenter of the lesion along the posterior petrous surface at the level of the vestibular aqueduct. Certain anatomical vascular variants in the temporal bone are a frequent cause of pulsatile tinnitus and a vascular appearing tympanic membrane. Some anatomical variants or anomalies of the jugular bulb have been related to venous pulsatile tinnitus. It remains unclear how or why these vascular anomalies cause sudden onset of pulsatile tinnitus.
This condition is an uncommon anomaly due to failure of formation of the proximal ICA (C1 segment) in fetal life. Intracranial dural arteriovenous fistulas are recognized as an abnormal channel from the artery(s) to the vein within the dura mater. Arteriovenous fistula of the transverse and sigmoid sinus is most frequently involved in pulsatile tinnitus. On imaging the typical finding is a network of tiny ("crack-like") vessels in the wall of a thrombosed dural venous sinus (figure 11). This appear as an abnormal network of vessels showing arterial flow inside the hypoglossal canal (Figure 13).
The imaging of choice in this clinical setting should be cervical Doppler ultrasound (Figure 14). Some investigators believe that compression of cranial nerve VIII can cause pulsatile tinnitus. It has been postulated that vascular compression of the nerve in the internal auditory canal (Figure 16) results in pusatile tinnitus due to a resonance effect in the petrous bone transmitted to the cochlea. The anterior inferior cerebellar artery often makes a normal redundant loop within the IAC without disrupt the CN VIII.
Intracraneal idiopathic hypertension comprises signs and symptoms of increased intracranial pressure without causative mass or hydrocephalus.
Otosclerosis(or more appropriately known as otospongiosis) is an idiopathic slowly progressive primary disorder of the bony labirynth. Thin sliced petrous temporal bone CT scans demonstrate replacement of the normally dense middle layer of the bony labyrinth with areas of  “spongy” Haversian bone (Figure 18). Thin-section CT demonstrates the covering defect of the superior semicircular canal (Figure 19). Tinnitus seems to be related to the intraosseous A-V shunting associated with the pagetic bone.
NPT is most frequently associated with functional injuries from exposure to environmental noise or the toxicity of certain medications. Vestibular schwannoma should be suspected in patients with unilateral persistent non-pulsatile tinnitus and progressive sensorineural hearing loss.
Them should be also aware thattinnitus may persist and even worsen after successful removal of the tumor. Solid component shows intense enhancement after intravenous contrast administration (Figure 21).
Myoclonic contractions of palatal muscles (Palatal myoclonus) may also cause objective tinnitus. 2 clicks for more privacy: On the first click the button will be activated and you can then share the poster with a second click. This study evaluated the incidence of various vascular anomalies and variants on the PT side and determined whether these lesions occurred as multiple or single entities.
Incidence of Vascular Anomalies and Variants Associated with Unilateral Venous Pulsatile Tinnitus in 242 Patients Based on Dual-phase Contrast-enhanced Computed Tomography. Angioplasty and stenting for intractable pulsatile tinnitus caused by dural venous sinus stenosis: A case series report.

Clinical characteristics of pulsatile tinnitus caused by sigmoid sinus diverticulum and wall dehiscence: A study of 54 patients. 3-Dimensional reconstruction of the venous system in patients suffering from pulsatile tinnitus. Endovascular treatment of two concomitant causes of pulsatile tinnitus: Sigmoid sinus stenosis and ipsilateral jugular bulb diverticulum. Imaging prevalence of sigmoid sinus dehiscence among patients with and without pulsatile tinnitus. Petrosquamosal sinus in the temporal bone as a cause of pulsatile tinnitus: A radiological detection.
Intracranial dural arteriovenous fistulas: Diagnosis and evaluation with 64-detector row CT angiography. Management of high jugular bulb with tinnitus: Transvenous stent-assisted coil embolization. Jugular bulb abnormalities in patients with Meniere's disease using high-resolution computed tomography. CT angiography as a screening tool for dural arteriovenous fistula in patients with pulsatile tinnitus: Feasibility and test characteristics. Idiopathic intracranial hypertension: The prevalence and morphology of sinovenous stenosis.
Sinus wall reconstruction for sigmoid sinus diverticulum and dehiscence: A standardized surgical procedure for a range of radiographic findings. 8: The right ICA shows a more lateral position than usual, allowing protrusion into the middle ear cavity (arrow). 11: Coronal (A) and sagittal (B) FFE-T1 post Gad MRI nicely show multiple small vessels (arrows) that converge on the wall of the thrombosed right transverse sinus (neoangiogenesis). Methods: The dual-phase contrast-enhanced computed tomography images of 242 patients with unilateral venous PT were retrospectively reviewed. Teplitzky Neuroimaging Clinics of North America. Eisenman Neuroimaging Clinics of North America.
Coronal FLAIR (A) and axial T2W (B) shows signal voids reflecting anomalous arterial flow in the superior left ophthalmic vein (arrows). The pathologic arterio-venous communication is established between various arterial dural branches and venous vessels inside the left hypoglossal canal. Left hypoglossal canal (red arrow) appears enlarged in comparison, with abnormal flow voids inside. The vascular anomalies and variants on the symptomatic and asymptomatic sides were analyzed, and the incidences of anomalies or variants on each side were compared. Thus far, previous studies on the incidence of these anomalies and variants of venous PT have notable limitations; they used small sample sizes and did not include several recently described venous PT anomalies, such as a dehiscent sigmoid plate and petrosquamosal sinus. Axial T1WI (C) and postcontrast coronal T1WI (D) show T1 hyperintesity of the mass (*) due to hemorrhagic components and heterogeneous enhancement (arrow).
However, inspection of the analogous location on the left side demonstrates absence of the horizontal carotid canal or internal carotid artery.
The number of anomalies and variants on the symptomatic side in each patient was calculated.
However, there are no studies indicating whether these venous PT anomalies and variants are multiple or single, which could significantly impact the prognosis of venous PT patients.Therefore, we sought to identify the incidence of vascular anomalies and variants of venous PT by retrospectively reviewing the DP-CECT images of 242 unilateral venous PT patients and determine whether these anomalies and variants occur as multiple or single lesions on the symptomatic side of each patient. Eisenman American Journal of Neuroradiology.
Of the 242 patients, 156 patients had right-sided venous PT, and 86 patients had left-sided venous PT. The arterial phase scan was trigged by the Bolus-Tracking program (Trigger Bolus Software; Philips, Best, The Netherlands) after administering the contrast agent and performed in a cephalocaudal direction. Standard algorithms were used to reconstruct all arterial phase images, and standard and bone algorithms were used in all venous phase images.
Multi-planar reconstruction images were generated on a workstation with a 1 mm slice thickness and no slice gap. The axial images were reconstructed by setting the position baseline parallel to the bilateral lateral semicircular canals; the coronal images were generated by setting the position baseline perpendicular to the bilateral lateral semicircular canals.

The vascular anomalies and variants on symptomatic and asymptomatic sides were analyzed and evaluated retrospectively. Axial CT image; (a) Sigmoid sinus diverticulum (arrow) accompanying with a dehiscent sigmoid plate (arrowhead). Axial CT image; (g) A filling defect (thrombosis) in the superior curve of right sigmoid sinus (arrow).
The vascular anomalies and variants on symptomatic sides and asymptomatic sides were counted and summed. The incidences of the anomalies and variants were compared on each side using the Chi-square test or the Fisher exact test.
In addition, number of findings on the symptomatic side in each patient was calculated to analyze the anomaly and variant diversification of venous PT. Spearman rank correlation test was used to evaluate the correlation between the side of PT and the side of dominant venous system.
Of these lesions, a dehiscent sigmoid plate, accounting for 86.4% of all venous PT patients, was the most frequent anomaly on the symptomatic side in this study. There were 155 patients with PT on the dominant side of the venous systems and 15 patients with PT on the opposite side. Co-dominant systems were diagnosed in 72 patients (36 with left-sided PT; 36 with right-sided PT).
Similarly, our results suggested that the sound of venous PT may be triggered by multiple lesions within the veins. This may explain why some venous PT patients experience no relief or report recurrence after a single surgery. This discordance reflects certain anomalies and variants measured in this study that were not analyzed in previous studies. Furthermore, PT patients in previous studies were evaluated using different imaging methods, some of which are unable to detect a dehiscent sigmoid plate effectively, such as digital subtraction angiography, magnetic resonance imaging, and magnetic resonance angiography.
In addition, the samples of venous PT patients in some studies were inadequate, which can compromise the validity of the results.
In a study based on 15 PT patients with a dehiscent sigmoid plate, 12 patients recovered completely postoperatively.
Therefore, it is essential to determine whether a dehiscent sigmoid plate exists.Based on the results of the present study, the symptomatic side was significantly more likely to have a vascular anomaly or variant than the asymptomatic side. Recent studies reported that the venous hum of venous PT is caused by turbulent and nonlaminar blood flow, which is then transmitted to the cochlea.
However, there is an ongoing debate on the role played by the high jugular bulb in causing venous PT because this lesion is also common in asymptomatic patients. However, PT also requires conditions that transmit the sound to the cochlea, like the dehiscent jugular bulb. Thus, a high jugular bulb should be considered a contributing factor to venous PT rather than a definitive cause.In other studies, the majority of patients with venous PT were female.
This characteristic is likely associated with benign intracranial hypertension, which is common in women and can present with PT as the only symptom.
In our study, the DP-CECT image demonstrated the details of each anatomic structure and ensured the accuracy of diagnosis.This study had some limitations, including intrinsic bias secondary to a retrospective review and selection bias due to patients being recruited from a single tertiary care center. A multi-center trial using a standardized imaging protocol would be ideal to evaluate venous PT patients. Second, in certain anomalies or variants, it was impossible to prove an association between venous PT and a therapeutic response in some cases. However, all of these lesions have been reported or confirmed as contributing factors or causes of venous PT in previous studies. Additional study performing a comparison of venous variation incidence to normal control subjects in a large patient population is needed. In addition, the weight of different vascular anomalies or variants in each patient was not analyzed in this study.
In addition, preliminary findings suggest that venous PT patients may have multiple vascular lesions on the symptomatic side, which implies venous PT could be a consequence of multiple factors within the veins.

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