Normal perfusion pressure breakthrough occurring during treatment of carotid and vertebral fistulas

Of the 185 carotid and vertebral fistulas treated by the authors over the past 10 years, five developed neurologic deficits after abrupt closure of their fistulas. The earliest case, treated initially by proximal surgical carotid occlusion, presented 32 years later with cerebral steal symptoms from the large, long-standing carotid cavernous fistula. Upon completion of a surgical trapping procedure, there was immediate massive cerebral edema, brain herniation, and death. In the remaining four patients (three vertebral fistulas and one with carotid cavernous fistula), all treated by transvascular embolization techniques, neurologic deficits occurred coincidentally with the abrupt closure of the fistula and resolved with reestablishment of fistula flow. This indicated that the cerebral vasculature is unable to tolerate the reestablishment of normal cerebral perfusion after abrupt closure of the fistula. All four patients were treated with staged or slow occlusion of their fistulas, which resulted in complete fistula closure without permanent neurologic sequelae. All five patients who developed symptoms consistent with normal perfusion pressure breakthrough had large, long-standing fistulas, ranging in duration from 9 to 32 years. Two of the five patients developed slowly progressive neurologic deficits consistent with cerebral steal prior to treatment. This sign was not observed in the 180 patients who did not develop symptoms during treatment. We conclude that patients with carotid or vertebral fistulas of long duration, particularly those with cerebral steal symptoms, are at risk to develop neurologic deficits related to perfusion breakthrough if their fistulas are abruptly closed. Staged or gradual closure may prevent this potentially devastating complication.     

Direct endovascular thrombolytic therapy for dural sinus thrombosis

Three patients, ages 51 to 71 years, sought treatment for symptomatic dural sinus thrombosis with occlusion and were treated by direct sinus perfusion with urokinase. All three patients had a dural arteriovenous fistula; one involved the inferior petrosal sinus and two involved the transverse sinus. Clinical findings included papilledema, diminished visual acuity, decreased mentation, and cranial nerve palsies. Diagnosis was made by cerebral arteriography and confirmed by sinus venography. All three patients were treated by a transjugular direct infusion of urokinase. In one patient, a transfemoral venous approach used initially was discontinued because of an infection. The period of continuous infusion for thrombolysis ranged between 4 and 10 days. In two patients, the clinical signs and symptoms improved with angiographic evidence of clot lysis and dural sinus recanalization. Angiography indicated that one patient had a partial resolution of a clot in the torcular herophili and transverse sinus but showed no clinical improvement. These preliminary results suggest that transjugular local infusion of thrombolytic agents can be an effective treatment for symptomatic, thrombosed dural sinuses. This selective lysis avoids thrombolytic effects that could aggravate or produce systemic hemorrhagic complications.     

Dural fistulas involving the cavernous sinus: results of treatment in 30 patients

Thirty symptomatic indirect carotid cavernous fistulas were treated between 1978 and 1986 with a variety of treatment modalities. Combined carotid artery and jugular vein compression resulted in a complete cure in seven of 23 patients (30%) and improvement in one additional patient. There were no complications from this treatment, which is performed by the patient on an outpatient basis. Patients in whom carotid jugular compression therapy failed or who demonstrated cortical venous drainage or visual decline were treated with intravascular embolization. Embolization resulted in complete cure in 17 of 22 (77%) and improvement in four of 22 (18%). One patient required surgical excision of the involved dura after embolization to achieve complete cure. There was one permanent complication (stroke), which resulted in mild weakness caused by clot formation on a catheter.     

Dural Arteriovenous Fistulas of the Foramen Magnum Region: Clinical Features and Angioarchitectural Phenotypes

BACKGROUND AND PURPOSE:AVFs of the foramen magnum region, including fistulas of the marginal sinus and condylar veins, have complex arterial supply, venous drainage, symptoms, and risk features that are not well-defined. The purpose of this study was to present the angioarchitectural and clinical phenotypes of a foramen magnum region AVF from a large, single-center experience.MATERIALS AND METHODS:We retrospectively reviewed cases from a 10-year neurointerventional data base. Arterial and venous angioarchitectural features and clinical presentation were extracted from the medical record. Venous drainage patterns were stratified into 4 groups as follows: type 1 = unrestricted sinus drainage, type 2 = sinus reflux (including the inferior petrosal sinus), type 3 = reflux involving sinuses and cortical veins, and type 4 = restricted cortical vein outflow or perimedullary congestion.RESULTS:Twenty-eight patients (mean age, 57.9 years; 57.1% men) had 29 foramen magnum region AVFs. There were 11 (37.9%) type 1, nine (31.0%) type 2, six (20.7%) type 3, and 3 (10.3%) type 4 fistulas. Pulsatile tinnitus was the most frequent symptom (82.1%), followed by orbital symptoms (31.0%), subarachnoid hemorrhage (13.8%), cranial nerve XII palsy (10.3%), and other cranial nerve palsy (6.9%). The most frequent arterial supply was the ipsilateral ascending pharyngeal artery (93.1% ipsilateral, 55.5% contralateral), vertebral artery (89.7%), occipital artery (65.5%), and internal carotid artery branches (48.3%).CONCLUSIONS:We present the largest case series of foramen magnum region AVFs to date and show that clinical features relate to angioarchitecture. Orbital symptoms are frequent when sinus reflux is present. Hemorrhage was only observed in type 3 and 4 fistulas.

Dural AVFs of the foramen magnum region (FMR) comprise a rare subgroup of intracranial arteriovenous shunts occurring at the marginal sinus and condylar veins.¹ These FMR AVFs are thought to represent between 1.5% and 4.2% of cranial shunting lesions.^2,3 These lesions are anatomically complex, owing to the functional and anatomic variability of venous drainage at the craniocervical junction.^4-6 The marginal sinus is an inconstant ringlike intradural sinus along the rim of the foramen magnum and is frequently undetectable on noninvasive imaging in normal physiologic states.⁷ The marginal sinus communicates with a network of venous channels, including the condylar veins (anterior, posterior, and lateral), the condylar confluence, and the inferior petrosal sinus, serving to redirect blood flow between the parallel venous egress pathways of the jugular vein and vertebral venous plexus (Fig 1). As a consequence, pressurization of this FMR venous network can manifest with a spectrum of symptoms ranging from pulsatile tinnitus to myelopathy. Retrograde pressurization of the cavernous sinus via the inferior petrosal sinus may also generate orbital chemosis and extraorbital muscle palsies that may masquerade as carotid cavernous fistulas.⁸Open in a separate windowFIG 1.Venous anatomy of the FMR from above. The marginal sinus (MS) lines the margin the foramen magnum and connects to the basilar plexus (BP) anteriorly, the anterior condylar vein (ACV) laterally via the hypoglossal canal (HGC), and the suboccipital cavernous sinus inferiorly (not shown). The anterior condylar vein (AVC) connects with the anterior condylar confluence (ACC), which, in turn, communicates with the inferior petrosal sinus (IPS) and inferior petroclival vein (IPCV) and posteriorly with the lateral condylar vein (LCV), and the jugular bulb and internal jugular vein (JB/IJV). The posterior condylar (emissary) vein (PCV) exits via the posterior condylar canal (PCC).An FMR AVF at high risk of hemorrhage or causing debilitating symptoms can be treated endovascularly with low morbidity.¹ Both transvenous and transarterial approaches have been described.^9-12 Successful treatment of FMR AVFs demands rigorous preparation and knowledge of both the arterial supply and venous drainage patterns to achieve a durable cure and avoid nontarget embolization. However, as with other classes of AVF, observation is appropriate for low-risk lesions.¹³ Therefore, knowledge of the holistic structure and behavior of the shunt, including comprehensive evaluation of the arterial and venous anatomy of the fistula, is essential for treatment planning and complication avoidance.McDougall et al¹ at the University of California, San Francisco proposed a grading system for FMR AVF, classifying shunts by their pattern of venous drainage. In this model, low-risk shunts (grade I) have unrestricted antegrade drainage via the internal jugular vein (IJV) system, whereas intermediate (grade II) lesions show partial or restricted IJV outflow. High-risk shunts (grade III) drain exclusively via superficial venous channels. Spittau et al¹⁴ proposed a modification to this taxonomy based on the dominant pattern of drainage, type 1: dominant antegrade flow (jugular or vertebral venous plexus), type 2: dominant retrograde flow (petrosal→cavernous), and type 3: dominant pial/perimedullary reflux. Because the current neuroendovascular literature is confined to small case reports and series, the validity of these proposed angiographic-clinical relationships is uncertain.The purpose of this study was to elucidate the relationship between vascular angioarchitecture and clinical presentation by retrospectively evaluating a large single-institution case series.     

Treatment of massive posterior epistaxis by detachable coil embolization of a cavernous internal carotid artery aneurysm

We present a case of massive posterior epistaxis caused by a cavernous internal carotid artery aneurysm. This lesion was treated with endovascular placement of electrolytically detachable platinum embolization coils. The treatment resulted in cessation of epistaxis until the patient's death 3 months following embolization. We discuss aspects of using these above coils for this condition.     

Interventional neurovascular treatment of a giant intracranial aneurysm using platinum microcoils

A 70-year-old woman presented with symptoms of progressive cerebellar dysfunction due to mass effect from a giant, expanding, posterior fossa aneurysm arising from the distal vertebral artery. The aneurysm contained thrombus and had a broad-based neck. From a transfemoral approach, with the patient under local anesthesia, a 2.2 French microcatheter was guided through the vertebral artery and placed directly into the aneurysm. Six 5 x 15-mm platinum microcoils were deposited into the residual lumen of the aneurysm, resulting in complete thrombosis with obliteration of the aneurysm and preservation of the parent artery. Endovascular coil embolization therapy by interventional neurovascular techniques may provide a therapeutic alternative in the management of surgically difficult symptomatic intracranial aneurysms.