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Traumatic Brain Injury 23.



  • Traumatic Brain Injury 23.
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  • Brain abnormalities found in victims of US embassy attack in Cuba
  • Brain Inj. Jan;22(1) doi: / MMPI-2 profiles 23 years after paediatric mild traumatic brain injury. Hessen E(1), Anderson. Traumatic brain injury (TBI) is a significant clinical problem with few Marklund N., and Hillered L. (). Animal modelling of traumatic brain injury in . Mounting evidence points to brain trauma as a risk factor for mental decline. Football players who've had multiple concussions perform worse on tests of brain .

    Traumatic Brain Injury 23.

    Each year, TBIs contribute to a substantial number of deaths and cases of permanent disability. Changes in the rates of TBI-related hospitalizations vary depending on age.

    For persons 44 years of age and younger, TBI-related hospitalizations decreased between the periods of — and — However, rates for age groups 45—64 years of age and 65 years and older increased between these time periods. In contrast, rates of TBI-related hospitalizations in youth 5—14 years of age fell from A severe TBI not only impacts the life of an individual and their family, but it also has a large societal and economic toll.

    This was the question that Lt. Tim Maxwell asked about his fellow marines being discharged from the hospital and left alone to recover from injuries of war. The Glasgow Coma Scale GCS , 5 a clinical tool designed to assess coma and impaired consciousness, is one of the most commonly used severity scoring systems. Despite their limitations, 6 these systems are crucial to understanding the clinical management and the likely outcomes of this injury as the prognosis for milder forms of TBIs is better than for moderate or severe TBIs.

    Indeed, evidence of delayed apoptosis of oligodendrocytes has been reported using immunocytochemical ICC analysis of brain tissues weeks to months after injury. Various strategies have been utilized to target apoptotic cell death after brain injury.

    Nonspecific apoptotic inhibitors have been reported, in some studies, to be protective after TBI and to be associated with improved behavioral outcome. Inflammatory processes have long been viewed as important secondary injury mechanisms after TBI. In clinical studies, biomarker analysis has also provided direct evidence for inflammatory processes being active in various TBI patients weeks to months after injury.

    A relatively new development in the area of inflammatory cascades after TBI is the discovery that inflammatory cells are relatively plastic and may participate in both neurodegenerative, as well as reparative, processes. Because recent clinical data have emphasized the high incidence of PTE and episodes of cortical spreading depolarization in TBI patients, these post-traumatic events require more investigation.

    More recent data have emphasized the incidence of subclinical nonconvulsive seizures after TBI that, although not routinely documented in the human population, can be recorded using monitoring procedures, including long-term electroencephalography surface recordings. In addition to PTE, episodes of cortical spreading depolarization CSD , as mentioned previously, are also observed in models of brain injury.

    Episodes of CSD have been shown to be sensitive to selective pharmacological treatments, including NMDA receptor and calcium antagonists. Subsequent to TBI, bleeding within the neuropil leads to hemolysis and the deposition of hemoglobin. TBI produces a prolonged activation of calpains resulting in the proteolysis of numerous cellular substrates, including cytoskeletal components and membrane receptors.

    Multiple strategies targeting calpain breakdown have been used to target the acute and more chronic consequences of CNS injury. Intravenous administration of calpain inhibitors, such as MDL, protect against axonal pathology, as well as neuronal damage, in some experimental models.

    WM injury is a hallmark of TBI, with pre-clinical and human autopsy data demonstrating axonal injury in conditions of both focal as well as diffuse brain injury. State-of-the-art imaging approaches clarifying WM damage using diffusion tension imaging and anisotropy are also providing evidence for subtle changes in the microenvironment and axonal structure, which could underlie some of the long-term progressive changes and prolonged functional disturbances reported in current animal models and in humans.

    In addition to axonal damage, evidence for abnormal axonal sprouting of specific neural populations is also reported in models of TBI. It is important to note that in the area of post-traumatic epilepsy, evidence for axonal sprouting has also been demonstrated in the hippocampal mossy fiber pathway.

    Several investigations have evaluated therapeutic interventions that may target axonal pathology. These include strategies targeting excitotoxicity, free radical generation, or combination approaches that may be directed at multiple pathomechanisms. Recent evidence has also indicated that therapeutic hypothermia may prevent axonal pathology in several models of TBI. As previously described, a variety of WM changes are observed after TBI in both experimental and clinical investigations.

    Subsequent to TBI, evidence for local demyelination associated with these WM changes has also been emphasized. Indeed, in a recent publication, oligodendrocyte cell death by apoptotic-dependent mechanisms was demonstrated after a moderate TBI injury. Importantly, because myelination is critical to the normal role of axons in terms of the complex function of neuronal circuits, demyelination could underlie many of the long-term functional consequences of brain injury.

    Emphasis needs to be placed on demonstrating evidence for demyelination in our TBI population using state-of-the-art imaging approaches determining the importance of this cellular response in terms of acute and more long-term TBI outcomes.

    Previous studies have emphasized the occurrence of ongoing neurogenesis in specific areas of the adult brain. Current research efforts are directed to evaluating the importance of adult neurogenesis on normal cognitive function and integration of new memories into our neural circuits.

    In this regard, several laboratories have reported that after TBI, there is a significant increase in cell proliferation and neurogenesis in the hippocampus using a variety of ICC approaches.

    In this regard, specific strategies, including exercise, motor rehabilitation, growth factor or hormonal, or other proneurogenic treatments, as well as therapeutic hypothermia, may enhance neurogenesis after brain injury. The fact that neurogenesis occurs in the adult brain and can be negatively impacted by TBI emphasizes that these reparative processes represent extremely important targets for treating the progressive nature of TBI.

    Early alterations in regional cerebral blood flow rCBF have been demonstrated in experimental and clinical models of TBI. Data are also available showing that, in addition to the acute changes in CBF, long-term alterations in rCBF are also observed in experimental and clinical models Fig. Moderate reductions in chronic blood flow can augment slow, evolving injury processes or aggravate events that were initiated by the acute insult. For example, inflammatory or excitotoxic processes could be aggravated by reduced blood flow.

    Strategies to improve blood flow include use of modifiers of vascular reactivity, such as nitric oxide or other strategies. The potential for cerebral emboli produced by the primary injury to occlude microvessels, abnormalities in coagulopathy, or whether microvascular vasospasm participates in reduced CBF needs to be addressed in future studies.

    In the CCI example shown, a large cystic lesion was observed encompassing both the cortex and hippocampus ipsilateral to the impact at 1 year after injury. That lesion is identified as a region of hyperintensity on both the T 2-weighted image A and the T 1obs map B and as a region lacking perfusion C. The corresponding histopathology cresyl-violet—stained section through the imaging plane confirms the location of the cystic cavity after CCI D , but not after sham surgery H.

    For figure presentation purposes, pixels outside the brain were assigned to zero intensity. Although the perfusion slice shown for injured rat C represents the best example of average for the overall effect of injury on CBF, it does not necessarily reflect the mean CBF for each individual region of interest.

    CBF, cerebral blood flow. Over the last several years, there has been an increased awareness that TBI can be an important risk factor for development of age-related neurodegenerative diseases, including AD and Parkinson's disease. In several studies, evidence for focal protein aggregation, as well as abnormal accumulation of beta-amyloid precursor or tau protein, has been demonstrated in experimental as well as clinical specimens.

    However, it is important to emphasize that a spectrum of TBI severities as well as repetitive mild concussions appear to produce similar cellular responses to injury and therefore may include common pathomechanisms occurring in the more chronic stages of TBI.

    Experimental and clinical research programs are targeting the devastating consequences of neurodegenerative diseases, including AD. Vaccine and antibody treatments are being tested to target abnormal protein aggregation and other neurodegenerative processes. Both experimental and clinical evidence indicates the multi-factorial nature of pathophysiological mechanisms that may underlie the progressive nature of TBI. Because the chronic consequences of TBI, including histopathological, physiological, and behavioral abnormalities, can be observed after mild, moderate, or severe injury, it may be difficult in the future to clarify whether any one dominant pathomechanism underlies the progressive nature of TBI.

    In addition, the acknowledgement of TBI being a possible risk factor for age-dependent neurodegenerative disease is also complicating the trauma field in terms of understanding pathophysiological events and treatment options.

    Hopefully, through genetic modeling approaches, combined with innovative cellular and functional approaches to evaluate novel pathomechanisms, a better understanding of how to best treat the chronic consequences of TBI will be achieved.

    Importantly, a greater understanding of the pathophysiological mechanisms associated with chronic TBI and the testing of novel therapeutic interventions using clinically relevant animal models will enhance the translation of new discoveries to the clinic.

    Past attempts to translate postive pre-clinical findings targeting acute neuroprotection have been unsuccessful in terms of improving functional outcome. Specifically, several conditions, including independent data replication, the critical evaluation of the quality of research data, and clinical relevance are now emphasized in the neurotrauma literature. It is anticipated that, in the future, pre-clinical findings will lead to successful clinical investigations potentially using novel combinatorial approaches, including neuroprotection, reparative approaches, and neurorehabilitation, to ultimately improve function in people living with the devastating consequences of TBI.

    The authors thank Jeremy Lytle for editorial support. National Center for Biotechnology Information , U. Author information Copyright and License information Disclaimer. Copyright , Mary Ann Liebert, Inc. This article has been cited by other articles in PMC. Abstract Traumatic brain injury TBI is a significant clinical problem with few therapeutic interventions successfully translated to the clinic.

    Introduction T raumatic brain injury TBI produces both acute and more chronic consequences that lead to permanent disabilities that increase long-term mortality and reduced life expectation. Open in a separate window. Excitotoxicity One of the initial pathomechanisms that was investigated to target neuronal vulnerability after cerebral ischemia or trauma was neuronal excitotoxicity. Reactive Oxygen Generation Experimental and clinical studies have emphasized the importance of generation of reactive oxygen species ROS and reactive nitrogen species RNS as occurring in the early post-traumatic stages of the injury process.

    Apoptosis Apoptosis is a mechanism underlying programmed cell death that has been characterized in models of brain injury and SCI. Inflammation Inflammatory processes have long been viewed as important secondary injury mechanisms after TBI. Calpain-Mediated Proteolysis TBI produces a prolonged activation of calpains resulting in the proteolysis of numerous cellular substrates, including cytoskeletal components and membrane receptors.

    Diffuse axonal injury WM injury is a hallmark of TBI, with pre-clinical and human autopsy data demonstrating axonal injury in conditions of both focal as well as diffuse brain injury.

    Adult Neurogenesis Previous studies have emphasized the occurrence of ongoing neurogenesis in specific areas of the adult brain. Neurodegenerative Processes Over the last several years, there has been an increased awareness that TBI can be an important risk factor for development of age-related neurodegenerative diseases, including AD and Parkinson's disease.

    Summary Both experimental and clinical evidence indicates the multi-factorial nature of pathophysiological mechanisms that may underlie the progressive nature of TBI. Author Disclosure Statement No competing financial interests exist. Neurotrauma 27 , — [ PubMed ]. Clinical rating of cortical atrophy and cognitive correlates following traumatic brain injury. Magnetic resonance imaging and computerized tomography in relation to the neurobehavioral sequelae of mild and moderate head injuries.

    Traumatic brain injury as a chronic health condition. A population-based study of seizures after traumatic brain injuries.

    Psychosocial functioning at 1 month after head injury. Neurosurgery 14 , — [ PubMed ]. Excessive daytime sleepiness in adults with brain injuries. Traumatic brain injury as a risk factor for Alzheimer's disease: Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: Head injury and Parkinson's disease risk in twins.

    Acute and chronic traumatic encephalopathies: Longterm consequences of traumatic brain injury , in: Gulf War and Health. The National Academies Press: Hormonal dysfunction in neurocritical patients. Care 19 , — [ PubMed ]. Chronic histopathological consequences of fluid-percussion brain injury in rats: Post-traumatic seizure susceptibility is attenuated by hypothermia therapy. Clinical trials in head injury.

    Emerging experimental therapies for intracerebral hemorrhage: Focus 34 , E9. Randomized controlled trials in adult traumatic brain injury. Cyclophilin-D inhibition in neuroprotection: Animal models of traumatic brain injury. Neuroprotection for traumatic brain injury: Dose-dependent neurorestorative effects of delayed treatment of traumatic brain injury with recombinant human erythropoietin in rats.

    Animal modelling of traumatic brain injury in preclinical drug development: An overview of the basic science of concussion and subconcussion: Focus 33 , E5. Blast-related traumatic brain injury.

    Consensus statement on concussion in sport—the 4th International Conference on Concussion in Sport held in Zurich, November PM R 5 , — [ PubMed ]. Chronic neuropathological and neurobehavioral changes in a repetitive mTBI model. Quantitative structural changes in white and gray matter 1 year following traumatic brain injury in rats.

    Progressive damage after brain and spinal cord injury: Spatial and temporal characteristics of neurodegeneration after controlled cortical impact in mice: Neurotrauma 22 , — [ PubMed ]. Enduring cognitive, neurobehavioral and histopathological changes persist for up to one year following severe experimental brain injury in rats. Neuroscience 87 , — [ PubMed ]. Progressive atrophy and neuron death for one year following brain trauma in the rat.

    Neurotrauma 14 , — [ PubMed ]. One-year study of spatial memory performance, brain morphology, and cholinergic markers after moderate controlled cortical impact in rats. Neurotrauma 16 , — [ PubMed ]. Light and electron microscopic assessment of progressive atrophy following moderate traumatic brain injury in the rat. Computed tomography and magnetic resonance imaging in mild to moderate head injury: Detection of brain atrophy following traumatic brain injury using gravimetric techniques.

    Ventricular dilation, cortical atrophy, and neuropsychological outcome following traumatic brain injury. Ventricle size, cortical atrophy and the relationship with neuropsychological status in closed head injury: Moderate-severe traumatic brain injury causes delayed loss of white matter integrity: Neurotrauma 30 , — [ PubMed ]. Neuroimaging and neuropathology of TBI. NeuroRehabilitation 28 , 63—74 [ PubMed ]. Systems biomarkers as acute diagnostics and chronic monitoring tools for traumatic brain injury , pps.

    Pathophysiology of cerebral ischemia and brain trauma: Alterations in AMPA receptor subunit expression after experimental spinal cord contusion injury. Glutamate release and free radical production following brain injury: Traumatic brain injury pathophysiology and treatments: Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.

    Changes in cortical extracellular levels of energy-related metabolites and amino acids following concussive brain injury in rats. Glutamate release and cerebral blood flow after severe human head injury. Acetylcysteine has been safely used to treat paracetamol overdose for over forty years and is extensively used in emergency medicine. It is important to begin emergency treatment within the so-called " golden hour " following the injury. In the acute stage the primary aim of the medical personnel is to stabilize the patient and focus on preventing further injury because little can be done to reverse the initial damage caused by trauma.

    Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center. Other methods to prevent damage include management of other injuries and prevention of seizures. Neuroimaging is helpful but not flawless in detecting raised ICP. Sedatives , analgesics and paralytic agents are often used. Endotracheal intubation and mechanical ventilation may be used to ensure proper oxygen supply and provide a secure airway.

    Failing to maintain blood pressure can result in inadequate blood flow to the brain. While they can be treated with benzodiazepines , these drugs are used carefully because they can depress breathing and lower blood pressure.

    Traumatic brain injury may cause a range of serious coincidental complications that include cardiac arrhythmias [99] and neurogenic pulmonary edema. Surgery can be performed on mass lesions or to eliminate objects that have penetrated the brain.

    Mass lesions such as contusions or hematomas causing a significant mass effect shift of intracranial structures are considered emergencies and are removed surgically. Once medically stable, people may be transferred to a subacute rehabilitation unit of the medical center or to an independent rehabilitation hospital.

    Physiatrists or neurologists are likely to be the key medical staff involved, but depending on the person, doctors of other medical specialties may also be helpful. Allied health professions such as physiotherapy , speech and language therapy , cognitive rehabilitation therapy , and occupational therapy will be essential to assess function and design the rehabilitation activities for each person. Treatment of neuropsychiatric symptoms such as emotional distress and clinical depression may involve mental health professionals such as therapists , psychologists , and psychiatrists , while neuropsychologists can help to evaluate and manage cognitive deficits.

    After discharge from the inpatient rehabilitation treatment unit, care may be given on an outpatient basis. Community-based rehabilitation will be required for a high proportion of people, including vocational rehabilitation; this supportive employment matches job demands to the worker's abilities. Pharmacological treatment can help to manage psychiatric or behavioral problems. The most effective research documented intervention approach is the activation database guided EEG biofeedback approach, which has shown significant improvements in memory abilities of the TBI subject that are far superior than traditional approaches strategies, computers, medication intervention.

    The TBI's auditory memory ability was superior to the control group after the treatment. Prognosis worsens with the severity of injury. Prognosis differs depending on the severity and location of the lesion, and access to immediate, specialised acute management.

    Subarachnoid hemorrhage approximately doubles mortality. The Functional Independence Measure is a way to track progress and degree of independence throughout rehabilitation.

    Medical complications are associated with a bad prognosis. Examples are hypotension low blood pressure , hypoxia low blood oxygen saturation , lower cerebral perfusion pressures and longer times spent with high intracranial pressures. Factors thought to worsen it include abuse of substances such as illicit drugs and alcohol and age over sixty or under two years in children, younger age at time of injury may be associated with a slower recovery of some abilities.

    Life satisfaction has been known to decrease for individuals with TBI immediately following the trauma, but evidence has shown that life roles, age, and depressive symptoms influence the trajectory of life satisfaction as time passes. Improvement of neurological function usually occurs for two or more years after the trauma. For many years it was believed that recovery was fastest during the first six months, but there is no evidence to support this. It may be related to services commonly being withdrawn after this period, rather than any physiological limitation to further progress.

    Complications are distinct medical problems that may arise as a result of the TBI. The results of traumatic brain injury vary widely in type and duration; they include physical, cognitive, emotional, and behavioral complications. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death , persistent vegetative state in which patients are unable to achieve a state of alertness to interact with their surroundings , [] and minimally conscious state in which patients show minimal signs of being aware of self or environment.

    Movement disorders that may develop after TBI include tremor, ataxia uncoordinated muscle movements , myoclonus shock-like contractions of muscles , and loss of movement range and control in particular with a loss of movement repertoire. Development of diabetes insipidus or an electrolyte abnormality acutely after injury indicate need for endocrinologic work up.

    Signs and symptoms of hypopituitarism may develop and be screened for in adults with moderate TBI and in mild TBI with imaging abnormalities. Children with moderate to severe head injury may also develop hypopituitarism. Screening should take place 3 to 6 months, and 12 months after injury, but problems may occur more remotely. Cognitive deficits that can follow TBI include impaired attention; disrupted insight, judgement, and thought; reduced processing speed; distractibility; and deficits in executive functions such as abstract reasoning, planning, problem-solving, and multitasking.

    About one in five career boxers is affected by chronic traumatic brain injury CTBI , which causes cognitive, behavioral, and physical impairments. It commonly manifests as dementia , memory problems, and parkinsonism tremors and lack of coordination.

    TBI may cause emotional, social, or behavioral problems and changes in personality. TBI also has a substantial impact on the functioning of family systems [] Caregiving family members and TBI survivors often significantly alter their familial roles and responsibilities following injury, creating significant change and strain on a family system.

    Typical challenges identified by families recovering from TBI include: In addition, families may exhibit less effective functioning in areas including coping, problem solving and communication. Psychoeducation and counseling models have been demonstrated to be effective in minimizing family disruption []. TBI is a leading cause of death and disability around the globe [2] and presents a major worldwide social, economic, and health problem.

    Findings on the frequency of each level of severity vary based on the definitions and methods used in studies.

    The incidence of TBI varies by age, gender, region and other factors. Biological, clinical, and demographic factors contribute to the likelihood that an injury will be fatal. The incidence of TBI is increasing globally, due largely to an increase in motor vehicle use in low- and middle-income countries. Regardless of age, TBI rates are higher in males. Socioeconomic status also appears to affect TBI rates; people with lower levels of education and employment and lower socioeconomic status are at greater risk.

    Head injury is present in ancient myths that may date back before recorded history. Medieval and Renaissance surgeons continued the practice of trepanation for head injury. It was first suggested in the 18th century that intracranial pressure rather than skull damage was the cause of pathology after TBI.

    Perhaps the first reported case of personality change after brain injury is that of Phineas Gage , who survived an accident in which a large iron rod was driven through his head, destroying one or both of his frontal lobes; numerous cases of personality change after brain injury have been reported since.

    The 20th century saw the advancement of technologies that improved treatment and diagnosis such as the development of imaging tools including CT and MRI, and, in the 21st century, diffusion tensor imaging DTI.

    The introduction of intracranial pressure monitoring in the s has been credited with beginning the "modern era" of head injury. In the s, awareness of TBI as a public health problem grew, [] and a great deal of progress has been made since then in brain trauma research, [98] such as the discovery of primary and secondary brain injury.

    No medication is approved to halt the progression of the initial injury to secondary injury. However, trials to test agents that could halt these cellular mechanisms have met largely with failure. In addition, drugs such as NMDA receptor antagonists to halt neurochemical cascades such as excitotoxicity showed promise in animal trials but failed in clinical trials. In addition to traditional imaging modalities, there are several devices that help to monitor brain injury and facilitate research.

    Microdialysis allows ongoing sampling of extracellular fluid for analysis of metabolites that might indicate ischemia or brain metabolism, such as glucose, glycerol, and glutamate.

    Research is also planned to clarify factors correlated to outcome in TBI and to determine in which cases it is best to perform CT scans and surgical procedures.

    The findings of a Cochrane systematic review does not justify the routine use of hyperbaric oxygen therapy to treat people recovering from a traumatic brain injury. As of , the use of predictive visual tracking measurement to identify mild traumatic brain injury was being studied.

    In visual tracking tests, a head-mounted display unit with eye-tracking capability shows an object moving in a regular pattern. People without brain injury are able to track the moving object with smooth pursuit eye movements and correct trajectory. The test requires both attention and working memory which are difficult functions for people with mild traumatic brain injury.

    The question being studied, is whether results for people with brain injury will show visual-tracking gaze errors relative to the moving target. Pressure reactivity index is an emerging technology which correlates intracranial pressure with arterial blood pressure to give information about the state of cerebral perfusion. From Wikipedia, the free encyclopedia. Traumatic brain injury CT scan showing cerebral contusions , hemorrhage within the hemispheres, subdural hematoma , and skull fractures [1] Specialty Neurosurgery Traumatic brain injury TBI , also known as intracranial injury , occurs when an external force injures the brain.

    Focal and diffuse brain injury. Primary and secondary brain injury. Complications of traumatic brain injury. Special issues of assessment and management".

    Occupational Therapy and Physical Dysfunction: Principles, Skills and Practice. Archives of Disease in Childhood.

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    Editor's note: Pending an FDA decision, 23andMe no longer offers new More than million people a year sustain a traumatic brain injury. Doctors say that traumatic brain injury (TBI) is a catastrophic condition, like Now her daughter is 23 and has no goals and she is worried about her future and . 04/23/, Behavioral and neurophysiological abnormalities during cued continuous performance tasks in patients with mild traumatic brain injury. 04/23/

    Brain abnormalities found in victims of US embassy attack in Cuba



    Editor's note: Pending an FDA decision, 23andMe no longer offers new More than million people a year sustain a traumatic brain injury.


    Doctors say that traumatic brain injury (TBI) is a catastrophic condition, like Now her daughter is 23 and has no goals and she is worried about her future and .


    04/23/, Behavioral and neurophysiological abnormalities during cued continuous performance tasks in patients with mild traumatic brain injury. 04/23/


    1 Brain Injury Association of America. (, January). Soldiers with Traumatic Brain Injury (TBI). 2 Deployment Health Clinical Center. (, April 23).


    Neuropsychological function 23 years after mild traumatic brain injury. A comparison of outcome after pediatric and adult head injuries. Brain Injury; 21(9): .

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