Endovascular Management of Intracranial Dural AVFs: Principles.

Intracranial dural AVFs are abnormal communications between arteries that supply the dura mater and draining cortical veins or venous sinuses. They are believed to form as a response to venous insults such as thrombosis, trauma, or infection. Classification and management are dependent on the presence of drainage/reflux into cortical veins because such drainage markedly elevates the risk of hemorrhage or venous congestion, resulting in neurologic deficits. AVFs with tolerable symptoms and benign drainage patterns can be managed conservatively. Intolerable symptoms, presentation with hemorrhage/neurologic deficits, or aggressive drainage patterns are indications for intervention. Treatment options include microsurgical disconnection, endovascular transarterial embolization, transvenous embolization, or a combination. This is the first in a series of 3 articles on endovascular management of intracranial dural AVFs, in which we outline the principles and outcomes of endovascular treatment.

Endovascular Management of Intracranial Dural AVFs: Transvenous Approach.

In this third review article on the endovascular management of intracranial dural AVFs, we discuss transvenous embolization approaches. Transvenous embolization is increasingly popular and now the first-line approach for ventral dural AVFs involving the cavernous sinus and hypoglossal canal. In addition, transvenous embolization is increasingly used in lateral epidural dural AVFs in high-risk locations such as the petrous and ethmoid regions. The advantage of transvenous embolization in these locations is the ability to retrogradely embolize the draining vein and fistula while reducing the risk of ischemic cranial neuropathy or brain parenchymal infarction commonly feared from a transarterial approach. By means of coils ± ethylene-vinyl alcohol copolymer, transvenous embolization can achieve angiographic cure rates of 80%-90% in ventral locations. Potential complications include transient cranial neuropathy, neurologic deterioration due to venous outflow obstruction, and perforation while navigating pial veins. Transvenous embolization should be considered when dural AVFs arise in proximity to the vasa nervosum or extracranial-intracranial anastomoses.

Endovascular Management of Intracranial Dural Arteriovenous Fistulas: Transarterial Approach.

In this second of 3 review articles on the endovascular management of intracranial dural AVFs, we discuss transarterial treatment approaches. The treatment goal is to occlude the fistulous point, including the most distal portion of the arterial supply together with the most proximal portion of the draining vein (ie, the "foot" of the vein), which can be accomplished with liquid embolic agents via transarterial access. Anatomic factors to consider when assessing the safety and efficacy of a transarterial approach using liquid embolic agents include location, angioarchitecture, and proximity of arterial feeders to both the vasa nervosum of adjacent cranial nerves and the external carotid-internal carotid/vertebral artery anastomoses. Anatomic locations typically favorable for transarterial approaches include but are not limited to the transverse/sigmoid sinus, cerebral convexity, and superior sagittal sinus. In this review article, we discuss the technical approaches, outcomes, potential complications, and complication avoidance strategies for transarterial embolization.

Facial Nerve Arterial Arcade Supply in Dural Arteriovenous Fistulas: Anatomy and Treatment Strategies.

BACKGROUND AND PURPOSE: Endovascular treatment of petrous dural AVFs may carry a risk of iatrogenic facial nerve palsy if the facial nerve arterial arcade, an anastomotic arterial arch that supplies the geniculate ganglion, is not respected or recognized. Our purpose was to demonstrate that the use of a treatment strategy algorithm incorporating detailed angiographic anatomic assessment allows identification of the facial nerve arterial arcade and therefore safe endovascular treatment. MATERIALS AND METHODS: This was a retrospective cohort study of consecutive petrous dural AVF cases managed at Toronto Western Hospital between 2006 and 2018. Our standard of care consists of detailed angiographic assessment followed by multidisciplinary discussion on management. Arterial supply, primary and secondary treatments undertaken, angiographic outcomes, and clinical outcomes were assessed by 2 independent fellowship-trained interventional neuroradiologists. RESULTS: Fifteen patients had 15 fistulas localized over the petrous temporal bone. Fistulas in all 15 patients had direct cortical venous drainage and received at least partial supply from the facial nerve arterial arcade. Following multidisciplinary evaluation, treatment was performed by endovascular embolization in 8 patients (53%) and microsurgical disconnection in 7 patients (47%). All patients had long-term angiographic cure, and none developed iatrogenic facial nerve palsy. CONCLUSIONS: By means of our treatment strategy based on detailed angiographic assessment and multidisciplinary discussion, approximately half of our patients with petrous AVFs were cured by endovascular treatment, half were cured by an operation, and all had preserved facial nerve function.

Artery of Davidoff and Schechter Supply in Dural Arteriovenous Fistulas.

The artery of Davidoff and Schechter is a dural branch of the posterior cerebral artery that can supply the meninges close to the falcotentorial junction. It is usually not identified on angiography except when enlarged in the setting of a dural AVF or meningioma. The impact on treatment of the artery of Davidoff and Schechter supply to a fistula is not well-described in the literature. Our retrospective analysis of patients with dural AVFs treated at the Toronto Western Hospital between 2006 and 2018 identified 6 patients with dural AVFs receiving supply from artery of Davidoff and Schechter (of a total of 173 patients with dural AVFs). All patients were initially treated by transarterial embolization using liquid embolic agents. Three patients required a second endovascular procedure partly due to residual supply from artery of Davidoff and Schechter, and in all cases, angiographic cure was obtained. The treatment approach, challenges encountered, and potential complications of treating such fistulas are described.

Acute Cortical Lesions in MELAS Syndrome: Anatomic Distribution, Symmetry, and Evolution.

BACKGROUND AND PURPOSE: Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome is a rare mitochondrial disorder affecting children and young adults. Stroke-like episodes are often associated with acute cortical lesions in the posterior cerebral cortex and are classically described as asymmetric and transient. In this study we assessed the anatomic distribution of acute cortical lesions, the incidence of symmetry, and the temporal evolution of lesions. MATERIALS AND METHODS: This was a retrospective cohort study of patients who had a confirmed genetic diagnosis of a pathogenic variant associated with MELAS and MR imaging performed at our center (2006-2018). Each MR imaging study was assessed for new lesions using T1, T2, FLAIR, DWI, ADC, and SWI. The anatomic location, symmetry, and temporal evolution of lesions were analyzed. RESULTS: Eight patients with the same pathogenic variant of MELAS (MT-TL1 m.3243A>G) with 31 MR imaging studies were included. Forty-one new lesions were identified in 17 of the studies (5 deep, 36 cortical). Cortical lesions most commonly affected the primary visual cortex, the middle-third of the primary somatosensory cortex, and the primary auditory cortex. Thirty of 36 cortical lesions had acute cortical diffusion restriction, of which 21 developed cortical laminar necrosis on subacute imaging. Six of 11 studies with multiple lesions showed symmetric cortical involvement. CONCLUSIONS: Acute cortical lesions in MELAS most commonly affect the primary visual, somatosensory, and auditory cortices, all regions of high neuronal density and metabolic demand. The most common pattern of temporal evolution is acute cortical diffusion restriction with subacute cortical laminar necrosis and chronic volume loss. Symmetric involvement is more common than previously described.