Pathology of blast-related brain injury. J Rehabil Res Dev

Yale University School of Medicine, Neuroscience Research Center (127A), VA CT Healthcare System, West Haven, CT 06516, USA.
The Journal of Rehabilitation Research and Development (Impact Factor: 1.43). 01/2009; 46(6):667-72. DOI: 10.1682/JRRD.2008.08.0100
Source: PubMed


Blasts are responsible for about two-thirds of the combat injuries in Operation Iraqi Freedom and Operation Enduring Freedom, which include at least 1,200 traumatic brain injuries. Blasts inflict damage to the brain directly and by causing injuries to other organs, resulting in air emboli, hypoxia, and shock. Direct injuries to the brain result from rapid shifts in air pressure (primary blast injury), from impacts with munitions fragments and other objects propelled by the explosion (secondary blast injury), and from collisions with objects and rapid acceleration of individuals propelled by the explosion (tertiary blast injury). Tertiary injury can occur from a building or other structure collapsing and from an individual being thrown by the blast wind. The pathological consequences of secondary and tertiary blast injuries are very likely to be similar to those of other types of mechanical trauma seen in civilian life. The damage attributable to the specific effects of a blast, however, has received little study, although it has been assumed to include the focal and diffuse lesions characteristic of closed head injuries. Available clinical studies of blast injuries show focal damage similar to that found in other types of closed head injuries but have not determined whether diffuse axonal injury also occurs. In this article, we will try to reach a better understanding of the specific pathology of blast-related brain injury by reviewing the available experimental studies and the autopsy reports of victims of terrorist attacks and military casualties dating back to World War I.

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    • "In order to test these proposed hypotheses and clarify the underlying pathophysiology in blast TBI, different preclinical methods have been developed using either shock or explosive blast tubes or open-field blast experiments (8, 19, 34). From these studies, extensive data has been amassed on blast shock wave–tissue interaction, blast exposure related cognitive, and behavior changes and brain pathology. "
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    ABSTRACT: Traumatic brain injury (TBI) due to explosive blast exposure is a leading combat casualty. It is also implicated as a key contributor to war related mental health diseases. A clinically important consequence of all types of TBI is a high risk for development of seizures and epilepsy. Seizures have been reported in patients who have suffered blast injuries in the Global War on Terror but the exact prevalence is unknown. The occurrence of seizures supports the contention that explosive blast leads to both cellular and structural brain pathology. Unfortunately, the exact mechanism by which explosions cause brain injury is unclear, which complicates development of meaningful therapies and mitigation strategies. To help improve understanding, detailed neuropathological analysis is needed. For this, histopathological techniques are extremely valuable and indispensable. In the following we will review the pathological results, including those from immunohistochemical and special staining approaches, from recent preclinical explosive blast studies.
    Frontiers in Neurology 04/2014; 5:47. DOI:10.3389/fneur.2014.00047
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    • "Primary blast component of blast injury is among the main contributors in developing neuropsychiatric impairments associated with the primary phase profile (30, 73). There had been an urgent quest to for future research examining the impact of blast concussion (particularly recurrent concussion) on neuropsychological performance. "
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    ABSTRACT: Among the U.S. military personnel, blast injury is among the leading causes of brain injury. During the past decade, it has become apparent that even blast injury as a form of mild traumatic brain injury (mTBI) may lead to multiple different adverse outcomes, such as neuropsychiatric symptoms and long-term cognitive disability. Blast injury is characterized by blast overpressure, blast duration, and blast impulse. While the blast injuries of a victim close to the explosion will be severe, majority of victims are usually at a distance leading to milder form described as mild blast TBI (mbTBI). A major feature of mbTBI is its complex manifestation occurring in concert at different organ levels involving systemic, cerebral, neuronal, and neuropsychiatric responses; some of which are shared with other forms of brain trauma such as acute brain injury and other neuropsychiatric disorders such as post-traumatic stress disorder. The pathophysiology of blast injury exposure involves complex cascades of chronic psychological stress, autonomic dysfunction, and neuro/systemic inflammation. These factors render blast injury as an arduous challenge in terms of diagnosis and treatment as well as identification of sensitive and specific biomarkers distinguishing mTBI from other non-TBI pathologies and from neuropsychiatric disorders with similar symptoms. This is due to the "distinct" but shared and partially identified biochemical pathways and neuro-histopathological changes that might be linked to behavioral deficits observed. Taken together, this article aims to provide an overview of the current status of the cellular and pathological mechanisms involved in blast overpressure injury and argues for the urgent need to identify potential biomarkers that can hint at the different mechanisms involved.
    Frontiers in Neurology 11/2013; 4:186. DOI:10.3389/fneur.2013.00186
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    • "Brain injuries are usually accompanied by injuries of other organs such as lung, bones, gastrointestinal tract, and heart, which can produce air emboli, fat emboli, and hypoxia/ischemia.14,24) The effects of blast injuries on the brain of animals include changes in small, unmyelinated axons that are characteristic of diffuse axonal injury, skull fractures, and extensive epidural, subdural, subarachnoid, and intracerebral hemorrhages, expanded perineuronal spaces, appearance of cytoplasmic vacuoles, myelin deformation, axoplasmic shrinkage, transient alternations in the distribution of neurofilament proteins.12,24,25) These changes such as expanded perineuronal spaces, appearance of cytoplasmic vacuoles, myelin deformation, axoplasmic shrinkage are due to the activation of inducible nitric oxide synthase and oxidative stress in the brain.12) "
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    ABSTRACT: The main objective of this study is to provide an overview of the basic mechanisms of blast induced hearing loss and review pharmacological treatments or interventions that can reduce or inhibit blast induced hearing loss. The mechanisms of blast induced hearing loss have been studied in experimental animal models mimicking features of damage or injury seen in human. Blast induced hearing loss is characterized by perforation and rupture of the tympanic membrane, ossicular damage, basilar membrane damage, inner and outer hair cell loss, rupture of round window, changes in chemical components of cochlear fluid, vasospasm, ischemia, oxidative stress, excitotoxicity, hematoma, and hemorrhage in both animals and humans. These histopathological consequences of blast exposure can induce hearing loss, tinnitus, dizziness, and headache. The pharmacological approaches to block or inhibit some of the auditory pathological consequences caused by blast exposure have been developed with antioxidant drugs such as 2,4-disulfonyl α-phenyl tertiary butyl nitrone (HXY-059, now called HPN-07) and N-acetylcysteine (NAC). A combination of antioxidant drugs (HPN-07 and NAC) was administered to reduce blast induced cochlear damage and hearing loss. The combination of the antioxidant drugs can prevent or treat blast induced hearing loss by reducing damage to the mechanical and neural component of the auditory system. Although information of the underlying mechanisms and treatment of blast induced hearing loss are provided, further and deep research should be achieved due to the limited and controversial knowledge.
    Korean Journal of Audiology 12/2012; 16(3):103-107. DOI:10.7874/kja.2012.16.3.103
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