scholarly journals The functional indexes of RBCs and microcirculation in the traumatic brain injury with the action of 2-ethil-6-methil-3-hydroxypiridin succinate

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
V. Polozova Anastasia ◽  
A. Boyarinov Gennadii ◽  
O. Nikolsky Viktor ◽  
V. Zolotova Marina ◽  
V. Deryugina Anna

Abstract Research aim To study the RBCs functional and metabolic parameters and the microcirculatory brain structure at traumatic brain injury (TBI) under the action of 2-ethyl-6-methyl-3-hydroxypyridine succinate. Methods A closed TBI was modeled by the free fall of a load on the parietooccipital regions of head. We made studies of the influence of 2-ethil-6-methil-3-hydroxipiridin succinate on aggregation and electrophoretic mobility of RBCs, catalase activity, malonic dialdehyde concentration, adenosine triphosphate and 2.3-biphosphoglycerate (2.3 – BPG) concentrations in RBCs. The state of parenchyma and microcirculatory brain mainstream in post-traumatic period of TBI have been studied on micro-preparations. Results The use of 2-ethyl-6-methyl-3-hydroxypyridine succinate under conditions of head injury leads to a decrease in MDA concentration and in aggregation of RBCs, to an increase in the 2.3—BPG concentration and RBC electrophoretic mobility compared to the control (group value). The most pronounced changes under the action of 2-ethyl-6-methyl-3-hydroxypyridine succinate were observed 3–7 days after the TBI. Significant indicators of the restoration of the microvasculature and brain tissue provoked by the use of 2-ethyl-6-methyl-3-hydroxypyridine succinate of were evident from the 7th day unlike the control group, where the restoration of structural morphological parameters was observed only on the 12th day of the post-traumatic period. Fast recovery of blood flow under the action of 2-ethyl-6-methyl-3-hydroxypyridine succinate ensured effective restoration of neurons and glia in comparison with the control group. Conclusions Early and long-term cytoprotective correction intensifies the oxygen transport function of the blood, prevents and / or reduces disorders of microvessels, neurons and glia in the post-traumatic period, thereby provides correction of hypoxic state and drives to the restoration of brain tissues homeostasis.

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Marc Fakhoury ◽  
Zaynab Shakkour ◽  
Firas Kobeissy ◽  
Nada Lawand

Abstract Traumatic brain injury (TBI) represents a major health concern affecting the neuropsychological health; TBI is accompanied by drastic long-term adverse complications that can influence many aspects of the life of affected individuals. A substantial number of studies have shown that mood disorders, particularly depression, are the most frequent complications encountered in individuals with TBI. Post-traumatic depression (P-TD) is present in approximately 30% of individuals with TBI, with the majority of individuals experiencing symptoms of depression during the first year following head injury. To date, the mechanisms of P-TD are far from being fully understood, and effective treatments that completely halt this condition are still lacking. The aim of this review is to outline the current state of knowledge on the prevalence and risk factors of P-TD, to discuss the accompanying brain changes at the anatomical, molecular and functional levels, and to discuss current approaches used for the treatment of P-TD.


2020 ◽  
pp. 1-12
Author(s):  
Cindy Santiago-Castañeda ◽  
Marysol Segovia-Oropeza ◽  
Luis Concha ◽  
Sandra Adela Orozco-Suárez ◽  
Luisa Rocha

Background: Severe traumatic brain injury (TBI), an important risk factor for Alzheimer’s disease, induces long-term hippocampal damage and hyperexcitability. On the other hand, studies support that propylparaben (PPB) induces hippocampal neuroprotection in neurodegenerative diseases. Objective: Experiments were designed to evaluate the effects of subchronic treatment with PPB on TBI-induced changes in the hippocampus of rats. Methods: Severe TBI was induced using the lateral fluid percussion model. Subsequently, rats received subchronic administration with PPB (178 mg/kg, TBI+PPB) or vehicle (TBI+PEG) daily for 5 days. The following changes were examined during the experimental procedure: sensorimotor dysfunction, changes in hippocampal excitability, as well as neuronal damage and volume. Results: TBI+PEG group showed sensorimotor dysfunction (p <  0.001), hyperexcitability (64.2%, p <  0.001), and low neuronal preservation ipsi- and contralateral to the trauma. Magnetic resonance imaging (MRI) analysis revealed lower volume (17.2%; p <  0.01) and great damage to the ipsilateral hippocampus. TBI+PPB group showed sensorimotor dysfunction that was partially reversed 30 days after trauma. This group showed hippocampal excitability and neuronal preservation similar to the control group. However, MRI analysis revealed lower hippocampal volume (p <  0.05) when compared with the control group. Conclusion: The present study confirms that post-TBI subchronic administration with PPB reduces the long-term consequences of trauma in the hippocampus. Implications of PPB as a neuroprotective strategy to prevent the development of Alzheimer’s disease as consequence of TBI are discussed.


2020 ◽  
Author(s):  
Xiangyi Yin ◽  
Jie Wu ◽  
Lihui Zhou ◽  
Chunyan Ni ◽  
Minyan Xiao ◽  
...  

Abstract Background: Tracheostomy is very common in patients with severe traumatic brain injury (TBI), and long-term nursing care are needed for those patients. We aimed to evaluate the effects of hospital-community-home (HCH) nursing in those patients. Methods: Tracheostomy patients with severe TBI needing long-term care were included. All patients underwent two months long follow-up. Glasgow coma score (GCS), Karnofsky, Self-Anxiety Scale (SAS) (SAS) and Barthel assessment at the discharge and two months after discharge were evaluated. The tracheostomy related complications were recorded and compared.Results: A total of 60 patients were included. There weren’t significant differences between two groups in the GCS, Karnofsky, SAS and Barthel index at discharge((all p>0.05), the GCS, Karnofsky and Barthel index was all significantly increased after two months follow-up for two groups (all p<0.05), and the GCS, Karnofsky and Barthel index at two months follow-up in HCH group was significantly higher than that of control group(all p<0.05), but the SAS at two months follow-up in HCH group was significantly less than that of control group(p=0.009). The incidence of block of artificial tracheal cannula and readmission in HCH group were significant less than that of control group (all p<0.05).Conclusion: HCH nursing care is feasible in tracheostomy patients with severe TBI, future studies are needed to further evaluate the role of HCH nursing care.


2020 ◽  
Vol 15 ◽  
pp. 263310552096890
Author(s):  
Son T Ton ◽  
Natalie S Adamczyk ◽  
Jack P Gerling ◽  
Ian C Vaagenes ◽  
Joanna Y Wu ◽  
...  

Background: Traumatic brain injury is a significant public health issue that results in serious disability in survivors. Traumatic brain injury patients are often intoxicated with alcohol when admitted to the hospital; however, it is not clear how acute intoxication affects recovery from a traumatic brain injury. Our group has previously shown that binge alcohol prior to traumatic brain injury resulted in long-term impairment in a fine sensorimotor task that was correlated with a decreased proliferative and neuroblast response from the subventricular zone. However, whether binge alcohol prior to traumatic brain injury affects the proliferative response in the hippocampal dentate gyrus is not yet known. Methods: Male rats underwent binge alcohol (3 g/kg/day) by gastric gavage for 3 days prior to traumatic brain injury. Cell proliferation was labeled by BrdU injections following traumatic brain injury. Stereological quantification and immunofluorescence confocal analysis of BrdU+ cells in the hippocampal dorsal dentate gyrus was performed at 24 hours, 1 week and 6 weeks post traumatic brain injury. Results: We found that either traumatic brain injury alone or binge alcohol alone significantly increased dentate gyrus proliferation at 24 hours and 1 week. However, a combined binge alcohol and traumatic brain injury regimen resulted in decreased dentate gyrus proliferation at 24 hours post-traumatic brain injury. At the 6 week time point, binge alcohol overall reduced the number of BrdU+ cells. Furthermore, more BrdU+ cells were found in the dentate hilar region of alcohol traumatic brain injury compared to vehicle traumatic brain injury groups. The location and double-labeling of these mismigrated BrdU+ cells was consistent with hilar ectopic granule cells. Conclusion: The results from this study showed that pre-traumatic brain injury binge alcohol impacts the injury-induced proliferative response in the dentate gyrus in the short-term and may affect the distribution of newly generated cells in the dentate gyrus in the long-term.


2005 ◽  
Vol 6 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Christine A. Bracy ◽  
Jacinta M. Douglas

AbstractThis study was undertaken to establish empirically whether couples in which the husband has sustained a severe traumatic brain injury (TBI) differed significantly, with respect to perceptions of husbands' interpersonal communication skills, from control couples in which the husband had sustained a traumatic orthopaedic injury (ORTHO) without injury to the brain. Fifty married couples (25 TBI dyads and 25 ORTHO dyads) were interviewed and completed a questionnaire for the study. Analysis of variance and planned comparisons were used to examine between- and within-group differences. TBI dyads were significantly different to control dyads with respect to perceptions of husbands' communication abilities. Both husbands and wives in long-term TBI dyads reported husbands to experience continuing interpersonal communication difficulties. As a group, TBI husbands self-reported significantly more communication difficulties than did ORTHO husbands. TBI wives and ORTHO wives also produced significantly different perceptions of their husbands' communication abilities. TBI wives perceived their husbands to have a number of interpersonal communication difficulties, while control group wives reported their husbands to be competent communicators.


2019 ◽  
Vol 7 (3) ◽  
pp. 47 ◽  
Author(s):  
Michael Oberholzer ◽  
René M. Müri

Traumatic brain injury (TBI) and its potential long-term consequences are of major concern for public health. Neurorehabilitation of affected individuals has some specific characteristics in contrast to neurorehabilitation of patients with acquired brain lesions of other aetiology. This review will deal with the clinical consequences of the distinct lesions of TBI. In severe TBI, clinical course often follows a typical initial sequence of coma; followed by disturbed consciousness; later, post-traumatic agitation and amnesia; and finally, recovery of function occurs. In the different phases of neurorehabilitation, physicians should be aware of typical medical complications such as paroxysmal sympathetic hyperactivity, posttraumatic hydrocephalus, and posttraumatic neuroendocrine dysfunctions. Furthermore, we address questions on timing and on existing evidence for different rehabilitation programmes and for holistic neuropsychological rehabilitation approaches.


Brain Injury ◽  
2006 ◽  
Vol 20 (7) ◽  
pp. 695-699 ◽  
Author(s):  
Elisabeth A. Wilde ◽  
Erin D. Bigler ◽  
Claudia Pedroza ◽  
David K. Ryser

Author(s):  
Serhii Antonenko

The problem of traumatic brain injury, its consequences in the long term is relevant for neurologists and doctors of related specialties involved in the treatment, diagnosis and rehabilitation of such a contingent of patients. There are about a dozen syndromes; yaks are most common after an injury. However, one of the most frequent and formidable consequences of traumatic brain damage is post-traumatic epilepsy, which is the main identified cause of symptomatic epilepsy at a young age. The work highlights the “trigger” mechanisms of traumatic brain injury, in particular, oxidative stress, which is an essential component both in the early and long-term periods of CNS damage and leads to the disintegration of all its levels, contributes to the development of basic neuropathological syndromes and primarily post-traumatic epilepsy. The problems of interpreting terminology are considered, when the diagnosis is based only on the fact of the presence of a brain injury, differentiation of this kind of symptomatic convulsive syndrome from other epileptic seizures, the dependence of development on the severity of a head injury (severe injury gives an increased risk of seizures 29 times higher than mild), staging and major risk factors for this type of epileptogenesis, as well as disorganization and damage to the antiepileptic system. A spectrum of convulsive seizures is described, in particular partial, taking into account the localization characteristic of a traumatic brain injury with the predominance of its lesion forms. It is necessary to take into account the occurrence of delayed brain damage, in particular disorders of the immune system, the correlation of the course of post-traumatic epilepsy with the degree of development of hydrocephalus, hypoperfusion of brain areas, glial barrier insufficiency, will contribute to the formation of convulsive activity. It is necessary to take into account the family history. Keywords: post-traumatic epilepsy, epileptogenesis, risk factors


2019 ◽  
Vol 21 (1) ◽  
pp. 83-89 ◽  
Author(s):  
L. B. Likhterman

In this article, we provide the definitions of “sequelae” and “complications” of traumatic brain injury (TBI). We have developed the classification principles for TBI consequences and described their clinical forms and morphological substrates. We also provide a radiological grading for assessing the severity of sequelae of focal and diffuse brain injuries. The article covers conceptual approaches, technologies, and results of their application related to leading surgically significant consequences of TBI, including carotid cavernous fistulas, chronic subdural hematomas, post-traumatic hydrocephalus, long-term basal liquorrhea, and skull defects. We have developed the doctrine of sequelae of TBI.


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