Neutralization of interleukin-1β reduces cerebral edema and tissue loss and improves late cognitive outcome following traumatic brain injury in mice

2011 ◽  
Vol 34 (1) ◽  
pp. 110-123 ◽  
Author(s):  
Fredrik Clausen ◽  
Anders Hånell ◽  
Charlotte Israelsson ◽  
Johanna Hedin ◽  
Ted Ebendal ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Edema ◽  
Cognitive Outcome ◽  
Interleukin 1Β ◽  
Tissue Loss

Blood Biomarkers Relate to Cognitive Performance Years after Traumatic Brain Injury in Service Members and Veterans

2020 ◽  
pp. 1-7
Author(s):  
Sara M. Lippa ◽  
Jessica Gill ◽  
Tracey A. Brickell ◽  
Louis M. French ◽  
Rael T. Lange
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Outcome ◽  
Service Members ◽  
Neurocognitive Performance ◽  
Blood Biomarkers ◽  
Post Injury ◽  
Blood Draw ◽  
Neurofilament Light ◽  
History Of

Abstract Objective: This study examines the relationship of serum total tau, neurofilament light (NFL), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), and glial fibrillary acidic protein (GFAP) with neurocognitive performance in service members and veterans with a history of traumatic brain injury (TBI). Method: Service members (n = 488) with a history of uncomplicated mild (n = 172), complicated mild, moderate, severe, or penetrating TBI (sTBI; n = 126), injured controls (n = 116), and non-injured controls (n = 74) prospectively enrolled from Military Treatment Facilities. Participants completed a blood draw and neuropsychological assessment a year or more post-injury. Six neuropsychological composite scores and presence/absence of mild neurocognitive disorder (MNCD) were evaluated. Within each group, stepwise hierarchical regression models were conducted. Results: Within the sTBI group, increased serum UCH-L1 was related to worse immediate memory and delayed memory (R2Δ = .065–.084, ps < .05) performance, while increased GFAP was related to worse perceptual reasoning (R2Δ = .030, p = .036). Unexpectedly, within injured controls, UCH-L1 and GFAP were inversely related to working memory (R2Δ = .052–.071, ps < .05), and NFL was related to executive functioning (R2Δ = .039, p = .021) and MNCD (Exp(B) = 1.119, p = .029). Conclusions: Results suggest GFAP and UCH-L1 could play a role in predicting poor cognitive outcome following complicated mild and more severe TBI. Further investigation of blood biomarkers and cognition is warranted.

Minocycline effects on cerebral edema: Relations with inflammatory and oxidative stress markers following traumatic brain injury in mice

2009 ◽  
Vol 1291 ◽  
pp. 122-132 ◽  
Author(s):  
Shadi Homsi ◽  
Fabiola Federico ◽  
Nicole Croci ◽  
Bruno Palmier ◽  
Michel Plotkine ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Edema ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
And Oxidative Stress

Hypothermia Attenuates the Normal Increase in Interleukin 1β RNA and Nerve Growth Factor Following Traumatic Brain Injury in the Rat

1995 ◽  
Vol 12 (2) ◽  
pp. 159-167 ◽  
Author(s):  
JAMES R. GOSS ◽  
SCOT D. STYREN ◽  
PETER D. MILLER ◽  
PATRICK M. KOCHANEK ◽  
ALAN M. PALMER ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Nerve Growth Factor ◽  
Brain Injury ◽  
Growth Factor ◽  
Interleukin 1Β ◽  
Nerve Growth ◽  
Normal Increase

Cognitive outcome in traumatic brain injury survivors

2005 ◽  
Vol 11 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Claire Helen Salmond ◽  
Barbara Jacquelyn Sahakian
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Outcome

Postural neurologic deficits after decompressive craniectomy: A case series of sinking skin flap syndrome in traumatic brain injury

2020 ◽  
pp. 1-10
Author(s):  
Emma A. Bateman ◽  
Jordan VanderEnde ◽  
Keith Sequeira ◽  
Heather M. MacKenzie
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rare Complication ◽  
Skin Flap ◽  
Case Series ◽  
Cognitive Outcome ◽  
Definitive Treatment ◽  
Care Providers ◽  
Neurologic Deficits ◽  
The Impact

BACKGROUND: Hemicraniectomy to manage raised intracranial pressure following traumatic brain injury (TBI) has improved survival but may increase the incidence of Sinking Skin Flap Syndrome (SSFS). SSFS is a clinical syndrome in which patients with craniectomy develop objective neurologic abnormalities due to the pressure of the atmosphere on the unprotected brain, often presenting with postural headaches and neurologic deficits that localize to the craniectomy site. Previously thought to be a rare complication of craniectomy after TBI, evidence suggests SSFS is under-recognized. OBJECTIVE: To describe the clinical and radiographic features leading to diagnosis and the impact of temporizing and definitive management of SSFS on outcomes in inpatients with moderate/severe TBI. METHODS: Two patients’ symptoms, qualitative behaviour observation, physical and cognitive outcome measures, and neuroimaging pre- and post-temporizing measures and cranioplasty are presented. RESULTS: Both patients demonstrated partial improvements with temporizing measures and substantial improvements in functional, cognitive, physical, and rehabilitation outcomes from the cranioplasty and resolution of SSFS. CONCLUSIONS: Rehabilitation care providers are critical to the timely diagnosis and management of SSFS, including the use of temporizing measures and advocacy for definitive treatment with cranioplasty. These cases highlight the diverse clinical presentations and importance of SSFS diagnosis to improve patient outcomes.

scholarly journals Activation of P2X7 Promotes Cerebral Edema and Neurological Injury after Traumatic Brain Injury in Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e41229 ◽  
Author(s):  
Donald E. Kimbler ◽  
Jessica Shields ◽  
Nathan Yanasak ◽  
John R. Vender ◽  
Krishnan M. Dhandapani
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Edema ◽  
Neurological Injury

scholarly journals Steroids for delayed cerebral edema after traumatic brain injury

2021 ◽  
Vol 12 ◽  
pp. 46
Author(s):  
G. Lakshmi Prasad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Head Injuries ◽  
Experimental Studies ◽  
Symptomatic Improvement ◽  
High Dose ◽  
The Mean ◽  
Key Aspects

Background: Brain edema is a common phenomenon after traumatic brain injury (TBI) resulting in increased intracranial pressure and subsequent neurological deterioration. Experimental studies have proven that brain edema is biphasic (cytotoxic followed by vasogenic). Till date, all studies, including the corticosteroid randomization after significant head injury (HI) trial, have used high-dose steroids in the acute period during which the edema is essentially cytotoxic in nature. No clinical data exist pertaining to delayed cerebral edema (vasogenic) and steroids. Methods: Patients who had received steroids for delayed cerebral edema after TBI were retrospectively analyzed over a 2-year period. Steroid dose, timing of steroid prescription, time to improvement of symptoms, and complications were noted. Results: There were six males and three females. Mean age was 41.1 years. There were no severe HI cases. All subjects had cerebral contusions on imaging. Dexamethasone was the preferred steroid starting with 12 mg/day and tapered in 5–7 days. The mean interval to steroid administration after trauma was 7 days. The mean duration of steroid prescription was 6.3 days. All patients had complete symptomatic improvement. The mean time to symptom resolution was 3.8 days. No patients experienced any complications pertinent to steroid usage. Conclusion: This is the first study to document efficacy of steroids for delayed cerebral edema after TBI, at least in mild/moderate head injuries. The timing of steroid usage and dose of steroids is key aspects that might determine its efficacy in TBI which was the drawbacks of the previous studies. Future prospective trials with the above factors in consideration may confirm/refute above findings.

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