28 Anterior Cerebral Artery Aneurysms
Abstract
Anterior cerebral artery is divided into five major segments, named A1 to A5 in order from proximal to distal—aneurysms in this arterial complex are classified accordingly. Anterior cerebral artery aneurysms (ACAAs) are rare lesions and account for less than 1% of all intracranial aneurysms (IAs). These aneurysms rupture at a smaller size and present frequently with intracerebral hematoma (ICH) and intraventricular hematoma (IVH). Patients carrying ACAAs usually have multiple IAs. These aneurysmal and patient characteristics make ACAAs suitable lesions for microneurosurgery. For A1 aneurysms, and A2 aneurysms, our preference is using a lateral supraorbital (LSO) approach. For distal ACAAs and for high-positioned A2 aneurysms projecting superiorly or posteriorly, we prefer to use a unilateral interhemispheric approach. The side of the approach for proximal ACAAs depends on rupture status, presence of ICH or IVH, size and projection of the aneurysm, A1 dominance, and orientation of both A2s. Endovascular treatment can be used to treat ACAAs. However, the anatomical characteristic of ACAAs many times requires flexible stents or stent-assisted coiling—this on the other hand requires dual-antiplatelet therapy, making ruptured aneurysm treatment challenging. Because ruptured ACAAs manifest often with ICH or/and IVH, microneurosurgical treatment is the treatment of choice.
Introduction
Anterior cerebral artery (ACA) aneurysms (ACAAs) arising from A1 to A5 and the frontobasal branches are rare and account for less than 1% of all intracranial aneurysms (IAs). In our experience, these aneurysms rupture at a smaller size relative to other locations. Lehechka et al found that ruptured A1 aneurysms present with an intracerebral hematoma (ICH) and intraventricular hematoma (IVH) of 25 and 17%, respectively. Distal ACAAs (DACAAs) include any distal to the A1–A2 junction; they present with a higher incidence of ICH and IVH when ruptured (52 and 33%, respectively) compared to A1 aneurysms. Patients with ACAAs commonly have multiple aneurysms.
Major controversies in decision making addressed in this chapter include:
Whether to not treatment is indicated.
Open versus endovascular treatment for ruptured and unruptured ACAA.
Management of ACAAs that present with ICH.
When should an advanced surgical technique (aneurysmorrhaphy, bypass) be considered?
Whether to Treat
Decision making in the face of unruptured IAs (UIAs) can be challenging. The latest American Heart Association (AHA) guidelines in 2015 reported a 0.25% annual rupture rate for UIAs. However, lifelong studies have demonstrated that approximately 25% of UIAs rupture. Since ACAAs are rare, specific epidemiological data are sparse for this location. Hypertension has been shown to have an impact on IA formation, whereas smoking induces inflammation and rupture. Thus, patients with UIAs with hypertension and a smoking history are at risk for UIA rupture as well as de novo aneurysm formation. There is well-described evidence that patients with multiple IAs have a higher tendency to rupture with resultant subarachnoid hemorrhage (SAH). Since ACAAs are often associated with multiple IAs and rupture at a smaller size, these patients should be treated early even if the aneurysm is small. We believe microsurgical treatment is the best first-line option as ACAAs are often located at the base of branches, have fragile walls, involve skull base perforators, and are associated with ICH. There are some instances in which endovascular treatment of ACAAs may be appropriate, though aneurysms in this location, particularly of the DACAA variety, are technically challenging.
Conservative Management
Unruptured Anterior Cerebral Artery Aneurysms
The main criteria for treatment have long been size and location. However, factors like aneurysm morphology, sex, hypertension, smoking, and immediate family member with SAH (familial does not necessarily means genetic) have been shown to strongly correlate with aneurysm formation and rupture. While prophylaxis is the best treatment method, intervention should be weighed against natural history of disease and potential risks of the procedure. The neurosurgeon has to keep in mind that treatment of small UIAs is far safer and more successful than treatment of larger UIAs. We recommend early treatment of ACAAs because they are less predictable: in our experience, they tend to rupture more frequently and at a smaller size than aneurysms in other locations ( 1 , 2 in algorithm ).
Anatomical Considerations
The ACA is one of the terminal branches of the internal carotid artery (ICA). It is divided into five major segments, named A1 to A5 in order from proximal to distal. The landmarks to take into consideration for this segmentation are the anterior communicating artery (ACoA), the region between the rostrum and the genu of the corpus callosum, and a virtual plane of division at the level of the coronary suture.
The A1 segment of the ACA arises in the carotid cistern. With a medial and anterior course superior to the optic nerve, it goes through a group of thick arachnoid bands extending from the olfactory triangle to the lateral side of the optic nerve and finally enters the cistern of lamina terminalis to join the opposite A1 to form the ACoA. The A2 segment ascends in the lamina terminalis cistern in front of the lamina terminalis, and enters the callosal cistern with an anterior trajectory that follows the surface of the rostrum of the corpus callosum inside the interhemispheric fissure before reaching to the genu of the corpus callosum where it turns superiorly and then posteriorly to continue as A3 to A5 segments. The medial lenticulostriate arteries that predominantly arise from the distal half of the A1 trunk and include the recurrent artery of Hubner should be preserved in all dissections. The same holds true for perforators of the ACoA complex.
Vascular anomalies frequently seen with A1 segment aneurysms (A1As) include hypoplasia (26% of the cases), aplasia, duplication, fenestration, and, very rarely, infraoptic course of the A1. Proximal ACAAs are associated with other aneurysms in 70% of the cases; however, the presence of mirror A1As is very rare.
The most common site of ACAAs is the ACoA (80–85%), followed by the A3 segment (10–15%). A1As (1–2% of the cases) are divided in proximal, medial, and distal parts of the A1 trunk, and they can project upward being embedded into the frontal lobe or backward behind the A1. Those aneurysms are often small and dangerous with high rate of rupture; therefore, unruptured A1As require therapy even at very small sizes ( 1 , 2 in algorithm ).
Classification
Aneurysms of the ACA can be classified into five different groups: aneurysms of the A1 segment or proximal ACAAs (A1As; ▶ Fig. 28.1 ), ACoAAs, aneurysms of the A2 segment and its frontobasal branches or proximal pericallosal aneurysms (A2As), aneurysms of the A3 segment or classical pericallosal aneurysms (A3As), aneurysms of the A4 and A5 segments, and distal cortical branches or distal pericallosal aneurysms (AdistAs). The last three groups are also called DACAAs and are further divided into seven subgroups according to microneurosurgical criteria.
Workup
Clinical Evaluation
Ruptured ACAAs present with SAH and its associated symptoms. Specific locations may show unique neurological deficits: ACoAAs may be associated with visual deficits and DACAA rupture can cause akinetic mutism, leg weakness, behavioral changes, and cognitive deficits.
Giant aneurysms produce mass effect in 75% of the patients causing headache, seizures, or visual defects; 25% of giant aneurysms rupture; and only 2 to 5% of them present with thrombosis or stroke. Unruptured aneurysms usually are diagnosed incidentally on imaging obtained for unrelated symptoms or in patients with multiple aneurysms.
Imaging
Computed tomography angiography (CTA) has a sensitivity and specificity comparable to digital subtraction angiography (DSA). Unlike DSA, CTA clearly characterizes luminal thrombosis, mural calcification (especially at the aneurysm neck), and the close relationship between the aneurysm and the skull bones (▶ Fig. 28.1 ). CTA with three-dimensional (3D) reconstruction makes the relationship between the aneurysm and related vessels and cranial bones even more clear to assist in the clinical management and planning of treatment (▶ Figs. 28.1 and 28.2 ). DSA was classically the gold standard for the detection of IAs (▶ Fig. 28.3 ). Magnetic resonance angiography (MRA) is very useful in some aneurysms with an immediate relation to the skull base, such as intracavernous or supraclinoid aneurysms. MRA is ideal for noninvasive follow-up after endovascular coiling.