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 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 Hypertonic Saline Compared to Mannitol for the Management of Elevated Intracranial Pressure in Traumatic Brain Injury: A Meta-Analysis

2022 ◽  
Vol 8 ◽  
Author(s):  
Chengchen Han ◽  
Fan Yang ◽  
Shengli Guo ◽  
Jianning Zhang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Hypertonic Saline ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Meta Analysis ◽  
Elevated Intracranial Pressure ◽  
Lower Treatment

Background: We performed a meta-analysis to evaluate the effect of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury.Methods: A systematic literature search up to July 2021 was performed and 17 studies included 1,392 subjects with traumatic brain injury at the start of the study; 708 of them were administered hypertonic saline and 684 were given mannitol. They were reporting relationships between the effects of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury. We calculated the odds ratio (OR) and mean difference (MD) with 95% confidence intervals (CIs) to assess the effect of hypertonic saline compared to mannitol for the management of elevated intracranial pressure in traumatic brain injury using the dichotomous or continuous method with a random or fixed-effect model.Results: Hypertonic saline had significantly lower treatment failure (OR, 0.38; 95% CI, 0.15–0.98, p = 0.04), lower intracranial pressure 30–60 mins after infusion termination (MD, −1.12; 95% CI, −2.11 to −0.12, p = 0.03), and higher cerebral perfusion pressure 30–60 mins after infusion termination (MD, 5.25; 95% CI, 3.59–6.91, p < 0.001) compared to mannitol in subjects with traumatic brain injury.However, hypertonic saline had no significant effect on favorable outcome (OR, 1.61; 95% CI, 1.01–2.58, p = 0.05), mortality (OR, 0.59; 95% CI, 0.34–1.02, p = 0.06), intracranial pressure 90–120 mins after infusion termination (MD, −0.90; 95% CI, −3.21–1.41, p = 0.45), cerebral perfusion pressure 90–120 mins after infusion termination (MD, 4.28; 95% CI, −0.16–8.72, p = 0.06), and duration of elevated intracranial pressure per day (MD, 2.20; 95% CI, −5.44–1.05, p = 0.18) compared to mannitol in subjects with traumatic brain injury.Conclusions: Hypertonic saline had significantly lower treatment failure, lower intracranial pressure 30–60 mins after infusion termination, and higher cerebral perfusion pressure 30–60 mins after infusion termination compared to mannitol in subjects with traumatic brain injury. However, hypertonic saline had no significant effect on the favorable outcome, mortality, intracranial pressure 90–120 mins after infusion termination, cerebral perfusion pressure 90–120 mins after infusion termination, and duration of elevated intracranial pressure per day compared to mannitol in subjects with traumatic brain injury. Further studies are required to validate these findings.

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

Trauma: Traumatic Brain Injury

2018 ◽  
pp. 95-100
Author(s):  
Ruchir Gupta
Keyword(s):  
Traumatic Brain Injury ◽  
Substance Abuse ◽  
Acute Respiratory Distress Syndrome ◽  
Cervical Spine ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Glasgow Coma Scale ◽  
Elevated Intracranial Pressure ◽  
Intraoperative Management ◽  
History Of

In this chapter the essential aspects of anesthesia for traumatic brain injury are discussed. Subtopics include manifestations and treatment of elevated intracranial pressure (ICP), Glasgow Coma Scale (GCS), drugs used to lower ICP, and patient monitoring. The case presented is an emergent craniotomy. The chapter is divided into preoperative, intraoperative, and postoperative sections with important subtopics related to the main topic in each section. Preoperative topics discussed are evaluation of trauma, use of the GCS in this case, assessing intracranial hypertension, history of substance abuse, and clearing the cervical spine. Issues related to intraoperative management in this case include induction and use of blood products. Postoperative concerns addressed include polyuria and acute respiratory distress syndrome.

Mesenchymal stem cell therapy for the treatment of traumatic brain injury: progress and prospects

2019 ◽  
Vol 30 (8) ◽  
pp. 839-855 ◽  
Author(s):  
Mahasweta Das ◽  
Karthick Mayilsamy ◽  
Shyam S. Mohapatra ◽  
Subhra Mohapatra
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Neuronal Loss ◽  
Tumor Formation ◽  
Functional Improvement ◽  
Preclinical Research ◽  
Mortality And Morbidity ◽  
Mesenchymal Stem Cell Therapy ◽  
Beneficial Effects

Abstract Traumatic brain injury (TBI) is a major cause of injury-related mortality and morbidity in the USA and around the world. The survivors may suffer from cognitive and memory deficits, vision and hearing loss, movement disorders, and different psychological problems. The primary insult causes neuronal damage and activates astrocytes and microglia which evokes immune responses causing further damage to the brain. Clinical trials of drugs to recover the neuronal loss are not very successful. Regenerative approaches for TBI using mesenchymal stem cells (MSCs) seem promising. Results of preclinical research have shown that transplantation of MSCs reduced secondary neurodegeneration and neuroinflammation, promoted neurogenesis and angiogenesis, and improved functional outcome in the experimental animals. The functional improvement is not necessarily related to cell engraftment; rather, immunomodulation by molecular factors secreted by MSCs is responsible for the beneficial effects of this therapy. However, MSC therapy has a few drawbacks including tumor formation, which can be avoided by the use of MSC-derived exosomes. This review has focused on the research works published in the field of regenerative therapy using MSCs after TBI and its future direction.

Computed Tomographic Brain Density Measurement as a Predictor of Elevated Intracranial Pressure in Blunt Head Trauma

2007 ◽  
Vol 73 (10) ◽  
pp. 1023-1026 ◽  
Author(s):  
Kenji Inaba ◽  
Pedro G.R. Teixeira ◽  
Jean-Stephane David ◽  
Carlos Brown ◽  
Ali Salim ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Injury Severity ◽  
Density Measurement ◽  
Elevated Intracranial Pressure ◽  
Icp Monitoring ◽  
Brain Ct ◽  
Blunt Head Trauma ◽  
Brain Density

There are no independent computed tomography (CT) findings predictive of elevated intracranial pressure (ICP). The purpose of this study was to evaluate brain density measurement on CT as a predictor of elevated ICP or decreased cerebral perfusion pressure (CPP). A prospectively collected database of patients with acute traumatic brain injury was used to identify patients who had a brain CT followed within 2 hours by ICP measurement. Blinded reviewers measured mean density in Hounsfield Units (HU) within a 100-mm2 elliptical region at four standardized positions. Brain density measurement was compared for patients with an ICP of 20 or greater versus less than 20 mm Hg and CPP of 70 or greater versus less than 70 mm Hg. During a 2-year period, 47 patients had ICP monitoring after brain CT. Average age was 40 ± 18 years old; 93.6 per cent were male; mean Injury Severity Score was 25 ± 10; and Glasgow Coma Scale was 6 ± 4. There was no difference in brain density measurement for observer 1, ICP less than 20 (26.3 HU) versus ICP 20 or greater (27.4 HU, P = 0.545) or for CPP less than 70 (27.1 HU) versus CPP 70 or greater (26.2, P = 0.624). Similarly, there was no difference for observer 2, ICP less than 20 (26.8 HU) versus ICP 20 or greater (27.4, P = 0.753) and CPP less than 70 (27.6 HU) versus CPP 70 or greater (26.2, P = 0.436). CT-measured brain density does not correlate with elevated ICP or depressed CPP and cannot predict patients with traumatic brain injury who would benefit from invasive ICP monitoring.

Long-term outcomes and prognostic factors in pediatric patients with severe traumatic brain injury and elevated intracranial pressure

2008 ◽  
Vol 2 (4) ◽  
pp. 240-249 ◽  
Author(s):  
Jay Jagannathan ◽  
David O. Okonkwo ◽  
Hian Kwang Yeoh ◽  
Aaron S. Dumont ◽  
Dwight Saulle ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Pediatric Patients ◽  
Elevated Intracranial Pressure ◽  
The Mean

Object The management strategies and outcomes in pediatric patients with elevated intracranial pressure (ICP) following severe traumatic brain injury (TBI) are examined in this study. Methods This study was a retrospective review of a prospectively acquired pediatric trauma database. More than 750 pediatric patients with brain injury were seen over a 10-year period. Records were retrospectively reviewed to determine interventions for correcting ICP, and surviving patients were contacted prospectively to determine functional status and quality of life. Only patients with 2 years of follow-up were included in the study. Results Ninety-six pediatric patients (age range 3–18 years) were identified with a Glasgow Coma Scale score < 8 and elevated ICP > 20 mm Hg on presentation. The mean injury severity score was 65 (range 30–100). All patients were treated using a standardized head injury protocol. The mean time course until peak ICP was 69 hours postinjury (range 2–196 hours). Intracranial pressure control was achieved in 82 patients (85%). Methods employed to achieve ICP control included maximal medical therapy (sedation, hyperosmolar therapy, and paralysis) in 34 patients (35%), ventriculostomy in 23 patients (24%), and surgery in 39 patients (41%). Fourteen patients (15%) had refractory ICP despite all interventions, and all of these patients died. Seventy-two patients (75%) were discharged from the hospital, whereas 24 (25%) died during hospitalization. Univariate and multivariate analysis revealed that the presence of vascular injury, refractory ICP, and cisternal effacement at presentation had the highest correlation with subsequent death (p < 0.05). Mean follow-up was 53 months (range 11–126 months). Three patients died during the follow-up period (2 due to infections and 1 committed suicide). The mean 2-year Glasgow Outcome Scale score was 4 (median 4, range 1–5). The mean patient competency rating at follow-up was 4.13 out of 5 (median 4.5, range 1–4.8). Univariate analysis revealed that the extent of intracranial and systemic injuries had the highest correlation with long-term quality of life (p < 0.05). Conclusions Controlling elevated ICP is an important factor in patient survival following severe pediatric TBI. The modality used for ICP control appears to be less important. Long-term follow-up is essential to determine neurocognitive sequelae associated with TBI.

Sign in / Sign up

Export Citation Format

Share Document