Эффективность препаратов эндогенного происхождения при комплексной патогенетической терапии черепно-мозговой травмы

Подані результати експериментальних досліджень, які мають на меті з’ясування механізму реалізації нейропротективної дії солкосерила за умов експериментальної черепно-мозкової травми (ЧМТ) з акцентом на його антиоксидантні ефекти. Показано, що після ЧМТ в сироватці крові щурів зростає концентрація проміжних продуктів ПОЛ – МДА і ДК, а також знижується активність антиоксидантних ферментів – каталази, СОД і ГП. Застосування солкосерилу сприяє нормалізації концентрації МДА і ДК та активності каталази, СОД і ГП. Максимальна антиоксидантна активність препарату відмічається на 14 добу після нанесення тваринам ЧМТ. Концентрація ДК, активність каталази і СОД під впливом солкосерилу нормалізувалися на 7 добу після ЧМТ. Результати даного експериментального дослідження показують, що одним з механізмів реалізації нейропротекторного ефекту солкосерилу за умов посттравматичного синдрому є антиоксидантна дія препарату.Authors describe the results of the experimental investigations aimed to solkoseryl antioxidant efficacy investigation in condition of experimental brain trauma. Brain trauma was shown to correspond with blood plasma peroxidation products – MDA and DK – levels increasing as well as antioxidant enzymes – catalase, SOD and GP – activity decreasing. Solkoseryl administration results in the investigated compound activity normalization with its maximal effectiveness revealed on the 14th day after brain trauma. It should be mentioned that solkoseryl resulted in DK level and catalase and SOD activity normalization on the 7 th day after brain trauma. These experimental results are in favour that antioxidant profile is one of the mechanism of solkoseryl neuroprotective effect in conditions of brain trauma

Neuroimaging in repetitive brain trauma

Sports-related concussions are one of the major causes of mild traumatic brain injury. Although most patients recover completely within days to weeks, those who experience repetitive brain trauma (RBT) may be at risk for developing a condition known as chronic traumatic encephalopathy (CTE). While this condition is most commonly observed in athletes who experience repetitive concussive and/or subconcussive blows to the head, such as boxers, football players, or hockey players, CTE may also affect soldiers on active duty. Currently, the only means by which to diagnose CTE is by the presence of phosphorylated tau aggregations post-mortem. Non-invasive neuroimaging, however, may allow early diagnosis as well as improve our understanding of the underlying pathophysiology of RBT. The purpose of this article is to review advanced neuroimaging methods used to investigate RBT, including diffusion tensor imaging, magnetic resonance spectroscopy, functional magnetic resonance imaging, susceptibility weighted imaging, and positron emission tomography. While there is a considerable literature using these methods in brain injury in general, the focus of this review is on RBT and those subject populations currently known to be susceptible to RBT, namely athletes and soldiers. Further, while direct detection of CTE in vivo has not yet been achieved, all of the methods described in this review provide insight into RBT and will likely lead to a better characterization (diagnosis), in vivo, of CTE than measures of self-report

On Brain Oedema

Traumatic brain injury and bacterial meningitis may at a glance appear as two different disease entities. The host reaction, however, to both trauma and infection involves a strong inflammatory response, with the classical symptomology of rubor, tumor, calor, dolor et functio laesa. Tumor, swelling, will increase the volume within the closed cranial vault, and may thereby raise the intracranial pressure to critical levels, affecting cerebral blood flow and oxygenation. In this thesis, brain oedema and its origins are investigated in experimental models of brain trauma and bacterial meningitis, and in patients suffering severe head injury. The studies are focused on fluid therapy, blood-brain barrier permeability changes, and their effects on oedema formation. In study I and II, it was shown that plasma volume expansion with crystalloid compared to colloid fluids resulted in increased cortical brain oedema after brain trauma in rats, and increased intracranial pressure in experimental meningitis in cats. Evidence is given that increased permeability of the blood-brain barrier is a key determinant of tissue water content after the insults. In study III, it was shown that post treatment with prostacyclin in experimental meningitis reduces systemic plasma volume loss, and may diminish the rise in intracranial pressure. In study IV, the effect of statin treatment after brain trauma in rats was investigated. No effect on brain oedema, cortical blood flow, or the transfer constant for a small molecule was detected, but capillary patency was better preserved in the statin group. Statin treatment was associated with increased plasma levels of nitric oxide, and decreased levels of prostacyclin. In study V, post-traumatic permeability changes of the blood-brain barrier in 17 brain trauma patients were quantified using contrast enhanced computerized tomography with multiple scanning during 25 minutes. It was shown that blood to brain transfer for iohexol was increased up to 20-fold in traumatized tissue. The relevance of these results regarding our understanding of the pathophysiology of post-traumatic brain oedema, and the implications for the clinical management of brain trauma patients are discussed

Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior

Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression, and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels are not available. Using controlled-cortical impact as an experimental model of brain trauma in adult mice, we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on the appearance of depressive-like behavior. We demonstrate that this alteration in behavior is associated with an impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in the expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission from hyperpolarizing to depolarizing after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.Peer reviewe

Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage

Background Traumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo. Findings Using [11C]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury. Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage. Conclusions These findings support a link between axonal damage and persistent inflammation after brain injury

Security oriented e-infrastructures supporting neurological research and clinical trials

The neurological and wider clinical domains stand to gain greatly from the vision of the grid in providing seamless yet secure access to distributed, heterogeneous computational resources and data sets. Whilst a wealth of clinical data exists within local, regional and national healthcare boundaries, access to and usage of these data sets demands that fine grained security is supported and subsequently enforced. This paper explores the security challenges of the e-health domain, focusing in particular on authorization. The context of these explorations is the MRC funded VOTES (Virtual Organisations for Trials and Epidemiological Studies) and the JISC funded GLASS (Glasgow early adoption of Shibboleth project) which are developing Grid infrastructures for clinical trials with case studies in the brain trauma domain

Distinctive Pattern Found in IED Survivors’ Brains

New research offers insight into brain trauma incurred by improvised explosive devices (IED), a problem affecting survivors of blast-related injuries since World War I

Consent and brain trauma in schools

In a recently published edition of the Journal of Physical Education, Recreation and Dance, we read with interest responses given by readers on ‘how should coaches, parents and participants be informed of the risks and rewards of their participation’ (2017: 54) in sports with a risk of head trauma. Over the past decade, increasing attention has been forthcoming on the issues of traumatic brain injuries, repetitive sub-concussive traumas and the long-term, and sometimes fatal, implications of concussion (McKee et al. 2014) often focusing on contact sports, such as American Football, Ice Hockey or the various codes of Rugby

E-infrastructures fostering multi-centre collaborative research into the intensive care management of patients with brain injury

Clinical research is becoming ever more collaborative with multi-centre trials now a common practice. With this in mind, never has it been more important to have secure access to data and, in so doing, tackle the challenges of inter-organisational data access and usage. This is especially the case for research conducted within the brain injury domain due to the complicated multi-trauma nature of the disease with its associated complex collation of time-series data of varying resolution and quality. It is now widely accepted that advances in treatment within this group of patients will only be delivered if the technical infrastructures underpinning the collection and validation of multi-centre research data for clinical trials is improved. In recognition of this need, IT-based multi-centre e-Infrastructures such as the Brain Monitoring with Information Technology group (BrainIT - www.brainit.org) and Cooperative Study on Brain Injury Depolarisations (COSBID - www.cosbid.de) have been formed. A serious impediment to the effective implementation of these networks is access to the know-how and experience needed to install, deploy and manage security-oriented middleware systems that provide secure access to distributed hospital based datasets and especially the linkage of these data sets across sites. The recently funded EU framework VII ICT project Advanced Arterial Hypotension Adverse Event prediction through a Novel Bayesian Neural Network (AVERT-IT) is focused upon tackling these challenges. This chapter describes the problems inherent to data collection within the brain injury medical domain, the current IT-based solutions designed to address these problems and how they perform in practice. We outline how the authors have collaborated towards developing Grid solutions to address the major technical issues. Towards this end we describe a prototype solution which ultimately formed the basis for the AVERT-IT project. We describe the design of the underlying Grid infrastructure for AVERT-IT and how it will be used to produce novel approaches to data collection, data validation and clinical trial design is also presented

Social network structure and composition in former NFL football players

Social networks have broad effects on health and quality of life. Biopsychosocial factors may also modify the effects of brain trauma on clinical and pathological outcomes. However, social network characterization is missing in studies of contact sports athletes. Here, we characterized the personal social networks of former National Football League players compared to non-football US males. In 303 former football players and 269 US males, we found that network structure (e.g., network size) did not differ, but network composition (e.g., proportion of family versus friends) did differ. Football players had more men than women, and more friends than family in their networks compared to US males. Black players had more racially diverse networks than White players and US males. These results are unexpected because brain trauma and chronic illnesses typically cause diminished social relationships. We anticipate our study will inform more multi-dimensional study of, and treatment options for, contact sports athletes. For example, the strong allegiances of former athletes may be harnessed in the form of social network interventions after brain trauma. Because preserving health of contact sports athletes is a major goal, the study of social networks is critical to the design of future research and treatment trials