Venous sinus stenosis (VSS) is the narrowing of the dural venous sinuses, which are large veins responsible for draining blood and cerebrospinal fluid (CSF) from the brain. These sinuses, primarily the transverse and sigmoid sinuses, are located within the dura mater. When these vessels narrow, the outflow of blood and CSF is obstructed, causing a buildup of pressure within the skull. This increased pressure can lead to various neurological symptoms, including severe headaches, vision changes, and pulsatile tinnitus (a rhythmic whooshing sound heard in the ear). The underlying causes range from intrinsic structural issues to external compression resulting from pressure dynamics.
Anatomical and Developmental Factors
Some VSS cases stem from inherent physical characteristics of the venous anatomy, meaning the structure is narrower from birth. Dural sinuses naturally show asymmetry; one side, typically the transverse sinus, is often larger than the other. This variation can predispose a person to symptoms if the smaller side becomes functionally compromised. A congenital variation known as hypoplasia (underdevelopment of a sinus) results in a vessel too small to handle normal blood flow. This structural limitation creates a bottleneck in the venous drainage pathway, causing relative stenosis. Another intrinsic factor is the presence of fibrous bands or septae within the sinus lumen. These internal structures, which are essentially scar tissue or embryonic remnants, restrict the vessel’s internal diameter, impeding blood flow.
The Role of Intracranial Pressure Dynamics
The relationship between VSS and elevated intracranial pressure (EIP), particularly in Idiopathic Intracranial Hypertension (IIH), is complex. IIH is characterized by high CSF pressure without an identifiable cause, and a significant portion of these patients also exhibit VSS. The debate centers on whether the sinus narrowing causes the EIP, or if chronically high CSF pressure causes the sinus to collapse.
Evidence suggests a vicious cycle: an initial rise in intracranial pressure compresses the highly compliant dural sinuses from the outside. This external compression, known as extrinsic stenosis, blocks venous outflow, causing further venous pressure to build up. The resulting increased venous pressure impairs the brain’s ability to absorb CSF, which elevates the EIP even more, perpetuating the cycle.
A major mechanism for this extrinsic compression involves the arachnoid granulations (AGs), small structures responsible for absorbing CSF into the venous bloodstream. In patients with IIH, these granulations can become enlarged and protrude into the venous sinus lumen. The increased pressure pushes the swollen AGs against the outer wall of the dural sinus, causing a functional narrowing. Reducing EIP, such as through CSF removal, can sometimes resolve the stenosis entirely.
Acquired Conditions and Secondary Blockages
Venous sinus stenosis can result from physical obstructions or inflammatory conditions acquired later in life. A primary acquired cause is Dural Sinus Thrombosis (DST), where a blood clot forms inside the venous sinus, creating a physical blockage. This clot formation obstructs the vessel lumen, leading to decreased venous flow and increased venous and intracranial pressure.
Thrombosis can be triggered by prothrombotic states, including inherited clotting disorders, hormonal factors like oral contraceptive use, or the postpartum period. Local infections, such as otitis media or mastoiditis, can also lead to thrombosis in the adjacent sinuses due to the spread of inflammation. This direct internal blockage is distinct from the external compression seen in IIH.
Stenosis can also result from a “mass effect,” which is external compression caused by a space-occupying lesion near the sinus. Tumors, abscesses, or hematomas (collections of blood) situated adjacent to the dural sinuses can physically squeeze the vessel, reducing its diameter. Furthermore, systemic inflammatory diseases, such as vasculitis or infections like meningitis, can cause swelling and thickening of the sinus walls, reducing the internal caliber and restricting flow.
Systemic and Modifiable Risk Factors
Systemic conditions and lifestyle choices significantly influence the likelihood of developing VSS or worsening an existing anatomical narrowing. Obesity and substantial weight gain are strongly recognized risk factors, particularly for IIH-associated VSS. For example, about 71% of adults with IIH are obese at diagnosis.
Increased abdominal fat elevates central venous pressure, which is transmitted up to the cerebral draining veins and sinuses. This elevation increases the pressure acting on the outside of the collapsible sinuses. Weight loss is a fundamental treatment strategy for IIH because it can reduce this transmitted pressure and alleviate secondary VSS. The link between obesity and VSS is especially pronounced in women, who are already more susceptible to IIH.
Certain medications are also implicated in pressure changes that can lead to secondary VSS. Some antibiotics, like tetracyclines, and hormonal therapies have been associated with changes in intracranial pressure that can initiate the positive feedback loop leading to stenosis. The systemic effects of these factors can lower the threshold at which a pre-existing, non-symptomatic anatomical variation becomes a clinically significant stenosis.