Sigmoid Sinus Dehiscence (SSD) is an anatomical finding where the bony plate (sigmoid plate) that normally covers the sigmoid sinus is absent or defective. The sigmoid sinus is a large, paired venous channel in the temporal bone that drains blood from the brain into the jugular vein. This dehiscence exposes the sinus wall directly to the air-filled mastoid cavity, often leading to pulsatile tinnitus. SSD results from a combination of inherent structural variations and acquired mechanical forces.
Structural Anatomy and Bone Variation
The initial susceptibility to SSD is rooted in an individual’s skull bone and venous anatomy. The sigmoid sinus is normally shielded by the sigmoid plate, a thin layer of cortical bone separating the vein from the mastoid air cells. If this protective bone is naturally thin or absent from birth, the sinus wall is vulnerable to forces that will develop later in life. This inherent weakness is often compounded by hyperpneumatization (extensive mastoid air cell development), which creates a larger adjacent cavity allowing the dehiscent sinus to protrude.
The positioning of the jugular bulb, the terminal portion of the sigmoid sinus, also plays a role. A high-riding jugular bulb is a common anatomical variant where the vein extends farther up into the temporal bone. If the overlying thin bony plate is missing, a dehiscent jugular bulb forms, exposing the vessel wall. Asymmetry is another factor, as the right transverse and sigmoid sinuses are often dominant, carrying a greater proportion of the brain’s venous outflow. This dominance results in increased flow and pressure on the dominant side, making it more prone to bone erosion.
The Dynamics of Intracranial Pressure
While structural factors create a weak spot, sigmoid sinus dehiscence is often the result of acquired, mechanical erosion driven by sustained high pressure within the venous system. Elevated intracranial pressure (ICP) translates directly to higher pressure inside the dural venous sinuses. This increased hydrostatic force, acting on a weak or thin sigmoid plate segment, physically pushes the vein wall outward. This continuous force eventually leads to bone lysis (bone resorption and destruction).
The primary mechanical driver is the turbulent, pulsatile flow of blood against the sinus wall, known as blood flow impingement. Under high venous pressure, the flow becomes chaotic, creating a vibrating force. This constant mechanical vibration against the thin bone causes the bone to resorb over time. The dehiscence is a pressure-driven remodeling process where the bone recedes from the expanding, high-pressure vein wall.
Surgical and imaging evidence supports this mechanism. Studies show that when high venous pressure is medically or surgically reduced, the sigmoid sinus diverticulum can decrease in size. New bone remodeling has been observed on follow-up imaging, demonstrating the body’s ability to repair the defect once the chronic erosive force is removed. This reversibility confirms that the bone defect is frequently an acquired pathology resulting from chronic pressure and turbulent flow acting on a vulnerable area.
Associated Systemic Conditions
The mechanical forces causing SSD are driven by systemic medical conditions that increase pressure within the skull. The most significant condition linked to SSD is Idiopathic Intracranial Hypertension (IIH). IIH is characterized by abnormally elevated cerebrospinal fluid (CSF) pressure, which is transferred to the dural sinuses because the CSF and venous systems are closely connected. The demographics of SSD patients closely mirror those of IIH patients, who are predominantly obese women of childbearing age.
A major contributor to high venous pressure in IIH patients is venous sinus stenosis, a narrowing of the large veins, most commonly the transverse sinuses, upstream of the sigmoid sinus. This stenosis acts as an obstruction, causing blood to back up and dramatically increasing venous pressure before the narrowing. The resulting pressure gradient and turbulent flow are then transmitted downstream to the sigmoid sinus, exacerbating the erosive process.
Obesity is another systemic factor contributing to the high venous pressure underlying IIH and SSD. Increased body mass, particularly in the abdomen, raises intra-abdominal and intra-thoracic pressure. This pressure is transmitted to the central venous system, hindering blood drainage from the head and elevating intracranial venous pressure. This cascade leads to local bone erosion and sigmoid sinus dehiscence.
Summary of Causal Factors
Sigmoid sinus dehiscence results from a convergence of pre-existing anatomy and acquired physiological stress. The condition requires an initial structural predisposition, such as a thin sigmoid plate or a high-riding jugular bulb, creating a vulnerable site. This vulnerability is exploited by an acquired pressure driver, most often Idiopathic Intracranial Hypertension (IIH). The resulting elevated venous pressure and turbulent blood flow mechanically erode the thin bone over time. Diagnosis and management require considering both the static anatomical configuration and the dynamic pressure forces acting on the sinus.