A Sigmoid Sinus Diverticulum (SSD) is a focal outpouching or ballooning of the sigmoid sinus, a large vein that drains blood from the brain. This structural anomaly is a major cause of pulsatile tinnitus, a disruptive symptom where a person hears a rhythmic whooshing or thumping sound synchronized with their heartbeat. The noise is caused by the audible flow of blood due to a defect in the bony structure surrounding the vein. Understanding the causes requires examining the anatomy, structural weaknesses, and dynamic forces that drive its expansion and symptoms.
Anatomical Relationship to the Inner Ear
The sigmoid sinus follows an S-shaped path along the inside of the skull, tracking a groove formed by the temporal bone, which houses the inner ear. This vein continues the cerebral venous system, carrying blood toward the neck where it becomes the internal jugular vein. Normally, a thin layer of bone, the sigmoid plate, separates the blood flow within the sinus from the delicate structures of the middle and inner ear. This bony plate acts as a natural sound barrier, muffling the normal sounds of rushing blood.
The temporal bone surrounding the sinus contains interconnected, air-filled spaces called mastoid air cells. When the structural integrity of the sigmoid plate is compromised, the sinus wall comes into direct contact with these air cells. This close proximity and the absence of the normal bony partition allow the mechanical sound of blood flow to be transmitted directly into the ear canal, causing pulsatile tinnitus.
Developmental and Structural Predisposition
The primary cause of a sigmoid sinus diverticulum lies in inherent structural weaknesses that develop during skull formation. This weakness is rooted in bony dehiscence, which is a gap or complete absence of the bone covering the sigmoid sinus. The diverticulum is the weakest part of the vein wall bulging outward into this unsupported area.
The degree of pneumatization, or air-filling, of the mastoid bone plays a significant role in this predisposition. Individuals with unusually large mastoid air cells extending close to the sigmoid sinus are more likely to experience this condition. These large air cells reduce the solid bone supporting the vein wall, creating a vulnerable area for the vein to push into and form an outpouching.
These structural variations are considered developmental anomalies present from birth. The sigmoid sinus is often dominant on one side, typically the right, handling a larger volume of blood flow. This naturally larger size and higher flow rate make the dominant side more susceptible to developing a diverticulum when a structural defect is present.
Hemodynamic and Pressure Contributions
While a structural defect provides the location for a diverticulum, dynamic forces related to blood flow and pressure drive its expansion and create the audible symptoms. One significant factor is turbulent blood flow within the sigmoid sinus. This turbulence is often caused by transverse sinus stenosis, an upstream narrowing of the vein that creates a high-velocity jet of blood directed toward the diverticulum. This turbulent flow creates swirling patterns and vortices, generating the noise heard as pulsatile tinnitus.
The constant, localized pressure from this erratic blood flow puts continuous stress on the weak sinus wall, contributing to gradual enlargement. The condition is also strongly linked to chronic or intermittent increases in intracranial pressure (ICP), such as in cases of Idiopathic Intracranial Hypertension (IIH). Elevated pressure inside the skull translates into higher pressure within the dural venous sinuses. This sustained pressure acts as a constant force, pushing against the structurally unsupported area of the vein wall. This combination of structural weakness and chronic pressure overload accelerates the formation and expansion of the diverticulum.