Pulsatile tinnitus refers to a perception of sound that coincides with the heartbeat. It may arise from a vascular lesion causing disruption of laminar flow, leading to turbulence that produces a bruit audible to the patient, or from normal sounds that are perceived as more intense because of proximity of vascular and auditory structures. Both venous and arterial anomalies may cause pulsatile tinnitus. Occasionally patients perceive intermittent clicking or pulsing sensations in their ear that are not consistently synchronized with the heartbeat and thus not true pulsatile tinnitus. These may be due to myoclonus of the muscles of the middle ear, and are seen in those with prior brainstem stroke or multiple sclerosis.
High-output cardiac states, such as thyrotoxicosis, severe anemia, or pregnancy, may cause pulsatile tinnitus, which will typically resolve along with the underlying condition.
Examine for an audible bruit, taking into consideration the patient’s description of the location from which they perceive the sound coming. If the patient notes the sound is enhanced with specific maneuvers or positions, be certain to auscultate under these conditions. Be sure to note if the patient perceives the pulsatile tinnitus during the examination. Objective pulsatile tinnitus (i.e., a bruit is audible to the examiner) is more likely to be associated with an identifiable underlying vascular abnormality.
An audible bruit over the posterior neck suggests vertebral artery disease such as atherosclerotic stenosis or dissection. Bruits may be transmitted from the intracranial circulation as well.
Cranial bruits indicate a high likelihood of significant and potentially dangerous pathology. Both brain and vascular imaging with magnetic resonance imaging/angiography (MRI/MRA) is indicated. Note that dural arteriovenous fistulas, an important cause of pulsatile tinnitus associated with a cranial bruit, may be occult on MRA or computed tomography angiography (CTA); catheter angiography is often necessary for diagnosis.
Anterior cervical bruits typically rise from either the carotid arteries or jugular veins. If the bruit disappears with gentle neck compression, a Valsalva maneuver, or change in position such as turning of the head, it is likely venous.
Carotid stenosis is the most common cause of an arterial bruit in the neck, most often due to atherosclerotic disease, which typically occurs at the carotid bifurcation and is usually easily diagnosed with carotid ultrasonography. Arterial dissection and segmental irregularity due to fibromuscular dysplasia may also cause pulsatile tinnitus but are not well-imaged by ultrasound. A very rare cause of pulsatile tinnitus is a carotid paraganglioma, a tumor of the carotid body. In these latter cases, MR or CT angiography is necessary for diagnosis.
Venous bruits in the neck most often represent a benign venous hum. However, abnormalities of venous drainage of the brain can cause pulsatile tinnitus, and cervical venous bruits are audible on occasion. Look for signs or symptoms suggestive of increased intracranial pressure; if present, MRI and MR venography of the brain is indicated. Lumbar puncture should be performed if MRI is normal and idiopathic intracranial hypertension (pseudotumor cerebri) is a consideration.
Otologic abnormalities may cause pulsatile tinnitus audible to the patient but not the examiner (subjective pulsatile tinnitus). If a middle ear effusion is present and the onset of symptoms coincides with a middle ear infection, capillary hyperemia from otitis media may be responsible. A visible retrotympanic mass on examination may indicate a paraganglioma (typically a red, pulsatile mass) or an anomalous vessel.
Autophony refers to an enhanced perception of bodily sounds, typically the patient’s own voice and breathing. Patients complaining of audible breathing or increased resonance of their own voice may have a persistently open or patulous Eustachian tube, allowing for excessive communication between the middle ear and the nasopharynx. In superior semicircular canal dehiscence syndrome there is thinning in the bony structures overlying the superior semicircular canal; patient’s may describe hearing their own eye movements, and in some cases may have vertigo triggered by loud noises (Tullio phenomenon).
Many patients with subjective pulsatile tinnitus have no obvious clinical diagnostic clues to point to a specific etiology, and thus deciding whether to pursue neuroimaging can be difficult. Duration of symptoms, associated systemic or neurologic symptoms, and medical history should all be considered. While most identified causes in these patients (e.g., anomalous or aberrant vessels, thinning of bony structures between vessels and inner ear) do not require specific treatment, this is not universally the case. Osseous abnormalities of the temporal bone, such as Paget disease and otosclerosis, invasive highly vascular tumors, dural arteriovenous fistulas, and vascular stenosis may all be important conditions to identify.