Treating posterior circulation aneurysms, particularly lesions of the distal basilar artery, remains as a major challenge to the cerebrovascular surgeon. Posterior circulation aneurysms range in severity from the small and relatively simple to the massive giant aneurysm with major brainstem distortion. This presentation will focus on the upper basilar artery, as most lesions in the proximal vertebral-basilar system are analogous to those in the anterior circulation.
After years of trial and error, a microsurgical approach to the upper basilar artery that may be termed the “extended lateral approach” has emerged as perhaps the safest and most efficient route with which to deal with the overwhelming majority of upper basilar aneurysms. When performed from the surgeon's dominant side, the resultant exposure provides all of the benefits of the subtemporal operation as well as the assets of the transsylvian exposure. This exposure, coupled with scalp and bony modifications when necessary, as well as the aggressive use of temporary arterial occlusion, provides a straightforward solution to most aneurysms in this area.
Giant basilar artery aneurysms carry a major toll, both through their natural history and operative complications. Temporary arterial occlusion is a constant component of open surgical treatment, but limitations emerge with excessively lengthy arterial occlusion. Endovascular techniques pose a relatively straightforward and potentially safer alternative for the patient at the time of the initial procedure. Fundamental problems with this approach, however, and early data suggesting an extremely high incidence of incomplete treatment and early aneurysm recurrence limit the applicability of these techniques. In the author's opinion, careful preoperative evaluation followed by a well thought out open surgical strategy represent the patient's best interest at the present time. Despite multidisciplinary approach to these lesions, our results over the past several years with giant posterior circulation aneurysms have been somewhat disappointing, with only 50% of the patients achieving a good outcome.

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We retrospectively analyzed operative results in 28 cases of intracerebral arteriovenous malformations (AVM's) operated on at the National Cardiovascular Center over the past three years. Intractable brain swelling and/or diffuse hemorrhage immediately after removal of an AVM was not experienced in the present series. There was one case of postoperative bleeding attributable to uncontrolled arterial hypertension just after the operation, in which total resection was confirmed by intraoperative angiography.
There was another case of a large high-flow AVM, in which discontinuance and resumption of hypotension after total resection showed brain swelling and shrinkage. This case was treated successfully with mild hypotension, hypothermia and barbiturate coma after the surgery. All the other cases were treated successfully.
Based on our limited experience of total resection of AVMs, we have concluded that when the surgery is technically successful and the perioperative blood pressure is appropriately controlled, uncontrollable hemodynamic state after resection of an AVM occurs very rarely.

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The treatment of large, high-flow cerebral arteriovenous malformations (AVMs) is one of the most difficult operations which a neurosurgeons will encounter, because of the complex surgery and the postoperative effects on the brain. We evaluated 25 patients with AVMs who underwent surgical resection. They were classified into three groups for the purpose of determining a therapeutic approach. They comprised of 9 cases with small AVMs (<3cm), 2 cases of medium AVMs (3 to 6cm) and 14 cases of large AVMs (>6cm). Patients were investigated with contrast-enhanced computed tomography (CECT) and magnetic resonance (MR) imaging, ¹²³I-IMP single photon emission computed tomography (SPECT) studies of cerebral flow and cerebral vasodilatory function, intraoperative Laser Doppler flowmetry, and conventional angiography.
SPECT imaging performed on the first postoperative day showed marked hyperperfusion in the brain tissue surrounding the resected nidus, and these regions were normal on images on the 7th postoperative day. Laser Doppler flowmetry showed sudden, and marked increase in CBF immediately following placement of temporary clips on the main feeding artery. Angiograms done 7-14 days following surgery showed a stagnating artery, fragile vessel, and a prolonged circulation time. Our results indicate that pre- and postoperative SPECT study, especially a dynamic SPECT study done on the first postoperative day, was the most useful examination for ascertaining the postoperative NPPB.

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We analyzed a series of 30 patients undergoing complete surgical resection of large arteriovenous malformations (AVM's) of the brain between 1986 and 1995 for intraoperative and postoperative complications. In 17 patients preoperative embolization for AVM was performed and the extent of embolization was about 20% to 80%.
First, in patients without preoperative embolization procedure, postoperative edema around the resected AVM on CT scan was analyzed. Remarkable or moderatice edema was seen more frequently in patients whose AVM consisted of the long feeding arteries and short draining veins. Normal perfusion pressure after AVM resection might cause the breakthrough of autoregulation (NPPB) and provoke edema of the brain.
In the patients undergoing preoperative embolization for AVMs, the extent of postoperatvie cerebral edema on CT scan was consistently smaller than in the patients without an embolization procedure. In two patients whose AVMs had long feeding arteries and short draining veins, intracerebral hemorrhage and remarkable cerebral edema were provoked postoperatively. The cause of these hemorrhages and edemas was considered to be secondary to venosinus thrombosis that occured after the AVM resection from postoperative serial angiographical and CT scan studies.
Based on these experiences, we concluded that NPPB after the AVM resection may enhance the cerebral postoperative edema, but remarkable postoperative edema or intracerebral hemorrhage are secondary to the venousinus thrombosis provoked by the venous blood flow reduction after AVM resection.

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The present study retrospectively analyzes cases of large arteriovenous malformation (AVM) that were treated surgically between 1975 and 1995. Our principle operative strategy for AVM is total removal under a one-stage operation without intravascular intervention procedures. Blood pressure is controlled during surgery and the post-operative course.
Fourteen out of 84 surgical cases of AVM during that period presented with AVM larger than 6cm in maximum diameter. The patients consisted of 3 females and 11 males, aged from 18 to 53 years (mean 36.8 yrs). Initial symptoms consisted of bleeding attacks in 7 cases, epilepsy in 5 cases and headaches in 2 cases. The patients were divided into two groups according to the presence of complicating hemorrhage; Group A consisted of 8 patients who showed no complication and Group B consisted of 6 patients with complications. Complicating hemorrhage can be manifested by an arterial component such as occlusion of high shunt flow (normal perfusion pressure breakthrough: NPPB) or by a venous mechanism such as occlusion hyperemia. Group B patients showed no posterior fossa AVM. All cases had more than 2 large feeding arteries and prominent draining veins. Stagnating arteries were detected in the post-operative angiography of 4 cases in Group A and in all cases in Group B. The outcome at the time of discharge was as follows: in Group A (ADL-1: 6 cases, ADL-2: 1 case, ADL-3: 1 case), in Group B (ADL-1: 3 cases, ADL-3: 2 cases, death: 1 case). There were no characteristic pre-operative findings in Group-B. The causes of poor clinical outcome in Group B included embolic complications associated with the intravascular procedure and hemorrhage due to NPPB. However, the recent development of staged surgical procedures, intravascular embolization and arterial pressure control may allow effective surgical treatment of large AVM.

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Surgery for high placed basilar bifurcation aneurysm is one of the most difficult neurological operations. There are special approaches for high basilar bifurcation aneurysms such as the temporopolar approach, zygomatic approach, transzygomatic subtemporal approach, transclinoid transsellar transcavernous approach, and transthird ventricular approach. In this paper, we will discuss some technical procedures that we have developed for the transcrista galli translamina terminalis approach in treating a small high basilar bifurcation aneurysm.
Case report
A 73-year-old woman was referred with a diagnosis of SAH Grade IV, and pulmonary effusion. Cerebral angiograms and helical 3D CT demonstrated an aneurysm arising at the bifurcation of the basilar artery. The aneurysm measured 7mm×10mm and the neck of the aneurysm was located 15mm high from the posterior clinoid process. The transcrista galli, interfalcine, translamina terminalis approach was selected because of the patient's old age and the highly placed basilar bifurcation aneurysm in the third ventricle. This approach requires less brain retraction. We will discuss some tactics of approaching this aneurysm, clipping techniques, and the surgical merits and demerits of this approach.

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We present an indirect revascularization technique using the dural arterial supply as the donor vessels. At surgery, the dura near the anterior and posterior branches of the middle meningeal artery was split into outer and inner layers, and the split surfaces of the outer layers were attached to the cortical surface of the frontal and parieto-occipital regions (Split duroencephalosynangiosis (Split DES)).
This procedure, combined with encephalo-duro-arterio-synangiosis (EDAS), was applied to 27 hemispheres in 19 patients with pediatric moyamoya disease (mean age, 6 years). All the patients were symptom free by 1.5 years after surgery. Postoperative superselective angiograms of the middle meningeal artery demonstrated effective cortical revascularization through the dural arteries in all cases.
Comparison of the sequential angiographic changes between EDAS and Split DES showed that the revascularization occurred as early as 2 weeks postoperatively with the split DES. The Split DES described here is a useful addition to indirect revascularization techniques, allowing extension of the area of revascularization.

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We report two patients who underwent cervical carotid ligation, without a revascularization procedure, for internal carotid aneurysms, focusing on various neuro-imaging findings obtained 14 and 11 years after ligation, respectively. Magnetic resonance (MR) angiography and digital subtraction angiography showed disappearance of the original aneurysms and no “de novo” aneurysm formation. MR imaging and computed tomographic (CT) scan demonstrated the aneurysms to be thrombosed. No major ischemic lesions were detectable in the cerebral parenchyma by means of MR imaging, stable xenon/CT cerebral blood flow, dynamic CT scan and single photon emission CT. Serial thin slice, bone window CT scans demonstrated that no changes in the caliber of the bony carotid canal may be produced by acquired hypoplasia of the internal carotid artery. These extensive neuro-imaging follow-up studies appear to be essential for proper evaluation of the long-term benefits, as well as potential untoward effects, of cervical carotid occlusion.

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Six patients with medium-sized arteriovenous malformation (AVMs, 3.0-6.0 cm in maximum diameter), treated by gamma knife radiosurgery without preceding embolization, are reported. The AVM manifested with intracranial hemorrhage in three cases and with seizure in the other three. The maximum nidus diameter ranged from 3.4 cm to 5.7 cm, with a mean and a median of 4.0 cm and 4.1 cm, respectively. Although total AVM coverage at the time of dose planning was feasible in four patients, the selected dose at the periphery of the nidus was limited to 7.2-14.0 Gy (total coverage and non-optimal dose treatment). The two remaining patients had only partial coverage; the part of the nidus adjacent to the major feeding artery was covered and a dose of 21.0-25.0 Gy was given within this limited area, although the remaining part of the nidus was irradiated with a dose of 5.0-7.0 Gy or less (partial coverage and optimal dose treatment). Neither hemorrhage nor significant radiation-induced complications occurred in any of the six cases during the postradiosurgical follow-up period which ranged from 18 to 85 months (mean 48 months). Complete nidus obliteration was angiographically confirmed 38 months after radiosurgery in one case, more than 90% obliteration of the treated nidus, respectively, 36 and 70 months after radiosurgery, in two cases. Magnetic resonance (MR) angiography demonstrated disappearance of the nidus in one case and remarkably decreased nidus volume in one, respectively, 30 and 18 months after radiosurgery. In the one remaining case, MR imaging obtained at 24 months after treatment showed a significantly diminished flow signal void, as well as the appearance of a gadolinium enhanced area within the treated nidus. In addition, a T2-weighted image showed hyperintense edema surrounding the AVM. These results indicate that single irradiation of a medium-sized AVM using a gamma knife, though not optimal, can produce complete nidus obliteration, or significant nidus shrinkage, for two-six years, or more, after radiosurgery. Even in the latter instance, the shrunken AVM can easily be re-treated using a gamma knife.

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Internal carotid artery (ICA) anterior wall aneurysm is relatively rare, but is well-known for its high risk of intraoperative rupture. Because of its characteristic clinical features, it has been suggested that its pathogenesis differs from other usual saccular aneurysms. We encountered 3 cases with this sort of aneurysm, which was considered to be caused by the dissection of the ICA.
Case 1 was 46-year-old female with subarachnoid hemorrhage due to rupture of the ICA anterior wall aneurysm. Trapping of the ICA and STA-MCA anastomosis were performed, and the aneurysm was resected together with the ICA. Its photomicrographs showed intramural hematoma at the aneurysm neck. Case 2 was 57-year-old female whose initial carotid angiography revealed a IC-posterior communicating artery aneurysm with a retention of the contrast media on C2 anterior wall portion. During operation, the blister-like aneurysm was seen on this portion, and bleeding occurred from the aneurysm. Case 3 was 32-year-old female whose initial carotid angiography revealed double lumen and a retention of the contrast media on C2 portion. It was confirmed operatively that the blister-like aneurysm was on the C2 anterior wall portion and that the bleeding occurred from this portion.
These cases suggest that some of such aneurysms are caused by the dissection of the ICA. As to the treatment, a preoperative Matas test is necessary, and the balloon catheter should be set at the ICA prior to surgery. And in the case with the findings suggesting the dissection of the ICA on angiography, trapping of the ICA must be taken into acount to avoid recurrent bleeding.

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We report 3 cases presenting with psycho-neurological symptoms after subarachnoid hemorrhage. The patients suffered from consciousness disturbance due to vasospasm. Although they recovered consciousness gradually from the apathetic state and became able to walk, they showed perseveration, compulsive behavior, oral tendency and Korsakoff's syndrome. These symptoms were almost transient and improved markedly.

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