9Vascular Causes (Pulsatile Tinnitus)
Pulsatile tinnitus is the one tinnitus that may be a sound the body really makes — and occasionally a sound the examiner can hear. This module separates arterial from venous causes, lists the lesions you must not miss, and maps the vascular imaging that finds them.
FPulsatile tinnitus: a symptom apart
Most tinnitus is a phantom; pulsatile tinnitus is often a real sound — turbulent or transmitted blood flow that the patient, and sometimes the clinician with a stethoscope, can actually hear. Because it can be objective, and because some of its causes are dangerous or curable, a rhythmic whooshing or pulsing in time with the heartbeat deserves a focused vascular work-up rather than the usual tinnitus counselling [2025].
The first and most powerful discriminator is rhythm. Ask the patient to take their pulse while listening: a sound that beats in synchrony with the pulse is vascular until proven otherwise, and the next job is to decide whether it is arterial or venous [2008].
TArterial versus venous: the bedside split
Arterial pulsatile tinnitus is sharply pulse-synchronous — a beating or whooshing locked to the heartbeat. Its causes include arteriovenous malformations, dural arteriovenous fistulas, carotid–cavernous fistulas and atherosclerotic stenosis of the internal carotid, all of which create turbulent high-velocity flow near the skull base [2024].
Venous pulsatile tinnitus is different in character: a lower-pitched continuous hum that is sensitive to posture and to manoeuvres. Two bedside tests help. Light ipsilateral neck compression over the jugular vein typically abolishes a venous hum but not an arterial sound, and turning the head or lying down often changes a venous tinnitus [2025]. Common venous culprits are a high-riding or dehiscent jugular bulb, sigmoid-sinus diverticulum/dehiscence, and the raised pressure of idiopathic intracranial hypertension [2025].
CThe dangerous and the curable: AVM, fistula, IIH
Some vascular causes are red flags. Dural arteriovenous fistulas and carotid–cavernous fistulas can carry a risk of haemorrhage or visual loss and may be treatable by endovascular embolisation, which can both cure the tinnitus and remove the hazard [2024]. They are therefore lesions actively to be sought, not merely explained.
Idiopathic intracranial hypertension deserves special attention: it classically produces bilateral pulsatile tinnitus, often in an overweight woman of childbearing age, alongside headache and visual obscurations, and the tinnitus stems from raised cerebrospinal-fluid pressure transmitted to the dural venous sinuses [2025]. Recognising it matters because untreated IIH threatens vision, and fundoscopy for papilloedema belongs in the pulsatile-tinnitus examination [2025].
CImaging the vascular ear
Because the lesions are vascular and structural, imaging is the heart of the work-up. A common strategy pairs cross-sectional vascular imaging — CT angiography/venography or MR angiography/venography — to display the arterial and venous anatomy of the skull base, with dedicated temporal-bone CT to reveal bony culprits such as a dehiscent jugular bulb or sigmoid-sinus wall defect [2008].
Catheter digital subtraction angiography remains the reference standard when a fistula or AVM is suspected and treatment is contemplated, because it shows flow dynamically and can be therapeutic in the same sitting [2024]. The clinical examination steers the choice: an arterial, pulse-synchronous sound points toward arterial imaging and DSA, whereas a position- and compression-sensitive venous hum directs attention to the venous sinuses and jugular bulb [2025].
TA practical algorithm
Pulling it together: confirm the sound is pulse-synchronous, then classify. Pulse-synchronous and abolished by nothing simple → treat as arterial and pursue CTA/MRA ± DSA for fistula, AVM or carotid disease [2008]. A hum that quiets with ipsilateral neck compression or changes with posture → treat as venous and look for jugular-bulb/sinus anomalies and IIH [2025].
Two examinations should never be skipped: auscultate the periauricular region, neck and orbit for an objective bruit, and perform fundoscopy to catch the papilloedema of IIH [2025]. A structured approach like this materially improves the diagnostic yield in pulsatile tinnitus and avoids both missed dangerous lesions and unnecessary scanning [2025].
Which diagnosis best fits, and what must be assessed urgently?
Which feature best distinguishes a venous from an arterial cause of pulsatile tinnitus at the bedside?
Which is a 'must-not-miss' vascular cause of pulsatile tinnitus that may be both dangerous and curable?
A patient has sharply pulse-synchronous tinnitus unchanged by neck compression, raising suspicion of an arteriovenous shunt. Which study is the reference standard and may also be therapeutic?