Positron emission tomography with Positome II using ⁶⁶Ga-EDTA was performed in cases with brain tumor and cerebral arteriovenous malformation. A significant focal uptake in static study and hemodynamic changes in dynamic study were noted in all cases except one case with intracranial lipoma.
Comparing this method with ^99mTc-pertechnetate cerebral image study and computerized axial tomography, the diagnostic rate for detecting brain tumor was almost equal in all of these three methods. However, detecting and localizing was easier and clearer in static positron emission tomography with ⁶⁸Ga-EDTA than in ^99mTcpertechnetate cerebral image and computerized axial tomography without infusion of contrast medium. Furthermore, static positron emission tomography with ⁶⁸Ga-EDTA was superior to computerized axial tomography without infusion of contrast medium for detecting cerebral arteriovenous malformation.
Concerning dynamic positron emission tomography with ⁶⁸Ga-EDTA, semiquantitative values obtained by this method correlated well with findings of computerized axial tomography and was thought to be more precise and in detail than the findings of ^99mTc-pertechnetate cerebral image study.
Summation of the previous studies about dynamic positron emission tomography with ⁷⁷Kr in occlusive cerebrovascular disease is also reported.
In conclusion, static positron emission tomography with ⁶⁸Ga-EDTA is a very useful diagnostic method for detecting and localizing brain tumor and cerebral arteriovenous malformation without any attendant complications. Furthermore, a good combination of static and dynamic positron emission tomography and computerized axial tomography appear to be outstandingly effective for not only detecting the lesion but also understanding the pathophysiological aspect in cases with various intracranial lesions.

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Forty-two cases of large pituitary adenomas (including 19 non-functioning adenoma cases, 8 PRL-secreting adenoma cases and 15 GH-secreting adenoma cases) were examined for pituitary insufficiency prior to treatment by operation and/or irradiation and more than 2 years thereafter.
PRL-secreting cases exhibited the highest degree of pre-treatment pituitary insufficiency, while non-functioning adenomas a medium degree, and GH-secreting adenomas a minor degree. These were in proportion to the dimensions of tumors. The incidence of disturbance in secretion of hormones were 100% in GH, about 50% in LH and TSH, and a mere 20% in ACTH, FSH and PRL. In GH secreting adenomas, however, TSH secretion was disturbed in about 70%.
A 2-year follow-up study after treatment revealed increased disturbances in LH, FSH and PRL compared to those before treatment, though no remarkable change was observed in ACTH and TSH. Irradiations were responsible for aggravation of disturbances and its influence was most dramatic in LH, FSH and PRL.
PRL levels in PRL-secreting cases decreased gradually for 2 years after treatment at rates of 19 to 49% (25.5% average) of the pre-treatment levels. In 2 of these cases, PRL levels showed a 10% decrease of the pre-treatment levels 4 years after treatment. In 3 out of 7 GH-secreting cases, which did not respond to surgery in terms of decrease in levels of GH and were further treated by irradiation, GH levels decreased below 10 ng/ml after a 2-year period. In addition, in 3 out of 4 GH-secreting cases treated by irradiation only, GH levels decreased below 10 ng/ml after a 2-year period. Irradiation seemed effective in GH-secreting adenomas.

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Human medulloblastomas obtained from 6 children were heterologously transplanted into the brains of Hy-3 strain mice with and without anti-thymocyte serum (ATS) treatment. Mice were sacrified 3 months after the inoculation of tumors. Active tumor growths were observed only in 7 out of 29 ATS treated mice (24%) while no tumor-growth was seen in the controls.
Tumor growths were always situated in the areas adjacent to the lateral ventricle or in the subarachnoid space. The histological pictures of these tumors were essentially similar to those of original tumors. Transplanted tumors were composed of two main tissue architectures. The major part of the tumor was composed of typical medulloblastoma cells with mitotic figures and pseudoresette formations, and there were scattered areas of the so-called “pale islands.” Tumor cells surrounding the “pale islands, ” however, did not show any specific patterns, such as trabecular arrangement of neoplastic cells which was observed in original tumors. Fibrous tissue around “pale islands” were much less than those seen in original tumors.
The electron microscopic study revealed that glial fibrils were present in the processes of the tumor cells and that many unmyelinated axons were encountered among the tumor cells.
The following might be concluded from the present study: 1) tumor growth may be promoted either directly or indirectly by the presence of CSF and presumably of choroid plexus; 2) fibrous areas of “pale island” seems to be reactive changes of the leptomeninges to the encroaching tumor since these findings disappeared completely in the transplanted tumors, though pale islands did exist. From this finding so-called “arachnoidal cerebellar sarcoma” is thought to be classified as one form of medulloblastoma modified by the interaction between medulloblastoma cells and fibrous tissue from arachnoid membrane; 3) medulloblastoma cells might have bipontentiality in differentiating toward either neurons or glial cells; and 4) it should be stressed that the heterologous transplantation of tumors could be a useful tool for the resolution of certain neuropathological problems.

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Modification of periventricular hypodensity in suspected communicating hydrocephalus was investigated by metrizamide CT cisternography. Six to eight ml of metrizamide isotonic solution with a concentration of 170 mgI/ml was given through lumbar puncture and scanning was conducted 1, 3, 6, 24 and 48 hrs after injection. In addition to visual analysis of images, mean value and standard deviation were calculated for Hounsfield units of the regions of interest at the anterolateral angle of frontal horn and the time courses of the attenuation values were statistically compared to each other at each scanning time. The results were classified into four groups: 1) periventricular low density zone with gradual penetration of metrizamide therein; 2) periventricular low density zone without penetration of metrizamide therein; 3) minimal periventricular low density zone with minimal metrizamide penetration; and 4) no periventricular low density zone and no penetration of metrizamide (Fig.1).
The presence of a periventricular low density zone with increase of the density after ventricular reflux of metrizamide would be an important criterion for CSF shunting operation in normal pressure hydrocephalus or communicating hydrocephalus.

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Hypothalamo-hypophyseal adrenal function of patients with neurogenic gastrointestinal hemorrhage in neurosurgery cases were studied. Measurement of circadian cortisol rhythm and insulin tolerance test were performed for patients with severe brain damage who had developed gastrointestinal hemorrhage under glucocorticoid administration.
The results showed : 1) circadian cortisol rhythm was abolished and cortisol levels were suppressed very easily by only 1 mg/day of Dexamethasone and they required two days to recover: and 2) endogenous cortisol response to hemorrhagic shock or hypoglycemia was completely suppressed by pharmacological doses of glucocorticoids (Dexamethasone 16-32 mg/day).
Therefore, if glucocorticoid administration was discontinued completly in patients with gastrointestinal hemorrhage, they may fall into acute adrenal insufficiency, which could be dangerous. We have been using pharmacological doses of glucocorticoids every 6 hours intravenously and have succeeded in decreasing the incidences of neurogenic gastrointestinal hemorrhage to 5.5%.
In conclusion, we propose that in cases of neurogenic gastrointestinal hemorrhage, pharmacological doses of glucocorticoids be provided every 6 hours.

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This paper describes our method in examining the source of subarachnoid hemorrhage and the results obtained in 630 subarachnoid hemorrhage patients who visited our clinic during the last 6 years.
Angiography was performed initially on the side corresponding with neurological findings. All cases underwent four-vessel angiography except for those in whom the source of hemorrhage was clearly noted as intracerebral hematoma or arteriovenous malformation. With the initial angiography, the source of hemorrhage was not clear in 119 cases (18.9%). Among them 72 patients showed a remarkable degree of hemorrhage and angiospasm in the main vessel. One to two weeks later, they were again subjected to four-vessel angiography, which revealed aneurysms in 5 cases and A-V malformations in 2 cases.
In 51 cases who showed ventricular dilatation in angiography and remarkable neurological findings, PEG, PVG, or CVG was performed. With these methods the source of hemorrhage became clear in 20 patients. During the last 10 months, CT scan has also been used and this has enabled us to find intracerebral hematomas in 5 cases and brain tumor in 1 case.
In cases of profuse subarachnoid hemorrhage with angiograms in main vessels at the base of the brain, ruptured aneurysm can be considered as the source of hemorrhage. However, in 5 cases in whom the source of hemorrhage was not found by angiography, craniotomy was performed. The arterial main trunk was examined and anterior communicating aneurysms were discovered in 3 patients and a middle cerebral aneurysm in 1 patient. No aneurysm was found in 1 case.
Autopsies were performed on 11 patients out of 13 who died of unknown source of hemorrhage. Intracerebral hematomas were found in 8 and aneurysms in 3 cases. In 69 patients (11%), the source of hemorrhage could not be found by these methods.
Among the 69 cases with unclear source of hemorrhage, two peaks of incidences were found; one in youth and the other in old age. Clinical symptoms were essentially the same as in these cases with clear sources of hemorrhage and the clinical courses and prognosis were clearly better in youth cases. There were no recurrences in follow-up studies and about 80% of the patients returned to completely normal life.

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Experimentally induced cerebral aneurysms in rats treated with unilateral ligation of the common carotid artery, deoxycorticosterone and salt hypertension, and β-aminopropionitrile (BAPN) have many similarities to spontaneous lesions in man in respect to the location, relation to the arterial fork and histological findings.
For the convenience of further studies, experimental conditions were reanalized. Male, adult SD rats were divided into four groups by different combinations of these three treatments. Cerebral aneurysms developed in rats treated with unilateral ligation of the common carotid artery and experimental hypertension with or without BAPN. Aneurysms developed more frequently in rats with BAPN than in those without BAPN. Aneurysms in these two groups were located on the anterior cerebral-anterior communicating arterial complex and on the proximal segment of the posterior cerebral artery on the side of carotid ligation. Aneurysms were found neither in rats treated with hypertension and BAPN nor in rats with carotid ligation and BAPN.
The results show that unilateral ligation of the carotid artery with hypertension is the minimal requirement for inducing cerebral aneurysms. BAPN increases the incidence of aneurysms. Furthermore, carotid ligation provides the site of aneurysms. It may be postulated that hypertension predisposes aneuirysmal formation chiefly with vascular changes caused by hypertension, such as increased permeability, but not with increased intraluminal pressure.

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(1) Fluorescein angiography (FAG), carbon perfusion (CP) and histological findings: At the end of the initial 3 hrs after restoration of blood pressure to normal, patchy non-filling area by carbon black was observed within the cortex which surface showed a complete or incomplete ischemia by FAG. By 6 hrs, a statistically significant increase in the ischemic area of the cerebral cortex was demonstrated in the territory of the clipped artery. Edema could then be demonstrated in the affected cerebral tissue. After 12 hrs, diapedesis and extravasation of carbon particles which had resulted from permeability changes in dilated long perforating vessels (i.e. subcortical veins) were observed. Neuronal shrinkage, characterized by angularity, cytoplasmic eosinophilia and nuclear pyknosis was also seen in the area of ischemia. Within 24 hrs, the involved cerebral tissue showed marked hemorrhagic infarction in which massive amounts of extravasated carbon particles were localized in the boundary zone between the deep cortical layer and the subcortical white matter. Prominent so-called incrustations were present.
(2) Water and electrolyte content: 30 minutes after the blood pressure was restored to normal level, a statistically significant decrease in the dry weight of the cerebral cortex was demonstrated in the territory of the clipped artery, and there was a further decrease with time. The accompanying changes in sodium and potassium were also extensive. Within 24 hrs the sodium and potassium were also extensive. Within 24 hrs the sodium content of the cortical tissue approached that of the plasma. The fall in potassium in cerebral cortex represented from the normal level of 108 mEq/kg of fresh weight to 45 mEq and 25 mEq after 5 and 24 hrs of restoration of blood pressure, respectively. These findings were clearly correlated with gross and histological evidence of massive necrosis and were interpreted as indicating cell death rather than tissue swelling.
In contrast, in the underlying white matter, there was no immediate effect on sodium and potassium, although there was a slight decrease in dry weight. With time, moderate delayed changes occurred compatible with the development of vasogenic edema: an increase in water and sodium content and a mostly dilutional decrease in potassium content.

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