Introduction

The outcome of giant intracranial aneurysm (GIA) is generally death, as a result of hemorrhage, neural compression, and thromboembolic episodes.19) The first case of GIA was reported in 1965.18) Various surgical strategies proposed to treat these lesions include wrapping, proximal vessel occlusion, thrombectomy, resection with or without bypass, or trapping with bypass.2) More recently, endovascular techniques used to treat GIAs have include a covered stent to reconstruct the parent arterial wall and biologically active coils that allow intra-aneurysmal thrombosis.6)16) However, endovascular treatment of GIAs is not optimal because of a lack of relief from the mass effect, the high rates of recanalization, and the low level of complete closure in broad-necked giant aneurysms.6)19) Treatment of GIAs should aim to arrest growth, eliminate the mass effect, and obliterate the abnormal vascular channel.1) In this way, trapping with bypass and aneurysm resection could be a better treatment option for thombosed GIA with mass effect.

We report a case of a partially thrombosed giant fusiform aneurysm with a blind sac, which was treated by trapping of the middle cerebral artery (MCA) aneurysm following extracranial-intracranial (EC-IC) arterial bypass surgery.

Case Report

A 62-year-old male presented with a 3-month history of gradually worsening motor dysphasia and headache. No neurological deficit was evident. An initial brain computed tomography (CT) demonstrated a round and well-defined high density mass on the left perisylvian area and surrounding low density lesions in the left frontoparietal cortex, subcortex and white matter. Magnetic resonance imaging (MRI) identified a 6.0x5.8x5.7 cm heterogeneous mass in the left perisylvian area, with focal peri-aneurysmal infarction of the distal MCA territory on diffusion MRI (Fig. 1). Cerebral angiography demonstrated a contrast-filling fusiform residual lumen of 2.5x0.5x 0.7 cm and MCA distal flow was not visualized (Fig. 2). Leptomeningeal collateral of the distal MCA territory from the anterior and posterior cerebral artery was noted. Brain perfusion CT revealed delayed mean transit time (MTT) in the peri-aneurysmal area and distal MCA territory (Fig. 2). These findings suggested a giant aneurysm that arose from the distal M1 portion of the MCA, with intraluminal thrombosis and peri-aneurysmal edema.

A simple superficial temporal artery (STA)-MCA bypass was planned to vascularize the distal MCA and trap the aneurysm. After the STA was dissected from the scalp, a pterional approach was used. After frontotemporal craniotomy and opening of the dura, a giant aneurysm was found within the sylvian fissure. The M1 segment of the MCA could not be exposed because a spherical, solid, and large aneurysmal sac obstructed the operative field of view. The usual STA-MCA end-to-side bypass surgery was carried out to preserve MCA distal flow. The temporary clipping time of the distal MCA was 33 min during bypass surgery. MCA distal flow was checked by intraoperative Doppler ultrasound. Aneurysmal thrombectomy was carried out using an ultrasonic suction device. At the end stage of thrombectomy, the aneurysmal sac was decompressed and, the proximal entrance of an aneurysm was exposed. Using a Sugita aneurysmal clip, the proximal and distal parent artery was trapped. The wall of the aneurysm could not be dissected because of tight adhesion to the surrounding brain tissue.

The patient awoke without any newly developed neurological deficit. Postoperative cerebral angiography showed excellent filling of the distal MCA from STA and the lumen of the aneurysm had disappeared (Fig. 3). Postoperative brain CT revealed a decreased mass effect in the left perisylvian area (Fig. 4). Significant improvement in symptoms was evident.

Discussion

Large and giant aneurysms are different groups of lesions. They should be considered as specific entities if they harbor partial thrombosis. The role played by the vasa vasorum, inflammation, and focal mural dissection in their pathogenesis is supported by clinical, pathological, and biological studies. In light of current reports, partially thrombosed aneurysms are related to subacute or chronic dissections and repeated intraluminal hematomas, proliferating vasa vasorum, and triggering of inflammatory mechanisms.3)

GIA usually manifests as an intracranial mass, rather than as hemorrhage. The symptoms relating to GIA depend on the aneurysm location, but predominant signs and symptoms are headache, hemiparesis, visual disturbance, cranial nerve paresis, dysphasia and aphasia, nausea, vomiting, seizures, and vertigo.1)2) In a study that reviewed the location of fusiform MCA aneurysms, 69% originated from the  proximal portion to the MCA genu, 21% were insular (M2 segment), and 10% were distal (M3 or M4 branches).8) The same authors also reported that 68% of all fusiform aneurysms were giant. Most fusiform aneurysms have good distal outflow and no blind sac. Presently, the distal outflow from an aneurysmal sac was not visualized by cerebral angiography. This means that the partially thrombosed aneurysm blocked the outflow, and delayed collateral circulation developed in the distal MCA territory. Upon preoperative assessment of mean transit time, perfusion CT revealed delayed circulation time in the distal MCA territory (Fig. 2). As a result of this evidence, we considered EC-IC bypass prior to aneurysm trapping.

Mortality and morbidity associated with GIAs are higher than those for smaller aneurysms, and surgical outcome for GIAs is still unsatisfactory.  Morbidity and mortality rates of 4% and 19%, respectively, have been reported in surgical patients.15) In a bypass group in the same study, the mortality and morbidity rates were 0% and 20%, respectively. A significant number of case reports with a satisfactory outcome regarding MCA revascularization with conventional bypassing of aneurysms have been published.4)5)9-11)13)17)20) Another study included 20 patients with an intracranial thrombosed aneurysm who were treated with bypass and parent artery occlusion.12) In seven of these patients, the MCA was revascularized, and one of the patients died. The authors reported 10% early bypass occlusion, 5% unintended branch occlusion, 90% good outcome, and 10% mortality.

Some GIAs have been treated successfully by endovascular procedures intended to induce thrombosis and shrinkage of the mass.7) The balloon remodeling technique, embolization with liquid embolic agents (such as Onyx), stent and coil combinations, and covered stents are used currently to treat complicated aneurysms.16) However, endovascular treatment for GIAs is generally not optimal, because of a lack of relief from the mass effect, cost, and the high complication rates in broad-necked giant aneurysms.  In a series of cases, two cases of GIA arising from the left MCA were complicated with aphasia after parent artery occlusion with an endovascular procedure.14)

GIAs arising from the MCA might be treated surgically with revascularization of the distal area by STA-MCA anastomosis. However, a spherical solid mass, including intraluminal thrombosis, may impede the operative field of view, and exposure of the proximal artery of a GIA might be difficult to achieve. In our case, the huge aneuysmal sac obstructed completely the field of vision, and the sylvian fissure could not be opened. After removal of intraluminal thrombus with an ultrasonic aspirator, the aneurysmal sac was shrunk, and the proximal entrance of the GIA was exposed. Intraoperative bleeding from the aneurysmal sac did not occur.

Preservation of the lenticulostriate arteries is particularly important during trapping of an MCA aneurysm. In our case, the lateral lenticulostriate arteries arose from the proximal portion of the GIA. The lenticulostriate arteries strongly adhered to the aneurysm; thus, the wall of the GSA was not removed from the surrounding brain tissue and post-operative cerebral angiogram showed these lenticulostriate arteries were well-preserved. A postoperative, follow-up brain CT revealed that the aneurysmal sac had shrunk gradually and the peri-aneurysmal brain edema was also decreased. In this GIA with a blind sac, the necessity for STA-MCA bypass was unclear. However, we believe that STA-MCA bypass surgery ameliorated delayed perfusion from the distal MCA branches, and may have prevented possible ischemia during surgery.

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