scholarly journals Traumatic Brain Injury

2002 ◽  
Vol 39 (6) ◽  
pp. 679-689 ◽  
Author(s):  
J. W. Finnie ◽  
P. C. Blumbergs

Animal models have played a critical role in elucidating the complex pathogenesis of traumatic brain injury, the major cause of death and disability in young adults in Western countries. This review discusses how different types of animal models are useful for the study of neuropathologic processes in traumatic, blunt, nonmissile head injury.

2012 ◽  
Vol 4 (3) ◽  
pp. 17
Author(s):  
Iván Legascue de Larrañaga

In western countries, accidents remain the leading cause of death in young adults. Worldwide, road traffic injuries in particular are increasing in incidence and injuries are projected to be the third leading cause of death and disability worldwide by 2020. Vehicle crashes are the leading cause of traumatic brain injury, while falls are second. Brain injury accounts for up to half of all deaths from trauma and often causes severe and long-lasting functional impairment in survivors. This article reviews the neuropsychiatric disturbances associated with traumatic brain injury, describing various psychiatric sequelae.


Author(s):  
Fardad T. Afshari ◽  
Antonio Belli ◽  
Peter C Whitfield

Traumatic brain injury is a potentially devastating condition that affects many young adults and is increasingly seen in older people. In addition to initial insult to the neuronal tissue at the time injury, patients with traumatic brain injury may suffer from many physical and psychological complications. These complications further protract the path of recovery and pose challenges in treatment of this group of patients. In this chapter we aim to discuss early and late phase complications following traumatic brain injury and summarize the role of neurorehabilitation in the care of patients with head injury, with the understanding that classification by timing is an inexact science and there is considerable overlap between early and late complications.


Diagnostics ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 4 ◽  
Author(s):  
Kristin A. Keith ◽  
Jason H. Huang

Traumatic brain injury is the leading cause of morbidity and mortality worldwide, with the incidence of post-traumatic epilepsy increasing with the severity of the head injury. Post-traumatic epilepsy (PTE) is defined as a recurrent seizure disorder secondary to trauma to the brain and has been described as one of the most devastating complications associated with TBI (Traumatic Brain Injury). The goal of this review is to characterize current animal models of PTE and provide succinct protocols for the development of each of the currently available animal models. The development of translational and effective animal models for post-traumatic epilepsy is critical in both elucidating the underlying pathophysiology associated with PTE and providing efficacious clinical breakthroughs in the management of PTE.


Author(s):  
Muhammad Reza Azriyantha ◽  
Syaiful Saanin ◽  
Hesty Lidya Ningsih

A B S T R A C TBackground: Traumatic brain injury is the main cause of death in the populationunder the age of 45 years, and the fourth leading cause of death in the entire ofpopulation. Based on the degree of traumatic brain injury, it is commonly categorizedbased on the Glasgow Coma Scale (GCS). Post-Concussion Syndrome (PCS) is theset of somatic, emotional / behavioral and cognitive symptoms that occur after atraumatic brain injury. The aim of this study was to find out the prevalence andcorrelation of the degree of traumatic brain injury based on the Glasgow Coma Scale(GCS) and the emersion of Post-Concussion Syndrome (PCS) acute onset in patientswith head injuries Method: This study was a cross-sectional analytic study ofpatients who experienced Post-Concussion Syndrome (PCS) after traumatic braininjury at DR. M. Djamil Hospital Padang in 2020 from June to November 2020. Datawere collected by filling in a questionnaire (The Rivermead Post ConcussionSymptoms Questionnaire) and medical record data of neurosurgical patients thatmet the inclusion and exclusion criteria. Result: : It indicated that 70 patients wereincluded in the inclusion criteria of this study. A total of 38 (54.3) respondents didnot undergo the acute onset of PCS, meanwhile respondents who experienced acuteonset of PCS were 32 (45.7) respondents. The results showed that 25 (67.6%)respondents with mild traumatic brain injury had PCS acute onset, while 4 (17.4%)respondents with moderate degree of traumatic brain injury had PCS acute onset,and 4 (17.4%) respondents had PCS acute onset PCS 3 (30%) respondentsexperienced severe traumatic brain injury with acute onset PCS and statistically thedifference in the proportion of data from each of these variables was significant witha p-value of 0.0001. The results of statistical tests showed that p value> 0.05 on thecorrelation between PCS and GCS, thus, it can be concluded that there was nocorrelation between the direction of the relationship between PCS and GCS.Conclusion There was no correlation between the degree of traumatic brain injurybased on GCS and the incidence of PCS acute onset, either it was unidirectional orvice versa in patients with head injuries at RSUP M. Djamil Padang.


2008 ◽  
Vol 9 (3) ◽  
pp. 214-215
Author(s):  
Andy Eynon

Traumatic brain injury (TBI) remains the commonest cause of death in the first four decades of life, accounting for 15–20% of deaths between 5 and 35 years.1 There is a ten-fold greater mortality in trauma patients with a head injury compared to those without.2 The effects of head injury for survivors, their families and for society can be devastating; TBI is the cause of severe disability for 150–200 people per million annually.3,4 Perhaps it is better if we do nothing, don't contact the neurosurgeons, don't admit them to specialist units, don't treat the pneumonia that develops – keep them comfortable, allow them some dignity? Or is this a situation where therapeutic nihilism leads to a self-fulfilling prophecy of poor outcome?


2013 ◽  
Author(s):  
Jinsheng Zhang ◽  
Anthony Cacace ◽  
E. M. Haacke ◽  
Bruce Berkowitz ◽  
Jiani Hu ◽  
...  

Author(s):  
Gopal Krishna ◽  
Varun Aggarwal ◽  
Ishwar Singh

Abstract Introduction Traumatic brain injury (TBI) affects the coagulation pathway in a distinct way than does extracranial trauma. The extent of coagulation abnormalities varies from bleeding diathesis to disseminated thrombosis. Design Prospective study. Methods The study included 50 patients of isolated TBI with cohorts of moderate (MHI) and severe head injury (SHI). Coagulopathy was graded according to the values of parameters in single laboratory. The incidence of coagulopathy according to the severity of TBI and correlation with disseminated intravascular coagulation (DIC) score, platelets, prothrombin time (PT), activated partial thromboplastin time (APTT), D-dimer, and fibrinogen was observed. The comparison was also made between expired and discharged patients within each group. It also compared coagulation derailments with clinical presentation (Glasgow Coma Scale [GCS]) and outcome (Glasgow Outcome Scale [GOS]). Results Road traffic accident was the primary (72%) mode of injury. Fifty-two percent had MHI and rest had SHI. Eighty-four percent of cases were managed conservatively. The mean GCS was 12.23 and 5.75 in MHI and SHI, respectively. Sixty-two percent of MHI and 96% of the patients with SHI had coagulation abnormalities. On statistical analysis, DIC score (p < 0.001) strongly correlated with the severity of head injury and GOS. PT and APTT were also significantly associated with the severity of TBI. In patients with moderate TBI, D-dimer and platelet counts showed association with clinical outcome. Fibrinogen levels did not show any statistical significance. The mean platelet counts remained normal in both the groups of TBI. The mean GOS was 1.54 and 4.62 in SHI and MHI, respectively. Conclusion Coagulopathy is common in isolated TBI. The basic laboratory parameters are reliable predictors of coagulation abnormalities in TBI. Coagulopathy is directly associated with the severity of TBI, GCS, and poor outcome.


Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 500
Author(s):  
William Brad Hubbard ◽  
Meenakshi Banerjee ◽  
Hemendra Vekaria ◽  
Kanakanagavalli Shravani Prakhya ◽  
Smita Joshi ◽  
...  

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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