Surgical Management of Anterior Communicating and Anterior Cerebral Artery Aneurysms

Nomenclature

The anterior cerebral artery (ACA) is divided into five segments ( Fig. 48.1 ). 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%). Some variants of the triplicated A2 (discussed later) can be understood as an extreme proximal bifurcation of the pericallosal and callosomarginal arteries.

Normal Anatomy

The A1 segment courses medially and anteriorly over the optic tract and chiasm to the ACoA complex. Numerous penetrating branches (average 8, range 2 to 15) 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 MCA. The most important source of ACA 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. The artery is almost always present (98%) and can be duplicated (2%). The artery follows a course parallel to the A1 segment, either superior (60%) or anterior (40%) to it. 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 arises from the embryologic lateral olfactory artery, perforators of which later coalesce to form the MCA. Subsequent migration onto the ACA results in its recurrent course. As a result, the recurrent artery of Heubner shares a similar territory to the M1 perforators, supplying 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.

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 approximately 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. The ACoA can be duplicated in one-third of patients and triplicated in 10% of patients but is always present. 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. 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. 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 the gyrus rectus. The recurrent artery is also typically small in caliber, with a diameter of approximately 1 mm. 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. 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 MCAs and posteriorly with posterior cerebral arteries in these watershed areas.

Variant Anatomy

Variations from the normal ACoA anatomy are common and probably contribute to the abnormal hemodynamic that forms aneurysms. Although 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), the 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. Smaller diameters are observed less frequently, with approximately 2% of patients having an A1 segment diameter of 1 mm. Aplastic A1 segments are rare, despite their suggestion of 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. 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.

Variations in ACoA anatomy include duplications, triplications, and fenestrations. ^, 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. Instead, the ACoA complex is usually rotated and/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 a 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. 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. 48.2 ). 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. 48.3 ). 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. 48.4 ). 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.

The MACC just mentioned originates during embryogenesis when elongating ACAs coalesce in the midline to form plexiform anastomoses at 44 days. Normally, the MACC regresses and disappears as the A2 segments mature, but vestigial remnants can account for the accessory ACA. The MACC will give rise to perforators which normally belong to the ACoA perforator complex, supplying the hypothalamus, subgeniculate cingulate cortex, and genu of the corpus callosum.