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K Takakura

Publications and source records attributed to K Takakura.

At least 433 records · Page 24Linked to original sources
PubMed1983

[Proposal for the definition of "foramen magnum syndrome"--foramen magnum tumor and abnormalities].

The clinical appearance of foramen magnum tumor is protean and, even at the stage when serious neurological deficits are present, the lesions are often misdiagnosed as another disease, especially cervical spondylosis and multiple sclerosis, and patients may undergo improper concervative or even surgical treatments. The best guarantee against misdiagnosis, we believed, was to establish a definition of "Foramen Magnum Syndrome" to facilitate the recollection of its peculiar clinical findings. "Foramen Magnum Syndrome" is composed of: 1. Cape distribution of sensory loss; 2. Atrophy of the intrinsic muscles of the hands; 3. Neck or suboccipital pain; 4. Dysesthesia of the hands (numbness, tingling, and cold sensation); 5. Eleventh cranial nerve palsy; 6. Stereoanesthesia. (Remember the mnemonic CANDES or DESCAN) Among these, cape distribution of sensory loss, eleventh cranial nerve palsy and cold dysesthesia (not numbness or tingling sensation) are of great importance for topological diagnosis. We also pointed out the similarities between the clinical picture of syringomyelia and that of the advanced stage of foramen magnum tumor. The syringomyelic syndrome, often seen in Arnold-Chiari malformation and basilar impression, has been attributed to the concurrent syrinx of cervical cord. But the clinical analysis of foramen magnum tumors showed that this is not always true and that compressive lesions at the foramen magnum alone can cause syringomyelic syndrome.

Accessory Nerve↗
PubMed1983

[Peroxidation of arachidonic acid and brain edema].

Recent studies suggest that peroxidation of arachidonic acid (AA) accumulating during ischemic insult, may be related to the occurrence of post-ischemic brain damage. Since the influence of the increased brain content of AA remains unclear, the present study was undertaken to explore whether the intracerebral injection of AA is associated with the injury of the surrounding brain tissues such as brain edema. Rats received the intracerebral injection of 10 microliters of test solution (160 microgram of AA emulsified in 1% bovine serum albumin, BSA) or the same volume of BSA as the control. The measurement of specific gravity (SG) (74 rats) and the local CBF by H2 clearance technique (21 rats), and electron microscopical studies with tracers (Evans blue and horseradish peroxidase, HRP) (24 rats) were carried out. The effect of pretreatment with indomethacin (PI, 10 mg/kg) was evaluated in separate groups. AA transiently produced a significant decrease in SG and in 1CBF adjacent to the injection sites (p less than 0.01). The increased pinocytotic transportation, an accumulation of edema fluid containing HRP in extracellular space and endothelial injuries were observed only after AA injection. The above-mentioned falls in SG and in 1CBF, and the extravasation of HRP were inhibited by PI. The fact that PI prevented the edema formation, 1CBF change and the disturbance of blood-brain barrier induced by AA, indicates that peoxidation of AA through the arachidonate cascade is involved in the mechanism of brain edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

[Effect of human fibroblast interferon on malignant brain tumors].

Since 1980, phase 1 and 2 clinical trials of Hu-IFN-beta have been done in the field of neurosurgery. In the present study, (1) the results of in vivo experiments of Hu-IFN-beta are reported and (2) the effectiveness of Hu-IFN-beta in patients with malignant brain tumors is also evaluated. (1) The antitumor activities of beta-IFN and poly ICLC in nude mice receiving subcutaneous transplants of human brain tumors (2 strains) were compared with those of conventional anticancer drugs. After 3 weeks of treatment with ACNU, vincristine, bleomycin, mitomycin C, beta-IFN and poly ICLC, tumor reduction rates were evaluated by the method of Battelle. The effectiveness of beta-IFN and poly ICLC was slightly inferior to that of ACNU and vincristine, although tumor reduction rates (treated/control values) of 43% and 39% were respectively obtained with beta-IFN and poly ICLC against one strain of glioblastoma. (2) Clinically, 7 patients with malignant brain tumors were given beta-IFN (4 by intratumor administration and 3 by intravenous injection) in a dose of 3 X 10(6) to 9 X 10(6) IU/day for 2 to 6 months to study the efficiency and side effects of IFN treatment. One of four patients given IFN intratumorally showed a reduction in tumor size (partial response) by CT scan; the three patients injected IFN intravenously were unchanged. There were no noteworthy side effects in the cases treated intratumorally except for fever occurring in one patient. In the patients treated intravenously, however, fever, general malaise, leukopenia and thrombocytopenia were noted.

Adolescent↗
PubMed1983

[Pneumocephalus induced by bromocriptine treatment in male prolactinoma--a case report].

The authors reported a case of pneumocephalus induced by bromocriptine (Bc) treatment for a recurrent invasive prolactinoma. The patient was a 38-year old man, who had been treated for 12 years, with three times of craniotomies and two times of irradiation therapies. CT scan showed the recurrence of the tumor, which extended into bilateral middle fossa, left orbit and left cerebellopontine angle. Serum prolactin levels elevated to 35,200 ng/ml. Then Bc was administered in a dose of 5 mg/day. Serum PRL concentration fell to 2,090 ng/ml one month after the initiation of the treatment, when he complained of headache, nausea and vomiting. Since these symptoms were considered as the side effects of Bc, the dose was reduced to 2.5 mg/day. Three weeks later, plain craniograms showed marked pneumocephalus, while no tumor was found on CT scan. The administration of Bc was stopped and he was prescribed a complete rest for a month. The air was collected again when he began to walk around. Therefore, the transsphenoidal operation was performed in order to pack the sella turcica and sphenoid sinus with muscle pieces. Since the pneumocephalus could not be cured, the muscle, taken from the thigh, was spread throughout the left middle fossa by the front-temporal craniotomy. When Bc reduces the size of the invasive prolactinomas, the intra- and extra-cranial spaces may be communicated. The greatest care should be taken for pneumocephalus, CSF rhinorrhea and/or meningitis during the Bc treatment of prolactinomas.

Adenoma↗
PubMed1983

Synchronization effect of cis-dichlorodiammineplatinum on a human neuroblastoma in vitro and in nude mice.

The effects of cis-dichlorodiammineplatinum (CDDP) on the cell kinetics of human neuroblastoma both in vitro and in vivo were analyzed by computer-aided flow cytometry. In the in vitro system, CDDP at the concentration of 1.0 microgram/ml of medium blocked early S phase and synchronized proliferating cells into the S phase within 24 hr. By 72 hr, cells in G2 + M phase reached the maximum level. CDDP at concentrations either lower or higher than 1.0 microgram/ml showed no synchronization effect. In the in vivo system, human neuroblastoma grown in nude mice had a larger proportion of cells in G0 + G1 phase than did in vitro cells of the same origin, explaining the refractory nature of the tumors to therapy. CDDP, when given as a single dose of 10 mg/kg of mouse weight showed a maximum synchronization of cells in the S phase by 48 hr, and caused an accumulation of cells in G2 + M phase by 72 hr. This accumulation of cells in G2 + M phase was thought to represent the overflow of cells from the S phase into G2 + M phase, resulting from the disappearance of the blocking effect of CDDP with time. Judging from these sequential changes in vivo, a second drug with specific cytocidal effect on S phase cells should work best 48 hr after the initial CDDP therapy, and drugs specific to G2 + M phase or radiotherapy should be added at 72 hr. Such preclinical experiments may be useful in the design of combination chemotherapy regimens against human neuroblastoma.

Animals↗
PubMed1982

[Male prolactin producing pituitary microadenoma -a case report (author's transl)].

A 27-year-old man was admitted to the Urological Department of Tokyo University, with complaints of delayed puberty and growth retardation. At the age of 14 years, he found his skeletal growth retarded. Since then he had not shown any development of secondary sex characters, such as change of voice, appearance of public and axillary hair and development of external genital organs. He had not experienced the ejaculation and libido, while the excretion has been maintained. This feminized patient showed poorly developed external genitalia, while there was no evidence of galactorrhea or gynecomastia. Ophthalmologic examinations were normal. Endocrinological studies revealed moderate hyperprolactinemia (185-200 ng/ml) and marked disorder for GH secretion. Gonadotropins were low normal and their responses to LH-RH were moderately disturbed. Serum testosterone level was extremely low and its responses to HCG were insufficient. Under the diagnosis of prolactinoma, he was referred to the Neurological Department. Plain skull film and tomography of the sella showed a deformed and slightly expanded sella, the measurement of which were within normal limits. No supra-sellar extention was demonstrated by pneumoencephalography and CT scan. A diagnosis of PRL producing microadenoma was made, and a radical removal of the tumor was performed through the transsphenoidal route. In most tumor cells the presence of PRL was revealed by immunohistochemical stains. Postoperatively, PRL levels returned to normal, while other hormonal deficiencies remained unchanged. With the administration of testosterone, he gradually became masculine and reportedly gained normal libido and potency.

Adenoma↗
PubMed1982

Selective destruction of the outer leaflet of the capillary endothelial membrane after intracerebral injection of arachidonic acid in the rat.

A peculiar ultrastructural change of the cytoplasmic membrane is described. It concerns selective destruction of the outer leaflet of the luminal side of the capillary endothelium in the white matter of the rat brain, 30 min and 3 h after intracerebral injection of arachidonic acid (AA). The cristae of the mitochondria disappeared in the endothelium of many capillaries. These changes were observed mainly in the central part of brain edema, where the extracellular space was markedly widened. The possible mechanism whereby these changes developed is discussed.

Animals↗
PubMed1982

Roles of subarachnoid blood clots and norepinephrine in cerebral vasospasm.

The content of norepinephrine (NE) in the ventricular, basal cisternal and lumbar cerebrospinal fluid (CSF) was determined in 19 patients with ruptured cerebral aneurysms. The cisternal CSF in patients with vasospasm contained a significantly higher level of NE (0.246 +/- 0.0490 ng/ml) compared with those without vasospasm (0.075 +/- 0.001 ng/ml) (p less than 0.001). However, this increase is not considered to be high enough to constrict cerebral arteries, unless there is an increased NE-sensitivity in subarachnoid haemorrhage. Vascular responses to NE in vivo were then studied after reversing blood-induced prolonged vasospasm of the rabbit's basilar artery through a transclival approach as well as a newly developed basal cisternal irrigation model. However, NE in molar concentrations between 1 x 10(-10) and 10(-2) failed to produce further contraction of the artery. In conclusion, the increase in NE with vasospasm might be only a secondary phenomenon, and not a causative factor of vasospasm. Early removal of subarachnoid blood clots seemed to prevent the development of vasospasm.

Animals↗
PubMed1982

Phase I-II trials of poly(ICLC) in malignant brain tumor patients.

Poly(ICLC) preparation, containing poly-L-lysine and poly(I) . poly(C) at a weight ratio of 1:2, was given intravenously at a dose of 0.05 to 0.2 mg/kg to 7 patients with malignant brain tumor. Poly(ICLC) induced significant serum interferon (more than 100 reference units/ml) in all patients. The highest interferon titer induced was 875 reference units/ml. Severe side effect was not observed except fever. Hypotension, leukopenia and elevation of liver enzyme levels were observed as side effects in a few cases.

Adult↗
PubMed1982

Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance.

Hemorrhage from brain tumor was confirmed clinically, surgically, or on autopsy in 94 of 1861 cases (5.1%) treated during the past 18 years: 49 of 311 pituitary adenomas (15.8%) and 45 of 1550 other brain tumors (2.9%). The higher incidence of hemorrhage from pituitary adenoma was statistically significant (p less than 0.001). In brain tumors other than pituitary adenoma, the incidence of hemorrhage was significantly higher in the patients under 14 years old (17 of the 322 cases, 5.3%) than in the patients over 15 years old (28 of the 1228 cases; 2.3%) (p less than 0.001). Nineteen patients showed no evidence of clinical symptoms related to bleeding. Twenty-six patients had a definite history of an acute episode that suggested sudden bleeding. In 11 of these, the apoplectic syndrome was the initial presenting symptoms. The incidence of hemorrhage was not statistically correlated with sex. The hemorrhage was intratumoral in 30 cases, intracerebral in 7, subarachnoid in 7, and subdural in 1. The tumors were supratentorial in 36 cases, pineal in 1, and infratentorial in 8. Primary and metastatic choriocarcinoma and primary embryonal carcinoma seemed to cause hemorrhage most frequently. The following precipitating factors were found in 7 of the 17 patients aged under 14: ventricular drainage in 2, ventriculoperitoneal shunt in 2, carotid angiography in 1, head injury in 1, and leukemia in 1. Seven of the 17 patients under 14 years old died of massive bleeding from the tumor. Unless there is evidence of vascular disease such as cerebral aneurysm, vascular malformation, or hypertensive cerebrovascular disease, intracranial hemorrhage should be suspected of being due to a brain tumor.

Adenoma↗
PubMed1982

Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor, OKY-1581.

The efficacy of thromboxane synthetase inhibitor in the prevention of cerebral vasospasm after subarachnoid hemorrhage (SAH) was evaluated in a prolonged experiment using dogs. Changes in the diameter of the basilar artery were followed by angiography, and morphological changes were studied by photomicroscopy and electron microscopy. As a thromboxane synthetase inhibitor, OKY-1581 (sodium-(E)-3-(4(-3-pyridylmethyl)phenyl)-2-methylacrylate) was used. Dogs received intravenous injections of 160 mg of OKY-1581 dissolved in 2 ml of physiological saline immediately after subarachnoid blood injection. Subsequently, the animals received continuous intravenous infusion of the drug at the rate of 4 gm/50 ml/24 hours until sacrifice 4 days after induction of SAH. Control dogs received subarachnoid blood injection without treatment with OKY-1581. Angiographic examination revealed that the late spasm was almost completely abolished by the treatment with OKY-1581. Early spasm was also prevented, but the drug's effect was less prominent than it was on the late spasm. Morphological study revealed degenerative changes in the endothelium and myonecrotic changes in the tunica media following SAH in the basilar arteries of the treated as well as the untreated dogs. However, corrugation of the internal elastic lamina was almost completely absent in the treated dogs. The above results indicate that a disproportionate synthesis of thromboxane A2 plays an important role in the evolution of chronic cerebral vasospasm following SAH, and that drugs such as OKY-1581 that selectively inhibit thromboxane synthetase might be useful in the prevention of vasospasm.

Acrylates↗
PubMed1982

[The role of immune RNA in the immunotherapy of malignant brain tumor (author's transl)].

At present, nonspecific immunotherapy using BCG or Picibanil is popular as an immunotherapy for malignant brain tumor. On the other hand, specific immunotherapy using lymphocytes which play an important role in the passive transmission of tumor immunity is also performed. But this therapy has some disadvantage such as the problem of blocking factor or histocompatibility. To compensate for this disadvantage, specific immunotherapy using the chemical mediater, immune RNA, extracted from immunized lymphocytes has started. We extracted immune RNA from the spleen of immunized rat using phenol and SDS, and observed the effect of normal lymphocytes preincubated with immune RNA in vitro and in vivo experiments. In in vitro experiment, following results were obtained. (1) Normal lymphocytes incubated with immune RNA revealed a significant cytotoxicity and this effect was disappeared by the pretreatment of immune RNA with RNase. (2) Cytotoxic effect of immune RNA seemed to be a tumor specific response. (3) Not only syngeneic RNA, but also xenogeneic RNA were effective. In addition to these results, we decided the optimal condition in which immune RNA transferred the cell mediated cytotoxicity to normal lymphocytes. Next, we tried the purification of immune RNA by way of sucrose density gradient centrifugation method and oligo (dT) cellulose affinity chromatography method. Active fraction of immune RNA was contained in 8-16 S fraction and in poly (A) containing fraction. As in vivo experiment, we injected immune RNA incubated lymphocytes intravenously to brain tumor-bearing rats and observed for death daily. In this experiments, significant prolongation of mean survival time was recognized in the group treated with immune RNA. We now consider the clinical application of immune RNA for malignant brain tumor by the following method: immune RNA is obtained from the lymphocytes of sheep which has immunized with patient's tumor cells. And then patient's own lymphocytes strengthened by incubation with immune RNA is injected intratumorally by way of Ommaya's reservoir. To do this therapy safely and effectively, further purification of immune RNA and solution of its physiochemical characteristics will be necessary.

Animals↗