|ECR 2019 / C-2645|
|Non-cavernous cranial dural arteriovenous fistulas: Imaging findings that suggest them and classification|
DAVF are a rare intracranial vascular malformation (10% to 15% of intracranial shunts) within the dural leaflets, characterized by abnormal connections between meningeal arteries and dural venous sinuses, meningeal veins, or cortical veins.
Fistulaes are distinguished from arteriovenous malformations by the lack of a parenchymal nidus and the existence of dural arterial supply.
Most reported intracranial DAVF involve the transverse-sigmoid sinuses (38%), and the cavernous sinus (35%), followed by the tentorium, superior sagittal sinus and dura of the anterior cranial fossa.
They are typically encountered in middle-aged adults with a median age of onset in the sixth decade.
In the paediatric population DAVF are frequently congenital, and often associated with structural venous abnormalities. In contrast adults they are thought to be acquired, most of them idiopathic (without any clear inciting event).
Nevertheless some patients with cranial DAVF have a history of previous venous or dural sinus thrombosis, chronic infection, trauma or craniotomy, so some of these events could be associated with the pathogenesis of dural fistulae.
The most commonly used classifications for DAVF are Cognard and Borden ones. The natural history of DAVF depends a lot on the venous drainage patterns and so, in both classifications, high-grade fistulaes are those with cortical venous drainage (CVD).
DAVF types I-IIa in Cognard classification, and type I in Borden classification, are confined to sinus and they do not show CVD, so we consider them as “benign”. While types IIb-V in Cognard and types II-III in Borden present CVD, and are the “aggressive” ones.
References: Hospital 12 de Octubre - Madrid/ES
We should be aware that these lesions have a dynamic nature, so the most indolent types at the beginning, could develop CVD at the end.
The risk of conversion is low, although we should be alert to any change in patient´s symptoms, which may denote exacerbations of the venous drainage pattern.
The anterior cranial fossa and tentorium locations have higher incidence of aggressive DAVF, probably because the lack of adjacent dural sinuses causes the shunt to cortical venous earlier than in other locations.
Most of the intracranial DAVF are asymptomatic, pulsatile tinnitus is often the only symptom in low-grade types. In contrast aggressive lesions are more likely to have an acute clinical presentation as a result of venous congestion (intracranial haemorrhage, seizure, focal neurological deficit, cognitive change, or altered level of consciousness).
Dural arteriovenous fistulas associated with cortical venous reflux, in particular those that present with clinical symptoms, are associated with poor outcome if left untreated. Their early detection can potentially avoid further progression or occurrence of complications.
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