title: Ischemic penumbra as a trigger for intracranial pressure rise - A potential cause for collateral failure and infarct progression?
abstract: We have recently shown that intracranial pressure (ICP) increases dramatically 24 h 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 (a) if choroid plexus damage contributes to the ICP elevation, (b) 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 and (c) if presence of ischemic penumbra (submaximal injury) is associated with ICP elevation. We found (a) no association between choroid plexus damage and ICP elevation, (b) animals with a good internal collateral supply through the AChA during MCAo had significantly larger penumbra volumes and (c) ICP elevation at ≈24 h post-stroke only occurred in rats with submaximal injury, shown in two different stroke models. We conclude that active cellular processes within the ischemic penumbra may be required for edema-independent ICP elevation.
authors.affiliation: School of Biomedical Sciences and Pharmacy, University of Newcastle, New South Wales, Australia Hunter Medical Research Institute, New Lambton, New South Wales, Australia.
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Beard
authors.affiliation: School of Biomedical Sciences and Pharmacy, University of Newcastle, New South Wales, Australia Hunter Medical Research Institute, New Lambton, New South Wales, Australia.
authors.forename: Caitlin L
authors.initials: CL
authors.lastname: Logan
authors.affiliation: School of Biomedical Sciences and Pharmacy, University of Newcastle, New South Wales, Australia Hunter Medical Research Institute, New Lambton, New South Wales, Australia.
authors.forename: Damian D
authors.initials: DD
authors.lastname: McLeod
authors.affiliation: School of Biomedical Sciences and Pharmacy, University of Newcastle, New South Wales, Australia Hunter Medical Research Institute, New Lambton, New South Wales, Australia.
authors.forename: Rebecca J
authors.initials: RJ
authors.lastname: Hood
authors.affiliation: School of Biomedical Sciences and Pharmacy, University of Newcastle, New South Wales, Australia Hunter Medical Research Institute, New Lambton, New South Wales, Australia.
authors.forename: Debbie
authors.initials: D
authors.lastname: Pepperall
authors.affiliation: School of Biomedical Sciences and Pharmacy, University of Newcastle, New South Wales, Australia Hunter Medical Research Institute, New Lambton, New South Wales, Australia.
authors.forename: Lucy A
authors.initials: LA
authors.lastname: Murtha
authors.affiliation: School of Biomedical Sciences and Pharmacy, University of Newcastle, New South Wales, Australia Hunter Medical Research Institute, New Lambton, New South Wales, Australia Department of Neurology, John Hunter Hospital, Hunter New England Local Health District, New South Wales, Australia Neil.Spratt@hnehealth.nsw.gov.au.
authors.forename: Neil J
authors.initials: NJ
authors.lastname: Spratt
mesh_terms: D000818:Animals; D020520:Brain Infarction / Q000473:pathology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology; D002831:Choroid Plexus / Q000293:injuries; D003097:Collateral Circulation; D018450:Disease Progression; D004487:Edema; D007427:Intracranial Pressure; D051381:Rats; D015424:Reperfusion
keywords: Collaterals; intracranial pressure; middle cerebral artery occlusion; penumbra; photothrombosis