scholarly journals Differential responses to increasing numbers of mild traumatic brain injury in a rodent closed‐head injury model

2019 ◽  
Vol 149 (5) ◽  
pp. 660-678 ◽  
Author(s):  
Brooke Fehily ◽  
Carole A. Bartlett ◽  
Stephen Lydiard ◽  
Michael Archer ◽  
Hannah Milbourn ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Mild Traumatic Brain Injury ◽  
Closed Head Injury ◽  
Injury Model ◽  
Closed Head ◽  
Differential Responses

scholarly journals Identification of Serum MicroRNA Signatures for Diagnosis of Mild Traumatic Brain Injury in a Closed Head Injury Model

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112019 ◽  
Author(s):  
Anuj Sharma ◽  
Raghavendar Chandran ◽  
Erin S. Barry ◽  
Manish Bhomia ◽  
Mary Anne Hutchison ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Mild Traumatic Brain Injury ◽  
Closed Head Injury ◽  
Serum Microrna ◽  
Injury Model ◽  
Closed Head

scholarly journals A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats

2019 ◽  
Vol 36 (11) ◽  
pp. 1683-1706 ◽  
Author(s):  
Colleen N. Bodnar ◽  
Kelly N. Roberts ◽  
Emma K. Higgins ◽  
Adam D. Bachstetter
Keyword(s):  
Systematic Review ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Mild Traumatic Brain Injury ◽  
Closed Head Injury ◽  
Closed Head ◽  
Injury Models

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.

scholarly journals Clinical Concerns in Counseling Clients with Traumatic Brain Injury

2019 ◽  
pp. 1-7
Author(s):  
Michael F. Shaughnessy ◽  
Aaron Johnson ◽  
Lela Rucker
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Closed Head Injury ◽  
Closed Head ◽  
Areas Of Concern ◽  
Counseling Clients ◽  
Goals And Objectives

Counseling clients who have experienced an open or closed head injury can be quite problematic and present challenges in different realms. This paper explores some of these disparate realms and offers some insights as to counseling strategies that may need to be explored and examined. Realistic goals and objectives are needed and attention to specific areas of concern are examined.

scholarly journals Multifactorial and closed head impact traumatic brain injuries cause distinct tactile hypersensitivity profiles

2020 ◽  
Author(s):  
A-S. Wattiez ◽  
W.C. Castonguay ◽  
O.J. Gaul ◽  
J.S. Waite ◽  
C.M. Schmidt ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Brain Injuries ◽  
Closed Head Injury ◽  
Sensory Profile ◽  
Nitric Oxide Donor ◽  
Relative Risks ◽  
Closed Head ◽  
Post Traumatic

AbstractChronic complications of traumatic brain injury (TBI) represent one of the greatest financial burdens and sources of suffering in society today. A substantial number of these patients suffer from post-traumatic headache (PTH), which is typically associated with tactile allodynia. Unfortunately, this phenomenon has been under-studied, in large part due to the lack of well-characterized laboratory animal models. We have addressed this gap in the field by characterizing the tactile sensory profile of two non-penetrating models of PTH. We show that multifactorial TBI, consisting of aspects of impact, acceleration/deceleration, and blast wave exposure, produces long term tactile hypersensitivity and central sensitization, phenotypes reminiscent of PTH in patients, in both cephalic and extracephalic regions. By contrast, closed head injury induces only transient cephalic tactile hypersensitivity, with no extracephalic consequences. Both models show more severe phenotype with repetitive daily injury for three days, compared to either one or three successive injuries in a single day, providing new insight into patterns of injury that may place patients at greater risk of developing PTH. Importantly, even after recovery from transient cephalic tactile hypersensitivity, mice subjected to closed head injury had persistent hypersensitivity to established migraine triggers, including calcitonin gene-related peptide (CGRP) and sodium nitroprusside, a nitric oxide donor. Our results offer new tools for studying PTH, as well as preclinical support for a pathophysiologic role of CGRP in this condition.SummaryTwo models of post-traumatic headache after traumatic brain injury provide novel laboratory tools and insights in relative risks of injury and therapeutic opportunities.

scholarly journals Elevated Intracranial IL-18 in Humans and Mice after Traumatic Brain Injury and Evidence of Neuroprotective Effects of IL-18—Binding Protein after Experimental Closed Head Injury

2002 ◽  
Vol 22 (8) ◽  
pp. 971-978 ◽  
Author(s):  
Ido Yatsiv ◽  
Maria C. Morganti-Kossmann ◽  
Daniel Perez ◽  
Charles A. Dinarello ◽  
Daniela Novick ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Binding Protein ◽  
Closed Head Injury ◽  
Specific Inhibitor ◽  
Published Data ◽  
Sham Operation ◽  
Neuroprotective Effects ◽  
Closed Head

Proinflammatory cytokines are important mediators of neuroinflammation after traumatic brain injury. The role of interleukin (IL)-18, a new member of the IL-1 family, in brain trauma has not been reported to date. The authors investigated the posttraumatic release of IL-18 in murine brains following experimental closed head injury (CHI) and in CSF of CHI patients. In the mouse model, intracerebral IL-18 was induced within 24 hours by ether anesthesia and sham operation. Significantly elevated levels of IL-18 were detected at 7 days after CHI and in human CSF up to 10 days after trauma. Published data imply that IL-18 may play a pathophysiological role in inflammatory CNS diseases; therefore its inhibition may ameliorate outcome after CHI. To evaluate the functional aspects of IL-18 in the injured brain, mice were injected systemically with IL-18–binding protein (IL-18BP), a specific inhibitor of IL-18, 1 hour after trauma. IL-18BP—treated mice showed a significantly improved neurological recovery by 7 days, accompanied by attenuated intracerebral IL-18 levels. This demonstrates that inhibition of IL-18 is associated with improved recovery. However, brain edema at 24 hours was not influenced by IL-18BP, suggesting that inflammatory mediators other than IL-18 induce the early detrimental effects of intracerebral inflammation.

scholarly journals The Ras Inhibitor S-Trans, Trans-Farnesylthiosalicylic Acid Exerts Long-Lasting Neuroprotection in a Mouse Closed Head Injury Model

2003 ◽  
Vol 23 (6) ◽  
pp. 728-738 ◽  
Author(s):  
Esther Shohami ◽  
Ido Yatsiv ◽  
Alexander Alexandrovich ◽  
Roni Haklai ◽  
Galit Elad-Sfadia ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Protein A ◽  
Closed Head Injury ◽  
Fold Increase ◽  
Lesion Size ◽  
Mk 801 ◽  
Neurologic Deficits ◽  
Closed Head

Traumatic brain injury activates N-methyl-D-aspartate receptors (NMDAR) inducing activation of the Ras protein (a key regulator of cell growth, survival, and death) and its effectors. Thus, trauma-induced increase in active Ras-GTP might contribute to traumatic brain injury pathology. Based on this hypothesis, a new concept of neuroprotection is proposed, examined here by investigating the effect of the Ras inhibitor S- trans, trans-farnesylthiosalicylic acid (FTS) in a mouse model of closed head injury (CHI). Mice subjected to CHI were treated systemically 1 h later with FTS (5 mg/kg) or vehicle. After 1 h, Ras-GTP in the contused hemisphere showed a significant (3.8-fold) increase, which was strongly inhibited by FTS (82% inhibition) or by the NMDA-receptor antagonist MK-801 (53%). Both drugs also decreased active (phosphorylated) extracellular signal-regulated kinase. FTS prevented the CHI-induced reduction in NMDAR binding in cortical, striatal, and hippocampal regions, measured by [3H]-MK-801 autoradiography, and decreased lesion size by 50%. It also reduced CHI-induced neurologic deficits, indicated by the highly significant ( P < 0.0001) 60% increase in extent of recovery. Thus, FTS provided long-term neuroprotection after CHI, rescuing NMDAR binding in the contused hemisphere and profoundly reducing neurologic deficits. These findings suggest that nontoxic Ras inhibitors such as FTS may qualify as neuroprotective drugs.

scholarly journals The Chemokine Fractalkine in Patients with Severe Traumatic Brain Injury and a Mouse Model of Closed Head Injury

2004 ◽  
Vol 24 (10) ◽  
pp. 1110-1118 ◽  
Author(s):  
Mario Rancan ◽  
Nicole Bye ◽  
Vivianne I. Otto ◽  
Otmar Trentz ◽  
Thomas Kossmann ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Closed Head Injury ◽  
Serum Levels ◽  
Barrier Dysfunction ◽  
Normal Ranges ◽  
Low Concentrations ◽  
Closed Head ◽  
Key Factor

The potential role of the chemokine Fractalkine (CX3CL1) in the pathophysiology of traumatic brain injury (TBI) was investigated in patients with head trauma and in mice after experimental cortical contusion. In control individuals, soluble (s)Fractalkine was present at low concentrations in cerebrospinal fluid (CSF) (12.6 to 57.3 pg/mL) but at much higher levels in serum (21,288 to 74,548 pg/mL). Elevation of sFractalkine in CSF of TBI patients was observed during the whole study period (means: 29.92 to 535.33 pg/mL), whereas serum levels remained within normal ranges (means: 3,100 to 59,159 pg/mL). Based on these differences, a possible passage of sFractalkine from blood to CSF was supported by the strong correlation between blood–brain barrier dysfunction (according to the CSF-/serum-albumin quotient) and sFractalkine concentrations in CSF (R = 0.706; P < 0.01). In the brain of mice subjected to closed head injury, neither Fractalkine protein nor mRNA were found to be augmented; however, Fractalkine receptor (CX3CR1) mRNA steadily increased peaking at 1 week postinjury ( P < 0.05, one-way analysis of variance). This possibly implies the receptor to be the key factor determining the action of constitutively expressed Fractalkine. Altogether, these data suggest that the Fractalkine-CX3CR1 protein system may be involved in the inflammatory response to TBI, particularly for the accumulation of leukocytes in the injured parenchyma.

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.

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