The effects of a novel calcium antagonist, NC-1100, on local cerebral blood flows (CBF) and brain tissue metabolites such as lactate, pyruvate and ATP were examined in spontaneously hypertensive rats (SHR) of which both carotid arteries were ligated (BCL). CBF in the cerebral and cerebellar cortices were measured by the hydrogen clearance method.
At rest, NC-1100 (0.2 and 1.0 mg/kg, IV) increased blood flows to the cerebrum by 25 and 22%, and to the cerebellum by 13 and 18%, respectively, while it transiently reduced mean atrial blood pressure (MABP) by 28 and 45%.
During BCL, CBF reduction in both cortices did not significantly differ between saline and NC-1100 treated SHR.
One hour after BCL, the increase in brain lactate was 26.6 ± 1.7 mmol/kg in the saline group, being larger than 23.5 ± 2.2 and 22.8 ± 2.3 in the NC-1100 0.2 and 1.0 mg/kg treated groups, respectively. In contrast, ATP levels remained higher in the NC-1100 treated groups (0.80 ± 0.19, 0.97 ± 0.24 mmol/kg in 0.2 and 1.0 mg/kg, respectively) than in the saline given group (0.61 ± 0.04 mmol/kg).
These results indicate that NC-1100 protects brain metabolism against acute ishcemia, suggesting a beneficial effect of this agent for treatment of acute cerebral infarction.

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Serial measurement of cerebral blood flow (CBF) was made in patients with aneurysmal subarachnoid hemorrhage (SAH) using ¹³³Xe inhalation method. CBF changes were analyzed in 50 patients who were in good outcome. In patients with good neurological grade the CBF significantly decreased in the first week after SAH and recovered in the 3rd to 4th week. The patients with poorer grade showed a greater and lasting decrease in CBF, and a significant decrease was observed even in the 4th week after SAH. Patients who developed symptomatic vasospasm showed a greater decrease in CBF than those who did not. The higher the patient's age was, the more marked and lasting was the decrease in CBF. Patients who were in their 30's and 40's restored normal CBF level by the 3rd week after SAH, and those who were in their 50's restored it in the 4th week. But the patients in their 60's showed a significant decrease in CBF even in the 4th week after SAH. The patients with the age of 50 years or older were found to have a significant decrease in CBF even in the follow-up period of 3 months to 1 year after SAH. The elderly patients should be carefully observed and managed after SAH even if they are apparently in good condition, since the physiological reserve is reduced in systemic and cerebral circualtions.

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I have investigated 102 vertebral arteries with Duplex ultrasonography in conjunction with angiograms. The 9 vertebral occlusions at the origin were characterized by ultrasonographic silence. The “distal occlusion pattern”, which was the absence of diastolic flow component in the ultrasonographic evaluation, was detected in all 4 vertebral occlusions before branching posterior inferior cerebellar artery (PICA), in 3 of 7 vertebral occlusions after branching PICA, and in the one basilar occlusion. The 7 retrograde vertebral blood flow was easily detected by Duplex ultrasonography. Vertebro-basilar stenoses could not be detected by Duplex ultrasonography.
The “distal occlusion pattern” was thought to be detected only in cases without a patent large branching artery, such as PICA and anterior inferior cerebellar artery (AICA). So Duplex ultasonography may not be able to detect basilar occlusion with patent large PICA or AICA. But if Duplex ultrasonography shows a distal occlusion pattern in bilateral vertebral arteries, it may be a basilar occlusion with poor collateral circulation. And if a distal occlusion pattern in unilateral vertebral artery is shown, it may be vertebral occlusion without PICA or with poor developing PICA.
Duplex ultrasonography could detect all vertebral occlusions at the origin and retrograde vertebral blood flow due to subclavian artery lesion. Thus, I believe that Duplex ultrasonography is very useful in the diagnosis of vertebro-basilar occlusion.

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A software is developed to automatically superimpose two cerebral angiograms to display a single synthesized image with the use of EFPACS-500. Two subtracted angiograms are degitized at 2048 × 2048 × 10 bits using a film laser scanner and stored in the 2.6 GByte optical disk. By simply indicating two reference points, Nasion and Inion, two films are automatically superimposed and displayed as a synthesized image with two different phases well delineated by positive-negative basis. Two illustrative cases of complete occlusion of the middle cerebral artery are presented to show this technique is of use in evaluating a basic hemodynamics on a single synthesized image.

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A 33-year-old man was admitted to our center due to gait disturbance one year after the attack of pontine hemorrhage. Right facial nerve palsy, right one-and-a-half syndrome, left hemi-hypalgesia, bilateral cerebellar ataxia (right<left) and palatal myoclonus were noted. Nineteen months after the onset, he noticed coarse tremorlike involuntary movement of left upper limb. As soon as he raised his arm voluntarily or tried the finger-to-nose test, coarse and rhythmic right-left movement of shoulder joint or extension-flexion movement of elbow joint appeared. During sleep or at rest, the movement disappeard. Superificial EMG recording of this movement revealed 2-3 Hz rhythmic reciprocal grouping discharges in biceps brachii and triceps brachii, occasionally in trunk and neck muscles. These movements were considered to be classified as action tremor or intension tremor resembling to “hyperkinésies vollitionelles”. Magnetic resonance imaging (MRI) showed a lesion in right tegmentum pontis and enlarged right inferior olive on T2-weighted image. These coarse action tremors were considered to be due to pontine tegmentum damage.

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Of 452 cases of ruptured intracranial aneurysm which have been treated in our clinic for the past 5 years, 24 cases (5.3%) presented re-rupture after hospitalization. These 24 cases were analyzed for the time and occasion of re-rupture, blood pressure control and prognosis.
The time interval from the onset to re-rupture was the day of onset most (10 cases), 27 days (4 cases), 814 days (6 cases) and not less than 15 days (4 cases).
Re-rupture was ascribable to body carrying, CT, angiography, ventricular drainage and urethral catheterization in 3, 2, 4, 4 and 1 cases, respectively.
In acute stage (13 days), 12 cases presented re-ruptured. In 10 cases, blood pressure control was unsatisafactory. On the other hand, we have no experience in re-rupture for systolic blood pressure below 100 mmHg. Depression of systolic blood pressure to 80100 mmHg had not aggravated the state of the patients.
In chronic stage (4 days-), satisfactory depression was difficult because of the coincidence with cerebral vasospasm.
Radical operation was received by only 9 cases. The mortality associated with re-rupture was 62.5%.
Thus, complete blood pressure control was considered to be important, though it probably has a limit.

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In order to investigate the changes of regional cerebral blood flow (rCBF) by the cold pressor test (CPT), it was carried out to 46 patients with cerebral thrombosis and 33 patients with cerebral hemorrhage in chronic stage, and to 16 cases with non-cerebrovascular disease.
After 15 min rest, rCBF on the affected side of the hemisphere was measured by the infusion method of ¹³³Xe into internal carotid artery. According to the mean of rCBF (m-rCBF), all of subjects with stroke were classified into 3 groups, namely, group I; m-rCBF≥40 ml/100 g/min, gruop II; 40 ml/100 g/min>m-rCBF≥30 ml/100 g/min, group III; 30 ml/100 g/min>m-rCBF.
Results were as follows.
1) Systolic blood pressure, diastolic blood pressure and heart rate increased clearly after the CPT in all of subjects.
2) m-rCBF of group III in the cerebral thrombosis and the cerebral hemorrhage increased markedly after the CPT. And also, autoregulation index of group III in the cerebral thrombosis was higher than those in other groups.
3) m-rCBF of group I in the cerebral hemorrhage decreased after the CPT, however in the cerebral thrombosis did not.
These results suggest that m-rCBF in the patients of lower cerebral blood flow with stroke is apt to increase by the cold stress, and the autoregulation in those patients with cerebral thrombosis disorders more.

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We report two cases of spontaneous dissection of the cervical internal carotid artery. Case 1 is a 48-year-old, right-handed man who felt transient left neck pain, dizziness, weakness of right upper extremity and blurred vision in the left eye on April 7, 1987. Two days later, he had weakness of the right upper and lower extremities, speech disturbance and blurred vision in the left eye again, and admitted to our hospital on April 11, 1987. Neurological examination on admission revealed slight motor aphasia, left incomplete Horner's syndrome, decrease of visual acuity of the left eye, dysarthria and mild right hemiparesis. He also showed left facial spasm which he had suffered for a few years. CT scan showed low density area in the white matter of the left middle cerebral artery region. Angiography, performed on the day of admission, showed irregular narrowing of left internal carotid artery from the level of the first cervical spine to the skull base (string sign). Also there was an aneurysm at the origin of right anterior choroidal artery. Left vertebral artery showed severe elongation and torsion and considered to be the cause of left facial spasm. After admission he developed total aphasia and complete right hemiparesis. Because of the contralateral aneurysm, we could not use heparin. And he was treated with dopamine and low molecular dextran. He recovered gradually. Angiography of two months later showed improvement of the narrowing of the left internal carotid artery and new formation of dissecting aneurysm. Three months later the narrowing improved further and dissecting aneurysm disappeared entirely. Case 2 is a 54-year-old, right-handed man who admitted due to transient ischemic attack and left neck pain on December 19, 1987. Neurological examination on admission revealed no abnormal findings. Angiography on December 23 showed irregular narrowing of the left cervical internal carotid artery (string sign). After angiography he developed transient ischemic attack of right hemiparesis, aphasia and Gerstmann's syndrome. Heparin and dopamine were administered. He gradually got better and recovered entirely. Angiography of four months later showed improvement of the narrowing of the left internal carotid artery and new formation of large dissecting aneurysm. Two months later the aneurysm and narrowing disappeared completely. He has no symptoms and signs now. There are many opinions about the therapy of the spontaneous dissection of the cervical internal carotid artery. From the experience of our two cases, we consider anticoagulant therapy should be tried first and surgical treatment is not necessary except when transient ischemic attack persists or neurological symptoms and signs get worse in spite of conservative therapies. Finally the case 1, who had an aneurysm of contralateral internal carotid artery, is very interesting when we consider the pathogenesis of spontaneous dissection of cervical internal carotid artery.

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The activity of acetylcholinesterase (AChE) G4 isozyme was measured in the serum of patients ith cerebrovascular diseases or with dementia and compared with that of healthy subjects. AChE G4 isozyme activity showed an increase in the serum of patients with cerebral infarction and a decrease in the serum of patients with Alzheimer-type dementia. The symptom, days after attack, size of the lesion or prognosis did not correlate the activity. However, the difference of the activity between vascular dementia and Alzhimer-type dementia may provide a useful tool for differential diagnosis of to types of dementia in consideration of the age.

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The metabolic relationship between one cerebral hemisphere and the opposite cerebellum was studied using positron emission tomography (PET) and a double-study method with [18-F] fluorodeoxyglucose (FDG). Subjects were 23 normal volunteers aged 46 to 78 years (mean ± S.D. : 61 ± 10).
All subjects were studied by a procedure incorporating two sequential scans carried out during different behavioral states. For the initial scan, the subjects were at rest, with eyes closed and lightly blindfolded. A bolus of 2.53.5 mCi of FDG was administered intravenously; 30 minutes later, a 20-minute PET scan was performed. Immediately thereafter, an activation paradigm (verbal memory task, described later) was commenced. Five minutes later, a second 2.53.5 mCi bolus of FDG was administered. The activation tesk was continued for the following 30 minutes. The subjects were then repositioned in the scanner in a manner identical to that in the first scan and a second 20-minute PET scan was performed.
In the verbal memory task, subjects were asked to read passages similar to those in the Wechsler Adult Intelligence Scale and immediately thereafter to recall what had been read. Before the scanning session, subjects were familiarized with the task and, during the actual session, were urged to attempt to recall the passages as thoroughly as possible.
Cerebral metabolic rate for glucose (CMRglc) was calculated in a total of 12 pairs of bilateral regions between 10 and 100 mm above the IOM line. Regional CMRglc was calculated by obtaining a mean value for all boxes in the prefrontal, premotor, orbitofrontal, motor, sensory, superior parietal, inferior parietal, superior temporal, medial temporal, occipital, deep grey (basal ganglia + thalamus) and cerebellar regions in each hemisphere.
During the 35-mimute period alloted to the task, the subjects read an average of 18.6 ± 2.6 passages. The number of recalled passages averaged 50.6 ± 14.5%. The mean CMRglc value at rest was 6.0 ± 1.3 mg/100 g/min and no significant right-left asymmetry in either cerebral or cerebellar CMRglc was noted. The CMRglc during activation was 7.1 ± 1.0 mg/100 g/min, showing an 18.3% increase. During activation, regional side-to-side asymmetries of CMRglc were produced. The premotor, orbitofrontal and motor regions in the left hemisphere showed significantly higher CMRglc increases than the corresponding regions in the right hemisphere, whereas the right cerebellum showed a significantly higher CMRglc increase than the left cerebellum.
The regional CMRglc increase data were analyzed in terms of regional (Left-Right) values of CMRglc increase. Correlations of these asymmetrical indices between various regions in the hemisphere and the cerebellum were examined. In Pearson correlation analysis, the motor region showed the highest correlation coefficient (r=-0.6, p=0.003) with cerebellum, followed by the premotor (r=-0.48, p=0.02), the prefrontal (r=-0.41, p=0.06) and the sensory (r=-0.41, p=0.06) regions. In multiple regression analysis, the only variable correlating with the cerebellum was the motor region (t=-2.6, p=0.02).
The clinical approach used here has provided one of the first quantitative demonstrations of highly specific metabolic coupling between the cerebral region and the cerebellum. Our finding suggests that the metabolic activation in the motor region during a verbal memory task is best coupled with the metabolic activation in the cerebellum.

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Surgical results were studied in a series of 42 patietns with an unruptured intracranial aneurysm who had not experienced a rupture from aneurysm. Aneurysms were found by cerebral angio-CT and/or cerebral MR angioimaging techniques in 25 patietns, by angiography for the evaluation of occulomoter palsy in 2 patients, and incidentally by angiography for the evaluation of various diseases other than subarachnoid hemorrhage in 15 patients. Twenty-two were men and 20 women. The patients had 49 unruptured aneurysms, 8 were anterior communicating (Acom) aneurysms, 16 middle cerebral artery (MCA) aneurysms, 16 internal carotid (IC) artery aneurysms, 5 anterior cerebral artery (ACA) aneurysms and 4 vertebro-basilar artery aneurysms. Nine aneurysms were smaller than 5 mm in the greatest diameter, 18 aneurysms from 5 to 10 mm, 16 aneurysms from 10 to 20 mm and 6 aneurysms lager than 20 mm.
Aneurysms were treated by neck clipping in 42, coating in 4, proximal ligation in 2 and aneurysmectomy in one. There were operative mortality in one patient (2%) who died one month after the surgery, and morbidity in two patients (5%) who developed a permanent neurological deficits after the surgery. In the patients with morbidity, one had a large MCA aneurysm. The middle cerebral artery was occluded due probably to the thrombus formation on an atheromatous plaque on the aneurysmal neck protruded into the lumen of the parent artery by neck clipping. The other one developed hemiparesis because of an internal carotid artery stenosis by neck clipping for a giant IC aneurysm. Our present result is superior than that in natural risk of unruptured aneurysms. It is considered that unruptured aneurysms should have a good indication for surgical treatment in careful consideration of patients medical conditions, regardless the size and location of aneurysms.

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It is well known that platelet dysfunction has a major role in the onset and progress of ischemic cerebrovascular disease. However, there are few reports describing morphological changes of platelets and, among other things, electron microscopic observations of them under such a pathological condition. In the present study, we made electron microscopic observations of platelets with ischemic cerebrovascular disease showing stenosis or occlusive lesions at the cerebral arteries.
The study involved patients who had been demonstrated to have stenosis or occlusion at single spot of the internal carotid artery or the middle cerebral artery by four vessels angiography. They were divided into the following types by the degree of stenosis. Type I : Patients with stenosis covering less than 75%. Type II : Patients wit stenosis covering 75% or more. Type III : Patients with complete occlusion. Blood samples were collected from each of them by puncturing the common carotid artery and jugular vein with 19G teflon sheath needle.
Pseudopod formation and surface folds were found to be the principal morphological changes of platelets in the blood of ischemic cerebrovascular disease. Pseudopod formation and surface folds were seen in 39%, 58% and 28% in type I, II and III respectively in the platelet of the jugular vein.
The incidence was 23% in the blood of the common carotid artery. Moreover, the platelets with deformation showed a decreased number of dense granules.
On the basis of the above findings, blood turbulence due to stenosis of blood vessels was presumed to play a more important role from the findings that platelet deformation was more remarkable in proportion to the increase in the severity index of vascular stenosis, whereas it became less in the patients with occlusion.

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The P300 or P3 component of the event-related brain potential (ERP) is generated when subjects discriminate stimulus events which differ from one another in some dimension. But there are few reports about correlation between P300 latency and rCBF in patiens with cerebral infarction. We studied the relationship between P300 latency and rCBF in patients with cerebral infarction.
Twenty-four non-demented patients (21 males, 3 females, mean age 65.0 years) with chronic cerebral infarction and 53 normal subjects (24 males, 29 females, mean age 64.1 years) who showed no abnormalities in neurological findings and MRI images were studied. An oddball stimulus paradigm was employed and ERP was elicited by rare target stimuli. Regional CBF was measured by a ¹³³Xe inhalation method. There was no significant difference between the two groups in P300 latency, but there as a significant difference between both groups in rCBF (p<0.05). Significant prolongation of P300 latency as observed with advancing age in the two groups. There was a significant negative correlation between P300 latency values and rCBF in patients with cerebral infarction (p<0.001).
It is concluded that P300 latency is related to rCBF in patients with cerebral infarction.

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The authors had experienced 13 cases of primitive arteries of 9 persistent primitive trigeminal arteries (PTA) and 4 persistent primitive hypoglossal arteries (PHA). Primary lesions, caused to be found incidentally of these 13 primitive arteries were 6 cases of cerebral aneurysms, 3 cases of intracranial tumors, 3 cases of cerebral infarctions and one case of arachnoid cyst. One of the infarction cases was also fond to have cerebral aneurysm. These experienced cases were analyzed on their characteristics and literatures on persistent carotid-basilar anastomoses were reviwed and discussed mainly on their embryology, coexistent lesions and clinical symptoms and signs. And also discussed the important point during and post operative care for the patient with persistent carotid-basilar anastomosis.

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A patient with neurofibromatosis associated with multiple aneurysms is presented.
A 51-year-old man was admitted for sudden onset of subarachnoid hemorrhage. He noticed subcutaneous tumors and pigmentations of the whole body at the time of junior high school. Cerebral angiography demonstrated a right distal anterior cerebral aneurysm and a left extracranial vertebral (V3 segment) aneurysm. Neck clipping of the right distal anterior cerebral aneurysm was performed because the rupture of this aneurysm caused subarachnoid hemorrhage. At the same time, biopsies of the subcutaneous tumor and superficial temporal artery were done. Histopathological examination of the tumor revealed a nurofibroma and the superficial temporal artery revealed intimal fibrosis, fragmentation of the internal elastic lamina and extrenal fibrosis.
Only thirteen cases of neurofibromatosis associated with cerebral aneurysms have been reported. Nine are with intracranial aneurysms, four with extracranial aneurysms and four with multiple aneurysms. It is considered that the pathogenesis of development of aneurysm is due to the elastic fragmentation.

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