CHAPTER 368 Anterior Communicating Artery Aneurysms
Surgical Management of Anterior Communicating Artery and Proximal Anterior Cerebral Artery Aneurysms
Landmark clinical studies have revealed the anterior communicating artery (ACoA) region as the most common site for intracranial aneurysms. In the original Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage (1958 to 1965), 30.3% of 2349 aneurysms were located in the ACoA region.1 Also in this study, the incidence of anterior cerebral artery (ACA) aneurysms proximal to the ACoA junction (on the A1 segment) was 1.5%, and the incidence of aneurysms distal to the ACoA junction was 2.8%. Therefore, the total incidence of A1 segment–ACoA–distal ACA aneurysms in the original Cooperative Study was 34.6%. This incidence has remained fairly constant over the years. In the more recent International Cooperative Study on the Timing of Aneurysm Surgery (1980 to 1983), the incidence of ACoA-ACA aneurysms was 39%.2
Embryology of the Anterior Communicating Artery Region
Basic understanding of the embryologic development of the ACoA region allows comprehension of its most common congenital anomalies. Our current understanding of the developmental anatomy of the intracranial arteries is based on Hager Paget’s 1948 article on this subject.3 At 35 days (12- to 14-mm stage), the primitive anterior division of the internal carotid artery (ICA) develops a distinct distal branch that is the stem of the ACA. By 40 days (16- to 18-mm stage), the stem of the ACA elongates medially toward its counterpart. It is at this stage that a midline cluster of plexiform anastomoses begins to form between the adjacent and elongating ACAs. At 44 days (20- to 24-mm stage), the channels of the midline cluster of plexiform anastomoses coalesce and form one or more ACoAs. In addition, the coalescing channels of the midline cluster of plexiform anastomoses give rise to a median ACA that originates from the ACoA.
Given this description, we can predict the most common congenital anomalies of this region, which are (1) multiple or fenestrated ACoAs, (2) triplicate A2 segments, and (3) the azygous A2 segment. Perlmutter and Rhoton4 found two or three ACoAs in 30% and 10%, respectively, of their 50 cadaver brain dissections. In addition, they confirmed that absence of the ACoA is exceedingly rare.5 Hager Paget calculated that the ACoA is absent in only 0.2% of cases (3 of 1803).6 Persistence of the median artery of the corpus callosum creates three A2 segments. Baptista identified triplicate ACAs in 13.1% of his specimens (50 out of 381),7 but Perlmutter and Rhoton found triplicate ACAs in only 2% of their specimens (1 out of 50).5 An azygous or solitary A2 segment arises when the paired ACAs regress after formation and enlargement of the median artery of the corpus callosum.3 An azygous A2 has been identified in only 0.26% of general autopsies7 and in only 0.22% of unselected angiograms.8 The higher incidence of azygous A2 segments in aneurysm series results from the fact that 41.1% of azygous A2 segments have a terminal aneurysm.8
Microsurgical Anatomy of the A1 Segment–Anterior Communicating Artery–A2 Segment Region
The anatomy of this region is reviewed in detail elsewhere in this book. Therefore, here we discuss only a few definitions and anatomic details that will serve as a background for our subsequent surgical discussion. The ACA is divided into five anatomic segments, A1 to A5.4 The A1 segment starts at the ICA termination and ends at ACoA junction. The A2 segment starts at the ACoA junction, follows the course of the rostrum of the corpus callosum, and terminates at the junction of the rostrum and genu of the corpus callosum. It is commonly referred to as the pericallosal artery. The A3 segment follows the curve of the genu of the corpus callosum and terminates where the ACA turns posteriorly above the genu. The A4 and A5 segments run over the body of the corpus callosum; the transition from A4 to A5 is arbitrarily set at the level of the plane defined by the coronal suture.4
A1 Segment
The average diameter of the A1 segment is 2.6 mm (range, 0.9 to 4 mm),5 about that of the middle cerebral artery (MCA) at the ICA bifurcation and about half that of the supraclinoid ICA at its origin (Fig. 368-1). Although absence of the A1 segment is extremely rare, hypoplasia of the A1 segment is recognized in about 10% of cases.5 Perlmutter and Rhoton chose a diameter of 1.5 mm as the threshold for labeling the A1 segment as hypoplastic, but it should be recognized that there is no agreed threshold below which an artery is labeled “hypoplastic.” They found that 10% of their specimens had A1 segments that were 1.5 mm or less in diameter and that 2% had A1 segments 1 mm or less in diameter.5 Another rare but surgically important anatomic variant is the duplication of the A1 segment (2%), which occurs only unilaterally.5
The paired A1 segments are of equal diameter in only half of cases. In 50% of cases, there is a difference of 0.5 mm or more between the diameters of the A1 segments. In 12% of cases, the difference is of 1 mm or more.5 This discrepancy in diameter between the paired A1 segments is even more prevalent when one considers cases with an ACoA aneurysm. In the presence of an ACoA aneurysm, the paired A1 segments are of unequal diameter in as many as 85% of cases.9 Typically, the base of the aneurysm arises on the side of the larger A1, and the dome points toward the side of the hypoplastic A1 segment.
Anterior Communicating Artery
The diameter of the ACoA is on average about half that of the A1 segment (see Fig. 368-1). The average diameter of the A1 segment is 2.6 mm, whereas that of the ACoA is 1.5 mm (range, 0.2 to 3.4 mm).5 There is a constant relationship between the diameter of the ACoA and the difference in the diameters of the A1 segments: the larger the difference between the A1 segments, the larger the ACoA.5 Because unequal A1 segments are typically found in the presence of an aneurysm and unequal A1 segments are typically associated with a larger ACoA, one can expect to always find a patent ACoA when exploring an aneurysm in this region, even when it is not demonstrated angiographically. The ACoA is rarely oriented in a strictly transverse plane, as depicted in most non-neurosurgical textbooks. At the level of the ACoA junction, the left ACA courses anterior to the right in 48% of cases, the right ACA courses anterior to the left in 34% of cases, and only in 18% of cases do they enter the interhemispheric fissure side by side.5 Because of the course of the ACAs, the ACoA is usually oriented in an oblique or sagittal plane. Absence of the ACoA is exceedingly rare (only 0.2% of cases).6
A2 Segment
Although most neurosurgeons refer to the A2 segment as the pericallosal artery and consider the callosomarginal artery a branch of the pericallosal artery, some use this term to define one of the two branches at the bifurcation of the distal A2 segment, the other branch being the callosomarginal artery. The main problem with this alternative nomenclature is that because the callosomarginal artery is absent in 18% of cases, it is difficult to define where the pericallosal artery starts.4 The callosomarginal artery originates most frequently (60% of cases) from the A3 segment, an average of 43 mm (range, 12 to 47 mm) from the ACoA junction, which places it beyond the junction of the rostrum and genu of the corpus callosum. It originates more proximally (from the A2 segment) in 10% of cases and more distally (from the A4 segment) in 12% of cases.4
Perforators of the A1 Segment, Anterior Communicating Artery, and A2 Segment
The A1 segment gives rise to an average of eight perforators (range, 2 to 15), 41% of which terminate in the anterior perforated substance.5 These perforators are sometimes identified as the medial lenticulostriate arteries to distinguish them from the lateral lenticulostriate arteries, which originate from the M1 segment and also terminate in the anterior perforated substance.10,11 Typically, the proximal half of A1 gives rise to twice as many perforators as the distal half. Another way of stating this is that of all the perforators of the A1 segment, two thirds arise from the proximal half and one third arise from the distal half. The proximal half gives rise to an average of 5.3 perforators (range, 1 to 11), whereas the distal half gives rise to an average of 2.5 perforators (range, 0 to 6).5 Most (86%) of the A1 perforators arise from the superior (54%) and posterior (32%) surfaces of this segment. Only rarely (14%) do they arise from the inferior (9%) and anterior (5%) surfaces of A1.5 Of all the A1 perforators, 41% terminate in the anterior perforated substance. These perforators branch into as many as 49 vessels as they reach the anterior perforated substance.12 Most enter the medial portion of the anterior perforated substance and typically course posterior to the branches of the medial striate artery of Heubner.12 The remaining A1 perforators terminate in the dorsal optic chiasm or suprachiasmatic hypothalamus (29%), inferior frontal lobe (10%), optic tract (11%), sylvian fissure (5%), dorsal optic nerve (2%), or interhemispheric fissure (2%).5
There have been conflicting anatomic reports concerning the number of ACoA perforators. Perlmutter and Rhoton,5 in their study of 50 brains, found that the ACoA may have no perforators or as many as four.5 By contrast, Dunker and Harris13 and Crowell and Morawetz14 examined 20 and 10 brains, respectively, and both concluded that the ACoA always has at least three perforators.
In a pattern similar to that seen on the A1 segment, most (90%) of the ACoA perforators arise from its superior (54%) and posterior (36%) surfaces, and only rarely (10%) from its anterior (7%) and inferior (3%) surfaces.5 Therefore, most ACoA perforators are hidden from the surgeon’s view. Of all the ACoA perforators, 51% terminate in the suprachiasmatic region, 21% terminate on the dorsal optic chiasm, and 15% reach the anterior perforated substance.5
Medial Striate Artery (Recurrent Artery of Heubner)
The most important perforator from the proximal A2 segment is the medial striate artery, better known as the recurrent artery of Heubner (see Fig. 368-1). We have reviewed elsewhere the anatomy of this vessel and the life and accomplishments of its discoverer, Johann Otto Leonhardt Heubner (1843-1926), a German pediatrician who described it in an article published in 1872.15 The medial striate artery of Heubner arises from the A2 segment in 78% of cases, from the A1 segment in 14% of cases, and at the level of the ACoA in 8% of cases.5 Perlmutter and Rhoton found that it originates within 4 mm of the ACoA junction (either proximal or distal to it) in 95% of cases.5 They also found this artery to be absent (only on one side) in 2% of cases and duplicated (also only on one side) in 2% of cases.5 By contrast, Gomes and colleagues found this artery to be absent in 3% of cases but duplicated in 12% of cases.16
The medial striate artery of Heubner courses anterior to the A1 segment in 60% of cases and superior to the A1 segment in 40% of cases.5 Therefore, this artery will be encountered before the A1 segment on initial retraction of the frontal lobe during surgery in most cases (60%). The length of the medial striate artery of Heubner is on average twice that of the A1 segment. Whereas the average length of the A1 segment is 12.7 mm,5 that of the medial striate artery is 23.4 mm (range, 12 to 38 mm).16 Its length therefore increases its exposure to injury during surgery.
The medial striate artery of Heubner should not be confused during surgery with the orbitofrontal artery, which is typically the second major branch of the A2 segment (see Fig. 368-1). The medial striate artery of Heubner is usually the first branch of the A2 segment immediately after the ACoA junction. It is also typically the largest vessel arising from the A2 segment. The orbitofrontal artery originates on average 5 mm (range, 0 to 15 mm) from the ACoA junction and has an average diameter of 0.9 mm (range, 0.4 to 2 mm).4 Based on diameter alone, the orbitofrontal artery can be mistaken for the medial striate artery of Heubner, which has an average diameter of 1 mm (range, 0.2 to 2.9 mm).5 Their courses, however, are very different. The medial striate artery of Heubner follows the course of the A1 segment, whereas the orbitofrontal artery courses perpendicularly over the gyrus rectus and across the olfactory tract11 (the subfrontal gyral and sulcal anatomy is depicted in Fig. 368-2). Another important anatomic distinction of the orbitofrontal artery is that it typically demarcates the boundary of the lamina terminalis cistern (where it originates) and the beginning of the callosal cistern.11
FIGURE 368-2 Anatomy of the subfrontal gyri and sulci in relation to the course of the olfactory nerve.
After the orbitofrontal artery, the third major branch of the A2 segment is the frontopolar artery. The frontopolar artery is a cortical branch that originates on average 14 mm (range, 2 to 30 mm) from the ACoA junction and has an average diameter of 1.3 mm (range, 0.6 to 1.8 mm).4 It courses anteriorly along the medial surface of the frontal lobe and crosses the subfrontal sulcus (see Fig. 368-2).4
The medial striate artery of Heubner supplies the anterior striatum (caudate nucleus and putamen), a portion of the outer segment of the globus pallidus, and the anterior limb of the internal capsule.5 Injury to this vessel typically results in a moderate paresis of the contralateral upper extremity and mild paresis of the contralateral face. It also causes dysfunction of the tongue and palate, which can only be documented during a careful swallowing evaluation. If the dominant hemisphere is involved, an expressive aphasia may be evident. In most patients, these deficits tend to resolve completely in a matter of months.
In addition to the medial striate artery of Heubner, the orbitofrontal artery, and the frontopolar artery, the proximal A2 segment gives rise to an average of 4.8 (range, 0 to 10) basal perforating branches. These branches supply the optic chiasm, anterior hypothalamus, medial portion of the anterior commissure, pillars of the fornix, and anterior-inferior portion of the striatum (caudate nucleus and putamen).4
Arachnoid Cisterns of the A1 Segment–Anterior Communicating Artery–A2 Segment Region
The sequential recognition and opening of three arachnoid cisterns (carotid, chiasmatic, and lamina terminalis) leads to the ACoA junction (Fig. 368-3). The A1 segment originates within the confines of the carotid cistern. It then courses within the lamina terminalis cistern over either the optic chiasm (70% of the time) or, less frequently, over the optic nerve (30% of the time).5 It enters into the interhemispheric fissure still within the confines of the lamina terminalis cistern.11 In addition to the origin of the A1 segment, the carotid cistern contains the supraclinoid ICA and the origins of its branches. The carotid cistern shares its medial wall with the chiasmatic cistern, which contains the optic nerves, optic chiasm, and infundibulum, but does not contain any major arteries. The lamina terminalis cistern is a midline structure that contains the paired A1 and proximal A2 segments, the ACoA, and the medial striate arteries of Heubner.11
Because the lamina terminalis cistern contains the A1-ACoA-A2 complex, ACoA aneurysms by definition arise within the confines of this cistern (see Fig. 368-3). A clear understanding of the boundaries of this cistern is therefore important microsurgically. Inferiorly, the lamina terminalis cistern stretches over the surface of the optic chiasm, where it apposes the chiasmatic cistern. Posteriorly, it is bounded by the lamina terminalis. Superiorly, it stretches into the interhemispheric fissure, where it is bounded by the rostrum of the corpus callosum. Its anterior surface stretches free over the A1-ACoA-A2 complex. Laterally, the lamina terminalis cistern surrounds the entire A1 segment after it emerges from the carotid cistern. Yaşargil points out that the lateral boundary of the lamina terminalis cistern is a thickened band of arachnoid fibers that stretch between the area immediately medial to the olfactory nerve and the optic nerve. The A1 segment enters the lamina terminalis cistern below this thickened band of arachnoid fibers. The medial striate artery of Heubner and the orbitofrontal artery originate within the confines of the lamina terminalis cistern.11
For the purpose of the arachnoid dissection during the approach to an ACoA aneurysm, it is important to remember that the optic nerves and chiasm are found in a separate cistern, namely the chiasmatic cistern. This means that if the aneurysm dome is oriented superiorly or posteriorly, one can dissect along the anterior edge of the optic chiasm and the optic nerves without entering the lamina terminalis cistern and potentially disturbing the aneurysm (Fig. 368-4).
In the sagittal plane, ACoA aneurysms may project superiorly, anteriorly, inferiorly, or posteriorly. Although most ACoA aneurysms do not fall neatly into one of these four categories, the recognition of the predominant sagittal projection of these aneurysms is useful in anticipating the complications associated with each projection. This helpful classification scheme for ACoA aneurysms was formulated by Yaşargil.40 It should be noted that our anterior/posterior and superior/inferior nomenclature refers to the standard anatomic orientation, not the surgical orientation of the lesion, as originally described by Yaşargil.
Most ACoA aneurysms (71.2%) project into the interhemispheric fissure, and only a minority (12.8%) project inferiorly into the chiasmatic cistern (16% of all ACoA aneurysms have complex, multilobulated projections).40 Whereas superior- and posterior-pointing aneurysms are found entirely within the interhemispheric fissure, anterior-pointing aneurysms are typically found only partially inside the interhemispheric fissure. Inferior-pointing aneurysms, the most treacherous of ACoA aneurysms if ruptured, are almost entirely outside the interhemispheric fissure and are typically adherent to the optic chiasm, the optic nerves, or the dura of the interoptic space. In terms of the initial subfrontal exposure of ACoA aneurysms, superior- and posterior-pointing aneurysms are the most favorable because they rarely rupture at this stage. By contrast, inferior-pointing aneurysms are the worst in this respect because elevation of the frontal lobes may avulse the dome from the optic chiasm, optic nerves, or the dura of the interoptic space early in the subarachnoid dissection.
History of Surgical Approaches for ACoA Aneurysms
The history of surgical treatment of aneurysms is reviewed in detail elsewhere in this book. Table 368-1 provides a chronology of the landmark surgical contributions pertinent to microsurgery of ACoA aneurysms. The modern frontosphenotemporal or “pterional” craniotomy as described by Yaşargil and Fox17,18 is the culmination of a 40-year neurosurgical refinement of a safe and efficient craniotomy to approach ACoA aneurysms. It is based on Dandy’s lateral subfrontal approach through a frontotemporal craniotomy,19–21 it incorporates elements of Kempe’s sphenoid wing removal,22 and it acknowledges the need to resect a portion of the frontal lobe as advocated by Norlén and Barnum,23 but only in a limited fashion (gyrus rectus resection) as advocated by Kempe and VanderArk.22,24 The pterional craniotomy is currently favored by most neurosurgeons around the world. A few neurosurgeons, however, still advocate a frontal interhemispheric approach as originally advocated by Tönnis25 and Pool26,27 through a frontal parasagittal craniotomy for some ACoA aneurysms.28–30
TABLE 368-1 Chronology of Landmark Surgical Contributions Pertinent to Microsurgery of Anterior Communicating Artery Aneurysms
| DATE | SURGEONS | CONTRIBUTION |
|---|---|---|
| 1918 | George J. Heuer | First description of frontotemporal craniotomy for lateral subfrontal approach to the circle of Willis19 |
| Walter E. Dandy | ||
| 1931 | Norman M. Dott | First direct surgical attack of an aneurysm (internal carotid artery bifurcation)60 |
| 1935 | W. Tönnis | Anterior interhemispheric approach first used for anterior communicating artery aneurysms25 |
| 1937 | Walter E. Dandy | First clipping of an aneurysm (posterior communicating artery)20 |
| 1941 | Walter E. Dandy | Frontotemporal approach first used for anterior communicating artery aneurysms21 |
| 1953 | Gösta Norlén | Transfrontal approach (partial frontal lobectomy) first used for anterior communicating artery aneurysms23 |
| Alec S. Barnum | ||
| 1956 | Valentine Logue | Proximal ligation of A1 segment44 |
| 1961 | Lawrence Pool | Bilateral anterior subfrontal/interhemispheric approach for large series of anterior communicating artery aneurysms26,27 |
| 1962 | Lyle French | Transfrontal approach (partial frontal lobectomy) for large series of anterior communicating artery aneurysms49 |
| 1968 | Ludwig Kempe | Sphenoid extension of frontotemporal craniotomy and gyrus rectus resection22 |
| 1971 | Ludwig Kempe, G. D. VanderArk | Gyrus rectus approach first used for anterior communicating artery aneurysms24 |
| 1975 | M. G. Yaşargil, John L. Fox | Frontolateral, spheno-orbital, or pterional craniotomy for aneurysms17,18 |
Clinical and Radiographic Presentation of Anterior Communicating Artery Aneurysms
The clinical presentation of aneurysmal subarachnoid hemorrhage (SAH) is reviewed in another chapter and elsewhere.31 Because the clinical presentation of ruptured ACoA aneurysms is in general not different from that of aneurysms in other locations, we will not discuss this issue in this chapter.
The radiographic evaluation of ACoA aneurysms, however, bears further discussion because there are two radiographic issues that are unique to ACoA aneurysms. The first is that not infrequently the diagnosis of an ACoA aneurysm can be made on the basis of the computed tomography (CT) scan alone because the CT scan may reveal either subarachnoid blood only in the interhemispheric fissure or a thicker clot in the interhemispheric fissure (Fig. 368-5A). Similarly, an intraparenchymal hemorrhage in the region of the gyrus rectus is indicative of an ACoA aneurysm (Fig. 368-6A).
