About 150 cases of supratentorial glioma were treated during the past 17 years. Based on functional status, 15 were judged to be cases of silent glioma (synonymous with Norman's inactive glioma). They were silent for from 5 to 17 years, for an average of 8.5 years.
Histologically, they included: Astrocytoma Grade I, 6 cases; Astrocytoma Grade II, 7 cases; Astrocytoma Grade III, 1 case, and Ependymoma, 1 case. Most of these silent gliomas were fibrillary or gemistocytic astrocytoma. Cystic formation was seen in 10 of the 15 tumors, and calcification in 7 of the 15 (46%). In other words, there were only 2 of 15 cases of silent glioma without either cystic formation or calcification.

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Glioma often recurs after apparently successful treatment and clinical remission. The effect of the host's immunologic status in such cases is unknown. In this study, the authors attempted to answer the following questions: 1) Is there a relationship between immunity and the recurrence of glioma? 2) Is immunologic monitoring useful in predicting the recurrence of glioma? 3) Which immunologic monitoring system is the most reliable? The subjects were 17 patients with gliomas who were treated between 1980 and 1985 and had tumor recurrence after an interval of clinical remission. They were evaluated during and after remission by means of clinical signs, computed tomography, and immunologic testing, which included measurement of purified protein derivative (PPD), phytohemagglutinin (PHA), the blastogenic response of T-lymphocytes to PHA, the OKT4 and OKT8 lymphocyte subsets, and serum complement CH50.
The patients were divided into two groups. Group 1 comprised five patients whose tumors showed malignant transformation from grade 2 to grade 3. Group 2 included patients whose tumors were of the same histologic grade initially and on recurrence. In Group 2, six tumors were grade 3 and six were grade 4.
Lowered immunity at the time of recurrence was demonstrated by the following: 1) a negative change in PPD and/or the PHA skin reaction in 80% of Group 1 and 75% of Group 2 patients; 2) elevation of CH50 in 40% of Group 1 and 58% of Group 2 patients; 3) a change in the blastogenic response of T-lymphocytes to PHA in 40% of Group 1 and 25% of Group 2 patients; and 4) an decrease in OKT4/OKT8 cell ratio in 60% of Group 1 and 38% of Group 2 patients. These patients were immunologically competent during remission. The immunologic changes at the time of tumor recurrence were accompanied by clinical deterioration. However, tumor recurrence could not be predicted from the immunologic parameters studied. Thus, it appears that extension or recurrence of the gliomas was responsible for lowered immunity in these patients, rather than the opposite.

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クモ膜下出血(SAH)後に発生する脳血管攣縮(spasm)の治療にballoon angioplastyを応用するため,血管の拡張機序・血管内壁への影響について組織学的検索を行った。SAH後,spasmで死亡した11例のヒト脳主幹動脈(約5cm)を11本採取し,このうち5本はin vitroで種々の条件下にballoon angioplastyを行い,術後,光学顕微鏡検査と走査電子顕微鏡検査で検討した。更に,残り6本は麻酔したイヌの頸動脈または大腿動脈に端々吻合し,この移植したspasm血管に対し吻合部の遠位端より透視下でcatheterを挿入し,in vitroの実験と同じ加圧条件下でangioplasty を施行し,検索した。結果はsilicon balloon catheterを用いて1気圧,10秒間,10回の加圧でspasmが十分解除出来,しかも血管内壁に損傷を加えることなく拡張できることが判明した。以上より,spasm血管に対するballoon angioplastyは,1気圧で,1分間の反復拡張術が安全で,効果的である。

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Fifty-five cases of brain tumors over the age of sixty were analysed. Classification as to the type of tumor gave 19 metastatic tumors, 11 gliomas, 11 meningiomas, 6 pituitary adenomas, 4 acoustic neurinomas and 4 miscellaneous tumors. Among gliomas 6 cases were glioblastoma multiforme. In cases of metastatic tumors, the lung came first as the primary site.
Difficulties in diagnosis of brain tumors in the aged which had been heretofore emphasized by many authors, could be solved by introduction of computed tomography. Among 47 surgical cases of the author's series, only 2 cases of metastatic brain tumors died within 1 month after operation. Postoperative mortality rate of brain tumors in the aged was 4.3 per cent. However, postoperative survival period of gliomas in this age groups was much shorter than that of total gliomas in whole adult groups. The cause of such poor prognosis was discussed.

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Both the Moyamoya Phenomenon and complete or incomplete occlusion of the internal carotid fork are essential neuroradiological findings of the true Moyamoya Disease of unknown etiology. However, the Moyamoya Phenomenon often is observed in occlusive diseases of the internal carotid fork whose etiologies are known, i. e., arteriosclerosis, tuberculous meningitis, sickle cell anemia, etc. Recently the authors observed the rather acute development of unilateral Moyamoya Phenomenon following severe vasospasm of the bilateral anterior cerebral and left middle cerebral arteries due to the rupture of an anterior communicating aneurysm. An autopsy of this case revealed the marked development of anastomotic small arteries and arteriolae in the basal part of the brain, and only on the left side. Such exteraordinarily dilated arteries mainly are branches of the posterior communicating, anterior choroidal and perforating arteries, and well correspond to the Moyamoya Phenomenon observed angiographically. There were no occlusive changes in the main intracranial arteries except for moderate stenosis of the A2 portion of the bilateral anterior cerebral arteries. Histologically, arteriosclerotic change generally was, very slight, and a slight thickening of the intima and edematous change of the media were observed only at the stenotic site. There was no histological change in the markedly dilated Moyamoya vessels. The following 4 factors have been suspected of contributing to development of the Moyamoya Phenomenon : 1. The chronology of arterial occlusion. 2. Location and extent of occlusion. 3. The cause of occlusion. 4. Anatomical and functional disposition of the basal circulation. As regards the chronology, chronic or slowly progressive arterial stenosis has been thought a mandatory factor in development of a Moyamoya network which plays an important role in the form of collateral channels. However, based on the findings outlined above, the congenital factor may be the most important of the 4 factors listed.

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症例の概要：患者は77歳，男性．過去に数度，義歯の再製作を繰り返したが咀嚼および発音時における義歯の安定が改善されず，義歯の不安定を主訴に来院した．初診時口腔内は，上下無歯顎であり，上顎と比較して下顎が前方位に位置していた．
考察：顕著な下顎前突症の無歯顎患者に対する補綴処置に際して，頭部 X線規格写真から上顎模型の咬合器装着基準を求めたが，それを基に構築された咬合関係により，最終補綴物の維持・安定性が改善され，良好な経過を得られたと考えられる．
結論：下顎前突を伴う上下無歯顎症例の補綴物製作に関して，頭部 X線規格写真を応用することは有用な診断基準となることが確認された．

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小児の頭部外傷後の植物状態について,4症例を中心に検討した.従来から小児の頭部外傷の予後は一般に良好で,死亡率も低く,意識障害も早期に回復するものが多いとされている.したがって外傷後の遷延昏睡例の報告も少ない.自験例のうち乳幼児にみられた3例は,いずれも外傷そのものは軽微で,続発した急性頭蓋内血腫または水腫による意識障害と考えられる.とくに1例では脳嵌入による脳幹損傷と,術中ショックによる脳低酸素症が遷延昏睡の原因と思われる.他の2例ではおそらく硬膜下水腫に伴う大脳皮質の広汎な萎縮が,重篤な痴呆状態を招いたものと思われる.年長児にみられた1例は,大脳の広汎な1次性損傷(脳挫傷)によるものと思われる.以上より頭部外傷後に意識障害が遷延する可能性は,小児でも成人でも同様と思われる.ただ乳幼児では重篤な痴呆状態と意識障害との区別が困難で,小児の植物状態の特殊性を形成している.なお重篤な脳損傷後に発生する植物状態の頻度が,果して小児と成人とで差があるかどうかは未解決であるが,小児脳損傷のすぐれた回復性・代償性は無視できない.したがって同じ植物状態でも,成人のように固定したままでなく,長期間の追跡により,緩徐ながら軽快の傾向があることも知られている.

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嚢胞形成craniopharyngiomaの直達手術前にOmmaya'sreservoirよりBLMの嚢胞内投与(合計30mg)を行ない,著明な臨床症状の改善と,組織学的変化(いわゆるhistologicalregression),ならびにBLMの腫瘍組織内とり込みを確認しえた.ただ残念ながらそれが腫瘍細胞内へのとり込みかどうかは不明である。しかしいずれにしても本法は嚢胞形成cra-niopharyngioma直達手術前またはいかなる時期においても必要により有力な補助療法であると考える.

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