Ischemic penumbra as a trigger for intracranial pressure rise: a potential cause for collateral failure and infarct progression?

We have recently shown that intracranial pressure (ICP) increases dramatically 24 hours after minor intraluminal thread occlusion with reperfusion, independent of edema. Some of the largest ICP rises were observed in rats with the smallest final infarcts. A possible alternate mechanism for this ICP rise is an increase of cerebrospinal fluid (CSF) volume secondary to choroid plexus damage (a known complication of the intraluminal stroke model used). Alternatively, submaximal injury may be needed to induce ICP elevation. Therefore we aimed to determine: i. if choroid plexus damage contributes to the ICP elevation; ii. If varying the patency of an important internal collateral supply to the middle cerebral artery (MCA), the anterior choroidal artery (AChA), produces different volumes of ischemic penumbra iii. if presence of ischemic penumbra (submaximal injury) is associated with ICP elevation. We found: i. no association between choroid plexus damage and ICP elevation; ii. animals with a good internal collateral supply through the AChA during MCAo had significantly larger penumbra volumes; iii. ICP elevation at ≈24 hours post-stroke only occurred in rats with submaximal injury, shown in 2 different stroke models. We conclude that active cellular processes within the ischemic penumbra may be required for edema-independent ICP elevation.