Management of vascular causes of pulsatile tinnitus

Abstract

Pulsatile tinnitus is a debilitating symptom affecting millions of Americans and can be a harbinger of hemorrhagic or ischemic stroke. Careful diagnostic evaluation of pulsatile tinnitus is critical in providing optimal care and guiding the appropriate treatment strategy. When a vascular cause of pulsatile tinnitus has been established, attention must be focused on the patient's risk of hemorrhagic stroke, ischemic stroke, or blindness, as well as the risks of the available treatment options, in order to guide decision-making. Herein we review our approach to management of the vascular causes of pulsatile tinnitus and provide a literature review while highlighting gaps in our current knowledge and evidence basis.

Keywords: blood flow; brain; fistula; intervention; intracranial pressure.

Figure 1.. Idiopathic intracranial hypertension.

A young woman presents with right pulse-synchronous pulsatile tinnitus, worse when laying down, exacerbated by right neck compression, with positional headaches and vision changes. (A) Axial balanced steady-state-free-precession (bSSFP; FIESTA) MRI demonstrates optic disc protrusion (asterisk). (B) Axial T1-weighted contrast-enhanced gradient-echo (FSPGR) demonstrates right transverse-sigmoid sinus junction stenosis (arrow). Lumbar puncture opening pressure was > 60 cm of water and she had decreased visual acuity on the right (20/100). Venous manometry gradient was 18 mm Hg. (C) Right transverse sinus venogram in lateral projection demonstrates stenosis (arrow). (D) Fundoscopy demonstrates Frisen grade 2 papilledema. (E) Venous sinus stenting of the right transverse-sigmoid sinus in lateral projection. (F) Cerebral angiogram in venous phase and lateral projection demonstrates no residual stenosis of the right transverse-sigmoid sinus. One week after stenting, visual acuity improved to 20/25 and (G) fundoscopy demonstrates improved papilledema to Frisen grade 1. At 3 months, lumbar puncture opening pressure was 11 cm of water and at 5 months, visual acuity had improved to 20/20 with no residual papilledema.

Figure 2.. Sigmoid sinus diverticulum.

A middle-aged woman presented with right-sided pulsatile tinnitus that was exacerbated by left neck compression and improved with right neck compression. Her lumbar puncture opening pressure was normal. (A) Coronal maximum intensity projection (MIP) reformat of time-resolved contrast-enhanced (TRICKS) MRA demonstrates right sigmoid sinus diverticulum (arrow). (B) Axial T1-weighted contrast-enhanced spin-echo (CUBE) MRI demonstrates signal void (arrow) due to flow in right sigmoid sinus diverticulum. (C) Axial T1-weighted contrast-enhanced gradient-echo (FSPGR) MRI demonstrates enhancement (arrow) of diverticulum contiguous with the right sigmoid sinus. (D) Left internal carotid arteriogram in venous phase and Townes projection demonstrates right sigmoid sinus diverticulum (arrow). (E) Volume rendering of 3D rotational cone beam CT in venous phase demonstrates sigmoid sinus diverticulum (arrow) and upstream venous stenosis (asterisk). (F) 4D flow MRI fluid dynamic modeling with streamlines demonstrates elevated velocity at the upstream venous sinus stenosis (asterisk), flow into the sigmoid sinus diverticulum (arrow), and vortex in the downstream sigmoid sinus (arrowhead). Reproduced with permission from reference [28] (G) Coil embolization of sigmoid sinus diverticulum (arrow) resulted in resolution of symptoms and abnormal 4D flow characteristics.

Figure 3.

Suggested algorithm for treatment approach to patient with a suspected vascular cause of pulsatile tinnitus. PT = pulsatile tinnitus; IIH = idiopathic intracranial hypertension; VSS = venous sinus stent; dAVF = dural arteriovenous fistula; FMD = fibromuscular dysplasia

Figure 4.. Left transverse-sigmoid sinus dural arteriovenous fistula.

A middle-aged woman presented with left pulsatile tinnitus that resolved one week ago, and has now developed headache, nausea, and incoordination. (A) Axial maximum intensity projection (MIP) of time-of-flight MRA demonstrates enlarged occipital arteries (asterisks) and flow-related enhancement in the left transverse (arrow) and sigmoid sinuses. (B) Axial TOF MRA demonstrates flow-related enhancement in the left transverse sinus (arrow) and enlarged bilateral occipital arteries. (C) Axial TOF MRA demonstrates flow-related enhancement in dural arteries of the left sigmoid sinus wall. (D) Left external carotid arteriogram in lateral projection demonstrates arteriovenous shunting into the left transverse sinus by enlarged occipital artery, middle meningeal artery, superficial temporal artery, and ascending pharyngeal artery branches. (E) Left internal carotid arteriogram in lateral projection demonstrates arteriovenous shunting into the left transverse sinus (arrow) by an enlarged lateral tentorial branch (asterisk) of the meningohypophyseal trunk. (F) Venous phase of left internal carotid arteriogram in frontal projection shows right-dominant venous system (arrow = right transverse sinus). Ethylene vinyl alcohol copolymer embolization via a left occipital artery transmastoid branch with intentional occlusion of the sinus (G) resulted in angiographic resolution of arteriovenous shunting on (H) post-embolization left common carotid arteriogram in lateral projection.