Skip to main content
NCBI home page
Journal of Neurological Surgery. Part B, Skull Base logoLink to Journal of Neurological Surgery. Part B, Skull Base
. 2021 Jan 14;83(3):248–253. doi: 10.1055/s-0040-1722670

Anatomical Variations of the Jugular Foramen Region in Patients with Pulsatile Tinnitus

Lifeng Li 1, Bentao Yang 2, Xiaobo Ma 1,✉, Pingdong Li 1, Francis X Creighton 3, Ricardo L Carrau 4, Nyall R London Jr 3
PMCID: PMC9236704  PMID: 35769801

Abstract

Objective  Structural anomalies of the jugular foramen (JF) and adjacent structures may contribute to development of pulsatile tinnitus (PT). The goal of this study was to assess anatomical variants in the ipsilateral JF region in patients with PT and to explore possible predisposing factors for PT.

Methods  One hundred ninety-five patients with PT who underwent CT angiography and venography of the temporal bone were retrospectively analyzed. Anatomic variants including dominance of the ipsilateral JF, bony deficiency of the sigmoid sinus and internal carotid artery canal, high riding or dehiscent jugular bulb, dehiscence of the superior semicircular canal, tumors in the JF region, or cerebellopontine angle were assessed.

Results  Of 195 patients with PT, the prevalence of a dominant JF on the ipsilateral side of patients with PT was 67.2%. Furthermore, the dominant JF demonstrated a significant correlation with the presence of ipsilateral PT ( p  < 0.001). No anatomical variants were present in 22 patients (11.3%), whereas in patients with structural variants, bony deficiency of the sigmoid sinus was most common (65.6%), followed by high riding (54.9%) or dehiscent jugular bulb (14.4%). Dehiscent internal carotid artery canal (3.1%) and superior semicircular canal (4.1%) were occasionally identified, while arteriovenous fistula, arterial aneurysm and tumors arising from the JF region or cerebellopontine angle were rarely encountered.

Conclusion  Structural abnormalities of the JF and adjacent structures may predispose to the development of PT. Knowledge of these anatomical variants in the JF region may help establish a clinical strategy for addressing PT.

Keywords: pulsatile tinnitus, jugular foramen, structural anomaly, sigmoid sinus, jugular bulb, dehiscent

Introduction

Pulsatile tinnitus (PT) is an uncommon condition manifested by perception of a rhythmic sound. It can be unilateral or bilateral hearing and can also be subjective or objective in nature. 1 2 PT is most common in middle-aged female patients and symptoms can range from minor to debilitating. 3 4 Multiple factors have been considered to contribute to the development of PT including bony deficiency of the sigmoid sinus, high riding or dehiscent jugular bulb, jugular foramen (JF), and cerebellopontine angle tumors. 5 6 7 Consequently, surgical interventions have been utilized to correct anatomical anomalies or reconstruct bony deficiencies, which have achieved satisfactory outcomes. 8 9 However, surgical intervention does not relieve PT in all patients. 10 Therefore, further investigation exploring potential underlying factors is desirable.

The JF is one of the most complex areas of the cranial base, including the lower cranial nerves (IX, X, and XI), jugular bulb and its transition portion with the sigmoid sinus, inferior petrous sinus, and meningeal branches of the ascending pharyngeal artery or occipital artery. 11 12 The JF is located near to the hypoglossal canal, which transmits the hypoglossal nerve, venous plexus, and tiny artery branches from the ascending pharyngeal artery or occipital artery. 13 The parapharyngeal segment of the internal carotid artery (ICA) is routinely located anterior or anteromedial to the JF when travelling superiorly before entry into the vertical petrous canal. 14 In addition to a deep location within the skull base, the complex neurovascular relationships within the JF region may also pose challenges for both investigation and surgical management of lesions arising in this area. 15

Given the location of the JF adjacent to the middle ear, structural anomalies of the JF region may contribute to clinical symptoms (i.e., PT, hearing loss, and vertigo). 16 However, to the authors' knowledge, a comprehensive radiographic investigation of the prevalence of anatomical variations or anomalies of the JF and adjacent structures in patients with PT has not been sufficiently explored.

The goal of this study was to assess anatomical variations of the ipsilateral JF region in patients with PT and to explore the possible predisposing factors for development of PT.

Methods

Clinical Data

Two hundred twenty-one patients with PT from January 1, 2018 to December 31, 2019 at a tertiary care hospital were retrospectively analyzed. Informed consent for scientific investigation was obtained from these patients upon admission for radiological examination, and the study protocol was approved by the Ethics Committee of Beijing Tongren Hospital, Capital Medical University (no. TRECKY2020–18).

Among these 221 patients, one hundred and ninety-five consecutive patients underwent a CT angiography and CT venography (CTA/CTV) images of the temporal bone as part of the workup for screening of possible structural variants were enrolled for analysis. The images including axial, coronal, and sagittal images were obtained in digital imaging and communications in medicine format. Patients with ipsilateral occurrence of otitis media, recurrent tumors of the temporal bone, or those with PT who did not undergo CTA/CTV examination of temporal bone were excluded from this study. The images of these patients were imported into Mimics 13.1 (Materialise, Leuven, Belgium) for measurement and analysis. Enrollment, patient exclusion, and measurement of study indices on CTA/CTV images were made simultaneously by a radiologist (B.T.Y.) and an ENT surgeon (L.F.L.).

All patients with suspicion of PT routinely underwent pure tune audiometry including frequencies of 250, 500, 1,000, 2,000, 4,000, and 8,000 Hz in our center. The average hearing value of 500, 1,000, and 2,000 Hz lower than 25 dB was considered normal, 26 to 40 dB was mild hearing loss (HL), 41 to 55 dB was moderate, 56 to 70 dB was moderately severe, 71 to 90 dB was severe, and more than 90 dB was profound HL.

Indices such as the ipsilateral dominance of the JF, bony deficiency of the sigmoid sinus and the ICA canal, high-riding or dehiscent jugular bulb, dehiscence of the superior semicircular canal, presence of tumors arising from the JF region or cerebellopontine angle, ICA aneurysm, arteriovenous (AV) fistula were assessed on CTA/CTV images and recorded.

Statistical Analysis

For patients with unilateral PT, comparison of structural variations or abnormalities—such as the bony deficiency of the sigmoid sinus and ICA canal, high-riding or dehiscent jugular bulb between the pulsatile, and the asymptomatic sides—was performed with a Student's t -test. The correlation between the laterality of PT with the ipsilateral dominance of jugular vein, high riding jugular bulb, dehiscent jugular bulb, and the bony deficiency of the sigmoid sinus and ICA canal was subject to a Chi-square test. The value was expressed as mean ± standard deviation, and a probability value of p <0.05 was considered to be statistically significant. Statistical analysis was performed using Statistica 16.0 software (StatSoft, Inc., Tulsa, Oklahoma, United States).

Results

Of 195 patients with PT reviewed, 155 patients were females (79.5%), and 40 patients were males (20.5%). The average age for these patients was 43.9 ± 13.2 years (range = 17–72 years). The duration of PT lasted from 7 days to 16 months when they consulted the otologic office and were admitted for CTA/CTV screening.

Of these 195 patients with PT, the right side dominant JF accounts for 66.2% (129/195), balanced distribution of JF for 20.5% (40/195), and left side dominant JF for 13.3% (26/195). Moreover, the vast majority of patients (192 patients, 98.5%) demonstrated unilateral PT, including the right side ( n  = 139, 72.4%) or left side ( n  = 53, 28.2%). The remaining three patients had bilateral PT (1.5%).

No structural variations surrounding the JF region were detected on CTA/CTV images in 22 patients (11.3%). In the remaining 173 patients, variable structural abnormalities or deficiency surrounding the JF region were identified. An ipsilateral dominant JF was identified in 131 patients (67.2%) with PT, including the right side (113, 58.0%) or left side (18, 9.2%); a balanced distribution of the reflux jugular bulb was present in another 40 patients (20.5%). In the remaining 24 patients (12.3%), a contralateral dominance of the JF was detected.

Bony deficiency of the sigmoid sinus occurred most commonly (128 patients, 65.6%) and was identified in the superior curving segment of the sigmoid sinus with a diverticulum protruding into the mastoid cavity ( Fig. 1A ). Subsequently, an ipsilateral high-riding jugular bulb ( Fig. 1B ) was identified in 107 patients with PT (54.9%), and a dehiscent jugular bulb ( Fig. 1C ) was detected in 28 patients (14.4%).

Fig. 1.

Fig. 1

Open in a new tab

( A ) Bony deficiency of the sigmoid sinus (green arrow), ( B ) high-riding jugular bulb (red arrow), and ( C, D ) dehiscent jugular bulb (blue arrows).

The petrosal ICA lies at the anteromedial aspect of the middle ear cavity, both of which were routinely separated by a thin bony canal. Deficiency of this bony separation was detected in six patients in this case series (3.1%; Fig. 2A ). Bony deficiency of the superior semicircular canal was identified in eight patients (4.1%), which was detected to travel intimately with the course of the superior petrous sinus ( Fig. 2B ).

Fig. 2.

Fig. 2

Open in a new tab

( A ) The bony deficiency of the internal carotid artery canal (red arrow) and ( B ) the bony deficiency of the superior semicircular canal (green arrow).

The abnormal early filling of the sigmoid sinus and the internal jugular vein during an CTA examination was identified in three patients (1.5%), which ultimately demonstrated to be an AV fistula.

Tumors arising from the JF region ( Fig. 3A and B ) or cerebellopontine angle ( Fig. 3C ) were detected in four (2.1%) and one patient (0.5%), respectively. However, the presence of a PT as the first or major symptom was not typically manifested. In one patient with the PT as the major symptom, however, petrosal ICA aneurysm was identified ( Fig. 3D ).

Fig. 3.

Fig. 3

Open in a new tab

( A, B ) Patients with pulsatile tinnitus have tumors arising from the jugular foramen (green arrows), ( C ) patients with tumors arising from the internal acoustic meatus with extension into the cerebellopontine angle (blue arrow), and ( D ) aneurysm of the petrous internal carotid artery (red arrow).

Normal hearing was detected in 176 patients (91.79%, within 25 dB). In the remaining 19 patients, 12 patients with bony deficiency of sigmoid sinus demonstrated a mild sensorineural HL (32.22 ± 2.52 dB HL); three patients with bony deficiency of the superior semicircular canal demonstrated a moderate (46.67 ± 2.50 dB HL) and one patient with severe sensorineural HL (85 dB HL); one patient with ICA aneurysm demonstrated a moderate HL (55 dB HL); one patient with tumor arising from the JF region demonstrated a moderate sensorineural HL (60 dB HL); one patient with a cerebellopontine angle tumor demonstrated a severe sensorineural HL (80 dB HL).

For 192 patients with unilateral PT, the occurrence of bony deficiency of the sigmoid sinus and ICA canal, high-riding, and dehiscent jugular bulb on the asymptomatic side was detected in 3, 0, 32, and 12 sides, respectively. Comparison of these indices between the pulsatile and asymptomatic sides was demonstrated in Table 1 . All four indices demonstrated a statistically significant difference comparing the symptomatic to asymptomatic side (all p  < 0.05). Analysis of the correlation between laterality of PT with the ipsilateral dominance of the jugular vein, high riding jugular bulb, dehiscent jugular bulb, and bony deficiency of the sigmoid sinus and ICA canal was demonstrated in Table 2 . A statistically significant difference was identified between the laterality of PT and the ipsilateral dominance of the JF ( p  < 0.001, Chi-square =35.96), whereas no statistically significant difference was noted between the laterality of PT with other anatomical variations (all p  > 0.05).

Table 1. The comparison of structural variations including the bony dehiscence of sigmoid sinus and internal carotid artery canal, high-riding, and dehiscent jugular bulb between the pulsatile side and the asymptomatic side in patients with unilateral pulsatile tinnitus.

Pulsatile side Asymptomatic side p -Value
SS Deficiency 125 3 <0.001
ICA Deficiency 6 0 0.014
High-riding JB 106 32 <0.001
Dehiscent JB 28 12 0.007
Open in a new tab

Abbreviations: ICA, internal carotid artery; JB, jugular bulb; SS, sigmoid sinus.

Table 2. Correlation analysis between the laterality of pulsatile tinnitus with the ipsilateral dominance of jugular foramen , high-riding jugular bulb, dehiscent jugular bulb, and the bony deficiency of the sigmoid sinus, and deficiency of internal carotid artery canal.

Laterality of pulsatile tinnitus
p -Value Chi-square
Dominant JF <0.001 35.96
High riding JB 0.187 1.744
Dehiscent JB 0.858 0.032
SS Deficiency 0.544 0.368
ICA Deficiency 0.557 0.346
Open in a new tab

Abbreviations: ICA, internal carotid artery; JB, jugular bulb; JF, jugular foramen; SS, sigmoid sinus.

Discussion

Distinguishing with the tinnitus caused by sensorineural dysfunction of inner ear, which mainly manifested as a consistent moderate-to-high frequency noise. 17 However, the predisposing factors for patients with PT are variable, 9 and the vast majority of patients with PT (91.79%) did not demonstrate a HL. Given that the JF region is in close proximity to the middle ear cavity, structural anomalies or lesions arising in close proximity to this region may consequently contribute to the development of PT. 18 This study demonstrated a comprehensive analysis of associated structural abnormalities or lesions surrounding the JF region in patients with PT, which may be beneficial for appreciation of the clinico-radiological characteristics and potentially aid in decision-making for patients with PT.

Bony deficiency of the great vessels (jugular bulb, sigmoid sinus, ICA) has been considered to be the main predisposing factor associated with the development of PT. 6 Therefore, reconstruction of the dehiscent bony wall has been employed to relieve the symptoms of PT and has achieved satisfactory outcomes. 10 A deficient bony wall may allow acoustic transmission of the cardiac heartbeat or arterial flow by way of the mastoid cavity into the middle ear cavity, which is subsequently objectively heard by the patient. Upon surgical repair, this transmission pathway may be occluded, and the sensation of PT thereby eliminated. Based on the investigations derived in the present study, bony deficiency of the sigmoid sinus was the most commonly encountered structural abnormality, which accounted for 65.6% in patients with PT. The occurrence of bony deficiency of sigmoid sinus on the symptomatic pulsatile side also demonstrated a statistically higher rate than that of the asymptomatic side ( Table 1 ). Therefore, surgical reconstruction of the deficient bony wall of the sigmoid sinus may be an option if present.

A high-riding or dehiscent jugular bulb is commonly encountered in clinical settings, most commonly identified incidentally and not resulting in clinical symptoms. 19 Although a high-riding or dehiscent jugular bulb might be causative factors for PT, only few published studies regarding surgical modification of the jugular bulb for addressing PT could be found. 20 In the present study, the prevalence of high-riding and dehiscent jugular bulb at the ipsilateral side of patients with PT was 54.9 and 14.4%, respectively. Despite the higher incidence of these structural abnormalities on the pulsatile side compared with the asymptomatic side ( Table 1 ), there was not a significant correlation with the ipsilateral occurrence of PT ( Table 2 ). Therefore, our study agrees with previous reports noting that the causative role of a high-riding or dehiscent jugular bulb may be limited, and therefore, associated procedures should be cautiously and critically selected. 20

The JF demonstrated a right-sided dominance pattern in majority of cases. 21 In this cohort, a similar fashion of right side dominated JF could also be detected in majority of patients with PT (66.2%), whereas a balanced type accounts for 20.5%, and left side dominance for 13.3%. To the authors' knowledge, however, literature with respect to the relation assessment between the dominance of JF and the ipsilateral occurrence of PT are sparse. Based on the clinico-radiological investigation derived in the present study, there was significant difference between the laterality of PT with the ipsilateral occurrence a dominant JF ( Table 2 ). It may imply that the dominance of the JF may potentially predispose to the development of PT to some extent, which might be associated with alterations of hemodynamics around the JF region. 22 23 However, this potential mechanism is still undefined and deserves further investigation.

The courses of parapharyngeal and petrosal segments of the ICA are intimately correlated with the middle ear cavity. 24 Deficiency of the bony wall can result in objective sensation of the pulsatile artery. 25 Isolated deficiency of the ICA canal is rarely encountered, and the incidence of ICA canal deficiency was detected to be 3.1% in the present study, whereas on the asymptomatic side no deficiency of the ICA canal or ICA aneurysm was detected. It is necessary to differentiate a solitary ICA canal deficiency from an aneurysm of the petrous ICA, which needs timely interventional or neurosurgical involvement. 26 Moreover, the petrous ICA also runs close to the cochlea, and decreased thickness of the bony septum between the ICA and the middle ear cavity may also contribute to pulsatile sensation. 27 Reconstructing ICA canal deficiency, however, is technically demanding and the efficacy deserves further validation. In addition, for those patients with tumors arising from the JF region, enclosing of the ICA or encroaching the ICA canal maybe coexist. 28 Although PT can be present as one of the symptoms in patients with JF tumors, it rarely emerged as the first or major symptom. 18

Due to the close proximity with the middle ear, tumors arising from the JF region and internal acoustic meatus may also contribute to the development of PT. 2 However, in accordance with previous reports, these tumors were rarely detected in patients included in the present study. Moreover, the deficiency of the superior semicircular canal and the AV fistula are uncommon reasons for the development of PT. The former may have an intimate relationship with the course of superior petrous sinus, which transmits the sound of arterial beat from elsewhere in association with its course. 29 In regard to AV fistula, the early abnormal filling of the venous system including the sigmoid sinus or jugular bulb during CTA examination was the typical sign, and the AV fistula may contribute directly to the sensation of a PT. 30 Therefore, we propose that the CTA/CTV of temporal bone is a valuable method for screening/exclusive diagnosis for patients with PT. The confirmation and embolization of the corresponding vessel, however, need to be employed by way of a vascular interventional method (e.g., DSA examination).

The authors recognized there are significant limitations to this study. It is a retrospective clinical radiological analysis; therefore, the strength of the evidence for analysis of the predisposing factors for PT is lower than that completed and confirmed by DSA examination, which may identify the concrete corresponding vessel and enhance the appreciation of individualized treatment. Moreover, the development of PT may be multifactorial. Although the predisposing factors such as bony dehiscence of the sigmoid sinus and the jugular bulb may be associated with PT, DSA examination should be routinely performed to exclude the corresponding nurturing vessels before surgical reconstruction. In addition, the JF is a deeply located region, radiological analysis of the potential relationship between the anomalies of JF and the occurrence of PT can only provide some clinical relevance, its mechanism still deserves further validation.

Conclusion

Structural abnormalities surrounding the JF region may predispose to the development of PT. Knowledge of anatomical variations in the JF region may help establish a clinical strategy for addressing PT.

Conflict of Interest N.R.L. holds stock in Navigen Pharmaceuticals and was a consultant for Cooltech Inc. The other authors report no conflict of interest.

*

These authors contributed equally to the article.

References

  • 1.Truesdale C M, El-Kashlan H K. Pulsatile tinnitus with imaging. JAMA Otolaryngol Head Neck Surg. 2018;144(05):451–452. doi: 10.1001/jamaoto.2018.0014. [DOI] [PubMed] [Google Scholar]
  • 2.Hofmann E, Behr R, Neumann-Haefelin T, Schwager K. Pulsatile tinnitus: imaging and differential diagnosis. Dtsch Arztebl Int. 2013;110(26):451–458. doi: 10.3238/arztebl.2013.0451. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Wang A C, Nelson A N, Pino C, Svider P F, Hong R S, Chan E. Management of sigmoid sinus associated pulsatile tinnitus: a systematic review of the literature. Otol Neurotol. 2017;38(10):1390–1396. doi: 10.1097/MAO.0000000000001612. [DOI] [PubMed] [Google Scholar]
  • 4.Berguer R, Nowak P. Treatment of venous pulsatile tinnitus in younger women. Ann Vasc Surg. 2015;29(04):650–653. doi: 10.1016/j.avsg.2014.12.039. [DOI] [PubMed] [Google Scholar]
  • 5.Lyu A R, Park S J, Kim D, Lee H Y, Park Y H. Radiologic features of vascular pulsatile tinnitus - suggestion of optimal diagnostic image workup modalities. Acta Otolaryngol. 2018;138(02):128–134. doi: 10.1080/00016489.2017.1385847. [DOI] [PubMed] [Google Scholar]
  • 6.Onder H. Sigmoid sinus dehiscence and suspected idiopathic intracranial hypertension in pulsatile tinnitus? Neuroradiology. 2018;60(04):355–356. doi: 10.1007/s00234-018-2009-1. [DOI] [PubMed] [Google Scholar]
  • 7.Mundada P, Singh A, Lingam R K. CT arteriography and venography in the evaluation of Pulsatile tinnitus with normal otoscopic examination. Laryngoscope. 2015;125(04):979–984. doi: 10.1002/lary.25010. [DOI] [PubMed] [Google Scholar]
  • 8.Monsell E M. Regarding evaluation and treatment of pulsatile tinnitus associated with sigmoid sinus wall anomalies. Laryngoscope. 2019;129(04):E127. doi: 10.1002/lary.27799. [DOI] [PubMed] [Google Scholar]
  • 9.Sismanis A. Pulsatile tinnitus: contemporary assessment and management. Curr Opin Otolaryngol Head Neck Surg. 2011;19(05):348–357. doi: 10.1097/MOO.0b013e3283493fd8. [DOI] [PubMed] [Google Scholar]
  • 10.Ma X B, Wang G P, Zeng R, Gong S S. Treatment of pulsatile tinnitus associated with multiple factors. Chin Med J (Engl) 2015;128(03):413–414. doi: 10.4103/0366-6999.150121. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Li L, London N R, Jr, Prevedello D M, Carrau R L. Endonasal endoscopic transpterygoid approach to the upper parapharyngeal space. Head Neck. 2020;42(09):2734–2740. doi: 10.1002/hed.26127. [DOI] [PubMed] [Google Scholar]
  • 12.Li L, London N R, Jr, Prevedello D M, Carrau R L. Anatomy based corridors to the infratemporal fossa: Implications for endoscopic approaches. Head Neck. 2020;42(05):846–853. doi: 10.1002/hed.26055. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Vaz-Guimaraes F, Nakassa A CI, Gardner P A, Wang E W, Snyderman C H, Fernandez-Miranda J C. Endoscopic endonasal approach to the ventral jugular foramen: anatomical basis, technical considerations, and clinical series. Oper Neurosurg (Hagerstown) 2017;13(04):482–491. doi: 10.1093/ons/opx014. [DOI] [PubMed] [Google Scholar]
  • 14.Tanjararak K, Upadhyay S, Thiensri T. Potential surgical exposure of the parapharyngeal internal carotid artery by endonasal, transoral, and transcervical approaches. J Neurol Surg B Skull Base. 2018;79(03):241–249. doi: 10.1055/s-0037-1607289. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Griessenauer C J, McGrew B, Matusz P, De Caro R, Loukas M, Tubbs R S. Surgical approaches to the jugular foramen: a comprehensive review. J Neurol Surg B Skull Base. 2016;77(03):260–264. doi: 10.1055/s-0035-1567863. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Ramina R, Maniglia J J, Fernandes Y B. Jugular foramen tumors: diagnosis and treatment. Neurosurg Focus. 2004;17(02):E5. doi: 10.3171/foc.2004.17.2.5. [DOI] [PubMed] [Google Scholar]
  • 17.Chari D A, Limb C J. Tinnitus. Med Clin North Am. 2018;102(06):1081–1093. doi: 10.1016/j.mcna.2018.06.014. [DOI] [PubMed] [Google Scholar]
  • 18.Isaacson B, Wick C C, Perez C, Cantrell S C, Killeen D E. Pathophysiology of sensorineural hearing loss in jugular foramen paraganglioma. Laryngoscope. 2019;129(01):67–75. doi: 10.1002/lary.27343. [DOI] [PubMed] [Google Scholar]
  • 19.Lee S Y, Song S K, Park S J. Jugular bulb resurfacing with bone cement for patients with high dehiscent jugular bulb and ipsilateral pulsatile tinnitus. Otol Neurotol. 2019;40(02):192–199. doi: 10.1097/MAO.0000000000002093. [DOI] [PubMed] [Google Scholar]
  • 20.DeHart A N, Shaia W T, Coelho D H. Hydroxyapatite cement resurfacing the dehiscent jugular bulb: Novel treatment for pulsatile tinnitus. Laryngoscope. 2018;128(05):1186–1190. doi: 10.1002/lary.26711. [DOI] [PubMed] [Google Scholar]
  • 21.Das S S, Saluja S, Vasudeva N. Complete morphometric analysis of jugular foramen and its clinical implications. J Craniovertebr Junction Spine. 2016;7(04):257–264. doi: 10.4103/0974-8237.193268. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Haraldsson H, Leach J R, Kao E I. Reduced jet velocity in venous flow after CSF drainage: assessing hemodynamic causes of pulsatile tinnitus. AJNR Am J Neuroradiol. 2019;40(05):849–854. doi: 10.3174/ajnr.A6043. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23.Kao E, Kefayati S, Amans M R. Flow patterns in the jugular veins of pulsatile tinnitus patients. J Biomech. 2017;52:61–67. doi: 10.1016/j.jbiomech.2016.12.008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24.Honkura Y, Hidaka H, Ohta J, Gorai S, Katori Y, Kobayashi T. Surgical treatment for the aberrant internal carotid artery in the middle ear with pulsatile tinnitus. Auris Nasus Larynx. 2014;41(02):215–218. doi: 10.1016/j.anl.2013.10.002. [DOI] [PubMed] [Google Scholar]
  • 25.Van Damme J P, Heylen G, Gilain C, Garin P. Pulsatile tinnitus associated with dehiscent internal carotid artery: an irremediable condition? Auris Nasus Larynx. 2017;44(05):612–615. doi: 10.1016/j.anl.2016.08.008. [DOI] [PubMed] [Google Scholar]
  • 26.Kim S M, Kim C H, Lee C Y. Petrous carotid aneurysm causing pulsatile tinnitus: case report and review of the literature. J Cerebrovasc Endovasc Neurosurg. 2018;20(01):35–39. doi: 10.7461/jcen.2018.20.1.35. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Sonmez G, Basekim C C, Ozturk E, Gungor A, Kizilkaya E. Imaging of pulsatile tinnitus: a review of 74 patients. Clin Imaging. 2007;31(02):102–108. doi: 10.1016/j.clinimag.2006.12.024. [DOI] [PubMed] [Google Scholar]
  • 28.Ginat D T, Gluth M B. Pulsatile tinnitus and a temporal bone mass. Eur Ann Otorhinolaryngol Head Neck Dis. 2016;133(06):441–442. doi: 10.1016/j.anorl.2015.06.010. [DOI] [PubMed] [Google Scholar]
  • 29.Liu Z, Bi W, Li J. Superior semicircular canal dehiscence in relation to the superior petrosal sinus: a potential cause of pulsatile tinnitus. Clin Radiol. 2015;70(09):943–947. doi: 10.1016/j.crad.2015.04.017. [DOI] [PubMed] [Google Scholar]
  • 30.Darvie P, Storey C, Nanda A, Cuellar-Saenz H. Dural arteriovenous fistula associated with a glomus jugulare tumour presenting with only pulsatile tinnitus. BMJ Case Rep. 2018 doi: 10.1136/bcr-2018-224860. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Journal of Neurological Surgery. Part B, Skull Base are provided here courtesy of Thieme Medical Publishers

RESOURCES