scholarly journals Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-αContents and by Stimulating Newly Formed Neurogenesis

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Chong-Un Cheong ◽  
Ching-Ping Chang ◽  
Chien-Ming Chao ◽  
Bor-Chih Cheng ◽  
Chung-Zhing Yang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Quantitative Determination ◽  
Enzyme Immunoassay ◽  
Immunofluorescence Staining ◽  
Motor Deficits ◽  
Etanercept Therapy ◽  
Cerebral Contusion ◽  
Brain Tissues

It remains unclear whether etanercept penetrates directly into the contused brain and improves the outcomes of TBI by attenuating brain contents of TNF-αand/or stimulating newly formed neurogenesis. Rats that sustained TBI are immediately treated with etanercept. Acute neurological and motor injury is assessed in all rats the day prior to and 7 days after surgery. The numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain injury that occurred during TBI were counted by immunofluorescence staining. Enzyme immunoassay for quantitative determination of TNF-αor etanercept in brain tissues is also performed. Seven days after systemic administration of etanercept, levels of etanercept can be detected in the contused brain tissues. In addition, neurological and motor deficits, cerebral contusion, and increased brain TNF-αcontents caused by TBI can be attenuated by etanercept therapy. Furthermore, the increased numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain tissues caused by TBI can be potentiated by etanercept therapy. These findings indicate that systemically administered etanercept may penetrate directly into the contused brain tissues and may improve outcomes of TBI by reducing brain contents of TNF-αand by stimulating newly formed neurogenesis.

scholarly journals Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jinn-Rung Kuo ◽  
Chong-Jeh Lo ◽  
Ching-Ping Chang ◽  
Mao- Tsun Lin ◽  
Chung-Ching Chio
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Oxidative Damage ◽  
Jugular Vein ◽  
External Jugular Vein ◽  
Motor Deficits ◽  
Sham Operation ◽  
Brain Cooling ◽  
Cerebral Contusion ◽  
Oxide Synthase

The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.

scholarly journals Determination of calorie and protein intake among acute and sub-acute traumatic brain injury patients

2020 ◽  
Vol 23 (5) ◽  
pp. 290-294
Author(s):  
Mohd Ibrahim Abdullah ◽  
Aryati Ahmad ◽  
Sharifah Wajihah Wafa Syed Saadun Tarek Wafa ◽  
Ahmad Zubaidi Abdul Latif ◽  
Noor Aini Mohd Yusoff ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protein Intake ◽  
Acute Traumatic Brain Injury

N-methyl-D-aspartate preconditioning improves short-term motor deficits outcome after mild traumatic brain injury in mice

2009 ◽  
pp. n/a-n/a ◽  
Author(s):  
Tayana Costa ◽  
Leandra C. Constantino ◽  
Bruna P. Mendonça ◽  
Josimar G. Pereira ◽  
Bruno Herculano ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Motor Deficits ◽  
Short Term

Traumatic brain injury: classification of initial severity and determination of functional outcome

2003 ◽  
Vol 25 (1) ◽  
pp. 9-18 ◽  
Author(s):  
B. Van Baalen ◽  
E. Odding ◽  
A. I. R. Maas ◽  
G. M. Ribbers ◽  
M. P. Bergen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcome ◽  
Initial Severity ◽  
Injury Classification

Reversible monoparesis following decompressive hemicraniectomy for traumatic brain injury

2008 ◽  
Vol 109 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Shirley I. Stiver ◽  
Max Wintermark ◽  
Geoffrey T. Manley
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebrospinal Fluid ◽  
Brain Injury ◽  
Motor Function ◽  
Ct Perfusion ◽  
Motor Deficits ◽  
Decompressive Hemicraniectomy ◽  
Number Of Patients ◽  
Motor Strength

Object The “syndrome of the trephined” is an uncommon and poorly understood disorder of delayed neurological deficit following craniectomy. From the authors' extensive experience with decompressive hemicraniectomy for traumatic brain injury (TBI), they have encountered a number of patients who developed delayed motor deficits, also called “motor trephine syndrome,” and reversal of the weakness following cranioplasty repair. The authors set out to study motor function systematically in this patient population to define the incidence, contributing factors, and outcome of patients with motor trephine syndrome. Methods The authors evaluated patient demographics, injury characteristics, detailed motor examinations, and CT scans in 38 patients with long-term follow-up after decompressive hemicraniectomy for TBI. Results Ten patients (26%) experienced delayed contralateral upper-extremity weakness, beginning 4.9 ± 0.4 months (mean ± standard error) after decompressive hemicraniectomy. Motor deficits improved markedly within 72 hours of cranioplasty repair, and all patients recovered full motor function. The CT perfusion scans, performed in 2 patients, demonstrated improvements in cerebral blood flow commensurate with resolution of cerebrospinal fluid flow disturbances on CT scanning and return of motor strength. Comparisons between 10 patients with and 20 patients (53%) without delayed motor deficits identified 3 factors—ipsilateral contusions, abnormal cerebrospinal fluid circulation, and longer intervals to cranioplasty repair—to be strongly associated with delayed, reversible monoparesis following decompressive hemicraniectomy. Conclusions Delayed, reversible monoparesis, also called motor trephine syndrome, is common following decompressive hemicraniectomy for TBI. The results of this study suggest that close follow-up of motor strength with early cranioplasty repair may prevent delayed motor complications of decompressive hemicraniectomy.

Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury*

2012 ◽  
Vol 40 (8) ◽  
pp. 2456-2463 ◽  
Author(s):  
Marcel J. H. Aries ◽  
Marek Czosnyka ◽  
Karol P. Budohoski ◽  
Luzius A. Steiner ◽  
Andrea Lavinio ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Optimal Cerebral Perfusion Pressure ◽  
Continuous Determination

Neuroimaging Patterns Associated with Motor Control in Traumatic Brain Injury

2006 ◽  
Vol 20 (1) ◽  
pp. 14-23 ◽  
Author(s):  
M. Lotze ◽  
W. Grodd ◽  
F. A. Rodden ◽  
E. Gut ◽  
P. W. Schönle ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Premotor Cortex ◽  
Blood Oxygenation ◽  
Motor Deficits ◽  
Healthy Controls ◽  
Cross Sectional ◽  
Fmri Signal ◽  
Signal Change ◽  
Motor Areas

Objective. To determine if patients with traumatic brain injury (TBI) and motor deficits show differences in functional activation maps during repetitive hand movements relative to healthy controls. Are there predictors for motor outcome in the functional maps of these patients? Methods. In an exploratory cross-sectional study, functional magnetic resonance imaging (fMRI) was used to study the blood-oxygenation-level-dependent (BOLD) response in cortical motor areas of 34 patients suffering from moderate motor deficits after TBI as they performed unilateral fist-clenching motions. Twelve of these patients with unilateral motor deficits were studied 3 months after TBI and a 2nd time approximately 4 months later. Results. Compared to age-matched, healthy controls performing the same task, TBI patients showed diminished fMRI-signal change in the primary sensorimotor cortex contralateral to the moving hand (cSM1), the contralateral dorsal premotor cortex, and bilaterally in the supplementary motor areas (SMAs). Clinical impairment and the magnitude of the fMRI-signal change in cSM1 and SMA were negatively correlated. Patients with poor and good motor recovery showed comparable motor impairment at baseline. Only patients who evolved to “poor clinical outcome” had decreased fMRI-signal change in the cSM1 during baseline. Conclusions. These observations raise the hypothesis that the magnitude of the fMRI-signal change in the cSM1 region could have prognostic value in the evaluation of patients with TBI.

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