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2 BIOLOGY OF TRAUMATIC BRAIN INJURY
Pages 19-58

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From page 19...
... PATHOBIOLOGY OF TRAUMATIC BRAIN INJURY Damage to the traumatized brain is a consequence of the initial mechanical insult and the subsequent activation of secondary pathogenic cascades that collectively influence the temporal progression of the primary insult (McIntosh, 1994; Werner and Engelhard, 2007)
From page 20...
... . Glutamate-mediated excitotoxicity leads to an increase in intracellular calcium and the subsequent induction of enzymes, such as nitric oxide synthase and xanthine oxidase, that produce free radicals.
From page 21...
... . Necrotic death and apoptotic cell death of neurons and glia have been identified in contused areas, the tissue bordering a contusion, and subcortical regions, including the hippocampus, cerebellum, and thalamus (Raghupathi et al., 2000; Raghupathi, 2004; Yakovlev and Faden, 2004)
From page 22...
... White matter injury is evidenced in part by axonal degeneration, oligodendrocyte death, and demyelination. White matter damage in relative isolation ("pure" diffuse axonal injury)
From page 23...
... Animal models are designed to produce a relatively homogeneous type of injury whereas a key feature of human TBI is heterogeneity. That distinction may partially account for differences in the kinetics of secondary pathogenic events when one compares findings in the animal model with the human condition.
From page 24...
... Posttraumatic ischemia has been demonstrated in both animal models and humans after TBI and is associated with poor neurologic outcome. The factors mediating posttraumatic ischemia include mechanical damage to blood vessels, hypotension in concert with autoregulatory failure, and lack of available endogenous vasomodulators, such as nitric oxide and prostaglandins (Werner and Engelhard, 2007)
From page 25...
... Those advanced technologies offer the opportunity to track the complex injury cascade that accompanies TBI and ultimately to generate a panel of biomarkers that can be applied to the brain-injured patient. TRADITIONAL CLASSIFICATIONS OF TRAUMATIC BRAIN INJURY TBI may be classified according to the extent of the pathology of the injury or according to the biomechanics of the injury.
From page 26...
... . Pathologic Features of Diffuse Traumatic Brain Injury Four pathologic conditions have been attributed to diffuse TBI: traumatic axonal injury, hypoxic brain damage, brain swelling, and vascular injury (Morales et al., 2005; Povlishock and Katz, 2005)
From page 27...
... Static loading occurs when a gradual force is applied to the brain whereas dynamic loading is characterized by rapid acceleration and deceleration. Static loading is not common in human head injury.
From page 28...
... . THERAPEUTICS AND TRAUMATIC BRAIN INJURY A number of recent reviews have addressed pharmacologic strategies of treatment for TBI (Faden, 2002; Morales et al., 2005; Thompson et al., 2005; Marklund et al., 2006; Schouten, 2007)
From page 29...
... , future efforts to develop and/or refine animal models will need to consider the findings that emerge from this clinical effort. SUMMARY OF PATHOBIOLOGY OF TRAUMATIC BRAIN INJURY The pathobiology of TBI can be summarized as follows: The traditional classifications of TBI have been based on the type of injury (focal vs.
From page 30...
... BLAST WAVE DEATH Injuries with immediate manifestation Hidden injuries with long-term consequences FIGURE 2.3 Potential consequences of blast exposure. In both civilian and military environments, exposure to a blast (see Figure 2.3)
From page 31...
... . The duration of the blast wave -- that is, the time that an object in the path of the shock wave is subjected to the pressure effects -- depends on the type of explosive and the distance from the point of detonation (Clemedson, 1956)
From page 32...
... The blast wave is the main determinant of the primary blast injury and consists of the front of high pressure that compresses the surrounding air and falls rapidly to negative pressure. It travels faster than sound and in a few milliseconds damages the surrounding structures.
From page 33...
... . Explosions may cause four major patterns of injury: primary blast injury caused by the blast wave itself, secondary injury caused by the fragments of debris propelled by the explosion, tertiary injury due to the acceleration of the body or part of the body by the blast wind, and flash burns due to the transient but intense heat of the explosion (Mellor, 1988)
From page 34...
... . Therefore, most research focused on the mechanisms of blast injuries within gas-containing organs or organ systems, primary BINT was underestimated, and safety recommendations (Table 2.1)
From page 35...
... . Because of the complexity of blast injury, its diagnosis should be based on a history of blast exposure, the presence of subjective symptoms characteristic of blast injuries, pathognomonic findings in a physical examination, and suggestive results of clinical tests (Cernak et al., 1999a, 1999b)
From page 36...
... Primary blast injury of the chest produces bradycardia, hypotension, and apnea via vagal reflexes, which may induce cerebral hypoxia and ischemia (Cernak et al., 1996a, 1997; Ohnishi et al., 2001)
From page 37...
... Although the damage might resemble the injury patterns that develop after mechanical TBI caused by direct interaction of a mechanical force and the skull, the injury manifestation, timeline, and complexity of pathologic changes make BINT a distinct health problem. Furthermore, frequency resonance between blast wave and electromagnetic pulse might also contribute to primary blast-induced neurologic disturbances (G.
From page 38...
... . Most shock and blast tubes used in current experimental models replicate the ideal blast wave from an open-air explosion without a capability to generate a nonideal blast wave with multiple shock and expansion fronts as seen in real-life conditions, and this limits the extent of comparability of experimental and clinical findings.
From page 39...
... reported that even veterans with a remote history of blast injury display permanent EEG changes similar to those often found after TBI, as well as persistent cognitive problems (Trudeau et al., 1998)
From page 40...
... . Penetrating Traumatic Brain Injury Penetrating TBI is generally inflicted by munitions fragments, high-energy bullets, or other fragments generated by an explosion.
From page 41...
... SEVERITY SCORING OF BLAST INJURIES AND TRAUMATIC BRAIN INJURY Severity Scoring of Blast Injuries The severity of injuries inflicted by explosive weaponry is usually scored by using the Abbreviated Injury Scale (AIS) or the Injury Severity Score (ISS)
From page 42...
... Experimental studies have often used the Walter Reed Army Institute of Research Blast Injury Subjective Score, which establishes blast-injury severity on the basis of the extent of lung damage (Jaffin et al., 1987; Mayorga, 1997) but does not take into account injuries in other organs or organ systems due to blast exposure.
From page 43...
... developed a head-injury severity scale for closed TBI, defining five GCS intervals: minimal head injury (GCS = 15, no LOC or amnesia) , mild head injury (GCS = 14, or 15 plus amnesia, or <5 minutes LOC, or impaired alertness or memory)
From page 44...
... . The Brief Traumatic Brain Injury Screen The Brief Traumatic Brain Injury Screen (BTBIS)
From page 45...
... It is recommended that beyond the use of the MACE other neurocognitive measures be implemented at level III to evaluate the cognitive state of an injured service member comprehensively. Severity Scoring of BINT Because moderate, moderate-to-severe, and severe BINTs are often part of complex polytrauma, proper diagnosis of BINT should include both classification of blast injuries and severity scoring of the head injury.
From page 46...
... 1989. Diffuse axonal injury in head injury: Definition, diagnosis and grading.
From page 47...
... http://www.bt.cdc.gov/masscasualties/pdf/explosions-blast injuries.pdf (accessed August 22, 2007)
From page 48...
... 2000. Characterization of plasma magnesium concentration and oxidative stress following graded traumatic brain injury in humans.
From page 49...
... 2006a. DVBIC Working Group on Acute Management of Mild Traumatic Brain Injury in Military Operational Setting: Washington, DC.
From page 50...
... 2007. Astroglia: Important mediators of traumatic brain injury.
From page 51...
... 2007. A review of pharmacological treatments used in experimental models of traumatic brain injury.
From page 52...
... 2007. The Mayo classification system for traumatic brain injury severity.
From page 53...
... 2005. Experimental models of traumatic brain injury: Do we really need to build a better mousetrap?
From page 54...
... 2004. Cell death mechanisms following traumatic brain injury.
From page 55...
... 2007. Gait rehabilitation with body weight-supported treadmill training for a blast injury survivor with traumatic brain injury.
From page 56...
... 1998. Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: A microdialysis study.
From page 57...
... 2005a. Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury.


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