Formation and resolution of white matter oedema in various types of brain tumours.

Department of Neurosurgery, Musashino Red-Cross Hospital, Tokyo, Japan.
Acta neurochirurgica. Supplement 02/1990; 51:149-51.
Source: PubMed


Following infusion of 200 ml of Iopamidol for 1 hour the propagation of extravasated contrast medium around different types of 12 brain tumours was examined and imaged via CT. Increasing volume of expanding peritumoural contrast enhanced brain tissue was measured by integrating volumes of planimetrically measured enhanced area on CT slice of 0.5 cm in thickness. So far our data failed to demonstrate differences in the peritumoural contrast expansion between the different types of tumours. Formation and resolution as well as the speed of oedema propagation were determined by calculation of the increasing volume of the enhanced peritumoural brain tissue. Average formation rate of oedema fluid from 1 cm3 of tumour was 0.06 ml/hr, and was lower in larger tumours, while formation rate of oedema fluid from whole tumour was higher in larger tumours. Average resolution rate of oedema fluid during the passage through 1 cm3 of the peritumoural white matter was 0.03 ml/hr, and was not affected by tumour size. Average speed of oedema propagation was 0.59 mm/hr, and was higher in larger tumours. The main therapeutic effect of steroid in peritumoural oedema was a reduction in formation rate of oedema fluid.

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    ABSTRACT: Peritumoural brain oedema is a prominent feature of malignant brain tumours. Glucocorticoids diminish the neurological symptoms and signs caused by the oedema and reduce the abnormally high cerebral water content. The exact mechanisms of action of the glucocorticoids are unknown. The present study investigates the influence of dexamethasone on NMR relaxation time T1 in peritumoural oedema in 13 patients with gliomas. It is shown that NMR T1 images can be used as a potent monitor of brain oedema, and that dexamethasone significantly reduces mean T1 after 1, 3, and 7 days of treatment by 2%, 6%, and 13% respectively. Using an image histogram analysis technique the term "super-oedema" was defined as the 50% of the total oedema area with the highest T1, corresponding to the highest water content. It is shown, that with this technique the treatment effect of steroids on super-oedema was a reduction of 13%, 33%, and 57% after 1, 3, and 7 days of treatment respectively. The mean change after 24 hours of treatment was statistically significant (p < 0.01). The method can be used in all situations where the anti-oedematous effect of a given treatment is to be monitored.
    Acta Neurochirurgica 02/1993; 122(3-4):218-24. DOI:10.1007/BF01405532 · 1.77 Impact Factor
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    ABSTRACT: Brain tumor-associated cerebral edema arises because tumor capillaries lack normal blood-brain barrier function; vascular permeability factor (VPF, also known as vascular endothelial growth factor, VEGF) is a likely mediator of this phenomenon. Clinically, dexamethasone reduces brain tumor-associated vascular permeability through poorly understood mechanisms. Our goals were to determine if suppression of permeability by dexamethasone might involve inhibition of VPF action or expression, and if dexamethasone effects in this setting are mediated by the glucocorticoid receptor (GR). In two rat models of permeability (peripheral vascular permeability induced by intradermal injection of 9L glioma cell-conditioned medium or purified VPF, and intracerebral vascular permeability induced by implanted 9L glioma), dexamethasone suppressed permeability in a dose-dependent manner. Since 80% of the permeability-inducing activity in 9L-conditioned medium was removed by anti-VPF antibodies, we examined dexamethasone effects of VPF expression in 9L cells. Dexamethasone inhibited FCS- and PDGF-dependent induction of VPF expression. At all levels (intradermal, intracranial, and cell culture), dexamethasone effects were reversed by the GR antagonist mifepristone (RU486). Dexamethasone may decrease brain tumor-associated vascular permeability by two GR-dependent mechanisms: reduction of the response of the vasculature to tumor-derived permeability factors (including VPF), and reduction of VPF expression by tumor cells.
    Journal of Clinical Investigation 10/1996; 98(6):1400-8. DOI:10.1172/JCI118927 · 13.22 Impact Factor
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