CHAPTER 136 Interventional Neuroradiology of the Skull Base, Head, and Neck
Interventional neuroradiologic techniques are essential in the management of certain disorders involving the skull base, face, and neck. These image-guided techniques are used for a variety of purposes, such as to test the potential effects of closing major arteries during surgery for lesions of the skull base, to occlude significant arterial feeders to neoplastic lesions preoperatively, to infuse a chemotherapeutic agent into a metastatic tumor, and to treat a variety of vascular disorders.
Rather than presenting an exhaustive discussion of the management of individual diseases, this chapter introduces the referring clinician to the use of the tools and the basic principles of endovascular and image-guided percutaneous management for lesions of the skull base and the face and neck. This knowledge should not only lead to an appreciation of the sophistication of the interventional techniques, including the capabilities, limitations, outcomes, and possible complications of these procedures, but it also should support the role of an interventionalist when dealing with difficult vascular and neoplastic lesions.
Before performing angiographic or percutaneous therapy, cross-sectional studies such as computed tomography (CT) or magnetic resonance imaging (MRI) are thoroughly analyzed to delineate the precise topography and extension of the lesion and its relationship to nearby structures, including displacements and alterations of blood vessels. It is essential that the goals of an interventional procedure are well defined by the entire therapeutic team to tailor the procedure to the overall treatment of a patient.
It is essential during endovascular interventional procedures to define the blood supply of a lesion with the highest possible resolution in all projections. Arteries or their collateral channels act as conduits for embolic material to the lesion. Of equal importance is the visualization of the many dangerous collateral vessels leading to the intracranial circulation or to the blood supply of the cranial nerves. Superb visualization and an excellent knowledge of the vascular anatomy are of paramount importance, as is an understanding of the potential clinical symptoms from embolization into an unwanted vascular territory and occlusion of the blood supply to normal tissues.1
The anatomic complexity of the neck, skull base, and face makes it essential that sophisticated C-arm positioners be used to allow variable projections of the area of interest. Biplane visualization is helpful for superselective catheterization of the small tortuous channels feeding the lesion. High-resolution techniques, including electronic “road-mapping,” are essential. Injection of embolic agents suspended or diluted in contrast material during real-time high-resolution subtracted fluoroscopy (road-mapping) permits visualization of the progressive occlusion of the vessels feeding the lesion. Monitoring the procedure with high-resolution fluoroscopy helps to avoid the complications of reflux of embolic material or flow to collateral branches, thus preserving the blood supply to normal tissues.
The catheters most commonly used for diagnostic angiography are 4F and 5F polyethylene catheters. Superselective catheterization of tiny arteries feeding tumors, fistulas, and other lesions facilitates the most effective embolization, frequently beyond sites of anastomoses to dangerous collaterals, and is achieved by the use of microcatheters. Wire-directed microcatheters approximately 2F to 3F in size have extremely flexible distal portions that are variable in length. They are used with microguidewires 0.008 to 0.018 inch in diameter. Flow-directed catheters also are used for tortuous vessels feeding high-flow lesions.
If it is impossible to catheterize feeders to a tumor selectively, percutaneous puncture of the hypervascular neoplasm can be performed under image guidance, gaining access to the intratumoral blood supply. Injections of contrast material during digital subtraction angiography are performed to ensure there is no filling of the arterial supply to normal tissues. Injections of the embolic agent are made under low pressure during fluoroscopy with road-mapping or digital subtraction angiography.
Several embolic agents are available for the various lesions found at the skull base and in the face and neck. The choice of the embolic material in a given patient depends on the goal of the procedure; the selectivity of the accomplished catheterization; the angioarchitecture and flow dynamics of the lesion; and the proximity of the catheter tip to the blood supply to vital structures such as the brain, cranial nerves, eyes, and skin, or to potential collateral channels to these organs. These embolic agents include particulate materials, metallic coils, liquid agents, and detachable balloons. Each has its own place in the interventionalist’s armamentarium.
Two commonly used particulate materials are Gelfoam (Upjohn Pharmaceuticals, Kalamazoo, MI) and polyvinyl alcohol (PVA) (PVA Foam, Cook, Inc., Bloomington, IN; Trufill, Cordis Endovascular Systems, Miami Lakes, FL; Ivalon, Inc., San Diego, CA; Contour Emboli, Boston Scientific/Target Therapeutics, Inc., Fremont, CA).2,3 Gelfoam breaks down 72 hours after embolization, and this lack of permanence detracts from its efficacy if surgery is not performed within a few days after the procedure. Gelfoam has been used as a preoperative embolization material for neoplasms that are to be operated on within 48 hours, and for patients with epistaxis in whom the goal is to slow the bleeding sufficiently so that the body’s normal hemostatic mechanisms stop the hemorrhage. Gelfoam powder always should be used with care because its particles (approximately 50 µm) in solution act as a liquid, easily passing through tiny arteries, which may result in skin necrosis or damage to cranial nerves, or through collateral channels communicating with the intracranial circulation.
PVA is more permanent than Gelfoam, but much of the efficacy of the vascular occlusion is a result of a combination of PVA plus intravascular thrombus. The stellate-shaped particles slow the intravascular flow, and thrombus forms.2–4 This thrombus may be metabolized before fibrosis occurs, however, resulting in partial or complete recanalization over weeks to months. PVA is easy to use, being supplied as uniform particles within a narrow range of size (150 to 1250 µm). In most patients with neoplasms, the smallest size (150 µm) is used because the particles can be easily injected through a small microcatheter placed selectively into tiny feeding arteries and penetrate into the tumoral vascular bed.
Because of the stellate shape of PVA particles, they do not form a tightly packed embolic mass, allowing recanalization as the interspersed thrombus undergoes lysis. Various types of beads and spheres have been produced to overcome that limitation, such as Embosphere Clear (Biosphere Medical, Inc., Rockland, MA). Their more uniform size and spherical geometry theoretically produce more complete and more permanent vascular occlusion. Similar spheres might also be filled with a chemotherapeutic or other agent for more prolonged treatment of a nonsurgical neoplasm. Microfibrillary collagen (Avitene; Avicon, Inc., Fort Worth, TX) is a hemostatic agent that may be mixed with contrast material for embolization5 or mixed with other embolic agents such as PVA and ethanol.6
There are two broad categories of metallic coils: coils that are pushed from a catheter with a metal coil pusher or guidewire, and coils that are released by breaking a bond between the coil and the pushing wire. The latter is the type used for treating intracranial aneurysms. In head and neck lesions, metallic coils are used for occluding vessels that measure a few millimeters to 1 cm or more in diameter. Their size prohibits their moving more distally into the embolized lesion. They are best used for occluding the feeding artery after particulate embolization; the particles are embolized deeply into the lesion, with the coil producing the final occlusion of the feeding artery. Coils have been used to occlude bleeding vessels, such as in epistaxis or after trauma.
Detachable balloons with a valve mechanism to keep the balloon inflated are currently unavailable in the United States, but should be available again in late 2009. They are used primarily for fistulas with a single artery-to-vein connection. Most experience was with intracranial post-traumatic carotid-cavernous sinus fistulas, but this technique was also used for vertebral artery–vertebral venous fistulas (usually post-traumatic) or for any other type of fistula in the face or neck.7–9 They were also used for occlusion of a parent artery leading to an unclippable aneurysm, a dissected carotid or vertebral artery producing embolization into intracranial vessels, or a carotid artery to be sacrificed at tumor surgery. Electrolytically detachable coils are used now instead of the currently unavailable detachable balloons. Many coils are usually necessary, however, to do what one balloon could accomplish, increasing the complexity and expense of the procedure.
There are numerous liquid embolic agents, the most commonly used being absolute alcohol (100% ethanol) and various tissue adhesives, including the cyanoacrylates and Onyx (MicroTherapeutics, Inc., Irvine, CA). Absolute ethanol is extremely toxic to the endothelium,10 and is highly effective at producing sclerosis of vascular lesions, such as venous and lymphatic malformations.11–13 Although it has also been used to treat arteriovenous malformations and dural arteriovenous fistulas, the problem with these fast-flowing lesions is the need to increase the “dwell time” of the ethanol to interact with the intima, often requiring temporary balloon occlusion more proximally. It has also been used for tumors, via endovascular and percutaneous access, particularly recurrent tumors that are surgically inaccessible.
The injection of ethanol is extremely painful, requiring deep sedation or, more commonly, general anesthesia. It is necessary to see where the embolic agent is going, and so opacification is necessary. Opacification of the ethanol with a liquid contrast agent produces dilution of the ethanol, however, decreasing its effectiveness, which is maximum if used undiluted. Metrizamide powder (Nycomed, Oslo, Norway) was used previously for opacification because a powder does not dilute the ethanol, but provides acceptable opacification. Metrizamide powder is no longer available in the United States, however.
Sodium tetradecyl sulfate (Sotradecol) 3% also is an excellent sclerosing agent, is less painful on injection than ethanol, and may be opacified, although it seems to be less effective than ethanol for venous malformations, and is not considered to be an acceptable alternative. Doxycycline, a tetracycline-like antibiotic, is an effective agent at producing sclerosis of venous, lymphatic, and other slow-flow vascular malformations in which there is an adequate “dwell time.” Tetracycline has been associated with darkening of the tooth enamel in young children, so this drug is usually reserved for patients older than 11 years, after the formation of the permanent teeth. Povidone-iodine (Betadine) can also be injected into lymphatic malformations, with less pain than with alcohol and with good success.
Cyanoacrylates such as isobutyl-2-cyanoacrylate (IBCA) or N-butyl-2-cyanoacrylate (NBCA) produce polymerization of rapidly flowing blood within seconds. They not only produce immediate thrombosis and have tissue adhesive properties, but they also initiate a giant cell inflammatory reaction of the vessel wall.14 These embolic liquids are excellent for lesions with rapidly flowing blood, such as an arteriovenous malformation or an arteriovenous fistula. Neoplasms have slow flow, so there is no need to use these agents, which are associated with more risk than particulate materials injected intra-arterially or other agents injected percutaneously.
The newest “liquid” agent is Onyx, which is an ethylene vinyl alcohol copolymer containing dimethyl sulfoxide as the agent facilitating absorption through endothelial barriers.15 This tissue adhesive is a needed new addition to the armamentarium of the neurointerventionalist because it slowly permeates into tiny vessels feeding a vascular lesion, “creeping” into these feeders during fluoroscopic visualization and control, without the rapid setup time of the cyanoacrylates.15,16
Any embolization procedure with a liquid agent should be approached with trepidation because occlusion of the end-arteries to the face, tongue, and cranial nerves may lead to necrosis, and intracranial embolization may occur as the liquid passes through tiny collateral channels to vessels feeding normal structures. Liquid embolization should be performed only when superselective catheterization can be done directly into the direct feeders to the lesion, or with percutaneous puncture of the lesion and direct visualization of the flow of the agent,17 to prevent unwanted extension to the blood supply of vital structures.
Two important techniques help to ensure the safety of vascular occlusion at the skull base. The first involves the injection of lidocaine (Xylocaine) 1% without preservatives into an arterial feeder that is considered a candidate for embolization, to predict the potential of permanent cranial nerve palsy from the embolization procedure.18 This provocative test anesthetizes the cranial nerve if there is blood supply leading to it from the vessel catheterized. Critics of this test suggest that a false-positive test may occur because a liquid anesthetic can be injected into the capillary bed, whereas particles used for embolization stop short of terminal arterioles so that devascularization is rare. It is likely that a negative test result is truly negative and reassuring.
The second provocative test is the temporary balloon occlusion test (BOT) of the internal carotid or vertebral artery, with the addition of blood flow measurement for precise quantification of the potential effects on cerebral blood flow during temporary or permanent occlusion of the artery during surgery or endovascular therapy. Carotid or vertebral artery occlusion might be necessary during the surgical removal of a skull base tumor, during the temporary occlusion of a major intracranial artery during surgical clipping of an aneurysm, for the thrombosis of an unclippable aneurysm via occlusion of the parent artery, or if carotid occlusion has to be performed to close a carotid-cavernous sinus fistula or any other type of traumatic vascular lesion.
First, a complete angiographic evaluation of all cerebral vessels is performed to evaluate their contribution to the particular lesion and the adequacy of collateral flow via the anterior and posterior communicating arteries. If communicating arteries are present, the traditional BOT is performed, consisting of occlusion of the internal carotid artery (ICA) with a nondetachable balloon catheter placed at the level of the future permanent occlusion. After systemic heparinization, the balloon is inflated, and the patient is evaluated for 30 minutes. Careful neurologic examinations are performed throughout the occlusion period, with special emphasis on the neurologic functions subserved by the vessel that is being tested. If the patient develops a neurologic deficit, the balloon is immediately deflated. If the patient has no neurologic deficit from the carotid occlusion, it is assumed that blood flow is adequate for permanent occlusion to occur. Such a qualitative test does not provide precise quantification of the blood flow to the hemisphere at risk, however. Blood flow values greater than 20 to 25 mL/100 g of tissue per minute allow normal neuronal function, with values less than that precipitating neuronal dysfunction. It is conceivable that blood flow values slightly greater than 20 to 25 mL/100 g/min would leave the patient without symptoms while on the angiography table, but superimposed intraoperative or postoperative hypotension, decreased cardiac output, or decreased oxygenation might precipitate cerebral infarction.
Different methods have been used during temporary occlusion to evaluate the physiologic effects of the BOT on cerebral blood flow to predict the risk of cerebral infarction after definitive occlusion. These methods include electric studies such as evoked potentials or electroencephalography,19 measurements of arterial stump pressures distal to the site of temporary occlusion,20 induced hypotensive challenges, and transcranial Doppler studies. Also, several cerebral blood flow imaging methods, including xenon-enhanced CT (Fig. 136-1),21 single photon emission computed tomography (SPECT), positron emission tomography, and MRI and CT perfusion studies, have been used to evaluate cerebral blood flow during BOT to determine the potential risk of ischemia after permanent occlusion.22,23 We prefer to use SPECT because it adds little to the basic BOT and easily provides the needed information. After the balloon has been inflated for a short time, the radionuclide is injected intravenously, and the patient is scanned a few hours after the completion of the angiographic study (the radiopharmaceutical “sticks” to the brain tissue during its initial circulation in proportion to the blood flow to that tissue).
Figure 136-1. Xenon-enhanced CT during balloon test occlusion. This 60-year-old patient with squamous cell carcinoma invading the skull base was to undergo skull base resection and probable permanent carotid occlusion. A Swan-Ganz catheter was placed in the right internal carotid artery. Temporary blockage of the internal carotid flow for 15 minutes did not produce neurologic deficit. A, Xenon-enhanced CT scan for the production of a blood flow map (left) at the midventricular level (right) during balloon deflation reveals symmetric flows to the middle cerebral artery distributions bilaterally. B, With the balloon inflated, there is a marked reduction in the blood flow to the right middle cerebral distribution (left) relative to the left middle cerebral distribution. Flows to the right middle cerebral distribution are approximately 22 mL/100 g/min. This case was early in the authors’ experience, and a bypass procedure was not performed after permanent carotid occlusion during the skull base tumor resection. C, Postoperatively, the patient became mildly hypotensive, resulting in infarction in the distribution predicted by the temporary carotid occlusion blood flow test.
Nevertheless, these techniques have turned out to be imperfect predictors of the ischemic risk associated with permanent carotid occlusion. Clinical deficits have been reported after permanent occlusion, even when there has been a negative BOT with accompanying normal physiologic or cerebral blood flow studies. Many, if not most, of these postocclusion deficits probably are a result of marginal cerebral perfusion accompanied by hypotension or decreased cardiac output, clot propagation from the residual stump, or de novo emboli at the time of vascular occlusion.
Paragangliomas, also known as chemodectomas or glomus tumors, are neoplasms related to chemoreceptor tissue. They usually are benign, but locally invasive and highly vascularized. Most glomus tumors originate within the temporal bone (48%), including lesions along the promontory of the middle ear (glomus tympanicum tumors) and lesions related to chemoreceptor tissue in the jugular bulb (glomus jugulare tumors). Tumors related to the vagus body (11%) in the high cervical region are called glomus vagale tumors, and tumors related to the carotid body (35%) at the common carotid artery bifurcation in the neck are called carotid body tumors. Multiple tumors are found in approximately 10% of patients (Fig. 136-2), and a familial form exists.24
Figure 136-2. Multiple chemodectomas. This 38-year-old woman was one of many members of a family with chemodectomas. There is a small glomus jugulare tumor (straight arrow), a glomus vagale tumor (curved arrow), and extension of tumor along the carotid sheath to end in a carotid body tumor (arrowhead).
The glomus tympanicum is a tiny tumor that usually manifests with pulsatile tinnitus and otoscopically is seen as a reddish blue mass behind the tympanic membrane. CT scanning allows the differentiation of this small tumor from an extension into the middle ear cavity of a larger glomus jugulare tumor. It also is necessary to exclude an aberrant ICA. In the former, the bony plate between the jugular foramen and the middle ear is destroyed, whereas in the latter, the posterior bony margin of the carotid canal is missing.25 This tumor is usually small enough for surgery to be performed without embolization.
A patient with a glomus jugulare tumor usually presents with dysfunction of cranial nerves IX, X, or XI, and XII if the tumor is large. Pulsatile tinnitus also is common. Contrast-enhanced CT or MRI usually is the first diagnostic test performed, with the diagnosis generally made and the extension of the tumor shown. The tumor begins in the region of the jugular foramen and may extend inferiorly into the upper neck, superolaterally into the middle ear by destroying bone, posteromedially and posterolaterally into the posterior fossa, and anteriorly to envelop the petrous ICA. Bone destruction can be extensive, simulating a malignant tumor, as the chemodectoma spreads through the skull base. Destruction around the foramen magnum may occur, with compression of the brainstem.26
The tumor is fed by multiple external carotid artery (ECA) branches, with each of these arteries feeding a specific compartment of tumor. The ascending pharyngeal (bilaterally at times) and middle meningeal (posterior division) arteries are the most commonly involved, with the stylomastoid branch of the occipital and the posterior auricular arteries providing supply less frequently (Fig. 136-3). If the tumor extends posteriorly around the foramen magnum, supply may be from the anterior and posterior meningeal branches of the vertebral artery. Intradural tumor within the posterior fossa may be fed from the anterior and posterior inferior cerebellar arteries. Tumor surrounding the high cervical or petrous portions of an ICA may parasitize tiny branches of these segments (see Fig. 136-3).27–29