scholarly journals Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury

2015 ◽  
pp. 1147-1160 ◽  
Author(s):  
Aric F. Logsdon ◽  
Brandon P. Lucke-Wold ◽  
Ryan C. Turner ◽  
Jason D. Huber ◽  
Charles L. Rosen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage

The Challenge of Mild Traumatic Brain Injury: Role of Biochemical Markers in Diagnosis of Brain Damage

2013 ◽  
Vol 34 (3) ◽  
pp. 503-531 ◽  
Author(s):  
Stefania Mondello ◽  
Kara Schmid ◽  
Rachel P. Berger ◽  
Firas Kobeissy ◽  
Domenico Italiano ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Mild Traumatic Brain Injury ◽  
Biochemical Markers

The Role of Neuroimaging in Assessing Neuropsychological Deficits following Traumatic Brain Injury

2011 ◽  
Vol 39 (4) ◽  
pp. 537-566 ◽  
Author(s):  
Benjamin J. Hayempour ◽  
Susan E. Rushing ◽  
Abass Alavi
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Brain Injuries ◽  
Neuropsychological Deficits ◽  
Prognostic Information ◽  
Specific Identification ◽  
Secondary Damage ◽  
Neuroimaging Techniques

Neuroimaging enables highly accurate and specific identification of treatable brain injuries for the purposes of preventing secondary damage as well as providing useful prognostic information. This article addresses the range of currently employed neuroimaging techniques and their utility in assessing legal claims involving the presence of brain damage.

Role of Vasopressin V1a and V2 Receptors for the Development of Secondary Brain Damage after Traumatic Brain Injury in Mice

2008 ◽  
Vol 25 (12) ◽  
pp. 1459-1465 ◽  
Author(s):  
Raimund Trabold ◽  
Sandro Krieg ◽  
Karsten Schöller ◽  
Nikolaus Plesnila
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Secondary Brain Damage

scholarly journals The Role of Bradykinin B1 and B2 Receptors for Secondary Brain Damage after Traumatic Brain Injury in Mice

2009 ◽  
Vol 30 (1) ◽  
pp. 130-139 ◽  
Author(s):  
Raimund Trabold ◽  
Christian Erös ◽  
Klaus Zweckberger ◽  
Jane Relton ◽  
Heike Beck ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcome ◽  
Brain Edema ◽  
Brain Damage ◽  
Secondary Brain Damage ◽  
Edema Formation ◽  
Receptor Mrna ◽  
B2 Receptors

Inflammatory mechanisms are known to contribute to the pathophysiology of traumatic brain injury (TBI). Since bradykinin is one of the first mediators activated during inflammation, we investigated the role of bradykinin and its receptors in posttraumatic secondary brain damage. We subjected wild-type (WT), B1-, and B2-receptor-knockout mice to controlled cortical impact (CCI) and analyzed tissue bradykinin as well as kinin receptor mRNA and protein expression up to 48 h thereafter. Brain edema, contusion volume, and functional outcome were assessed 24 h and 7 days after CCI. Tissue bradykinin was maximally increased 2 h after trauma ( P<0.01 versus sham). Kinin B1 receptor mRNA was upregulated up to four-fold 24 h after CCI. Immunohistochemistry showed that B1 and B2 receptors were expressed in the brain and were significantly upregulated in the traumatic penumbra 1 to 24 h after CCI. B2R−/− mice had significantly less brain edema (−51% versus WT, 24 h; P<0.001), smaller contusion volumes (∼50% versus WT 24 h and 7 d after CCI; P<0.05), and better functional outcome 7 days after TBI as compared with WT mice ( P<0.05). The present results show that bradykinin and its B2 receptors play a causal role for brain edema formation and cell death after TBI.

scholarly journals Angiotensin Receptor Type 1 Inhibition in Lymphopenia and in Neutropenia After Traumatic Brain Injury In Mice: a Randomized Controlled Study (ATLANTIS)

2021 ◽  
Author(s):  
Ralph Timaru-Kast ◽  
Shila P. Coronel-Castello ◽  
Tobias Krämer ◽  
André V. Hugonnet ◽  
Michael K.E. Schäfer ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Receptor Type ◽  
Wild Type ◽  
Secondary Brain Damage ◽  
Neutrophil Depletion ◽  
Cerebral Inflammation

Abstract Background: Cerebral inflammation with invasion of neutrophils and lymphocytes is an important factor in the process of secondary brain damage expansion after traumatic brain injury (TBI). Depletion of neutrophils in mice has been shown to reduce neurologic impairment after TBI. The intrinsic cerebral renin-angiotensin system is an important mediator of cerebral inflammation, as inhibition of the angiotensin II receptor type 1 (AT1) with candesartan improves neurologic recovery, and reduces secondary brain damage and cerebral neutrophil invasion after TBI. The present study was therefore designed to determine the role of immune cells in AT1 inhibition-mediated neuroprotection after TBI. Methods: In study A we assessed the effect of neutrophil depletion in mice after TBI. In study B we investigated the impact of RAG1 deficiency (RAG1-/-; mice without mature B- and T-lymphocytes) after TBI. In study C we investigated the role of neutrophils in candesartan mediated protection after TBI in wild-type mice with and without neutrophil depletion. In study D we examined the role of lymphocytes in AT1 inhibition mediated neuroprotection after TBI in RAG1-/-.Results: Neutropenic and RAG1-/- mice showed reduced brain damage compared to control groups. In control antibody treated wild type mice AT1 inhibition reduced lesion volumes and inflammation compared to vehicle, while in neutropenic mice, candesartan had no effect. In RAG1-/- mice AT1 inhibition resulted in reduction of brain damage and neuroinflammation compared to vehicle group. Conclusion: The present results demonstrate, that reduction of neutrophils and of lymphocytes as well as AT1 inhibition in wild type and RAG1-/- mice reduce brain damage and inflammation after TBI. However, AT1 inhibition was neuroprotective in RAG1-/- mice, but not in neutropenic mice. Therefore, the results indicate that AT1 inhibition mediated neuroprotection may be exerted by anti-inflammatory effects on neutrophils, with a subsequent reduction of neutrophil invasion.

scholarly journals Role of Cortical Spreading Depressions for Secondary Brain Damage after Traumatic Brain Injury in Mice

2008 ◽  
Vol 28 (7) ◽  
pp. 1353-1360 ◽  
Author(s):  
Louisa von Baumgarten ◽  
Raimund Trabold ◽  
Serge Thal ◽  
Tobias Back ◽  
Nikolaus Plesnila
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Low Frequency ◽  
Lesion Size ◽  
Secondary Brain Damage ◽  
Ipsilateral Hemisphere ◽  
Temporary Decrease ◽  
Electroencephalogram Eeg

In recent years, several studies have unequivocally shown the occurrence of cortical spreading depressions (CSDs) after stroke and traumatic brain injury (TBI) in humans. The fundamental question, however, is whether CSDs cause or result from secondary brain damage. The aim of the current study was, therefore, to investigate the role of CSDs for secondary brain damage in an experimental model of TBI. C57/BL6 mice were traumatized by controlled cortical impact. Immediately after trauma, each animal showed one heterogeneous direct current (DC) potential shift accompanied by a profound depression of electroencephalogram (EEG) amplitude, and a temporary decrease of ipsi- and contralateral regional cerebral blood flow (rCBF) suggesting bilateral CSDs. Within the next 3 h after TBI, CSDs occurred at a low frequency (0.38 CSD/h per animal, n = 7) and were accompanied by rCBF changes confined to the ipsilateral hemisphere. No significant relationship between the number of SDs and lesion size or intracranial pressure (ICP) could be detected. Even increasing the number of posttraumatic CSDs by application of KCl by more than six times did not increase ICP or contusion volume. We therefore conclude that CSDs may not contribute to posttraumatic secondary brain damage in the normally perfused and oxygenated brain.

THE ROLE OF CHEMOKINES AND ADHESION MOLECULES IN TRAUMATIC BRAIN INJURY: SELECTIVE EXPRESSION IN FOCAL VERSUSDIFFUSE BRAIN DAMAGE

Shock ◽  
2004 ◽  
Vol 21 (Supplement) ◽  
pp. 77
Author(s):  
M C Morganti-Kossmann ◽  
M Rancan ◽  
N Bye ◽  
P Nguyen ◽  
T Kossmann
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Adhesion Molecules ◽  
Brain Damage ◽  
Selective Expression

scholarly journals Role of Secondary Brain Damage Factors in Activation of VascularPlatelet Hemostasis in Traumatic Brain Injury

2016 ◽  
Vol 12 (5) ◽  
pp. 42-51 ◽  
Author(s):  
G. A. Boyarinov ◽  
L. V. Boyarinova ◽  
A. V. Deryugina ◽  
O. D. Solov'eva ◽  
R. R. Zaytsev ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Secondary Brain Damage

scholarly journals Role of CCL2 (MCP-1) in Traumatic Brain Injury (TBI): Evidence from Severe TBI Patients and CCL2−/− Mice

2009 ◽  
Vol 30 (4) ◽  
pp. 769-782 ◽  
Author(s):  
Bridgette D Semple ◽  
Nicole Bye ◽  
Mario Rancan ◽  
Jenna M Ziebell ◽  
M Cristina Morganti-Kossmann
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Closed Head Injury ◽  
Lesion Volume ◽  
Cellular Mechanisms ◽  
Cytokine Network ◽  
Secondary Brain Damage ◽  
Severe Tbi

Cerebral inflammation involves molecular cascades contributing to progressive damage after traumatic brain injury (TBI). The chemokine CC ligand-2 (CCL2) (formerly monocyte chemoattractant protein-1, MCP-1) is implicated in macrophage recruitment into damaged parenchyma after TBI. This study analyzed the presence of CCL2 in human TBI, and further investigated the role of CCL2 in physiological and cellular mechanisms of secondary brain damage after TBI. Sustained elevation of CCL2 was detected in the cerebrospinal fluid (CSF) of severe TBI patients for 10 days after trauma, and in cortical homogenates of C57Bl/6 mice, peaking at 4 to 12 h after closed head injury (CHI). Neurological outcome, lesion volume, macrophage/microglia infiltration, astrogliosis, and the cerebral cytokine network were thus examined in CCL2-deficient (−/−) mice subjected to CHI. We found that CCL2−/− mice showed altered production of multiple cytokines acutely (2 to 24 h); however, this did not affect lesion size or cell death within the first week after CHI. In contrast, by 2 and 4 weeks, a delayed reduction in lesion volume, macrophage accumulation, and astrogliosis were observed in the injured cortex and ipsilateral thalamus of CCL2−/− mice, corresponding to improved functional recovery as compared with wild-type mice after CHI. Our findings confirm the significant role of CCL2 in mediating post-traumatic secondary brain damage.

Sign in / Sign up

Export Citation Format

Share Document