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Treatment of Venous Pulsatile Tinnitus in Younger Women
Clinical Research Treatment of Venous Pulsatile Tinnitus in Younger Women Ramon Berguer,1 and Peggy Nowak,2 Ann Arbor and Royal Oak, Michigan
Background: We present 7 cases of pulsatile tinnitus (PT) of venous origin in younger women seen over a period of 24 years and treated by Internal Jugular Bulb ligation. Methods: All patients had a pulsatile bruit in one side of the neck that disappeared when gentle pressure over the internal jugular vein (IJV) caused it to collapse as seen in a duplex scan. Their computed tomography showed a dominant venous system with a high jugular bulb on the side of the bruit. Results: The IJV was ligated under local anesthesia. Five patients in whom the ligation was done above the facial vein were cured. Two patients in whom the ligation was done below the facial vein experienced a decrease but not disappearance of the PT. Conclusions: Once other possible causes for PT have been discarded, ligation of the IJV above the facial vein cures this condition.
INTRODUCTION Only a small percentage (5e10%) of tinnitus is pulsatile, and with rare exceptions, the latter has a vascular origin. The source for pulsatile tinnitus (PT) can be arterial (carotid fibrodysplasia, intrapetrosal carotid aneurysm, and arteriovenous fistula) or venous (high jugular bulb [HJB]) because both the intrapetrosal carotid and the jugular bulb are in close proximity to the inner ear. The source of the PT is blood flow turbulence that may originate in the carotid artery or in the internal jugular vein (IJV) that is transmitted to the adjacent inner ear through a thin bone plate, or when the plate is absent, by direct contact of the jugular wall with the semicircular canal (SCC).
1 Department of Vascular Surgery, University of Michigan Medical Center, Ann Arbor, MI. 2 Department of Otolaryngology, Beaumont Health System, Royal Oak, MI.
Correspondence to: Ramon Berguer, Department of Vascular Surgery, 1500 East Medical Center Dr, CVC 5463, Ann Arbor, MI 48109, USA; E-mail: [email protected] Ann Vasc Surg 2015; 29: 650–653 http://dx.doi.org/10.1016/j.avsg.2014.12.039 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: August 27, 2014; manuscript accepted: December 31, 2014; published online: March 6, 2015.
650
There are reports of ‘‘symptomatic venous hums’’ in the medical literature dating back to 1961. Hentzer1 reported on 13 cases of pulsatile venous tinnitus, and in 3 patients, he ligated the IJV. The hum disappeared temporarily in 2 and permanently in 1. Gary2 used a prosthetic device that pressed over the IJV to obliterate the ‘‘venous hum.’’ Chandler,3 Hardison et al.,4 and Nehru et al.5 in separate case reports noted the disappearance of the venous hum with pressure over the IJV and reported that ligation of the IJV in their patients cured the symptom. None of the patients had had a previous angiogram or a computed tomography (CT) scan. Golueke et al.6 reported a successful case of IJV ligation that cured the PT in a patient who had both of these tests. The PT in patients with a HJB characteristically disappears when the IJV is compressed to occlusion. This is documented by applying gentle pressure over the vein during duplex imaging and having the patient report the disappearance of the bruit as soon as the IJV is seen to collapse and reappear when the vein expands. The bruit may increase when the contralateral IJV is compressed. Patients report that the bruit is more bothersome at night. The first manifestation of PT is sometimes reported during pregnancy, when blood volume and cardiac output increase. The average age of the women reported in the cited references was 40 years. The PT may be the
Vol. 29, No. 4, May 2015
Treatment of venous PT in younger women 651
Fig. 1. CT venogram showing a higher jugular bulb and a larger, dominant venous system on the left side.
source of anxiety and has been described in reports as ‘‘incapacitating’’ or being a source of ‘‘great worry.’’ This disturbance can be serious enough that complex transtemporal operations have been done to cure the bruit by interposing a pad of surgical wax between the dome of the jugular bulb and the SCC.7,8 The pulsatility of the bruit could be generated by an adjacent internal carotid artery pulsating against a distended jugular bulb or more likely be the consequence of variations of the venous flow in the proximity of the heart caused by the contraction of the atrium and the opening and closing of the pulmonary valve. HJB is used synonymously with enlarged or dehiscent jugular bulb although the last 2 denominations actually describe the progressive evolution of a HJB. The jugular bulb itself is not a stable anatomic structure. A HJB is rarely seen in children, and it has shown to continue enlarging in patients who have been followed with periodic temporal CT scans.9,10 The histologic studies of the jugular bulb10 show that its vascular wall is devoid of adventitia and is much thinner than that of the lateral sinus that precedes it or of the jugular vein that follows it. The higher the jugular bulb the thinner its wall, and this finding is consistent with what happens to an expanding venous wall. The diverticula that extend medially from a HJB are essentially monolayer vascular structures that can be described as venous aneurysms. What constitutes a HJB varies for different authors depending on the landmarks used to define it. The one used most frequently is when the dome of the jugular bulb extends above the inferior part of the round window (Fig. 1). Its incidence in a general population11 is 6%. Others have found the incidence of HJB in temporal bone scans12 (in selected patients referred to radiology for various neuro-otologic conditions) to be as high as 24%.
Fig. 2. Proximity of the semicircular canal to the IJV bulb. Yellow line: site of the thin bony plate separating both structures.
The jugular bulb is separated from the SCC by a bone septum (Fig. 2). As the jugular bulb expands, this septum becomes very thin (0.1 mm), more like a membrane. In other cases, the septum is absent (dehiscence), and the bluish bulb can be seen with the otoscope behind the tympanic membrane. The bruit is caused by flow turbulence in the large HJB. The venous blood exiting the lateral sinus enters the large jugular bulb, and the sudden expansion of the flow stream generates turbulent vortices.
MATERIALS AND METHODS This retrospective review of a 24-year experience was not submitted to an institutional review board. All operations had been preceded by discussion leading to informed consent. The 7 patients summarized in Table I, had had multiple studies that included hearing test, duplex examination of the neck, CT scan of the head, and arteriography. The only anatomic abnormality found in their CT was a HJB. Their only symptom was a pulsatile noise synchronous with the heart frequency. The bruit interfered with their quality of life to the point that 2 of 7 were at the time undergoing psychiatric treatment after other known causes for their PT (tumor, carotid aneurysm, fistula, and so forth) had been ruled out.
652 Berguer and Nowak
Annals of Vascular Surgery
Table I. Ligature level and outcome for the 7 patients included in this report. Patient#
Age, years
Side
Ligature level
Outcome
1 2 3 4 5 6 7
34 29 47 44 55 23 55
Left Right Right Left Right Right Right
Above facial Above facial Above facial Below facial Above facial Below facial Below facial
Cured Cured Cured Some improved Cured Some improved Cured
All 7 patients had noted that certain maneuvers that resulted in pressure on the neck on the side of the PT made the latter disappear. The PT was perceived as more intense during the night. To obtain relief during night rest, 1 patient taped an elastic strip around the symptomatic side of the neck, another put pressure under her neck with a rolled small pillow, and a third jammed her hand between her neck and the pillow. The pulsatile bruit disappeared in all when the duplex scan showed the IJC being compressed to occlusion and returned as soon as the flow resumed in the IJV. After demonstrating the integrity of the contralateral venous system and ruling out the diagnosis of benign intracranial hypertension (BIH), the 7 patients underwent IJV ligation under local anesthesia. The IJV was ligated below the facial vein in 2 patients with the intention of avoiding a possible thrombosis of the IJV above the facial vein. The other 5 underwent ligation above the facial vein.
RESULTS Follow-up ranged from 2 to 10 years. The PT disappeared immediately and permanently in the 5 patients in whom the ligation was done above the facial vein. In the 2 patients in whom the ligature was done below the facial vein, the bruit disappeared immediately but returned with lesser intensity after 2 and 3 days. In these 2 patients, the remaining softer bruit disappeared when IJV was collapsed under duplex imaging. Both of them had patency of the IJV below the facial vein maintained by a medial thyroid vein. A reoperation or an occlusion of the large facial vein by endovascular means was offered, but the recommendation was not accepted.
DISCUSSION PT has been reported to be associated with BIH and a HJB.13 BIH is a rare condition (incidence 1:105)
Fig. 3. Schematic representation of the volume flow (arrow) of the IJV in normal conditions, after its ligation above the facial vein and after its ligation below the facial vein.
more commonly reported in overweight black women who develop cephalic venous hypertension secondary to increased intrathoracic pressure.14 The venous hypertension results in intracerebral edema, which is evidenced by the CT findings of empty sella and small ventricular size and the clinical manifestations of papilledema, headache, and occasional diplopia from VI nerve palsy. The etiology of the PT in patients with BIH has been postulated as a consequence of the high-velocity jet of venous blood exiting a lateral sinus that is compressed by the intracranial hypertension against the unyielding bone. But this explanation is not consistent with the facts that patients with BIH do not develop bilateral bruits and that many other conditions associated with increased intracranial pressure (brain tumor and infarction) do not result in PT. The PT in patients with BIH is always unilateral and more likely is determined by the concomitant presence of a HJB in these patients. In the selection of patients for ligation, it is necessary to rule out BIH as the ligation of the IJV may very well suppress the PT but could only further increase the venous cerebral hypertension. For this reason, one should ensure that there is no evidence of intracranial hypertension (papilledema, headache, and VI nerve palsy) and that the CT scan is normal. An association has also been reported7,8 between Meniere’s syndrome, a dehiscent HJB and PT. This association of a HJB and Meniere’s syndrome is explained to be the consequence of a dilated HJB, or the diverticulum arising from it, pressing against the inner ear structures that are responsible for the resorption of endolymph. The HJB is thought to be the etiology of the Meniere syndrome in these patients. These patients have undergone
Vol. 29, No. 4, May 2015
mastoidectomy7,8 and the insertion of a tab of surgical wax to separate the jugular bulb from the inner ear structures. Their vertigo was cured in 92% of cases and the PT disappeared in 23% and improved in 31%. The bruit intensity is a function of the venous flow velocity that generates turbulence as it enters the jugular bulb. When flow in the IJV is arrested by external pressure, the noise disappears. If the IJV is ligated below a well-developed facial vein, the flow rate through the bulb will decrease and so will the intensity of the bruit, at least temporarily, but it may not disappear as it happened in 2 of our patients. Ligation of the IJV above the facial results in a large decrease in outflow and the disappearance of the PT (there remain small branches at the hypoglossal level and at C2 that provide enough outflow to preclude thrombosis of the lateral sinus). Figure 3 shows schematically the volume flow through the IJV under normal conditions and after ligation at 2 different sites. The almost exclusive incidence of this condition in younger adult women remains unexplained. There is no significant gender difference in the incidence of HJB, with the exception of one report14 that found HJB to be more frequent (68%) in women. Anemia increases the cardiac output and consequently the production of turbulence but it was not present in any of our patients. In addition, most patients in the published reports of PT secondary to HJB are within the age bracket of 25e40 years, but the anatomic studies of temporal bones show that the incidence of HJB increases with age and peaks at the 61e70 years interval.
CONCLUSIONS A specific case of PT found in younger women without any other symptom or sign of disease can be cured by ligation of the IJV above the level of the facial vein. Once the source of the bruit has been located in the jugular bulb and before an
Treatment of venous PT in younger women 653
intervention is carried out, other conditions, capable of producing PT or being associated with it, must be ruled out. Prominent among these is BIH that could be aggravated by ligation of the IJV. The integrity of the opposite venous system must also be proven before ligating the IJV on the symptomatic side.
REFERENCES 1. Hentzer E. Objective tinnitus of the vascular type: a followup study. Acta Otolaryngol 1968;66:273e81. 2. Gary FH. Symptomatic venous hum. Report of a case. N Engl J Med 1961;264:869e70. 3. Chandler JR. Diagnosis and cure of venous hum tinnitus. Laryngoscope 1983;93:892e5. 4. Hardison JE, Smith RB, Crawley IS, et al. Self-heard venous hums. JAMA 1981;245:1146e7. 5. Nehru VI, al-Khaboori MJ, Kishore K. Ligation of the internal jugular vein in venous hum tinnitus. J Laryngol Otol 1993;107:1037e8. 6. Golueke PJ, Panetta T, Sclafani S, et al. Tinnitus originating from an abnormal jugular bulb: treatment by jugular vain ligation. J Vasc Surg 1987;6:248e51. 7. El-Begermy MA, Rabie AN. A novel surgical technique for management of tinnitus due to high dehiscent bulb. Otolaryngol Head Neck Surg 2010;142:576e81. 8. Couloigner V, Grayeli AB, Bouccara D, et al. Surgical treatment of the high jugular bulb in patients with Meniere’s disease and pulsatile tinnitus. Eur Arch Otorhinolaryngol 1999;256:224e9. 9. Graham MD. The jugular bulb: its anatomic and clinical considerations in contemporary otology. Laryngoscope 1977;87: 105e25. 10. Kawano H, Tono T, Schaachern P, et al. Petrous high jugular bulb: a histological study. Am J Otolaryngol 2000;21:161e8. 11. Overton SB, Ritter FN. A high placed jugular bulb in the middle ear: a clinical and temporal bone study. Laryngoscope 1973;83:1986e91. 12. Atilla S, Akpek S, Uslu S, et al. Computed tomographic evaluation of surgically significant vascular variations related with the temporal bone. Eur J Radiol 1995;20:52e6. 13. Herraiz C, Aparicio JM. Diagnostic clues in pulsatile tinnitus (Somatosounds). Acta Otorrinolaryngol Esp 2007;58: 426e33. 14. Vachata P, Petrovicky P, Sames M. An anatomical and radiological study of the high jugular bulb on high-resolution CT scans and alcohol-fixed skulls of adults. J Clin Neurosci 2010;17:473e8.
Background: We present 7 cases of pulsatile tinnitus (PT) of venous origin in younger women seen over a period of 24 years and treated by Internal Jugular Bulb ligation. Methods: All patients had a pulsatile bruit in one side of the neck that disappeared when gentle pressure over the internal jugular vein (IJV) caused it to collapse as seen in a duplex scan. Their computed tomography showed a dominant venous system with a high jugular bulb on the side of the bruit. Results: The IJV was ligated under local anesthesia. Five patients in whom the ligation was done above the facial vein were cured. Two patients in whom the ligation was done below the facial vein experienced a decrease but not disappearance of the PT. Conclusions: Once other possible causes for PT have been discarded, ligation of the IJV above the facial vein cures this condition.
INTRODUCTION Only a small percentage (5e10%) of tinnitus is pulsatile, and with rare exceptions, the latter has a vascular origin. The source for pulsatile tinnitus (PT) can be arterial (carotid fibrodysplasia, intrapetrosal carotid aneurysm, and arteriovenous fistula) or venous (high jugular bulb [HJB]) because both the intrapetrosal carotid and the jugular bulb are in close proximity to the inner ear. The source of the PT is blood flow turbulence that may originate in the carotid artery or in the internal jugular vein (IJV) that is transmitted to the adjacent inner ear through a thin bone plate, or when the plate is absent, by direct contact of the jugular wall with the semicircular canal (SCC).
1 Department of Vascular Surgery, University of Michigan Medical Center, Ann Arbor, MI. 2 Department of Otolaryngology, Beaumont Health System, Royal Oak, MI.
Correspondence to: Ramon Berguer, Department of Vascular Surgery, 1500 East Medical Center Dr, CVC 5463, Ann Arbor, MI 48109, USA; E-mail: [email protected] Ann Vasc Surg 2015; 29: 650–653 http://dx.doi.org/10.1016/j.avsg.2014.12.039 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: August 27, 2014; manuscript accepted: December 31, 2014; published online: March 6, 2015.
650
There are reports of ‘‘symptomatic venous hums’’ in the medical literature dating back to 1961. Hentzer1 reported on 13 cases of pulsatile venous tinnitus, and in 3 patients, he ligated the IJV. The hum disappeared temporarily in 2 and permanently in 1. Gary2 used a prosthetic device that pressed over the IJV to obliterate the ‘‘venous hum.’’ Chandler,3 Hardison et al.,4 and Nehru et al.5 in separate case reports noted the disappearance of the venous hum with pressure over the IJV and reported that ligation of the IJV in their patients cured the symptom. None of the patients had had a previous angiogram or a computed tomography (CT) scan. Golueke et al.6 reported a successful case of IJV ligation that cured the PT in a patient who had both of these tests. The PT in patients with a HJB characteristically disappears when the IJV is compressed to occlusion. This is documented by applying gentle pressure over the vein during duplex imaging and having the patient report the disappearance of the bruit as soon as the IJV is seen to collapse and reappear when the vein expands. The bruit may increase when the contralateral IJV is compressed. Patients report that the bruit is more bothersome at night. The first manifestation of PT is sometimes reported during pregnancy, when blood volume and cardiac output increase. The average age of the women reported in the cited references was 40 years. The PT may be the
Vol. 29, No. 4, May 2015
Treatment of venous PT in younger women 651
Fig. 1. CT venogram showing a higher jugular bulb and a larger, dominant venous system on the left side.
source of anxiety and has been described in reports as ‘‘incapacitating’’ or being a source of ‘‘great worry.’’ This disturbance can be serious enough that complex transtemporal operations have been done to cure the bruit by interposing a pad of surgical wax between the dome of the jugular bulb and the SCC.7,8 The pulsatility of the bruit could be generated by an adjacent internal carotid artery pulsating against a distended jugular bulb or more likely be the consequence of variations of the venous flow in the proximity of the heart caused by the contraction of the atrium and the opening and closing of the pulmonary valve. HJB is used synonymously with enlarged or dehiscent jugular bulb although the last 2 denominations actually describe the progressive evolution of a HJB. The jugular bulb itself is not a stable anatomic structure. A HJB is rarely seen in children, and it has shown to continue enlarging in patients who have been followed with periodic temporal CT scans.9,10 The histologic studies of the jugular bulb10 show that its vascular wall is devoid of adventitia and is much thinner than that of the lateral sinus that precedes it or of the jugular vein that follows it. The higher the jugular bulb the thinner its wall, and this finding is consistent with what happens to an expanding venous wall. The diverticula that extend medially from a HJB are essentially monolayer vascular structures that can be described as venous aneurysms. What constitutes a HJB varies for different authors depending on the landmarks used to define it. The one used most frequently is when the dome of the jugular bulb extends above the inferior part of the round window (Fig. 1). Its incidence in a general population11 is 6%. Others have found the incidence of HJB in temporal bone scans12 (in selected patients referred to radiology for various neuro-otologic conditions) to be as high as 24%.
Fig. 2. Proximity of the semicircular canal to the IJV bulb. Yellow line: site of the thin bony plate separating both structures.
The jugular bulb is separated from the SCC by a bone septum (Fig. 2). As the jugular bulb expands, this septum becomes very thin (0.1 mm), more like a membrane. In other cases, the septum is absent (dehiscence), and the bluish bulb can be seen with the otoscope behind the tympanic membrane. The bruit is caused by flow turbulence in the large HJB. The venous blood exiting the lateral sinus enters the large jugular bulb, and the sudden expansion of the flow stream generates turbulent vortices.
MATERIALS AND METHODS This retrospective review of a 24-year experience was not submitted to an institutional review board. All operations had been preceded by discussion leading to informed consent. The 7 patients summarized in Table I, had had multiple studies that included hearing test, duplex examination of the neck, CT scan of the head, and arteriography. The only anatomic abnormality found in their CT was a HJB. Their only symptom was a pulsatile noise synchronous with the heart frequency. The bruit interfered with their quality of life to the point that 2 of 7 were at the time undergoing psychiatric treatment after other known causes for their PT (tumor, carotid aneurysm, fistula, and so forth) had been ruled out.
652 Berguer and Nowak
Annals of Vascular Surgery
Table I. Ligature level and outcome for the 7 patients included in this report. Patient#
Age, years
Side
Ligature level
Outcome
1 2 3 4 5 6 7
34 29 47 44 55 23 55
Left Right Right Left Right Right Right
Above facial Above facial Above facial Below facial Above facial Below facial Below facial
Cured Cured Cured Some improved Cured Some improved Cured
All 7 patients had noted that certain maneuvers that resulted in pressure on the neck on the side of the PT made the latter disappear. The PT was perceived as more intense during the night. To obtain relief during night rest, 1 patient taped an elastic strip around the symptomatic side of the neck, another put pressure under her neck with a rolled small pillow, and a third jammed her hand between her neck and the pillow. The pulsatile bruit disappeared in all when the duplex scan showed the IJC being compressed to occlusion and returned as soon as the flow resumed in the IJV. After demonstrating the integrity of the contralateral venous system and ruling out the diagnosis of benign intracranial hypertension (BIH), the 7 patients underwent IJV ligation under local anesthesia. The IJV was ligated below the facial vein in 2 patients with the intention of avoiding a possible thrombosis of the IJV above the facial vein. The other 5 underwent ligation above the facial vein.
RESULTS Follow-up ranged from 2 to 10 years. The PT disappeared immediately and permanently in the 5 patients in whom the ligation was done above the facial vein. In the 2 patients in whom the ligature was done below the facial vein, the bruit disappeared immediately but returned with lesser intensity after 2 and 3 days. In these 2 patients, the remaining softer bruit disappeared when IJV was collapsed under duplex imaging. Both of them had patency of the IJV below the facial vein maintained by a medial thyroid vein. A reoperation or an occlusion of the large facial vein by endovascular means was offered, but the recommendation was not accepted.
DISCUSSION PT has been reported to be associated with BIH and a HJB.13 BIH is a rare condition (incidence 1:105)
Fig. 3. Schematic representation of the volume flow (arrow) of the IJV in normal conditions, after its ligation above the facial vein and after its ligation below the facial vein.
more commonly reported in overweight black women who develop cephalic venous hypertension secondary to increased intrathoracic pressure.14 The venous hypertension results in intracerebral edema, which is evidenced by the CT findings of empty sella and small ventricular size and the clinical manifestations of papilledema, headache, and occasional diplopia from VI nerve palsy. The etiology of the PT in patients with BIH has been postulated as a consequence of the high-velocity jet of venous blood exiting a lateral sinus that is compressed by the intracranial hypertension against the unyielding bone. But this explanation is not consistent with the facts that patients with BIH do not develop bilateral bruits and that many other conditions associated with increased intracranial pressure (brain tumor and infarction) do not result in PT. The PT in patients with BIH is always unilateral and more likely is determined by the concomitant presence of a HJB in these patients. In the selection of patients for ligation, it is necessary to rule out BIH as the ligation of the IJV may very well suppress the PT but could only further increase the venous cerebral hypertension. For this reason, one should ensure that there is no evidence of intracranial hypertension (papilledema, headache, and VI nerve palsy) and that the CT scan is normal. An association has also been reported7,8 between Meniere’s syndrome, a dehiscent HJB and PT. This association of a HJB and Meniere’s syndrome is explained to be the consequence of a dilated HJB, or the diverticulum arising from it, pressing against the inner ear structures that are responsible for the resorption of endolymph. The HJB is thought to be the etiology of the Meniere syndrome in these patients. These patients have undergone
Vol. 29, No. 4, May 2015
mastoidectomy7,8 and the insertion of a tab of surgical wax to separate the jugular bulb from the inner ear structures. Their vertigo was cured in 92% of cases and the PT disappeared in 23% and improved in 31%. The bruit intensity is a function of the venous flow velocity that generates turbulence as it enters the jugular bulb. When flow in the IJV is arrested by external pressure, the noise disappears. If the IJV is ligated below a well-developed facial vein, the flow rate through the bulb will decrease and so will the intensity of the bruit, at least temporarily, but it may not disappear as it happened in 2 of our patients. Ligation of the IJV above the facial results in a large decrease in outflow and the disappearance of the PT (there remain small branches at the hypoglossal level and at C2 that provide enough outflow to preclude thrombosis of the lateral sinus). Figure 3 shows schematically the volume flow through the IJV under normal conditions and after ligation at 2 different sites. The almost exclusive incidence of this condition in younger adult women remains unexplained. There is no significant gender difference in the incidence of HJB, with the exception of one report14 that found HJB to be more frequent (68%) in women. Anemia increases the cardiac output and consequently the production of turbulence but it was not present in any of our patients. In addition, most patients in the published reports of PT secondary to HJB are within the age bracket of 25e40 years, but the anatomic studies of temporal bones show that the incidence of HJB increases with age and peaks at the 61e70 years interval.
CONCLUSIONS A specific case of PT found in younger women without any other symptom or sign of disease can be cured by ligation of the IJV above the level of the facial vein. Once the source of the bruit has been located in the jugular bulb and before an
Treatment of venous PT in younger women 653
intervention is carried out, other conditions, capable of producing PT or being associated with it, must be ruled out. Prominent among these is BIH that could be aggravated by ligation of the IJV. The integrity of the opposite venous system must also be proven before ligating the IJV on the symptomatic side.
REFERENCES 1. Hentzer E. Objective tinnitus of the vascular type: a followup study. Acta Otolaryngol 1968;66:273e81. 2. Gary FH. Symptomatic venous hum. Report of a case. N Engl J Med 1961;264:869e70. 3. Chandler JR. Diagnosis and cure of venous hum tinnitus. Laryngoscope 1983;93:892e5. 4. Hardison JE, Smith RB, Crawley IS, et al. Self-heard venous hums. JAMA 1981;245:1146e7. 5. Nehru VI, al-Khaboori MJ, Kishore K. Ligation of the internal jugular vein in venous hum tinnitus. J Laryngol Otol 1993;107:1037e8. 6. Golueke PJ, Panetta T, Sclafani S, et al. Tinnitus originating from an abnormal jugular bulb: treatment by jugular vain ligation. J Vasc Surg 1987;6:248e51. 7. El-Begermy MA, Rabie AN. A novel surgical technique for management of tinnitus due to high dehiscent bulb. Otolaryngol Head Neck Surg 2010;142:576e81. 8. Couloigner V, Grayeli AB, Bouccara D, et al. Surgical treatment of the high jugular bulb in patients with Meniere’s disease and pulsatile tinnitus. Eur Arch Otorhinolaryngol 1999;256:224e9. 9. Graham MD. The jugular bulb: its anatomic and clinical considerations in contemporary otology. Laryngoscope 1977;87: 105e25. 10. Kawano H, Tono T, Schaachern P, et al. Petrous high jugular bulb: a histological study. Am J Otolaryngol 2000;21:161e8. 11. Overton SB, Ritter FN. A high placed jugular bulb in the middle ear: a clinical and temporal bone study. Laryngoscope 1973;83:1986e91. 12. Atilla S, Akpek S, Uslu S, et al. Computed tomographic evaluation of surgically significant vascular variations related with the temporal bone. Eur J Radiol 1995;20:52e6. 13. Herraiz C, Aparicio JM. Diagnostic clues in pulsatile tinnitus (Somatosounds). Acta Otorrinolaryngol Esp 2007;58: 426e33. 14. Vachata P, Petrovicky P, Sames M. An anatomical and radiological study of the high jugular bulb on high-resolution CT scans and alcohol-fixed skulls of adults. J Clin Neurosci 2010;17:473e8.