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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of benign intracranial hypertension due to prolonged administration of a low dose of Vitamin A is described in a young male investigated as a brain tumor suspect. Computerized axial tomography showed small and symmetrical lateral ventricles which was consistent with the diagnosis. The syndrome of benign intracranial hypertension and its relationship to chronic Vitamin A toxicity is discussed.
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PMID:Vitamin A induced benign intracranial hypertension. 13 Feb

The pattern and pathogenesis of nonlocalizing visual disturbances, associated with optic disc edema (ODE). raised cerebrospinal fluid pressure, and intracranial space-taking lesions were investigated experimentally in rhesus monkeys with simulated progressive brain tumor and clinically in patients with benign intracranial hypertension. The visual disturbances occurring in one of both eyes were of three types: recurrent attacks of transient obscuration, permanent blindness, and various types of visual field defects. The studies indicate that the visual disturbances are usually due to two mechanisms. The most common is ischemia of the optic disc secondary to ODE. The other, rarer mechanism probably consists of the space-taking lesion causing downward herniation of the parahippocampal gyrus into the tentorial notch, producing compression of the lateral geniculate body and optic tract.
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PMID:Optic disc edema in raised intracranial pressure. VI. Associated visual disturbances and their pathogenesis. 40 82

Two cases of delayed radiation necrosis of the brain were reported. Case 1 was a 50-year-old man who had right hemiparesis and disorientation 26 months after Linac irradiation (5,000 rad), preceded by the operation for right maxillar carcinoma. A left carotid angiogram demonstrated a left temporal mass lesion, extending the frontal lobe. Case 2 was a 41-year-old man who had previously the operation for right intraorbital plasmocytoma, followed by two times Co irradiation (6,400 rad, and 5,000 rad). He had the signs and symptoms of intracranial hypertension 36 months after last irradiation. A left carotid angiogram demonstrated a left temporal mass lesion. Both cases were treated by administration of steroid hormone, which alleviated the signs and symptoms, followed by the temporal lobectomy. Microscopic examinations showed necrosis of the brain tissues associated with hyaline degeneration of blood vessel walls and perivascular cell infiltration. The signs and symptoms of intracranial hypertension subsided postoperatively. The other thirteen cases as same as ours were collected from literature, which showed the signs and symptoms simulating a brain tumor (like a metastic brain tumor) after the irradiation to extracranial malignant tumors, and the diagnosis of radiation necrosis were made by the operation or autopsy. A follow-up for a long time is necessary, because the pathological changes in the brain may be progressive and extending in some cases, although the decompressive operations for mass lesion are excellent in result.
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PMID:[Delayed radiation necrosis of the brain simulating a brain tumor--report of two cases (author's transl)]. 103 40

We evaluated the hospital records of 412 patients with isolated or combined ocular nerve palsies in a retrospective study. Palsies of the oculomotor nerve (n = 172) and of the abducens nerve (n = 165) were more frequent than those of the trochlear nerve (n = 25). Combined ocular nerve palsies (n = 50) were generally combinations of the 3rd and 6th cranial nerves (n = 21) or pareses of all three ocular nerves (n = 17). 165 ocular nerve palsies were due to vascular causes: in 135 of these cases diabetes mellitus and hypertension were present. The oculomotor nerve was most frequently affected; in 63% there was no involvement of the pupil. In inflammatory disease and brain tumor the abducens nerve was most frequently affected, with aneurysm of the oculomotor nerve. The origin of ophthalmoplegia was unclear in 73 patients. Ocular nerve paralysis was most common with tumors, aneurysm, and vascular processes and in 206 cases was only partial. Pain was associated with tumor, trauma and aneurysm. In trochlear nerve palsies concomitant pain was much less frequent than in palsies of the other two ocular nerves. The clinical course was followed for 3 weeks in 352 patients; in 191 patients there was a complete regression of the pareses and in 59 only a partial recovery. The most favorable prognosis was with inflammatory and vascular lesions; in the latter the outcome was improved by the administration of non-steroidal anti-inflammatory drugs.
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PMID:Isolated and combined pareses of cranial nerves III, IV and VI. A retrospective study of 412 patients. 186 22

Regional blood flow of brain tumors and normal brain tissue of rats before and during angiotensin II (AT II)-induced hypertension were measured using an electrolytic flowmeter and a laser flowmeter. Etoposide concentration in the tumor and brain tissue after intracarotid administration were also measured in brain tumor bearing rats with or without AT II-induced hypertension. A suspension of 5 x 10(5)/10 microliters 9L gliosarcoma cells was inoculated into the left caudate-putamen of CD Fischer 344 rats. Before induced hypertension, regional blood flow of the tumor (28.2 +/- 2.6 ml/100 g/min; mean +/- SEM) and the contralateral caudate-putamen (23.0 +/- 1.8 ml/100g/min) in the tumor bearing rats were significantly lower than that of the caudate-putamen (43.9 +/- 4.1 ml/100g/min) in the normal rats (p less than 0.01). Intravenous administration of AT II at a dose of 0.4-0.6 microgram/body/min increased the mean arterial blood pressure from 96.5 +/- 4.7 mmHg to 138.0 +/- 3.6 mmHg. AT II-induced hypertension resulted in an approximate 1.8(1.1 - 3.6)-fold increase in the regional tumor blood flow. On the other hand the regional blood flow of the contralateral caudate-putamen was slightly decreased at the rate of 6%. The mean concentration of etoposide with AT II-induced hypertension in the tumor tissue was 2.2-fold higher than that without AT II-induced hypertension. However, etoposide delivery to normal brain tissue was small. From these results, induced hypertension with intravenously administrated AT II selectively increase the tumor blood flow and drug delivery to brain tumor tissue. Intracarotid chemotherapy with AT II-induced hypertension might contribute to enhance therapeutic effect of malignant brain tumors.
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PMID:[Selective enhancement of tumor blood flow and drug delivery to brain tumors in experimental rat gliomas under angiotensin II-induced hypertension]. 191 Sep 50

The incidence of mycotic infection of C.N.S. seems to have increased in the last few years and the diagnosis is being made more and more frequently. The authors are reporting a case of a 27 year old man, admitted with severe intracranial hypertension, very poor visual acuity and right motor weakness. The C.T. Scan showed a massive space occupying lesion in the left hemisphere. Only the biopsy, then the surgical removal of the lesion revealed the true histological nature. It turned out to be aspergilloma. The patient expired 13 hours later. Up to date, 25 cases of Aspergillus granulomas have been reported. This disease is included in the entity of neuromycosis. Its specificity compared to the other types of cerebral mycotic localization as for example abscess, meningitis, mycotic aneurysm, lies in the fact that it presents as granulomatous mass in the hemisphere, mimicking a brain tumor without any specific neuroradiological findings. In the light of so far published literature, the authors draw the attention to the fact of the difficulty of diagnosis of this dreadful benign disease due to the lack of specific clinical and radiological findings. They are stressing the necessity of early and vigorous diagnosis mainly in patients with a risk factor to try to reduce the high mortality that has been universally reported in almost all cases.
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PMID:[Cerebral aspergilloma. Review of the literature apropos of a case]. 219 Dec 35

Blood flow was measured in transplanted rat gliomas before and during a constant intravenous infusion of angiotensin II using hydrogen clearance methods. The brain tumor models were produced in syngeneic Wister-King-Aptekman male rats with stereotaxic inoculation of ethylnitrosourea-induced glioma cells (KEG-1). Induced hypertension up to 150 mmHg (mean arterial pressure) with the infusion of angiotensin II resulted in a significant increase of blood flow to tumor center compared to the normotensive state (p less than 0.001). Blood flow measured simultaneously in brain tissue of tumor-free contralateral hemisphere did not change. The therapeutic effect of administration of the simultaneous 1-(4-Amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and angiotensin II was evaluated in four experimental groups with the tumor-bearing rats. Twelve days after tumor implantation, the rats were administered angiotensin II to increase the mean arterial blood pressure to 150 mmHg, followed by intravenous injection of ACNU injection. The increased blood pressure was steadily maintained for 20 minutes. The ACNU/induced hypertension group showed a median survival time of 27.0 days, which was significant longer (p less than 0.02) than that of an ACNU treatment group (22.0 days), a hypertension treatment group (19.0 days), or a no treatment group (18.5 days). The enhanced therapeutic effect can be attributed to improving chemotherapeutic drug delivery due to increased blood flow in the tumor.
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PMID:Modification of tumor blood flow and enhancement of therapeutic effect of ACNU on experimental rat gliomas with angiotensin II. 235 53

In 7 patients with a brain tumor and intracranial hypertension treated by ventriculosubcutaneous drainage, intracranial pressure and cerebral perfusion pressure were continuously monitored during induction of anesthesia with fentanyl 1.5 micrograms/kg, propofol 2.5 mg/kg and vecuronium 0.1 mg/kg. End-tidal pCO2 was kept constant by manual ventilation and arterial pCO2 was verified before induction and before and after intubation. Five minutes after induction the patients were intubated and measurements continued for five more minutes. Mean arterial pressure decreased from 102 (+/- 9.8) mmHg to 57 (+/- 11.6) mmHg (p less than 0.01). Intracranial pressure did not change significantly before intubation. However in two patients intracranial pressure increased before intubation due to a significant rise in arterial pCO2. In 4 of the 7 patients an important increase to 25 (+/- 4.6) mmHg in intracranial pressure was observed during intubation. Cerebral perfusion pressure decreased from 88 (+/- 4.6) to 45 (+/- 9.8) mmHg (p less than 0.01) before intubation, but did not differ from the baseline during and after intubation. It is concluded that propofol 2.5 mg/kg in a bolus injection does not increase ICP but can produce a significant decrease of the cerebral perfusion pressure due to a marked decrease in mean arterial pressure in patients with a brain tumor.
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PMID:The effects of propofol on intracranial pressure and cerebral perfusion pressure in patients with brain tumors. 280 Oct

The Cushing, or ischemic response, is a useful mechanism in intracranial hypertension because it restores normal cerebral perfusion pressure and cerebral circulation. In patients with acute intracranial hypertension due to mass-expanding lesions such as brain edema, hydrocephalus or brain tumor, cerebral perfusion pressure decreases and plateau waves occur. In experimental animals, spontaneous or induced arterial hypertension can compensate for the reduction of cerebral perfusion pressure. The interrelation between arterial pressure, intracranial pressure and cerebral perfusion pressure in an experimental model of hydrocephalus in dogs was investigated. Plateau waves were preceded by a decrease in cerebral perfusion pressure and a Cushing response was seen 5 to 15 seconds before abolition of the wave. Arterial hypertension, induced by intravenous infusion of Aramin, restored cerebral perfusion pressure and intracranial pressure became normal. Arterial hypertension appears to be an efficient stimulus to abort plateau waves. Hypertensive patients in whom subarachnoid bleeding develops from ruptured aneurysm are at high risk of bleeding again and need antihypertensive treatment together with drainage of cerebrospinal fluid. Induced arterial hypertension is the most effective treatment of vasospasm but increases the danger of aneurysmal rebleeding and can only be safe after clipping of the aneurysm. This is one of the strongest arguments for early operation on cerebral aneurysms.
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PMID:Arterial hypertension in neurosurgical emergencies. 291 56

The authors report two cases of contralateral intratumoral hemorrhage after tumor biopsy in patients with bilateral glioblastoma multiforme. There was no evidence of systemic hypertension during either procedure. The occurrence of hemorrhage distant to the site of biopsy may be related to some aspect of the surgical procedure and should be recognized as a possible complication of brain tumor biopsy procedures.
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PMID:Contralateral intracerebral hemorrhage as a complication of tumor biopsy. 302 82


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