Impact of pre-existing neuroendocrine tumors on brain tissue compliance following intracerebral hemorrhage in old spontaneously hypertensive rats

Conditions associated with mass effect, such as intracranial tumors and hemorrhagic stroke (intracerebral hemorrhage; ICH), disrupt intracranial pressure (ICP) regulation by exhausting the brain’s compliance reserves. Displacement of cerebrospinal fluid, blood, and brain tissue (“tissue compliance”) can buffer ICP elevations, but these reserves are limited. Brain tumor patients face elevated ICH risk, yet how pre-existing mass effect influences acute intracranial compliance remains unclear. This study examined how chronic intracranial mass effect alters tissue compliance following acute ICH. In an aged spontaneously hypertensive rat (SHR) cohort, a high incidence of spontaneous intracranial tumors were discovered. This prompted an exploratory analysis in 18 SHRs (n = 6/group: ICH-24 h, ICH-72 h, sham) to evaluate the impact of chronic mass effect on post-ICH tissue compliance. Following collagenase striatal hemorrhage, brains were collected for macroscopic and microscopic volumetric morphological analysis. Tissue compliance persisted in tumor-bearing animals, reflected by reduced contralateral hemisphere volume (∼6% at 24; ∼14 % at 72 h) and neuronal soma shrinkage in hippocampal and cortical regions. Despite smaller hematoma volumes, rats with tumors exhibited nearly twofold greater tissue compliance responses than non-tumor animals. Pre-existing mass effect may modify the recruitment of intracranial compliance reserves following stroke in aged animals.

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Publication Details

Journal
Brain Hemorrhages
Published
2025-11-05
DOI
https://doi.org/10.1016/j.hest.2025.10.005
Citations
1
Primary Topic
Intracerebral and Subarachnoid Hemorrhage Research
Type
article
Field-Weighted Citation Impact
1.39
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article

Impact of pre-existing neuroendocrine tumors on brain tissue compliance following intracerebral hemorrhage in old spontaneously hypertensive rats

Frederick Colbourne, Anna C. J. Kalisvaart
1 citations
Brain Hemorrhages
Intracerebral and Subarachnoid Hemorrhage Research
1.39
article

Impact of pre-existing neuroendocrine tumors on brain tissue compliance following intracerebral hemorrhage in old spontaneously hypertensive rats

Frederick Colbourne, Anna C. J. Kalisvaart
article en
1 citations

Abstract

Conditions associated with mass effect, such as intracranial tumors and hemorrhagic stroke (intracerebral hemorrhage; ICH), disrupt intracranial pressure (ICP) regulation by exhausting the brain’s compliance reserves. Displacement of cerebrospinal fluid, blood, and brain tissue (“tissue compliance”) can buffer ICP elevations, but these reserves are limited. Brain tumor patients face elevated ICH risk, yet how pre-existing mass effect influences acute intracranial compliance remains unclear. This study examined how chronic intracranial mass effect alters tissue compliance following acute ICH. In an aged spontaneously hypertensive rat (SHR) cohort, a high incidence of spontaneous intracranial tumors were discovered. This prompted an exploratory analysis in 18 SHRs (n = 6/group: ICH-24 h, ICH-72 h, sham) to evaluate the impact of chronic mass effect on post-ICH tissue compliance. Following collagenase striatal hemorrhage, brains were collected for macroscopic and microscopic volumetric morphological analysis. Tissue compliance persisted in tumor-bearing animals, reflected by reduced contralateral hemisphere volume (∼6% at 24; ∼14 % at 72 h) and neuronal soma shrinkage in hippocampal and cortical regions. Despite smaller hematoma volumes, rats with tumors exhibited nearly twofold greater tissue compliance responses than non-tumor animals. Pre-existing mass effect may modify the recruitment of intracranial compliance reserves following stroke in aged animals.

Brain HemorrhagesVol. 6(6)
University of Alberta (CA), Cornell University (US), Burke Medical Research Institute (US), Women and Children’s Health Research Institute (CA), Weill Cornell Medicine (US)
Openalex Percentile: Top 14%
Intracerebral and Subarachnoid Hemorrhage Research
1.39
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