Microsurgery of Paraclinoid Aneurysms

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CHAPTER 366 Microsurgery of Paraclinoid Aneurysms

Rose Du, Arthur L. Day

Paraclinoid aneurysms are defined as aneurysms arising from the internal carotid artery (ICA) in close proximity to the anterior clinoid process. Using the broadest definition, such aneurysms could include those arising from the intracavernous, clinoidal, ophthalmic, and posterior communicating ICA segments.1–3 The ensuing chapter, however, addresses only those lesions arising beyond the venous lumen of the cavernous sinus and proximal to the origin of the posterior communicating artery—the clinoidal and ophthalmic segments. More proximal and distal aneurysm variants are discussed in other chapters.

The complex relationship of the vascular, neural, dural, and osseous structures surrounding the paraclinoid aneurysm often makes operative obliteration challenging. With experience and proper understanding of these relationships, however, most can be treated surgically with very reasonable risks.

Anatomy

Osseous Anatomy

The anterior clinoid process (ACP), formed by the medial extension of the lesser wing of the sphenoid bone, provides a bony roof to the superior orbital fissure (SOF) and the anterior cavernous sinus (Fig. 366-1). The optic strut extends from the inferomedial surface of the ACP to the body of the sphenoid bone, separating the optic canal from the SOF. The ACP and optic strut define and obstruct access to the anterior and lateral borders of the ascending ICA as it exits the cavernous sinus to enter the subarachnoid space.

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FIGURE 366-1 Paraclinoid osseous anatomy, dorsal (A) and posterior oblique (B) views. The anterior clinoid process (ACP) is the most medial extension of the lesser wing of the sphenoid bone. The ACP provides a bony boundary to many structures in the region, including a roof to the superior orbital fissure (SOF), an anterolateral border to the clinoidal segment (ClinSeg) of the internal carotid artery (ICA), and an anterolateral margin to the superior aspect of the cavernous sinus. The optic strut (OS) extends from the inferomedial surface of the ACP to the body of the sphenoid body, and separates the optic canal (OpCan) superomedially from the SOF inferolaterally. DS, dorsum sella.

The superomedial portion of the ACP is connected to the planum sphenoidale by the roof of the optic canal, the most posterior portion of which is formed by a dural fold called the falciform ligament. The anterior clinoid process is thus connected to the skull at three main points: the medial aspect of the lesser sphenoid wing, the optic strut, and the roof of the optic canal.

Dural Anatomy

The relevant dural structures in this region represent dural reflections off the ACP, which primarily include the falciform ligament, the (distal) dural ring, and the carotid-oculomotor membrane (COM; Fig. 366-2).4 The dural ring represents the circular point of attachment of the dura to the ICA as the vessel penetrates the dura to enter the subarachnoid space. This dural attachment extends radially from the ICA and is continuous with the periosteum covering the superomedial aspect of the anterior clinoid process, the diaphragma sella, and the floor of the optic canal.5–9 The plane of the dural ring slopes downward from anterior-to-posterior and lateral-to-medial directions. The subarachnoid space diverticulum medial to the ICA created by this slant is called the carotid cave.6–10 The COM is formed by dura from the inferior surface of the ACP that extends from the ICA medially to the oculomotor nerve laterally.4 This membrane marks the point of exit of the ICA from the cavernous sinus main lumen.

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FIGURE 366-2 Paraclinoid dural, vascular, and neural anatomy (schematic): lateral (A), dorsal (B), and anteroposterior (C) views. The cavernous segment (CavSeg), clinoidal segment (ClinSeg), and ophthalmic segment (OphSeg) of the internal carotid artery (ICA) are all in close proximity to the anterior clinoid process (ACP). The CavSeg lies within the venous channels of the cavernous sinus. The ClinSeg has an interdural location between the dural ring (DR) and the carotid-oculomotor membrane (COM). The OphSeg is entirely subarachnoid. Note the paraclinoid branches of the ICA: (1) the ophthalmic artery (OphArt), which arises just past the dural ring and projects beneath the optic nerve (ON) as it travels to the orbit; and (2) the superior hypophyseal artery (SupHypArt), which arises distal to the OphArt along the medial aspect of the OphSeg projecting to the pituitary gland. Note also the location of the oculomotor (III), trochlear (IV), and first division of the trigeminal (V1) nerves within the lateral sinus wall, and the abducens nerve (VI) within the venous lumen. AChorArt, anterior choroidal artery; CavSin, cavernous sinus; PComArt, posterior communicating artery; PetSeg, petrous segment; Pit, pituitary gland.

Neural Structures

The cranial nerves within the cavernous sinus (CN III, IV, V, and VI) are rarely clinically affected by paraclinoid aneurysms because these lesions generally project superiorly or medially away from the superior orbital fissure and lateral cavernous sinus wall (see Fig. 366-2). Nonetheless, their close proximity to the ACP makes knowledge of their anatomy mandatory so as to avoid injury during its removal.

The oculomotor nerve is located within the superior lateral cavernous sinus wall and courses anteriorly just beneath the ACP to enter the orbit through the SOF. The trochlear nerve is also located within the lateral cavernous sinus wall, traveling just beneath and parallel to the oculomotor nerve. The first division of the trigeminal nerve (V1) courses several millimeters below the oculomotor and trochlear nerves within the lateral sinus wall, whereas the abducens nerve courses within the cavernous venous compartment between the cavernous segment and V1. Finally, sympathetic fiber bundles course as a plexus along the cavernous and clinoidal ICA, eventually departing the ICA proximal to the dural ring to project into the orbit. Disruption of these fibers can occur from operative manipulation of the clinoidal segment, causing mild postoperative ptosis or miosis without facial anhidrosis.

In contrast, the optic nerves and chiasm are often directly in line with aneurysm expansion and are commonly distorted by aneurysms arising from this region. The optic nerve courses posteriorly and medially from the back of the globe, runs through the optic canal, and then enters the subarachnoid space superior and medial to the ICA. At the posterior end of the optic canal, the optic nerve is bounded superiorly by the falciform ligament. Most of the floor of the posterior optic canal is created by the optic strut. Both the falciform ligament and the optic strut may play important roles in the production of visual loss, either by the aneurysm itself or during the surgical procedure for aneurysm obliteration. The specific types of visual deficits created by lesions in this region and their relationships to these structures are discussed later in this chapter.

Vascular Structures

Arterial Segments

The paraclinoid ICA is herein composed of two regions—the clinoidal and ophthalmic segments (see Fig. 366-2).11 The clinoidal segment, the distal portion of the anterior ascending vertical segment of the cavernous carotid artery, is located below and medial to the ACP, above the major venous lumen of the cavernous sinus. This region is a transitional ICA segment found between the COM and the dural ring.4,9,10 The clinoidal segment is located neither within the venous channels of the cavernous sinus nor within the subarachnoid space, and is essentially “interdural.”4,9,10 The ophthalmic segment, the distal portion of the paraclinoid ICA region, lies entirely within the subarachnoid space above and medial to the ACP. Beginning at the dural ring, the ophthalmic segment extends to the origin of the posterior communicating artery, and generally represents the longest subarachnoid ICA segment.11

Arterial Bends and Branches

Saccular aneurysms typically form at points of hemodynamic stress where a bend in the vessel and a branch site coincide.12 Two major bends in the paraclinoid ICA region predispose this region to aneurysm formation. The first bend, seen best on lateral angiogram, is the posteriorly projecting turn that begins at the anterior genu of the cavernous segment and continues as the vessel ascends through the dural ring. This bend creates a strong superior vector on the anterior and dorsal wall of the clinoidal and ophthalmic segments. A less conspicuous second bend, seen best from an anteroposterior or dorsal view, is the gentle lateral-to-medial-to-lateral curve beginning at the anterior genu of the cavernous segment and continuing as the ICA travels toward its terminal bifurcation. This medially projecting hemodynamic vector places significant stress upon the medial aspect of the clinoidal and ophthalmic ICA segments.

The ophthalmic segment harbors several prominent arterial branches that predispose this region to aneurysm formation. The ophthalmic artery is the most prominent and clinically significant branch, and typically arises from the dorsomedial carotid surface just above the dural ring and below the inferolateral portion of the optic nerve.13,14 This branch projects anterolaterally to run through the optic canal beneath the optic nerve, and supplies the optic nerve through perforating branches and the retina through the central retinal artery. The superior hypophyseal artery is the second major branch (or series of branches), usually arising from the medial or inferomedial ICA surface just distal to the dural ring, medial and unrelated to the take-off of the ophthalmic artery along the medial-to-lateral ICA bend within the ophthalmic segment.15,16 This vessel projects medially to supply the superior aspect of the pituitary stalk and gland, a portion of the cavernous sinus dura, and the posterior optic nerve and chiasm.

The clinoidal segment is usually devoid of named arterial perforators. On occasion, however, the ophthalmic or superior hypophyseal arteries originate from this segment, typically reaching their end organs through alternate anatomic pathways. The ophthalmic artery, for example, can originate from the distal cavernous segment or clinoidal segment in up to 10% of cadaveric specimens, usually entering the orbit through the SOF or an orifice within the optic strut.4,17,18

Aneurysm Classification

Paraclinoid aneurysms are classified according to the segment of origin of the aneurysm into clinoidal or ophthalmic segment types. Each segment has several subtypes or variants. The classification of aneurysms into their respective subtypes has important implications for the management of and operative approach to the aneurysm.

Clinoidal Segment Aneurysms

Two clinoidal segment aneurysm variants can be differentiated according to their site of origin, direction of projection, and relationships to arterial bends and branches and the adjacent dural and osseous structures within the segment (Fig. 366-3).

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FIGURE 366-3 Clinoidal segment (ClinSeg) aneurysm types (schematic): lateral (A), dorsal (B), and anteroposterior (C) views. D, Anterolateral variant of ClinSeg aneurysm: arteriogram (anteroposterior [top left], lateral [top right], and three-dimensional [bottom left] views) and axial magnetic resonance image (bottom right). E, Medial variant ClinSeg aneurysm: arteriogram (anteroposterior [top left], lateral [top right], and three-dimensional bottom left views) and coronal computed tomographic angiography (bottom right). Anterolateral variant ClinSeg aneurysms (hatched area 1) originate from the dorsolateral aspect of the ClinSeg and project toward the anterior clinoid process (ACP), whereas medial variant ClinSeg aneurysms (hatched area 2) originate from the medial aspect of the ClinSeg and project toward the sella. Small ClinSeg aneurysms (<1 cm) typically remain interdural apart from the subarachnoid space, whereas larger lesions (≥1 cm) tend to breach the overlying dura and enter the subarachnoid space. OphArt, ophthalmic artery; SupHypArt, superior hypophyseal artery; DR, dural ring; COM, carotid-oculomotor membrane; ON, optic nerve.

Anterolateral Variant

The anterolateral variant arises from the anterolateral surface of the clinoidal segment as it obliquely ascends toward the dural ring underneath the ACP.1 The superiorly and slightly medially directed course of the segment promotes an aneurysm that expands lateral and anterior to the ascending ICA, superiorly projecting toward and into the ACP. When small, the anterolateral variant may erode the optic strut and undersurface of the ACP to cause monocular visual loss from ipsilateral optic nerve compression within the optic canal. Larger lesions may secondarily compress the visual system (nerve or chiasm) within the subarachnoid space after extension through the dura medial to the ACP. These aneurysms can sometimes arise in association with a clinoidal segment origin of the ophthalmic artery but are more often associated just with the hemodynamic stress associated with the anterior ascending vertical segment of the cavernous ICA.

Medial Variant

The medial variant extends from the medial surface of the clinoidal segment and enlarges toward the sphenoid sinus and sella as the ICA turns from lateral to medial to lateral during its ascent toward and through the dural ring.1 Initially, this aneurysm type expands beneath the diaphragma sella into the pituitary fossa. Gradual enlargement may cause hypopituitarism; rarely, aneurysm rupture into the pituitary gland may simulate pituitary apoplexy. Extension and rupture into the sphenoid sinus may cause life-threatening epistaxis. Large or giant lesions may extend through the diaphragma sella to enter the subarachnoid space. Visual loss from this aneurysm type does not occur with small lesions, but field cuts resembling those of pituitary tumors may occur with large or giant lesions that extend into the suprasellar space.

Ophthalmic Segment Aneurysms

Three ophthalmic segment aneurysm variants can be differentiated according to their site of origin, direction of projection, and relationships to arterial bends and branches and the adjacent dural and osseous structures within the segment (Fig. 366-4).

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FIGURE 366-4 Ophthalmic segment (OphSeg) aneurysm types (schematic): lateral (A), dorsal (B), and anteroposterior (C) views. D, Ophthalmic artery (OphArt) aneurysm: arteriogram (anteroposterior [top left], lateral [top right], and three-dimensional [bottom left], views) and axial magnetic resonance image [bottom right]. E, Superior hypophyseal artery (SupHypArt) aneurysm: arteriogram (anteroposterior [top left], lateral [top right], and three-dimensional [bottom left] views) and axial magnetic resonance image [bottom right]. OphArt origin (black arrow) is proximal to aneurysm, and posterior communicating artery (white arrow) is distal to aneurysm. F, Dorsal variant internal carotid artery (ICA) aneurysm: growing blister aneurysm, arteriogram (anteroposterior view on post–subarachnoid hemorrhage [SAH] days 0 [top left], 13 [top right], and 17 [bottom left]; lateral view on post-SAH day 17 [bottom right]). Note the distance between OphArt origin (black arrow) and the aneurysm. OphArt aneurysms (hatched area 1) arise from the dorsomedial ICA surface just distal to the OphArt origin, whereas SupHypArt aneurysms (hatched area 2) arise from the inferomedial ICA surface independent of the OphArt origin, in close association with the perforators that supply the optic chiasm and parasellar dura. Dorsal OphSeg aneurysms (hatched area 3) are rare and arise from the dorsal ICA surface well distal to the OphArt origin. ACP, anterior clinoid process; COM, carotid-oculomotor membrane; DR, dural ring; ON, optic nerve; Pit, pituitary gland.

Ophthalmic Artery Aneurysms

Ophthalmic artery aneurysms arise immediately distal to and in relation to the origin of the ophthalmic artery.1,2,19–22 These lesions typically arise along the posterior bend of the ICA just distal to the ophthalmic artery and dural ring, project dorsally or dorsomedially, and elevate the lateral edge of the nerve against the falciform ligament. The pressure from the falciform ligament against the superior surface of the nerve results in an inferior nasal field defect. A monocular inferior nasal field defect is initially produced; as the lesion enlarges, however, the entire nasal field can become affected, followed by a superior temporal field loss in the contralateral eye. If the clinical course is protracted, ipsilateral blindness with marked contralateral deficits can occur. Larger ophthalmic artery aneurysms tend to thicken or even calcify along their anterior portion, a factor that must be accommodated during clip placement.

Superior Hypophyseal Artery Aneurysms

Superior hypophyseal artery aneurysms arise in association with the superior hypophyseal artery along the medial surface of the ICA, usually just distal to the dural ring.2,20 There are two main variants. The parasellar variant projects inferiorly toward the sella into the carotid cave, whereas the suprasellar variant projects superiorly into the suprasellar space. Parasellar superior hypophysal artery aneurysms are usually asymptomatic. Because they project into the dura of the sella or cavernous sinus, purely parasellar aneurysms are unlikely to rupture.1 Their medial projection and proximity to ICA perforators also makes them more difficult to treat. Suprasellar or large lesions have a much higher tendency to rupture. When large or giant, these aneurysms tend to elevate the optic chiasm and produce visual changes and relationships to the visual system similar to those seen with pituitary tumors. Larger superior hypophyseal artery aneurysms tend to develop thickenings or calcifications along the anterior-medial aspect, near their origin from the ICA, similar to ophthalmic artery aneurysms. Because these lesions extend medially underneath the optic chiasm, they can result in bilateral visual field defects.

Many small lesions burrow inferiorly and medially toward and beneath the diaphragma sella, expanding the carotid cave. These lesions, termed parasellar variant superior hypophyseal artery aneurysms, have also been called carotid cave aneurysms.1,2,7,20 When small, the fundus of this variant is invested by adjacent lateral parasellar dura, and their risk for subarachnoid hemorrhage is quite low. With growth, however, these lesions expand superomedially above the diaphragma sella into the suprasellar space, where the hemorrhage risk becomes greater. A second type, the suprasellar variant superior hypophyseal artery aneurysm, projects medially above a shallow carotid cave and expands into the medial suprasellar space above the diaphragm, without investment by the parasellar dura. Superior hypophyseal artery lesions cause their visual compression by expansion into the suprasellar space and elevation of the optic chiasm, producing superior bitemporal or other patterns of visual loss more suggestive of pituitary tumors.

Dorsal Variant Aneurysms

Dorsal variant aneurysms are rarer, and arise along the dorsal surface of the ICA distinctly distal to the ophthalmic artery origin, unrelated to any arterial branch point.1,2,19,20 Many are the result of hemodynamic forces produced by an accentuated bend in the ICA as the vessel courses laterally to become the communicating segment. Others appear as “blisters” on the dorsal carotid surface of the ophthalmic segment. With a genesis likely related to dissection, blister aneurysms are very fragile and rupture easily during surgery.23 Visual loss or a reliable relationship with the optic nerve or chiasm is not consistently seen with the dorsal variant.14,17

Indications for Treatment

Aneurysms from both of these carotid segments are much more common in women, with ratios as high as 9 : 1 female-to-male predominance.20,22,24 Most present during the fifth and sixth decades of life, usually as either incidental lesions or with mass effect.20,24,25 These segments have a propensity for aneurysm multiplicity; up to half of ophthalmic segment aneurysm patients harbor at least one additional intracranial aneurysm.2,26,27 With the exception of the dorsal variant, which often represents an unstable dissection, most paraclinoid aneurysms have a lower rupture risk compared with those at other intracranial subarachnoid sites.

Because both clinoidal segment variants are located interdurally below the dural ring and subarachnoid space, the risk for hemorrhage associated with small lesions (<1 cm) is extremely low. Once this size is exceeded, however, these lesions may erode through the dura adjacent to the dural ring and extend into the subarachnoid space, at which time they assume the same or greater hemorrhage risk as those of the ophthalmic segment. In addition to subarachnoid hemorrhage, clinoidal segment aneurysms also present with visual disturbance, with headaches, or as incidentally discovered lesions. Headaches from clinoidal segment aneurysms are generally limited to the ipsilateral V1 and retroorbital regions, presumably because of pulsatile distortion of the dura overlying this segment. Much less commonly, clinoidal segment lesions may produce facial numbness or diplopia from compression against the lateral cavernous sinus wall, but a full-blown cavernous sinus syndrome is rare from these lesions.

Indications for treatment of clinoidal segment aneurysm are largely dictated by the size of the offending lesion and its associated symptoms. Small asymptomatic aneurysms (<1 cm) are interdural below the subarachnoid space and are therefore generally treated conservatively with periodic clinical and radiographic follow-up. Small symptomatic lesions (visual deficits or focal, unrelenting headaches) and lesions whose protective ACP roof has been removed for treatment of another aneurysm in the region should be treated. Most large (≥1 cm) clinoidal segment aneurysms have extended through the overlying dural coverings into the subarachnoid space and carry an increased risk for intracranial hemorrhage, and stronger consideration for intervention is therefore given to such lesions even if asymptomatic. Small clinoidal segment aneurysms may be cured with endovascular coiling only because many have a narrow neck-to-fundus ratio that facilitates this methodology. Large or giant clinoidal segment lesions often require coiling combined with stenting to achieve satisfactory aneurysm obliteration. Direct surgical obliteration is also a reasonable option but requires broad removal of the ACP and optic strut and opening of the dural ring and COM to gain satisfactory exposure for accurate clip placement. Lesions presenting with epistaxis should be obliterated urgently.

All ophthalmic segment aneurysms are located within the subarachnoid space and have at least some risk for rupture and intracranial hemorrhage. Patients presenting with visual loss should be treated urgently, ideally with surgery if the patient’s risk factors and the experience of the operative team are reasonable, to acutely decompress the visual system. Many small unruptured ophthalmic segment lesions appear to have very low risk for rupture, particularly the parasellar superior hypophyseal artery variant, and conservative or endovascular treatment is often preferable to surgery, particularly in older patients with higher surgical risks. When surgery is done, early sectioning of the falciform ligament is helpful to prevent iatrogenic optic nerve injury. Carotid sacrifice should be considered only as a secondary alternative to surgical clipping and endovascular stent or coiling.

Preoperative Evaluation

Computed tomography (CT) is the best imaging modality for diagnosing subarachnoid hemorrhage and may also diagnose the aneurysm, particularly when CT angiography is added. Bony details delineated by CT, such as focal erosion of the ACP or optic strut, can help differentiate particular proximal aneurysm subtypes. CT imaging may also reveal aneurysm features that potentially increase treatment complexity (i.e., ACP or optic strut pneumatization, aneurysm wall calcification), factors that may prompt further studies such as awake trial balloon occlusion testing before intervention. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) often provide adjunctive anatomic detail that can help determine an aneurysm’s relationship to soft tissue structures such as the optic apparatus and pituitary gland, or whether a portion of a clinoidal segment lesion enters the subarachnoid space.

Four-vessel transfemoral cerebral angiography remains the “gold standard” for aneurysm diagnosis and is generally recommended in all patients harboring proximal carotid artery aneurysms if intervention is being considered. The cervical carotid artery should be carefully inspected for atherosclerotic plaque that may make proximal temporary clamping hazardous, and the superficial temporary artery should be evaluated for its applicability as a bypass conduit. An awake trial balloon occlusion test with induced hypotension and cerebral blood flow studies (i.e., single-photon emission CT or xenon CT) should be considered for complex lesions that may require long temporary or permanent ICA occlusion during aneurysm obliteration.

Because of its dorsal projection, the anterolateral variant can sometimes be mistaken for a low-lying ophthalmic artery aneurysm. The distinction can often be made by noting several features on CT, MRI, or arteriography: (1) focal bony erosion evident on CT or MRI, (2) origination proximal to the typical take-off of the ophthalmic artery, (3) a subtle “double density” along the anterolateral ICA wall indicating the lesion’s proximal nature, (4) aneurysm projection dorsal and lateral to the ICA (in contrast to the dorsal or dorsomedial projection of an ophthalmic artery aneurysm), and (5) an angiographic “waist” marking the penetration of the lesion through the overlying dural coverings into the subarachnoid space.

Differentiating a medial variant clinoidal segment from a superior hypophyseal artery aneurysm can also be difficult. The distinction can often be made by several features noted on CT, MRI, or arteriography: (1) Although both lesions project medially, the clinoidal segment subtype originates beneath the diaphragma sella and has an intimate association with the pituitary gland; this low origin often displaces the aneurysm down into the sella, and the diaphragm flattens its superior margin. In contrast, the superior hypophyseal artery type arises above the diaphragma sella into the parasellar or suprasellar space. (2) Medial variant clinoidal segment lesions typically have a narrow neck, owing to the origin of the aneurysm between the COM and the dural ring, whereas superior hypophyseal artery aneurysms, free of such dural restraints, usually have a wide neck. (3) On a lateral view, the medial variant clinoidal segment lesion originates proximal to the ophthalmic artery and creates a subtle double density along the anterior genu below the plane of the ACP, indicating the lesion’s proximal origin. Superior hypophyseal artery lesions appear to arise on the posterior or posteromedial ICA wall opposite the ophthalmic artery origin. Neither type produces significant bony erosion seen on CT scan.

Operative Technique

See Figures 366-5 through 366-7 for illustrations of the operative techniques described next. Video 366-1 image demonstrates anterior clinoidectomy and clipping of an ophthalmic artery.

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FIGURE 366-5 Bony and dural resection for paraclinoid aneurysm surgery (schematic). A, Extradural bone exposure includes a frontotemporal craniotomy (hatched area 1), along with resection of the sphenoid ridge, posterior orbital roof, and medial floor of the superior orbital fissure (SOF) (hatched area 2). Intradural bone removal includes resection of the remaining medial sphenoid wing and drilling of the anterior clinoid process (ACP) and optic strut (OS) (area 3). B, The dashed lines represent the dural incisions used during intradural anterior clinoidectomy. The incision is extended through the falciform ligament and optic nerve (ON) ensheathment to decompress and mobilize the ON as needed. C, Exposure following intradural ACP removal and drilling of the OS. Aneurysms arising from the clinoidal segment (ClinSeg) and ophthalmic segment (OphSeg) of the internal carotid artery (ICA) are well accessed through this approach. D, Operative view. Opening of the carotid-oculomotor membrane (COM) between the ClinSeg and oculomotor nerve (III) provides excellent exposure to the anterior genu of the cavernous ICA segment. DR, dural ring; OphArt, ophthalmic artery; PComArt, posterior communicating artery.

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FIGURE 366-6 Operative view of clinoidal segment (ClinSeg) aneurysms (schematic). Anterolateral variant. A, Exposure: note that the anterior clinoid process (ACP) and optic strut (OS) have been extensively removed to expose the ClinSeg. Also note the constriction of the aneurysm—a sign that the lesion has entered the subarachnoid space. B, Clipping: a gently curved clip is placed along the long axis of the internal carotid artery (ICA), paralleling the curve of the ICA. Medial variant. C, Exposure: note that the ACP and OS have been extensively removed to expose the ClinSeg. Also note the projection of the medial variant ClinSeg aneurysm beneath the diaphragma sella into the pituitary fossa. D, Clipping: a fenestrated clip is placed parallel to the ICA with the tips abutting or extending past the carotid-oculomotor membrane (COM), carefully sparing the ophthalmic and superior hypophyseal arteries. AN, aneurysm; DR, dural ring; ON, optic nerve; OphArt, ophthalmic artery; OphSeg, ophthalmic segment; SupHypArt, superior hypophyseal artery.

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FIGURE 366-7 Operative view of ophthalmic segment aneurysms (schematic). Ophthalmic artery (OphArt) aneurysm. A, Exposure: note that the anterior clinoid process (ACP) has been extensively removed to expose the clinoidal segment (ClinSeg). B, Clipping: the deep blade of a side-angled clip is placed into the interval between the OphArt and the aneurysm (AN), then rotated medial to the aneurysm, ending in a plane closely parallel to the long axis of the internal carotid artery (ICA). Superior hypophyseal artery (SupHypArt) aneurysm. C, Exposure: note the aneurysm’s inferior and medial position to the intimately associated SupHypArt. D, Clipping: a fenestrated clip is placed parallel to the ICA to reconstruct the carotid lumen. The dural ring (DR) has been circumferentially sectioned to allow access of the clip blades to the ClinSeg. The butt of the clip must spare the posterior communicating artery (PComArt), while the tips are advanced proximally beyond the dural ring. COM, carotid-oculomotor membrane; FalcLig, falciform ligament; ON, optic nerve; OphSeg, ophthalmic segment; OS, optic strut.

Preoperative Preparation

Patients with paraclinoid aneurysms are generally managed in the same way as other intracranial aneurysms. Those patients with visual field deficits should undergo preoperative visual field testing if possible to evaluate the degree of visual compromise. The cervical carotid bifurcation and the branches of the external carotid artery should be evaluated to assess the safety of temporary clipping and the availability of a donor vessel should bypass become a consideration.

Prophylactic antibiotics and steroids are given preoperatively. Blood pressure is continuously monitored with an arterial line. Continuous somatosensory evoked potential and electroencephalographic monitoring is used. Before temporary clipping, barbiturates are administered to achieve burst suppression as determined by the electroencephalogram. Mild hypertension is also maintained during the temporary clipping. Patients who present with subarachnoid hemorrhage are also given mannitol to relax the brain 20 minutes before dural opening.

Positioning and Exposure

The patient is positioned supine on the table with a shoulder roll. The head is elevated above the heart, fixed in a radiolucent head frame for intraoperative angiography, and turned 45 to 60 degrees toward the contralateral side. The vertex is lowered so that the maxilla is at the highest point to facilitate gravitational retraction of the frontal and temporal lobes.

The cervical carotid region should always be draped out even if the surgeon does not initially intend to expose the cervical bifurcation. Cervical ICA exposure is advisable for most large, giant, or ruptured clinoidal segment aneurysms and should include 2 cm of the ICA high in the neck to allow temporary clipping without disruption of any atheromatous plaque.

The skin incision is made from the midline to the zygoma, just behind the hairline. The temporalis muscle and fascia are elevated using the Yasargil interfascial technique to allow for a better basal exposure without undue brain retraction. The muscle and fascia are mobilized and retracted posteriorly and inferiorly, carefully avoiding injury to the frontalis branch of the facial nerve. A pterional craniotomy is performed up to the edge of the orbital rim to allow an unobstructed view of several centimeters of the orbital roof. An orbital osteotomy can also be performed to provide additional exposure for large aneurysms. The lateral sphenoid ridge and the posterior portion of the orbital roof and the lateral orbital wall are then removed down to the superior orbital fissure. The lesser sphenoid wing is then removed down to the base of the anterior clinoid process.

Anterior Clinoidectomy

Anterior clinoidectomy has great value in the surgical exposure and treatment for most paraclinoid aneurysms and can be performed either extradurally or intradurally. Extradural removal is done by using a high-speed diamond drill, burring down the anterior clinoid process until it is disconnected at its three points of bony fixation. The ACP can then be freed up from the attached dura and removed. Cavernous sinus bleeding can be controlled with packing.

Although the extradural clinoidectomy can often be done safely, the intradural anterior clinoidectomy is preferable in most instances because it allows the surgeon to see the optic nerve and aneurysm during the entire dissection. In this technique, the craniotomy and posterior orbital roof and lesser sphenoid wing are removed in a manner similar to the technique used for the extradural approach, down to the base of the ACP. Then, the dura is opened and the sylvian fissure widely split, allowing the aneurysm to be partially visualized along with its relationship to the anterior clinoid process and optic nerve.

A dural incision is then made along the lesser sphenoid wing extending from the tip of the ACP laterally beyond the edge of the prior ridge resection. A second dural incision made perpendicular to the first near the clinoid tip extends to and includes sectioning of the falciform ligament. The ACP is exposed by retracting the dural leaflets, and then is removed in a similar fashion as the extradural removal, but with better visualization of the optic apparatus and the aneurysm. After ACP removal is complete, the optic canal is unroofed, and the optic strut is drilled, down to the base of the sphenoid bone for clinoidal segment lesions. The optic nerve sheath is then sectioned laterally to allow further mobilization of the optic nerve. If needed, the distal dural ring can be sectioned circumferentially to further expose the clinoidal segment.

Aneurysm Clipping

Clinoidal Segment Aneurysms

Exposure of clinoidal segment aneurysms requires extensive anterior clinoidectomy and optic strut removal before aneurysm dissection. Because these aneurysms arise below the ACP, and the anterolateral variant actually erodes and may extend through this bony process, extradural removal of the ACP is not recommended for this aneurysm type. Proximal control in the cervical region for most lesions is advisable, especially for those presenting with hemorrhage. Circumferential sectioning of the dural ring allows for more accurate viewing and dissection of the aneurysm’s adherence to the adjacent dura and cavernous sinus and also facilitates unimpeded clip blade passage from the proximal ophthalmic segment to span the entire clinoidal segment.

The anterolateral variant is usually best clipped with a gently curved or side-angled clip that runs parallel to the anterolateral surface of the clinoidal ICA. To eliminate the proximal neck, the clip blades must pass up to or proximal to the COM, using great care to avoid injuring the oculomotor nerve, which courses in the lateral edge of the COM. Opening the COM and gentle packing of the cavernous sinus lumen with Gelfoam or Surgicel will achieve the desired meticulous hemostasis to permit accurate clip placement and avoid ICA luminal compromise.

The medial variant projects beneath the diaphragma sella into the pituitary fossa. Circumferential section of the dural ring allows placement of a fenestrated clip whose blades run parallel to the curvature of the clinoidal segment medial wall. The dome of the aneurysm may be adherent to the pituitary stalk and surrounding dura. These attachments must be sufficiently dissected and relaxed to allow aneurysm wall to partially collapse, thereby reducing the risk for avulsion of the aneurysm neck during clip placement. Care must be taken to spare the ophthalmic and any superior hypophyseal or other perforating vessels that arise from either the clinoidal segment or ophthalmic segment.

Ophthalmic Segment Aneurysms

Ophthalmic artery aneurysms are the least hazardous of the different types of paraclinoid aneurysms to clip, owing to the lack of associated perforators and its relatively distal and superior location on the ICA, especially if the ACP is removed as outlined previously. Before aneurysm dissection, the falciform ligament should be sectioned to relax any compression on the superior optic nerve surface. After ACP removal, this cut can be extended along the lateral aspect of the optic nerve into the optic canal, thereby allowing much easier exposure of the proximal neck and ophthalmic artery origin. The distal neck is usually easily identified and typically free of perforators. A gently curved or side-angled clip directed parallel to the plane of the ICA, sparing the ophthalmic artery, obliterates most lesions. Ophthalmic artery aneurysms are frequently calcified along their anterior wall, and the wall thickening and rigidity can prevent complete clip closure. Fenestrated clips are then used to encircle the calcified portion of the aneurysm without the need to do an aneurysmal endarterectomy. Clipping too close to the aneurysm neck in such circumstances can lead to ICA luminal stenosis.

Superior hypophyseal artery aneurysms are often more complex because of their medial burrowing nature; the most difficult part of the dissection is usually in the inferior and medial aspect of the aneurysm, where the dome projects into the carotid cave or parasellar dura. Perforator injury during superior hypophyseal artery aneurysm clipping can lead to visual loss and rarely pituitary dysfunction. The superior hypophyseal arteries usually arise proximally, just above the dural ring on the medial ICA surface. After ACP removal, circumferential sectioning of the dural ring allows ICA mobilization sufficient to identify the superior hypophyseal artery origins and avoid injury during clip placement. Most superior hypophyseal artery aneurysms are best clipped using fenestrated clips. With simpler lesions, one or more right-angled fenestrated clips, with blades parallel to and encircling the ICA, can reconstruct the ICA lumen while sparing the superior hypophyseal artery perforators. For more complex lesions, especially those with atheroma or calcification near their proximal base, stacked straight fenestrated clips applied to the proximal neck can avoid incorporating the superior hypophyseal perforators within in the clip blades. The posterior communicating artery and its thalamus-perforating branches, as well as other ICA branches, must also be identified and preserved.

Dorsal carotid wall aneurysms are clipped in a similar fashion to ophthalmic artery aneurysms, with easier identification of the proximal neck. Because they are not in such close proximity to the ACP, dural ring, and optic apparatus, these aneurysms are often easier to expose. They also tend to be more fragile, however, and can rupture easily during clip placement. When the blister variety is identified, the clip should be applied only after trapping of the affected segment between temporary clips to reduce pulsations and pressure in the affected vessel segment; the clip blades should ideally be placed parallel to the long axis of the ICA to avoid any twisting or torque on the fragile parent vessel.

Giant and Complex Aneurysms

Paraclinoid aneurysms are frequently gigantic in size, and specific techniques are often employed to ensure safe and complete surgical obliteration. Temporary proximal cervical carotid ligation, accomplished under barbiturate-induced electroencephalography burst suppression and mild hypertension, greatly facilitates clip placement for complex lesions. Further aneurysm relaxation or collapse may be achieved with trapping and retrograde cervical or intra-aneurysmal suction decompression as needed. Once controlled, the lesion is then opened, allowing removal of intraluminal thrombus before final clip placement. Opening the lesion at least 180 degrees of its circumference allows favorable flattening and collapse of any intramural calcification.

Many larger paraclinoid aneurysms have significant thickening within the aneurysm wall or neck, which can cause an initial aneurysm clip to migrate downward and partially occlude the parent vessel lumen. In such circumstances, a temporary clip is often placed proximally on the neck, in the desired plane for final clipping, to serve as a place-holder for the parent vessel to ensure its patency. Then, sequential clips are added distally in the same plane until the aneurysm is completely obliterated. The proximal temporary clip is then removed. Fenestrated clips facilitate closure of calcified lesions by encircling the affected segment of the aneurysm neck. An intraoperative angiogram through direct common carotid artery puncture (if the cervical carotid is already exposed) or through a preoperatively placed transfemoral catheter is highly recommended before closure to ascertain parent vessel patency and complete aneurysm obliteration. The use of indocyanine green injected into the venous system allows visualization of perforator patency and can substitute for arteriography in some instances.28

Closure

After ICA patency is ensured, dural closure begins. A pneumatized optic strut is found in about 10% of patients; any communication between the optic strut and the sphenoid sinus must be identified and sealed with muscle, Gelfoam, and methylmethacrylate. The dural leaves covering the medial sphenoid wing are then closed primarily, followed by watertight closure of the more superficial dural opening. The bone flap is returned and secured, and the temporalis muscle and fascia are reapproximated. A subgaleal drain is left in place, and the skin closed.

Surgical Complications and Outcome

Patients who undergo surgical treatment of paraclinoid aneurysms usually have good or excellent outcomes, particularly when the surgery is done by experienced surgeons and the secondary effects of vasospasm are negated.2,29–31

Complications generally revolve around the anatomic structures present within the region—the ICA, arterial perforators, and neighboring cranial nerves. Even though intraoperative angiography may demonstrate initial ICA patency, delayed stenosis or thrombosis can still occur. Any evidence of hemibody neurological deficits should be emergently addressed with CT and angiography, with a return trip to the operating room for emergent re-exploration and clip adjustment strongly considered.

Visual deterioration following paraclinoid aneurysm surgery is usually attributable to excessive optic nerve manipulation or arterial perforator compromise during aneurysm exposure. In patients who present with visual field defects, visual symptoms improved in 50% to 74%, remained stable in 26% to 42%, and are worsened in 0% to 8% after surgical clipping.2,29 The cause of worsened vision (or failure of improvement) can be mechanical, thermal, or vascular. Mechanical injury may occur from manipulation of the optic nerve against the falciform ligament, which can be reduced by sectioning the ligament and unroofing the optic canal before manipulation of the aneurysm or optic nerve. Thermal injury can occur during drilling of the anterior clinoid process and is prevented by generous irrigation to dissipate the heat or by using the newer ultrasonic bone aspirators. Finally, perforator injury can be avoided by wide exposure and dural ring sectioning, to see the perforators clearly and avoid inadvertent clipping or kinking of their origins. Re-exploration and clip adjustment should be considered if intraoperative events do not adequately explain any postoperative visual deficit.

Postoperative oculomotor, trochlear, and abducens palsies, as well as ptosis and miosis secondary to sympathetic fiber disruption, are generally the result of surgical trauma during anterior clinoidectomy, clip blade advancement, cranial nerve manipulation, or cavernous sinus packing. These deficits are usually partial and transient in nature and are best avoided through careful dissection and retraction of these nerves.

Suggested Readings

Batjer HH, Kopitnik TA, Giller CA, et al. Surgery for paraclinoidal carotid artery aneurysms. J Neurosurg. 1994;80:650.

Cawley CM, Zipfel GJ, Day AL. Surgical treatment of paraclinoid and ophthalmic aneurysms. Neurosurg Clin N Am. 1998;9:765.

Dawson BH. The blood vessels of the human optic chiasma and their relation to those of the hypophysis and hypothalamus. Brain. 1958;81:207.

Day A. Clinicoanatomic features of supraclinoid aneurysms. Clin Neurosurg. 1990;36:256.

Day AL. Aneurysms of the ophthalmic segment. A clinical and anatomical analysis. J Neurosurg. 1990;72:677.

Day AL, Morcos JJ, Revilla R. Management of aneurysms of the anterior circulation, 4th ed. Youmans JR, editor. Neurological Surgery, Vol 2. Philadelphia: Saunders. 1996:1272-1309.

Dolenc VV. A combined epi- and subdural direct approach to carotid-ophthalmic artery aneurysms. J Neurosurg. 1985;62:667.

Drake CG, Vanderlinden RG, Amacher AL. Carotid-ophthalmic aneurysms. J Neurosurg. 1968;29:24.

Gibo H, Kobayashi S, Kyoshima K, et al. Microsurgical anatomy of the arteries of the pituitary stalk and gland as viewed from above. Acta Neurochir (Wien). 1988;90:60.

Gibo H, Lenkey C, Rhoton ALJr. Microsurgical anatomy of the supraclinoid portion of the internal carotid artery. J Neurosurg. 1981;55:560.

Harris FS, Rhoton AL. Anatomy of the cavernous sinus. A microsurgical study. J Neurosurg. 1976;45:169.

Inoue T, Rhoton ALJr, Theele D, et al. Surgical approaches to the cavernous sinus: a microsurgical study. Neurosurgery. 1990;26:903.

Knosp E, Muller G, Perneczky A. The paraclinoid carotid artery: anatomical aspects of a microneurosurgical approach. Neurosurgery. 1988;22:896.

Kobayashi S, Kyoshima K, Gibo H, et al. Carotid cave aneurysms of the internal carotid artery. J Neurosurg. 1989;70:216.

Meling TR, Sorteberg A, Bakke SJ, et al. Blood blister–like aneurysms of the internal carotid artery trunk causing subarachnoid hemorrhage: treatment and outcome. J Neurosurg. 2008;108:662.

Nutik SL. Removal of the anterior clinoid process for exposure of the proximal intracranial carotid artery. J Neurosurg. 1988;69:529.

Nutik SL. Ventral paraclinoid carotid aneurysms. J Neurosurg. 1988;69:340.

Perneczky A, Knosp E, Vorkapic P, et al. Direct surgical approach to infraclinoidal aneurysms. Acta Neurochir (Wien). 1985;76:36.

Raco A, Frati A, Santoro A, et al. Long-term surgical results with aneurysms involving the ophthalmic segment of the carotid artery. J Neurosurg. 2008;108:1200.

Rhoton ALJr. Anatomy of saccular aneurysms. Surg Neurol. 1980;14:59.

Yasargil MG, Gasser JC, Hodosh RM, et al. Carotid-ophthalmic aneurysms: direct microsurgical approach. Surg Neurol. 1977;8:155.

References

1 Cawley CM, Zipfel GJ, Day AL. Surgical treatment of paraclinoid and ophthalmic aneurysms. Neurosurg Clin N Am. 1998;9:765.

2 Day AL. Aneurysms of the ophthalmic segment. A clinical and anatomical analysis. J Neurosurg. 1990;72:677.

3 Day AL, Morcos JJ, Revilla R. Management of aneurysms of the anterior circulation, 4th ed. Youmans JR, editor. Neurological Surgery, Vol 2. Philadelphia: Saunders. 1996:1272-1309.

4 Inoue T, Rhoton ALJr, Theele D, et al. Surgical approaches to the cavernous sinus: a microsurgical study. Neurosurgery. 1990;26:903.

5 Dolenc VV. A combined epi- and subdural direct approach to carotid-ophthalmic artery aneurysms. J Neurosurg. 1985;62:667.

6 Knosp E, Muller G, Perneczky A. The paraclinoid carotid artery: anatomical aspects of a microneurosurgical approach. Neurosurgery. 1988;22:896.

7 Kobayashi S, Kyoshima K, Gibo H, et al. Carotid cave aneurysms of the internal carotid artery. J Neurosurg. 1989;70:216.

8 Nutik SL. Removal of the anterior clinoid process for exposure of the proximal intracranial carotid artery. J Neurosurg. 1988;69:529.

9 Perneczky A, Knosp E, Vorkapic P, et al. Direct surgical approach to infraclinoidal aneurysms. Acta Neurochir (Wien). 1985;76:36.

10 Nutik SL. Ventral paraclinoid carotid aneurysms. J Neurosurg. 1988;69:340.

11 Gibo H, Lenkey C, Rhoton ALJr. Microsurgical anatomy of the supraclinoid portion of the internal carotid artery. J Neurosurg. 1981;55:560.

12 Rhoton ALJr. Anatomy of saccular aneurysms. Surg Neurol. 1980;14:59.

13 Hayreh S. The ophthalmic artery. In: Newton T, Potts D, editors. Radiology of the Skull and Brain. St. Louis: Mosby; 1974:1333-1350.

14 Nishio S, Matsushima T, Fukui M, et al. Microsurgical anatomy around the origin of the ophthalmic artery with reference to contralateral pterional surgical approach to the carotid-ophthalmic aneurysm. Acta Neurochir (Wien). 1985;76:82.

15 Dawson BH. The blood vessels of the human optic chiasma and their relation to those of the hypophysis and hypothalamus. Brain. 1958;81:207.

16 Gibo H, Kobayashi S, Kyoshima K, et al. Microsurgical anatomy of the arteries of the pituitary stalk and gland as viewed from above. Acta Neurochir (Wien). 1988;90:60.

17 Harris FS, Rhoton AL. Anatomy of the cavernous sinus. A microsurgical study. J Neurosurg. 1976;45:169.

18 Kyoshima K, Oikawa S, Kobayashi S. Interdural origin of the ophthalmic artery at the dural ring of the internal carotid artery. Report of two cases. J Neurosurg. 2000;92:488.

19 Batjer HH, Kopitnik TA, Giller CA, et al. Surgery for paraclinoidal carotid artery aneurysms. J Neurosurg. 1994;80:650.

20 Day A. Clinicoanatomic features of supraclinoid aneurysms. Clin Neurosurg. 1990;36:256.

21 Drake CG, Vanderlinden RG, Amacher AL. Carotid-ophthalmic aneurysms. J Neurosurg. 1968;29:24.

22 Yasargil MG, Gasser JC, Hodosh RM, et al. Carotid-ophthalmic aneurysms: direct microsurgical approach. Surg Neurol. 1977;8:155.

23 Meling TR, Sorteberg A, Bakke SJ, et al. Blood blister–like aneurysms of the internal carotid artery trunk causing subarachnoid hemorrhage: treatment and outcome. J Neurosurg. 2008;108:662.

24 Kupersmith MJ, Hurst R, Berenstein A, et al. The benign course of cavernous carotid artery aneurysms. J Neurosurg. 1992;77:690.

25 Linskey ME, Sekhar LN, Hirsch WLJr, et al. Aneurysms of the intracavernous carotid artery: natural history and indications for treatment. Neurosurgery. 1990;26:933.

26 al-Rodhan N. Aneurysms within the cavernous sinus and transitional cavernous aneurysms. In: Wilkins R, Rengachary S, editors. Neurosurgery. 3rd ed. New York: McGraw-Hill; 1996:2283-2289.

27 al-Rodhan NR, Piepgras DG, Sundt TMJr. Transitional cavernous aneurysms of the internal carotid artery. Neurosurgery. 1993;33:993.

28 de Oliveira JG, Beck J, Seifert V, et al. Assessment of flow in perforating arteries during intracranial aneurysm surgery using intraoperative near-infrared indocyanine green videoangiography. Neurosurgery. 2008;62:1300.

29 Baccin CE, Krings T, Alvarez H, et al. Multiple mirror-like intracranial aneurysms. Report of a case and review of the literature. Acta Neurochir (Wien). 2006;148:1091.

30 Nonaka T, Haraguchi K, Baba T, et al. Clinical manifestations and surgical results for paraclinoid cerebral aneurysms presenting with visual symptoms. Surg Neurol. 2007;67:612.

31 Raco A, Frati A, Santoro A, et al. Long-term surgical results with aneurysms involving the ophthalmic segment of the carotid artery. J Neurosurg. 2008;108:1200.

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