A sigmoid sinus diverticulum forms when part of the sigmoid sinus, a major vein that drains blood from the brain, pouches outward through a weakness or gap in the surrounding bone. The exact mechanism is still debated, but several factors appear to work together: thinning of the protective bone plate, narrowing of the vein upstream, elevated pressure inside the skull, and the constant force of pulsing blood against the vessel wall. This rare vascular condition is one of the more common treatable causes of pulsatile tinnitus, accounting for roughly 32% of cases in patients who seek care for a heartbeat sound in their ear.
The Role of the Sigmoid Plate
The sigmoid sinus sits in a groove carved into the mastoid bone behind your ear. A thin layer of bone called the sigmoid plate separates the vein from the air-filled spaces of the mastoid. When this plate thins out or disappears entirely (a condition called dehiscence), the sinus wall loses its structural backing. Without that bony support, the soft wall of the vein can bulge outward into the surrounding bone, forming the pouch known as a diverticulum.
Dehiscence tends to occur in predictable spots. It most often appears along the outer wall of the upper curve and the descending segment of the sigmoid sinus, exactly where blood hits the vessel wall with the greatest force. This pattern has led researchers to propose that the bone doesn’t simply vanish on its own. Instead, years of forceful, pulsatile blood flow may gradually wear the plate thinner until it breaks down entirely. Once the bone is breached, the sinus wall is free to stretch outward under pressure.
Whether sigmoid plate dehiscence is something you’re born with or something that develops over time remains an open question. Some people may start with a naturally thinner plate that becomes vulnerable earlier in life, while others may develop thinning gradually from hemodynamic stress.
Upstream Venous Narrowing
In nearly every documented case of sigmoid sinus diverticulum studied with advanced imaging, narrowing (stenosis) of the vein upstream from the diverticulum has been present. This narrowing typically occurs in the transverse sinus, the large channel that feeds into the sigmoid sinus. The consistency of this finding has led many specialists to view upstream stenosis as a likely contributor to diverticulum formation, not just an incidental finding.
The proposed mechanism is straightforward. When the vein narrows at one point, blood accelerates through the tight spot and creates turbulent, high-pressure flow downstream. That turbulent flow hammers the sinus wall in a concentrated area. Over time, this force can weaken the wall and the overlying bone, eventually allowing a pouch to form. Think of it like water pressure building behind a partially kinked garden hose: the flow that escapes past the kink hits whatever is downstream with extra force.
Elevated Intracranial Pressure
There is a notable overlap between sigmoid sinus diverticulum and idiopathic intracranial hypertension (IIH), a condition where the pressure of the fluid surrounding the brain is abnormally high. In one study, 41% of temporal bones in patients with IIH showed sigmoid plate dehiscence, compared with 27% in controls. Diverticula themselves were twice as common in IIH patients (8% versus 4%), though that particular difference did not reach statistical significance due to the small number of cases.
The connection makes physiological sense. Elevated cerebrospinal fluid pressure pushes outward on the walls of the venous sinuses from the outside. At the same time, changes in venous pressure from the inside can compound the stress on the vessel wall. Some researchers believe that chronically raised intracranial pressure is a direct cause of both dehiscence and diverticulum formation. Others suggest that many people with diverticula may have a subclinical form of IIH, meaning their intracranial pressure is elevated but not high enough to produce the classic symptoms of headache and vision changes.
This association is particularly strong in patients with higher body mass indices, which is itself a well-known risk factor for IIH. The link suggests that weight-related pressure changes inside the skull may set the stage for bone thinning and diverticulum development over months or years.
How the Diverticulum Produces Pulsatile Tinnitus
The intact sigmoid plate normally acts as an acoustic insulator, blocking the sound of blood flowing through the sinus from reaching the inner ear. Once the bone barrier is gone and a diverticulum protrudes into the mastoid air cells, that insulation disappears. The turbulent blood flow inside the pouch is now close enough to the cochlea for you to hear it as a rhythmic whooshing or thumping that matches your heartbeat.
The turbulence itself is amplified by the shape of the diverticulum. Blood swirling into and out of the pouch creates chaotic flow patterns that are noisier than the smooth flow in a normal sinus. When upstream stenosis is also present, the already-turbulent blood entering the diverticulum makes the sound even louder. This is why some patients notice that their pulsatile tinnitus worsens with physical exertion, lying down, or anything else that increases blood flow or venous pressure in the head.
How It Is Diagnosed
Sigmoid sinus diverticulum is typically identified on a high-resolution CT scan of the temporal bone, which can show both the bony defect and the soft tissue pouch extending through it. Contrast-enhanced MR angiography provides additional detail about the size of the diverticulum, the width of its neck (the opening connecting it to the main sinus), and whether there is upstream narrowing. In documented cases, diverticula have ranged from about 6 to 9 millimeters in their longest dimension, with neck widths between 3 and 7 millimeters. They most commonly point laterally or anteriorly and are slightly more often found on the right side.
Identifying the upstream stenosis is just as important as finding the diverticulum itself, because it can change the treatment approach. If a significant pressure difference is measured across the narrowed segment during a catheter-based study, treating that narrowing may be the key to resolving symptoms.
Treatment Options and Success Rates
Two main approaches exist for treating a symptomatic sigmoid sinus diverticulum: endovascular (catheter-based) procedures and surgery.
Endovascular treatment, which can include placing a stent to open the upstream narrowing or packing the diverticulum with coils to close it off, has shown strong results. In a systematic review, complete or near-complete resolution of pulsatile tinnitus occurred in 100% of patients treated this way, with 85% achieving full relief after a single procedure. Complications were rare, occurring in about 4% of cases, and all resolved without lasting effects. In many patients with both a diverticulum and upstream narrowing, stenting alone was enough to eliminate the tinnitus, likely because reducing the turbulent flow removed the sound source.
Surgical treatment typically involves opening the mastoid bone to access the area and either resurfacing the dehiscent bone or reconstructing the sinus wall. This approach resolves pulsatile tinnitus completely in about 78% of patients, with another 11% experiencing partial improvement. However, roughly 11% see no improvement at all, and significant complications occur in about 9% of surgical cases. Around 7% of surgical patients require a second operation. When sigmoid plate dehiscence alone is the target (without addressing upstream stenosis), failure rates have been reported as high as 50%, which underscores how important the upstream narrowing is in generating the symptom.
The choice between approaches depends on the specific anatomy. Endovascular treatment has the advantage of being able to address the upstream narrowing directly, while surgery can physically rebuild the missing bone barrier. In some cases, both problems need to be addressed for lasting relief.