We report the results of a nationwide questionnaire investigating the current therapeutic strategy for carotid artery stenosis in Japan sent to 1102 neurosurgical institutes. Of them, 445 (40.4%) replied. The mean number of carotid endarterectomies (CEAs) performed in 1997 was 1.9. CEAs for both symptomatic and asymptomatic carotid stenosis are increasing in number, but remain few compared with North America or Europe. Endovascular surgery for carotid artery stenosis is still uncommon in Japan. More than half of Japanese neurosurgeons considered that CEA is necessary for asymptomatic carotid artery stenosis of more than 60% if the patient is less than 70 years old and in good general condition. About 90% of institutes used intraoperative monitoring such as electroencephalography, stump pressure and somatosensory evoked potentials. The operative microscope was used in 71% of institutes. Intraoperative shunting was used for all cases in 40% of institutes, for selected cases in 32% and for no cases in 16%. Tacking suture was used in all cases in 41% of institutes.
It is somewhat difficult to do CEA for Japanese patients, because Japanese carotid artery stenosis has a tendency to have a higher position of the carotid bifurcation and relatively harder plaque than in Western patients. A nationwide prospective study will evaluate the optimum therapeutic strategy.

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Since the results of ACAS were first reported, carotid endarterectomy (CEA) in patients with asymptomatic carotid stenosis has been increasing in Japan. In this report, we evaluate our results of CEA in patients with asymptomatic carotid stenosis and complications, and discuss the indication of CEA in Japanese patients with asymptomatic carotid stenosis.
From January 1975 to December 1998, 318 CEAs were performed. Of these, 116 CEAs in 107 patients were carried out for asymptomatic carotid stenosis. Overall mortality was 4/116 (3.4%). There was 1 permanent morbidity (0.9%). Therefore, the mortality and morbidity rate was 4.3%. Twenty-one patients (19.6%) were over 70 years old (range 70-75 years old) and mortality and morbidity in these patients was 0%. Ultrasonography was applied to 54 patients prior to CEA, showing ulcer in 50% of them. Intraplaque hemorrhage was found in 7 of 15 with hypoechoic plaque. Coronary angiography was performed in 54 patients. The patients with a history of ischemic heart disease (IHD) showed more severe coronary stenosis than patients without any history of IHD. However, 60.5% of the patients without any history of IHD showed some degree of coronary stenosis. No patient who underwent coronary angiography suffered IHD during CEA and postoperative course.
Based on these results, we conclude that the indications of CEA for asymptomatic patients are as follows: 1) ICA stenosis of more than 70%, 2) patients under 75 years old who can be expected to live more than 5 years, 3) patients with plaque showing hypoechoic and ulcer by Ultrasonography and 4) patients who have undergone coronary examination or treatment for IHD and can tolerate general anesthesia.

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We analyzed surgical results of carotid endarterectomy (CEA) for asymptomatic carotid stenosis to clarify factors related to stroke mortality and morbidity.
In the past 13 years (1986-1998), CEA was performed in 91 patients with symptomatic carotid stenosis and 54 patients with 56 asymptomatic carotid stenosis. Surgical indication was confirmed by angiographic high-grade stenosis (>70%) estimated using the NASCET criterion in both groups. CEA was performed under general anesthesia (normotension and normocapnia), and internal shunting was carried out under general heparinization. Cerebral ischemic events during operation was monitored by SEP and intraoperative DSA. To determine recent results of CEA, we investigated the ratio of CEA for symptomatic and asymptomatic group, and perioperative mortality and morbidity in both groups. Since 1995, resting and acetazolamide-activated CBF, and severity of hemodynamic cerebral ischemia (Stage 0-II) was quantified using ¹²³I-IMP ARG method and preoperative cerebral hemodynamics was compared in both symptomatic patients (n=30) and asymptomatic patients (n=24). Additionally, we estimated which surgical procedure related to stroke morbidity.
The ratio of CEA for symptomatic lesion and asymptomatic lesion was 91 lesions (62%) vs. 56 lesions (38%) in 1986-1998, 33 lesions (55%) vs. 27 lesions (45%) in 1995-1998 and 13 lesions (45%) vs. 17 lesions (55%) in 1998, respectively. The number of CEAs for asymptomatic lesions has increased in recent years. Overall surgical morbidity and mortality was 5 cases (3.4%) and 0% in 147 lesions, and morbidity was 4 cases (4.4%) in 91 symptomatic lesions, and 1 case (1.8%) in 56 asymptomatic lesions. A significant difference in resting CBF was observed between symptomatic patients (31.8±6.1ml/100g/min) and asymptomatic patients (37.6±6.6ml/100g/min) (P<0.002, t-test). The severity of hemodynamic cerebral ischemia based on resting and acetazolamide-activated CBF did not differ significantly between groups (χ²-test). However, Stage II ischemia (hemodynamically compromised state) was 20% in symptomatic patients and 8% in asymptomatic patients. Hemodynamic cerebral ischemia was generally mild in asymptomatic patients.
Perioperative morbidity in one patient with asymptomatic lesion was connected with careless compression of the internal carotid artery with ulcerated plaque during exposure of carotid system. No morbidity and mortality was observed in connection with manipulation of internal shunting and reperfusion of carotid system.
In CEA for asymptomatic carotid stenosis, confirmation of strict surgical indication, risk evaluation based on cerebral hemodynamics and standardization of surgical procedures (especially exposure and handling carotid system) may be essential for reducing perioperative morbidity and mortality.

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Several large randomized multicenter trials have demonstrated the beneficial effects of carotid endarterectomy (CEA) for prevention of strokes in patients with severe symptomatic or asymptomatic carotid artery stenosis. On the other hand, endovascular treatments are rapidly evolving as alternatives to CEA, but indication for endovascular treatment remain uncertain and long-term results have not yet been established. We experienced 59 consecutive patients with asymptomatic carotid artery stenosis treated with CEA in 5 recent years, and 14 patients with asymptomatic carotid artery stenosis treated with stenting since 1997. One minor stroke (1.7%, hemiparesis and aphasia) and 1 transient neurological event occurred after CEA, and one major stroke (7.1%, hemiplegia) occurred during stenting by distal embolic occlusion of MCA and ACA. There were no neurological events after either CEA or stenting, but distal embolic signals were detected in all patients with TCD during stenting, and embolic lesions were detected in more than half the patients with MRI/DWI after stenting.
We consider that cerebral protection by means of balloon is mandatory to eliminate embolic complication in the endovascular treatment of carotid artery stenosis. Stenting for asymptomatic carotid artery stenosis can now be indicated only for surgically high-risk patients who are very old, have severe heart or pulmonary disease, contraindication to general anesthesia, high-positioned stenosis, restenosis after CEA or PTA, or radiation-induced stenosis.

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We present 5 cases among 728 quantitative serial CBF studies in 342 patients at 42 hospitals. CBF studies were performed with ^99mTc-ethyl cysteinate dimer (ECD) and a simple Patlak plot-method before and after surgical treatment. CBF values are reliable. Compared with qualitative images, quantitative images give clinically useful information corresponding to clinical status even in cases with diffusely reduced CBF. This method is convenient for daily clinical practice.

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We retrospectively analyzed clinical courses of 69 giant intradural aneurysms before treatments in 68 patients who admitted to our institute between April 1965 and December 1998 in order to determine the natural history of intradural giant aneurysms. The aneurysms were located on the internal carotid artery in 31, the middle cerebral artery in 9, the anterior cerebral artery in 9, the posterior cerebral artery in 2, the basilar artery in 14, and the vertebral artery in 4. Sixteen presented with hemorrhage, 35 with mass signs, and 18 with others (headache in 7, seizure in 4, embolism in 2, asymptomatic in 5). Between the initial presentation and the treatment (0-360 months), 11 hemorrhages occurred in 69 aneurysms, and 5 were fatal (annual bleeding rate 5.2%, annual death rate 2.4%). Re-bleedings occurred in 7 out of 16 hemorrhagic cases (fatal in 3) during 0-360 months of follow up periods. In 35 massive aneurysms, mass signs remained progressive in 28 and bleeding occurred in 3 (fatal in 1) during 1-288 months of follow up periods. In 18 aneurysms without hemorrhage or mass signs as initial symptoms, bleeding occurred in 1 (fatal) during 1-264 months of follow-up periods. The presence of thrombosis did not prevent subarachnoid hemorrhage.
Giant intradural aneurysms with hemorrhage or mass signs should be treated considering high risks of re-bleeding in ruptured cases and progressive neurological deficits in massive cases, and those without hemorrhage or mass signs should be treated depending on the progression of symptoms and surgical morbidities.

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With the introduction of Guglielmi detachable coils (GDC), endovascular treatment of intracranial aneurysms is rapidly gaining popularity as an alternative approach to surgical clipping, especially for unruptured aneurysms. In our institute, priority has been given to endovascular treatment for unruptured aneurysms since 1995. However, 18 patients were referred to direct surgical treatment because of difficulty in endovascular treatment or complications during the procedure. In this study, we analyze characteristics of these aneurysms and discuss surgical problems. The locations of aneurysms were the middle cerebral artery in 10, the anterior communicating artery in 5 and the internal carotid artery in 3. The reasons of referral from endovascular surgery were broad neck aneurysms in 10, too small size in 4, fusiform shape in 3 and complications during procedures in 3. Surgical methods were simple neck clipping in only 6, while a combination of neck clipping and wrapping was employed in 9 and multiple clipping reconstructing the parent artery in 3. The postoperative course was uneventful except for two cases-one had delayed arterial occlusion probably due to angitis by the wrapping material, the other had bleeding from the aneurysm after multiple clipping reconstructing the parent artery and wrapping. All direct surgeries after complications of endovascular treatment were done for aneurysms of the anterior communicating artery. Bleeding by endovascular procedure occurred in 2, and anterior cerebral arterial occlusion in 1. The bleeding point was the side wall of the aneurysm in 1 case. Recanalization of the occluded artery was difficult even after direct embolectomy.
In conclusion, it was also difficult to obtain satisfactory results with direct surgery for unruptured aneurysms, which were referred from endovascular surgery because of difficulty or complications. These cases had to be managed more carefully to minimize complications.

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Management in patients with ruptured cerebral aneurysms remain controversial. However, endovascular treatment of ruptured cerebral aneurysms with Guglielmi Detachable Coils (GDC) is gaining favor as an attractive alternative to surgical clipping. We analyze the experience with endovascular embolization to determine the safety and efficacy of endovascular treatment of ruptured cerebral aneurysms. We retrospectively analyzed 32 consecutive patients harboring 33 cerebral aneurysms. Patients with ruptured aneurysms are managed according to the following protocol: the primary treatment recommendation is endovascular embolization with GDC. Surgical clipping is recommended after failed attempts at embolization or in the presence of angiographical features that contraindicate endovascular treatment, such as a broad neck. Of 33 cerebral aneurysms, 9 (27.3%) were completely embolized, 8 (24.2%) were almost embolized but had a small neck remnant, and 16 (48.5%) showed a body filling. Symptomatic complications after endovascular treatment were found in 3 (9.4%) patients such as parent artery occlusion. Permanent morbidity and mortality related to the procedure were 6.3%and 3.1%respectively. Reembolization was performed in 7 (21.9%) patients and surgical clipping in 4 (12.1%) patients. After the treatment, 25 (78.1%) patients showed a favorable outcome such as good recovery and moderate disability, and 7 (21.9%) patients showed an unfavorable outcome such as severe disability, persistent vegetative state, and death. The results of this study suggest that short-term results of the embolization of ruptured aneurysms are favorable. However, the long-term investigation is important to clarify the significance of this treatment.

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We present the case of a 74-year-old woman with middle cerebellar peduncular AVM (Spetzler-Martin grade II) resulting in fourth ventricular hemorrhage. CT scans revealed fourth ventricular hemorrhage complicated with small hematoma in the right middle cerebellar peduncle. MRI demonstrated that the right middle cerebellar peduncle showed high signal intensity in T2-weighted and FLAIR images. Vertebral angiogram revealed the nidus of AVM supplied by the right superior cerebellar artery (SCA) and anterior inferior cerebellar artery (AICA) and draining in the right superior petrous sinus (SPS) with a varix.
Gamma knife radiosurgery was performed. A maximum dose of 50 Gy was delivered with a marginal dose of 25 Gy. We considered two hypotheses for why AVM located in the middle cerebellar peduncle has caused fourth ventricular hemorrhage. One is that the hemorrhage of the right middle cerebellar peduncle perforated into the fourth ventricle. The other is that a rupture of vein of lateral recess of fourth ventricle (VLR) caused by retrograde venous hypertension resulted in fourth ventricular hemorrhage.

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To prevent recurrent rupture, proximal occlusion or trapping of the lesion has commonly been advocated for unilateral vertebral dissecting aneurysms that occur with subarachnoid hemorrhage (SAH). Although the results of proximal occlusion were generally excellent, this procedure does not guarantee prevention of rebleeding. Therefore, trapping of the lesion should be considered for the primary treatment of choice to assure its obliteration.
However, trapping of vertebral aneurysms may result in postoperative ischemic complications. We describe two cases in which the lesion was successfully trapped using intraoperative Doppler sonography. Both cases presented with SAH and were admitted to our institution on the day of rupture. One case, whose posterior inferior cerebellar artery (PICA) was involved in the aneurysmal wall, was treated by trapping with the PICA involved in the trapped segment. Existence of blood flow in the PICA was confirmed by microprobe using the intraoperative Doppler method. Postoperatively the patient suffered transient mild brainstem ischemia, but eventually recovered completely.
The other patient, whose contralateral vertebral artery was smaller than the ipsilateral vertebral artery, was treated by trapping and suffered no postoperative ischemia. Intraoperatively, a test occlusion of the vertebral artery was performed to confirm the safety of permanent occlusion. A microprobe for the Doppler sonography was applied to the lower basilar artery after occluding the lesional dominant vertebral artery, and no significant reduction of the blood flow in the basilar artery was confirmed.
The intraoperative Doppler method is not a quantitative technique for measuring blood flow. However, intraoperative test occlusion of the vertebral artery using the microvascular Doppler method or confirmation of the PICA blood flow by the Doppler method may be an important technique in the treatment of selected vertebral dissecting aneurysms.

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We report a case of a large aneurysm of left posterior cerebral artery presenting with intraluminal thrombosis or intramural hemorrhage. A 49-year-old female was admitted to our department suffering from severe headache and vomiting. CT scan did not show subarachnoid hemorrhage but demonstrated a round high density mass of 1.5 cm in diameter in the left ambient cistern. MRI demonstrated that the intensity of the inside of the mass was low and that of the outer wall was somewhat high in the both Ti and T2 weighted image. Cerebral angiography showed crescent opacification of supero-lateral part of the aneurysm while medial-inferior part was not visualized, indicating thrombus formation.
We carried out surgery via the left extended subtemporal approach. No evidence of subarachnoid hemorrhage was observed during the operation. The wall was dark-blue colored. The parent artery was clipped at the proximal side of the aneurysm and disappearance of the aneurysm was confirmed by the intraoperative angiography. The postoperative course was uneventful and CT scan showed no abnormal low-density area. PCA aneurysms were overviewed literary, and mechanisms of intraluminal thrombosis and intramural hemorrhage were considered.

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