SUMMARY:Intracranial DAVFs are pathologic dural-based shunts and account for 10%-15% of all intracranial arteriovenous malformations. These malformations derive their arterial supply primarily from meningeal vessels, and the venous drainage is either via dural venous sinuses or through the cortical veins. DAVFs have a reported association with dural sinus thrombosis, venous hypertension, previous craniotomy, and trauma, though many lesions are idiopathic. The diagnosis is dependent on a high level of clinical suspicion and high-resolution imaging. Cross-sectional imaging techniques by using CT and MR imaging aid in the diagnosis, but conventional angiography remains the most accurate method for complete characterization and classification of DAVFs. The pattern of venous drainage observed on dynamic vascular imaging determines the type of DAVF and correlates with the severity of symptoms and the risk of hemorrhage.ABBREVIATIONS: CVD ϭ cortical venous drainage; DAVF ϭ dural arteriovenous fistula; DMSO ϭ dimethyl-sulfoxide; FPCT ϭ flat panel detector CT; n-BCA ϭ n-butyl 2-cyanoacrylate; NHND ϭ non-hemorrhagic neurologic deficit; SRS ϭ stereotactic radiosurgery; TAE ϭ transarterial embolization; TVE ϭ transvenous embolization
Variability of measurements was reduced with the computer-assisted perimeter method compared with the diameter method, which suggests that changes in volume can be detected more accurately with the perimeter method. The differences between these techniques seem large enough to have an impact on grading the response to therapy.
Carotid-cavernous fistulas (CCFs) are abnormal arteriovenous communications in the cavernous sinus. Direct CCFs result from a tear in the intracavernous carotid artery. Indirect CCFs generally occur spontaneously and cause more subtle signs. Direct CCFs, which typically have high flow, usually present with ocular-orbital venous congestive features and cephalic bruit. Indirect CCFs, which typically have low flow, present with similar but more muted clinical features. Direct CCFs are always treated with endovascular methods. The goal is to occlude the fistula but preserve the patency of the internal carotid artery (ICA). Agents include detachable coils or liquid embolic agents delivered transarterially or transvenously. Arterial porous or covered stents are often used adjunctively. In rare cases, the ICA must be occluded. Indirect CCFs are only treated if symptoms are intractable or intolerable or if vision is threatened. The goal is to interrupt the fistulous communications and decrease the pressure in the cavernous sinus. The traditional approach has been transarterial embolization with liquid agents, particularly n-butyl cyanoacrylate (n-BCA). However, the multiplicity of arterial feeders and the low success rate in occluding indirect CCFs by the arterial route has led to a preference for transvenous embolization, most commonly via the inferior petrosal sinus. If that sinus is impassable, alternative routes include the pterygoid venous plexus, superior petrosal sinus, facial vein, or ophthalmic veins. The cavernous sinus is occluded with coils, liquid embolic agents, or both. The use of ethylene vinyl alcohol copolymer (Onyx), an agent that may be superior to n-BCA because it may allow better distal fistula penetration. However, more safety and efficacy data must be accumulated. When experienced interventionalists are involved, the success rate for closing direct fistulas is 85%-99% and for closing indirect fistulas is 70%-78%. Serious complications are relatively infrequent.
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