Management of venous pulsatile tinnitus with normal otoscopic findings.
We conducted a retrospective study to analyze the therapeutic effects of ligation of the internal jugular vein in a series of adults with pulsatile tinnitus of venous origin. Our study group was made up of 12 patients--all women, aged 27 to 61 years (mean: 40 [+ or -] 6.1)--who had been diagnosed with venous pulsatile tinnitus and who were treated with jugular vein ligation. Follow-up had been conducted by telephone interviews for 1 to 6 years postoperatively to assess tinnitus status over the long term. Seven patients achieved complete relief of their tinnitus immediately after surgery, but 5 of them experienced a recurrence within 2 years. The remaining 5 patients received no relief from surgery, including 1 patient who actually experienced a worsening of her tinnitus to the point that it became an intolerable roar. We conclude that treatment of pulsatile tinnitus of venous origin by ligation of the internal jugular vein should be avoided because of poor outcomes and in view of the possibility of complications. In addition to our study findings, we discuss 2 of our cases in more detail.
Pulsatile tinnitus in a patient with normal findings on otoscopic examination often poses a diagnostic challenge to the otolaryngologist. The causes of pulsatile tinnitus can be divided into vascular and nonvascular factors. Characteristically, pulsation is temporarily muted or even eliminated by relatively gentle compression of the ipsilateral internal jugular vein (IJV). This type of compression is used to differentiate venous pulsatile tinnitus from arterial pulsatile tinnitus.
Pulsatile sounds are reported by less than 10% of tinnitus patients. (1) These patients typically describe their tinnitus as "uncomfortable." One method of relieving pulsatile tinnitus is ligation of the IJV. A few clinicians have tried to achieve relief of PT with this procedure, and some subsequently reported an immediate resolution of symptoms. (2-4) Others have warned against the use of venous ligation because of the possibility of serious complications, such as florid pseudotumor cerebri. (5)
In this article, we describe our study of the therapeutic effects of IJV ligation on pulsatile tinnitus, and we discuss the proper management of pulsatile tinnitus of venous origin.
Patients and methods
We conducted a retrospective study of patients who had been diagnosed with venous hum (idiopathic pulsatile tinnitus of a venous origin) and treated with IJV ligation over a 6-year period at the Eye and ENT Hospital of Fudan University in Shanghai, China. Our study population was made up entirely of women, aged 27 to 61 years (mean: 40 [+ or -] 6.1).
All 12 patients complained of a unilateral pulsating sound that correlated with their heartbeat. Nine patients were affected in the right ear and 3 in the left. During evaluation, the tinnitus was eliminated by digital compression of the ipsilateral jugular vein.
Patients provided a detailed history. No specific cause of their tinnitus--such as trauma, infection, or high fever--was evident. Two patients had a history of hypertension, and 1 patient was overweight, with a body mass index (BMI) of 27.
Otoscopic findings were normal in all cases, which ruled out middle ear pathology such as a retrotympanic lesion (e.g., a glomus tumor or persistent stapedial artery). (6) All patients also underwent temporal bone computed tomography (CT). In addition, 6 patients were evaluated by craniocerebral magnetic resonance imaging (MRI). Imaging detected an ipsilateral high-riding jugular bulb in 6 patients; the results of radiologic examinations were normal in the other 6 patients.
Patients were followed by telephone interviews over a period of 1 to 6 years to assess their condition after the surgery.
After surgery, a comparison of the pre- and postoperative degree of tinnitus revealed that the loudness:
* decreased immediately after surgery in 7 patients (58%);
* was unchanged in 4 patients (33%); and
* increased to an intolerable roar in 1 patient (8%).
However, 5 of the 7 patients who reported immediate relief after surgery developed a recurrence of their tinnitus within 2 years. The loudness of the recurrence was unchanged from the preoperative level.
No patient experienced any complications during or after surgery.
Two of the 12 cases are particularly noteworthy in that they illustrate the importance of carefully excluding other possible causes of PT before making a diagnosis of venous hum.
Patient 1. This 54-year-old woman had a 7-year history of pulsatile tinnitus in her right ear that interfered with her hearing. She was also hypertensive (160/100 mm Hg). Her weight was normal (BMI: 24.7). Her complaint of a mild hearing loss was not substantiated by the results of her audiologic examination. CT had demonstrated a high jugular bulb and laterally placed and enlarged sigmoid sinuses.
The patients symptoms did not improve after surgery. Furthermore, she reported experiencing several incidents of cerebral vascular insufficiency and angina. In our opinion, there were two possible causes of her pulsatile tinnitus: atherosclerotic carotid artery disease (ACAD) or the high jugular bulb.
Patient 2. This 35-year-old woman presented with a 1-year history of intermittent left-sided pulse-synchronous tinnitus. Otherwise, she had been in good health. The sudden onset of her symptoms had been accompanied by the onset of constipation and left-sided headaches after strenuous exercise. Her blood pressure was 120/80 mm Hg, and her BMI was 27 (overweight). She had no hearing deficit, and her CT was normal.
The patient's tinnitus was relieved immediately after surgery. However, she experienced a recurrence within 6 months. In our opinion, the most probable cause of her tinnitus was benign intracranial hypertension.
Most causes of pulsatile tinnitus are vascular. Pulsatile tinnitus of vascular origin results from turbulent blood flow, which is caused by an increase in flow volume or a lumen irregularity. (7)
Most researchers agree that venous causes of pulsatile tinnitus can be differentiated from arterial causes by gently compressing the jugular vein ipsilateral to the tinnitus. This maneuver results in immediate resolution of tinnitus of venous origin, and it amplifies pulsatile tinnitus of arterial origin. (8)
Arterial causes of pulsatile tinnitus include carotid artery stenosis, carotid occlusion, dissection, fibromuscular dysplasia, a persistent stapedial artery, and an aberrant or lateralized internal carotid artery course. Among the venous causes of pulsatile tinnitus, the most frequently reported is benign intracranial hypertension. (7) Other causes include jugular bulb abnormalities, dural sinus stenosis, sigmoid sinus diverticulum, and venous hum. (7)
Pulsatile tinnitus should be diagnosed as venous hum only after all other differential diagnoses have been ruled out. IJV ligation should be considered as a treatment only for venous hum and only after careful exclusion of benign intracranial hypertension or other causes of raised intracranial pressure. (7) Sismanis published a diagnostic algorithm for patients with pulsatile tinnitus that we think is very useful. (8)
Our study showed that 7 of our 12 patients (58%) experienced relief of tinnitus immediately following surgery. However, symptoms recurred within 2 years in 5 of these patients, meaning that only 2 patients experienced a complete resolution of symptoms on extended follow-up.
In our opinion, there are two possible explanations for the failure of IJV ligation to effect a cure:
* Misdiagnosis. Our patients had been diagnosed with venous hum without the careful exclusion of the other possible causes of pulsatile tinnitus.
* Ineffectiveness. Ligation of the IJV simply may not offer permanent correction of pulsatile tinnitus.
Possible causes. In the Results section, we documented 2 cases in which the possibility of misdiagnosis of venous hum exists. It is possible that benign intracranial hypertension, ACAD, or a high jugular bulb might have been the underlying cause of the pulsatile tinnitus in these 2 cases.
Benign intracranial hypertension. Among the venous causes of pulsatile tinnitus, the most frequently reported is benign intracranial hypertension, especially in young and obese women. (8) Benign intracranial hypertension is of unknown etiology and, as its name implies, it has a benign and self-limiting course in most patients. It classically presents as pulsatile tinnitus alone or in association with hearing loss, dizziness, and/or aural fullness; other manifestations include headaches and vision disturbances. (9)
Funduscopic examination is recommended when benign intracranial hypertension is suspected. However, it has been well documented that the absence of papilledema does not exclude this entity. (10-12) A diagnosis of benign intracranial hypertension begins with an MRI of the head to exclude other etiologies, and it is confirmed when lumbar puncture shows a cerebrospinal fluid (CSF) pressure greater than 200 mm [H.sub.2]O.
ACAD. ACAD is a common cause ofpulsatile tinnitus in patients older than 50 years, especially in smokers and in those with hypertension, angina, hyperlipidemia, and/ or diabetes. (9) While atherosclerotic plaques are usually located distant from the skull base in the extracranial carotid artery, they still can cause tinnitus. (13) Ipsilateral carotid bruits can often be detected. The diagnosis of ACAD can be established by carotid artery Doppler ultrasonography and cranial CT.
In a study of 74 patients with pulsatile tinnitus, Sonmez et al found atherosclerotic changes of different levels and degrees in the extracranial carotid arteries of 16 patients (21.6%) on Doppler ultrasonography. (14) Sismanis evaluated 145 patients with pulsatile tinnitus over a 15-year period and found that 24 (16.6%) had ACAD; 23 were diagnosed by Duplex ultrasonography, and 1 by cerebral angiography. (8)
In 1995, the Executive Committee for the Asymptomatic Carotid Atherosclerosis Study recommended that carotid endarterectomy be considered for patients with ACAD when artery obstruction is greater than 60%. (15) Still, current management of asymptomatic carotid stenosis remains the subject of controversy. In a joint guideline published in 2011, the American College of Cardiology Foundation, the American Heart Association, and the American Stroke Association stated that it is reasonable to perform an endarterectomy in asymptomatic patients who have more than 70% stenosis of the internal carotid artery if the perioperative risks of stroke, myocardial infarction, and death are low. (16)
The same year, the European Society of Cardiology stated that endarterectomy may be considered for asymptomatic patients with greater than 60% carotid stenosis if their perioperative risk of stroke or death is less than 3% and if the patients life expectancy exceeds 5 years. (17) Other authors have reported the successful treatment and relief of pulsatile tinnitus with carotid artery stenting, (18,19) as well as carotid endarterectomy. (20)
High jugular bulb. The incidence of high jugular bulb ranges from 3.5 to 20% on temporal bone studies. (21-24) Pulsatile tinnitus affects approximately 4.5% of patients who have a high bulb. (24) Sonmez et al considered a jugular bulb and its variants to be a positive finding in patients with tinnitus. (14) However, it is unclear exactly how often jugular bulbs are the true cause of tinnitus. Jugular bulbs are better seen on high-resolution CT than on MRI. Yoon et al reported a case of transvenous stent-assisted coil embolization to treat tinnitus with a high jugular bulb. (25)
Management. Weight loss is typically the most important management strategy for pulsatile tinnitus. Patients may respond to medical management with acetazolamide at 250 mg three times a day or furosemide 20 mg twice a day; both agents reduce CSF production. (10,26) If conservative management fails, two surgical procedures are recommended: placement of a lumbar-peritoneal shunt and weight-reduction surgery.
While our series showed that ligation of the IJV did not effect a permanent cure in a high percentage of cases, successful surgery has been described in a few isolated case reports. Golueke et al reported the case of a patient with pulsatile tinnitus and a high jugular bulb who noted an immediate cessation of tinnitus and the return of normal hearing following IJV ligation. (2) Rothstein et al (4) and Hardison et al (27) also reported successful resolution of venous hum in patients who underwent IJV ligation.
On the other hand, Hentzer reported 13 cases of pulsatile tinnitus; 4 of these patients underwent ligation of the ipsilateral IJV, but only 1 achieved a permanent cure. (28) Similarly, in another series of 13 patients, Overton and Ritter found that only 1 of 3 patients who underwent IJV ligation benefited permanently; the other 2 patients experienced a return of their pulsatile tinnitus within a few days. (22)
Duvillard et al argued that IJV ligation should be avoided because the vein represents the dominant channel for cerebral venous outflow, and therefore IJV ligation poses a theoretical risk of causing intracranial hypertension. (29) Instead, they treated their patient with a mastoidectomy, which successfully suppressed the tinnitus without a single recurrence during a 2-year follow-up.
Another reason to avoid IJV ligation is that contralateral tinnitus may arise when the entire blood flow is diverted to the remaining side. Buckwalter et al reported the case of a patient who developed transient pulsatile tinnitus after ligation of the contralateral jugular vein, probably because of increased venous flow on the nonligated side. (30)
Our findings are consistent with those of others who have found that IJV ligation yields inconsistent results and overall poor outcomes. Moreover, Jackler et al warned surgeons against undertaking this procedure because it also presents a risk of serious neurologic injury. (5) Over the past decade, an increasing amount of research has been targeted toward selecting the most effective and least aggressive treatment for venous hum. Ligation of the IJV does not appear to meet this goal. Before we find a new treatment for venous hum, we can only help patients alter their selective attention to the tinnitus.
In conclusion, it has been reported that the underlying pathology of pulsatile tinnitus can be detected in more than 70% of patients with objective tinnitus. (14) Therefore, the evaluation of pulsatile tinnitus should be individualized, and it should include a thorough history, physical examination, funduscopic examination, imaging studies including ultrasonography and, if necessary, lumbar puncture. Diagnosis of venous hum should be made only after careful exclusion of other disorders, such as benign intracranial hypertension, ACAD, high jugular bulb, and other rare vascular anomalies, including dural arteriovenous fistulas and sigmoid sinus diverticulum. We believe ligation of the IJV should be avoided in view of the risk of poor outcomes and unpredictable complications.
(1.) Kircher ML, Leonetti JP, Marzo SJ, Standring B. Neuroradiologic assessment of pulsatile tinnitus [abstract], Otolaryngol Head Neck Surg 2008;139(Suppl 2):144.
(2.) Golueke PJ, Panetta T, Sclafani S, Varughese G. Tinnitus originating from an abnormal jugular bulb: Treatment by jugular vein ligation. J Vase Surg 1987;6(3):248-51.
(3.) Aikoye AA, Tang TY, Meyer FJ. Local anaesthetic surgical treatment of severe objective pulsatile tinnitus: A useful technique. Ann R Coll Surg Engl 2012;94(4):e139-40.
(4.) Rothstein J, Hilger PA, Boies LR Jr. Venous hum as a cause of reversible factitious sensorineural hearing loss. Ann Otol Rhinol Laryngol 1985;94(33):267-8.
(5.) Jackler RK, Brackmann DE, Sismanis A. A warning on venous ligation for pulsatile tinnitus [letter]. Otol Neurotol 2001;22(3):427-8.
(6.) Dietz RR, Davis WL, Harnsberger HR, et al. MR imaging and MR angiography in the evaluation of pulsatile tinnitus. AJNR Am J Neuroradiol 1994;15(5):879-89.
(7.) Liyanage SH, Singh A, Savundra P, Kalan A. Pulsatile tinnitus. J Laryngol Otol 2006;120(2):93-7.
(8.) Sismanis A. Pulsatile tinnitus. A 15-year experience. Am J Otol 1998; 19(4):472-7.
(9.) Sismanis A. Pulsatile tinnitus. Otolaryngol Clin North Am 2003;36(2):389-402, viii.
(10.) Spence JD, Amacher AL, Willis NR. Benign intracranial hypertension without papilledema: Role of 24-hour cerebrospinal fluid pressure monitoring in diagnosis and management: Neurosurgery 1980;7(4):326-36.
(11.) Lipton HL, Michelson PE. Pseudotumor cerebri syndrome without papilledema. JAMA 1972;220(12):1591-2.
(12.) Marcelis J, Siberstein SD. Idiopathic intracranial hypertension without papilledema. Arch Neurol 1991;48(4):392-9.
(13.) Sismanis A, Stamm M A, Sobel M. Objective tinnitus in patients with atherosclerotic carotid artery disease. Am J Otol 1994;15(3):404-7.
(14.) Sonmez G, Basekim CC, Ozturk E, et al. Imaging of pulsatile tinnitus: A review of 74 patients. Clin Imaging 2007;31 (2): 102-8.
(15.) Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273(18):1421-8.
(16.) Guideline on the Management ofPatients with Extracranial Carotid and Vertebral Artery Disease. American College of Cardiology Foundation, American Heart Association, American Stroke Association. https://my.americanheart.Org/idc/groups/ahamah-public/@wcm/@ sop/@spub/documents/downloadable/ucm_430166.pdf. January 2011. Accessed June 21, 2015.
(17.) European Stroke Organisation; Tendera M, Aboyans V, Bartelink ML, et al; ESC Committee for Practice Guidelines. ESC guidelines on the diagnosis and treatment of peripheral artery diseases: Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries: The Task Force on the Diagnosis and Treatment of Peripheral Artery Diseases of the European Society of Cardiology (ESC). Eur Heart J 2011;32(22):2851-2906.
(18.) Carlin RE, McGraw DJ, Anderson CB. Objective tinnitus resulting from internal carotid artery stenosis. J Vase Surg 1997;25(3):581-3.
(19.) lhn YK, Jung WS, Kim BS. Disappeared pulsatile tinnitus related to petrous segment stenosis of the ICA after relief of the stenosis by stenting. Interv Neuroradiol 2013;19(1):97-101.
(20.) Singh DP, Forte AJ, Brewer MB, Nowygrod R. Bilateral carotid endarterectomy as treatment of vascular pulsatile tinnitus. J Vase Surg 2009;50(1):183-5.
(21.) Lin D J, Hsu CJ, Lin KN. The high jugular bulb: Report of five cases and a review of the literature. J Formos Med Assoc 1993;92(8):745-50.
(22.) Overton SB, Ritter FN. A high placed jugular bulb in the middle ear: A clinical and temporal bone study. Laryngoscope 1973;83(12):1986-91.
(23.) Subotic R. The high position of the jugular bulb. Acta Otolaryngol 1979;87(3-4):340-4.
(24.) Kang M, Escott E. Imaging of tinnitus. Otolaryngol Clin North Am 2008;41 (1): 179-93, vii.
(25.) Yoon BN, Lee TH, Kong SK, et al. Management of high jugular bulb with tinnitus: Transvenous stent-assisted coil embolization. Otolaryngol Head Neck Surg 2008;139(5):740-1.
(26.) Sismanis A. Otologic manifestations of benign intracranial hypertension syndrome: Diagnosis and management. Laryngoscope 1987;97(8 Pt 2 Suppl 42):1-17.
(27.) Hardison JE, Smith, RB III, Crawley IS, Battey LL. Self-heard venous hums. JAMA 1981;245(11):1146-7.
(28.) Hentzer E. Objective tinnitus of vascular type. A follow-up study. Acta Otolaryngol 1968;66(4):273-81.
(29.) Duvillard C, Ballester M, Redon E, Romanet P. Pulsatile tinnitus cured by mastoidectomy Ann Otol Rhinol Laryngol 2004;113(9):730-3.
(30.) Buckwalter JA, Sasaki CT, Virapongse C, et al. Pulsatile tinnitus arising from jugular megabulb deformity: A treatment rationale. Laryngoscope 1983;93(12):1534-9.
Lei Jin, MD; Yucheng Wang, PhD
From the Department of Otorhinolaryngology-Head and Neck Surgery, Shanghai Childrens Hospital, Shanghai Jiao Tong University, Shanghai, China (Dr. Jin); and the Department of Otorhinolaryngology-Head and Neck Surgery, Eye and ENT Hospital, Fudan University, Shanghai (Dr. Wang). The study described in this article was conducted at the Eye and ENT Hospital.
Corresponding author; Dr. Yucheng Wang, Eye and ENT Hospital, Fudan University, 83 Fenyang Rd., Xu Hui District, Shanghai, China 200031. Email: email@example.com
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|Title Annotation:||ORIGINAL ARTICLE|
|Author:||Jin, Lei; Wang, Yucheng|
|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Clinical report|
|Date:||Sep 1, 2015|
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