Pathophysiology of Dural Arteriovenous Fistula
Core Pathophysiologic Mechanism
Dural arteriovenous fistulas (DAVFs) are acquired abnormal direct connections between meningeal arteries and dural venous sinuses or cortical veins within the dura mater, lacking a parenchymal nidus that distinguishes them from brain AVMs 1.
The fundamental pathologic lesion involves abnormal communications between dural arteries and dural veins through small dilated venules (approximately 30 microns in diameter, termed "crack-like vessels") within the venous sinus wall 2. These represent the essential anatomic substrate of DAVFs rather than sinus thrombosis itself 2.
Initiating Factors and Development
Primary Triggers
The development of DAVFs appears triggered by venous sinus hypertension caused by stenocclusive disease of the venous sinuses, which promotes formation of fistulous connections between arteries and veins in the dural wall 2. This venous hypertension leads to progressive dilation of venules and eventual DAVF formation 2.
Predisposing Conditions
Multiple factors can initiate DAVF development 3:
- Head trauma - mechanical injury to dural structures 3
- Venous sinus thrombosis - though not essential for DAVF formation, acts as a predisposing factor 2, 3
- Prior neurosurgery - surgical manipulation of dural structures 3
- Hypercoagulable states - promoting venous stasis and hypertension 3
- Hormonal influences - less well-characterized mechanism 3
Hemodynamic Consequences
High-Flow Shunting
DAVFs create abnormal high-flow shunts between the high-pressure arterial system and low-pressure venous system 1. This arteriovenous shunting occurs without the normal intermediary capillary bed 1.
Venous Drainage Patterns
The aggressiveness and clinical risk of DAVFs is determined primarily by the pattern of venous drainage, specifically the presence of cortical venous reflux 4, 5, 6. When arterial blood is shunted directly into cortical veins rather than dural sinuses, venous hypertension develops in the brain parenchyma 1.
Venous Hypertension and Stenosis
Venous outflow obstruction and stenosis are critical pathophysiologic features 1:
- Venous stenosis/occlusion creates impedance to normal drainage 1
- Venous ectasia (>2-fold caliber change) indicates abnormal venous pressure 1
- Reversal of normal venous flow direction occurs away from the closest venous sinus 1
These venous abnormalities are associated with hemorrhagic presentation and increased morbidity 1.
Clinical Manifestations Based on Pathophysiology
Location-Dependent Symptoms
Symptoms directly correlate with fistula location and venous drainage patterns 1:
- Transverse/sigmoid sinus DAVFs - pulsatile tinnitus from turbulent flow 1
- Cavernous sinus DAVFs - exophthalmos, chemosis, cranial nerve palsies 1
- Cortical venous drainage - seizures, focal neurological deficits, cognitive impairment 1
Hemorrhagic Risk
DAVFs with cortical venous drainage carry significant hemorrhage risk due to venous hypertension transmitted to fragile cortical veins 4, 5, 6. The presence of venous ectasia further increases bleeding risk by indicating severe venous hypertension 1, 4.
Progressive Nature
Unlike congenital vascular malformations, DAVFs are acquired lesions that can progress over time 4, 5. Continued venous hypertension promotes recruitment of additional arterial feeders and worsening of venous drainage abnormalities, creating a self-perpetuating cycle 2.
Key Pathophysiologic Distinctions
DAVFs differ fundamentally from brain parenchymal AVMs in several critical ways 1:
- Arterial supply derives exclusively from meningeal (dural) arteries rather than pial arteries 4
- No parenchymal nidus exists - the fistula occurs within dural leaflets 5, 6
- DAVFs are acquired rather than congenital 4, 2
- Location is within dura mater, most commonly at transverse and cavernous sinuses 4
This distinction is clinically important because DAVFs are often amenable to curative endovascular treatment, unlike many brain AVMs 1.