scholarly journals COMPLEX FORENSIC MEDICAL EVALUATION OF THE TRAUMATIC BRAIN INJURY: CASE OF PRACTICE

2021 ◽  
Vol 121 (1) ◽  
pp. 65-69
Author(s):  
Svіtlana Diachenko ◽  
Roksolana Dіduk ◽  
Nailia Kashapova ◽  
Alina Pletenetska

The problem of studying the mechanisms of the occurrence of traumatic brain injury remains a very urgent issue for forensic medicine. The high incidence and high mortality rate of head injuries underlines its importance to experts. The article presents a case from the practice of a forensic medical examination of a traumatic brain injury. This case is indicative, since it clearly demonstrates the difficulties that forensic doctors face when examining craniocerebral injuries, when determining the mechanism of damage and the severity of bodily injuries. In this case, there is damage to the head and a concussion. The cited several conclusions of the experts of the bureau of forensic medical examination and the commission examination of the Main Bureau of Forensic Medical Examination of the Ministry of Health of Ukraine regarding the forensic medical assessment in the case of traumatic brain injury with damage to the head. When conducting an investigative experiment, it was determined that the simultaneous occurrence of an abrasion and a concussion of the brain with one traumatic effect in the glabellar region is unlikely. After all, a concussion of the brain and abrasions in the glabellar area were formed by different mechanisms. The results of this assessment of the characteristics of traumatic brain injury can be useful for preventing difficulties in establishing the mechanism of damage in further expert practice.

Author(s):  
Ian Whittle

Head injury or traumatic brain injury is a ubiquitous phenomenon in all societies and affects up to 2 per cent of the population per year (Bullock et al. 2006). Although the causes of head injury and its distribution within populations vary, it can have devastating consequences both for the patient and family (Tagliaferri et al. 2006). In some countries severe traumatic brain injury is the commonest cause of death in people under 40 years (Lee et al. 2006), and it is estimated that the sequelae of head injury cost societies billions of dollars per year. Understanding of the pathophysiology, diagnosis, and management have all improved dramatically in the last few decades (Steudel et al. 2005). However within western society, perhaps one of the greatest benefits has been the reduction in severe craniocerebral injuries following motor vehicle accidents. This has arisen because of increased safety in car design, seat-belt legislation, the introduction of air-bags, enforcement of speed limits, and the societal conformity to drink-driving legislation. For instance, because of these changes, in the last 15 years the number of severe head injuries managed in the Clinical Neuroscience unit in Edinburgh has decreased by around 66 per cent. Unfortunately in some developing countries one legacy of increased traffic, particularly of motor cycles, is an epidemic of head injuries amongst young adults (Lee et al. 2006). With the number of severe head injuries declining in many countries the challenge will be to provide better care for patients with minor head injury, about 10 times more common than severe injury (Steudel et al. 2005).Ageing patients who tend to fall over, falls associated with increased alcohol consumption, and domestic or social assaults probably now contribute to the majority of head injuries (Flanagan et al. 2005; Steudel et al. 2005; Tagliaferri et al. 2006). Sporting injuries are fortunately uncommon as a cause of severe craniocerebral injury, although horse riding accidents can sometimes be devastating particularly in teenage girls. In some countries injuries from hand guns and other missiles are common (Aryan et al. 2005), but in European countries many such injuries are self-inflicted. Prompt management of intracranial haematoma, which occurs in 25–45 per cent of severe head injuries, 3–12 per cent of moderate injuries, and 0.2 per cent of minor injuries, and the rehabilitation of patients with head injury are now important areas in clinical neuroscience (Flanagan et al. 2005; Bullock et al. 2006b, c).


2021 ◽  
Vol 12 ◽  
Author(s):  
Rodrigo G. Mira ◽  
Matías Lira ◽  
Waldo Cerpa

Traumatic brain injury (TBI) is a heterogeneous disorder that involves brain damage due to external forces. TBI is the main factor of death and morbidity in young males with a high incidence worldwide. TBI causes central nervous system (CNS) damage under a variety of mechanisms, including synaptic dysfunction, protein aggregation, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Glial cells comprise most cells in CNS, which are mediators in the brain’s response to TBI. In the CNS are present astrocytes, microglia, oligodendrocytes, and polydendrocytes (NG2 cells). Astrocytes play critical roles in brain’s ion and water homeostasis, energy metabolism, blood-brain barrier, and immune response. In response to TBI, astrocytes change their morphology and protein expression. Microglia are the primary immune cells in the CNS with phagocytic activity. After TBI, microglia also change their morphology and release both pro and anti-inflammatory mediators. Oligodendrocytes are the myelin producers of the CNS, promoting axonal support. TBI causes oligodendrocyte apoptosis, demyelination, and axonal transport disruption. There are also various interactions between these glial cells and neurons in response to TBI that contribute to the pathophysiology of TBI. In this review, we summarize several glial hallmarks relevant for understanding the brain injury and neuronal damage under TBI conditions.


2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.


2018 ◽  
pp. 110-119

Primary Objectives: By extending the scope of knowledge of the primary care optometrist, the brain injury population will have expanded access to entry level neurooptometric care by optometric providers who have a basic understanding of their neurovisual problems, be able to provide some treatment and know when to refer to their colleagues who have advanced training in neuro-optometric rehabilitation.


2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.


2021 ◽  
Vol 7 (10) ◽  
pp. eabe0207
Author(s):  
Charles-Francois V. Latchoumane ◽  
Martha I. Betancur ◽  
Gregory A. Simchick ◽  
Min Kyoung Sun ◽  
Rameen Forghani ◽  
...  

Severe traumatic brain injury (sTBI) survivors experience permanent functional disabilities due to significant volume loss and the brain’s poor capacity to regenerate. Chondroitin sulfate glycosaminoglycans (CS-GAGs) are key regulators of growth factor signaling and neural stem cell homeostasis in the brain. However, the efficacy of engineered CS (eCS) matrices in mediating structural and functional recovery chronically after sTBI has not been investigated. We report that neurotrophic factor functionalized acellular eCS matrices implanted into the rat M1 region acutely after sTBI significantly enhanced cellular repair and gross motor function recovery when compared to controls 20 weeks after sTBI. Animals subjected to M2 region injuries followed by eCS matrix implantations demonstrated the significant recovery of “reach-to-grasp” function. This was attributed to enhanced volumetric vascularization, activity-regulated cytoskeleton (Arc) protein expression, and perilesional sensorimotor connectivity. These findings indicate that eCS matrices implanted acutely after sTBI can support complex cellular, vascular, and neuronal circuit repair chronically after sTBI.


CNS Spectrums ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 178-179
Author(s):  
John L. Sherman ◽  
Laurence J. Adams ◽  
Christen F. Kutz ◽  
Deborah York ◽  
Mitchell S. Szymczak

AbstractTraumatic brain injury (TBI) is a complex phenomenon affecting multiple areas of the brain in multiple ways. Both right and left hemispheres are affected as well as supratentorial and infratentorial compartments. These multifocal injuries are caused by many factors including acute mechanical injury, focal intracranial hemorrhage, blunt and rotational forces, epidural and subdural hematoma, hypoxemia, hypotension, edema, axonal damage, neuronal death, gliosis and blood brain barrier disruption. Clinicians and patients benefit by precise information about the neuroanatomical areas that are affected macroscopically, microscopically and biochemically in an individual patient.Standard imaging studies are frequently negative or grossly underestimate the severity of TBI and may exacerbate and prolong patient suffering with an imaging result of “no significant abnormality”. Specifically, sophisticated imaging tools have been developed which reveal significant damage to the brain structure including atrophy, MRI spectroscopy showing variations in neuronal metabolite N-acetyl-aspartate, elevations of membrane related Choline, and the glial metabolite myo-inositol is often observed to be increased post injury. In addition, susceptibility weighted imaging (SWI) has been shown to be more reliable for detecting microbleeds versus calcifications.We have selected two TBI patients with diffuse traumatic brain injury.The first patient is a 43-year-old male who suffered severe traumatic brain injury from a motorcycle accident in 2016. Following the accident, the patient was diagnosed with seizures, major depression, and intermittent explosive disorder. He has attempted suicide and has neurobehavioral disinhibition including severe anger, agitation and irritability. He denies psychiatric history prior to TBI and has negative family history. Following the TBI, he became physically aggressive and assaultive in public with minimal provocation. He denies symptoms of thought disorder and mania. He is negative for symptoms of  cognitive decline or encephalopathy.The second patient is a 49-year-old male who suffered at least 3 concussive blasts in the Army and a parachute injury. Following the last accident, the patient was diagnosed with major depressive disorder, panic disorder, PTSD and generalized anxiety disorder. He denies any psychiatric history prior to TBI including negative family history of psychiatric illness. In addition, he now suffers from nervousness, irritability, anger, emotional lability and concurrent concentration issues, problems completing tasks and alterations in memory.Both patients underwent 1.5T multiparametric MRI using standard T2, FLAIR, DWI and T1 sequences, and specialized sequences including susceptibility weighted (SWAN/SWI), 3D FLAIR, single voxel MRI spectroscopy (MRS), diffusion tensor imaging (DTI), arterial spin labeling perfusion (ASL) and volumetric MRI (NeuroQuant). Importantly, this exam can be performed in 30–45 minutes and requires no injections other than gadolinium in some patients. We will discuss the insights derived from the MRI which detail the injured areas, validate the severity of the brain damage, and provide insight into the psychological, motivational and physical disabilities that afflict these patients. It is our expectation that this kind of imaging study will grow in value as we link specific patterns of injury to specific symptoms and syndromes resulting in more targeted therapies in the future.


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