Vincristine and vinblastine possess antimitotic activities with arrest of cycling cells in metaphase. These drugs were utilized to analyze the growth characteristics of 12 human gliomas (6 glioblastomas, 4 anaplastic astrocytomas, 2 well differentiated gliomas). The patients received ³H-thymidine and mitostatic agents (either 0.1 mg/kg of Velban or 3 mg/m² of Oncovin) prior to tumor biopsy. To allow for more convenient comparison of the mitotic index (MI) and the labeling index (LI) in the prognosis of patients, a normalized value (MI/t) was computed by dividing the MI by the lapsed time between drug administration and biopsy. Most malignant gliomas had a MI/t value of 4-5×10^-3, a LI of 5-15%, and a potential doubling time of 8.7±3.3 days. In contrast, well differentiated gliomas had a MI/t value of <0.6×10^-3 and a LI of 1.9% or less. Patients whose tumors had a MI/t value of > 2×10^-3 and/or a LI of > 5% died within 6 months after biopsy. Postmortem examination of specimens from 4 glioblastomas revealed very few, inconsistent mitoses (MI ?? <0.5×10^-3). Thus, MI/t values obtained with the use of mitostatic agents should have prognostic significances similar to the LI. Although many uncertainties still exist, the use of mitostatic agents in the study of human brain tumor growth kinetics offers some advantages such as: mitostatic agents are not radioactive; single doses of these drugs are virtually harmless; the method is simple to apply; and, the results can be obtained very quickly.

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The relation between tissue coagulating, fibrinolytic system and cyst-formation of brain tumors was studied. Twenty-nine cases of brain tumor, which contained 1 1 cases with cystic tumor and 18 cases with solid tumor, were examined. Four pieces of normal brain which were obtained by operation were examined as control.
The levels of fibrinolytic activities of contents of cystic tumors were measured by plasmin activity, SK-activated plasmin activity using fibrin plate (Kowa Co., Japan) and FDP values using FDP Kit (Wellcome, England). Plasmin activity was found in 7 cases of cystic tumor. SK-activated plasmin activity was also found in 9 cases of cystic brain tumor. The FDP values measured in 7 cases of cystic tumor were 40-800 ug/ml. In only 2 cases with cystic brain tumors, the activities of plasmin and SK-activated plasmin were not found. In one of these FDP value was 160 ug/ml. Thus, cystic content of most cystic brain tumor had fibrinolytic activities.
The levels of tissue thromboplastin of 29 cases of brain tumor were measured by a modified Astrup's method. Coagulation time of normal brain tissues was 14.8 sec. (thromboplastin content in 100 mg. tissues: 100%), that of tumor tissues with cyst was 12.5 sec. (215%), and that of tumor tissues without cyst was 19.3 sec. (29.9%). Hence, the levels of tissue thromboplastin of cystic brain tumors were higher than those in normal brain tissues and the levels of solid brain tumors were much lower than those of normal ones. The tissue local fibrinolytic activities were measured by Permis' method, using fibrin plate, and the levels of tissue plasminogen activator were measured by a modified Astrup's method. Trypsin solution was used as control and fibrinolytic activity of normal brain tissues were 0.80±1.78 TU, those of cystic brain tumor tissues were 4.35±3.25 TU, and those of solid brain tumor tissues were 0.14±0.64 TU. These results showed that the levels of tissue fibrinolytic activity of cystic brain tumor were much higher than those of normal brains and brain tumors without cysts (p<0.05, p<0.01). However, the levels of plasminogen activator of the tissues of cystic brain tumor were almost the same compared with normal brains. The levels of tissue plasminogen activator of solid brain tumor were much lower than those of normal brains and of cystic brain tumors (p<0.01).
Both local coagulating system and fibrinolytic system of brain tumor tissues might be concerned with the cyst formation of the tumor.

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This is a case of primary glioblastoma multiforme in the cerebellum of a 33-year-old female with four months' clinical history. One month prior to admission, she had a sudden onset of severe vertigo, diplopia and headache, and then became unconscious. When admitted to the hospital on December 24, 1974, she was somnolent, and showed respiratory distress, stiff neck, bilateral papilledema, upward gaze palsy, bilateral abducens palsy, tetraparesis, and cerebeller signs such as ataxia and hypotonus of all limbs. Angiography and conray ventriculography disclosed a mass in the cerebellum. Posterior fossa exploration uncovered the mass in the inferior vermis. Partial removal of the tumor was performed. While irradiated by Linac in doses of 2, 600 rads, when she became dyspneic. The patient's condition deteriorated rapidly and she died two months after the operation.
Autopsy revealed that the tumor was situated in the inferior vermis and had infiltrated the bilateral cerebeller hemispheres. Meningeal dissemination in the basal cistern and in the spinal subarachnoidal space, and ventricular seeding were observed. Subcapsular tumor metastases to the liver were also recognized, probably via blood stream. Histological diagnosis of the cerebeller tumor was typical glioblastoma multiforme.
Approximately 44 cases of cerebellar glioblastoma, including our case, have been reported in assorted literature. Clinical features and pathological characteristics are critically reviewed.

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The authors present a case of a 9-year-old boy who had had generalized seizures of focal onset. Plain skull films demonstrated large nodular dense calcification situated deeply in the left parietal region. Clinical investigations did not detect the nature of the lesion. Serial cerebral angiography showed no specific abnormalities except for postero-inferior displacement of a parieto-occipital branch of the left posterior cerebral artery. The mass was removed and was found to be a venous angioma with extensive calcification and thrombosis. The seizures were well controlled with anticonvulsant and he was discharged without neurological deficits. The reason of nonvisualization of the venous angioma with serial angiography is discussed and the literature describing this rare entity is reviewed.

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A total of 128 cases with ruptured cerebral aneurysms were operated on within two weeks after subarachnoid hemorrhage (SAH) . Postoperatively, cerebrospinal fluid (CSF) was continuously drained from the lateral ventricle and the basal cistern. Using the intraventricular catheter, intracranial pressure (ICP) was monitored for an average of three weeks after operation. The development of normal pressure hydrocephalus (NPH) was estimated from ICP pattern and other diagnostic studies such as CT scan, infusion test and RI cisternography.
NPH developed in 26% of these cases. Patients who had a large volume of CSF drainage of over 200 ml daily underwent shunt surgery in a higher proportion (56%). It was postulated that the defect of the subarachnoid space might be aggravated by CSF drainage.
A total of 49 long-term recordings of ICP was obtained in 31 cases. Within two weeks after SAH, ICP was usually higher than 20 mmHg, but thereafter became lower. This early high pressure was mostly due to acute hydrocephalus and not to the so-called acute brain swelling. However, when mildly elevated ICP with B-wave lasted beyond the third week of SAH, almost all patients developed NPH. This characteristic pattern of ICP plays an important role in the development of NPH and is useful for selecting patients for shunt surgery.
Vasospasm was a frequent concomitant of increased ICP, and patients with vasospasm underwent shunt surgery in rather high incidences (34%). Both vasospasm and hydrocephalus could be explained to be the result of blood clots in the subarachnoid space.

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The patient, a 48-years-old housewife, was admitted with complaints of severe headache, intractable nausea and vomiting. She had been treated as a case of alveolar pyorrhea till one month ago. She had suffered from chills and was shivering with high fever about 10 days ago.
On admission, physical examination showed dehydration and cachexia, and laboratory data revealed inflammation. There were left hemihypesthesia and mild papilledema. Spinal puncture revealed watery clear fluid with initial pressure of over 500 mm H₂O. Computed tomogram (CT) demonstrated a high density area suggesting hemorrhage which was surrounded with low density area in the right temporal lobe. Bilateral carotid angiogram showed no filling of superior sagittal sinus and right transverse sinus. Despite use of hypertonic mannitol solution, steroid and antibiotics, she became semicoma tose with right hemiparesis. Emergent right temporal craniectomy disclosed massive brain swelling and intracerebral hematoma in the temporal lobe. Post-operative course was unfavorable. CT revealed multiple intracerebral hematomas in both hemispheres. She died at the eighth day after operation.
At autopsy, revealed swelling of right cerebral hemisphere with right uncal herniation. Horizontal section showed massive multiple hemorrhages in the subcortical white matter and numerous petechiae in both cerebral hemispheres. Superior sagittal sinus and right transverse sinus were thrombosed.
Few reports of computed tomogram related to sinus thrombosis are found. In our case, CT revealed the multiple foci of increased absorption surrounded with a relatively large low density area. These foci, examinated by print out data, were not homogeneous nor regular, characteristic of hemorrhagic infarction.

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Pathophysiology of preoperative and postoperative angiospasm in cases with ruptured intracranial aneurysm was studied.
Twenty-three cases of ruptured intracranial aneurysm who had neurological signs and symptoms of ischemic lesions caused by cerebral angiospasm (spasm-syndrome) were selected on the basis of symptomatology from 184 consecutive cases with ruptured intracranial aneurysm. These cases were divided into two groups according to the time of development of spasm-syndrome and surgery of aneurysm; those in which spasm-syndrome developed in the preoperative period and those in which spasm-syndrome developed in the postoperative period.
In all cases angiospasm in variable degrees was demonstrated on angiograms which were performed after the development of spasm-syndrome. In the cases with preoperative spasm-syndrome clinical signs and symptoms did not become worse after surgery when operation was delayed until spasm-syndrome was improved. Operative results in these cases were fairly good. Postoperative spasm-syndrome frequently occurred in cases in which operation was performed within 10 days after the episode of subarachnoid hemorrhage (SAH). Neurological signs and symptoms in these cases were much worse than those in the cases with preoperative spasm-syndrome. Characteristic features of postoperative spasm-syndrome at early stages of postoperative periods were extensive diffuse angiospasm together with a round shift of major arteries from the surgically affected side to the opposite on angiograms, and an extensive low density area with compression and deformity of ventricles on computed tomograms, suggesting extensive brain edema on the surgically affected cerebral hemisphere. And then, these findings seen on computed tomograms became cerebral infarction at a later postoperative period. On the other hand, abnormal findings on computed tomograms were not found in 11 of 12 operated cases of ruptured intracranial aneurysm who did not have spasm-syndrome in their clinical courses. Preoperative rCBF measurements showed a marked decrease of cerebral blood flow in the cases with postoperative spasm-syndrome.
From this study, it is likely that postoperative spasm-syndrome is the result of cerebral ischemic lesions caused by angiospasm following SAH and surgical influences.

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Ulcerative changes and stenotic lesions in the cervical portion of the carotid artery are being noted as lesions responsible for the development of TIA and RIND. As a result thromboendarterectomy of the carotid artery is recently being actively performed to prevent stroke. The authors' device for this operation is presented.
The device consists of T-shaped internal shunt tubes, two angled bulldog clamps and a retractor. The T-shaped internal shunt tubes are made of polyvinyl chloride (PVC) material. PVC is the most appropriate material for the tube, because it is flexible and does not kink. We made tubes with three different outer diameter sizes and in the same lengths of 30 cm. A side arm mainly to check the patency of the blood flow was also designed in the middle of the tube. Bulbs with smooth surface were provided at both ends so that the intima would not be injured and to prevent the tube from slipping out of the vessel. From the differences in diameter of the common and internal carotid arteries, the tube on the proximal side was provided with a bulb 1-2 mm larger than its distal side and was colored so as to make it easy to distinguish. To permit easy insertion and removal of the tube and its fixation to the vessel, small bulldog-like clamps with jaws angled at a 30° were used. The ringed jaws were provided in three sizes so as to fit the three different outer diameter tubes. To date endarterectomies have been performed with satisfactory results and without complications.

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