Almost all causes of pulsatile tinnitus can be diagnosed by magnetic resonance imaging and magnetic resonance angiography, except for the most frequent cause of pulsatile tinnitus : Benign Intracranial Hypertension.

 

Benign Intracranial Hypertension is a clinical entity usually afflicting obese women who suffer from a venous hum, headache and blurry vision. Importantly the venous hum, even unilaterally, can be the only presenting symptom.

Clinically it can be diagnosed by compressing the ipsilateral jugular vein causing the venous hum to disappear. Except for the rarely diagnosed condition of sinus thrombosis. Magnetic resonance angiography and magnetic resonance imaging are usually negative and the diagnosis is confirmed by lumbar puncture (pressure > 20 cm water).

Treatment consists of weight loss, diuretics or ventriculoperitoneal or lumboperitoneal shunting.

 

 Pre-operative

Postoperative with shunt
 

Carotid Stenosis is the most frequent cause of arterial pulsatile tinnitus. The pulsatile tinnitus disappears on compressing the ipsilateral, internal carotid artery. Diagnosis can be confirmed by angiography. Treatment of the extracranial carotid artery stenosis consists of dilation and stenting or carotid endartrectomy.

As for the rarer intracranial carotid artery stenosis two approaches can be followed. An initial balloon occlusion test under transcranial doppler and E.E.G. monitoring can verify whether the ipsilateral carotid artery can be sacrificed. If so, one option is to ligate the symptomatic carotid artery. The other option is to dilate and stent the intracranial portion of carotid artery resulting in a disappearance of the arterial pulsatile tinnitus.

A major problem still faced today is that stents tend to occlude, and thus this elegant technique still remains experimental until the coagulation problems are better controlled.
 

 

Glomus Tumours, or paraganglioma, are found in women presenting with unilateral hearing loss and pulsatile tinnitus. As they are benign lesions growing to less than 2 cm in five years, treatment options are a "wait and see" policy or embolisation and surgery.

Other Vascular Lesions of the Petrous Bone or Skull Base such as hemangiopericytoma, plasmacytoma, giant cell tumours amongst others are also known to generate a treatable pulsatile tinnitus.

 
 

Dural Arteriovenous Malformations (A.V.M.) result from chronic mastoiditis or other causes leading to occlusion of the sigmoid-transverse sinus. Vascular bypasses develop around the occlusion resulting into a dural A.V.M. If the dural A.V.M. is symptomatic or if it is asymptomatic with leptomeningeal drainage these lesions should be embolized, usually in multiple sessions. If intractable with endovascular treatment surgical excision of the A.V.M. and dura can be proposed.
 

The High Jugular Bulb can generate a venous hum, as a result of intimate direct contact with the cochlea. This venous hum disappears on compressing the ipsilateral jugular vein and can be diagnosed by CT imaging. Surgically ligating or lowering the jugular bulb and interposing teflon or bonewax can abolish or diminish this form of tinnitus.

 
A Brain Tumour compressing the auditory cortex can cause a non-pulsatile tinnitus as the sole symptom, probably due to a direct influence on normal cortical sound processing. Removal of the lesion results in abolishing the tinnitus. Tumours elsewhere along the auditory tract, for example the brainstem, usually give rise to additional symptoms, related to the closeness of other neural structures.

Microvascular Compressions of the cochlear nerve can cause incapacitating high pitch non-pulsatile tinnitus, unless the vascular loop enters the internal auditory canal, in which case the osseous conduction gives rise to an arterial pulsatile tinnitus. This difficult diagnosis is based on the clinical picture and confirmed by auditory brainstem evoked potentials and magnetic resonance imaging.

Results of microsurgical vascular decompression are related to the surgical delay, the preoperative hearing status, MRI imaging and gender. In general we can state that if the tinnitus has been present for less than three years, if there is a useable or normal hearing, and the MRI demonstrates a vascular compression - in women - the results can be good. Vascular compressions of the vestibulocochlear nerve are found in many asymptomatic patients (12.5% and 21.5% respectively) but this discrepancy is also noticed in trigeminal neuralgia (14%) and even in herniated lumbar discs (36%), where this is not considered an argument to doubt about the pathophysiological importance of the neural compression.

After surgery, the tinnitus can be expected to disappear completely if there is a significant amelioration within the first 72 hours. If this rapid amelioration does not occur, it can take several weeks or even months before the tinnitus improves, but complete resolution is usually not expected.