SURVEY IN SERUM ADH CONCENTRATION IN TRAUMATIC BRAIN INJURY PATIENTS

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.

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

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/01.wcb.0000133470.91843.72 ◽

2004 ◽

Vol 24 (10) ◽

pp. 1110-1118 ◽

Cited By ~ 36

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.

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Differences between open and closed head injury: evaluation of weight-drop model in experimental traumatic brain injury

Intrinsic Activity ◽

10.25006/ia.5.s2-a2.22 ◽

2017 ◽

Vol 5 (Suppl. 2) ◽

pp. A2.22

Author(s):

Einars Kupats

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Head Injury ◽

Closed Head Injury ◽

Closed Head ◽

Weight Drop ◽

Experimental Traumatic Brain Injury

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Differential Leukocyte and Platelet Profiles in Distinct Models of Traumatic Brain Injury

Cells ◽

10.3390/cells10030500 ◽

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.

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The closed head injury with the hematoma formation of stroke: the analysis of the clinical case

East European Journal of Neurology ◽

10.33444/2411-5797.2015.5(5).15-19 ◽

2015 ◽

pp. 15-19

Author(s):

N. K. Svyrydova ◽

N. O. Kravchuk ◽

N. l. Ingula ◽

S. O. Lishnevskyi ◽

A. S. Bondarenko ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Clinical Case ◽

Closed Head Injury ◽

World Health ◽

Hematoma Formation ◽

The World ◽

Closed Head ◽

Causes Of Mortality ◽

Health Organization

According to the World Health Organization (WHO) annually in the world traumatic brain injury (TBI) are about 10 million people, of whom 1.5 million die (9.0% of all causes of mortality), and another 2.4 million are disabled. The incidence of TBI is 1,8-5,4 per 100 thousand population, according to WHO, every year it increases by 2%. In Ukraine there is a TBI each year almost 100-200 thousand. Victims, about 1 million. Establish disability due to TBI. In 50-90% of patients after brain injury neurological symptoms persist or new emerging neurological syndromes that cause disability in 45% of them. Every year in Ukraine die from TBI 10-11 thousand citizens, in accordance mortality of 2.4 cases per 10 thousand population (USA- 1.8-2.2 per 10,000 per year).

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Sodium-Based Osmotherapy in Continuous Renal Replacement Therapy: a Mathematical Approach

Kidney360 ◽

10.34067/kid.0000382019 ◽

2020 ◽

Vol 1 (4) ◽

pp. 281-291 ◽

Cited By ~ 2

Author(s):

Jerry Yee ◽

Naushaba Mohiuddin ◽

Tudor Gradinariu ◽

Junior Uduman ◽

Stanley Frinak

Keyword(s):

Brain Injury ◽

Sodium Concentration ◽

Plasma Sodium ◽

Hypotonic Stress ◽

End Stage Liver Disease ◽

Vulnerable Patients ◽

Plasma Sodium Concentration ◽

Strategic Solution ◽

End Stage ◽

Rapid Correction

Cerebral edema, in a variety of circumstances, may be accompanied by states of hyponatremia. The threat of brain injury from hypotonic stress-induced astrocyte demyelination is more common when vulnerable patients with hyponatremia who have end stage liver disease, traumatic brain injury, heart failure, or other conditions undergo overly rapid correction of hyponatremia. These scenarios, in the context of declining urinary output from CKD and/or AKI, may require controlled elevations of plasma tonicity vis-à-vis increases of the plasma sodium concentration. We offer a strategic solution to this problem via sodium-based osmotherapy applied through a conventional continuous RRT modality: predilution continuous venovenous hemofiltration.

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Clinical Concerns in Counseling Clients with Traumatic Brain Injury

Journal of Advances in Medicine and Medical Research ◽

10.9734/jammr/2019/v29i130047 ◽

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.

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

10.1101/2020.06.01.127944 ◽

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.

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