Intracranial Elastance Research Articles

Effects of steroids on behavior, electrophysiology, water content and intracranial pressure in cerebral cytotoxic edema

The effect of therapy with methylpredisolone sodium succinate (5.33 mg/kg/day) and dexamethasone sodium phosphate (1 mg/kg/day) on grey matter of rabbits rendered edematous by a metabolic blocker, 6-aminonicotinamide, is presented. Methylprednisolone was observed to significantly reduce the water content of the grey matter ( p<0.001), whereas dexamethasone had little effect. Both agents, however, were equally effective in reducing intracranial pressure ( p<0.001) and improving intracranial elastance, when compared to untreated animals. However, in the dexamethasone-treated group, there was improved behavior and EEG findings in 50% of the animals when compared to the untreated controls, and similar improvement was present in less than 15% of the methylprednisolone group. The disparity between the effects on water content, behavior and EEG supports the thesis that in cerebral edema these agents have a metabolic effect out of proportion to their effect on tissue water.

Hypocapnia and intracranial volume-pressure relationship. A clinical and experimental study.

The effect of induced hypocapnia was observed, during intraventricular pressure monitoring, in five patients with chronically increased intracranial pressure (ICP) and in five baboons with acutely raised ICP. The volume-pressure response (VPR) was used as a measure of intracranial elastance (inverse compliance), an index of residual compensatory capacity. The VPR is the acute increase in mean ICP that occurs in response to a constant volume increment to ventricular cerebrospinal fluid. In the patients, hypocapnia produced a decrease in the VPR that was proportional to the decrease in ICP; in the baboons, ICP was substantially decreased with minimal change in the VPR. Both observations indicate that hypocapnia, though it decreases ICP, does not selectively decrease intracranial elastance. This may be a limiting factor in the use of hypocapnia in the management of raised ICP.