Intracranial Pressure Monitoring in Experimental Traumatic Brain Injury: Implications for Clinical Management

Abstract

Traumatic brain injury (TBI) is often associated with long-term disability and chronic neurological sequelae. One common contributor to unfavorable outcomes is secondary brain injury, which is potentially treatable and preventable through appropriate management of patients in the neurosurgical intensive care unit. Intracranial pressure (ICP) is currently the predominant neurological-specific physiological parameter used to direct the care of severe TBI (sTBI) patients. However, recent clinical evidence has called into question the association of ICP monitoring with improved clinical outcome. The detailed cellular and molecular derangements associated with intracranial hypertension (IC-HTN) and their relationship to injury phenotype and neurological outcomes are not completely understood. Various animal models of TBI have been developed, but the clinical applicability of ICP monitoring in the pre-clinical setting has not been well-characterized. Linking basic mechanistic studies in translational TBI models with investigation of ICP monitoring that more faithfully replicates the clinical setting will provide clinical investigators with a more informed understanding of the pathophysiology of IC-HTN, thus facilitating development of improved therapies for sTBI patients.

Post-injury ventricular enlargement associates with iron in choroid plexus but not with seizure susceptibility nor lesion atrophy—6-month MRI follow-up after experimental traumatic brain injury

“…In the rat lateral FPI model we found a growth of ipsilateral ventricles up to 1340% (14-fold) as compared to the volume in shams, and contralateral ventricles up to 703% (eightfold) over the 6 months follow-up, which were not related to the extent off the cortical atrophy. Previous studies with measurements of intracerebral pressure (ICP) have showed only acute increases in ICP, up till 24 h post-FPI (recent review by (Glushakova et al 2020 ) with no evidence of chronic increase in the ICP (to our knowledge). Brain swelling due to transient acute and subacute edema is mostly resolved by 9-day post-FPI, and FPI-craniectomy acts as ‘decompressive craniectomy’.…”

Intravenous Immunomodulatory Nanoparticle Treatment for Traumatic Brain Injury

“…The global injury produced in the CHI model leads to edema and increased intracranial pressure (ICP) in rodents, similar to human injuries . We therefore used a quantitative R2* sequencing modality on MRI to evaluate tissue edema at 24 hpi, a time of peak edema.…”

“…The global injury produced in the CHI model leads to edema and increased intracranial pressure (ICP) in rodents, similar to human injuries. 24 We therefore used a quantitative R2* sequencing modality on MRI to evaluate tissue edema at 24 hpi, a time of peak edema. Even with only 1 infusion of IMP/vehicle at 2 hpi, there was attenuated volume of R2* hyperintensity in the IMP group at 24 hours ( Fig 6).…”

Effects of increased intracranial pressure on cerebrospinal fluid influx, cerebral vascular hemodynamic indexes, and cerebrospinal fluid lymphatic efflux

“…Three levels of IICP were investigated in this study: 1) mild IICP (5 mm Hg-10 mm Hg), 2) moderate IICP (10 mm Hg-20 mm Hg), and 3) severe IICP (20 mm Hg-30 mm Hg). The classification standard was based on a previous study, 37 which illustrated that ICP elevation to critical levels (i.e., >20 mm Hg) was clinically significant in human TBI and reflected severe TBI in experimental TBI. Sham group received the incision and thinned skull window preparation, and their ICP was recorded continuously in the same ways as the IICP groups.…”