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urgical Management of Giantnterior Cerebral Artery Aneurysms

amuel Barnett, MD,* and Duke Samson, MD†

Giant aneurysms of the anterior cerebral artery are uncommon lesions that present uniquesurgical challenges. Although they occasionally rupture, they more frequently present withfrontal lobe dysfunction, visual loss, hydrocephalus, and pituitary dysfunction secondary tomass effect. Successful surgical treatment is dependent upon a thorough preoperativeevaluation and a careful operative plan. Neurosurgeons dealing with these complex lesionsneed to be prepared to utilize multiple surgical strategies including direct clip reconstruc-tion, proximal ligation, trapping and excision, bypass or a combination thereof.Oper Tech Neurosurg 8:93-97 © 2005 Elsevier Inc. All rights reserved.

KEYWORDS aneurysm, anterior communicating artery, giant aneurysm

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iant aneurysms of the anterior cerebral arteries aredistinctly uncommon, representing 5 to 10% of all

eported giant lesions.1 The most frequent area of involve-ent is the anterior communicating artery complex;1-3 less

requently, giant aneurysms occur along the A1 segmentr distally, usually at the junction of A2 and A3. Clinicalresentation may be subarachnoid hemorrhage1 or symp-oms related to aneurysmal mass effect such as visualoss,1,4,5 pituitary dysfunction,1 dementia or all three.1

reoperative Evaluationreoperative medical evaluation should include a com-lete neuro-ophthalmological assessment, and an assess-ent of mental capacity. When aneurysms involve the A1

egment, pituitary function should also be evaluated. Use-ul imaging studies include both computed tomographyCT) and magnetic resonance imaging (MRI), completeerebral angiography to include carotid cross-compres-ion views. In certain patients, balloon trial occlusionBTO) of one or both proximal anterior cerebral arteries iseeded.1 It is critical to obtain a complete bilateral assess-ent of the exact nature and competency of the anterior

erebral-anterior communicating artery system from an-iography. Angiography also may provide potentiallyaluable information about the presence or absence of

Department of Neurological Surgery, The University of Texas Southwest-ern Medical School, Dallas, TX.

Department of Neurological Surgery, 5323 Harry Hines Blvd., Dallas, TX.ddress reprint requests to Samuel Barnett, MD, Chief Resident, Department of

Neurological Surgery, The University of Texas Southwestern Medical

rSchool, Dallas, TX; E-mail: samuel.barnett@UTSouthwestern.edu.

092-440X/05/$-see front matter © 2005 Elsevier Inc. All rights reserved.oi:10.1053/j.otns.2005.09.008

eptomeningeal collaterals from the territories of the mid-le cerebral artery and posterior cerebral artery.

haracteristicshe distinguishing characteristics of these aneurysms are

heir size (�24 mm), their almost inevitable intramuralalcification, the presence of intraluminal thrombosis inore than 80% of cases,1 and the unique morphology of

n individual aneurysm’s base or neck.Aneurysms of the A1 segment tend to involve most if not

ll of the anterior cerebral artery distal to its origin. Theylso frequently engulf the ipsilateral A1-A2 junction. Typ-cally, they project medially and inferiorly with resultantressure on the ipsilateral optic apparatus,6 mesial orbitalortex, hypothalamus and pituitary stalk.

Aneurysms of the anterior communicating artery complexan project in any direction in the sagittal plane. When muchf the aneurysmal enlargement is directed superiorly, theass may obstruct one or both foramina of Monro thereby

ausing hydrocephalus.2 The low midline location of theseiant aneurysms results in early bilateral compression of therbital cortex and septal areas. Consequently, these lesionsften reach clinical attention through investigation of alteredental status. With giant aneurysms involving the anterior

ommunicating region, hypothalamic perforating arteriesypically arise from the anterior communicating artery andhe proximal A2 segments and are tightly adherent to theorsal surface of the aneurysm.Lesions located distal to the anterior communicating

rtery typically involve the A2-A3 junction. They are oftenssociated with having an azygos A2 and may occur as a

emote consequence of traumatic herniation of the ante-

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94 S. Barnett and D. Samson

ior cerebral arteries beneath the falx. They too can man-fest with dementia, subarachnoid hemorrhage, or infre-uently hydrocephalus.

urgical Considerationss is true with all giant aneurysms, these lesions are bestperated on after a lengthy study of their anatomical andorphological features and of the flow dynamics of the ca-

otid circulation bilaterally. The several available therapeuticptions (direct reconstruction, proximal ligation, trappingnd excision, revascularization, or combinations of two orore approaches) must then be considered carefully. Realis-

ic goals for the operative procedure should be establishedased on the patient’s presentation, comorbidities, and aneu-ysm characteristics.

The operating surgeon’s experience and expertise, partic-larly with revascularization procedures, should be consid-red. An entire armamentarium of contemporary neurosur-ical devices should be available, and intraoperativengiography should be used routinely. Scalp flaps should beashioned to optimize revascularization options. Bony expo-ures should be constructed to minimize brain tissue retrac-ion. Temporary proximal occlusion is almost uniformly nec-ssary and should be performed in conjunction with allossible physical and pharmacological methods to minimizehe effects of iatrogenic ischemia.

1 Segment Aneurysmsroutine unilateral subfrontal or frontotemporal surgical

xposure is adequate for the management of these aneu-ysms. Primary reconstruction with preservation of both af-

igure 1 Coronal MRI demonstrating giant A1 aneurysm with pul-atility artifact.

igure 2 Giant A1 aneurysm seen on angiography. Note jet effect and

lling of both A2 segments. fi

erent and efferent branches represents the optimal anatom-cal result. However, giant aneurysms in this location oftennvolve the entire A1 segment and the absence of a normalrtery precludes definitive clip reconstruction. Confrontedith this situation, the surgeon’s knowledge of the collateral

irculation determines which of several options is most ad-isable. If both distal A2 segments can be supplied by theontralateral A1, simple trapping and excision of the aneu-ysm may suffice. If the dominant A1 segment is aneurysmal,roximal occlusion of its origin (Hunterian ligation) may beolerated if collateral circulation via the contralateral A1 in-ow and distal MCA-ACA leptomeningeal complex is ade-uate. This possibility can often be evaluated safely by BTO ofhe involved A1.

When the contralateral anterior cerebral artery is absentr its size is inadequate to supply both distal circulationsFigs. 1 and 2), a more predictable approach involves re-ection of the aneurysmal A1. It is replaced with a shortnterposition graft, usually a saphenous vein or radial ar-ery. The proximal anastomosis (end-to-side) can usuallye performed without occlusion of the internal carotidrtery (Fig. 3). The distal anastomosis, which is performedn the interhemispheric fissure (Fig. 4), can be challeng-ng. However, the lateral aspect of the A1-A2 junction

igure 3 Intraoperative view of proximal anastamosis. (Color ver-ion of figure is available online.)

igure 4 Intraoperative view of distal anastamosis. (Color version of

gure is available online.)

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Managing giant anterior cerebral artery aneurysms 95

sually provides an acceptable arteriotomy site once theneurysmal A1 has been transected. After flow has beenestored (Fig. 5), it is important to deflate and, if possible,emove the aneurysmal sac itself. If the fundus is denselydherent to the chiasm and hypothalamus, the sac shoulde opened widely. Its lumen is then carefully inspected for

igure 5 Intraoperative view of completed interposition graft withneurysms sac excised. (Color version of figure is available online.)

igure 6 Post-operative angiogram demonstrating patent interposi-

ion graft. F

vidence of delayed retrograde filling via small arteriesuch as the recurrent artery of Huebner.

Postoperative angiography (Fig. 6) shows a slight mis-atch between the size of the graft and the host but goodlling of bilateral distal anterior cerebral arteries.

nterior Communicatingegment Aneurysmshe common anatomical denominators of these difficult an-urysms are almost invariably intraluminal thrombus (Fig. 7)

igure 7 Head CT demonstrating giant AComm aneurysm with in-raluminal thrombus.

igure 8 Angiogram demonstrating giant AComm aneurysm.

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96 S. Barnett and D. Samson

nd the great distances between sites of entry of the A1 vesselsnd the sites of origin of the A2 segments bilaterally (Fig. 8).ommonly, the entire region of the communicating artery is

ransformed into a giant aneurysmal mass whose afferent andfferent vessels arise at remote intervals. Consequently, com-lete exposure of all aspects of the relevant arterial anatomyay require extensive bilateral subfrontal interhemispheric

pproaches (Fig. 9).The use of a large bifrontal craniotomy, generous bilateral

yrus rectus resections and, on occasion, simultaneous bilat-ral surgical exposures (Fig. 10) can improve visualization,ecrease the length of iatrogenic ischemia, and facilitate clipeconstruction. The high incidence of extensive intramuralalcification, coupled with the expansive nature of the aneu-ysm’s neck, often mitigates against precise anatomic recon-truction. In these situations, the surgeon should be contentith elimination of the bulk of mass effect and preservationf branch vessel origins, even if one A1 segment must beacrificed or significant residual aneurysm persists. Some-imes the origin of an A2 branch (Figs. 11 and 12) can beccluded inadvertently because of dense calcification but notause clinical sequela because the MCA-ACA collateral circu-ation is exuberant. If, however, such occlusion is identifiedntraoperatively, an A2-A2 bypass should be strongly consid-red.

igure 9 Large bifrontal craniotomy for simultaneous bilateral expo-ure. (Color version of figure is available online.)

igure 10 Simultaneous bilateral approach using two microscopes.

Color version of figure is available online.) p

Successful Hunterian ligation of the dominant A1 segmentr of both A1s has been reported when clip reconstructionas deemed impossible.2 However, in addition to potentialistal ischemia, postoperative aneurysmal subarachnoidemorrhage2 and unrelieved or recurrent mass effect also canccur.

igure 11 Angiogram demonstrating A1 occlusion but robust MCA-CA collaterals.

igure 12 Post-operative head CT after simultaneous, bilateral ap-

roach for giant aneurysm.

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Managing giant anterior cerebral artery aneurysms 97

2 Segment Aneurysmshese rare lesions, located at the A2-A3 junction, almostlways require bilateral interhemispheric surgical exposure.n lesions lying inferior to the rostrum of the corpus callo-um, the mass effect makes proximal control (of both A1egments or the most proximal ipsilateral A2 segment) quiteifficult. The bifrontal interhemispheric exposure may needo be combined with a lateral subfrontal approach to thenterhemispheric fissure. Especially when located on azygosnterior cerebral arteries, the efferent origins of A3 tend to bear from each other. In the presence of dense wall calcifica-ion, this configuration makes clip reconstruction with pres-rvation of antegrade flow in both distal branches very diffi-ult. In such situations an excellent alternative involvesransposing A3. The patency of this vessel is compromised bylip reconstruction in such a fashion that it fills via a distalnd-to-side anastomosis with its contralateral partner.

onclusionsiant aneurysms of the anterior cerebral-anterior communi-ating artery complex are uncommon lesions that may reachlinical attention with subarachnoid hemorrhage. Typically,owever, they become symptomatic via local mass effect.epending on size and projection, these aneurysms can pro-uce visual loss, pituitary dysfunction, anosmia, dementia,

ydrocephalus, or all of these symptoms. Their successful

reatment is based on in-depth evaluation of the pertinentascular anatomy followed by thoughtful prioritization of aumber of potential therapeutic options, which include re-onstruction, trapping, proximal ligation, and surgical revas-ularization.7-9

eferences. Lownie SP, Drake CG, Peerless SJ, Ferguson GG, Pelz DM: Clinical

presentation and management of giant anterior communicating regionaneurysms. J Neurosurg 92:267-277, 2000

. Rosta L, Battaglia R, Pasqualin A, et al. Italian cooperative study on giantintracranial aneurysms: Part 2. Radiological data. Acta Neurochir Suppl42:53-59, 1988

. Sundt TM Jr., Piepgras DG: Surgical approach to giant intracranial an-eurysms. Operative experience with 80 cases. J Neurosurg 51:731-742,1979

. Lawton MT, Spetzler RF: Surgical management of giant intracranial an-eurysms: Experience with 171 patients. Clin Neurosurg 42:245-266,1995

. Peiris JB, Ross Russell RWR: Giant aneurysms of the carotid systempresenting as visual field defect. J Neurol Neurosurg Psychiatry 43:1053-1064, 1980

. Versavel M, Witmer JP, Matricali B: Giant aneurysm arising from theanterior cerebral artery and causing an isolated homonymous hemianop-sia. Neurosurgery 22:560-563, 1988

. Kodama N, Suzuki J: Surgical treatment of giant aneurysms. NeurosurgRev 5:155-160, 1982

. Maxwell RE, Chou SN: Aneurysmal tumors of the basifrontal region.J Neurosurg 46:438-445, 1977

. Symon L: Surgical experiences with giant intracranial aneurysms. Acta

Neurochir 118:53-58, 1992