Twenty-four h after permanent occlusion of the middle cerebral artery (MCA) in the cat, the hemispheric swelling due to edema is markedly reduced under treatment with large doses of dexamethasone than is the case with the untreated group. The increase of regional water and sodium content in the MCA territory is less in the dexamethasone treated group, whereas the potassium changes in the ischemic tissue showed only small differences between the two groups. The potassium content of the non-ischemic tissue is slightly increased in the dexamethasone treated animals when comparing with the untreated group. RISA activity in the tissue is increased in the grey and the white matter of both groups. The less marked RISA-131 activity in the cortical grey matter of the treated animals indicates blood-brain barrier damage of a smaller degree due to dexamethasone. These findings indicate a beneficial effect of dexamethasone on local ischemic edema. Regarding our results and the pharmacokinetics of this steroid the dexamethasone loading of a patient has to be in the range of about 100 mg per day for the adult, and has to be started immediately after the onset of a stroke.

The authors present the results of an investigation studying the resolution of vasogenic brain edema using cold injury in cats. The appearance of RISA-I TM and sucrose-C 14 labeled edema fluid in the ventricular cerebrospinal fluid (CSF) was assessed by means of ventriculocisternai perfusion. The effect of low-or high-pressure perfusion on edema spread was determined by measuring the water, sodium, RISA-1181, and sucrose-C 14 content of serial tissue blocks taken from the injured cortex through the white matter to the ventricular ependyma. The findings indicate that increasing the hydrostatic pressure gradient between edematous brain and CSF enhances the clearance of edema fluid into the ventricular CSF. This was conclusively demonstrated with low-pressure ventricular perfusion which markedly diminished the amount of edema close to the ventricles compared to the controls. The concentration of albumin, sodium, and potassium in the fluid removed from the tissue during lowpressure perfusion indicates that bulk flow was the primary method of edema movement through the extracellular space. With high-pressure perfusion the concentration profiles suggested alternative mechanisms of edema resolution, such as diffusion and reabsorption into capillaries.

The development of the intracranial pressure after a subarachnoid haemorrhage was evaluated in 21 patients. A statistically significant relation between the intracranial pressure and the neurological findings was found, whereas vasospasms did not influence the intracranial pressure. In patients in a clinically critical condition, rhythmic pressure waves of a frequency of 1/minute were repeatedly observed.

No abstract

Summary24 hours after a circumscribed cold injury of the cortex dog brains were perfused from the lateral ventricle and the frontal subaraehnoidal space to the eisterna magna with an artificial CSF containing trace amounts of 35S-labelled thiosulphate. Simultaneously the extraeellular tracer was administered intravenously.Extracellular fluid volume was estimated and found to be increased from 10 to 15% in the oedematous cortex and from 10 to 27% in the oedematous white matter. The actual size of ECS in oedematous white matter, however, must be larger as indicated by the relative alterations of thiosulphate distribution, tissue water, sodimn and chloride. Apparently a small part of the fluid accumulation affects the cellular compartment in oedematous white matter. It may be concluded from the close spatial correspondence of the spreading of 1181 albumin mad Evans blue, the increase in water and sodium content, and the enlargement of the TSS that the dilated extraeellular channels are filled with a plasma like oedema fluid, derived from blood.The oedema resulting from a local cold injury to the cortex produces all experimental model bearing similarities to the oedema following traumatic brain injury. This model has often been used to study the disturbance of blood-brain barrier to various compounds 3, G, 11, 13, 14 as well as the morphological 3, 4, 5, 15, 22 and chemical changes 3, 6, 16 that occur in oedematous tissue. In contrast, the sequence of events oeeuring during the formation of oedema and the physiochemieal forces (in terms of diffusior~ and driving forces) involved in the formation and resolution of brain oedema are not adequately kaowm Of