The temporopolar approach to the basilar apex aneurysm has the advantage of offering a wide working space for clipping but has the disadvantage of sacificing a draining vein from the superficial sylvian vein to the sphenoparietal sinus. We analyze methods that have been employed in our institution to provide a wide working space.
The techniques are divided into 3 categories based on the depth of surgical procedure: A, superficial layer; B, middle layer; and C, deep layer. Techniques in the superficial layer are zygomatic (n=9) or orbitozygomatic (n=3) osteotomy. Techniques in the middle layers include sectioning or dissection of the anterior temporal artery (n=5), retraction of the temporal lobe (n=18), and a combined approach (n=2). Techniques in the deep layer are optic unroofing (n=7), removal of the anterior (n=4) or posterior clinoid process (n=8), separation of tentorium (n=8), direct retraction in the posterior circulation (n=16), and sectioning of the posterior communicating artery (n=9). These techniques were used in 58 of 107 cases of basilar apex aneurysms.
When the temporal bridging veins developed well, the extended pterional approach or combined approach is effective to secure a wide working space. The extended pterional approach enables retraction of the temporal lobe without sacrificing the venous system. In the combined approach, the pterional and subtemporal approaches are undertaken through the same craniotomy. These methods were employed in 5 cases with successful clipping avoiding brain damage related to the occlusion of the venous system. These techniques were found to be beneficial to preserve the temporal bridging vein and also to provide a wide working space and access from various directions when approaching a basilar apex aneurysm.

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We report the case of a 65-year-old man with intracerebral hemorrhage accompanying carotid endarterectomy.
Preoperative angiography demonstrated very high-grade stenosis of the right internal carotid artery, with limited collateral flow. In the perioperative period, hypertension was well controlled. One clay after the operation, mild SAH and brain swelling was recognized in the right hemisphere on CT scan. On the third postoperative day, fatal intracerebral hemorrhage on the ipsilateral side of the CEA suddenly developed. Postoprative angiography showed wide patency of the right carotid artery without stenosis.
Although a low dose of aspirin was medicated from the second postoperative day, it was considered that postoperative-hyperperfusion played the most important role. To determine the factors that predict the occurrence of hyperperfusion syndrome after CEA, we reviewed the literature and discussed the perioperative managements to avoid postoperative hyperperfusion syndrome in some tightly stenosed internal carotid arteries, we propose stepwise revascularization with a preliminary extra-intracranial bypass followed by a carotid endarterectomy.

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We do not have enough knowledge concerning the process from the non-ruptured aneurysm to the ruptured aneurysm. Hemodynamic stress is one of the important factors that influence the growth and rupture of cerebral aneurysm. The hemodynamic stress affects vascular endothelium inside of the aneurysm. We investigated the morphology of the vascular endothelial cells of 5 ruptured aneurysms. These aneurysms were surgically obtained in the acute stage, and the specimens were processed for the scanning electron microscope. The inner surface of the aneurysmal sac was examined.
In one patient, the endothelial cell layers were relatively preserved. However, the gap between endothelial cells was enlarged where leukocytes adhered. We found defects of endothelium where the extracellular matrix of the wall became exposed, and blood cells invaded into the aneursmal wall in 2 patients. In those 2 patients, there were relatively well preserved endothelium in other areas.
Blood cells also adhered to the enlarged gap between endothelial cells. There was no layer of the endothelial cells within the specimen obtained from the other 2 patients. We found damage of the endothelial cell layer inside the aneurysm and blood cells invasion into the aneurysmal wall in the ruptured aneurysm. One possible explanation is that increases in hemodynamic stress injure the endothelium inside of the aneurysm, and then, leukocytes, platelets, and blood plasma invade the aneurysm wall before the rupture. These processes can cause the destruction and rupture of the aneurysmal wall.
Acom, anterior communicating artery; ICA, internal carotid artery; MCA, middle cerebral artery; SAH, subarachnoid hemorrhage.

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We report of a case of systemic lupus erythematosus (SLE) complicated by multiple ruptured cerebral aneurysms. The patient was a 33-year-old female with a 5-year history of SLE. The onset of the complication was marked by a headache, and subsequent cerebral angiography revealed multiple aneurysms in the vertebro-basilar system.
A clipping of aneurysms was performed on the day of hospitalization, but the patient died on the 31st day due to renal insufficiency. Although SLE complicated by cerebrovascular disease is not rare, SLE associated with ruptured cerebral aneurysm is encountered less often than expected.
As for the prognosis, 15 of 23 reported cases, including the present one, were fatal. In addition, 6 of 8 patients suffering from multiple aneurysms died, indicating an extremely poor prognosis for this type of disease. Further deterioration of the prognosis may be explained by the difficulty in identifying a ruptured aneurysm as well as the extended vasculitis and fragility of such a lesion.

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The overall results of 217 patients with subarachnoid hemorrhage (SAH) for the past three years and 33 poor outcome patients in comparison with the grade on admission were analyzed. The sites of aneurysm in poor outcome cases were ICPC in 12 cases (36.4%), Acom in 6 cases (18.2%), MCA in 5 cases (15.2%), BAtip in 5 cases (15.2%), and others in 3 cases (9.1%).
The causes of poor outcome cases were vasospasm in 11 cases (33.3%) intraoperative complication in 8 cases (24.3%), preoperative rebleeding in 6 cases (18.2%), and complication in 5 cases (15.1%).
Although cisternal irrigations were performed in 9 cases in the vasospasm cases, they were not effective. The causes of intraoperative complications were perforating artery injury in 5 cases (62.5%), premature rupture, incomplete clipping, and embolization from aneurysm in 1 case (12.5%).
The preoperative rebleeding rate was 31.2% in Grade 5, 27.8% in Grade 4, 10.0% in Grade 3, 11.2% in Grade 2, and 0% in Grade 1. Considering these analyses of overall management results and poor outcome cases, we suggest the following to improve the SAH outcome: 1) the development of essential therapy for the severe vasospasm; 2) the preservation of perforating artery in the operation; 3) the careful management for the rebleeding in risky period.

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We chronologically measured the platelet aggregations in 28 cases after surgery of cerebral aneurysm. Thirteen cases were constantly in normal or slightly increased range of platelet aggregability, and 15 cases showed significant increases. These latter cases evidenced arterial spasm in the course but no spasm in a few cases. Platelet aggregation inhibitors were administrated to the cases that showed increased platelet aggregability. After administration of these drugs, the platelet aggregabilities immediately decreased. Then we tried to control aggregations within the normal or slightly inhibited range. There were no complications by means of bleeding associated with administration of these drugs.
It seems to be a common practice to administrate the platelet aggregation inhibitors after aneurysm surgery. In our study, some of the patients did not show increased platelet aggregability through the postoperative course, so it might not be necessary to give platelet aggregation inhibitors to these patients. Therfore, it is important to measure the platelet aggregation chronologically to decide whether to administer platelet aggregation inhibitors. Platelet aggregation should be controlled within the suitable ranges of platelet aggregability if these drugs are administrated in the postoperative aneurysm patients.

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We investigated clinical features in elderly patients with ruptured intracranial aneurysm in comparison with younger patients. A total of 199 patients older than 50 years underwent surgical treatment within 72 hours of the first onset. The patients were classified into three groups: those aged 50 to 59 years (Group A: 98 patients, 49%), those aged 60 to 69 years (Group B: 71 patients, 36%), and those aged 70 years or older (Group C: 30 patients, 15%)
We defined the“elderly”patients as those aged 70 years or older, because the management outcome in Group C was significantly worse than that in Group B (p<0.05), while no significant difference was shown between that in Group A and B. In Group C, the patients in Hunt and Kosnik Grades I and II were significantly fewer than those in Group A or B (p<0.05).
No significant difference was observed in the incidence of symptomatic vasospasm between Group C and other groups. The incidence of hydrocephalus in Group C was significantly higher than that in Group B (p<0.05). The main obstacles to the induced hypertension therapy were systemic complications in Group C, in which only 4 patients underwent this treatment. The overall outcome of the patients with preoperative hypertension was significantly poorer than those without it (p<0.01), and the mortality rate was higher in Group C (50%, 6 in 12 patients). In Group C, the outcome was obviously poor in the patients with postoperative complications (pneumonia, myocardial infarction, severe systemic infection, and so on), and all the patients remained disabled or died.
In elderly patients, brief and effective therapies should be administered in the treatment of symptomatic vasospasm to prevent systemic complications that might confine patients to bed for a long time.

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Seventeen patients with aneurysms of the internal carotid bifurcation were treated by direct microsurgery.
Two patients had unruptured and asymptomatic aneurysms. Six patients were operated on in the acute stage, while the remaining 9 patients were operated on in the chronic stage. Fifteent (88%) of the 17 patients had a good result. There was no mortality.
However, 6 patients had postoperative neurological deficits, though 4 of them were transient. In 4 of the 6 patients, circulatory disturbance of the anterior choroidal artery or perforating arteries was responsible for such operative complications.
We stress that direct surgery should be performed for patients not only with ruptured aneurysms of the internal carotid bifurcation but also with unruptured, incidentally discovered ones, because they tend to bleed at a younger age, compared with aneurysms at other sites.
Furthermore, based on our experiences, surgical consideration for aneurysms at this location includes (1) wide opening of sylvian fissure, especially in patients with large aneurysms or long internal carotid artery, (2) dissection strategy pertinent to the projection of the aneurysm, (3) gentle but complete dissection of aneurysm neck, (4) temporary or tentative clipping in difficult cases, (5) careful and reasonable application of clip to aneurysm neck, and (6) preservation of perforating arteries of the anterior and middle cerebral, and posterior communicating arteries, Heubner's artery, and the anterior choroidal artery.

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It is well-known that outcomes of the ruptured dissecting aneurysms are quite poor, and that rebleeding of the aneurysms is one of the important prognostic factors in this disease. We conducted this study to elucidate the clinical and radiological features of the patients with rebleeding.
Forty-two patients with ruptured dissecting aneurysms in the vertebrobasilar system were analyzed. Ages ranged from 35 to 73 years (mean=50.9±8.4 years). Twenty-eight patients were treated surgically and the other 14 were treated conservatively. Among these 42 patients, 12 (29%) had rebleeding. The rebleeding was confirmed on CT scan. The outcome was evaluated by a Glasgow Outcome Scale. The mean follow-up period was 6.8±4.4 years.
Results: Among 42 patients, 25 (60%) achieved a good recovery, and 6 (14%) had died at 6 months after onset. The causes of death were rebleeding in 4 and vasospasm in 2. These outcomes were well correlated with the neurological severity (Hunt and Hess grade on admission). None, except for 1 aged patient, had deteriorated on long-term follow-up. Twelve patients with rebleeding had significantly poorer outcomes than the other 30 without it (p<0.01). The significant clinical and radiological features in the patients with rebleeding were as follows: poorer neurological grade (p<0.025), higher incidence of right vertebral artery dissection (p<0.05), and pearl and string sign as the angiographical finiding (p<0.01). Proximal occlusion was the most common procedure (68%) in the 28 surgically treated patients. Seventeen (60%) recovered well and none had been aggravated after the operation in these patients. Among the 14 conservatively treated patients, 8 (57%) made a good recovery on long-term follow-up.
These results suggest that the patients with rebleeding had poorer outcomes and might have the specific clinical and radiological features. It should be important to recognize these features, when considering the management strategy, because most of the patients who were treated conservatively made a good recovery on long-term follow-up in ruptured dissecting aneurysms of the vertebrobasilar system.

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Hypervolemic hemodilution (H-H) therapy for neurological deficit due to delayed cerebral vasospasm has been shown to be effective. The purpose of the present study was to monitor the hemorrheological and hemodynamic states (Ht, RBC-aggregation, cardiac output (CO), cardiac index (CI), pulmonary capillary wedge pressure (PCWP), serum albumin, a₂-macroglobulin (a₂-MG), circulating blood volume (CirBV) and cerebral blood flow (CBF) with patients with aneurysmal SAH and to assess how H-H therapy improved these factors during cerebral vasospasm.
We studied 50 patients who underwent early clipping surgery for aneurysmal SAH at our institution between January 1994 and December 1994. Twenty-one (42%) patients developed clinical vasospasm. The Ht of the patients with vasospasm was decreased significantly from 37.7% to 31.6% by H-H therapy. The RBC aggregation rate increased during day 4-6 and was significantly reduced by the therapy. The serum albumin decreased and a₂-MG increased at the same periods. CirBV data showed that the patients tend to be hypovolemic a few days after ictus, and that the patients receiving H-H therapy became normovolemic to hypervolemic. CO (4.7±0.4) and CI (3.1±0.3) at the onset of vasospasm, increased significantly to 6.8±1.1 and 4.1±0.5 respectively after H-H therapy. At the onset of vasospasm, the CBF (44.7±1.2 ml/100g/min) on the side of surgery was significantly lower than that on the contra-lateral side. During H-H therapy the CBF increased to 56.6±3.2 ml/100g/min.
After H-H therapy, 15 patients (71.5%) had good recovery, 4 (19.0%) had moderate disability, 2 (9.5%) had severe disability. Death and vegetative state were not present. Severe disability from clinical vasospasm occurred in 4% of all patients with SAH.
Our study showed that H-H therapy including albumin decreased the Ht and RBC aggregability and increased CirBV and CO, consequently increased CBF. We conclude that the improvement of hemorrheological and hemodynamic parameters by H-H therapy effectively reversed progressive neurological deterioration due to cerebral vasospasm.

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