A new experimental model of cerebral sinus occlusion was devised, using 16 mongrel dogs to study the regional cerebral blood flow (r-CBF) change in intracranial venous hypertension. A mixture of α-cyanoacrylate monomer and pantopaque was injected through a catheter introduced into the superior sagittal sinus (SSS). According to the extent of the sinus occlusion, the animals were divided into three groups: group A, SSS occlusion only; group B, SSS occlusion+ transverse sinus (TS) occlusion; group C, SSS occlusion+TS occlusion+cortical vein occlusion. To make a model of the dural arteriovenous malformation, normal saline was infused under constant pressure through a catheter introduced into the SSS and the sinus pressure was elevated from 10 mmHg to 60 mmHg in group D. Changes in intracranial pressure (ICP), SSS pressure (SSSP), and r-CBF and histological changes were evaluated in these groups. Before sinus occlusion, ICP and SSSP were 9±3.2 mmHg and 4±2.5 mmHg, respectively. After sinus occlusion, ICP and SSSP were 20±5.5 mmHg and 27±4.5 mmHg in group A, 30±5.4 mmHg and 38± 5.1 mmHg in group B, and 65±7.9 mmHg and 74±6.1 mmHg in group C. No ICP change was noted in group D. r-CBF showed no change in group A or D, and minimal reduction for a short period in group B. In group C, r-CBF decreased to 20-30% of the value prior to sinus occlusion due to marked venous congestion, which was complicated by subarachnoid hemorrhage and intracerebral hematoma.
From the above results, it may be concluded that cortical veins play an important role as a collateral channel in sinus occlusion.

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A fundamental study was made on the possibility of applying hyperthermia using interstitial induction heating for deep seated brain tumors. This method uses a piece of thermosensitive magnetic metal or thermoseed, implanted in the tumor by direct surgery or stereotactic maneuver. Induction heating is performed by an extracranially placed magnetic coil which produces a high frequency magnetic field by means of a generator. The thermoseed must generate enough heat by loss of eddy current or hysteresis. It is also desirable to have the proper degree of Curie temperature to automatically regulate the temperature of the seed itself. Three kinds of implanting material [ferrite, stainless steel, and nickel-palladium (Ni-Pd) alloy] were developed and tested for the relationship between heat production and Curie temperature. Ni-Pd alloy was thought to be the best so far for this purpose, producing enough heat and a low Curie temperature, between 40 and 60 centigrade degrees. In vivo experiments were performed on a malignant brain tumor (T₉) which was inoculated intracutaneously in the backs of CDF rats. When the tumors measured as large as 10 × 10 mm, the animals were subjected to local hyperthermia by induction heating. Three stainless steel needles (0.8 × 15 mm) were implanted in the tumor and a magnetic field was produced by a generator with a maximum power of 100 W and a field frequency of 250 kHz. The heating was continued for 60 minutes by controlling the magnetic field so that the temperature of the periphery of the tumor was maintained at 42°C. During the heating, the temperatures of the center of the tumor, a point 1 cm away from the tumor, and the skin over the tumor were measured, and were found to be steady at 45°C, 39°C and 38°C, respectively. Four tumors were treated by this method. Three tumors completely disappeared by the end of four weeks and another was markedly reduced in size compared to the control. In conclusion, magnetic induction heating using a ferromagnetic implant with low Curie temperature will be a useful method of interstitial hyperthermia for deep seated or unresectable brain tumors.

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Na⁺-K⁺-stimulated adenosine triphosphatase (Na⁺-K⁺ATPase) activities were measured in 12 human brain tumors and surrounding tissue (white matter and cortex) by the colorimetric determination of hydrolyzed inorganic phosphorus (Pi) from adenosine triphosphate (ATP). In glioma cases, the brain microvessels, filial component, and neurons were isolated from the cortex by the methods of Brendel, et al., and Nagata, et al. In each sample, Na⁺-K⁺ATPase activity was measured in the presence of various K⁺ ion concentrations.
In 8 glioma cases, the lowest value was obtained in the glioblastoma multiforme. Decrease in Na⁺-K⁺ATPase activity in the tumor or in the surrounding tissue was roughly proportional to the pathological malignancy of the tumor. In 2 cases of glioma with an epileptic focus shown by electroencephalography, activity of the enzyme was decreased in the epileptic cortex. In one case of glioma without epileptic focus, decrease of the enzyme activity was mainly attributed to decrease in the glial component. The kinetic parameters, maximum velocity (Vmax) and activation constant for K⁺ (Ka) were also calculated in each sample to determine the effect of the K⁺ ion on the Na⁺-K⁺ATPase activity. Vmax in the tumor region was significantly decreased compared with the surrounding tissue. On the other hand, differences in Ka were not so significant. Disturbed buffering action for the extracellular K⁺ ions observed in the glioma group might result in lowered ability to maintain the electrolytic milieu, and might play a significant role in the development of the epileptic focus.

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Cellular estrogen receptors in cryostat sections of human glioma tissue were determined in 34 patients by a histochemical method with 17β-estradiol-6-carboxymethyl oxime-bovine serum albumin-fluorescein isothiocyanate conjugate. Estrogen receptor protein was found in all cases of glioblastoma multiforme (7), anaplastic astrocytoma (5), benign astrocytoma (7), pilocytic astrocytoma (2), ependymoma (5), and a case of mixed oligodendroglioma, but in no cases of medulloblastoma (5) or pure oligodendroglioma (2). These findings suggest the possibility of hormone therapy for human glioma.

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The effect of multidisciplinary therapy is discussed, focusing on the results of the combined use and single use of intracarotid injection of 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU), fractionated irradiation by ⁶⁰Co, and subcutaneous injection of OK-432 on brain tumor-bearing rats as well as on 31 human glioma cases.
The experiments using brain tumor-bearing rats demonstrated the dose dependency of ACNU, and ACNU combined with ⁶⁰Co irradiation resulted in an additive promoting effect, compared with the results of single use of each therapy. As for the mechanism of this effect, in addition to cell synchronization, the cell-killing effect of ACNU enforced by the circulatory disturbance due to irradiation was shown by the histological study. Multidisciplinary therapy for clinical cases, on the other hand, demonstrated good results among 60% of glioblastoma patients and 73% of benign astrocytoma patients, resulting in an improved survival rate. In in vivo study, OK-432 showed no cytocidal effect; however, OK-432 was an important agent for clinical use as it was effective in maintaining the general condition, or in reducing side effects induced by the combined use of ACNU and ⁶⁰Co irradiation.

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Combination therapy with radiation and (1-4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)3-nitrosourea hydrochloride (ACNU) and/or N₁-(2'-tetrahydrofuryl)-5-fluorouracil (5-FU) was given to 102 patients with malignant gliomas. The purpose of this study was to evaluate the efficacy of two treatment protocols after operative resection as compared with the control treatment, radiotherapy+5-FU. The three protocols were (A): adequate operation (OP)+radiation (R) (40-60 Grey/6-7 weeks)+ACNU [1-3 mg/kg, intravenously (IV) or intraarterially (IA), two times with a week interval, and repeated after 6 months]±OK-432 (2.0 “Klinische Einheit” or clinical unit/week, intramuscularly), (B): OP+R+ACNU (1-3 mg/kg, IV or IA, two times with 6-8 weeks interval, and repeated after 6 months)+5-FU (8-16 mg/kg/day orally)±OK-432, (C): OP+R+5-FU.
The combination therapy with ACNU and radiation significantly improved survival time as compared with protocol (C) (p<0.01). Malignant gliomas treated with protocol (A) had 40.5 months mean survival time (MST) and (B) had 25.7 months MST. On the other hand (C) group had a MST of 11.3 months (A:B, not significant, A:C p=0.00, B:C p=0.0002). Several important prognostic factors were identified. Histological type, initial performance status and operative resections were significant factors but ACNU total dosage, administration route and OK-432 had no influence on the survival after surgery. Nausea and vomiting were noticed immediately after ACNU administration, and later myelosuppression occurred in 25-29% of the patients. No relationship was observed between toxicity, and the single dosage of ACNU or administration routes.

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Subdural pressure (SDP) was measured in 25 patients with head injury and intracerebral hematoma, by a subtemporaly placed Gaeltec catheter-tip pressure transducer. The SDP was well correlated with the ventricular fluid pressure. Correct and prompt responses to SDP and pulse wave were observed during head elevation, hyperventilation, and intravascular administration of the osmo-diuretic agents.
This transducer seemed to be beneficial in measuring SDP of various portions, and calibrating zero-point repeatedly during measurement. As intracranial pressure (ICP) is said to be variable in the different intracranial portions, the importance of measuring subtemporal ICP of the ipsilateral hemisphere to the lesion is discussed.

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It is important for adequate treatment after subarachnoid hemorrhage (SAH) to estimate objectively the disturbed cerebrospinal fluid (CSF) circulation and the intracranial spatial compensatory capacity. This paper reports the results of a preliminary trial to apply infusion studies as a method of quantifying the amount of CSF circulatory disturbance and the elasticity of the brain. The infusion studies (bolus injection, bolus withdrawal and steady-state infusion) were performed in 14 adult SAH patients for a total of 19 times. In 12 patients, studies were carried out under two spinal taps (one for CSF manipulation and the other for a pressure transducer). Two other patients received the tests through ventricular drainage. Pressure changes were recorded by a polygraph and a data recorder, and were later analysed by the methods of Marmarou, et al. and Katzman, et al. to calculate three parameters, namely, pressure-volume index (PVI), CSF outflow resistance (Ro) and CSF formation rate. These parameters were compared with computed tomography (CT) findings, radioisotope cisternographic findings (6 cases) and the effectiveness of therapeutic procedures (external decompression in 4 cases and CSF shunt in 9 cases). PVI values showed statistically significant differences between the decompressed group (44.62±30.33 ml) and nondecompressed group (22.23±9.02 ml) (p<0.001, F test). Ro values recorded their peak from 10 to 20 days after SAH, and tended to be higher among the patients who showed a reflux-stasis pattern in cisternography and in whom the shunt procedure was effective. Patients who developed periventricular lucency in the CT scan tended to show higher Ro values. However, there was one case which did not develop hydrocephalic symptoms despite a high Ro value. In some cases Ro remained low despite the fact that other examinations suggested advanced disturbance of CSF absorption. These discrepancies were thought mainly to have occurred because Marmarou's theory did not consider interactions between another two intracranial components (the vascular bed and the brain parenchyme) on volume loading or withdrawal into CSF space. If this problem were solved, the bolus infusion test could be a much more useful and practical method than steady-state infusion.

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A case of multiple cerebral aneurysms associated with so-called moyamoya disease is reported. The patient was a 52-year-old male attacked by subarachnoid hemorrhage. The patient was confused and signs of meningeal irritation were noted. Computed tomography (CT) scan showed the ventricular hemorrhage. Right carotid angiogram showed moyamoya vessels in the basal ganglia. The other angiograms showed three aneurysms, which were located at the origin of the posterior communicating artery (ICA-PCA) on the left, at the posterior cerebral-posterior communicating artery origin (PCA-PcomA) on the right, and the distal site of the posterior choroidal artery (PchA) on the left. Two aneurysms located at the origin of PCA and ICA were clipped by the transsylvian approach, the former being reached through the moyamoya vessels. Spontaneous regression of an aneurysm at the peripheral portion of PchA were angiographically documented 10 days after the second operation. There were no changes around the basal ganglia on post-operative CT. Histological examination of a part of the flat and small middle cerebral artery (M₁) gained during operation revealed proliferation of intima, elongated elastica interna and loss of media.
Forty-four reported cases of so-called moyamoya disease with aneurysm were discussed. As for operative indication of the aneurysm associated with moyamoya vessels, the authors consider that the aneurysm classified after Okamoto, et al. as Type III or major artery aneurysm, was almost saccular and the operative approach does not always injure moyamoya vessels.

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Diffuse lymphocytic infiltration of the pituitary gland occurring in temporal relation to gestation was found in a 30-year-old female who had a suprasellar mass that caused bitemporal hemianopsia. The histology and pathogenesis of this lesion is discussed. Endocrinological examination showed a lower value of prolactin and growth hormone in her serum, but the other pituitary hormones were normal. From the results of these clinicopathological examinations it is unable to propose any opinion as to whether this is an autoimmune disease or not at the present time. However, it seemed that the hypopituitarism was present following destruction of the hormone secreting cells by lymphocytic infiltration. This observation suggests that hormone replacement therapy is required at an early stage.

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Intracranial aneurysms found in three out of eight siblings in one family are presented, with a review of ninety-six sibling cases in the literature.
The eight siblings comprised four brothers and four sisters. Patients suffering from subarachnoid hemorrhage were the third sister, aged 57 years, and the eldest brother, aged 65 years. They were successfully treated by clipping of the ruptured aneurysms. The eldest sister, aged 72 years, was shown to have an unruptured aneurysm by angiography.
Ninety-nine reported cases of sibling aneurysms including the present three cases were analyzed from the view points of familial relationship, age at onset, sex incidence, and location of aneurysm. Compared with intracranial aneurysms in the general population, aneurysms in sibling cases had a lower incidence of anterior cerebral or anterior communicating artery aneurysms, and a higher incidence of middle cerebral artery aneurysms. In cases where more than two siblings suffered from subarachnoid hemorrhage, other members were reported to have an increased risk of intracranial aneurysm. An angiographical investigation should be considered in such cases.

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A 52-year-old male sustained subarachnoid hemorrhage and ventricular hemorrhage due to a ruptured anterior communicating artery aneurysm. Ventriculo-peritoneal shunting was performed 3 weeks later. The aneurysm was clipped 1 month after the onset. During the operation, the aneurysm ruptured prematurely causing marked swelling of the brain. Enlargement of the fourth ventricle was detected by computerized tomography (CT) scan the next day. Four days postoperatively the fourth ventricle was opacified by metrizamide injected into the lateral ventricle, showing patency of the aqueduct of Sylvius. However, the fourth ventricle increased in size on serial CT scans. Since the patient was in ataxic respiration and tetraplegia, an external fourth ventricular drainage was placed 5 days postoperatively, and the fourth ventricle became smaller. The patient died of pneumonia 1 month postoperatively.
It is suggested that the mechanism of the trapped fourth ventricle in the present case is the oneway block of the aqueduct, resulting from the ependymal change due to the ventricular hematoma and brain edema compressing the midbrain after the operation for the aneurysm.

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