scholarly journals Defining Ischemic Burden after Traumatic Brain Injury Using 15O PET Imaging of Cerebral Physiology

2004 ◽  
Vol 24 (2) ◽  
pp. 191-201 ◽  
Author(s):  
Jonathan P Coles ◽  
Tim D Fryer ◽  
Peter Smielewski ◽  
Kenneth Rice ◽  
John C Clark ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Brain Injury ◽  
Head Injury ◽  
A Priori ◽  
Oxygen Metabolism ◽  
Oxygen Extraction Fraction ◽  
Statistical Accuracy ◽  
Positron Emission ◽  
Cerebral Physiology

Whereas postmortem ischemic damage is common in head injury, antemortem demonstration of ischemia has proven to be elusive. Although 15O positron emission tomography may be useful in this area, the technique has traditionally analyzed data within regions of interest (ROIs) to improve statistical accuracy. In head injury, such techniques are limited because of the lack of a priori knowledge regarding the location of ischemia, coexistence of hyperaemia, and difficulty in defining ischemic cerebral blood flow (CBF) and cerebral oxygen metabolism (CMRO2) levels. We report a novel method for defining disease pathophysiology following head injury. Voxel-based approaches are used to define the distribution of oxygen extraction fraction (OEF) across the entire brain; the standard deviation of this distribution provides a measure of the variability of OEF. These data are also used to integrate voxels above a threshold OEF value to produce an ROI based upon coherent physiology rather than spatial contiguity (the ischemic brain volume; IBV). However, such approaches may suffer from poor statistical accuracy, particularly in regions with low blood flow. The magnitude of these errors has been assessed in modeling experiments using the Hoffman brain phantom and modified control datasets. We conclude that this technique is a valid and useful tool for quantifying ischemic burden after traumatic brain injury.

scholarly journals Incidence and Mechanisms of Cerebral Ischemia in Early Clinical Head Injury

2004 ◽  
Vol 24 (2) ◽  
pp. 202-211 ◽  
Author(s):  
Jonathan P. Coles ◽  
Tim D. Fryer ◽  
Piotr Smielewski ◽  
Doris A. Chatfield ◽  
Luzius A. Steiner ◽  
...  
Keyword(s):  
Head Injury ◽  
Oxygen Metabolism ◽  
Jugular Bulb ◽  
Emission Tomography ◽  
Oxygen Extraction Fraction ◽  
Ischemic Brain ◽  
Cerebral Oxygen Metabolism ◽  
Extraction Fraction ◽  
Positron Emission ◽  
The Brain

Antemortem demonstration of ischemia has proved elusive in head injury because regional CBF reductions may represent hypoperfusion appropriately coupled to hypometabolism. Fifteen patients underwent positron emission tomography within 24 hours of head injury to map cerebral blood flow (CBF), cerebral oxygen metabolism (CMRO2), and oxygen extraction fraction (OEF). We estimated the volume of ischemic brain (IBV) and used the standard deviation of the OEF distribution to estimate the efficiency of coupling between CBF and CMRO2. The IBV in patients was significantly higher than controls (67 ± 69 vs. 2 ± 3 mL; P < 0.01). The coexistence of relative ischemia and hyperemia in some patients implies mismatching of perfusion to oxygen use. Whereas the saturation of jugular bulb blood (SjO2) correlated with the IBV ( r = 0.8, P < 0.01), SjO2 values of 50% were only achieved at an IBV of 170 ± 63 mL (mean ± 95% CI), which equates to 13 ± 5% of the brain. Increases in IBV correlated with a poor Glasgow Outcome Score 6 months after injury (ρ = −0.6, P < 0.05). These results suggest significant ischemia within the first day after head injury. The ischemic burden represented by this “traumatic penumbra” is poorly detected by bedside clinical monitors and has significant associations with outcome.

scholarly journals Alterations in Cerebral Oxygen Metabolism after Traumatic Brain Injury in Children

2012 ◽  
Vol 33 (1) ◽  
pp. 48-52 ◽  
Author(s):  
Dustin K Ragan ◽  
Robert McKinstry ◽  
Tammie Benzinger ◽  
Jeffrey R Leonard ◽  
Jose A Pineda
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Mitochondrial Dysfunction ◽  
Oxygen Metabolism ◽  
Metabolic Dysfunction ◽  
Noninvasive Measurements ◽  
Metabolic Defects ◽  
Severe Tbi

Traumatic brain injury (TBI) is the most common cause of acquired disability in children. Metabolic defects, and in particular mitochondrial dysfunction, are important contributors to brain injury after TBI. Studies of metabolic dysfunction are limited, but magnetic resonance methods suitable for use in children are overcoming this limitation. We performed noninvasive measurements of cerebral blood flow and oxygen metabolic index (OMI) to assess metabolic dysfunction in children with severe TBI. Cerebral blood flow is variable after TBI but hypoperfusion and low OMI are predominant, supporting metabolic dysfunction. This finding is consistent with preclinical and adult clinical studies of brain metabolism and mitochondrial dysfunction after TBI.

scholarly journals Early Nonischemic Oxidative Metabolic Dysfunction Leads to Chronic Brain Atrophy in Traumatic Brain Injury

2009 ◽  
Vol 30 (4) ◽  
pp. 883-894 ◽  
Author(s):  
Yueqiao Xu ◽  
David L McArthur ◽  
Jeffry R Alger ◽  
Maria Etchepare ◽  
David A Hovda ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Metabolic Rate ◽  
Oxidative Metabolism ◽  
Brain Atrophy ◽  
Occipital Lobe ◽  
Oxygen Extraction Fraction ◽  
Metabolic Dysfunction ◽  
Cerebral Metabolic Rate ◽  
Positron Emission

Chronic brain atrophy after traumatic brain injury (TBI) is a well-known phenomenon, the causes of which are unknown. Early nonischemic reduction in oxidative metabolism is regionally associated with chronic brain atrophy after TBI. A total of 32 patients with moderate-to-severe TBI prospectively underwent positron emission tomography (PET) and volumetric magnetic resonance imaging (MRI) within the first week and at 6 months after injury. Regional lobar assessments comprised oxidative metabolism and glucose metabolism. Acute MRI showed a preponderance of hemorrhagic lesions with few irreversible ischemic lesions. Global and regional chronic brain atrophy occurred in all patients by 6 months, with the temporal and frontal lobes exhibiting the most atrophy compared with the occipital lobe. Global and regional reduction in cerebral metabolic rate of oxygen (CMRO2), cerebral blood flow (CBF), oxygen extraction fraction (OEF), and cerebral metabolic rate of glucose were observed. The extent of metabolic dysfunction was correlated with the total hemorrhage burden on initial MRI ( r=0.62, P=0.01). The extent of regional brain atrophy correlated best with CMRO2 and CBF. Lobar values of OEF were not in the ischemic range and did not correlate with chronic brain atrophy. Chronic brain atrophy is regionally specific and associated with regional reductions in oxidative brain metabolism in the absence of irreversible ischemia.

scholarly journals Association of Age and Sex With Multi-Modal Cerebral Physiology in Adult Moderate/Severe Traumatic Brain Injury: A Narrative Overview and Future Avenues for Personalized Approaches

2021 ◽  
Vol 12 ◽  
Author(s):  
C. Batson ◽  
A. Gomez ◽  
A. S. Sainbhi ◽  
L. Froese ◽  
F. A. Zeiler
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
High Frequency ◽  
Biological Sex ◽  
Severe Tbi ◽  
Cerebral Physiology ◽  
Age And Sex

The impact of age and biological sex on outcome in moderate/severe traumatic brain injury (TBI) has been documented in large cohort studies, with advanced age and male sex linked to worse long-term outcomes. However, the association between age/biological sex and high-frequency continuous multi-modal monitoring (MMM) cerebral physiology is unclear, with only sparing reference made in guidelines and major literature in moderate/severe TBI. In this narrative review, we summarize some of the largest studies associating various high-frequency MMM parameters with age and biological sex in moderate/severe TBI. To start, we present this by highlighting the representative available literature on high-frequency data from Intracranial Pressure (ICP), Cerebral Perfusion Pressure (CPP), Extracellular Brain Tissue Oxygenation (PbtO2), Regional Cerebral Oxygen Saturations (rSO2), Cerebral Blood Flow (CBF), Cerebral Blood Flow Velocity (CBFV), Cerebrovascular Reactivity (CVR), Cerebral Compensatory Reserve, common Cerebral Microdialysis (CMD) Analytes and their correlation to age and sex in moderate/severe TBI cohorts. Then we present current knowledge gaps in the literature, discuss biological implications of age and sex on cerebrovascular monitoring in TBI and some future avenues for bedside research into the cerebrovascular physiome after TBI.

scholarly journals Traumatic Brain Injury by a Closed Head Injury Device Induces Cerebral Blood Flow Changes and Microhemorrhages

2015 ◽  
Vol 5 ◽  
pp. 52 ◽  
Author(s):  
Srinivasu Kallakuri ◽  
Sharath Bandaru ◽  
Nisrine Zakaria ◽  
Yimin Shen ◽  
Zhifeng Kou ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Head Injury ◽  
Corpus Callosum ◽  
Closed Head Injury ◽  
Susceptibility Weighted Imaging ◽  
Closed Head ◽  
Flow Changes

Objectives: Traumatic brain injury is a poly-pathology characterized by changes in the cerebral blood flow, inflammation, diffuse axonal, cellular, and vascular injuries. However, studies related to understanding the temporal changes in the cerebral blood flow following traumatic brain injury extending to sub-acute periods are limited. In addition, knowledge related to microhemorrhages, such as their detection, localization, and temporal progression, is important in the evaluation of traumatic brain injury. Materials and Methods: Cerebral blood flow changes and microhemorrhages in male Sprague Dawley rats at 4 h, 24 h, 3 days, and 7 days were assessed following a closed head injury induced by the Marmarou impact acceleration device (2 m height, 450 g brass weight). Cerebral blood flow was measured by arterial spin labeling. Microhemorrhages were assessed by susceptibility-weighted imaging and Prussian blue histology. Results: Traumatic brain injury rats showed reduced regional and global cerebral blood flow at 4 h and 7 days post-injury. Injured rats showed hemorrhagic lesions in the cortex, corpus callosum, hippocampus, and brainstem in susceptibility-weighted imaging. Injured rats also showed Prussian blue reaction products in both the white and gray matter regions up to 7 days after the injury. These lesions were observed in various areas of the cortex, corpus callosum, hippocampus, thalamus, and midbrain. Conclusions: These results suggest that changes in cerebral blood flow and hemorrhagic lesions can persist for sub-acute periods after the initial traumatic insult in an animal model. In addition, microhemorrhages otherwise not seen by susceptibility-weighted imaging are present in diverse regions of the brain. The combination of altered cerebral blood flow and microhemorrhages can potentially be a source of secondary injury changes following traumatic brain injury and may need to be taken into consideration in the long-term care of these cases.

Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study

1997 ◽  
Vol 86 (2) ◽  
pp. 241-251 ◽  
Author(s):  
Marvin Bergsneider ◽  
David A. Hovda ◽  
Ehud Shalmon ◽  
Daniel F. Kelly ◽  
Paul M. Vespa ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Brain Injury ◽  
Head Injury ◽  
Fdg Pet ◽  
Emission Tomography ◽  
Content Type ◽  
Cerebral Metabolic Rate ◽  
Positron Emission ◽  
Fine Print

✓ Experimental traumatic brain injury studies have shown that cerebral hyperglycolysis is a pathophysiological response to injury-induced ionic and neurochemical cascades. This finding has important implications regarding cellular viability, vulnerability to secondary insults, and the functional capability of affected regions. Prior to this study, posttraumatic hyperglycolysis had not been detected in humans. The characteristics and incidence of cerebral hyperglycolysis were determined in 28 severely head injured patients using [18F]fluorodeoxyglucose—positron emission tomography (FDG-PET). The local cerebral metabolic rate of glucose (CMRG) was calculated using a standard compartmental model. In six of the 28 patients, the global cerebral metabolic rate of oxygen (CMRO2) was determined by the simultaneous measurements of arteriovenous differences of oxygen and cerebral blood flow (xenon-133). Hyperglycolysis, defined as an increase in glucose utilization that measures two standard deviations above expected levels, was documented in all six patients in whom both FDG-PET and CMRO2 determinations were made within 8 days of injury. Five additional patients were found to have localized areas of hyperglycolysis adjacent to focal mass lesions. Within the 1st week following the injury, 56% of patients studied had presumptive evidence of hyperglycolysis. The results of this study indicate that the metabolic state of the traumatically injured brain should be defined differentially in terms of glucose and oxygen metabolism. The use of FDG-PET demonstrates that hyperglycolysis occurs both regionally and globally following severe head injury in humans. The results of this clinical study directly complement those previously reported in experimental brain-injury studies, indicating the capability of imaging a fundamental component of cellular pathophysiology characteristic of head injury.

scholarly journals Prospective Analysis of Coagulopathy Associated with Isolated Traumatic Brain Injury and Clinical Outcome

2021 ◽  
Author(s):  
Gopal Krishna ◽  
Varun Aggarwal ◽  
Ishwar Singh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Clinical Outcome ◽  
Road Traffic ◽  
Statistical Significance ◽  
Platelet Counts ◽  
Coagulation Abnormalities ◽  
The Mean ◽  
D Dimer

Abstract Introduction Traumatic brain injury (TBI) affects the coagulation pathway in a distinct way than does extracranial trauma. The extent of coagulation abnormalities varies from bleeding diathesis to disseminated thrombosis. Design Prospective study. Methods The study included 50 patients of isolated TBI with cohorts of moderate (MHI) and severe head injury (SHI). Coagulopathy was graded according to the values of parameters in single laboratory. The incidence of coagulopathy according to the severity of TBI and correlation with disseminated intravascular coagulation (DIC) score, platelets, prothrombin time (PT), activated partial thromboplastin time (APTT), D-dimer, and fibrinogen was observed. The comparison was also made between expired and discharged patients within each group. It also compared coagulation derailments with clinical presentation (Glasgow Coma Scale [GCS]) and outcome (Glasgow Outcome Scale [GOS]). Results Road traffic accident was the primary (72%) mode of injury. Fifty-two percent had MHI and rest had SHI. Eighty-four percent of cases were managed conservatively. The mean GCS was 12.23 and 5.75 in MHI and SHI, respectively. Sixty-two percent of MHI and 96% of the patients with SHI had coagulation abnormalities. On statistical analysis, DIC score (p < 0.001) strongly correlated with the severity of head injury and GOS. PT and APTT were also significantly associated with the severity of TBI. In patients with moderate TBI, D-dimer and platelet counts showed association with clinical outcome. Fibrinogen levels did not show any statistical significance. The mean platelet counts remained normal in both the groups of TBI. The mean GOS was 1.54 and 4.62 in SHI and MHI, respectively. Conclusion Coagulopathy is common in isolated TBI. The basic laboratory parameters are reliable predictors of coagulation abnormalities in TBI. Coagulopathy is directly associated with the severity of TBI, GCS, and poor outcome.

scholarly journals Differential Leukocyte and Platelet Profiles in Distinct Models of Traumatic Brain Injury

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 500
Author(s):  
William Brad Hubbard ◽  
Meenakshi Banerjee ◽  
Hemendra Vekaria ◽  
Kanakanagavalli Shravani Prakhya ◽  
Smita Joshi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Closed Head Injury ◽  
Diffuse Brain Injury ◽  
Blood Brain ◽  
Closed Head ◽  
Leukocyte Counts ◽  
Neutrophil Aggregation ◽  
Blood Leukocyte

Traumatic brain injury (TBI) affects over 3 million individuals every year in the U.S. There is growing appreciation that TBI can produce systemic modifications, which are in part propagated through blood–brain barrier (BBB) dysfunction and blood–brain cell interactions. As such, platelets and leukocytes contribute to mechanisms of thromboinflammation after TBI. While these mechanisms have been investigated in experimental models of contusion brain injury, less is known regarding acute alterations following mild closed head injury. To investigate the role of platelet dynamics and bioenergetics after TBI, we employed two distinct, well-established models of TBI in mice: the controlled cortical impact (CCI) model of contusion brain injury and the closed head injury (CHI) model of mild diffuse brain injury. Hematology parameters, platelet-neutrophil aggregation, and platelet respirometry were assessed acutely after injury. CCI resulted in an early drop in blood leukocyte counts, while CHI increased blood leukocyte counts early after injury. Platelet-neutrophil aggregation was altered acutely after CCI compared to sham. Furthermore, platelet bioenergetic coupling efficiency was transiently reduced at 6 h and increased at 24 h post-CCI. After CHI, oxidative phosphorylation in intact platelets was reduced at 6 h and increased at 24 h compared to sham. Taken together, these data demonstrate that brain trauma initiates alterations in platelet-leukocyte dynamics and platelet metabolism, which may be time- and injury-dependent, providing evidence that platelets carry a peripheral signature of brain injury. The unique trend of platelet bioenergetics after two distinct types of TBI suggests the potential for utilization in prognosis.

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