Relationship between systemic glucose and cerebral glucose is preserved in patients with severe traumatic brain injury, but glucose delivery to the brain may become limited when oxidative metabolism is impaired

2012 ◽  
Vol 40 (6) ◽  
pp. 1785-1791 ◽  
Author(s):  
Sandra Magnoni ◽  
Cecilia Tedesco ◽  
Marco Carbonara ◽  
Mauro Pluderi ◽  
Angelo Colombo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Oxidative Metabolism ◽  
The Brain

scholarly journals Engineered glycomaterial implants orchestrate large-scale functional repair of brain tissue chronically after severe traumatic brain injury

2021 ◽  
Vol 7 (10) ◽  
pp. eabe0207
Author(s):  
Charles-Francois V. Latchoumane ◽  
Martha I. Betancur ◽  
Gregory A. Simchick ◽  
Min Kyoung Sun ◽  
Rameen Forghani ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Large Scale ◽  
Growth Factor Signaling ◽  
Neuronal Circuit ◽  
Reach To Grasp ◽  
Function Recovery ◽  
Cellular Repair ◽  
The Brain

Severe traumatic brain injury (sTBI) survivors experience permanent functional disabilities due to significant volume loss and the brain’s poor capacity to regenerate. Chondroitin sulfate glycosaminoglycans (CS-GAGs) are key regulators of growth factor signaling and neural stem cell homeostasis in the brain. However, the efficacy of engineered CS (eCS) matrices in mediating structural and functional recovery chronically after sTBI has not been investigated. We report that neurotrophic factor functionalized acellular eCS matrices implanted into the rat M1 region acutely after sTBI significantly enhanced cellular repair and gross motor function recovery when compared to controls 20 weeks after sTBI. Animals subjected to M2 region injuries followed by eCS matrix implantations demonstrated the significant recovery of “reach-to-grasp” function. This was attributed to enhanced volumetric vascularization, activity-regulated cytoskeleton (Arc) protein expression, and perilesional sensorimotor connectivity. These findings indicate that eCS matrices implanted acutely after sTBI can support complex cellular, vascular, and neuronal circuit repair chronically after sTBI.

Keep the Brain Cool—Endovascular Cooling in Patients With Severe Traumatic Brain Injury: A Case Series Study

Neurosurgery ◽  
2011 ◽  
Vol 68 (4) ◽  
pp. 867-873 ◽  
Author(s):  
Marlene Fischer ◽  
Peter Lackner ◽  
Ronny Beer ◽  
Raimund Helbok ◽  
Stephanie Klien ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Case Series ◽  
Brain Cool ◽  
Case Series Study ◽  
Endovascular Cooling ◽  
Series Study ◽  
The Brain

scholarly journals Decompressive Craniectomy for Elevated Intracranial Pressure and Its Effect on the Cumulative Ischemic Burden and Therapeutic Intensity Levels After Severe Traumatic Brain Injury

Neurosurgery ◽  
2010 ◽  
Vol 66 (6) ◽  
pp. 1111-1119 ◽  
Author(s):  
Gregory M. Weiner ◽  
Michelle R. Lacey ◽  
Larami Mackenzie ◽  
Darshak P. Shah ◽  
Suzanne G. Frangos ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Decompressive Craniectomy ◽  
Severe Traumatic Brain Injury ◽  
Intensity Level ◽  
Before And After ◽  
Severe Tbi ◽  
Therapeutic Intensity ◽  
The Brain

Abstract BACKGROUND Increased intracranial pressure (ICP) can cause brain ischemia and compromised brain oxygen (PbtO2 ≤ 20 mm Hg) after severe traumatic brain injury (TBI). OBJECTIVE We examined whether decompressive craniectomy (DC) to treat elevated ICP reduces the cumulative ischemic burden (CIB) of the brain and therapeutic intensity level (TIL). METHODS Ten severe TBI patients (mean age, 31.4 ± 14.2 years) who had continuous PbtO2 monitoring before and after delayed DC were retrospectively identified. Patients were managed according to the guidelines for the management of severe TBI. The CIB was measured as the total time spent between a PbtO2 of 15 to 20, 10 to 15, and 0 to 10 mm Hg. The TIL was calculated every 12 hours. Mixed-effects models were used to estimate changes associated with DC. RESULTS DC was performed on average 2.8 days after admission. DC was found to immediately reduce ICP (mean [SEM] decrease was 7.86 mm Hg [2.4 mm Hg]; P = .005). TIL, which was positively correlated with ICP (r = 0.46, P ≤ .001), was reduced within 12 hours after surgery and continued to improve within the postsurgical monitoring period (P ≤ .001). The duration and severity of CIB were significantly reduced as an effect of DC in this group. The overall mortality rate in the group of 10 patients was lower than predicted at the time of admission (P = .015). CONCLUSION These results suggest that a DC for increased ICP can reduce the CIB of the brain after severe TBI. We suggest that DC be considered early in a patient's clinical course, particularly when the TIL and ICP are increased.

scholarly journals Different Methods and Technical Considerations of Decompressive Craniectomy in the Treatment of Traumatic Brain Injury: A Review

2017 ◽  
Vol 06 (01) ◽  
pp. 036-040 ◽  
Author(s):  
Amit Ghosh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Decompressive Craniectomy ◽  
Severe Traumatic Brain Injury ◽  
Surgical Procedure ◽  
Surgical Decompression ◽  
Brain Swelling ◽  
The Brain ◽  
Technical Considerations

Decompressive craniectomy, which is performed worldwide for the treatment of severe traumatic brain injury (TBI), is a surgical procedure in which part of the skull is removed to allow the brain to swell without being squeezed. On 1901, Kocher was the first surgeon to promote surgical decompression in posttraumatic brain swelling. In this article, different methods of decompressive craniectomy and its technical considerations have been reviewed.

scholarly journals Correlation of Cerebral and Subcutaneous Glycerol in Severe Traumatic Brain Injury and Association with Tissue Damage

2021 ◽  
Author(s):  
Linda Hägglund ◽  
Magnus Olivecrona ◽  
Lars-Owe D. Koskinen
Keyword(s):  
Computed Tomography ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Injury Severity Score ◽  
Severe Traumatic Brain Injury ◽  
Tissue Damage ◽  
Injury Severity ◽  
Health Evaluation ◽  
Brain Tissue Damage ◽  
The Brain

Abstract Background This study is a substudy of a prospective consecutive double-blinded randomized study on the effect of prostacyclin in severe traumatic brain injury (sTBI). The aims of the present study were to investigate whether there was a correlation between brain and subcutaneous glycerol levels and whether the ratio of interstitial glycerol in the brain and subcutaneous tissue (glycerolbrain/sc) was associated with tissue damage in the brain, measured by using the Rotterdam score, S-100B, neuron-specific enolase (NSE), the Injury Severity Score (ISS), the Acute Physiology and Chronic Health Evaluation Score (APACHE II), and trauma type. A potential association with clinical outcome was explored. Methods Patients with sTBI aged 15–70 years presenting with a Glasgow Coma Scale Score ≤ 8 were included. Brain and subcutaneous adipose tissue glycerol levels were measured through microdialysis in 48 patients, of whom 42 had complete data for analysis. Brain tissue damage was also evaluated by using the Rotterdam classification of brain computed tomography scans and the biochemical biomarkers S-100B and NSE. Results In 60% of the patients, a positive relationship in glycerolbrain/sc was observed. Patients with a positive correlation of glycerolbrain/sc had slightly higher brain glycerol levels compared with the group with a negative correlation. There was no significant association between the computed tomography Rotterdam score and glycerolbrain/sc. S-100B and NSE were associated with the profile of glycerolbrain/sc. Our results cannot be explained by the general severity of the trauma as measured by using the Injury Severity Score or Acute Physiology and Chronic Health Evaluation Score. Conclusions We have shown that peripheral glycerol may flux into the brain. This effect is associated with worse brain tissue damage. This flux complicates the interpretation of brain interstitial glycerol levels. We remind the clinicians that a damaged blood–brain barrier, as seen in sTBI, may alter the concentrations of various substances, including glycerol in the brain. Awareness of this is important in the interpretation of the data bedside as well in research.

scholarly journals Pathophysiology of severe traumatic brain injury and management of intracranial hypertension

2019 ◽  
Vol 18 (2) ◽  
pp. 62-71
Author(s):  
Raimondas Juškys ◽  
Vaiva Hendrixson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Hypertension ◽  
Severe Traumatic Brain Injury ◽  
Current Treatment ◽  
Secondary Brain Injury ◽  
Management Options ◽  
Treatment Protocols ◽  
Improved Outcomes ◽  
The Brain

It is well recognized that severe traumatic brain injury causes major health and socioeconomic burdens for patients their families and society itself. Over the past decade, understanding of secondary brain injury processes has increased tremendously, permitting implementation of new neurocritical methods of care that substantially contribute to improved outcomes of such patients. The main objective of current treatment protocols is to optimize different physiological measurements that prevent secondary insults and reinforce the ability of the brain to heal. The aim of this literature review is to uncover the pathophysiological mechanisms of severe traumatic brain injury and their interrelationship, including cerebral metabolic crisis, disturbances of blood flow to the brain and development of edema, putting emphasis on intracranial hypertension and its current management options.

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