A surgical technique based on the authors' experience with the use of the long saphenous vein bypass graft for anterior circulation revascularization is reported in this paper. In this technique, a vein graft is taken from the thigh with meticulous care. The proximal end-to-end anastomosis of the vein graft to the proximal portion of the a. thoracoacromialis, a branch of the axillary artery, is preferred. The vein graft is passed subcutaneously posterior to the tragus of the ear from the infraclavicular region to the craniotomy site. The distal end-to-side anastomosis to the angular artery of the middle cerebral artery provides the enough graft flow to maintain a good graft patency. In the postoperative period great care must be taken to keep the blood pressure normal to avoid the danger of hyperperfusion breakthrough and of graft occlusion due to hypoflow through the graft.
The safety, long term patency and reliability of the vein bypass procedures have been demonstrated. An immediate post-operative large volume of blood flow through the graft is an absolute advantage over the conventional STA-MCA anastomosis. A generous length of vein will make any revascularization procedure viable in both anterior and posterior circulation.

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Case histories of 44 patients with overlapped cerebrovascular diseases are presented in this paper. Combinations were mainly as follows: 11 cases of ruptured intracranial aneurysm-cervical internal carotid artery stenosis, eight cases of cerebral infarction-unruptured intracranial aneurysm, eight cases of intracerebral hematoma-unruptured intracranial aneurysm, and five cases of arteriovenous malformation-intracranial aneurysm. There were 20 surgical cases for main cerebrovascular diseases and 20 for coexisting cerbrovascular diseases. Surgical treatment for both main and coexisting cerbrovascular disease was performed in nine patients. Postoperative sequelae occurred in six cases. This was the result of coexisting ischemic cerebrovascular disease in five cases. Ischemic cerebral symptoms contralateral to the site of operation were especially observed in three patients. It should be noted that, in case of coexisting ischemic cerebrovascular disease, the postoperative sequela occurred, even when measures were taken to prevent lowering systoric blood pressure, to prevent hypovolemia, and when anticoagulants were administered during the operative procedure.

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Twenty-four cases of intracranial aneurysms associated with cerebral infarction were studied. The types of infarction were as follows: Five cases of TIA, five of RIND and fourteen completed strokes. Ten cases had unruptured aneurysms and fourteen cases had ruptured aneurysms. Aneurysm surgery was performed in fifteen out of twenty four cases. EC-IC bypass or carotid endarterectomy for the responsible occlusive vascular lesion was performed in five cases. Operative results on discharge were as follows: Eight cases showed excellent results, two good, four fair and one poor. Operative complication was observed in only case. This was the occlusion of the perforating branch of the middle cerebral artery caused by the neck clipping of the aneurysm. The operative results were not as bad as in previous reports, which would seem to indicate that revascularization can be useful for preventing postoperative ischemic complications.

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Intracranial aneurysm in elderly patients seem to differ in many aspects from those in patients their thirties, forties and fifties. During the past five years, the authors have experienced 42 cases of intracranial aneurysm (s) in patients over 60. These patients were divided into two groups. The first group consisted of those with moderate or marked arteriosclerosis and/or occlusive changes in the cerebral arteriography or CT scan (arteriosclerotic group). Cases without sclerotic or occlusive changes in the artery were included in second group (non-arteriosclerotic group). Prognosis was undoubtedly worse in the first group.
The authors analysed several factors affecting the prognosis. These included the patient's age, site of the aneurysm, grade of arteriosclerosis and occulusive changes, mode of surgical intervention, timing of operation and skillfulness of the operator. Our conclusion was as follows: (1) intentionally delayed operation is recommendable in cases with marked arteriosclerostic changes. Prognosis was poor in these cases if an operation was carried out in the acute stage. (2) surgical manipulation of the brain and vessels should be as protective as possible. Forceful and prolonged retiaction of these structures must be avoided. Operation should be done by skillful hands. (3) in patients with multiple aneurysms, only the ruptured aneurysm should be operated upon in the first operation. Unruptured aneurysm (s) should be left, or should be clipped at the second stage if feasible. (4) prudence is required in deciding on surgical intervention and the timing of the operation in patients with cerebral infarction. Conservative treatment is recommended in many such cases.

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During the past ten years, 583 cases of cerebral infarction were investigated angiographically in our institute. Incidental unruptured aneurysms were demonstrated in 14 cases (2.4%). In two cases the aneurysm was clipped to prevent TIA due to microemboli from the aneurysmal dome itself. Three cases with RIND and one case with a minor completed stroke underwent neck clipping; however, cases of RIND with incidental aneurysms on the same side as the ischemic lesion developed cerebral infarction adjacent to the old ischemic area during the post-operative period. Three cases developed subarachnoid hemorrhage in the follow-up period, which ranged from eight months to 2.2 years after ischemic ictus. Two cases were operated on in the acute stage. The outcome was poor due to newly emerged ischemic deficits. Meticulous decision and evaluation one necessary for operative treatment of incidental infarction.

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Surgery was performed in particular cases of ruptured intracranial aneurysms accompanied by the insidious occlusion of the main cerebral artery. Such surgery was performed in 1.14% of 701 patients found to have ruptured intracranial aneurysms after the introduction of a CT scanner in our institute.
There were eight men and one woman, whose mean age was 58. In these nine patients, three of the ruptured aneurysms were located in the anterior communicating artery, five at the internal carotid-posterior communicating junction, and one at the internal carotid-anterior choroidal junction.There were four cases with multiple aneurysms.
There were five internal carotid occlusions, three middle cerebral (at the horizontal portion) occlusion and one occlusion of the common carotid artery. The site of the aneurysms and the previous occlusion of the main cerebral artery appeared well correlated, indicating a hemodynamic process for aneurysmal formation. None of the patients had ever experienced a cerebral ischemic event before the attack of aneurysmal subarachnoid hemorrhage.
Surgical treatment for five of these patients consisted of aneurysmal clipping, and that for the remaining four consisted of aneurysmal clipping + STA-MCA bypass. One patient died, four were fully recovered at the time of discharge, and four needed further treatment. Clinical deterioration of these cases was chiefly due to the severe cerebral ischemia at the occluded site after the development of vasospasms. When the degree of subarachnoid hemorrhage seemed too severe to avoid subsequent spasms, bypass surgery, in addition to acute aneurysmal clipping, was considered suitable.

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Special strategic consideration is necessary for the surgical treatment cases of complicated occlusive cerebro-vascular disease with intracranial aneurysm because the direct approach for such an aneurysm can easily give rise to cerebral infarction due to impending cerebral ischemia.
A total 22 cases of complicated occlusive cerebro-vascular disease with intracranial aneurysm have been treated in our hospital in the past 10 years. Of those, nine started with apparent subarachnoid hemorrhage, and complicated occlusive cerebro-vascular disease was incidentally identified later (Group 1). In 13 other cases cerebral ischemic symptoms were first noted and incidental intracranial aneurysms were found by cerebral angiography later (Group 2).
The ages of the patients ranged from 23 to 78 years old, with 15 of them being over 60 years old.(The average of group one was 65 and that of group two was 60.2).
Of the patients in group one, neck clipping was the only surgical treatment necessary in four cases while three other cases required vascular reconstruction after neck clipping. Only three vascular reconstruction was done in one case. Another patient was simply treated conservatively. Postoperative symptomatic vasospasm was noted in three cases. The final results were excellent in three cases, good in two, poor in two and two cases the patient died. Apprent operative complication was seen in two patients; both had cerebral infarction due to injury of the arteriosclerotic small branch.
The patients in group two were examined by cerebral angiography because of TIA in five cases, because of a minor stroke in 16 cases and because of a major stroke on one cases. Sixteen of those patients had surgical treatment of some sort: eight had neck clipping, five had coating of an aneurysm, one had STA-MCA anastosis, and two had neck clipping with additional STA-MCA anastomosis. The surgical results were good in 12 cases, poor in one and one patient died by because of late bleeding after coating.
The surgical results give us warning that ruptured intracranial aneurysm complicated by occlusive cerebro-vascular disease should be operated on by careful and gentle maneuver, while an incidental intracranial aneurysm still requires radical operation in order to prevent subarachnoid hemorrhage.

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There are some differences of opinion regarding the management of intracranial aneurysms associated with internal carotid occlusive disease. Therapeutic approaches, e.g. whether to operate or not to operate on an intracranial aneurysm and whether to operate on an intracranial aneurysm first or secondarily are discussed in this paper.
The authors have experienced eight cases with both intracranial aneurysms and internal carotid occlusive disease. Four of these patients had ischemic attacks and coexisting intracranial aneurysms. The other four presented symptoms referable to an aneurysm and significant carotid or middle cerebral artery stenosis or occlusion on angiography. Five of these patients first underwent successful clipping of the aneurysm and one patient first underwent carotid endarterectomy and then clipping of the contralateral IC-ophthalmic aneurysm. Post-operative minor ischemic complication was present in one patient who had transient ischemic attacks three times and showed unilateral carotid occlusion with ipsilateral moyamoya vessels and an asymptomatic contralateral saccular aneurysm on angiography. The other five patients did not suffer from significant ischemic complications.
When the blood flow is decreased by carotid stenosis or occlusion, an intracranial approach to an aneurysm has been thought to carry an increased risk. Advance of operative technique, anesthesia and brain protective agents is expected to lead to lower operative morbidity without mortality.
The authors recommend that a patients with an intracranial aneurysm in the anterior circulation associated with internal carotid occlusive disease should be treated by clipping of the aneurysm first, except where the patient has a symptomatic carotid stenosis and an asymptomatic IC-ophthalmic aneurysm on the contralateral side that may need the ligation of the internal carotid artery at aneurysm surgery.

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Of 27 patients suffering from overlapped cerebrovascular disease with whe underwent both types of surgical treatment, 16 cases in which the disease was combined with cervical carotid arterial occlusive disease are discribed in this paper, comparing the results of simultaneous operations with the results obtained when the operations were carried out separately. In the simultaneous operations, the combined cerebrovascular diseases consisted of three aneurysm and four middle cerebral arterial occlusions, five unilateral and two bilateral lesions, and two emergency cases. The symptoms were recurrent TIA, hemiparesis, aphasia and so on, caused by occlusive diseases.
In the simultaneous operations, clinical considerations and surgical devices were adopted. 1), In the cases combined with aneurysms, the aneurysm was first clipped and carotid endarterectomy was performed to prevent premature rupture. On the other hand, in combined middle cerebral arterial occlusion, carotid endarterectomy was first performed, followed by STA-MCA anastomosis in order to avoid clotting or reccurent occlusion at the anastomotic portion. In carotid endarterectomy, mannitol and plasm expander were administrated without internal shunt. Blood pressure was closely monitored to prevent premature rupture in the aneurysmal operations and to prevent lowering systolic pressure in operations for occlusive disease.
About 100mmHg of systolic pressure was maintained for aneurysmal clipping and then more than 130mmHg during carotid endarterectomy or STA-MCA anastomosis.
With separate operations, more than three weeks interval should elapse between the first and second operations to allow recovery from effects of the trauma and anesthesia of the first operation.
No other special considerations or surgical device are necessary.
In the cases reported here, prognosis was good with simultaneous operations because main brain damage occurred only once. Prognosis was not so good with separate operations because each disease had its own main symptom and damage. It was especially noted that pseudobulbar palsy disturbed improvement of the ADL in bilateral cases.

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Posterior circulation aneurysms, especially aneurysms of the posterior cerebral artery-posterior communicating artery junction (PA-Pcom AN), with agenesis or occlusion of the internal carotid artery (ICA) are rare. We experienced two such cases. One patient had lt. PC-Pcom AN with ipsilateral ICA occlusion, the other blt. PC-Pcom ANs with blt. ICAs occlusion.
Case 1, a 27-year-old man who had been treated for homocystinuria, suffered from subarachnoid hemorrhage (SAH) on January 26, 1980. He was admitted with no neurological deficit three days after the SAH. Carotid angiography revealed complete occlusion of the lt. ICA at its origin. A saccular aneurysm was recognized at the junction of PCA and dilated PcomA. Thirty-one days after the onset the aneurysm was clipped, but he showed disturbance of consciousness and rt. hemiplegia after the operation. He died of sepsis fifty-one days later. Postoperative angiography had shown disappearance of the aneurysm and poor filling of the PcomA.
Case 2, a 52-year-old man suffered from SAH on March 25, 1986 and the next day he was admitted in a drowsy state with signs of meningeal irritation. Blt. ICAs were not opacified intracranially by carotid angiography. Anterior and middle cerebral arteries of both sides were supplied with vertebro-basilar system and blt. PC-Pcom ANs were recognized. Thirty-five days after admission clipping of the responsible lt. PC-Pcom AN and lt. STA-MCA anastomosis were performed. He had temporary lt. hemiparesis but was discharged twenty-three days after the operation without neurological deficits. Postoperative angiography showed disappearance of the aneurysm and good patency of the anastomosis, but the lt. PcomA was not opacified.
We suppose the change of hemodynamics by the occlusion of ICA as the cause of the formation and growth of such aneurysm.
During the operation, the dilated and tortuous PcomA disturbed the procedures and both patients showed neurological deficits inspite of an uneventful operation. In such cases, therefore, considering the difficulty of the operative procedures and the subtle balance of hemodynamics, we should perform the operation more carefully. We think the STA-MCA anastomosis is a good means of preventing complications in these operations.

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In this paper, we described a patient with a basilar tip aneurysm complicated by bilateral carotid occlusions and a patient with the formation of the vertebrobasilar dolichoectasia following bilateral carotid occlusions.
The patient with a basilar tip aneurysm had had no ischemic symptoms following bilateral carotid occlusions because the vertebrobasilar artery supplied enough blood flow for both cerebral hemispheres through both posterior communicating arteries. We performed a craniotomy and coated the aneurysm.
In the second patient, the bilateral carotid occlusion had caused moderate ischemic symptoms of the left cerebral hemisphere. The vertebrobasilar artery completely perfused the right cerebral hemisphere through the right posterior communicating artery. Six years after the left STA-MCA bypass surgery, we found the devolopment of the dolichoectasia in the vertebrobasilar artery. A right STA-MCA bypass was performed to reduce the hemodynamic stress to the dolichoectasia. Digital subtraction angiography revealed the reduction of the dolichoectasia and good patencies of both STA-MCA bypasses 10 months after right STA-MCA bypass surgery.
The mechanism and therapeutic problems of aneurysmal formation in the posterior circulation following bilateral carotid occlusion are discussed.

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In patients with internal carotid artery occlusion, blood flow through the vertebro-basilar system and the posterior communicating artery as a collateral flow becomes much greater than the normal state, and aneurysms might be formed at these arteries as a result of increased hemodynamic stress, subsequently causing subarachnoid hemorrhage. The authors have experienced two such cases with asymptomatic carotid occlusion and ruptured vertebro-basilar artery aneurysms, including posterior communicating artery aneurysms. The first case, a 46-year-old female, had slowly progressive dementia for five years, prior to the episode of subarachnoid hemorrhage (SAH) of Hunt and Hess's grade III. A CT scan revealed moderate SAH, and a 4-vessel study angiography showed a left posterior cerebral-posterior communicating artery (P1-P2) aneurysm and a basilar-superior cerebellar artery aneurysm on the left side. Also it showed bilateral carotid artery occlusion in the neck, and the collateral flow from the left ophthalmic artery and the bilateral posterior cerebral arteries through the posterior communicating arteries was also documented. On the 20th day of SAH, an operation was performed. At first, superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis was performed on the right side which had less collateral flow than on the left side. This was followed by neck-clipping of the two aneurysms through the subtemporal route on the left side. Immediately after the operation, the patient had left hemispheric symptoms, though no major lesions were detected on the CT scan. Volume expansion and hypertensive therapy were started. On the third day, the revascularized area became low in density on the CT scan and it progressed into hemorrhage, resulting in tetraparesis and a vegetative state. This event could be explained by assuming that the so-called normal perfusion pressure breakthrough phenomenone from the bypass site occurred as a result of local hyperperfusion in chronically ischemic brain tissue under the postoperative control of volume expansion and hypertension.
The second case, a 59-year-old male, had SAH of grade H, and angiography revealed a posterior cerebral-posterior communicating artery aneurysm with asymptomatic carotid occlusion in the cavernous portion, and a dominant collateral flow through the posterior communicating artery was also noted. After surviving a symptomatic vasospasm, STA-MCA anastomosis and neck-clipping of the aneurysm via fronto-temporal approach on the right side was uneventfully performed on the 21st day of SAH with a favorable outcome.
In this paper, we discuss the mechanism of aneurysmal formation as a result of increased hemodynamic stress, and the operative procedures, including timing, that are necessary for safe operation. Finally, the pathogenesis of hemorrhage into the revascularized area seen in case one is discussed.

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A few cases of ruptured intracranial aneurysms associated with pulseless disease have been reported previously. In such cases the aneurysms arose on the cerebral arteries serving as collateral pathways. The role of hemodynamic factors in the pathogenesis of these aneurysms has been emphasized.
In this paper, we report three cases of ruptured intracranial saccular aneurysms associated with pulseless disease.
Case 1: A 54 year-old woman had three episodes of subarachnoid hemorrhage 15 years, four years, and one year previously. Right vertebro-angiograms showed a giant aneurysm at the terminal bifurcation of the basilar artery. She died during the operation.
Case 2: A 55 year-old man had a sudden attack of severe occipital headaches due to a subarachnoid hemorrhage. Right vertebro-angiograms revealed an intracranial aneurysm located at the junction of the right vertebral-posterior inferior cerebellar artery. Aneurysmal neck clipping was performed via the right suboccipital approach.
Case 3: A 64 year-old woman had severe headaches and motor weakness in both legs. Left carotid angiograms revealed multiple intracranial aneurysms (at the junction of the left IC-Ophth and IC-PC arteries, and at the top of the basilar artery). She died due to bleeding from the basilar top aneurysm. In addition to the three intracranial saccular aneurysms discovered by arteriography, autopsy revealed another small saccular aneurysm at the junction of the basilar and left anterior inferior cerebellar arteries.
Surgical treatment for ruptured saccular aneurysms associated with pulseless disease should be carried out insofar as the patient's general condition allows for the operation. In some cases, reconstruction of the artery may be helpful for the relief of cerebral ischemic symptoms.

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In this paper, the authors describe three cases of extremely rare aneurysm which were located in the C₂ portion of the internal carotid artery and had no relation to arterial branches. From the operative findings, these aneurysms looked like “chimame” (blood blister) because of their extremely thin wall. Moreover, this aneurysm was not saccular but merely a protrusion. Because it has not been reported previously in the medical literature, the authors advocate calling it a “chimamelike aneurysm.” This aneurysm has a extremely high tendency to rupture prematurely during a radical operation. Special care should be taken to prevent tragic results.
All of the three patients were middle aged females who had a past history of hypertension. One of the most characteristic angiographic appearances was a small protrusion emerging from the upper wall of the internal carotid artery with more or less arteriosclerotic changes adjacent to the aneurysm. Complete angiographic investigation and careful analysis of the angiograms were necessary for the accurate preoperative detection of this type of unusual aneurysm.
The aneurysms were small protrusions without a distinctive neck. Because of the high tendency of premature rupture, it is advisable to occlude the proximal internal carotid artery temporarily during the brain protection using “Sendai cocktail”.Sometimes it is necessary to use multiple temporary clips in order to control the bleeding during surgery. These clips tend to disturb the operative field. Intravascular temporary balloon occlusion was very useful. As this aneurysm has a very thin and fragile wall and no distinct neck, it might be advisable to treat it by wrapping with a muscle piece, using Aron alpha adhesives (alkyl-alpha-cyanoacrylate monomer). Complete wrapping, including the portion behind the aneurysm, is also recommended.

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Since no signal for flowing blood is obtained in magnetic resonance imaging (MRI), a normal blood vessel is imaged in black as low-signal intensity. With attention focused on this advantage, we studied vascular occlusion by MRI in occluded intracranial main arteries in the acute stage.
The subjects were six patients with occlusion of the internal carotid artery (ICA) and four with occlusion of the trunci of the middle cerebral arteries (MCA).
The following findings were obtained: (1) In all 10 cases the horizontal portion of the MCA on the occluded side was invaded with the same signal intensity as the peripheral brain tissues, resulting in poor identification of the blood vessels; (2) In the six cases of occluded ICA, iso- or high-signal intensity was observed in a vascular lumen at the intracranial running of the ICA on the occluded side; (3) in the four cases of occluded MCA, a signal for ICA on the occluded side showed normal low-signal intensity, whereas the horizontal portion of the MCA on the occluded side was located in a more peripheral site than the occluded part, resulting in poor identification of the blood vessel.
These findings are considered to be characteristic of occluded main arteries in the acute stage as seen in MRI. Findings (2) and (3) also suggest the possibility of MRI differentiation of occluded MCA and occluded ICA in the acute stage.

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In this paper, 45 cases of cerebral aneurysm accompanied with cerebro-vascular-diseases are reported. Sixteen of the cases were accompanied with cerebral infarction including TIA and RIND, 18 cases with hypertensive intracerebral hematoma, two with moyamoya disease, four with AVM, two with SLE, and three with chronic subdural hematoma. The clinical characteristics and surgical indications are discussed.
1) There is no correlation between the side on which the cerebral infarction occurs and the site of the cerebral aneurysm, however there is a tendency for the site of the cerebral aneurysm to exist on the same side as a hypertensive intracerebral hematoma (14/18, 78%). Such sites are especially observed with bifurcation or trifurcation of the middle cerebral artery (9/14, 64%).
2) It is likely that surgery is indicated for a ruptured cerebral aneurysm with cerebro-vascular-diseases in patients showing Hunt-Kosnik grade I~III in the preoperative stage. It is necessary to delay the operation for two weeks after controling systemic blood pressure.
3) Surgery is indicated for an unruptured cerebral aneurysm with cerebro-vascular-diseases in patients showing ADL1-3 in the preoperative stage more than one month after the first operation or first attack of cerebro-vascular-disease.
4) Some post-operative complications, such as epidural hematoma, convulsion, subdural effusion and temporary focal ischemic symptom due to hypo-perfusion, are seen in case of unruptured aneurysms with cerebral infarction.

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As operative therapy for intracerebral hematoma and craniotomy for hematoma removal, CT guided stereotaxic operation is familiar.
In spite of its effeciency, institutions rarely use ultrasound guidance in operations to remove hematoma.
Advantages of intraoperative ultrasound monitoring are;.
1. Real-time display is available during the operation.
2. Scanning sections are freely selective.
3. Intermittent and/or continuous monitoring is available.
4. The probe is small and does not obstruct the operative field.
5. Precise information can be obtained, which can reduce operation time.
We used ultrasound monitoring for intracerebral acute and chronic hematoma removal operations using a 12 mm diameter 5 MHz probe. For this monitoring, we developed a probe holder in order not to obstruct the FOV under the microscope. We also made a puncture needle guide attachment to do ultrasound monitoring even for microscopic surgery, such as a cerebral tumor operation.
We made a special needle using an eight gauge, silicon puncture needle with two side holes at the tip and 10 mm from the tip and with this equipment proceeded to remove hematoma.

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Many reports have been presented on the treatment of idiopathic carotid-cavernous fistula (CCF); however, there is scarcely any literature on idiopathic CCF harbouring cerebral aneurysms. In this paper, we report three cases of idiopathic CCF associated with cerebral aneurysm. The first case was a 57-year-old woman complaining of right proptosis and conjunctival congestion. Right carotid angiography demonstrated a direct type CCF associated with a small aneurysm arising from the cavernous portion of the internal carotid artery. The second case was a 64-year-old woman with left ptosis and orbital bruit. Carotid angiography showed a CCF supplied by the right internal maxillary artery and the left internal carotid artery. An aneurysm was found in the horizontal portion of the right middle cerebral artery. The third case was a 72-year-old woman with left proptosis, conjunctival congestion and ptosis. Left carotid angiography revealed a CCF fed by the dural branches of the internal carotid and external carotid arteries. An aneurysm was shown in the left middle cerebral artery. Of eight cases, our three cases and five previously reported cases, all were females above 45 years of age. Aneurysms in five cases arose from the cavernous portion of the internal carotid artery; in three cases they arose from the middle cerebral artery. It has been widely considered that the pathogenesis of idiopathic CCF's was of congenital origin, namely rupture of dural AVM or dural AV fistula. However, we speculate that non-congenital pathological conditions, such as rupture of a cerebral aneurysm or acquired vulnerability of dural vessels due to arteriosclerosis and hypertension might contribute to the development of idiopathic CCF in some cases.

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