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Diagnostic Approach to Pulsatile Tinnitus

the body are likely being perceived more intensely because of inner ear alterations to sound conduction, or loss of masking abil ity. Low-pitch PT (“buzzing” or “humming”) is frequently venous, whereas higher-pitch PT (“whooshing,” “hissing,” or “fetal heart beat”) is frequently arterial, and very high-pitch PT (“ringing” or a continuous high-pitch that takes breaks with each heartbeat) is not likely to be vascular. A “drum beat” or “suction cup” sound that is not synchronous with the pulse is most likely related to palatal or middle ear myoclonus. Pulsatile tinnitus is usually per ceived unilaterally, although some systemic and vascular condi tions can cause bilateral PT. A detailed otologic history is also helpful, including hearing loss, prior ear surgery, ear infections, and ear pain or drainage. In particular, symptoms such as autophony (hearing bodily sounds loudly such as voice, eyes moving, or heel-strike), aural pressure, or sound-induced vertigo can suggest superior canal dehiscence. Pulsatile tinnitus is often divided between that which can be heard by an examiner (termed “objective PT”), and that which the exam iner cannot hear (termed “subjective PT”). Objective PT can be per ceived by the examining physician with cranial auscultation. Objec tive PT should raise suspicion for an arterial cause of PT, but cranial auscultation alone should not be used for diagnosis because objec tive PT can also result from venous causes. Subjective PT is more common; in this case, sound may nevertheless be generated by a blood vessel, but the examiner may be unable appreciate it with a stethoscope. One should maintain a strong suspicion for a vascular cause of PT even in subjective PT. Auscultation during the physical examination should include the heart, neck, and orbits, as well as over the venous sinuses, specifically at the vertex over the superior sagittal sinus, at the occiput over the torcula, over the transverse si nuses, and at the mastoid over the sigmoid sinuses (eTable 1 in the Supplement; top panel). Auscultation of the frontal and temporal calvarium should also be performed because high-flow vascular mal formations of the scalp can produce PT. Manual compression of the cervical blood vessels can exacerbate or improve vascular PT (eTable 1 in the Supplement; bottom panel). Specifically, jugular vein com pression, occipital artery compression, and head turning can be help ful during physical examination. If neck compression (usually jugu lar vein compression) ipsilateral to symptoms improves PT, an ipsilateral venous cause should be suspected. Specifically, a low pitch, pulse-synchronous hum that improves with ipsilateral jugu lar compression or Valsalva maneuver is highly suggestive of a ve nous cause of PT. However, if neck compression ipsilateral to symptoms worsens PT, one should suspect increased ipsilateral con dylar vein flow (increased jugular venous resistance can divert ad ditional venous flow into enlarged ipsilateral condylar veins) or an arterial cause (owing to narrowing of the artery without complete occlusion resulting in increased velocity of blood flow). Higher pitched PT heard over a dural venous sinus with a bounding pulse palpable in a scalp artery is highly suspicious for a dural arteriove nous fistula (dAVF). A complete neurologic, cranial nerve, and oto scopic examination should also be performed. The otoscopic ex amination should particularly assess for compacted cerumen, middle ear fluid, cholesteatoma, and glomus tumor. If intracranial hyper tension is suspected, fundoscopic examination should also be per Assessment Physical Examination

Table. Causes of Pulsatile Tinnitus: Groups a Group Cause Diagnosis Structural Neoplasm

Paraganglioma Schwannoma Skull base meningioma

Endolymphatic sac neoplasm Skull base vascular metastasis Semicircular canal dehiscence Sigmoid plate dehiscence Otospongiosis Carotid canal dehiscence

Temporal bone pathologic abnormality

Metabolic Ototoxic medications

Aminoglycosides Cisplatin

Vitamin toxic effects

VitaminB6

Myoclonus

Tensor tympani Stapedius Soft palate

High cardiac output

Hyperthyroidism Anemia Valvular heart disease

Vascular Venous

Idiopathic intracranial hypertension Dural venous sinus stenosis Jugular vein stenosis Dural venous sinus diverticulum

Jugular bulb diverticulum High-riding jugular bulb Dural arteriovenous fistula Carotid-cavernous fistula Arteriovenous malformation Aneurysm Dissection Fibromuscular dysplasia Carotid stenosis Aberrant arterial course Dolichoectasia

Arterial

a Causes of pulsatile tinnitus organized into groups. This organization facilitates practical evaluation, referral, and treatment in patient-centered fashion rather than focusing on anatomic compartments.

formed to evaluate for papilledema, particularly if the patient has an abducens nerve palsy, headaches that are worse when supine, history of vitamin A analog ingestion, sleep apnea, obesity, or PT that is worst in the morning. Audiologic Testing Standard audiometric testing consists of measuring air and bone con duction thresholds, tympanometry, acoustic reflex testing, and speech audiometry. This allows hearing loss to be characterized as conductive, sensorineural, or mixed (both conductive and sensori neural). Almost every cause of conductive hearing loss is thought to cause PT, owing to increased audibility of bone-conducted sounds. For example, otospongiosis can result in PT with an ipsilateral con ductive hearing loss. Unilateral or asymmetric sensorineural hear ing loss on the same side as PT should prompt evaluation for dis eases that cause both, such as paraganglioma, schwannoma, or other

(Reprinted) JAMA Otolaryngology–Head & Neck Surgery May 2022 Volume 148, Number 5 477

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