Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six children are reported in whom subarachnoid hemorrhage was an initial symptom of brain tumor. In our neurosurgical clinics, this represented 3.6% of pediatric brain tumors and showed a frequency equal to aneurysmal rupture among nontraumatic subarachnoid hemorrhage of children. In pediatric patients, hemorrhages from brain tumors occur predominantly in the posterior fossa. The medulloblastoma, which had been believed to bleed rarely, is now realized to be a common source of tumor hemorrhages in such cases. The introduction of CT scan facilitates early recognition of hemorrhagic stroke from brain tumors and prompt management for acute intracranial hypertension and brainstem dysfunction. Although the patients achieve favorable recovery from their initial catastrophic condition, the ultimate prognosis, in the majority of cases, is still rather poor because such hemorrhages usually develop from a malignant tumor. The present and other recent reports indicate that the incidence of hemorrhagic stroke from brain tumors in pediatric patients is much higher than has been thought and is an important cause of subarachnoid hemorrhage in this age group.
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PMID:Subarachnoid hemorrhage from brain tumors in childhood. 304 Feb 48

The authors examined 30 patients with intracranial hypertension caused by brain tumor who received 1 g/kg mannitol for dehydration. It was found that dehydration improves the function of the brain in the stage of subcompensation but makes it worse in the stage of decompensation. This has an effect both on the patients' general condition and on the EEG. The response of the healthy hemisphere to the administration of mannitol differed significantly from that of the involved hemisphere. Indications were determined for prescribing dehydration therapy according to the clinical stage of intracranial hypertension.
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PMID:[EEG changes in response to dehydration depending on the extent of intracranial hypertension]. 314 64

The authors reported the clinical course and the postmortem examination of a unique case of neurocutaneous melanosis with numerous anomalies and complications, which included congenital dislocation of lenses, hypogonadism, ectopia of prostatic duct, genuine phimose, retentio testis, psina bifida and neurogenic bladder. This 13-year-old boy with a large hairy nevus in a bathing trunk configulation and multiple small nevi over the whole body since his birth was admitted to our hospital for evaluation of headache and vomiting. Neurological examination showed bilateral papilledema and slight left hemiparesis. A CT scan revealed a large right frontal mass and craniotomy was performed with subtotal removal of this tumor which was confirmed as a malignant leptomeningeal melanoma. He initially made uneventful postoperative recovery, and two courses of chemotherapy with DTIC, ACNU and VCR were given; however, the currence of brain tumor ensued shortly thereafter, and he died in approximately six months after the onset of intracranial symptoms despite of the third course of chemotherapy. Thirty five cases of neurocutaneous melanosis associated with or without malignant melanoma have been reported in Japan. Twenty-eight cases were male and 7 female. Two cases showed the evidence of primary malignant melanoma outside of the central nervous system, whereas twenty eight leptomeningeal melanoma, in which 22 were solid and 6 diffuse, were shown intracranially. Other 5 cases had epileptic seizure and/or hydrocephalus caused by wide spreaded leptmeningeal melanosis. This high incidence of intracranial malignant melanoma in this disorder was remarkable compaired with the previous reports in other countries. Mean duration between deaths and the onset of symptoms of intracranial hypertension or focal neurological signs was 7 months, ranging from 1 to 24 months, showing the rapidly deteriorating course in this disorder.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of neurocutaneous melanosis associated with intracerebral malignant melanoma]. 332 33

The author reports on a number of cases of bilateral papilledema of unknown etiology. The condition was presumably caused by a formen virus infection. The symptoms were indicative of increased intracranial pressure; the possibility of a brain tumor therefore had to be ruled out. The results of the neurological examinations were negative and a benign intracranial hypertension was diagnosed. In 20 out of 22 cases neither lasting disturbances of visual nor visual field defects developed as a result of conservative treatment. In two cases--children in whom therapy was only instituted at a late stage--a partial atrophy of the optic nerve developed in spite of the treatment.
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PMID:[Bilateral papilledema of unknown etiology in childhood]. 343 Oct 10

Blood flow of transplanted intracerebral rat gliomas was measured before and after a constant I.V. infusion of angiotensin II-induced arterial hypertension using hydrogen clearance method. The brain tumor model was produced in syngeneic Wistar-King-Aptekman male rats by stereotaxic inoculation of ethylnitrosourea-induced glioma cells (KEG-1). Induced hypertension by angiotensin II infusion resulted in a significant increase in tumor blood flow compared with control levels (P less than 0.001). In addition, the therapeutic effect of administration of 3-[(4-amino-2-methyl-5-pyrimidinyl) ethyl] -1-(2-chloroethyl)-1-nitrosourea (ACNU) during angiotensin II-induced hypertension was evaluated. At 12 days after implantation, tumor-bearing rats were administrated angiotensin II as the mean blood pressure reached 150 mmHg, followed by ACNU injection, maintained the same blood pressure for 20 minutes. ACNU with induced hypertension group showed a median survival time of 27.0 days, which was significantly (P less than 0.02) longer than that of ACNU alone (22.0 days). It is therefore suggested that chemotherapy with angiotensin II-induced hypertension has a enhancing effect on chemotherapy for improving the drug delivery to tumor tissue by a increased tumor blood flow.
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PMID:[Experimental studies on induced hypertension chemotherapy of intracerebral inoculated gliomas in rats]. 346 30

A retrospective analysis of clinical manifestations of verified brain tumors in 1542 patients showed that the onset of the disease was acute in 5.8%, subacute in 12.3% and gradual in 81.9% while its further course was progressing in 60.5%, progression in 26.9%, remittent in 10.4% and even relatively stable in 2.2%. In 70.4% of the cases the brain tumor developed according to the classic "blastomatous" variant while in the remaining cases it developed atypically, i. e., as an inflammatory (13.1%) or vascular (10.7%) cerebral process, epilepsy (3.3%) or the syndrome of intracranial hypertension without focal symptoms (2.5%). or the syndrome of intracranial hypertension without focal symptoms (2.5%).
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PMID:[Variants in the onset and development of the clinical manifestations of brain tumors]. 373 77

We reviewed the computed tomographic findings after 1055 intracranial operations to determine the incidence of postoperative extradural hematomas. There were 11 medium and 5 large hematomas after 1055 operations (1.0%). Ten of the 16 hematomas were operated upon (10/1055, 0.9%). Four of the 10 hematomas were seen after 278 brain tumor removals (1.4%), another four after 190 aneurysmal operations (2.1%), one after 14 intracerebral hematoma removals (7.1%), and the last one after 251 ventricular shunting or drainage procedures (0.4%). In 4 of the 10 operated hematomas, sites were regional, in five sites were adjacent, and in one the site was distant. All of the five adjacent hematomas extended downward from a lower rim of the operative locus. Causes were analyzed in the three types of the hematomas. In case of the regional hematomas, the causes were incomplete hemostasis of the dura mater or the bone in all four patients, nonperformance of central stay sutures in three, systemic hypertension in one, and hypofibrinogenemia in one. In the adjacent hematomas, we could find dural separation at an edge of craniotomy in all five patients, abrupt collapse of the brain in all, ventricular dilatation in two, and systemic hypertension during immediate postoperative period in two. In one distant hematoma, ventricular dilatation and ventricular shunting procedure were themselves thought to be the causal factors.
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PMID:Postoperative extradural hematomas: computed tomographic survey of 1105 intracranial operations. 378 96

Multiple intracranial aneurysms have been reported in association with polycystic disease of the kidney, brain tumor, pituitary adenoma and coarctation of the aorta. We report the association of multiple aneurysms with primary hyperaldosteronism due to bilateral adrenal hyperplasia in an 18 year old left-handed man who presented with subarachnoid hemorrhage and arterial hypertension. We report the excellent outcome of this patient in spite of a difficult and surgical management. Ligation of all three intracranial aneurysms was performed after an extra-intracranial arterial bypass was done as a protective measure.
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PMID:[Multiple intracranial aneurysms associated with primary hyperaldosteronism]. 398 19

Results of surgical treatment in 85 cases with metastatic brain tumors are reviewed. The lung was the most frequent site of primary lesion and the following sites were GI tract and the breast. Adequate treatment consisted of total removal of tumor, irradiation and/or chemotherapy were carried out in 51 cases. The remaining 34 cases had an unsuccessful treatment because of their poor physical condition. Mean survival time after adequate treatment was 8.75 months in the former group and 3.06 months in the latter group. Of 51 patients (86.3%) in the former group, 44 showed improvement of the neurological signs after treatment. In the latter group, only 14 patients (41.2%) revealed neurological improvement. Total removal of tumor was carried out in 55 of 85 cases. The one-month operative mortality for all patients was 19.2%. Postoperative one-year survival rate was 12.5% in 16 cases with multiple metastases and in 36 cases with single metastasis was 25.6%. Follow-up study of 77 cases showed 31.2% of survival rate in 6 months, 18.2% in one-year and 5.2% in two-years. Only four patients survived more than 3 years after treatment. The direct causes of death in cases of total removal were attributed in recurrence of primary lesion or remote metastases to other organs. This study revealed that the prognosis of the patient with metastatic brain tumor was influenced by existence of intracranial hypertension due to brain edema or metastatic tumor itself and metastases to other organs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of the surgical treatment of metastatic brain tumors]. 405 62

The transfer of cefoperazone (CPZ) into cerebrospinal fluid (CSF), brain or brain tumor tissue was studied in 13 cases with brain tumor, chronic subdural hematoma and benign intracranial hypertension in 1982. The peak values of CPZ in serum came up immediately after its rapid intravenous administration and then decreased exponentially. The concentration of CPZ in CSF started to increase with a long delay of about 60 min. The average peak level in CSF remained 21.6 micrograms/ml and corresponded to 10.3% of the peak level in serum. The best transfer of chloramphenicol into CSF has been reported, while that of CPZ would be one of the next. The CPZ levels in CSF showed a slower decay than in serum. The concentration of CPZ in brain reached the peak level in less than 30 min and the average peak level was 36.5 micrograms/g cerebral tissue. The brain to blood rate of the CPZ concentration was 11.1%. The CPZ levels in the brain showed a rapid decrease like the transition of antibiotic levels in serum. The antibiotic levels in brain tumors were divided into two groups. The one showed sharp peak about one tenth of the values in serum. The other was of a slowly increasing type.
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PMID:[Concentration of antibiotics (cefoperazone) in human brain, brain tumor tissue and cerebrospinal fluid]. 608 80


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