The anterior communicating complex formed by the ACA, ACoA and adjacent branches is a common site for aneurysm formation (1). Microvascular reconstruction procedures used to manage aneurysms require thorough knowledge of the vascular anatomy and variations for planning of surgical strategy (14). Previous reports intimate variations in the vascular anatomy including ACA hypoplasia (1,6), single (Azygos) or triple ACAs (10). The callosomarginal artery may be missing (3) and when present the PerA-CMA junction may be superior, anterior or inferior to the genu of the corpus callosum (4). As data from Africa is scarce, this paper aims to report the variant anatomy of the anterior cerebral artery in Kenyans.
MATERIALS AND METHODS
Thirty six cadaveric brains (72 hemispheres) for routine dissection at the Department of Human Anatomy, University of Nairobi, were used in the study. Any subject with evidence of pathology or trauma of the brain and its supplying vessels that may have affected the topography of the arteries was excluded from the study. Each calvarium was opened using a saw, the dura incised and the brain detached at the spino-medullary junction then carefully lifted out. The arachnoid mater was peeled off to expose the vessels at the base of the brain and their branches identified. The origin, course, termination and variable anatomy of the anterior cerebral and anterior communicating arteries were noted and recorded. The dissection was done with the aid of a hand lens (x10) and representative photographs taken using a digital camera (Sony cybershot 7.2 megapixels). Fenestration of the ACoA was defined as an incomplete separation of the anterior communicating artery while two separate ACoAs were considered duplicated.
Seventy two cases (41 males and 31 females) were available for study. The anterior cerebral artery was the smaller terminal branch of the internal carotid artery and was joined to its fellow ACA by an anterior communicating artery in all the cases. In 66 hemispheres (92%) the A2 segment coursed round the genu of the corpus callosum and terminated as the pericallosal and callosomarginal arteries. Most of the PerA-CMA junctions were supracallosal (60%) while others were infracallosal (27%) or precallosal (5%). In 6 cases (8%) the callosomarginal artery was absent and there was thus no PerA-CMA junction. An accessory ACA was documented in one brain (Fig. 1). It was given off from the anterior communicating artery communicating artery and accompanied the right and left ACAs around the genu of the corpus callosum. This vessel terminated midway above the body of the corpus callosum by giving branches to both hemispheres. Early termination of the pericallosal artery was observed in four hemispheres (6%). In these cases, the left pericallosal artery ended in the cingulate sulcus at the level of the genu of the corpus callosum and a collateral branch of the right pericallosal artery vascularised the posterior territory of both hemispheres. This “bihemispheric pericallosal artery” originated at the level of the genu of the corpus callosum and ran backward in the midline within the callosal cistern (Fig 2). In one case the A2 segments of both ACAs had an intertwining course. Following communication at the ACoA, the right anterior cerebral artery crossed the midline superior to the left ACA and then traversed forwards along the orbital surface. It then recrossed to its own side and had a standard subsequent course (Fig 3). The ACoA had a variable pattern in 14 hemispheres (40%). Fenestration was observed at an incidence of 26% (Fig 4) while that of complete duplication of the ACoA was 14% (Fig 5).
In the present study, a normal terminal ACA bifurcation was recorded in 66 (92%) cases. The callosomarginal artery (CMA) was absent in 8% of the hemispheres. Previous studies have reported disparate rates for the absence of the callosomarginal artery (Table 1), raising questions as to its value as a landmark in the nomenclature of the distal ACA. This difference in reported incidences may be in part due to variable definitions of the callosomarginal artery. According to Rhoton (9), PerA is the primary extension of the ACA beyond ACoA and the CMA is its largest cortical branch. For other authors, CMA comes into existence after its bifurcation point with the PerA (3,8,10,12). In the current study, CMA as the artery originating from the distal ACA, coursing in the cingulate sulcus, and producing cortical branches. The pericallosal-callosomarginal junction (perA-CMA) in the current study was above, below or in front of the genu of the corpus callosum in 60%, 28%, and 4% of the cases respectively. Most aneurysms of the distal ACA arise at the perA-CMA junction (4,13). This anatomical detail may dictate exploration of the interhemispheric fissure above the corpus callosum for aneurysms of distal ACA in a significant proportion of brains. Four (6%) of 62 hemispheres had a “bihemispheric pericallosal artery” which ran backward within the callosal cistern supplying both hemispheres. The data by Ture denotes a much higher incidence of 13.3% (12). In one case a third ACA was observed arising from the ACoA and accompanying the two normal ACAs around the genu of the corpus callosum. Acessory ACAs are rare in literature. Bihemispheric pericallosal and accessory anterior cerebral arteries may be explained by the embryological development of the cerebral arteries. Padget observed an embryonic median artery of the corpus callosum which was a branch of the ACoA directed toward the commissural plate (7). Persistence of the median artery of the corpus callosum into adulthood forms an accessory ACA. However, if one of the two A2 segments is underdeveloped, its territory may be vascularized either by the median artery of the corpus callosum or by the contralateral pericallosal arteries (7). This variation corresponds to the bihemispheric pericallosal artery observed in the current study. The observed incidence of duplication of the ACoA (14%) in the present study is much lower than reported in literature (Table 2). The presence of variations in the ACoA may also be explained by the embryological development of the ACAs. The ACoA has not yet formed in the 21 mm stage embryo. It is a single large canal in embryos of 23mm, and is large and plexiform in the 24mm stage embryo (7). Incomplete fusion of this plexiform anastomosis may lead to a fenestration or a doubling or tripling of the ACoA (2,7). Gomez et al reported mean diameter values of 1.8± 0.1 mm in the case of a single trunk and of 1.1±0.1 mm in the case of a double trunk (2). Thus, in patients with a double trunk, the mean ACoA resistance could be slightly higher than that of patients with a single trunk (2). It follows that collateral flow would probably be better in individuals with single than double ACoAs. Further, Matsumura and Nojiri (5) reported a high incidence of coexisting fenestration and aneurysms of the ACoA and suggested that congenital factors may play a role in the pathogenesis of cerebral aneurysm.
Majority of CMA terminations were supracallosal. ACA were either duplicated or fenetrated in a significant proportion of brains. These anatomical features may form important considerations in the pathogenesis and surgical approach to ACA aneurysms.
Table 1: Table showing the incidence of absence of callosomarginal artery
Table 2: Table showing the incidence of duplicated ACoA
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