scholarly journals Increased Intracranial Pressure after Diffuse Traumatic Brain Injury Exacerbates Neuronal Somatic Membrane Poration but not Axonal Injury: Evidence for Primary Intracranial Pressure-Induced Neuronal Perturbation

2012 ◽  
Vol 32 (10) ◽  
pp. 1919-1932 ◽  
Author(s):  
Audrey D Lafrenaye ◽  
Melissa J McGinn ◽  
John T Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Neuronal Damage ◽  
Axonal Injury ◽  
Somatic Membrane ◽  
Increased Intracranial Pressure ◽  
Baseline Levels ◽  
Membrane Poration

Increased intracranial pressure (ICP) associated with traumatic brain injury (TBI) is linked to increased morbidity. Although our understanding of the pathobiology of TBI has expanded, questions remain regarding the specific neuronal somatic and axonal damaging consequences of elevated ICP, independent of its impact on cerebral perfusion pressure (CPP). To investigate this, Fischer rats were subjected to moderate TBI. Measurements of ICP revealed two distinct responses to injury. One population exhibited transient increases in ICP that returned to baseline levels acutely, while the other displayed persistent ICP elevation (>20 mm Hg). Utilizing these populations, the effect of elevated ICP on neuronal pathology associated with diffuse TBI was analyzed at 6 hours after TBI. No difference in axonal injury was observed, however, rats exhibiting persistently elevated ICP postinjury revealed a doubling of neurons with chronic membrane poration compared with rats exhibiting only transient increases in ICP. Elevated postinjury ICP was not associated with a concurrent increase in DNA damage; however, traditional histological assessments did reveal increased neuronal damage, potentially associated with redistribution of cathepsin-B from the lysosomal compartment into the cytosol. These findings indicate that persistently increased ICP, without deleterious alteration of CPP, exacerbates neuronal plasmalemmal perturbation that could precipitate persistent neuronal impairment and ultimate neuronal death.

scholarly journals Moderately Elevated Intracranial Pressure after Diffuse Traumatic Brain Injury is Associated with Exacerbated Neuronal Pathology and Behavioral Morbidity in the Rat

2014 ◽  
Vol 34 (10) ◽  
pp. 1628-1636 ◽  
Author(s):  
Audrey D Lafrenaye ◽  
Thomas E Krahe ◽  
John T Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Neuronal Damage ◽  
Neuronal Loss ◽  
Global Ischemia ◽  
Neuronal Membrane ◽  
Elevated Intracranial Pressure ◽  
Membrane Perturbation

Traumatic brain injury (TBI)-induced elevated intracranial pressure (ICP) is correlated with ensuing morbidity/mortality in humans. This relationship is assumed to rely mostly on the recognition that extremely elevated ICP either indicates hematoma/contusions capable of precipitating herniation or alters cerebral perfusion pressure (CPP), which precipitates global ischemia. However, whether subischemic levels of elevated ICP without hematoma/contusion contribute to increased morbidity/mortality remains unknown. To address this knowledge gap, we utilized a model of moderate diffuse TBI in rats followed by either intraventricular ICP monitoring or manual ICP elevation to 20 mm Hg, in which CPP was above ischemic levels. The effects of ICP elevation after TBI on acute and chronic histopathology, as well as on behavioral morbidity, were evaluated. ICP elevation after TBI resulted in increased acute neuronal membrane perturbation and was also associated with reduced neuronal density at 4 weeks after injury. Somatosensory hypersensitivity was exacerbated by ICP elevation and was correlated to the observed neuronal loss. In conclusion, this study indicates that morbidity and increased neuronal damage/death associated with elevated ICP can occur without concurrent global ischemia. Therefore, understanding the pathologies associated with subischemic levels of elevated ICP could lead to the development of better therapeutic strategies for the treatment and management of TBI patients.

scholarly journals Brain Temperature Influences Intracranial Pressure and Cerebral Perfusion Pressure After Traumatic Brain Injury: A CENTER TBI Study

2020 ◽  
Author(s):  
Tatiana Birg ◽  
Fabrizio Ortolano ◽  
Eveline J.A. Wiegers ◽  
Peter Smielewski ◽  
Yan Savchenko ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Brain Temperature ◽  
Mixed Effects ◽  
Wilcoxon Test ◽  
Brain Physiology

Abstract BackgroundAfter Traumatic Brain Injury (TBI) fever is frequent. Brain temperature, which is directly linked to body temperature, may influence brain physiology. Increased body and/or brain temperature may cause secondary brain damage, with deleterious effects on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and outcome. MethodsCENTER-TBI, a prospective, multicenter, longitudinal study on TBI in Europe and Israel, includes a high resolution (HR) cohort of patients with data sampled at high-frequency (from 100 Hz to 500 Hz). In this study, simultaneous BT, ICP and CPP recordings were investigated. A mixed effects linear model was used to examine the association between different BT levels and ICP. We additionally focused on changes of ICP and CPP during the episodes of BT changes (delta BT ≥0.5 °C, lasting from 15 minutes to 3 hours) up or down-wards. The significance of ICP and CPP variations was estimated with the paired samples Wilcoxon test. Results Twenty-one patients with 2435 hours of simultaneous BT and ICP monitoring were studied. All patients reached a BT of 38° and experienced at least one episode of ICP above 20 mmHg. The linear mixed effects model revealed an association between BT above 37.5°C and higher ICP levels that was not confirmed for lower BT. We identified 149 episodes of BT changes. During BT elevations (n=79) ICP increased while CPP was reduced; opposite ICP and CPP variations occurred during episodes of BT reduction (n=70). All these changes were of moderate clinical relevance, even if statistically significant (p<0.0001). It has to be noted, however, that a number of therapeutic interventions against intracranial hypertension was documented during those episodes.ConclusionPatients after TBI usually develop BT> 38° soon after the injury. Brain temperature may influence brain physiology, as reflected by ICP and CPP. An association between BT exceeding 37.5°C and a higher ICP was identified. The relationship between BT, ICP and CPP become clearer during rapid temperature changes.Trial registration: The core study was registered with ClinicalTrials.gov, number NCT02210221, registered on July 29, 2014

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