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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steroids reduce permeability of the blood-brain barrier and inhibit active sodium transport by brain capillaries in vitro. Since the rate of edema formation during the early stages of ischemia is related to the rate of sodium transport from blood to brain, this study was designed to determine whether steroids reduce ischemic edema formation by inhibiting blood-brain barrier sodium transport. Dexamethasone was compared with progesterone since the latter is a more potent inhibitor of sodium transport in isolated capillaries. Sprague-Dawley rats were treated with vehicle (n = 22) or 2 mg/kg of either dexamethasone (n = 22) or progesterone (n = 17) 1 hour before occlusion of the middle cerebral artery. After 4 hours of ischemia, brain water content and blood-brain barrier permeability to [3H] alpha-aminoisobutyric acid and sodium-22 were determined. In controls, mean +/- SEM water content of tissue in the center of the ischemic zone was 82.4 +/- 0.2%. Brain edema was significantly reduced following pretreatment with either dexamethasone (80.6 +/- 0.1%, p less than 0.001) or progesterone (81.5 +/- 0.3%, p less than 0.05). There was also a significant reduction in blood-brain barrier permeability to alpha-aminoisobutyric acid in normal brain following either treatment (e.g., 2.21 +/- 0.19 and 1.37 +/- 0.10 microliters/g/min, p less than 0.001, for control and dexamethasone treatments, respectively), but no effect on the permeability to sodium (e.g., 1.19 +/- 0.05 and 1.12 +/- 0.11 microliters/g/min for control and dexamethasone treatments, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of steroids on edema and sodium uptake of the brain during focal ischemia in rats. 238 1

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

Cerebellar masses are a heterogenous group of conditions that can cause compression of the aqueduct or fourth ventricle, resulting in obstructive hydrocephalus, brainstem compression, and upward/downward herniation as a direct result of mass effect. Untreated lesions can be fatal in a few hours, but prompt and appropriate treatment of the mass effect can produce very good outcomes. These patients should be closely followed in a critical care setting that has rapid access to neurosurgical expertise. Medical measures to decrease brain edema should be taken, including elevation of the head of the bed and avoidance of hypo-osmolar solutions, hypercarbia, or hyperthermia. Osmotic diuretics should be initiated promptly in patients with clinical worsening and radiographic evidence of edema resulting in mass effect. However, medical measures should not delay surgical intervention, which should proceed as rapidly as possible when indicated. Cerebellar hemorrhages more than 3 cm in diameter and cerebellar hemispheric strokes involving more than one third of the hemisphere should be considered for early suboccipital craniotomy with decompression. Regardless of lesion size, neurologic deterioration and radiologic signs of obstructive hydrocephalus should call for emergency decompressive surgery with resection of hematoma or necrotic brain tissue. Ventriculostomy should be considered as a bridge to surgical decompression, given the theoretical concern of upward herniation mediated by supratentorial drainage in the face of an underlying posterior fossa mass lesion. Steroids are not indicated for cerebrovascular disease but should be used to treat vasogenic edema induced by tumor. Anticoagulation is reserved for cerebellar venous and dural sinus thrombosis. Specific treatments targeting the underlying pathology should be used aggressively: thrombolysis and endovascular interventions for eligible stroke patients, antibiotic therapy for abscesses, and radiotherapy, chemotherapy, or both for tumors.
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PMID:Treatment of cerebellar masses. 1833 36