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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今日脳動脈瘤に対し, 頭蓋外頸動脈結紮術が選択される例は限られている. しかしながら, 本術式が全く歴史的なものとなった訳ではない. 本稿ではこの術式が行われて10年以上 (症例1は14年, 症例2は11年) を経過した2例における, 最近のCT, MRI, MRA, USなどの静的画像所見, およびSPECTやXe-CTなどの動的検査所見を報告する. ここに述べる2例では血管吻合などの血行再建術は施行されていない. 症例1は1937年生まれの女性. 1980年左視力・視野障害で発症. 左巨大内頸動脈瘤に対し総頸動脈結紮術施行. 1986年症状増悪かつ脳血管撮影で動脈瘤の増大を認め, 左内頸動脈結紮術施行. 視神経障害持続するも57歳の今日まで経過. 症例2は1916年生まれの男性. 1983年クモ膜下出血. 左内頸動脈瘤に対しclippingを試みるも, 技術的困難により左内頸動脈結紮術施行. 術後神経症状なく77歳の今日まで経過. ここに報告した2例に関する限り, 画像診断上, 動脈瘤の血栓化は10年以上を経た今日でも満足すべき状態にある. また動的検索でも結紮側での血流低下は著明ではなかった. 骨条件のCT上, 内頸動脈管径に左右差はなく, 後天的な内頸動脈径の変化では内頸動脈管には変化をきたさないことが示唆された.

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従来gamma knife (GK) 治療の適応外と考えられていた, 最大径3～6cm (Spetzler & Martinのsize分類で“medium-size”) のAVMに対するGK治療経験を報告した. 対象は1978年以来AVMに対しGK治療がなされた41例中, 最大径3～6cmの6例で, これらの症例では治療前に栓塞術や放射線治療はなされていない. 3例は出血で発症しており, 他の3例は痙攣発作で発症した. 病巣の最大径は3.4～5.7cmで平均4.0cmであった. 照射計画では4例でtotal coverageが可能で, 辺縁線量7.2～14.0Gyで治療されたが (total coverage, non-optimal dose treatment), 他の2例ではfeeding artery近傍の病巣のみ25Gy以上とし, 辺縁線量としては5.0～7.0Gy以下で治療された (partial coverage, optimal dose treatment). 治療後の追跡期間中 (18～85カ月, 平均48カ月), 再出血やsymptomaticな放射線障害はないが, 1例で照射野を中心にcyst formationを認めている. 血管撮影では1例で完全閉塞 (治療後38カ月, 以下無名数で表示), 2例で90%以上の縮小を認め (36, 37), この2例ではGKによる再照射が行われた. 他の3例では血管撮影は未施行なるも, 1例でMRA上病巣は認められなくなっており (30), 残る2例でもMRAまたはMRIで病巣の明らかな縮小を認めている (18, 24). 従来GK治療の適応外とされていたやや大きめのAVMでも, 安全性を考慮した低線量治療で著明な縮小が期待でき, 中には完全閉塞に至る例もある. 少なくとも初回治療で著明な縮小が得られれば, GK再治療の確実性と安全性は飛躍的に高まると考えられ, 栓塞術が不可能か, もしくは栓塞術により十分なvolume reductionが得られない例では, GKによるstaged treatmentが有効と考えられる.

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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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