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Traumatic Brain Injuries

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Traumatic Brain Injuries PRIMEVIEW TRAUMATIC BRAIN INJURIES For the Primer, visit doi:10.1038/nrdp.2016.84 Axonal injury is considered a Traumatic brain injuries (TBIs) are a DIAGNOSIS MECHANISMS key mechanism of Axonal injury major cause of disability and death damage following TBIs, worldwide. Clinically subdivided into mild, as the severity of axonal TBIs are classified based on several clinical factors, moderate and severe forms, mild TBI (also Brain damage injury correlates including the Glasgow Coma Scale score, results known as concussion) accounts for 80–90% Microhaemorrhages Activation of microglia in TBIs is caused with the extent of radiographic imaging (CT or MRI) and the of cases. Insights from severe TBI and by rotational and/or of disability presence of neurological symptoms and amnesia. chronic traumatic encephalopathy (CTE) linear acceleration forces, Newer radiographic imaging techniques, such as can probably shed light on the underlying or blunt trauma with impact diffusion tensor imaging, can be used to detect cellular and molecular processes involved deceleration, which generate axonal injury in patients with TBI. PET ligands that in mild TBI. forces that stretch and bind to Aβ plaques and tau can be used to monitor damage axons Tau aggregation the deposition of these molecules in the brain and could be used to assess the pathology of TBIs. EPIDEMIOLOGY Biomarkers are emerging to assess Approximately 10 million TBIs occur each year Aβ accumulation the severity of brain damage, worldwide. The most common causes are falls TRAUMA predict prognosis and guide clinical and road traffic accidents, which account management. Candidates include markers for >50% of cases. Contact sports athletes and Reactive oxygen of neuronal damage, immune response and military service personnel are unique, increasingly and nitrogen astrocyte function. studied risk groups for TBIs; the incidence of species formation sports-related TBI visits to emergency rooms is 152 cases per 100,000 individuals in the United States. MANAGEMENT Several studies suggest At the scene of injury or in the emergency a relationship between room, patients have a brief interview and a repetitive TBI and CTE, neurological examination. If indicated, patients a neurodegenerative condition Aside from can undergo radiographic characterized by perivascular axonal injury, a imaging. The standard tau deposition, axonal damage range of other of care for patients Few guidelines and variable amounts pathophysiological with TBI is rest, for the diagnosis findings can also of astroglial scarring observation for be observed or management of and Aβ plaques 24 hours following TBIs athletes with potential and verbal and CTE are available. However, QUALITY OF LIFE written many clinicians would advise instructions an athlete to retire from Levels of cognitive and physical disability in New treatments for for identifying OUTLOOK sports after sustaining patients with TBI depend on the severity of TBIs include those that the possible multiple concussions. injury, and can affect mood, fatigue and social target cerebral oedema, prevent complications participation. 12 months after mild TBI, patients More research is required to underlies CTE. In addition, studies are secondary tissue damage and of TBIs. have a similar quality of life to controls, but this understand the number needed to elucidate the precise role promote neuroprotection can decrease over time, owing to a loss of life and/or severity of TBIs that initiate of tau aggregates and amyloid- (A ) β β or neuroregeneration. roles and the development of depression. the neurodegeneration that deposits in TBIs and CTE. Written by Louise Adams; designed by Laura Marshall Article number: 16085; doi:10.1038/nrdp.2016.85; published online 17 Nov 2016 ©2016 Mac millan Publishers Li mited, part of Spri nger Nature. All ri ghts reserved. .
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  • Blunt and Blast Head Trauma: Different Entities
    International Tinnitus Journal, Vol. 15, No. 2, 115–118 (2009) Blunt and Blast Head Trauma: Different Entities Michael E. Hoffer,1 Chadwick Donaldson,1 Kim R. Gottshall1, Carey Balaban,2 and Ben J. Balough1 1 Spatial Orientation Center, Department of Otolaryngology, Naval Medical Center San Diego, San Diego, California, and 2 Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA Abstract: Mild traumatic brain injury (mTBI) caused by blast-related and blunt head trauma is frequently encountered in clinical practice. Understanding the nuances between these two distinct types of injury leads to a more focused approach by clinicians to develop better treat- ment strategies for patients. In this study, we evaluated two separate cohorts of mTBI patients to ascertain whether any difference exists in vestibular-ocular reflex (VOR) testing (n ϭ 55 en- rolled patients: 34 blunt, 21 blast) and vestibular-spinal reflex (VSR) testing (n ϭ 72 enrolled patients: 33 blunt, 39 blast). The VOR group displayed a preponderance of patients with blunt mTBI, demonstrating normal to high-frequency phase lag on rotational chair testing, whereas patients experiencing mTBI from blast-related causes revealed a trend toward low-frequency phase lag on evaluation. The VSR cohort showed that patients with posttraumatic migraine- associated dizziness tended to test higher on posturography. However, an indepth look at the total patient population in this second cohort reveals that a higher percentage of blast-exposed patients exhibited a significantly increased latency on motor control testing as compared to pa- tients with blunt head injury ( p Ͻ .02). These experiments identify a distinct difference be- tween blunt-injury and blast-injury mTBI patients and provide evidence that treatment strategies should be individualized on the basis of each mechanism of injury.
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