Normal adult Sprague-Dawley rats were used to demonstrate enzymatic activity on capillaries of the cortex. Fixation was performed by intracardiac perfusion of 2% glutaraldehyde in a 0.1 M cacodylate buffer of pH 7.2 with 8% sucrose. After perfusion for 2 min from 1.5 m in height, the brain was removed. Coronal slices (1.0 mm thickness) of the frontal cerebral cortex were fixed for an additional period of 10 to 30 min by immersion in the same fixative and then washed overnight in the same buffer solution. Frozen sections of 40 μm in thickness were obtained from the washed tissues. The sections were immersed at 37°C for 30 min in the incubation media for acid phosphatase, alkaline phosphatase (ALPase), glucose-6-phosphatase, thiamine pyrophosphatase (TPPase), Mg⁺⁺-ATPase, Na⁺, K⁺-ATPase substituted for measuring K⁺-dependent p-nitrophenylphosphatase, 5'-nucleotidase (5'-Nase), and nucleoside diphosphatase (NDPase). Among them, ALPase, Mg⁺⁺-ATPase, TPPase, and NDPase demonstrated positive staining on the capillary walls when viewed with light microscope. The ultrastructural localization of these four enzymes on the capillary walls was investigated.
The cytochemical findings gave the following results. All four enzymatic activities were found on the abluminal surfaces of the endothelial cells and on the surfaces of the pericytes. Electron dense precipitations on the luminal surfaces of endothelial cells were infrequently seen and were considered an artefact. Intense reaction products of ALPase and Mg⁺⁺-ATPase were evenly distributed on the surfaces of the astrocytic processes in contact with the thick basal lamina. Heavy, dotted reaction products of TPPase and NDPase were found in the basal lamina.
The ultrastructural localization of ALPase, TPPase, Mg⁺⁺-ATPase, and NDPase were also briefly discussed in connection with cerebral microcirculation and the blood-brain barrier.

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Hepatoma cells from ascitic fluid were injected into peripheral nerves of rats. Involvement of the central nervous system was observed in 6 of 41 animals. Five of these 6 rats showed subarachnoid dissemination of tumor, and in 3 of these there was involvement of both the brain and spinal cord. None showed parenchymal lesions. It is concluded that diffuse leptomeningeal carcinomatosis may result from involvement of peripheral nerves by tumor.

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In order to clarify the mechanisms of action of CB-154 and TRH, ultrastructural studies using cationized ferritin as a ligand for anionic sites of membrane constituents of human adenoma cells were performed. Adenoma cells were cultured for a certain period with intermittent incubation with either CB-154 or TRH. The effects of these agents were ascertained by hormonal analysis of the culture media. We examined 7 GH-producing adenomas, 4 PRL-producing ones, and 2 non-functioning ones. In functioning adenoma cells, hormone secretion was confirmed to be increased by TRH activation and decreased by CB-154 incubation. Hormonal examination of cultured media revealed autonomous secretion of PRL but not of GH in dispersed cell cultures of human pituitary adenomas.
When activated by TRH, both GH and PRL adenoma cells contained abundant cationized ferritin (CF) particles in the cytoplasm in the form of densely packed small vacuoles, endoplasmic reticulum (ER), and Golgi cisternae. In CB-154 treated cells, internalization of CF was rarely observed, as if inhibited by the action of CB. Internalization of CF particles in the control study seemed to lie in degree between the TRH activated cells and the CB-154 treated ones. It was made clear in this study that TRH activated the recovery or recycling of surface membrane in functioning adenoma cells, while CB 154 seemed to suppress the internalization of anionic sites of the surface membrane.

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In the modern treatment of subarachnoid hemorrhage due to a ruptured cerebral aneurysm, the prevention of rebleeding and the management of cerebral ischemia induced by delayed cerebral vasospasm are the greatest problems. Since these morbid processes have not yet been sufficiently elucidated, opinions vary on the timing of surgery for these aneurysms. Although early surgery is generally favored in Japan, we, in this hospital and its affiliated clinics, have made it a principle to use a regimen based on intentionally delayed surgery.
This study was conducted to compare the results of early surgery with those of delayed surgery. The sources of data were the report on 4, 238 cases of cerebral aneurysm (1974-1975) in major neurosurgical clinics across Japan (118 hospitals)—a report made by the Research Group on Cerebrospinal Vascular Abnormalities and designated for intensive studies by the Health and Welfare Ministry—and the records on 906 cases (1972-1979) experienced in Juntendo University Hospital and its branches (10 hospitals). We chose for analysis 1, 288 cases from the former group (hereafter the JNSC group) and 520 from the latter one (the Juntendo group), which were all “acute” cases, hospitalized within 1 week after the bleeding attack. There was no statistically significant difference between the two groups with respect to such variable factors as the patients' backgrounds and quality of surgical treatment.
Non-surgical cases amounted to 29.0% of the JNSC group and 32.1% of the Juntendo group, the opportunity for surgery being missed more frequently in the latter. Surgery was performed within 2 weeks of the bleeding attack in 66.0% of the JNSC group and in 24.8% of the Juntendo group, which clearly shows the difference in therapeutic principle between the two groups. The operative mortality was 26.8% in the JNSC group, as compared with 15.0% in the Juntendo group: significantly higher (p ¹0.01) in the former. This difference applied equally irrespective of severity of case.
The overall mortality in the combined surgical and non-surgical cases was 41.3% in the JNSC group, as against 39.7% in the Juntendo group, in which respect there was little difference between the groups. Investigation of the surviving patients' daily activities disclosed, however, that the rate of post-operative restoration to society was 66.3% in the JNSC group and 77.9% in the Juntendo group: significantly higher (p ¹0.01) in the latter.

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Pituitary neuroadenolysis was performed 136 times on 102 terminally ill patients with intractable cancer pain. Through the aid of televised fluoroscopy, one or two needles were inserted manually through a nostril into the sella turcica, and 1.0-2.4 ml of pure ethanol was instilled. Excellent relief of cancer pain was ultimately obtained almost instantaneously in 82 (80%) out of 102 cases; 95% in 43 cases with hormone-dependent tumors and 69% in 59 cases with non-hormone-dependent tumors. In some cases, pain relief continued over a period of more than 2 years.
Tumor regression was also observed in three cases (6.9%) with carcinoma of the breast and prostate gland. Visual field defects were complained of in 10 cases, and temporary ophthalmoplegia was observed in four. Diabetes insipidus was documented in half of the cases. Euphoria and increased appetite were observed in most cases, which suggested hypothalamic involvement. There was no death ascribed to NALP. Transsphenoidal surgical hypophysectomy was also performed on 18 other cases with carcinoma of the breast and prostate gland. Cancer pain relief was obtained in 88% of 16 cases with intractable pain, and objective tumor regression was achieved in 55% out of 18 cases. Subsequent to surgery, diabetes insipidus (16 cases), mental changes (4 cases), cerebrospinal fluid rhinorrhea (4 cases), and meningitis (2 cases) were documented in the early postoperative stage. The operative mortality rate was 5.6%. The results indicate that NALP is favorably indicated for the relief of intractable cancer pain in the terminally ill, even in high-risk patients who suffer from hormone-dependent, as well as non-dependent, malignant tumors. Surgical hypophysectomy should be performed in low-risk patients when the treatment is aimed at the regression of hormone-dependent tumors.

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During performance of pituitary neuroadenolysis for relief of cancer pain, metrizamide solution was injected through the same needle used for ethanol instillation into the sella turcica in 8 cases. In half of the cases, the contrast material flowed out along the pituitary stalk immediately after it reached the sellar cavity, and delineated the third ventricle, the aqueduct, and the fourth ventricle, suggesting spread of ethanol along the same route. Autopsies performed in 18 cases which had been subjected to neuroadenolysis revealed widespread necrosis in all pituitaries, but no gross or histological alterations were observed in any of the hypothalamus, thalamus, brain stem, or pituitary stalk, except for a localized necrotic focus in the stalk and/or infundibulum in one-third of the cases. These findings indicate that the ethanol instilled into the sella turcica induces necrosis of the pituitary gland, and also acts as a destructive as well as a stimulative agent on the nervous structure around the ventricle. It is assumed that cancer pain is relieved through these effects of ethanol on the hypothalamopituitary axis which would influence the related structure of the central nervous system.

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Two young female patients developed mild hyperprolactinemia with galactorrhea several years after surgery for polycystic ovaries and were found to have an extremely rare type of pituitary tumor composed of mixed tissue elements of Rathke's cleft cysts and prolactin-secreting adenoma previously termed cystic prolactinoma. Clinical and pathologic features of this unique combination of lesions in two closely related endocrine organs were described with special emphasis on the pathogenesis of prolactinomas. It is possible that continuous estrogenic stimulation via pertinent receptors in the pituitary prolactin-secreting cells may be related to the development of prolactinoma in these patients.

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A 16-year-old girl with prolactin secreting pituitary adenoma was treated with 2.5 to 30 mg/day of bromocriptine for about eight months, followed by transsphenoidal surgery. The preadministration baseline value of prolactin (PRL) was 13, 886 ng/ml, which markedly decreased to 6.6 ng/ml after bromocriptine treatment. Computed tomography (CT) performed before bromocriptine administration showed the presence of a large, irregularly shaped suprasellar extension of the tumor. About eight months after bromocriptine treatment, reduction of tumor size was revealed by CT scans, but a small enhanced mass was still present in the sella turtica and suprasellar areas. Postoperatively, administration of bromocriptine was suspended for about two weeks and the blood PRL value increased rapidly to 2, 960 ng/ml. Histology of the tumor tissue consisted mainly of two components, i.e., island-like, shrunken tumor cell nests and acellular spaces which surrounded these tumor cell nests. The acellular spaces were considered to be the spaces left after the majority of the prolactinoma cells had died and disappeared. Thus, the marked tumor size reduction and marked decrease of blood PRL level in this case can be explained by the “cytocidal” and “cytostatic” effects of bromocriptine on prolactinoma cells.

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A peculiar case of abnormally tangled cerebral artery with complete defect of the terminal portion of the internal carotid artery is reported. The patient suffered from an intraventricular hemorrhage. Preoperative angiography suggested an aneurysm at the junction of the right internal carotid and posterior communicating arteries and also an occlusion of the terminal portion of the right internal carotid artery which was thought to have developed asymptomatically prior to the hemorrhage. The right cerebral hemisphere was supplied mainly by an artery arising from the anterior cerebral artery and partly by several cortical arteries of the anterior and posterior cerebral arteries. Abnormal fine arteries originating from the internal carotid artery also supplied the basal part of the hemisphere. Operative findings, however, revealed that the aneurysm-like mass was not a true aneurysm, but rather was abnormally elongated tangled arteries composed of the posterior communicating and posterior cerebral arteries. Furthermore, no vessels were found where the terminal portion of the internal carotid artery and the horizontal portion of the anterior and middle cerebral arteries were considered to exist. This case offers the first example in which the complete defect was localized at the terminal portion of the internal carotid artery. The radiological findings and the pathogenesis of these peculiar lesions are discussed.

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A 62-year-old man with an asymptomatic ossified plaque in the cranial arachnoid was reported. The lesion was removed; histology confirmed it to be well-formed osteoid tissue with lamellated bone formation. Intracranial calcified and ossified lesions were discussed.

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A 74-year-old female developed a subdural hematoma in association with a large hemorrhagic infarct. The hemorrhagic infarct was treated conservatively by steroid and a dehydrating agent. The subdural hematoma enlarged over a 10-day period and it was evacuated through a burr hole. The patient survived with residual neurological deficits. Although subdural hematomas associated with cerebrovascular lesions are not uncommon, ones with intracerebral hemorrhage or hemorrhagic infarct are rare.

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