Oedema, brain

Hartman A, Dettmers C, Schott H, Beyenburg S. Cerebral blood flow and rheologic alterations by hyperosmolar therapy in patients with brain oedema. Acta Neurochir Suppl (Wein) 1990 51 168-169. 

A series of dihydrodibenzoxepines, represented by AJ3941, was tested in animal models of global ischaemia and hypoxia, and found to be protective. AJ3941 is an inhibitor of lipid peroxidation (Kurakawa etal., 1991). A novel quinazoline fumarate (KB56666, was found to inhibit lipid peroxidation in rat brain homogenates and isolated mitochondria. In a rat focal stroke model, KE56666 prevented brain oedema and neuronal damage in the ischaemic zone (Hara etal., 1991). 

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a condition in which secretion of ADH continues despite serum hypo-osmolarity. This results in fluid retention and hyponatremia that can lead to brain oedema, mental confusion and coma. The causes are hypothalamic-pituitary tumours or an ectopic vasopressin-secreting tumour. 

Breen JC, Caplan LR, Dewitt LD et al. (1996). Brain oedema after carotid surgery. Neurology 46 175-181... 

Ikeda Y, Teramoto A, Nakagawa Y, Ishibashi Y, Yoshii T (1997b) Attenuation of cryogenic induced brain oedema by arginine vasopressin release inhibitor RU51599. Acta Neuiochir (Wien) 139 1173-1180... 

Ikeda Y, Toda S, Kawamoto T, Teramoto A (1997a) Arginine vasopressin release inhibitor RU51599 attenuates brain oedema following transient forebrain ischaemia in rats. Acta Neurochir (Wien) 139 1166-1172... 

Mittal S, Wu Z, Neelavalli J, Haacke EM (2009) Susceptibility-weighted imaging technical aspects and clinical applications, part 2. AJNR Am J Neuroradiol 30 232-252 Molnar AH, Varga C, Berko A, Rojik 1, Parducz A, Laszlo F, Laszlo FA (2008a) Prevention of hypoxic brain oedema by the administration of vasopressin receptor antagonist OPC-31260. Prog Brain Res 170 519-525... 

In HE due to acute liver failure, marked brain oedema is predominantly evident with a spongy loosening of the tissue, capillary proliferation and a hypoxia-related loss of function of the ganglion cells (F. Erbsloeh, 1958). In... 

We observed a lethal case (treatment with doxycycline was unsuccesful) showing massive amounts of leptospirae in the serum and in the centrifuged urine under dark-field examination. Maximum values were GPT 4,200 Ull, GOT 2,290 Ull, GDH 1,080 Ull, serum bilirubin 11 mgldl and Quick s value 17%, but with normal AP ( ) such pathological levels have repeatedly been reported in the literature. Autopsy revealed severe interstitial nephritis, tubular necrosis (laboratory findings corresponding to severe renal insufficiency), brain oedema (680 g), severe... 

This syndrome was described by W.R. Brain et at in 1929. (81) In 1963 it was differentiated as a clinical pathological entity by R. D. K. Reye et at and defined as a feverish disease of unclear aetiology in infancy. Almost half the children died of cerebral manifestations including brain oedema. (91)... 

Silibinin [inn] (silybin sllybum substance E6 silymarin and many other names) is a polycyclic structure isolated from Silybum mahanum. It has antioxidant and hepatoprotective properties, and has been used clinically for the treatment of brain oedema and liver disorders. 

Sharma, H. S., Nyherg, F, Cervos-Navarro, J., and Dey, P. K. (1992). Histamine modulates heat stress-induced changes in blood-brain barrier permeability, cerebral blood flow, brain oedema and serotonin levels An experimental study in conscious young rats. Neuroscience 50, 445-454. 

Dexamethasone may increase the acute hepatotoxicity of high-dose methotrexate. A retrospective comparison in children with brain tumours given methotrexate alone (24 patients), or with dexamethasone (33 patients), found that no serious brain oedema occurred in either of the groups... 

A patient, dependent on dexamethasone due to brain oedema caused by a tumour, deteriorated rapidly, with headache and lethargy, when aminoglutethimide was also given. The problem was solved by withdrawing the aminoglutethimide and temporarily increasing the dexamethasone dosage from 6 to 16 mg daily. ... 

Schnittger, C., Weissenborn, K., Boker, K., Kolbe, H., Dengler, R., Manns, M.R 1997. Continuous noninvasive cerebral perfusion monitoring in fulminant hepatic failure and brain oedema. In Advances in Hepatic Encephalopathy Metabolism in Liver Disease, eds C. Record and H. A1 Mardini (eds.)., pp. 515-519. New Castle upon Tyne Medical Faculty of the University of Newcastle upon Tyne... 

Brain tissue levels of interleukin-8, a potent neutrophil chemotactic cytokine (chemokine), increased significantly at 6h after reperfusion, but without a noticeable elevation of plasma IL-8 levels (Matsumoto et al. 1997). IL-8 protein was detected immunohistochemically in the vascular wall and, to a lesser degree, in infiltrated neutrophils, suggesting a local production of IL-8 in reperfused brain tissues. A neutralising anti-IL-8 antibody significantly reduced brain oedema and infarct size in comparison to rabbits receiving a control antibody. 

Brain oedema in humans may be a sequelae to a variety of conditions such as tumour, injuries, hypertension, infarct or hypercapnic hypoxia. In some instances there is overlapping of mechanisms, such as tumour causing increased intracranial pressure followed by haemorrhage. Brain oedema may be focal or diffuse, frequently occurring with exclusion of the arcuate fibres. It is now recognized by most authors that two types of brain oedema can be differentiated vasogenic and cytoxic [1]. Their chemical parameters can be elucidated better in experimental models and tend to differ with the type of the oedema. The term demyelination in this condition refers to the pallor of white matter seen in sections stedned for demonstration of myelin. 

Ultrastructural studies in acute cytotoxic oedema obtained by TET application [14, 15] reveal separation of myelin lamellae and splitting of the intraperiod line but no evidence of destruction of myelin. In contrast, in brain oedema induced by insertion of PPD (vasogenic type), [16] there is myelin damage, and macrophages with phagocytosed myelin are found. 

An hypothesis on the mechanism of production and spread of vasogenic brain oedema has been advanced based upon... 

Two less frequent types of brain oedema merit mentioning in cases of severe hypoglycaemia, due to insulin shock, oedema associated with pallor of white matter in corresponding myelin stains has been demonstrated [19]. This may find its explanation in the decrease of cerebral phospholipids demonstrated in rats subjected to experimental hypoglycaemia [20]. Brain oedema has also been observed in children afflicted with galactosaemia. In these cases, it is ascribed to osmotic action of the accumulated galactitol (dulcitol) [21,22]. 

Branston, N. M., Bayhan, M., Harris, R. J., Watson, A., Symon, L., 1981 Indomethacin increases ischaemic brain oedema in the primate. J. Cereb. Blood Flow Metab. (Suppl. 1) 1, S143-S144. 

---