Chapter 74 Surgical Management of Anterior Communicating and Anterior Cerebral Artery Aneurysms
The anterior communicating artery (ACoA) aneurysm is the most common aneurysm encountered in neurosurgical practice, accounting for one quarter to one third of all microsurgically treated aneurysms in published experiences1–3 and 21% of the senior author’s experience with 2320 aneurysms. This aneurysm has a propensity to hemorrhage, often at or below size limits considered safe for conservative management and often in younger patients for whom microsurgical clipping might be favored over endovascular coiling.2,4 Consequently, neurosurgeons must be prepared to deal with this lesion. This particular aneurysm, more than any other, has an unusually wide variety of complexity and technical difficulty that depends on variations in parent artery anatomy, aneurysm projection, and clinical presentation. In addition, the ACoA complex is adjacent to the hypothalamus, optic apparatus, and cognitive/emotional centers in the basal frontal lobes, while arteries emanating from the ACoA complex affect the basal ganglia, internal capsule, and motor/sensory cortex. Therefore, surgery for ACoA aneurysms is associated with elevated risks. This chapter discusses the factors and techniques that facilitate surgical management of ACoA aneurysms and help improve patient outcome.
The anterior cerebral artery (ACA) is divided into five segments (Fig. 74-1). The A1 segment, also known as the precommunicating or horizontal segment of the ACA, originates with the ACA at the internal carotid artery (ICA) bifurcation and extends to the junction with the ACoA. The A2 segment, also known as the postcommunicating segment, originates at the ACoA and extends to the genu of the corpus callosum, following the contour of the rostrum. The A3 segment curves around the genu and extends to the body of the corpus callosum, where it assumes a posterior course. The A4 and A5 segments continue over the body of the corpus callosum, the division between them being located at the plane of the coronal suture. Contrary to popular opinion, this nomenclature is not defined by the bifurcation into pericallosal and callosomarginal arteries. This bifurcation is usually located along the A3 segment (approximately 60% of patients), but it can be more proximal on the A2 segment (10%), it can be more distal on the A4 segment (12%), or the pericallosal artery can be absent (18%).5
FIGURE 74-1 Microsurgical anatomy of the ACA. Anterior (A) and oblique (B) views, showing the five ACA segments and 12 arteries that can enter the surgical field around an ACoA aneurysm. The five ACA segments are: A1, precommunicating or horizontal segment; A2, postcommunicating or infracallosal segment; A3, precallosal segment; A4, supracallosal segment; and A5, postcallosal segment. CmaA, callosomarginal artery; FpA, frontopolar artery; LSA, lenticulostriate artery; OfA, orbitofrontal artery; PcaA, pericallosal artery; RAH, recurrent artery of Heubner.
(From Lawton, MT. Seven Aneurysms: Tenets and Techniques for Clipping. New York: Thieme, 2010.)
The A1 segment courses medially and anteriorly over the optic tract and chiasm to the ACoA complex. Numerous penetrating branches (average 8, range 2-15)5 originate from this segment and course superiorly to supply the anterior perforated substance, subfrontal area, dorsal surface of the optic apparatus, hypothalamus, anterior commissure, septum pellucidum, and paraolfactory structures. Collectively, these perforators are also known as the medial lenticulostriate arteries, as opposed to the lateral lenticulostriate arteries that originate from the M1 segment of the middle cerebral artery (MCA). The most important of these perforators is the recurrent artery of Heubner, which originates from the proximal A2 segment on its lateral wall, just distal to the ACoA. This artery can arise from the distal A1 segment, just proximal to the ACoA, in 14% of patients or at the level of the ACoA in 8% of patients but is within 4 mm of the ACoA in 95% of patients.5 The artery is almost always present (98%) and can be duplicated (2%).5 The artery follows a course parallel to the A1 segment, either superior (60%) or anterior (40%) to it.5 The recurrent artery is typically seen before the A1 segment when the frontal lobe is retracted, making it a useful landmark to identify the A1 segment and the ACoA. The recurrent artery of Heubner supplies the head of the caudate nucleus, putamen, outer segment of the globus pallidus, and anterior limb of the internal capsule. Therefore, arterial injury can produce weakness involving the contralateral face and arm and expressive aphasia in the dominant hemisphere.6
The ACoA joins the two ACAs as they arrive in the interhemispheric fissure, completing the anterior part of the circle of Willis. Normally, the ACoA diameter is about half that of the A1 segments, but there is a direct correlation between asymmetry in the A1 segments and ACoA diameter. In other words, the ACoA diameter increases as the caliber of a hypoplastic A1 segment decreases, thereby compensating for the asymmetry in the A1 inflow.7 The ACoA can be duplicated in one third of patients, and triplicated in 10% of patients, but is always present.5 An ACoA that is not visualized angiographically is usually explained by an absence of cross-filling rather than an absence of the ACoA itself, and it can be visualized by a carotid cross-compression maneuver during angiography. The ACoA gives rise to important perforating arteries, which originate from its superior (54%) and posterior (36%) surfaces.5 These perforators course to the hypothalamus, median paraolfactory nuclei, genu, columns of the fornix, septum pellucidum, and anterior perforated substance. There can be perforators originating from the anterior and inferior aspects of the ACoA, supplying the dorsal optic chiasm, but these are few in number.
After making a right-angle turn from the horizontal A1 ACA, the A2 ACA runs superiorly in the interhemispheric fissure, coursing in front of the lamina terminalis and tracing the curvature of the genu. The branches arising from this segment are important more for correctly deciphering the anatomy of the ACoA complex than for their vascular supply. The orbitofrontal artery is the first cortical ACA branch, arising from the A2 segment approximately 5 mm distal to the ACoA from the anterolateral surface and coursing perpendicularly over the gyrus rectus and olfactory tract.6 This artery supplies the gyrus rectus, orbital gyri (anterior, posterior, medial, and lateral), and olfactory bulb/tract. It is important to avoid mistaking the recurrent artery of Heubner for this orbitofrontal artery. Both can be seen on the medial aspect of the gyrus rectus, but their origins from the A2 segment are separated and their courses are different, with the recurrent artery of Heubner eventually rejoining the A1 segment, even if it meanders under the gyrus rectus along its more proximal course. Correctly identifying the recurrent artery is especially important when resecting gyrus rectus. The recurrent artery is also typically small in caliber, with a diameter of approximately 1 mm.5 The orbitofrontal artery is often encountered draped over or adherent to the dome of a superiorly projecting aneurysm, which can tether the dome and make it more difficult to mobilize. The course of the orbitofrontal artery can also lead it across the neck of an ACoA aneurysm, requiring additional dissection before clipping.
The last relevant branch artery is the frontopolar artery, which originates from the A2 segment 14 mm, on average, from the ACoA near the genu.5 This artery courses anteriorly in the interhemispheric fissure and supplies the ventromedial frontal lobes. Rarely, it can originate from a common trunk with the orbitofrontal artery. Like the orbitofrontal artery, the frontopolar artery can be draped over the dome of a superiorly projecting aneurysm and should not be misinterpreted.
The terminal branches of the ACA are the pericallosal and callosomarginal arteries, bifurcating at a variable point along the genu of the corpus callosum. The callosomarginal artery is usually the smaller of the two, and it runs across the cingulate gyrus to the cingulate sulcus, where it continues posteriorly. It gives rise to the anterior, middle, and posterior internal frontal arteries, which supply the medial frontal lobes back to the precentral gyrus. The pericallosal artery courses over the corpus callosum, giving rise to the paracentral, superior internal parietal (precuneal), and inferior internal parietal arteries. These cortical branches extend over the convexity to supply the superomedial surfaces of the hemisphere, anastomosing laterally with middle cerebral arteries and posteriorly with posterior cerebral arteries in these watershed areas.
Variations from the normal ACoA anatomy are common and probably contribute to the abnormal hemodynamic that forms aneurysms. While the effects of variant anatomy on aneurysm pathogenesis are poorly understood, the anatomy itself must be thoroughly understood by the neurosurgeon to correctly interpret the anatomy intraoperatively and safely clip an aneurysm. Variations can be categorized as involving the afferent arteries (A1 segments), efferent arteries (A2 segments), or the ACoA.
Asymmetry in the caliber of the A1 segments is seen in approximately 10% of patients, with a hypoplastic segment defined arbitrarily as having a diameter of 1.5 mm.5 Smaller diameters are observed less frequently, with approximately 2% of patients having an A1 segment diameter of 1 mm.5 Aplastic A1 segments are rare, despite their suggestion on angiography with a contralateral A1 ACA that fills both distal ACAs. At surgery, a small A1 segment is typically found. The dominance of an A1 segment is relevant to aneurysm formation, projection of the dome, site of hematoma, and choice of side. Dominant A1 segments are frequently seen in association with ACoA aneurysms, which typically project in the direction of blood flow in that segment.7 As discussed later, it is usually advantageous to surgically approach these aneurysms from the side of the dominant A1 ACA, both for easier proximal control of the aneurysm and for better clipping of the neck. One final variant, the duplicated A1 segment, is rare (2%) and almost always unilateral.5
Variations in ACoA anatomy include duplications, triplications, and fenestrations.8,9 Accessory ACoAs are typically small and without significant perforators, making it important to recognize the primary ACoA and preserve both it and its perforators. Fenestrations can be the site of aneurysm formation and require special attention to differentiate the normal artery from the pathology. More important than these structural variations in the ACoA is its orientation. In only 18% of patients is the ACoA oriented in the transverse plane, as illustrated in anatomic textbooks.5 Instead, the ACoA complex is usually rotated or tilted, causing the A2 ACAs to course obliquely to one another in the interhemispheric fissure. This variation in orientation can direct an A2 segment more posteriorly, making its visualization more difficult. Rotation of the ACoA can shift the location of perforators from posterior to lateral, again making visualization more difficult, particularly when the aneurysm lies between the neurosurgeon and the perforators. These subtle changes in angles can be misleading, particularly when visualization is compromised by factors such as a swollen brain, a large aneurysm, and thick hematoma.
Variant anatomy in the efferent arteries can be the most difficult to deal with and is best understood in terms of the classification by Baptista.10 After analyzing 381 brain specimens, he defined three types of efferent artery anatomy. The type I anomaly, referred to as the azygos or “unpaired” ACA, is a single midline vessel arising from the confluence of the A1 segments (Fig. 74-2). Distally, the azygos ACA divides into pericallosal and callosomarginal arteries, with bifurcations, trifurcations, and quadrifurcations having been reported. This variant occurs in 0.3% to 2% of patients. The type II anomaly, referred to as the bihemispheric ACA, is an A2 ACA that transmits branches across the midline to supply both hemispheres, usually in the presence of a contralateral A2 segment that is hypoplastic or terminates early in its course toward the genu. This anomaly can be seen in as many as 12% of patients. The type III anomaly, referred to as an accessory ACA, is defined as a third artery originating from ACoA, in addition to the paired A2 segments and usually between them (Fig. 74-3). This accessory ACA variant is the most difficult one surgically because it results in some of the most unusual anatomic puzzles. If this variation is not appreciated, then a critical A2 ACA could be missed or, worse, sacrificed inadvertently during the aneurysm clipping (Fig. 74-4). The accessory ACA varies in caliber from a small remnant of the median artery of the corpus callosum (MACC) to a hyperplastic ACA that can resemble an azygos ACA when the two A2 segments are small in caliber and terminate early. A careful analysis of the angiogram preoperatively can alert the neurosurgeon to this challenging variant.
FIGURE 74-2 A 67-year-old woman, with chronic headaches, underwent left carotid artery angiography that demonstrated a 1.5-cm-diameter azygos ACA aneurysm and a 7-mm ophthalmic artery aneurysm in oblique (A) and anterior–posterior (AP) (B) views. The ophthalmic artery aneurysm was coiled, and the azygos ACA aneurysm was clipped through a bifrontal craniotomy and anterior interhemispheric approach. No residual aneurysms were seen on postoperative lateral (C) and AP (D) projection angiograms.
FIGURE 74-4 A, This small, ruptured anteriorly projecting ACoA aneurysm appeared to have classic anatomy at first glance. B, Additional dissection revealed an accessory A2 ACA. C, The neck was clipped with one straight clip that preserved flow through all three efferent A2 ACAs.
(From Lawton, MT. Seven Aneurysms: Tenets and Techniques for Clipping. New York: Thieme, 2010.)
The MACC just mentioned originates during embryogenesis when elongating ACAs coalesce in the midline to form plexiform anastomoses at 44 days.11 Normally, the MACC regresses and disappears as the A2 segments mature, but vestigial remnants can account for the accessory ACA.
ACoA aneurysms, as a group, arise from the complex of arteries around the ACoA, but their precise location can be subdivided into true ACoA aneurysms, A1–A2 junction aneurysms, A1 ACA aneurysms, and variant aneurysms associated with the anatomic variants described earlier. In addition, the distal ACA aneurysms, notably the pericallosal artery aneurysms, are often included in this group.
The true ACoA aneurysm arises from ACoA and is defined further by the projection of its dome in an anterior, superior, posterior, or inferior direction. In Yasargil’s experience with ACoA aneurysms, the superiorly and anteriorly projecting aneurysms were the most common (34% and 23%, respectively), while posteriorly and inferiorly projecting aneurysms were the least common (14% and 13%, respectively).12 Some aneurysms (approximately 16%) have mixed projection or multiple lobes.
The anteriorly projecting aneurysm is a favorable one from the neurosurgeon’s perspective because the parent arteries are separated from the aneurysm. The two A2 ACAs course at right angles to the aneurysm’s axis, making their identification in the interhemispheric fissure straightforward. The neurosurgeon has a good view across the neck of the aneurysm, with the dome and its likely rupture site removed from where this critical dissection takes place. Posteriorly projecting perforators are well away from the aneurysm and are easily preserved. The anterior projection of the dome typically leaves room under the neck to view across to the contralateral A1 segment to complete the exposure for proximal control of the aneurysm. This orientation often adheres the dome to the frontal lobes, which can limit the mobility of the aneurysm, but the dome can be freed as a final step in the dissection if greater mobility is needed to see contralateral anatomy or to increase the aneurysm’s maneuverability for clip application. In addition to their anterior projection, these aneurysms typically tilt to one side, most commonly away from the dominant A1 segment.
The superiorly projecting aneurysm is less favorable than the anterior projecting aneurysm, mainly because of the contralateral A2 ACA and the perforators (Fig. 74-5). Proximal control is straightforward, as the aneurysm is away from the A1 segments and the view to the contralateral side is unobstructed. However, the aneurysm is interposed between the neurosurgeon and the contralateral A2 ACA, requiring some manipulation of the aneurysm to locate this artery. Furthermore, larger aneurysms can displace perforators laterally or posteriorly, and their adherence to the aneurysm necessitates some delicate dissection. In addition, the A2 segments can be adherent, requiring aggressive dissection along the plane between this efferent artery and the fundus to fully expose the neck. Unlike the anteriorly projecting aneurysms, where the view behind the aneurysm is panoramic, the view behind a superiorly projecting aneurysm requires more extensive dissection. The ipsilateral A2 ACA must be mobilized anteriorly and can require dissection of its branches (i.e., the orbitofrontal and frontopolar arteries). The clip application is often more complex with these aneurysms, sometimes requiring fenestrated clips that encircle the ipsilateral A2 ACA.
FIGURE 74-5 Cerebral angiograms demonstrate the different projections of ACoA aneurysms: inferiorly (A) and anteriorly (B) projecting aneurysms. C, A CTA demonstrates a superiorly projecting right A1–A2 junction aneurysm at the ACoA complex.
Posteriorly projecting ACoA aneurysms are arguably the most challenging to clip. With these lesions, the A1 and A2 segments can be identified readily, but the perforators are markedly more difficult to visualize and preserve. They are often displaced laterally, where they become obstacles to the clip blades during clip application, and/or they are displaced posteriorly, where they can easily elude detection. In addition, the parent arteries of the ACoA complex are interposed between the surgeon and the aneurysm neck, making it more difficult to dissect and apply the clips to the neck. Fortunately, these aneurysms are uncommon.12
The inferiorly projecting aneurysm is another favorable aneurysm, with the one caveat: its dome often adheres to the optic apparatus, making it susceptible to avulsion and rupture early in the dissection with frontal lobe retraction. From that standpoint, it can be treacherous, because at that point in the dissection, proximal control is inadequate and the aneurysm anatomy has not been analyzed or even exposed. However, care in retracting the frontal lobe can avert this complication, and the advantages of an inferior projection make it a relatively straightforward aneurysm. Like the anteriorly projecting aneurysm, the ipsilateral A1 and bilateral A2 segments are easily visualized. The contralateral A1 segment can be obscured, which could compromise proximal control of the aneurysm, but the other critical anatomy is accessible. Perforators are rarely a problem, and the necks of these aneurysms are easily closed. These aneurysms can be adherent to the optic nerves and/or chiasm, and often it is preferable to leave the dome undissected or amputate it after clipping the neck, rather than manipulating the optic nerves with unnecessary dissection.
A1–A2 junction aneurysms arise at the bifurcation of the A1 segment into the ACoA and A2 ACA, with a distinctly separate ACoA. These aneurysms have the same variability in their projection (anterior, superior, posterior, and inferior) but also tend to have a lateral projection leftward or rightward. This lateral deviation can result in rupture into frontal lobe parenchyma opposite from the dominant A1 ACA. The perforators tend to be more manageable with these aneurysms than with the ACoA aneurysms.
A1 segment aneurysms are uncommon and tend to be located more proximally toward the carotid bifurcation than the ACoA complex. They are associated with the perforators from this segment, or with curves and bends in the artery as it courses to the ACoA complex.
Variant aneurysms include aneurysms that arise from a fenestration, duplicated or accessory ACoA, accessory A2 ACA, or azygos ACA. Accessory anatomy can pose additional risks, because it can mislead the surgeon and result in inadvertent arterial occlusions if not carefully protected. For example, the neurosurgeon might erroneously clip an important accessory A2 segment if an ipsilateral and contralateral A2 segment have already been identified. Therefore, thorough preoperative review of the anatomy and intraoperative dissection is critical before the final clipping is performed. Infundibuli arising from the ACoA have been observed, particularly with other vascular lesions such as arteriovenous malformations. These infundibuli, like those at the posterior communicating artery and elsewhere, can appear on angiography like aneurysms but transmit normal arteries and must be preserved. Dissection along the course of these arteries distinguishes them from aneurysms. ACoA aneurysms can be giant, atherosclerotic, calcified, or thrombotic. Aneurysms at this location can also be nonsaccular and due to other causes, including infection, trauma, and dissection.
Aneurysm rupture is the most common presentation of patients with ACoA aneurysms, with the classic headache characterized by its sudden onset and severity.1 Patients can present in much worse neurologic condition, with obtundation or coma depending on the extent of hemorrhage and presence or absence of hydrocephalus. ACoA aneurysms are notoriously small, often rupturing at sizes smaller than those that would be considered a threshold for treatment. Therefore, advance symptoms are uncommon. When large or giant, ACoA aneurysms can produce symptoms from mass effect on the optic apparatus (visual field deficits), hypothalamus (endocrine dysfunction), hydrocephalus (obstruction of the foramen of Monro), or frontal lobes (cognitive dysfunction, memory impairment, and seizure).13,14