Kinetics of the specific immune status was studied in experimental brain tumor of rats. To produce intracerebral tumors, the KEG-1. Cell line of mixed glioma induced by ethylnitrosourea in a WKA/HKM rat was inoculated into the caudate nucleus of the syngeneic rats with a stereotaxic technique. Such inoculation induced a 100% incidence of intracerebral tumors, and killed all the rats in about 20 days after the inoculation. The specific cellular immunity against KEG-1 was examined with a ⁵¹Cr-release cytotoxic assay at various stages of the tumor development. Cellular cytotoxic activity was observed from the 4th day after inoculation with KEG-1, and reached a peak on the 7th day and then declined as tumor growth until the death of the rats. Its activity was well correlated with the result of a tumor neutralization assay. The onset, peak, and decline of cellular cytotoxic activity corresponded closely to that of the cytotoxic antibody detected by a complement-dependent cytotoxic assay. The kinetics of the immune status in these brain tumor bearing rats were essentially similar to those in other tumor models. These results suggest that this brain tumor model may serve as a useful immunological parallel for the human brain tumor.

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It is generally regarded to be very difficult to establish an experimental animal model of chronic subdural hematoma (CSH).
The subdural space was inoculated with fresh blood in 9 dogs (Group I), blood clot in 10 dogs (Group II), and CSF-blood mixture in 13 dogs (Group III). In both Group I and II, the subdural mass showed high or mixed density in the early stage and the mass showed shrinkage of the volume with decrease of its density in the chronic stage by CT. Histological examination revealed rapid organization process of the mass from granulation tissue to firm fibrous connective tissue. In Group III, inoculated subdural masses showed low or iso-density in the early stage and then, the densities variably reduced afterwards. Histological examination revealed neomembrane formation in the subdural space about 2-3 weeks after the inoculation which were consisted of the sinusoidal channel layer and the fibrous layer. Structures of this neomembrane quite resembled to those of clinical cases of CSH. However, there was no expansive subdural lesions so far. In Group IV of 13 dogs, CSF-blood mixture was inoculated into the subdural space and daily doses of D-Mannitol of 3 g/kg and Heparin of 200u./kg were given intravenously from Day 7 after inoculation. In 10 dogs, the subdural collections diminished with increase of the density. In 2 dogs, however, the subdural mass showed significant expansive character with high density in CT from Day 14 to 21. Pathological examination revealed massive hemorrhage from capillaries of the fibrous layer of the neomembrane into the capsular lumen. In the remaining one dog, the subdural mass showed expanding low density area due to dissolution of the hematoma. These three cases resembled human cases of CSH clinico-pathologically.
The result suggested that subdural collection of mixture of CSF and blood participated in the neomembrane formation of CSH and that enlargement of the content of subdural hematoma was brought forth by hemorrhages from capillaries of the fibrous layer, or by dissolution of the hematoma.

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Regional cerebral blood flow values (rCBF values) were measured during the resting state and during 5% CO₂ inhalation by the Xe-133 clearance method in 11 cases with moyamoya disease and in 5 cases with unilateral moyamoya phenomenon. Electro-encephalography and cerebral angiography were simultaneously carried out. Examinations were performed in the chronic phase more than 3 months after the last subarachnoid hemorrhage or transient ischemic attack. Of the 11 cases with moyamoya disease, 3 were children under 20 years old. The 5 patients with unilateral moyamoya phenomenon were all adult. In the resting state, the rCBF values were normal in 5 and abnormally low in 3 out of the 8 adult cases, and were abnormally low in all 3 young cases of moyamoya disease. In the patients with unilateral moyamoya phenomenon, the rCBF values were normal in 3 and slight low in 2 cases. There were no obvious differences between the young and adult cases in their clinical features or in their electroencephalographic and cerebral angiographic findings. rCBF measurement during 5% CO₂ inhalation were carried out in 9 cases with moyamoya disease and in 4 cases with unilateral moyamoya phenomenon. Increase in the rCBF values was noted in 3 out of 7 adult cases with moyamoya disease and in all 4 cases with unilateral moyamoya phenomenon, but was not observed in the 2 young cases with moyamoya disease.
These results indicate that there are differences in the hemodynamic condition between cases with moyamoya disease and cases with unilateral moyamoya phenomenon. Furthermore, a discrepancy also exists between adult and young cases of moyamoya disease. The reason for these discrepancies can not be fully explained as yet. It is supposed that they are mainly due to differences of extent of the anastomotic process in small cortical branches.

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Among 293 cases admitted from May 1976 to December 1980, due to ruptured intracranial aneurysms, 219 cases (91 anterior communicating, 67 internal carotid, and 61 middle cerebral aneurysms) admitted within 14 days after the onset without intracerebral hematoma, sudden death, or troubled operation were chosed for analysis. Among which 153 cases (70%) developed angiographically detectable vasospasm, 56 cases (26%) presented symptomatic vasospasm and 44 cases (20%) showed cerebral infarction due to vasospasm. 14 (32%) of these 44 cases revealed hemorrhagic infarction confirmed by CT. Detection of hemorrhagic infarction by CT occurred between 13 and 42 days after the onset (average: 24±7 days). This period almost coincided with that of the maximum contrast enhancement of the infarcted region (23±4 days) and that of angiographical relaxation of vasospasm (21±4 days). Among these 14 cases, 71% showed capillary blush and 64% revealed early venous filling just before the appearance of hemorrhagic infarction. The incidence of these phenomena were clearly higher than in the cases with ischemic infarction only. On CT examination, 11 cases revealed a high density area mainly in the cortical area, 2 cases in the subcortical area, and one case accompanied ventricular hematoma. Twelve cases developed hemorrhagic infarction without a worsening of the neurological signs with a slight increase of brain swelling. However, one case died due to severe brain swelling and another case needed ventricular drainage because of intraventricular hematoma. The case who died was of the “swelling stage type”. Severe brain swelling due to ischemia and increased perfusion pressure due to a slight release of vasospasm with concomitant arterial hypertension must have caused the hemorrhagic infarction. The other 13 cases fell into the “neovascularization stage type”. Here, increased perfusion pressure following relaxation of vasospasm and development of neovascularization lacking blood brain barrier after ischemic cerebral infarction might explain the cause of hemorrhagic infarction. These phenomena coincided with the decreasing stage of brain swelling and the stage of marked contrast enhancement on CT. In both types, increase of cerebral blood flow despite low metabolism in the damaged brain—the concept of “luxury perfusion syndrome”—may explain the development of hemorrhagic infarction. Concerning the management of vasospasm, care should be paid not to worsen hemorrhagic infarction by monotonus methods for the increase cerebral blood flow such as the induced hypertensive-hypervolemic therapy. Appropriate evaluation of the ischemic stage is important for suitable treatment.

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Correlations between the patterns of spread of hypertensive intracranial hemorrhages and their outcome were studied. The subjects were 236 patients with hypertensive intracranial hematoma hospitalized during the period from October 1975 (when CT was introduced) through September 1981. Breakdown of the cases was: 141 (59.7%) putaminal hemorrhages, 67 (28.4%) thalamic hemorrhages, 18 (7.6%) pontine hemorrhages, and 10 (4.3%) cerebellar hemorrhages.
In putaminal hemorrhage, the outcome was well correlated to the CT grading of the Japanese cooperative study groups, except in Type III (hematoma extending to the posterior limb of the internal capsule). The definition and details of Type III should therefore be reconsidered, as this type is the hematoma most indicated for surgery. The worst factor for the prognosis was extension of the hematoma to the subthalamic areas. Therefore, Type I (external capsular hematoma) and those cases in which the hematoma has spread to the subthalamic areas should not be operated. Thalamic hemorrhage were roughly divided into three groups. Outcome of the hematoma limited within the thalamus was good, while that of the hematoma extending beyond the internal capsule was poor. The hematoma reaching the internal capsule showed variable outcome, and its therapeutic principle has yet to be established. Pontine hemorrhages were classified into two groups; one localizing in the pons and the other extending to the midbrain. Generally, the hematoma extending to the midbrain showed poor outcome, but those extending upward to the midbrain unilaterally along the pons showed moderately good outcome. Some cerebellar hemorrhages treated conservatively showed good outcome, even when the diameter of the hematoma was over 3 cm. Discrepancies between CT findings and autopsy findings were 58.8% in the putaminal hemorrhages and 50% in the thalamic hemorrhages. Death was most frequent in cases with subthalamic extension.

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When a sitting operation is performed, early detection and prevention of air embolism are important. Air flow into the right heart system was monitored by a real-time two-dimensional echocardiograph in combination with a video-recorder. The heart was observed from the apical four chamber view by a ditector placed under the xiphisternum and directed towards the base of heart. The echocardiography showed two types of air flow; one was the single-bubble type in which several bubbles flowed from the right atrium to the right ventricle, and the other was the stormy-bubble type in which a great number of air bubbles flowed en masse. The single-bubble type was observed during surgery involving the skin, muscle, or bone, and the air flow in this type could be interrupted by electrocoagulation, bone wax, etc. The stormy-bubble type was noted during surgery involving the muscle or dura mater. The air flow from the dura mater was most frequently observed. Retroflexion of the dura mater and then electrocoagulation would be required to prevent the air flow from the cut end of the dura mater. If electrocoagulation does not control the air flow from the cut end of the muscle, massive muscle suture by thick threads could prevent the air flow. Air flow into the right heart system in a sitting operation was more frequent than has previously been believed, and a small amount of air flow was noted even during minor surgery. Therefore, application of. a sitting operation should be carefully undertaken.
Ultrasonic tomographic monitoring of the heart was useful in the early detection of air embolism because of its non-invasive technique and its high sensitivity.

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Five patients, all females, had meningiomas of the optic nerve sheath. The tumor was located in the right in four and in the left in one. Three had severe visual disturbance. All had proptosis of more than 3 mm. Three had disc edema and one had optic atrophy. Opticociliary veins were observed in only one case. Ocular movement was mildly impaired in two patients. Plain films were normal in all patients. Arteriographic abnormalities were present within the orbit in all of the four cases examined, an actual tumor blush occurring in three. Orbital venography showed evidence of the lesion within the muscle cone in 4/4. Computed tomography showed enlargement of the optic nerve in 3/3. All five cases were operated. The surgical approach for the tumors was the combined frontal intra- and extradural approach. All of the meningiomas in this series were of the meningothelial type.

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Two cases with cerebral aneurysms and bilateral carotid occlusion are described. They had no cerebral ischemic attack prior to aneurysmal subarachnoid hemorrhage because of sufficient collateral blood flow from the posterior circulation. The cerebral aneurysms were both located in the posterior circulation where the hemodynamic stress might have occurred.
Case 1. A 54-year-old hypertensive man was admitted with headache. Computerized tomography scan and cerebral angiography revealed subarachnoid hemorrhage, bilateral internal carotid occlusion, and two saccular aneurysms of the right posterior cerebral artery at the junction of the posterior communicating artery. The blood flow for both cerebral hemispheres was mainly supplied through the posterior circulation via the right posterior communicating artery. Physical examination on admission was unremarkable except for moderate nuchal rigidity and headache. He was discharged after clipping of the aneurysms.
Case 2. A 81-year-old woman was admitted because of sudden loss of consciousness. She had an unremarkable an history except for a short term loss of consciousness three months prior. On admission she was in a semicomatose state, and showed no lateralizing signs. Computerized tomography scan revealed subarachnoid hemorrhage. On aortography, the innominate artery and the left common carotid artery were not opacified from their origin. The left vertebral artery, which was enlarged and elongated, supplied most of the cerebral hemispheres through both posterior communicating arteries. The saccular aneurysm was located at the lower part of the basilar artery where the hemodynamic stress might have occurred. She died without recovery.
The present report indicates that the hemodynamic stress caused by bilateral carotid occlusion in combination with hypertension or aging may play an important role in aneurysmal formation in the posterior circulation.

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CT scans of 26 cases of subdural hematomas were carefully reviewed with particular emphasis on their densities. All the five cases of verified infantile chronic subdural hematoma, and four out of 15 cases of adult chronic subdural hematomas showed accumulations of CSF-dense fluid over the hemispheres, as well as in the cerebral sulci and cisterns, which were clearly demarcated from the overlying, rather highdense, subdural hematomas. The accumulation over the hemisphere was thicker where the underlying brain was severely atrophied. One of these had been erroneously diagnosed as ‘brain atrophy’. This and one adult case later progressed to a lentiform chronic subdural hematoma without CSF accumulation. Among six acute infantile subdural hematoma cases, three clinically mild cases showed accumulation of fluid in the sulci, fissures, and over the hemispheres, which gave the appearance of ‘brain atrophy’. Among three cases of severe form acute subdural hematomas, one showed a localized accumulation of CSF-dense fluid underneath the clot and over the hemisphere with sulcal patterns.
In two cases of adult subdural effusions, metrizamide CT cisternography was performed. In both cases the dye not only filled the widely open cisterns and sulci, but also showed the existence of the subarachnoid space over the hemispheres and even beneath the subdural fluid space.
From these observations it seemed logical that the subdural effusion (hematoma) was usually accompanied by enlargement of the subarachnoid spaces. In the acute phase, either primary subarachnoid hemorrhage or secondary bleeding from permeation of the subdural blood would cause blockage of the arachnoid villi, and the subsequent evolution of communicating hydrocephalus. In the chronic phase, however, hydrocephalus ex vacuo should play an important role, since the CSF accumulation appeared to have increased under decreased intracranial pressure with brain atrophy and/or enlargement of the calvarium, i.e., craniocerebral disproportion. Previous reports such as benign subdural collection of fluid, should be interpreted as the combination of subdural fluid with enlargement of the subarachnoid spaces. Similarly, in case termed benign enlargement of the subarachnoid spaces, benign communicating hydrocephalus, etc., the coexistence of subdural fluid must be considered and sought.

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A case of primary cerebral ganglioneuroblastoma of the anterior skull base was reported.
The patient, a 19-year-old male, suffered from visual disturbance and fatigability. Obesity, hypogonadism, disturbance of visual acuity, visual field defect, and bilateral choked discs were revealed and moderate panhypopituitarism was found. Plain craniograms showed signs of increased intracranial pressure and demineralization of the anterior skull base. Left carotid angiograms showed a left to right displacement of the anterior cerebral artery and an oval vascular stain in the left frontal region. EEG revealed a polyphasic slow wave focus in the left frontal region. Partial removal of the tumor was performed and Linac therapy with a tumor dose of 4, 000 rads was given. The histological dignosis was ganglioneuroblastoma, which showed small, uniform, spherical cells with abundant nuclear chromatin and large cells with some processes and Nissl granules. At follow-up studies 3, 5, and 6 years after the operation, only a slight decrease of visual acuity was noted and no enlargement of the tumor was found in CT scans or cerebral angiograms. A histological maturation of this tumor may have occurred.

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The pathological findings and clinical course of a case of primary cerebellar neuroblastoma was reported.
The patient, a two-month-old girl, showed sun-set phenomenon and bilateral foot-clonus. Retrobrachial angiography and CT scan showed hydrocephalus and a large tumor in the posterior fossa. Partial removal of the tumor and a ventriculo-peritoneal shunt were performed. Thereafter, radiotherapy was given (whole brain 2, 940 rads, total spinal 2, 000 rads), and methotrexate was injected intrathecally through the ventricular tube of the shunt every 6 months. On discharge, CT scan did not reveal tumor and 29 months after the operation the patient showed no signs of tumor recurrence on CT scan or in neurological examination. Histologically, the tumor was lobulated by narrow vascular stroma. The tumor cells had little cytoplasm, a round or oval nucleus, and were arranged in groups of variable sizes or in single rows, separated by varying amounts of fibrillary matrix. Ultrastructurally, the extracellular spaces were occupied by varying amounts of intricate networks of slender cytoplasmic processes which lay mostly parallel each other and contained many microtubules and clear vesicles of about 40-50 nm in diameter. These clear vesicles occasionally aggregated in groups and assumed a presynaptic configuration associated with a postsynaptic membrane thickening. These findings established the diagnosis of neuroblastoma. This case, as confirmed by the literature, indicates that the prognosis of cerebellar neuroblastoma is better than for medulloblastoma.

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