19 Cavernous Carotid Artery Aneurysms
Abstract
Cavernous carotid aneurysms (CCAs) account for 2 to 9% of all intracranial aneurysms. Their position in the extradural space and within dural walls limits their growth and risk of rupture. The majority of CCAs are asymptomatic. If CCAs are large, patients can present with cranial nerve palsies, and if CCAs are ruptured, patients can present with carotid-cavernous fistula, severe epistaxis, or occasionally with subarachnoid hemorrhage. CCAs are generally considered to be lower-risk aneurysms compared to other intracranial aneurysms. Digital subtraction angiography is the gold standard for aneurysm visualization and characterization. Small asymptomatic CCAs should remain under observation. Large or giant CCAs with irregular features, extending into subarachnoid space, bony erosion, or documented growth should be considered for treatment. Symptomatic and ruptured CCAs must be treated. Endovascular procedures have become the preferred method of treatment, including coiling, stent-assisted coiling, flow diversion, or parent vessel occlusion. Flow diversion has become the first-line therapy for most CCAs. Nowadays, open cerebrovascular techniques are rarely used. Complete obliteration rates with flow diversion are 66 to 100%, with a recent meta-analysis demonstrating an occlusion rate of 76%.
Introduction
Cavernous carotid aneurysms (CCAs) are located within the cavernous segment of the internal carotid artery (ICA). According to Bouthillier′s classification, the cavernous segment begins at the petrolingual ligament and extends to the proximal dural ring. CCAs account for 2 to 9% of all intracranial aneurysms, with a high proportion of wide-necked aneurysms. Their position in the extradural space of the cavernous sinus, with the dural walls isolating the cavernous segment from the brain, limits growth and lowers the risk of rupture. However, their proximity to multiple cranial nerves can lead to mass effect symptoms. When a rupture does occur, CCAs can present with carotid-cavernous fistulas, severe epistaxis, or, in rare cases, subarachnoid hemorrhage (SAH). The location of the cavernous ICA within the cavernous sinus relative to several cranial nerves and postganglionic sympathetic fibers makes CCAs difficult to manipulate via microsurgical techniques. Therefore, endovascular procedures have become the preferred method of treatment, most notably with flow diversion devices such as the Pipeline Embolization Device (PED; eV3). Given the current widespread acceptance of flow diversion as a first-line therapy for most CCAs, this chapter will focus on the details of this approach.
Major controversies in decision making addressed in this chapter include:
Whether or not treatment is indicated.
Open versus endovascular treatment for ruptured and unruptured cavernous ICA aneurysms.
The role of flow diversion stents and other endovascular techniques.
Whether an advanced surgical technique is indicated (ICA sacrifice and bypass) and, if so, when.
Whether to Treat
CCAs are generally considered to be lower-risk aneurysms compared with other intracranial aneurysms, with an estimated cumulative annual risk of rupture of 0 to 1.6% and a reported cumulative annual risk of SAH of 0.2 to 0.4%. According to the International Study of Unruptured Intracranial Aneurysms (ISUIA), the 5-year cumulative rupture rate for CCAs with no previous history of SAH is 0% for aneurysms less than 7 mm, 0% for aneurysms 7 to 12 mm, 3% for aneurysms 13 to 24 mm, and 6.4% for aneurysms larger than 25 mm. Therefore, the decision making for CCAs relies heavily on the presence of symptoms, size, and rupture status of the aneurysm ( 1 –5 in algorithm ). In general, unruptured asymptomatic CCAs should be handled on a case-by-case basis, with the morphology and size of the aneurysm taken into consideration along with serial imaging results. Small asymptomatic CCAs should remain under observation ( 2 in algorithm ). Large or giant aneurysms with irregular features or extension into the subarachnoid space, bony erosion, or lesions exhibiting significant growth over interval imaging should be considered for treatment ( 3 in algorithm ). Patients with ruptured CCAs who present with either SAH or carotid-cavernous fistulas should be treated to preserve the function of the proximate cranial nerves and prevent future repeated rupture ( 4 in algorithm ). Most cases will require formal angiography for definitive diagnosis, with treatment often carried out in the same setting. Patients with unruptured symptomatic CCAs may present with cranial nerve palsies affecting vision (e.g., diplopia and blurred vision), headaches, facial pain and numbness, and embolic complications. These symptoms can be secondary to both mass effect and acute thrombotic changes. Patients with unruptured CCAs who present with intolerable symptoms should be considered for treatment ( 5 in algorithm ).
Anatomical Considerations
CCAs form on the cavernous segment of the ICA, which is located within the extradural space of the cavernous sinus, bounded anteriorly by the superior ophthalmic fissure and posteriorly by the petrous apex. The cavernous segment sits adjacent to several cranial nerves, most notably cranial nerves II, III, V, and VI. Thus, CCAs may present with cranial neuropathy as a result of mass effect or arterial pulsations. The orientation of the segment within the ICA is superior to the petrous segment and inferior to the supraclinoid segment. After passing through the carotid bifurcation and petrous segment, blood flows through the foramen lacerum, exits the skull, and passes the petrolingual ligament before entering the cavernous segment known as the C4 segment in Bouthillier′s classification. This segment is one of the few to feature nonmajor separate branches, supplying the posterior pituitary and portions of the clivus, cranial nerves III, IV, V, and VI, pituitary gland, tentorium cerebelli, and adjacent dura. The meningohypophyseal trunk consists of the lateral tentorial artery, marginal tentorial artery, inferior hypophyseal artery, and lateral clival artery. This branch of the cavernous segment is easily seen on angiographic imaging. The inferolateral trunk, which arises from the lateral aspect of the cavernous segment, supplies adjacent dura and cranial nerves and has extensive anastomoses with the extracranial circulation.
Workup
Clinical Evaluation
Although most CCAs are discovered incidentally during diagnostic imaging for other indications, some may produce intolerable symptoms. Patients with symptomatic CCAs commonly present with cranial nerve palsies, including symptoms such as diplopia, decreased visual sharpness, and facial pain or loss of sensation. Very rarely are these aneurysms discovered because of rupture or SAH.
Imaging
Initial noninvasive imaging workup typically consists of computed tomography angiography (CTA) or magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA). Digital subtraction angiography, combined with three-dimensional rotational angiography, is the gold standard for aneurysm visualization. Computed tomography (CT) without contrast allows for identification of SAH.
Differential Diagnosis
The differential diagnosis for CCAs depends largely on the imaging method. On studies without contrast, large space-occupying lesions in the region of the cavernous segment of the ICA or the cavernous sinus can include primary or metastatic neoplasms. Opacification on CTA in the region of the cavernous segment can also represent a carotid-cavernous fistula.
Treatment
Choice of Treatment and the Influence of Intracerebral Hematoma
Small unruptured CCAs are generally managed conservatively ( 2 in algorithm ). For patients with large or giant asymptomatic CCAs requiring treatment and for patients with symptomatic unruptured CCAs who have no contraindications to dual antiplatelet therapy, flow diversion should be considered as the first-line treatment ( 3, 6 in algorithm ). If dual antiplatelet therapy is contraindicated, a balloon test should be performed ( 7 in algorithm ). Surgical ligation or coiling should be considered if the test indicates tolerance for carotid artery occlusion ( 8 in algorithm ); bypass surgery should be considered for patients unable to tolerate the test occlusion ( 9 in algorithm ). Given that CCAs rarely present with intracranial or intracerebral hemorrhage/hematoma, this is seldom a consideration in the choice of treatment.
Conservative Management
Most asymptomatic unruptured CCAs are found incidentally during noninvasive imaging for other disorders. Decisions on management must take into account the natural history and etiology of the aneurysm, patient age and smoking history, and risk to the patient. Because of their low risk of rupture, asymptomatic aneurysms smaller than 13 mm are managed conservatively with periodic follow-up imaging, most commonly angiography and MRI, to monitor growth ( 2 in algorithm ). Asymptomatic CCAs 13 mm or larger may be kept under observation or flow diversion may be considered ( 3 in algorithm ).
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