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

Clinical and computerized tomography findings in patients with miliary infestation of cysticerci in brain parenchyma are presented. Cysticercotic encephalitis produces a severe and frequently fatal neurological disorder. Although parenchymal cysticercosis is common in endemic areas, in the cases reported here, the pathology is induced by a severe inflammatory response in brain parenchyma rather than by the physical presence of multiple cysts. As a result of diffuse brain edema, all cases develop subacute severe intracranial hypertension and compromise of visual function. One important feature of this form of neurocysticercosis is that it particularly affects young women.
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PMID:Cysticercotic encephalitis: a severe form in young females. 382 97

Acute arterial hypertension was studied in normal cats to determine its role in the formation of brain edema. Arterial hypertension was induced for 30 minutes by inflation of a balloon catheter situated in the descending aorta. Cerebral edema was evaluated by gross and microscopic observations, tissue water content by wet/dry weights, and blood-brain barrier (BBB) permeability by extravasation of horseradish peroxidase (HRP) and Evans blue dye. For 1 hour after the hypertensive insult, tissue pressure and regional cerebral blood flow (rCBF) were measured from the arterial boundary zone and from a non-boundary region, and intracranial pressure was recorded from the lateral ventricle as ventricular fluid pressure. Focal lesions with increased BBB permeability to Evans blue dye or HRP were usually located symmetrically in the cortex, corresponding to the occipitoparietal parts of the arterial boundary zones. The increase in water content was found only in areas of increased permeability. Tissue pressure increased simultaneously with the abrupt rise in blood pressure, and an increase in rCBF paralleled the elevation of blood pressure. Tissue pressure and rCBF returned to a steady state when blood pressure returned to normal. There were no differences in tissue pressure or rCBF between the arterial boundary zone and the non-boundary zone, even during arterial hypertension. In cerebral hemispheres examined 48 hours after the hypertensive challenge, brain edema had not continued to develop. The data indicate that acute arterial hypertension may produce focal brain edema with increased permeability of the BBB in the cortex of normal brain, particularly in the arterial boundary zones. The authors postulate that increased cerebral blood volume, high intraluminal pressure, and breakthrough of autoregulation play an important role in the formation of hypertensive brain edema.
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PMID:Focal brain edema associated with acute arterial hypertension. 395 Jul 47

Changes in water and electrolyte content of the brain and edema formation after acute, drug-induced hypertension were studied in albino rabbits. Blood-brain and blood-cerebrospinal fluid (CSF) barriers opened to Evans blue-albumin when systemic blood pressure was elevated abruptly to more than 160 mm Hg by i.v. injection of Aramin. No statistically significant changes in sodium and potassium content of brain, muscle, and CSF were observed. Measurable brain edema did not develop. The results suggest that short-lasting hypertensive barrier opening does not cause brain edema, but may enhance a tendency for brain edema.
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PMID:Water and electrolyte content of rabbit brain after opening the blood-brain barrier by acute hypertension. 396 6

The present studies were performed to determine whether cerebral edema will develop as a consequence of arterial hypertension and/or craniectomy. Arterial hypertension was induced for 30 minutes by inflation of a balloon catheter situated in the descending aorta, and a parietal craniectomy was performed. The cerebral edema noticed was evaluated by macroscopic and microscopic observations, BBB permeability of HRP and Evans blue and water content. In addition, ICP was measured in the cisterna magna and ICPP by a catheter-tip transducer. In arterial hypertension or craniectomy alone, some small areas of Evans blue extravasation with increased water content were seen in the cortex, which corresponded to the occipito-parietal parts of the arterial boundary zones. In contrast, when arterial hypertension was combined with craniectomy, these lesions extended further into underlying white matter with increased water content. Forty-eight hours later, extensive brain edema with a shift of midline structures developed on the side of craniectomy which differed from that in arterial hypertension or craniectomy alone. It is suggested that some hydrostatic pressure gradients, particularly between blood vessel and surrounding extracellular space and among different areas within the brain parenchyma, may play an important role in the development of brain edema.
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PMID:Cerebral edema associated with craniectomy and arterial hypertension. 402 78

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

Experimental colibacillary (Escherichia coli) enterotoxemia as described in this report mimics natural edema disease both clinically and in gross pathology. The histopathology is characterized by accumulations of non-inflammatory edema and by arteriopathy. The smaller arterial and arteriolar changes recorded here are similar to those described in natural edema disease. The vascular changes described in recovered cases of experimental colibacillary enterotoxemia concur with those reported in so-called subacute and chronic edema disease. The arteriolar changes that occur in colibacillary enterotoxemia of swine are comparable to those associated with hypertension. Thin sections of cerebral cortex from four pigs with acute experimental edema disease were examined by electron microscopy in an attempt to demonstrate brain edema. Sections from one pig taken during the convulsive phase of disease revealed dilatation of perivascular glial processes. However, examination of sections taken from three other pigs during an earlier phase of the neurological disturbance revealed no significant lesions. We were unable to ascertain the role of brain edema in the pathogenesis of the nervous system disturbance in these experiments.
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PMID:Experimental edema disease of swine (E. coli enterotoxemia). 3. Pathology and pathogenesis. 427 56

Vasogenic edema was induced in mongrel cats by cold injury to study uptake and activation of the plasma-kallikrein-kinin system in central nervous system (CNS) tissue. A method was developed for quantitative assessment of kinin formation in affected brain tissue areas. Gross disruption of the blood-brain barrier by focal trauma causes marked penetration of plasma kininogens into necrotic and edematous brain tissue. Moreover, the kallikrein-kinin (KK) system was activated in both necrotic and perifocal edematous areas, and was markedly enhanced by additional cerebral ischemia. Formation of kinins in necrotic brain tissue led to consumption of approximately 60% to 80% of the amount of kininogens being taken up. In perifocal edematous tissue, formation of kinins was less pronounced, or even absent. However, if cerebral ischemia evolved after severe intracranial hypertension, kinins were also formed in the perifocal edematous brain. The intravascular origin of kininogens found in pathological tissue areas secondary to injury was deduced from the observation that cerebral tissue of the contralateral hemisphere with an intact blood-brain barrier had no measurable quantities of kininogens. Consumption of plasma kininogens or formation of kinins were assessed as the difference of the total amount of plasma kininogens taken up into the tissue minus the amount of kininogens found in the brain at postmortem examination. The data indicate that uptake and activation of the plasma-KK system might occur under all pathological conditions in which blood-brain barrier damage permits cerebral penetration of plasma proteins, such as with cerebral contusion, focal ischemia, and tumors. The potent pathophysiological mechanisms induced by kinins in CNS tissue, such as formation of brain edema, microcirculatory dysfunction, and enhancement of blood-brain barrier permeability, together with their formation in focal and perifocal pathological brain tissue, provide further support for a mediator function of the KK system. Methods that specifically interfere with the formation of kinins in damaged brain should therefore be expected to attenuate vasogenic edema.
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PMID:The kallikrein-kinin system as mediator in vasogenic brain edema. Part 2: Studies on kinin formation in focal and perifocal brain tissue. 656 63

In rabbits subjected to bicuculline (BC)- or pentylenetetrazole (PTZ)-seizures of 3 or 20 min duration or to adrenaline-induced hypertension, specific gravity (SG) was measured bilaterally in 15 regional brain areas in order to detect possible associations between the regionally limited blood-brain barrier openings due to these insults (see Nitsch and Klatzo 1983) and the presence of brain edema. In controls, a large variation between regional SG levels became evident: between 1.0467 in cerebellum and 1.0417 in preoptic area. A seizure duration of only 3 min was not sufficient to change SG significantly. After 20 min of seizures independent from the inducing agent, SG increased in all brain areas. The degree of increase seemed to be unrelated to presence or absence of a blood-brain barrier opening. In an attempt to avoid the influence of blood impregnation on the SG value, blood was replaced by saline before measurement. In controls, saline perfusion decreased SG only in the two areas with the highest original levels, thus documenting the partial dependency of the regional SG on the hematisation of the tissue. After 20 min of PTZ-induced seizures, SG in saline-perfused rabbits increased, but no longer significantly in all brain areas. This suggests that a part of the seizure-induced SG increase can be attributed to the hyperemia of the brain during the convulsions. On the other hand, an increase in flow volume due to hypertension did not change SG with the exception of the septum, preoptic area and hypothalamus. The direct measurement of water content with the classical wet/dry method in 4 gross brain areas showed that early seizure periods are in fact associated with a dehydration of the brain. This phenomenon could be explained by a glucose- and lactate-induced rise in blood osmolarity which in turn might cause a dehydration of the brain tissue.
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PMID:Specific gravity increases and brain water content decreases during short epileptiform seizures in discrete rabbit brain areas. 674 60

Intracranial hypertension is caused by various pathologic processes. From oncologic point of view, they are 1) intracranial space-occupying lesions, especially malignant tumors, 2) leptomeningeal tumors, 3) hemorrhage in the brain tumors, 4) intracranial hemorrhage due to hemorrhagic diathesis related to the malignant tumors, and 5) cerebral thrombosis or embolism due to increased blood coagulability secondary to malignancy. In the increase of intracranial pressure, brain edema or disturbance of cerebrospinal fluid (CSF) circulation due to the presence of brain tumors play more important role than the tumor bulk itself. CT scan is useful for demonstrating the process causing the intracranial hypertension. Therapeutic measures in all patients with increased intracranial pressure are initiated promptly to restore the cardiopulmonary dysfunction if any. Hyperventilation and intravenous infusion of hyperosmolar agents such as mannitol and glycerol have an immediate effect in reducing intracranial pressure when brain edema plays role in increasing it. Steroids are also very effective in reducing brain edema; the effect is less immediate but long lasting. CSF drainage or shunt operation is necessary when dilated ventricular system plays role in the intracranial hypertension. The radical treatment of the intracranial hypertension is a removal of the tumor causing it; however, if not indicated, the second choice is the internal or external decompressions. Postoperative radiotherapy and chemotherapy are also indicated for the malignant brain tumors.
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PMID:[Intracranial hypertension]. 688 68

Neurocysticercosis is a major public health problem in the developing countries. Previous to the CT scan era its diagnosis was very restricted and conventional diagnostic methods were unreliable. It was also frequently necessary to submit patients to costly and dangerous surgical procedures to confirm the precise nature of the disease. The most striking type of neurocysticercosis diagnosed by CT is the acute or edematous type (Table 1). Patients with this type of neurocysticercosis are referred for examination with intracranial hypertension, in general with suspicion of space-occupying lesion. In the authors' experience it is possible to obtain a dramatic reduction of the brain edema in the acute stages of neurocysticercosis using corticosteroids, the use of which completely changes the clinical picture and the CT images.
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PMID:[Effect of corticoids in the acute phase of neurocysticercosis: preliminary note]. 709 7


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