Venous hum tinnitus is also known as objective tinnitus, pulsatile tinnitus; rhythmic tinnitus or vascular tinnitus.
The perception of sound heard with a regular rhythm in concert with the heart beat that can often be modified by external movements and/or position changes.
It is estimated that one of every five people experience some form of tinnitus during their lifetime, and 25% of those with tinnitus have their lives severely affected (Otto et al. 2007). Approximately 50 million US adults report having any tinnitus, and 16 million US adults report having frequent tinnitus in the past year (Shargorodsky et al. 2010). The prevalence of frequent tinnitus increases with increasing age (Shargorodsky et al. 2010).
Pulsatile tinnitus represents a small portion of those presenting with tinnitus, and is thought to approximate 4%. Pulsatile tinnitus has a number of etiologies. Sismanis (1998) found Benign Intracranial Hypertension to be the most frequent cause of pulsatile tinnitus in review of his 15-year experience; however, venous anomalies were not closely investigated (Sismanis 1998). In 2008, Mattox et al. discovered 43% of patients presenting with objective pulsatile tinnitus were found to have a venous anomaly (Mattox and Hudgins 2008) and a quarter were found to be due to a diverticulum of the sigmoid sinus (Mattox and Hudgins 2008).
The first patient with a venous hum was described in the literature by Cary in 1961 (Cary 1961). A prosthetic device was worn around the neck to silence an idiopathic symptomatic venous hum heard by a 37-yearold woman. Reports followed in 1968 by Hardison and Hentzer, who both described men and women with idiopathic symptomatic venous sounds (Hardison 1968; Hentzer 1968).
Tinnitus is defined as the perception of sound not present in the external environment, and can be categorized as either auditory or somatosounds. Auditory tinnitus is subjective and originates within the central or peripheral auditory system. A somatosound is a sound that originates from any structure surrounding the ear, and often may be objectively perceived by the examiner depending on circumstance and examination techniques. The most common causes of somatosounds are vascular bruits, palatal myoclonus, patulous eustachian tube, and the temporal mandibular joint (Jastreboff et al. 1998).
Pulsatile tinnitus is a type of rhythmic somatosound, and has an extensive list of causes including non-vascular, neoplasms, and vascular anomalies. The source of the tinnitus can be discerned based on specific details from the patient’s history and clinical exam findings, and is confirmed by imaging studies. Vascular bruits are the most common cause of pulsatile tinnitus. The characteristic description of a vascular bruit is a rhythmic murmur that is in synchrony with the patient’s heartbeat. Venous anomalies account for a large portion of vascular bruits. A venous bruit can also be described as a venous hum.
If a vascular source is suspected as the cause of pulsatile tinnitus, the next step in evaluation is to determine if the bruit is from a venous or arterial source. This can be accomplished by compressing each side of the neck with enough pressure to occlude the venous system and assessing if the patient perceives an increase or decrease in the sound. In young patients arterial occlusion may be tried if venous does not alter the sound perception, however this should not be attempted if vascular disease is suspected or in elderly patients.
A computed tomography angiography (CTA) is recommended if the tinnitus is believed to be from a venous source, with adequate delay of contrast material for careful examination of the temporal bone in both the venous and arterial phases. The CTA allows examination of the arterial and venous anatomy of the neck and skull base but also the bony anatomy of the middle ear, skull base, and temporal bone, and is superior to magnetic resonance angiography (MRA) for these areas. However, four-vessel arteriography may be needed for identification of small arteriovenous malformations (AVM) if the CTA is negative. For patients in whom an arterial source is suspected, a carotid ultrasound is recommended, followed by CTA if the ultrasound fails to identify the pathology and a high index of suspicion is present.
Despite the sensitivity of current imaging techniques, it is often difficult to arrive at a definitive diagnosis in these patients. The literature reports that only approximately 68–72% of patients achieve a definitive diagnosis of the origin of their symptoms (Mattox and Hudgins 2008; Sonmez et al. 2007).
Prior to diagnosing a venous hum, other causes of pulsatile tinnitus must be ruled out based on physical exam and imaging results.
The combination of autophony with pulsatile tinnitus suggests either patulous eustachian tube or superior semicircular canal dehiscence. The major distinguishing factor is the presence of audible breathing with a patulous eustachian tube that is not typically present in a patient with superior semicircular canal dehiscence. These two entities can be further evaluated by nasal endoscopy and thin cut computed tomography (CT) of the temporal bone, respectively. Benign intracranial hypertension should be suspected when a patient presents with pulsatile tinnitus and is obese, although this entity does not occur exclusively in these patients. An MRI for evaluation of the sella and ventricles as well as an opthalmologic evaluation is performed when this diagnosis is suspected. The final diagnosis is achieved with lumbar puncture showing an elevated opening pressure.
Once a vascular bruit is suspected as the etiology of pulsatile tinnitus, the source of the bruit must be identified as arterial or venous in origin. Arterial causes for pulsatile tinnitus include carotid artery atherosclerosis, carotid artery aneurysm, carotid cavernous fistula, carotid dissection, aberrant carotid artery, or paraganglioma, and can be identified by neck ultrasound or CTA.
The differential for venous hum includes a highriding or dehiscent jugular bulb, diverticula of the sigmoid sinus or jugular bulb, or turbulent flow in the region of the sigmoid sinus or jugular bulb with otherwise normal anatomy. A high-riding jugular bulb is a common vascular anomaly, found in 2.4–7% of temporal bones. The jugular bulb is not present at birth and develops over time along with the temporal bone (Friedmann et al. 2010), and therefore morphology can be highly variable. However, not all patients with high-riding jugular bulbs present with pulsatile tinnitus. A jugular bulb diverticulum is an outpouching of the jugular bulb that occurs less frequently than a highriding jugular bulb. Most often the diverticulum protrudes into the middle ear causing pulsatile tinnitus with or without a conductive hearing loss. Sigmoid sinus diverticula can also occur, and are a relatively new reported cause of pulsatile tinnitus that can be managed surgically (Otto et al. 2007).
The anatomy of the venous system within the skull base and cerebral dural sinuses is highly variable, and can lead to a number of anomalies that may contribute to a venous hum. Venous bruits originate from turbulent flow in an otherwise smooth-walled vein. This turbulent flow may be secondary to stenosis or tortuosity of the venous structures, or from a diverticulum of the venous system. The pathogenesis of these lesions is thought to be due to the erosion of bone overlying the sinus, facilitated by turbulent flow within the diverticulum (Otto et al. 2007). The sound may become louder with physical exertion or with particular head position, such as turning the head away from the ipsilateral side.
Idiopathic venous hum may also occur due to a hyperdynamic circulatory state, such as pregnancy, thyrotoxicosis, or anemia. Idiopathic venous hum may also be diagnosed in a patient with increased awareness of blood flow in the ear with a normal venous system.
Treatment of venous hum varies depending on the etiology. A high-riding jugular bulb or idiopathic venous hum requires no treatment. Ligation of the internal jugular vein has been reported as treatment for venous hum, but is not routinely performed and risks causing intracranial hypertension if the contralateral venous system is inadequate.
If a diverticulum is identified, surgical intervention aimed at providing a smooth reconstructed wall of the vessel eliminates the audible turbulence. For jugular or sigmoid diverticula, the diverticulum is skeletonized and reduced, and the wall is reconstructed with extraluminal placement of either temporalis muscle and fascia, bone substitute, or titanium plate.
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Friedmann DR, Le BT, Pramanik BK, Lalwani AK (2010) Clinical spectrum of patients with erosion of the inner ear by jugular bulb abnormalities. Laryngoscope 120(2): 365–372
Hardison JE (1968) Cervical venous hum: a clue to the diagnosis of intracranial arteriovenous malformations. N Engl J Med 278:587–590
Hentzer E (1968) Objective tinnitus of the vascular type. Acta Otolaryngol 66:273–281
Jastreboff PW, Mattox DE, Gray WC et al (1998) Tinnitus and hyperacusis. In: Cummings CW, Fredrickson JM, Harker L, Krause CJ, Schuller DE (eds) Otolaryngology Y head and neck surgery, vol 4, 3rd edn. Mosty, St. Louis, p 3198Y222, chap 165
Mattox DE, Hudgins P (2008) Algorithm for evaluation of pulsatile tinnitus. Acta Otolaryngol 128(4):427–431
Otto KJ, Hudgins PA, Abdelkafy W, Mattox DE (2007) Sigmoid sinus diverticulum: a new surgical approach to the correction of pulsatile tinnitus. Otol Neurotol 28(1):48–53
Shargorodsky J, Curhan GC, Farwell WR (2010) Prevalence and characteristics of tinnitus among US adults. Am J Med 123(8):711–718
Sismanis A (1998) Pulsatile tinnitus. A 15-year experience. Am J Otol 19(4):472–477
Sonmez G, Basekim CC, Ozturk E, Gungor A, Kizilkaya E (2007) Imaging of pulsatile tinnitus: a review of 74 patients. Clin Imaging 31:1028