Association of Baseline Body Weight with Neurological Deficits, Histology, and Death after Repetitive Closed Head Traumatic Brain Injury in the Mouse

2021 ◽  
Author(s):  
Aydan Kahriman ◽  
James Bouley ◽  
Daryl A. Bosco ◽  
Nils Henninger
Keyword(s):  
Traumatic Brain Injury ◽  
Body Weight ◽  
Brain Injury ◽  
Neurological Deficits ◽  
Baseline Body Weight ◽  
Closed Head

Possible protective effect of endogenous opioids in traumatic brain injury

1990 ◽  
Vol 72 (2) ◽  
pp. 252-261 ◽  
Author(s):  
Ronald L. Hayes ◽  
Bruce G. Lyeth ◽  
Larry W. Jenkins ◽  
Richard Zimmerman ◽  
Tracy K. McIntosh ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Body Weight ◽  
Brain Injury ◽  
Endogenous Opioids ◽  
Neurological Deficits ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Drug Treatments

✓ Naloxone (0.1, 1.0, or 20.0 mg/kg), morphine (1.0 or 10.0 mg/kg), or saline was administered systemically intraperitoneally to rats 15 minutes prior to moderate fluid-percussion brain injury. The effects of the drugs were measured on systemic physiological, neurological, and body-weight responses to injury. The animals were trained prior to injury and were assessed for 10 days after injury on body-weight responses and neurological endpoints. Low doses of naloxone (0.1 or 1.0 mg/kg) significantly exacerbated neurological deficits associated with injury. Morphine (10.0 mg/kg) significantly reduced neurological deficits associated with injury. The drugs had no effect on neurological measures or body weight in sham-injured animals. Drug treatments did not significantly alter systemic physiological responses to injury. Data from these experiments suggest the involvement of endogenous opioids in at least some components of neurological deficits following traumatic brain injury and suggest the possibility that at least some classes of endogenous opioids may protect against long-term neurological deficits produced by fluid-percussion injury to the rat.

SURVEY IN SERUM ADH CONCENTRATION IN TRAUMATIC BRAIN INJURY PATIENTS

2014 ◽  
pp. 83-89
Author(s):  
Dung Ngo ◽  
Thi Nhan Nguyen ◽  
Khanh Hoang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Osmotic Pressure ◽  
Negative Correlation ◽  
Closed Head Injury ◽  
Serum Levels ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Plasma Sodium Concentration ◽  
Closed Head

Objective: Study on 106 patients with closed head injury, assessment of serum ADH concentration, correlation with Glasgow score, sodium and plasma osmotic pressure. Patients and methods: Patients with closed head injuries were diagnosed determined by computerized tomography, admitted to the Hue Central Hospital 72 hours ago. Results: (i) Serum concentration of ADH 42.21 ± 47.80 pg/ml. (ii) There is a negative correlation between serum levels of ADH with: (1) Glasgow point r = -0.323, p <0.01; (2) Plasma sodium concentration r = - 0.211, p > 0.05; (3) Plasma osmotic pressure r = - 0.218, p> 0.05. Conclusion: There is a negative correlation between serum levels of ADH with Glasgow scale, plasma sodium concentration and osmotic pressure in plasma. Key words: ADH traumatic brain injury.

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.

Sidestream Smoke Affects Dendritic Complexity and Astrocytes After Model Mild Closed Head Traumatic Brain Injury

2021 ◽  
Author(s):  
Whitney A. Ratliff ◽  
Jessica N. Saykally ◽  
Kristen L. Keeley ◽  
David C. Driscoll ◽  
Kathleen E. Murray ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sidestream Smoke ◽  
Closed Head ◽  
Dendritic Complexity

scholarly journals Rhein Protects Against Neurological Deficits After Traumatic Brain Injury in Mice via Inhibiting Neuronal Pyroptosis

2020 ◽  
Vol 11 ◽  
Author(s):  
Fangfang Bi ◽  
Huaifen Ma ◽  
Chen Ji ◽  
Cuicui Chang ◽  
Wenbo Liu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Deficits
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