Pulsatile tinnitus

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Pulsatile tinnitus requires hearing, as there is usually a genuine physical source of the sound.

Pulsatile tinnitus is therefore included under the umbrella terms “physical tinnitus” and “somatosounds”.

Less than 10% of tinnitus patients suffer from pulsatile tinnitus

Pulsatile tinnitus (PT) may be due to a spectrum of cerebrovascular etiologies, ranging from benign venous turbulence to life threatening dural arteriovenous fistulas.

Most cases are due to vascular lesions.

1. pulse synchronous:

a) carotid cavernous fistula

b) AVM:

● cerebral (pial) AVM

● dural AVM

c) glomus jugulare tumor

d) cerebral aneurysm: (rare) possibly with turbulent flow in a giant aneurysm

e) hypertension

f) hyperthyroidism

g) idiopathic intracranial hypertension (pseudotumor cerebri)

h) transmitted bruit: from heart (e.g. aortic stenosis), carotid artery stenosis (especially external carotid)

i) dehiscent jugular bulb or high riding jugular bulb: normal venous variant

j) rarely with posterior fossa tumors: CP-angle tumors e.g. vestibular schwannoma or meningioma, vascular intraparenchymal tumors e.g. hemangioblastoma (especially in CPA)

k) lesions that can present with a red tympanic membrane

● aberrant carotid artery in the middle ear

● persistent stapedial artery: rare. Arises from aberrant ICA or from junction of horizontal and vertical petrous ICA. Foramen spinosum is absent on the affected side. Enlargement of anterior tympanic segment of seventh nerve canal

● glomus tympanicum tumor

l) sigmoid sinus diverticulum

2. non pulse-synchronous: asymmetrical enlargement of sigmoid sinus and jugular vein may pro- duce a low grade hum

There are two plausible causes of pulsatile tinnitus:

Bloodflow accelerates, or changes in bloodflow disrupt laminar flow, and the resulting local turbulence is audible. Normal flow sounds within the body are perceived more intensely, either as a result of alterations in the inner ear with increased bone conduction or as a result of disturbance of sound conduction leading to loss of the masking effect of external sounds.

Pulsatile tinnitus is usually unilateral, unless the underlying vascular pathology is bilateral. Recently, a disorder known as “somatosensory pulsatile tinnitus” has been discussed. This is bilateral tinnitus with no vascular cause.

It is often possible to identify the cause of pulsatile tinnitus. In addition to the patient’s medical history and targeted clinical examination, imaging procedures also play an important role in diagnosis. However, despite careful examination, no cause is found in up to 30% of patients.

Pulsatile tinnitus of vascular origin may arise in arterial or venous structures. Many authors have reported the association of pulsatile tinnitus with anomalies of dural venous sinuses and the jugular bulb.

see Venous sinus diverticulum.

Venous pulsatile tinnitus

Obstructive hydrocephalus secondary to enlarged Virchow Robin space (VRS) is a rare entity, with only a handful of cases reported in the literature. Presenting symptoms vary widely from headaches, to dizziness.

Donaldson et al. report a 31-year-old male who presents with pulsatile tinnitus and an MRI showing obstructive hydrocephalus secondary to tumefactive VRS. After a CSF diversion procedure in the form of an ETV he had almost complete resolution of his symptoms.

This is the first case of obstructive hydrocephalus secondary to enlarged Virchow-Robin spaces, presenting with pulsatile tinnitus ¹⁾.

Patients with idiopathic intracranial hypertension most frequently present with headaches, transient visual obscurations, papilledema, and/or pulsatile tinnitus, but may also be asymptomatic ²⁾.

1. MRI without and with enhancement: to look for tumors, e.g. glomus jugulare

2. angiogram: include internal and external carotid injections

3. tests that are usually not helpful and should not be ordered routinely

a) carotid ultrasound: nonspecific, not sensitive

b) MRI/MRV: may miss small dural fistulas and do not give details needed for treatment for large ones.

In patients with Pulsatile tinnitus, clinical history and physical examination can achieve high performance at detecting a shunting lesion. Potentially treatable venous etiologies may also be suggested by relief with neck compression ³⁾.

A 26-year-old male with a history of blunt trauma presented delayed PT with direct AVF between the ascending pharyngeal artery (APA) and the internal jugular vein (IJV). The patient underwent occlusion of the fistula with transarterial embolization using coils and PT was completely resolved, confirming the successful treatment. The delayed manifestation of PT in the APA-IJV fistula is probably due to the gradual formation of a pseudoaneurysm and subsequent AVF. This case highlights the importance of investigating PT in head trauma patients, as it can be a sign of AVF and possible complications. Overall, this case contributes to understanding delayed PT with AVF and emphasizes the importance of prompt diagnosis and treatment of AVF in patients with head and neck trauma ⁴⁾