The anterior cerebral artery (ACA) is a paired major artery of the brain, arising as a terminal branch of the internal carotid artery (ICA), and it primarily supplies oxygenated blood to the medial surfaces of the frontal and parietal lobes, the corpus callosum, and anterior portions of the basal ganglia.[1] It plays a critical role in vascularizing regions responsible for motor and sensory functions of the lower extremities, executive functions, and interhemispheric communication.[2] The ACA forms part of the anterior circulation of the circle of Willis, connecting to its contralateral counterpart via the anterior communicating artery, which provides collateral circulation in cases of occlusion.[3]The ACA is divided into segments along its course: the A1 (pre-communicating) segment extends from the ICA bifurcation to the anterior communicating artery; the A2 (post-communicating) segment begins at the anterior communicating artery and ascends over the optic chiasm toward the genu of the corpus callosum; subsequent segments include A3 (pre-callosal), A4 (supra-callosal), and A5 (postero-callosal), collectively forming the pericallosal artery as it runs posteriorly along the corpus callosum within the interhemispheric fissure.[1] This trajectory allows the ACA to course superiorly and medially, parallel to the midline, supplying the cingulate gyrus and adjacent structures while avoiding the lateral cerebral convexities, which are primarily served by the middle cerebral artery.[4]Key branches of the ACA include the recurrent artery of Heubner (arising from the A1 or proximal A2 segment), which supplies the anterior striatum, anterior internal capsule, and uncinate fasciculus; medial lenticulostriate (basal perforating) arteries that vascularize the anterior basal ganglia, including the head of the caudate nucleus, anterior putamen, and globus pallidus; and cortical branches such as the orbitofrontal, frontopolar, internal frontal, paracentral, and parietal arteries, which distribute to the medial frontal lobe, superior frontal gyrus, and anterior two-thirds of the medial hemispheric surface.[1] Additional small perforators from the ACA and anterior communicating artery nourish the anterior perforated substance, hypothalamus, and optic chiasm.[3]Clinically, the ACA's territory is vulnerable to infarction from embolism or thrombosis, often resulting in contralateral lower limb weakness or paralysis (paraparesis), urinary incontinence, abulia, and grasp reflexes due to involvement of the leg-foot area of the motor cortex and frontal association areas; unilateral occlusion distal to the anterior communicating artery spares the upper body but impairs lower extremity sensorimotor function, while bilateral stem occlusion can lead to profound frontal lobe syndromes including personality changes and akinetic mutism.[4] The ACA's anatomical variants, such as azygos configurations, can influence surgical approaches in aneurysms or strokes affecting the anterior circulation.[1]
Anatomy
Origin and Course
The anterior cerebral artery (ACA) originates from the internal carotid artery (ICA) as the smaller terminal branch at its bifurcation, typically at the level of the anterior clinoid process.[5]The proximal portion, designated the A1 or pre-communicating segment, extends from this origin to the anterior communicating artery and measures approximately 12-14 mm in length with a typical diameter of 1.5-3 mm.[6][7] This horizontal segment courses superiorly and medially over the optic chiasm and optic nerve, traversing the anterior perforated substance while deviating toward the midline.[8][9]The A2 or post-communicating segment arises at the anterior communicating artery—which interconnects the ACAs bilaterally as a component of the circle of Willis—and ascends anterior to the lamina terminalis before entering the interhemispheric fissure.[8]
Branches
The anterior cerebral artery (ACA) is divided into segments, with its branches arising primarily from the A1 (precommunicating) and A2 (postcommunicating) segments, as well as more distal portions.[8]From the A1 segment, which extends from the internal carotid artery bifurcation to the anterior communicating artery, the principal branches are the medial striate arteries. These small perforating vessels originate along the superior or posterior aspect of the A1 segment and course medially or posteromedially toward the anterior perforated substance. The recurrent artery of Heubner, a prominent medial striate branch, typically arises from the proximal A2 segment but can originate variably from the distal A1; it directs posteriorly and laterally, parallel to the anterior communicating artery.[4][8]The A2 segment, beginning at the anterior communicating artery and ascending over the corpus callosum, gives rise to several cortical and central branches. The orbitofrontal artery emerges from the inferior aspect of the proximal A2 and extends anteriorly and inferiorly toward the orbital surface of the frontal lobe. The frontopolar artery branches from the anterior portion of the A2 and proceeds superiorly and anteriorly along the medial frontal pole. More distally, the A2 continues as the pericallosal artery, which runs posteriorly along the superior surface of the corpus callosum, following its genu and body. Arising from the superior aspect of the A2 or early pericallosal artery, the callosomarginal artery courses posteriorly over the cingulate gyrus, parallel to the pericallosal trunk.[4][8]Deep penetrating branches of the ACA include the subcallosal and precuneal arteries. The subcallosal artery typically originates near the anterior communicating artery junction or proximal A2 and directs posteriorly beneath the rostrum of the corpus callosum.[10] The precuneal artery emerges from the distal ACA (A4 or A5 segments) and courses toward the precuneus.[11] Perforators from the anterior communicating artery, arising near the ACA junction, supply the hypothalamus and optic chiasm.[12]In standard anatomy, the terminal branches of the distal ACA consist of the posterior extensions of the pericallosal and callosomarginal arteries, which arborize over the medial parietal and occipital surfaces; in some configurations, these include distinct posterior parietal and parieto-occipital arteries arising near the splenium of the corpus callosum.[8]
Relations
The anterior cerebral artery (ACA) maintains specific spatial relationships with surrounding neurovascular and dural structures throughout its course, which are critical for understanding its anatomical positioning within the intracranial space. In the A1 segment, the ACA originates from the internal carotid artery and travels superiorly over the optic chiasm and optic nerve, forming its primary anterior relation, while also lying inferior to the anterior perforated substance through which its medial striate branches penetrate.[13][14] This configuration positions the vessel in close proximity to the optic apparatus, with the A1 segment typically coursing over the ipsilateral optic nerve and chiasm in the standard Osborn classification.[8]Superiorly and medially, the A2 segment of the ACA ascends within the longitudinal cerebral fissure, paralleling the falx cerebri and arching around the genu of the corpus callosum before continuing posteriorly along its body.[13][15] The vessel remains adjacent to the falx cerebri medially, occasionally giving rise to a meningeal branch from the precallosal A3 segment that supplies the anterior falx.[8] Inferiorly, the ACA relates to the lamina terminalis and the rostrum of the corpus callosum, particularly near the anterior communicating artery complex, where it maintains a position above these midline structures.[13][15]Along its course, the ACA exhibits venous and neural proximities that highlight its integration into the interhemispheric environment. The anterior cerebral veins run parallel to the ACA, particularly the pericallosal vein, which accompanies the artery posteriorly and drains into the vein of Galen.[15][13] Neural structures such as the olfactory tracts lie in close anterior proximity, with the ACA's orbitofrontal branches supplying these tracts as they course forward.[14][15]Asymmetry between the left and right ACAs is common, often manifesting in the A1 segment where one side may be hypoplastic (diameter ≤1.5 mm in about 10% of cases) or longer and more tortuous, potentially altering their relative positions to midline structures like the falx cerebri due to inherent anatomical variations.[13][14] This bilateral difference can influence the vessel's trajectory in the interhemispheric fissure without pathological midline shifts.[15]
Development and Variations
Embryological Development
The anterior cerebral artery (ACA) derives from the primitive internal carotid artery (ICA) system during early embryonic development, emerging as a cranial branch around weeks 4 to 6 of gestation. At approximately 28-29 days (Padget stage 1, embryo size 4-5 mm), the primitive ICA forms from the cranial portion of the dorsal aorta and the third aortic arch, with the ACA initially appearing as an olfactory artery curving around the optic vesicle to supply the developing olfactory region and basal forebrain.[16][17] By week 5 (Padget stage 4, 12-14 mm), the ACA develops as a distal extension of the ICA's cranial division, termed the primitive olfactory artery (pOlfA), which provides initial vascularization to the nasal fossa and olfactory nerve roots.[17]The formation of the circle of Willis precursor involves the fusion of carotid sprouts with the bilateral longitudinal neural arteries, establishing a foundational anastomotic network by week 8. During week 5 (Padget stage 2-3, 5-12 mm), the caudal branches of the primitive ICA extend posteriorly to anastomose with the longitudinal neural arteries, forming the precursors to the posterior communicating arteries, while anterior extensions contribute to the ACA's bilateral symmetry.[16] By Carnegie stage 23 (approximately week 8, 20-40 mm), this fusion process typically closes the circle of Willis in most embryos, creating a polygonal arterial ring that links the anterior and posterior circulations.[18] The anterior communicating artery (AComA) plays a critical role in this midline fusion, arising from plexiform anastomoses between medial branches of the bilateral ICAs around week 5, thereby connecting the paired ACAs and ensuring balanced perfusion across the midline.[16][17]Maturation of the ACA's A1 and A2 segments occurs concurrently with the regression of primitive olfactory artery remnants during weeks 6 to 8. The A1 segment, representing the pre-communical portion from the ICA bifurcation to the AComA, derives from the primitive ventral ophthalmic artery and stabilizes by week 6 (Padget stage 5, 16-18 mm), as the pOlfA becomes more prominent in supplying the olfactory nerve.[16] The A2 segment, the post-communical portion, emerges along the developing cerebral hemispheres by week 5 (Padget stage 3), with further branching to the medial frontal lobe by week 7-8 (Padget stages 6-7), coinciding with the reduction of the pOlfA to a minor remnant branch supplying the olfactory nerve.[17] This regression reflects hemodynamic remodeling, where dominant pathways persist while transient embryonic vessels atrophy.[15]Key developmental processes are regulated by signaling pathways such as vascular endothelial growth factor (VEGF) and Notch, which drive angiogenesis and arterial specification in the ACA. VEGF promotes endothelial cell proliferation and differentiation during the initial sprouting from the primitive ICA around weeks 4-5, facilitating vessel elongation toward the telencephalon.[16]Notch signaling, active from early stages, influences arterial-venous fate decisions and smooth muscle recruitment, ensuring proper maturation of the A1 and A2 segments by week 8 and contributing to the stability of AComA connections.[16]
Anatomical Variations
The anterior cerebral artery (ACA) displays several anatomical variations, most notably in its A1 (pre-communicating) and A2 (post-communicating) segments, which can affect cerebral perfusion patterns and are critical for accurate interpretation in neuroimaging studies such as magnetic resonance angiography (MRA) or digital subtraction angiography (DSA). These variants arise from incomplete regression or persistence of embryonic vessels and are typically asymptomatic but may influence surgical planning or endovascular interventions by altering expected vascular dominance or collateral flow pathways.[19][8]A common variation involves hypoplasia or absence of the A1 segment, with hypoplasia reported in 1-13% of cases and complete absence in 1-6% of the general population based on angiographic and autopsy data.[20] This asymmetry often results in contralateral A1 dominance, where the larger A1 segment supplies both ACAs via the anterior communicating artery (ACoA), providing compensatory flow; such configurations are identified in up to 10-25% of individuals when combining hypoplastic and aplastic forms, emphasizing the need for bilateral vessel assessment in imaging to avoid misdiagnosis of occlusions.[20][21]Rarer distal variants include the azygos ACA, in which bilateral A1 segments fuse into a single midline trunk that continues as an unpaired A2 without an ACoA, exhibiting a pooled prevalence of 1.5% (95% CI: 0.01-0.02) across imaging and autopsy studies.[19] Similarly, bihemispheric ACA occurs when one ACA irrigates both hemispheres due to hypoplasia or absence of the contralateral ACA and ACoA, with a prevalence of approximately 1% in MRA evaluations.[21] These midline variants can mimic midline shifts or tumors on imaging if not recognized, potentially complicating aneurysm detection near the ACoA complex.[19]Additional uncommon configurations encompass triple A2 segments, where three A2 branches arise from the ACoA, with prevalence ranging from 0.4% to 3% in angiographic series, and fenestrations (duplications) of the A1 or A2 segments, occurring in 0-4% anatomically and 0.058% angiographically.[21][22] Overall, symmetric bilateral A1 segments predominate in 80-90% of adults per large-scale angiographic studies, underscoring the infrequency of variants while highlighting their relevance for personalized imaging protocols.[20][21]
Function
Vascular Territories
The anterior cerebral artery (ACA) supplies the medial surfaces of the frontal and parietal lobes, as well as key midline structures. Its cortical branches, including the frontopolar and anterior frontal arteries arising from the A2 segment, perfuse the medial frontal lobe, encompassing the superior frontal gyrus and the anterior two-thirds of the cingulate gyrus.[14] These branches ensure oxygenation of regions involved in executive functions and emotional processing, though the focus here is on anatomical distribution.[23]The callosomarginal artery, a major branch of the distal ACA, extends along the cingulate sulcus to supply the paracentral lobule on the medial hemispheric surface. This territory includes the motor and sensory cortices for the lower extremities, located at the junction of the frontal and parietal lobes. Additionally, the pericallosal artery, often the continuation of the ACA, perfuses the genu, rostrum, and body of the corpus callosum, providing essential blood flow to this interhemispheric commissure.[15][13]Subcortically, the recurrent artery of Heubner (also known as the medial striate artery) originates from the proximal A2 segment and supplies the anterior basal ganglia, including the head of the caudate nucleus and anterior putamen, along with portions of the anteroinferior internal capsule. Small perforating branches from the ACA's proximal segments (A1 and early A2) deliver blood to the olfactory bulb, anterior perforated substance, and adjacent structures such as the septal nuclei and anterior commissure.[24][25] The ACA territory interfaces with the middle cerebral artery domain along the medial cortical surface, defining a watershed zone vulnerable to hypoperfusion in borderline flow states.[3]
Physiological Role
The anterior cerebral arteries (ACAs), arising from the internal carotid arteries and interconnected via the anterior communicating artery, contribute approximately 10-20% of total cerebral blood flow as part of the anterior circulation within the circle of Willis, with each ACA typically supplying around 80-90 mL/min in healthy adults.[26] This flow supports critical hemodynamic stability in the medial frontal and superior parietal regions. Hemodynamic assessments via transcranial Doppler ultrasonography reveal typical mean flow velocities of 40-60 cm/s in the A1 segment of the ACA, reflecting efficient laminar flow under normal conditions.[27]Autoregulation in the ACA territory maintains constant blood flow despite fluctuations in systemic pressure, primarily through myogenic and metabolic mechanisms that adjust arteriolar tone. This process operates effectively within a mean arterial pressure (MAP) range of 50-150 mmHg, preventing hypoperfusion or hyperperfusion.[28] Additionally, the ACA responds to changes in arterial partial pressure of carbon dioxide (PaCO₂), with each 1 mmHg increase eliciting approximately a 4% rise in regional blood flow via vasodilation, enhancing oxygen delivery during hypercapnic states.[28]The ACA's perfusion enables key brain functions, including executive processes in the prefrontal cortex such as planning and decision-making, which rely on medial frontal networks for cognitive control.[29] It also supports micturition control through the medial frontal lobe, where excitatory projections from the anterior cingulate and medial prefrontal cortex inhibit the micturition reflex to maintain urinary continence.[30] Furthermore, the ACA supplies the paracentral lobule for motor and sensory processing of the lower extremities, facilitating coordinated leg movements and proprioception.[9]In scenarios of hemodynamic stress, the ACA interacts with leptomeningeal collaterals—thin anastomotic vessels connecting distal branches of the ACA, middle cerebral artery, and posterior cerebral artery—to redistribute flow and preserve perfusion in adjacent territories.[31] These collaterals provide retrograde flow pathways, mitigating potential ischemia by augmenting collateral circulation when primary ACA inflow is compromised.[31]
Clinical Significance
Occlusion and Infarction
Occlusion of the anterior cerebral artery (ACA) typically results from thromboembolism originating from the internal carotid artery or cardiac sources such as atrial fibrillation, atherosclerosis in the A1 segment, or embolism specifically to the recurrent artery of Heubner, leading to ischemic stroke in the ACA territory.[24][32][33] These etiologies account for the majority of cases, with cardioembolism identified as the primary mechanism in up to 63% of ACA infarctions in some cohorts.[34]The clinical presentation of ACA occlusion often includes contralateral lower extremity weakness or paralysis due to involvement of the paracentral lobule, urinary incontinence from medial frontal lobe dysfunction, and behavioral changes such as abulia or akinetic mutism arising from ischemia in the cingulate gyrus and supplementary motor area.[24][32] Motor deficits with a crural (leg-predominant) distribution are particularly characteristic, occurring in approximately 86-91% of patients.[35][36]On imaging, ACA infarctions appear as wedge-shaped lesions in the medial frontal and parietal lobes on computed tomography (CT) or magnetic resonance imaging (MRI), with diffusion-weighted MRI particularly effective for delineating acute ischemic boundaries in this territory.[24][37]Major risk factors for ACA occlusion mirror those of broader anterior circulation strokes and include hypertension, diabetes mellitus, hypercholesterolemia, smoking, and atrial fibrillation, with ACA infarcts comprising approximately 5-10% of anterior circulation ischemic events.[24][38]Hypertension is the most prevalent, affecting over 80% of patients in reported series.[39]Acute management focuses on rapid reperfusion, with intravenous thrombolysis using tissue plasminogen activator (tPA) recommended within 4.5 hours of symptom onset for eligible patients, and mechanical thrombectomy indicated for large vessel occlusions to achieve recanalization rates exceeding 70% in ACA cases.[24][40] These interventions improve functional outcomes when performed promptly, though ACA-specific data emphasize the need for tailored endovascular approaches due to anatomical challenges.[41]
Aneurysms
Aneurysms of the anterior cerebral artery (ACA) primarily occur at the anterior communicating artery (ACoA) junction, accounting for approximately 30-37% of all intracranial aneurysms.[42] These represent the most common site for ACA-related aneurysms, with about 85% located at the ACoA complex due to hemodynamic stresses from asymmetric A1 segment flow or hypoplasia.[43] Less frequent predilection sites include the A1 segment origin (rare, often saccular at perforator branches, ~1% of all intracranial aneurysms) and A2 segment bifurcations (~1.5-9%), with aneurysms on the ACA proper (excluding ACoA) comprising approximately 3-5% of all intracranial cases overall.[44][45] Intracranial aneurysms are more prevalent in women at a ratio of about 1.5-2:1 compared to men, though ACoA subtypes show a slight male predominance in some cohorts.[46]The predominant type is saccular (berry) aneurysms, which form 90% of cerebral cases and arise from congenital medial defects at arterial bifurcations, exacerbated by pulsatile flow and wall shear stress.[47]Fusiform aneurysms are rarer in the ACA, typically associated with atherosclerosis or dissection, and present as elongated dilations rather than focal outpouchings.[48]Aneurysm growth is influenced by hemodynamic factors, such as turbulent flow at the ACoA due to A1 hypoplasia, which increases wall tension per Laplace's law.[49]Connective tissue disorders like vascular Ehlers-Danlos syndrome (type IV) predispose to ACA aneurysms through collagen defects, leading to multifocal arterial fragility and higher rupture propensity.[50]Unruptured ACA aneurysms smaller than 7 mm carry an annual rupture risk of 0.5-1%, rising to 1-2% for ACoA locations due to their anterior circulation exposure and irregular morphology.[51] Larger or irregularly shaped aneurysms (>7 mm) elevate this to 2-5% annually, influenced by factors like hypertension and smoking.[52] Rupture typically manifests as subarachnoid hemorrhage (SAH), presenting with sudden severe headache ("thunderclap"), nuchal rigidity, photophobia, and altered consciousness in 70-80% of cases.[53]Diagnosis relies on computed tomography angiography (CTA) or magnetic resonance angiography (MRA), which delineate aneurysm dome, neck width (>4 mm increases complexity), and perforator involvement with >95% sensitivity for aneurysms >5 mm.[54] Digital subtraction angiography confirms flow dynamics if endovascular planning is considered. For ruptured cases, severity is graded using the Hunt-Hess scale (grades I-V), where grade I (mild headache) predicts better outcomes than grade IV-V (coma, deficits) with mortality up to 50%.[55]Management of unruptured ACA aneurysms involves observation for low-risk (<7 mm, no symptoms) lesions with serial imaging, while intervention is recommended for higher-risk features like growth or family history.[56] Ruptured aneurysms require urgent securing via microsurgical clipping (preferred for wide-neck ACoA lesions to preserve perforators) or endovascular coiling/stenting, achieving 90-95% occlusion rates and reducing rebleeding to <3%.[44] Postoperative care includes nimodipine for vasospasm prevention, with overall SAH mortality from ACA aneurysms at 20-40%.[53]
Surgical and Interventional Approaches
Endovascular treatments for anterior cerebral artery (ACA) pathologies, particularly anterior communicating artery (ACoA) aneurysms, primarily involve coil embolization, which achieves complete or near-complete occlusion in approximately 85-89% of cases immediately post-procedure and maintains similar rates long-term.[57][58] Stent-assisted coiling is employed for complex or wide-necked ACoA aneurysms, while stenting alone addresses dissections, as seen in cases of ACA dissecting aneurysms where it preserves vessel patency and prevents hemorrhage.[59]Angioplasty, often with conditional stenting, is used for symptomatic ACA stenosis, reducing long-term stroke risk by improving luminal diameter and cerebral perfusion.[60]Microsurgical approaches for ACA lesions typically utilize pterional craniotomy for proximal ACoA aneurysm clipping, providing direct visualization and secure occlusion with low morbidity in unruptured cases (around 4%).[61][62] For distal ACA aneurysms or those with unfavorable projections, the anterior interhemispheric approach offers better access to superiorly directed lesions, minimizing brain retraction and achieving successful clipping without added complications.[62][63]Bypass procedures, such as superficial temporal artery (STA) to ACA anastomosis, are indicated for chronic ACA occlusion, providing reliable revascularization in symptomatic cases like isolated ACA insufficiency or moyamoya variants, with variants including STA-radial artery graft extensions for enhanced flow.[64][65] These STA-ACA bypasses demonstrate patency rates exceeding 90% and reduce ischemic events in the ACA territory.[66]Common complications across these interventions include cerebral vasospasm, occurring in 5-10% of post-procedure cases following subarachnoid hemorrhage-related treatments, potentially leading to delayed ischemia.[67] Surgical clipping risks infarction from clip malposition or temporary occlusion, with rates up to 13% in some series, while endovascular procedures may cause periprocedural thromboembolism in 5-13% of patients.[68][69]Outcomes for ruptured ACoA aneurysm treatment favor endovascular coiling over clipping, with 70-80% of patients achieving good recovery (modified Rankin Scale 0-2) at one year, as adapted from the International Subarachnoid Aneurysm Trial (ISAT) results showing reduced mortality and dependency (23% vs. 30%).[70][71] For unruptured cases, both modalities yield favorable neurological outcomes in over 90%, though coiling demonstrates lower morbidity (<1%).[61]