Fig. 14.1
(a) CT scan shows hemorrhagic PA extending locally to the suprasellar cisterns. (b) Postoperative CT scan after pituitary removal
When SAH is secondary to a preexisting intracranial aneurysm, it can produce a pituitary apoplexy when the rupture of the aneurysm is into the pituitary tumor (Suzuki et al. 2001; Sasagawa et al. 2012); this condition can occur in large aneurysms of ICA and ACoA that extend into the pituitary gland. SAH is an uncommon complication in cases of cavernous carotid artery (CCA) aneurysms (German and Black 1965; Kupersmith et al. 1984; Vasconcellos et al. 2009). Spontaneous thrombosis of ICA due to vascular compression is the most frequent complication in patients with aneurysm of CCA, most commonly in cases of giant aneurysms (Kupersmith 1993; Stiebel-Kalish et al. 2005). In the situation of a rupture of aneurysm of CCA it can present in different ways, as massive epistaxis (Davies et al. 2011) or as an acute cavernous sinus syndrome (Fernández-Real et al. 1994). In both cases an endovascular procedure is the best treatment option.
14.3 Pituitary Adenomas and Intracranial Aneurysms
In 1912, Dr. Harvey Cushing was the first to suggest a possible association between intrasellar aneurysms and pituitary neoplasms (Cushing 1912). This relationship is frequently described in the recent literature (Handa et al. 1976; Wakai et al. 1979; Mangiardi et al. 1983; Weir 1992; Borges et al. 2006; Locatelli et al. 2008; Wang et al. 2009). In the clinical series reported by Wakai et al. (1979), the incidence of aneurysms associated with 95 pituitary tumors was 7.4 %. In a more recent retrospective study (Pant et al. 1997) of 467 cases of pituitary adenomas, the incidence of associated intracranial aneurysms was 5.4 %. In general, the consensus is that the incidence of an intracranial aneurysm associated with pituitary adenomas is low (Nakagawa and Hashi 1994) from 3.7 to 7.4 % (Housepian and Pool 1958; Pant et al. 1997), and it is more common than with other intracranial tumors (1.1 %).
Regarding the location of intracranial aneurysms that coexists with a pituitary tumor, the ICA and the ACoA are the most frequent arteries affected because they supply the pituitary region (Locatelli et al. 2008). In one retrospective study (Pant et al. 1997), 48 % of intracranial aneurysms associated with pituitary adenoma were observed in the cavernous segment of the ICA artery followed by ICA-ophthalmic aneurysms in 19 % and ICA bifurcation in 13 %. Moreover, 60 % of aneurysms are near the parasellar region and 40 % at distant locations (Pant et al. 1997).
Several hypotheses to explain the association of aneurysm and pituitary adenoma have been proponed. A radiation-induced arterial damage, in cases where radiation was used to treat pituitary adenomas, has been suggested (Bulsara et al. 2007), which leads to loss of arterial muscle with necrosis and fibrosis of the tunica intima and media, thus causing dilation of the arterial walls. Different studies have also attempted to link the coexistence of pituitary adenomas and intracranial aneurysms to mechanical factors. In their study of 116 cases (Pia et al. 1972) reported that microanatomical changes in the cerebral circulation secondary to compression or traction might lead to increase in blood flow and aneurysmal formation. Recently, a series of 800 patients who underwent transsphenoidal surgery for pituitary apoplexy was reported and concluded that the existence of a cavernous sinus invasion was correlated with an increased incidence of intracranial aneurysms in patients with pituitary adenoma (Oh et al. 2012). Hormonal and microcirculatory influences have also been proposed as a major etiological factor. There have been many studies with growth hormone pituitary adenomas and intracranial aneurysms (Acqui et al. 1987). They studied 62 cases of pituitary adenomas and intracranial aneurysms and stated that mechanical, microcirculatory, and hormonal factors, especially growth hormone, play an important role in the formation of intracranial aneurysms (Acqui et al. 1987). In their review of the literature, they reported that 50 % of the pituitary adenomas associated with intracranial aneurysms were growth hormone secreting (Acqui et al. 1987).
Large or giant ICA aneurysms, in association or not with a pituitary adenoma, have been previously documented to mimic pituitary tumors and pituitary apoplexy (Arseni et al. 1970; Raymond and Tew 1978; Mangiardi et al. 1983; Mindel et al. 1983; Weir 1992; Borges et al. 2006), especially when they expand to the sellar and suprasellar area. This situation can suppose a tremendous risk to the patient, particularly when the aneurysm lies near the operative field (Pant et al. 1997). There is a recent review the literature regarding cerebral aneurysm with sellar extension (Hanak et al. 2012). The most common artery of origin for intrasellar aneurysms was the ICA, which gave rise to 90 % of reported aneurysms, with the remaining 10 % originating from the ACoA.
14.4 Carotid Artery Aneurysms
14.4.1 Aneurysmal Classification
ICA aneurysms can expand to the sellar region mimicking a pituitary adenoma or pituitary apoplexy depending on their clinical presentation. There are two primary growth patterns by which aneurysms extend into the sellar region: (1) infradiaphragmatic, extends medially through the cavernous sinus dura and under the diaphragma sellae, and (2) supradiaphragmatic, extends inferomedially from above the diaphragma sellae (Hanak et al. 2012). The majority of infradiaphragmatic aneurysms are considered “cavernous segment” ICA aneurysms in the literature (Kupersmith et al. 1992; Hahn et al. 2000; Stiebel-Kalish et al. 2005; Kasliwal et al. 2008; Davies et al. 2011). Nevertheless, recent studies (Hanak et al. 2012) concluded that the clinoid ICA segment is the most frequent origin for these aneurysms, extending into the sella turcica through the thin medial cavernous sinus wall. These aneurysms tend to be smaller at the time of presentation than supradiaphragmatic ones (Fig. 14.2), because extensive growth is greatly limited by the dural and bony confines of the sella turcica (Table 14.1).
Fig. 14.2
MRI T1 sequence shows a small medial clinoid aneurysm compressing the pituitary stalk
Table 14.1
Sellar aneurysm classification
Infradiaphragmatic | Supradiaphragmatic | |
|---|---|---|
Location | Cavernous or clinoidal | Sup. hypophysial or ACoA |
Size | Small to large | Large to giant |
Thrombosed wall | (++) | (+) |
Rupture/SAH | (−) | (+) |
ICA thrombosis | (+) | (−) |
Supradiaphragmatic intrasellar aneurysms are typically large or giant superior hypophysial aneurysms that grow into the suprasellar space (Fig. 14.3a, b). With enlargement, they depress the diaphragma sellae into the pituitary fossa but do not generally erode through this membrane to contact the actual pituitary gland itself.
Fig. 14.3
(a) CT scan demonstrates a giant carotid aneurysm with sellar/suprasellar extension. Calcification is demonstrated on the aneurysm wall. (b) Carotid angiography shows a giant superior hypophysial artery aneurysm
Occasionally, large inferiorly projecting ACoA aneurysms can extend anteriorly and inferiorly into the sella turcica, displacing the diaphragma sellae downwards. Whereas they do not originate in the ICA artery, they are considered supradiaphragmatic aneurysms with extension to the sella (Hanak et al. 2012), both the ICA and ACoA artery aneurysms. Aneurysms of CCA typically reach very large or giant proportions before extending into the sella turcica (Lemole et al. 2000; Wang et al. 2009; Szmuda and Sloniewski 2011).
14.4.2 Epidemiology and Clinical Presentation
14.4.2.1 Infradiaphragmatic Aneurysms
Infradiaphragmatic aneurysms represent approximately 3–5 % of all intracranial aneurysms and 15 % of those originated in the ICA (German and Black 1965). Aneurysms of CCA can arise from any segment of cavernous ICA, most commonly in the horizontal segment (Goldenberg-Cohen et al. 2004). Morbidity and mortality indices of aneurysms of CCA are low; however, pain and neuro-ophthalmologic deficits due to neurovascular compression are frequent (Roederer et al 1984; Seckhar and Heros 1981; Wiebers et al. 2003). Spontaneous thrombosis of ICA is a complication in patients with aneurysm of CCA, frequently associated with giant aneurysm (Kupersmith 1993; Barth and de Tribolet 1994; Stiebel-Kalish et al. 2005; Hahn et al. 1992; Krings et al. 2005), due to vascular compression (Fig. 14.4a–c). The occlusion of ICA can be a dangerous complication to patients without a patent collateral circulation (Autret et al. 1987; Linskey et al. 1990; Van der Zwan et al. 1992; Vasconcellos et al. 2009; Busuttil et al. 1981; Juvela et al. 2005; O’Donell et al. 1985; Reilly et al. 1983) manifested as an ischaemic scenario, with a devastating cerebrovascular accident, or results in spontaneous therapeutic with a patent collateral circulation.
Fig. 14.4
(a) CT scan shows a large round hyperdense lesion centered in the left cavernous sinus. (b) Angio-CT demonstrates a giant partially thrombosed CCA with a small area of contrast enhancement. (c) MRI identifies a giant CCA complicated with an acute spontaneous thrombosis extending to the sellar area and compressing the pituitary gland
In an uncommon event a giant and thrombosed sellar aneurysm of CCA can present an acute expansion causing a compression of the residual pituitary gland and the cavernous sinus. This situation can manifest as a pituitary apoplexy: acute hypopituitarism, headache, and ophthalmoplegia (Torres et al. 2009). The intrasellar compression might inflict direct tissue damage to the pituitary gland or stalk or instigate ischemic changes attributable to compression of the superior hypophysial arteries and/or meningohypophysial trunk, thereby presenting the symptoms of pituitary apoplexy.
Aneurysms of CCA rarely present with a SAH, due to the fact that cavernous sinus is composed by dural slices, which lay over the body of the sphenoid bone and are, infrequently, projected towards the subarachnoid space (German and Black 1965; Kupersmith et al. 1984). In the unfortunate situation of a rupture of aneurysm of CCA, it can present in different ways. A massive epistaxis can be the clinical manifestation of a rupture of aneurysm of CCA that can be managed with endovascular ablation technique of the feeding ICA (Davies et al. 2011). An atypical case was reported by Fernández-Real et al. (1994) of a patient harboring a giant ICA that presented with a SAH, left ophthalmoplegia, and left hemiparesis. The MRI showed a giant ICA aneurysm ruptured into the cavernous sinus. Again an endovascular procedure is the best option to treat this critical situation.
Symptoms of neurovascular compression are frequently associated to aneurysms of CCA (Lees et al. 1984; Locksley 1966; McCormick and Acosta-Rua 1979), being the most prevalent diplopia due to the cranial nerve VI lesions (Vasconcellos et al. 2009). The association with other cranial nerves (III, IV, V1, and V2) located in the lateral wall of the cavernous sinus characterizes the complete cavernous sinus syndrome (Stiebel-Kalish et al. 2005).
Medial clinoid ICA aneurysms have been recently considered infradiaphragmatic aneurysms (Hanak et al. 2012). The clinoid ICA segment ascends beneath and just medial to the anterior clinoid process before passing through the dural ring to enter the subarachnoid space; this curvature places a hemodynamic vector on the medial surface of the carotid artery aimed toward the contents of the sella turcica. Aneurysms in this region presumably arise in association with small branches that supply the parasellar dura or pituitary gland. Termed “medial variant clinoid segment aneurysms,” these lesions expand into the confines of the sella turcica normally occupied by the pituitary gland and, with sufficient enlargement, cause compression of the gland and resultant hypopituitarism. On rare occasions (similar to aneurysms of CCA), these lesions can rupture into the pituitary fossa, creating a clinical picture similar to pituitary apoplexy (Hanak et al. 2012).
14.4.2.2 Supradiaphragmatic Aneurysms
Supradiaphragmatic ICA aneurysms are typically giant superior hypophysial aneurysms that grow into the suprasellar area. They are a subset of ophthalmic segment aneurysms that arise from the ventromedial wall of the ICA just after it becomes intradural. Because the dural ring slants from lateral to medial (higher laterally), a small diverticulum of CSF is evident medially, termed the carotid cave, from which the most proximal superior hypophysial arteries originate.
Occasionally, large inferiorly projecting ACoA aneurysms can extend anteriorly into the sella turcica, usually in association with long optic nerves and postfixed chiasms, an anatomical situation that allows the aneurysm to reach the sella by displacing the diaphragma sellae downward.
Both superior hypophysial aneurysms and inferiorly projecting ACoA aneurysms are more likely to present with visual field cuts and/or decreased visual acuity than infradiaphragmatic aneurysms (Hanak et al. 2012). Hypopituitarism (due to mass effect on the hypothalamo-pituitary axis or the pituitary gland itself) is reported in the literature (Cartlidge and Shaw 1972; Heshmati et al. 2001; Tungaria et al. 2011; Lawson et al. 2008). Among 4,087 patients with hypopituitarism, an intrasellar aneurysm was observed in only seven patients (0.17 %) (Hanak et al. 2012). The patients reported in the literature usually have additional neurological/visual deficits secondary to brain or visual pathway compression (Cartlidge and Shaw 1972; Ooi and Russell 1986; Fernández-Real et al. 1994; Ray et al. 2002; Gondim et al. 2004; Fujii et al. 2008; Kasliwal et al. 2008). Pituitary dysfunction due to an ICA aneurysm involves the pituitary-gonadal axis, followed by the pituitary-adrenal and pituitary-thyroid axis (Tungaria et al. 2011). Diabetes insipidus and pituitary stalk compression causing elevated serum prolactin levels is a rare event (Heshmati et al. 2001). A detailed list of symptoms is shown in Table 14.2.
Table 14.2
Aneurysmal symptoms
Mass effect symptoms | Vascular symptoms |
|---|---|
Hypopituitarism | Spontaneous thrombosis ICA |
Diabetes insipidus | Embolic/ischemic events |
Pituitary stalk effect | Rupture and SAH |
Neuro-ophthalmologic deficit | Rupture and CSS |
Visual pathway defect | Rupture and pituitary apoplexy |
14.4.3 Neuroradiological Appearances
Aneurysms of the cavernous/medial clinoid and supraclinoid ICA make up nearly 5 and 15 %, respectively, of all intracranial aneurysms. When they are large to giant, they can present as masses in the sellar and parasellar region and may compress the contents of the cavernous sinus, optic chiasm, and pituitary gland.
Although the neuroradiological diagnosis is usually done with carotid arteriogram or computed tomography (CT) angiography, in cases where the patient presents a clinical syndrome of pituitary apoplexy (headache, vomit, and visual impairment), a CT scan or cranial MRI is the first radiological image obtained in order to rule out a pituitary tumor. Special attention has to be paid to the radiological findings on CT scan and cranial MRI not to misdiagnose an aneurysm as a pituitary apoplexy or a pituitary adenoma.
CT scan may show erosion of the adjacent bony wall around the cavernous sinus, with circumferential or lamellar calcification within the wall of the aneurysm. In a non-thrombosed giant aneurysm on CT, the mass intensely enhances following contrast administration, and this represents the true lumen of the aneurysm (Fig. 14.5a–d). This may simulate the appearance of other masses in the sellar/parasellar region as pituitary macroadenomas. If the aneurysm is partially thrombosed, a focal area on enhancement surrounded by a low-density area is shown (Eisenberg and Al-Mefty 2000).
