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            "title": "Combat TBI: History, Epidemiology, and Injury Modes",
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                    "creatorType": "author",
                    "firstName": "Ralph G.",
                    "lastName": "DePalma"
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                    "firstName": "Firas H.",
                    "lastName": "Kobeissy"
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            "abstractNote": "Although types and modes of combat injury have changed over the centuries as weapons of war evolved, details about combat traumatic brain injury (TBI) date from the earliest accounts of warfare. This chapter provides a brief historical overview of combat TBI resulting from primitive blunt and penetrating head injuries to current blast-related injuries. Updated numbers of TBI events and injuring mechanisms will be considered. Brain injury causes loss or alteration of consciousness, prograde and retrograde amnesia, and immediate physical and neurological effects ranging from mild to severe. These injuries, in certain cases, cause varying chronic physical, cognitive, and behavioral issues. The most common form of brain injury, acute mild TBI or concussion (mTBI/concussion), has multiple definitions derived from various sources. Vasterling et al. have provided a useful summary of these iterations (Vasterling, 2012). The operative definition selected for this review includes loss or alteration consciousness for up to 30 minutes at the time of injury, a confused or disoriented state lasting less than 24 hours, memory loss lasting less than 24 hours, and normal structural brain imaging on computed tomographic scanning. Glasgow Coma Scale scores of 13–15 characterize acute mTBI, whereas lower Glasgow Coma Scale scores, 9–12, designate acute moderate TBI. Glasgow Coma Scale scores of 3–8 designate acute severe TBI (Teasdale and Jennett, 1974). Current combat or military TBI/concussions most frequently are classified as mild. Although recovery from mTBI/concussion is said to be the norm, in about 15% (estimates range from 10%–25%) of cases, physical disabilities and symptoms persist beyond three months to become a chronic condition, also known as postconcussion syndrome (Vasterling, 2012). Chronic sequelae of postconcussion syndrome include headache, insomnia, fatigue, sensory, balance, and other neurologic defects as well as cognitive and emotional disorders. Symptoms can be subtle and variable in severity and frequency over time; mTBI and concussion are often used clinically as synonyms. This chapter focuses on mTBI/concussion as a combat injury. Diagnosis of posttraumatic stress disorder (PTSD), first accepted as a formal diagnosis in 1980 (Horowitz et al., 1980), and other mental illness including depression are reportedly more common in combatants as compared with nondeployed service members during current ongoing military operations (Blakely, 2013). The methods used to obtain estimates affect data concerning numbers of cases of TBI, PTSD, and other mental disorders. Individuals usually are reported only once as a case within a category; data can be presented as the number of diagnoses (prevalence), rate of new diagnoses in a population (incidence), or total number of cases in a population. The total number of diagnoses changes in relation to population size, which for military conditions increases over time with continued combat activities (Blakely, 2013). This chapter uses numbers available from public sources for the Department of Defense (DOD) and updated data through 2013 from the tracking tool used by the Department of Veterans Affairs (VA). PTSD results from exposure to a traumatic event with risk of serious injury or bodily harm to self or others and a response to that event involving intense fear, horror, or helplessness. Symptoms include reexperiencing of the traumatic event, including nightmares and distressing recollections, avoidance of stimuli associated with the trauma with diminished responsiveness and loss of interest in activities, and hyperarousal including irritability, anger, hypervigilance, insomnia, and concentration difficulties. Cognitive and behavioral symptoms of PTSD and depression overlap with those of mTBI; mTBI sustained during the stress of battle is believed to predispose to or accentuate PTSD (Bryant, 2011; Vasterling, 2012). Historical narratives reveal connections or associations between past and current relationships (Rabins, 2013). Vignettes from past and present conflicts yield insights into the causes and sequelae of combat injuries affecting the brain. Currently, blast injuries predominate among combatants in Operations Enduring Freedom, Iraqi Freedom, and New Dawn (OEF/OIF/OND). Recognition of the importance of mTBI and PTSD relates to enhanced surveillance and clinical guidelines initiated by the DOD and the VA (Management of Concussion/mTBI Working Group 2009). Incidence and prevalence data from both sources provide ongoing estimates of the numbers of service members affected by TBI; the frequency of this particular injury has become a matter of increasing concern. Although the long-term effects of brain damage caused by differing modes of head injury seem to appear identical in the long term (Belanger et al., 2009), recent observations suggest that differing modes of combat injury—for example, blunt as compared with blast injuries—result in differing vestibular-ocular and spinal reflexes (Hoffer et al., 2009) and neural activation responses (Fischer et al., 2013). Behavioral disorders appear to be more common with blast as opposed to blunt injury (Mendez et al., 2013). Repeated injuries, particularly sports-related, have become a public health concern because of their long-term consequences (Jordan, 2013). These emerging observations are important for assessing treatments, outcomes, and disability determinations.",
            "bookTitle": "Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects",
            "series": "Frontiers in Neuroengineering",
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            "shortTitle": "Combat TBI",
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            "rights": "© 2015 by Taylor & Francis Group, LLC.",
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            "title": "The pathobiology of blast injuries and blast-induced neurotrauma as identified using a new experimental model of injury in mice",
            "creators": [
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                    "creatorType": "author",
                    "firstName": "Ibolja",
                    "lastName": "Cernak"
                },
                {
                    "creatorType": "author",
                    "firstName": "Andrew C.",
                    "lastName": "Merkle"
                },
                {
                    "creatorType": "author",
                    "firstName": "Vassilis E.",
                    "lastName": "Koliatsos"
                },
                {
                    "creatorType": "author",
                    "firstName": "Justin M.",
                    "lastName": "Bilik"
                },
                {
                    "creatorType": "author",
                    "firstName": "Quang T.",
                    "lastName": "Luong"
                },
                {
                    "creatorType": "author",
                    "firstName": "Theresa M.",
                    "lastName": "Mahota"
                },
                {
                    "creatorType": "author",
                    "firstName": "Leyan",
                    "lastName": "Xu"
                },
                {
                    "creatorType": "author",
                    "firstName": "Nicole",
                    "lastName": "Slack"
                },
                {
                    "creatorType": "author",
                    "firstName": "David",
                    "lastName": "Windle"
                },
                {
                    "creatorType": "author",
                    "firstName": "Farid A.",
                    "lastName": "Ahmed"
                }
            ],
            "abstractNote": "Current experimental models of blast injuries used to study blast-induced neurotrauma (BINT) vary widely, which makes the comparison of the experimental results extremely challenging. Most of the blast injury models replicate the ideal Friedländer type of blast wave, without the capability to generate blast signatures with multiple shock fronts and refraction waves as seen in real-life conditions; this significantly reduces their clinical and military relevance. Here, we describe the pathophysiological consequences of graded blast injuries and BINT generated by a newly developed, highly controlled, and reproducible model using a modular, multi-chamber shock tube capable of tailoring pressure wave signatures and reproducing complex shock wave signatures seen in theater. While functional deficits due to blast exposure represent the principal health problem for today's warfighters, the majority of available blast models induces tissue destruction rather than mimic functional deficits. Thus, the main goal of our model is to reliably reproduce long-term neurological impairments caused by blast. Physiological parameters, functional (motor, cognitive, and behavioral) outcomes, and underlying molecular mechanisms involved in inflammation measured in the brain over the 30 day post-blast period showed this model is capable of reproducing major neurological changes of clinical BINT.",
            "publicationTitle": "Neurobiology of Disease",
            "publisher": "",
            "place": "",
            "date": "Feb 2011",
            "volume": "41",
            "issue": "2",
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            "partNumber": "",
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            "pages": "538-551",
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            "journalAbbreviation": "Neurobiol. Dis.",
            "DOI": "10.1016/j.nbd.2010.10.025",
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            "extra": "PMID: 21074615",
            "tags": [
                {
                    "tag": "Animals",
                    "type": 1
                },
                {
                    "tag": "Atmosphere Exposure Chambers",
                    "type": 1
                },
                {
                    "tag": "Atmospheric Pressure",
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                    "tag": "Blast Injuries",
                    "type": 1
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            "abstractNote": "Objective\nThe purpose of this study is to provide a review of the ocular injuries sustained by survivors of the April 19, 1995, bombing of the Alfred P. Murrah Federal Building in Oklahoma City.\nDesign\nRetrospective, noncomparative case series.\nParticipants\nThe authors retrospectively evaluated data collected on all surviving persons receiving ocular injuries during the bombing and on all at-risk occupants of the federal building and four adjacent buildings.\nMethods\nInjury data from survivors were collected from multiple sources to include hospital medical records, a physician survey, emergency medical services run reports, written survivor accounts, building occupant survey, telephone interviews, and mail surveys.\nMain outcome measures\nThe types of ocular injuries, the associated systemic injuries, and the location of the injured at the time of the blast were evaluated.\nResults\nFifty-five (8%) of the 684 injured bombing survivors sustained an ocular injury. Persons injured in the Murrah building were more than three times more likely to sustain an ocular injury than other injured persons. Seventy-one percent of ocular injuries occurred within 300 feet of the point of detonation. The most common serious ocular injuries included lid/brow lacerations (20 patients, 23 eyes), open globe injuries (12 eyes), orbital fractures (6 eyes), and retinal detachment (5 eyes). A retained intraocular foreign body accounted for only two of the injuries (4%). Glass accounted for nearly two thirds of the ocular injuries.\nConclusions\nBlasts involving explosions inflict severe ocular injury, mostly as a result of secondary blast effects from glass, debris, etc. Eye injuries in bombings can probably be prevented by increasing the distance from and orientation away from windows (i.e., by facing desks away from windows). Use of such products as laminated glass, toughened window glazing, and Mylar curtains may reduce glass projectiles in the blast vicinity.",
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            "abstractNote": "Aim: The potential causes of the optic nerve injury as a result of blunt object trauma, were investigated using a computer model.\nMethods: A finite element model of the eye, the optic nerve, and the orbit with its content was constructed to simulate blunt object trauma. We used a model of the first phalanx of the index finger to represent the blunt body. The trauma was simulated by impacting the blunt body at the surface between the globe and the orbital wall at velocities between 2–5 m/s, and allowing it to penetrate 4–10 mm below the orbital rim.\nResults: The impact caused rotations of the globe of up to 5000°/s, lateral velocities of up to 1 m/s, and intraocular pressures (IOP) of over 300 mm Hg. The main stress concentration was observed at the insertion of the nerve into the sclera, at the side opposite to the impact.\nConclusions: The results suggest that the most likely mechanisms of injury are rapid rotation and lateral translation of the globe, as well as a dramatic rise in the IOP. The strains calculated in the study should be sufficiently high to cause axonal damage and even the avulsion of the nerve. Finite element computer modelling has therefore provided important insights into a clinical scenario that cannot be replicated in human or animal experiments.",
            "publicationTitle": "British Journal of Ophthalmology",
            "publisher": "",
            "place": "",
            "date": "06/01/2006",
            "volume": "90",
            "issue": "6",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "778-783",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Br J Ophthalmol",
            "DOI": "10.1136/bjo.2005.086538",
            "citationKey": "",
            "url": "http://bjo.bmj.com/content/90/6/778",
            "accessDate": "2015-09-25T16:23:20Z",
            "PMID": "",
            "PMCID": "",
            "ISSN": ", 1468-2079",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "en",
            "libraryCatalog": "bjo.bmj.com",
            "callNumber": "",
            "rights": "",
            "extra": "PMID: 16421184",
            "tags": [
                {
                    "tag": "IOP, intraocular pressure",
                    "type": 1
                },
                {
                    "tag": "Optic Nerve",
                    "type": 1
                },
                {
                    "tag": "avulsion",
                    "type": 1
                },
                {
                    "tag": "blunt injury",
                    "type": 1
                },
                {
                    "tag": "computer model",
                    "type": 1
                },
                {
                    "tag": "traumatic neuropathy",
                    "type": 1
                }
            ],
            "collections": [],
            "relations": {},
            "dateAdded": "2015-09-25T16:23:20Z",
            "dateModified": "2015-09-25T16:23:20Z"
        }
    }
]