Cranial meninges of humans were studied by electron microscopy after fixation in situ and histochemical demonstration of nicotinamide-adenine dinucleotide diaphorase within mitochondria.
There was an intimate fusion between the innermost portion of the dura mater (dural border cells) and the outermost portion of the arachnoid (arachnoid barrier layer). Cranial meninges did not contain a true subdural space, when specimens were well prepared with spatial relationships preserved. If cleavage had occurred during preparation, the subdural space was artificially formed by the separation of dural border cells, because the latter showed a paucity of intercellular contacts and weak collagenous reinforcements.
The arachnoid barrier layer was a squamous layer of elongated cells with numerous tonofilaments, desmosomes and tight junctions. There was a lining of junctional devices between the innermost two cell layers. There was a number of extracellular lacunae, being separated by interdigitations and containing collagen fibrils, elastins, granular material and matrix vesicles with or without psammoma bodies. The mitochondrial enzymes of this layer showed negative activity in intact specimens, but a positive one in cleaved dural border cells and arachnoid trabecular cells. An incomplete basement membrane covered the innermost aspect of this layer.
The arachnoid trabecular cells generally had electron-lucent cytoplasm with a few tonofilaments. The cells beneath the arachnoid barrier layer had oval nuclei and wide cytoplasm containing numerous mitochondria. This layer was anchored by flattened or button-shaped pedicles, otherwise these cells formed an epithelial cluster. The cells lying within the subarachnoid space had elongated nuclei and cytoplasmic projections. The arachnoid trabeculae consisted of both a network of arachnoid trabecular cells and interwoven collagen fibrils. Alternating with these cells were numerous resting macrophages.

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The combined effect of 1-(4-amino 2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (AC NU) and 5-fluorouracil (5-Fu) on cells grown exponentially as a monolayer and multicell spheroids of rat glioma clone-6 (RG cells) was analyzed by the colony forming assay in order to obtain a more effective way of the combination.
Mature spheroids (500-600 μm in diameter) with central necrosis resembled the solid tumors in vivo in histological appearance and in the distribution of cells labeled by ³H-thymidine. Both mature spheroids and cells in monolayer were exposed to ACNU for 2 hours and to 5-Fu for 24 hours. After the drug exposure, spheroids and cells in the monolayer were trypsinized and single cells were plated for the colony forming assay. The dose survival curves for 5-Fu, for ACNU and for the combination of ACNU and 5-Fu were obtained for both spheroids and cells in the monolayer. The dose survival curve for ACNU showed an exponential cell killing following a shoulder for both cells in the monolayer and spheroids. However, the terminal slope of the curve expressed as the reciprocal of Co (concentration of drug to reduce the surviving fraction to e^-1) was steeper for spheroids than for cells in the monolayer. The dose survival curve for cells in monolayer treated by 5-Fu again showed an exponential cell killing following a shoulder. On the other hand, the dose survival curve for spheroids treated by 5-Fu showed a biphasic curve. This suggested that a proportion of cells in these spheroids was resistant to treatment by 5-Fu.
The cytotoxic effect of ACNU was enhanced by the combined treatment with 5-Fu for cells both in monolayer and spheroids. The enhancement was more marked when 5-Fu was administered before ACNU. The combined treatment also reduced the fraction of cells in spheroids resistant to 5Fu, suggesting that ACNU may be more effective for quiescent cells. The enhancement by the combined treatment on spheroids was compared with that on cells in the monolayer, based on the ratio of the surviving fraction to the concentration of the drug. The results indicated that there was a concentration range, which was more effective for spheroids than for cells in the monolayer. That was 10-35 μg/ml of ACNU and 2-15 μg/ml of 5-Fu.

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Multicellular spheroids of rat glioma clone-6 cells were developed in a spinner flask. The histological appearance of these mature spheroids was similar to that of tumor cord structure of solid tumors in vivo. Namely, spheroids showed a central necrosis surrounded by a viable rim. The viable rim was composed of actively proliferating cells (P cells) in the outer cell-layers and of non-proliferating cells (Q cells) in the inner layers.
The X-ray dose-survival curve of cells in the mature spheroids was biphasic, indicating the presence of hypoxic cells, whereas the dose-survival curve of single cells from the same batch of the spheroids was monophasic.
Mature spheroids were killed more effectively with 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) treatment than cells grown as a monolayer. Response of small spheroids without necrosis to ACNU was intermediate. Comparison of ACNU treatment under various conditions indicated that single cells from mature spheroids were most sensitive to ACNU. These results suggest that cells highly sensitive to ACNU may be located close to the central necrosis.

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Germ cell tumors have been classified into germinoma, embryonal carcinoma, choriocarcinoma and teratoma by a World Health Organization proposal, although this subgrouping is still controversial. This paper reviews clinical, computed tomographic (CT) and angiographic data of 14 patients with histologically verified germ cell tumors. These 13 males and one female, ranging from 5 to 34 years in age, included 6 cases of teratoma, 5 of germinoma and 3 of embryonal carcinoma. On plain CT, perifocal edema was never seen in cases with teratoma or germinoma, but was usual in those with embryonal carcinoma. Teratoma, although often containing calcium deposits, was isodense in most parts of the mass, while germinoma was always hyperdense in the solid part. CT with intravenous iodine demonstrated some enhancing effect within the tumor mass in all cases, but it differed in intensity from one group to another. Enhancement was less intense or slight in germinoma, whereas it was marked in all of embryonal carcinoma and most of teratoma. Cerebral angiography showed abnormal tumor vessels and dense tumor stain in embryonal carcinoma, but these were not observed in teratoma and faintly in rare occasions of germinoma.

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In the past 4 years, the authors operated on 120 cases of trigeminal neuralgia. It is noteworthy that among the series there were 13 cases (11 %) of cerebellopontine (CP) angle epidermoid. This report discusses the clinical significance of this tumor and the surgical approach. The age distribution ranged from 22 to 70 years, with a mean age of 45 years, which is considerably lower than the mean age of 59 years in the series. There were no characteristic findings regarding sex, laterality or distribution of pain. The patients were classified into 3 groups from the nature of the neuralgia and associated neurological findings; 8 patients were classified into Group I with genuine tic douloureux, 3 patients into Group II with atypical trigeminal neuralgia, 2 patients into Group III with trigeminal neuralgia and other neurological signs. The duration of the symptoms was from 6 months to 10 years, with a mean of 5 years. Previous treatments were varied. According to the extent of epidermoid, the posterior fossa approach was used in 11 cases and the subtemporal transtentorial approach in 2 cases. Computerized tomography (CT) and metrizamide CT cisternography were very useful and characteristic in the diagnostic procedure, but there were 4 cases in which the high resolution CT findings were negative and the diagnosis of CP angle epidermoid was made by craniectomy aimed for microvascular decompression. The epidermoid was extending from the lower cranial nerves up to the midbrain or the hypothalamus and to the middle fossa. In all 13 cases the tumor was totally removed microsurgically and postoperative follow-up disclosed complete disappearance of trigeminal neuralgia in all cases. The permanent postoperative deficit were decreased hearing in 1 case and hearing loss in 1 case.
The relatively high frequency of epidermoid in this series (11 %) should be kept in mind when treating trigeminal neuralgia even by some other procedure, particularly in younger patients.

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The purpose of this study is to report the serial changes of the coagulation activity in patients with head injuries. The coagulation activity studied included the Urokinase (UK) resistance test modified from thromboelastography, the prothrombin time (PT) and the active partial thromboplastin time (APTT). The basic part of this study indicated that a prolongation of the UK resistance time (UKRT) reflected a decrease in the plasminogen activity due to hypercoagulability of the systemic blood and that the UKRT had no close correlation with antithrombin III. A marked prolongation of the UKRT (longer than 90 minutes under 100 I.U. UK) was found in 7 out of 16 head injury patients (7 craniotomized and 9 non-operated). The prolongation lasted for several days after the injury. On the other hand, only one of 10 controls without head injury (5 craniotomized and 5 laparotomized, all electively) showed a transient prolongation of the UKRT. In all the head injury patients, whether operated or not, the degree of the prolongation of the UKRT was grossly proportional to the clinical signs of brain damage after the injury. The prolongation of PT was observed only in the craniotomized head injury group while APTT was not specific to any groups studied.
The result suggests that monitoring the UKRT after head injury is a useful and quick method for predicting the degree of brain damage and an anticoagulant therapy after head injury, though still controversial, must be considered.

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A 25-year-old woman experienced visual field defects in the 39th week of gestation. A pituitary mass with a suprasellar extension was demonstrated by computerized tomography (CT). The visual impairment improved after delivery and a repeated CT showed that the pituitary mass had undergone a spontaneous regression in size. The postpartum pituitary function tests revealed that the pituitary is preserved for thyroid stimulating hormone, luteinizing hormone and follicle stimulating hormone but not for growth hormone, adrenocorticotropic hormone and prolactin. Although the nature of the lesion in this patient was conjecturable, lymphoid hypophysitis seemed to be a good possibility. This case suggests that some pituitary masses during pregnancy are not always pituitary adenomas and may not require surgical intervention but can be treated by hormone replacement alone with close observation.

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A 33-year-old male was admitted unconscious. Computerized tomography scan disclosed an intracerebral hematoma with ventricular penetration. Angiography demonstrated the characteristic appearance of moyamoya disease as well as aneurysms in the peripheral portion of the lenticulostriate artery. The patient died of re-rupture of the aneurysms fourteen days after the onset. At autopsy, these aneurysms proved to be true aneurysms.
Possible hemodynamic mechanisms of cerebral aneurysms associated with moyamoya disease are discussed.

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A case of ependymoma with extracranial metastasis was reported. This patient was a 28-year-old female who had had a right parietal tumor removed fifteen months prior to admission. The second operation was performed under diagnosis of recurrence of the tumor in February 1977. A few months later, she noticed a painful scalp tumor around the lower margin of the external decompression area. Repeated computerized tomographic scan revealed a recurrence of the tumor and a separate scalp tumor, for which the third operation was performed and radiation therapy was applied. Eighteen months later, she complained of cough and another scalp tumor again at the external decompression area. Chest X-ray showed multiple metastases, and bone scintigram showed abnormal uptake in Th7, 8 and L4, 5 of the spines. After February 21, 1981, she noticed gait disturbance. At that time, neurological examination revealed paraparesis and hyperalgesic and hypesthetic levels at the Th10 dermatome. The patient died of respiratory insufficiency. At autopsy the residual intracerebral tumor was white and elastic soft, attached to the right lateral ventricle, penetrating the dura and continued to the scalp tumor. Lungs were entirely replaced by metastatic tumors. Other metastases were found in the pleura, hilar, right axillar, right supraclavicular and paraaortic lymphnodes and spine (Th7, 8 and L4, 5). Histological diagnosis was ependymoma. The mode of metastases is discussed with a review of the literature.

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A case of Hand-Schuller-Christian disease with involvement of the central nervous system is reported. The patient was a 13-year-old girl, admitted with cerebellar ataxia, polydipsia and polyuria, exophthalmos and visual impairment. Computerized tomography (CT) scan with contrast enhancement revealed a high-density mass at the left cerebellopontine angle, brachium pontis, cerebellar hemisphere, ambient cistern, superior cerebellar cistern, quadrigeminal cistern and posterior third ventricle. High-density masses along the bilateral optic nerves were also revealed. Left vertebral angiography showed no tumor stain. Suboccipital craniectomy was performed after the Stein's approach, and the tumor which adhered strongly to the cerebellum was partially removed. The tumor was yellowish in color, fibrous, and elastic hard. Histological examination showed histiocytosis X. It was supposed from the clinical course that the disease began in the hypothalamic region and spread through the subarachnoid and Virchow-Robin spaces to the optic nerve sheath and posterior cranial fossa. Only twenty-five cases of Hand Schüller-Christian disease with cerebellar signs or cerebellar involvement have been reported in the literature. CT findings of Hand Schuller-Christian disease with cerebellar involvement has not been reported.

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Surgical treatment of the symptomatic carotid stenosis associated with ipsilateral intracranial aneurysm requires special strategic consideration. A 56-year-old housewife was admitted to a local hospital with a history of mild hypertension and recent episodes of recurrent transient ischemic attacks of the right cerebral hemisphere. Carotid angiography revealed bilateral stenosis of the carotid artery, 90% stenosis with ulcer on the right and 50% smooth surfaced stenosis on the left, middle cerebral trifurcation aneurysm on the right, internal carotid aneurysm in the left cavernous portion, and aplasia of the left anterior cerebral artery at its horizontal portion. She was referred for surgery. Neurological examination revealed a slightly disturbed mentality. During hospitalization she developed left hemiparesis and computerized tomography scan demonstrated right frontal watershed infarction. One month after the onset of cerebral infarction, operative treatment was attempted with special care to prevent lowering systolic blood pressure during procedure. The right middle cerebral artery aneurysm was first clipped, and right carotid endarterectomy was performed, while mannitol and barbiturate were administered without resort to internal shunt. Postoperatively the left hemiparesis improved gradually.
Twenty-seven cases of the carotid stenosis associated with intracranial aneurysm(s) were collected from the literature and the strategic problems of these cases are discussed.

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