Evidence for Decreased Brain Parenchymal Volume After Large Intracerebral Hemorrhages: a Potential Mechanism Limiting Intracranial Pressure Rises

Michael R Williamson,Frederick Colbourne

doi:10.1007/s12975-017-0530-x

Abstract

Potentially fatal intracranial pressure (ICP) rises commonly occur after large intracerebral hemorrhages (ICH). We monitored ICP after infusing 100–160 μL of autologous blood (vs. 0 μL control) into the striatum of rats in order to test the validity of this common model with regard to ICP elevations. Other endpoints included body temperature, behavioral impairment, lesion volume, and edema. Also, we evaluated hippocampal CA1 sector and somatosensory cortical neuron morphology to assess whether global ischemic injury occurred. Despite massive blood infusions, ICP only modestly increased (160 μL 10.8 ± 2.1 mmHg for <36 h vs. control 3.4 ± 0.5 mmHg), with little peri-hematoma edema at 3 days. Body temperature was not affected. Behavioral deficits and tissue loss were infusion volume-dependent. There was no histological evidence of hippocampal or cortical injury, indicating that cell death was confined to the hematoma and closely surrounding tissue. Surprisingly, the most severe hemorrhages significantly increased cell density (~15–20%) and reduced cell body size (~30%) in regions outside the injury site. Additionally, decreased cell size and increased density were observed after collagenase-induced ICH. Parenchymal volume is seemingly reduced after large ICH. Thus, in addition to well-known compliance mechanisms (e.g., displacement of cerebrospinal fluid and cerebral blood), reduced brain parenchymal volume appears to limit ICP rises in rodents with very large mass lesions.

Highlights

After intracerebral hemorrhage (ICH), the mass effect from the hematoma and edema, among other factors, can raise intracranial pressure (ICP) [1]
Striatal blood infusion caused volume-dependent lesions (Fig. 3a, b; P = 0.003, ANOVA; P = 0.002, Tukey, 100 vs. 160 μL) that were largely confined to the striatum and corpus callosum, with some crossing to the contralateral hemisphere (2/5 100, 4/5 130, and 3/5 160-μL animals;
We show that large hemorrhages induced by striatal blood infusion are readily accommodated for, causing ICP to increase only modestly and transiently

Summary

Introduction

After intracerebral hemorrhage (ICH), the mass effect from the hematoma and edema, among other factors, can raise intracranial pressure (ICP) [1]. High ICP predicts poor outcome and death [2, 3] and is linked to impaired consciousness [4]. ICP and related compensatory changes in response to large hemorrhagic mass lesions have not been well studied in animal models. The Monro-Kellie hypothesis predicts that mobile cranial fluids, blood and cerebrospinal fluid (CSF), are displaced to maintain ICP in response to a change in the volume of the cranial contents (e.g., from hemorrhage) [5, 6]. The exhaustion of rapid compensatory mechanisms (displacement of blood and/or CSF) due to a large insult causes ICP to increase, resulting in brain displacement or herniation and impaired cerebral blood flow [6,7,8]

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