scholarly journals The synapse in traumatic brain injury

Brain ◽  
2020 ◽  
Author(s):  
Aimun A B Jamjoom ◽  
Jonathan Rhodes ◽  
Peter J D Andrews ◽  
Seth G N Grant

Abstract Traumatic brain injury (TBI) is a leading cause of death and disability worldwide and is a risk factor for dementia later in life. Research into the pathophysiology of TBI has focused on the impact of injury on the neuron. However, recent advances have shown that TBI has a major impact on synapse structure and function through a combination of the immediate mechanical insult and the ensuing secondary injury processes, leading to synapse loss. In this review, we highlight the role of the synapse in TBI pathophysiology with a focus on the confluence of multiple secondary injury processes including excitotoxicity, inflammation and oxidative stress. The primary insult triggers a cascade of events in each of these secondary processes and we discuss the complex interplay that occurs at the synapse. We also examine how the synapse is impacted by traumatic axonal injury and the role it may play in the spread of tau after TBI. We propose that astrocytes play a crucial role by mediating both synapse loss and recovery. Finally, we highlight recent developments in the field including synapse molecular imaging, fluid biomarkers and therapeutics. In particular, we discuss advances in our understanding of synapse diversity and suggest that the new technology of synaptome mapping may prove useful in identifying synapses that are vulnerable or resistant to TBI.

2012 ◽  
Vol 15 (3) ◽  
pp. 253-263 ◽  
Author(s):  
Karen M. O’Connell ◽  
Marguerite T. Littleton-Kearney

Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.


Author(s):  
Richard A. Bryant

One of the more hotly debated issues in the field of post-traumatic stress disorder (PTSD) is the role of traumatic brain injury (TBI), and particularly mild traumatic brain injury (mTBI). This topic became increasingly the focus of attention in the context of recent wars in Iraq and Afghanistan, where many troops suffered PTSD and mTBIs. Over three-quarters of injuries sustained in these conflicts arose from encounters with explosive devices, and accordingly it was often claimed that the “signature injuries” of the wars in Iraq and Afghanistan were both PTSD and mTBI. Clinicians and researchers have thus given renewed attention to the interplay of these two conditions. This chapter reviews definitional issues of PTSD and mTBI, how PTSD can develop after mTBI, the impact mTBI may have on stress responses, the distinctive role of postconcussive syndrome, and how to manage PTSD following mTBI.


2017 ◽  
Vol 31 (3) ◽  
pp. 319-334
Author(s):  
Hector Rolando Romero-Rivera ◽  
Marticela Cabeza-Morales ◽  
Enrique Soto-Zarate ◽  
Guru Dutta Satyarthee ◽  
Huber Padilla-Zambrano ◽  
...  

Abstract Oxidative stress constitute one of the commonest mechanism of the secondary injury contributing to neuronal death in traumatic brain injury cases. The oxidative stress induced secondary injury blockade may be considered as to be a good alternative to improve the outcome of traumatic brain injury (TBI) treatment. Due to absence of definitive therapy of traumatic brain injury has forced researcher to utilize unconventional therapies and its roles investigated in the improvement of management and outcome in recent year. Antioxidant therapies are proven effective in many preclinical studies and encouraging results and the role of antioxidant mediaction may act as further advancement in the traumatic brain injury management it may represent aonr of newer moadlaity in neurosurgical aramamentorium, this kind of therapy could be a good alternative or adjuct to the previously established neuroprotection agents in TBI.


2000 ◽  
Vol 6 (1) ◽  
pp. 33-44
Author(s):  
Peter Stebbins ◽  
Kenneth I. Pakenham ◽  
Paul Leung

The provision of care to a relative with a traumatic brain injury (TBI) has been shown to be distressing for the primary caregiver (usually the spouse or parent). Much research has examined factors which affect caregiver adjustment to brain injury. However, the impact of caregiver cognitions, in particular irrational beliefs, as a potential factor in poor adjustment, has received little if any attention in the TBI caregiving literature. This article provides a review of predictors of TBI caregiver adjustment and a discussion of the cognitive model and the impact of irrational beliefs on adjustment. As caregivers are central to the rehabilitation process, there is a need for research into irrational beliefs and TBI caregivers as well as the development of interventions which focus specifically on the caregiver's beliefs and perceptions of events.


Neurosurgery ◽  
2013 ◽  
Vol 73 (2) ◽  
pp. 305-311 ◽  
Author(s):  
Rahul Raj ◽  
Jari Siironen ◽  
Riku Kivisaari ◽  
Juha Hernesniemi ◽  
Päivi Tanskanen ◽  
...  

Abstract BACKGROUND: Markers of coagulation have shown to have important value in predicting traumatic brain injury outcome. OBJECTIVE: To externally validate and investigate the role of markers of coagulation for outcome prediction by using the International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) model while adjusting for overall injury severity. METHODS: A retrospective chart analysis of traumatic brain injury patients admitted to Helsinki University Central Hospital between 2009 and 2010 was performed. Outcome was estimated by using the criteria of the IMPACT model. Admission international normalized ratio (INR) and platelet count were used as markers of coagulation. Overall injury severity was categorized with the injury severity score (ISS). Variables were added to the calculated IMPACT risk, generating new models. Model performance was assessed by analyzing and comparing the area under the curve (AUC) of the models. RESULTS: For 342 included patients, 6-month mortality was 32% and unfavorable neurological outcome was 36%. Patients with a poor outcome had lower platelets and higher INR and ISS than those with good outcome (P < .001). The IMPACT model had an AUC of 0.85 for predicting mortality and 0.81 for neurological outcome. Addition of INR but not ISS or platelets to the IMPACT predicted risk improved the predictive validity for mortality ([INCREMENT]AUC 0.02, P = .034) but not neurological outcome ([INCREMENT]AUC 0.00, P = .401). In multivariate analysis, INR remained significant for mortality but not for neurological outcome when adjusting for IMPACT risk and ISS (P = .012). CONCLUSION: The IMPACT model showed excellent performance, and INR was an independent predictor for mortality, independent of overall injury severity.


2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Mehar Naseem ◽  
Suhel Parvez

Brain and spinal cord are implicated in incidences of two of the most severe injuries of central nervous system (CNS). Traumatic brain injury (TBI) is a devastating neurological deficit involving primary and secondary injury cascades. The primary and secondary mechanisms include complex consequences of activation of proinflammatory cytokines, cerebral edema, upregulation of NF-κβ, disruption of blood-brain barrier (BBB), and oxidative stress. Spinal cord injury (SCI) includes primary and secondary injury cascades. Primary injury leads to secondary injury in which generation of free radicals and oxidative or nitrative damage play an important pathophysiological role. The indoleamine melatonin is a hormone secreted or synthesized by pineal gland in the brain which helps to regulate sleep and wake cycle. Melatonin has been shown to be a versatile hormone having antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. It has a special characteristic of crossing BBB. Melatonin has neuroprotective role in the injured part of the CNS after TBI and SCI. A number of studies have successfully shown its therapeutic value as a neuroprotective agent in the treatment of neurodegenerative diseases. Here in this review we have compiled the literature supporting consequences of CNS injuries, TBI and SCI, and the protective role of melatonin in it.


2006 ◽  
Vol 12 (5) ◽  
pp. 609-621 ◽  
Author(s):  
KALAICHELVI GANESALINGAM ◽  
ANN SANSON ◽  
VICKI ANDERSON ◽  
KEITH OWEN YEATES

This study examined the impact of childhood traumatic brain injury (TBI) on self-regulation and social and behavioral functioning, and the role of self-regulation as a predictor of children's social and behavioral functioning. Participants included 65 children with moderate to severe TBI and 65 children without TBI, all between 6 and 11 years of age. Self-regulation and social and behavioral functioning were assessed 2 to 5 years following injury. Children with TBI displayed deficits in self-regulation and social and behavioral functioning, after controlling for socioeconomic status (SES), although the magnitude of the deficits was not related to injury severity. Self-regulation accounted for significant variance in children's social and behavioral functioning, after controlling for SES and group membership. Self-regulation may be an important determinant of children's social and behavioral functioning following TBI. (JINS, 2006,12, 609–621.)


Sign in / Sign up

Export Citation Format

Share Document