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Review

Diffuse Axonal Injury

In: Translational Research in Traumatic Brain Injury. Boca Raton (FL): CRC Press/Taylor and Francis Group; 2016. Chapter 3.
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Review

Diffuse Axonal Injury

Erik Su et al.
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Excerpt

Traumatic brain injury (TBI) is the leading cause of death in the United States in people between the ages of 1 and 44 years and occurs in hundreds of thousands of subjects yearly. Recently, the importance of apparently mild injuries has been recognized as a public health crisis for soldiers in the combat theater, children and young adults in sport activities, and others throughout their normal life. Our understanding of the pathology of TBI is rudimentary despite years of study. This chapter will summarize an important aspect of TBI pathology—diffuse axonal injury (DAI)—that is increasingly recognized as an important cause of long-term disability and mortality. DAI describes a process of widespread axonal damage in the aftermath of acute or repetitive TBI, leading to deficits in cerebral connectivity that may or may not recover over time. It is a component of injury in 40% to 50% of hospital admissions for traumatic brain injury (TBI) and one of the most common pathologies in all closed-head trauma.– DAI is typically characterized by coma without focal lesion, on presentation and pathologically defined by axonal damage in multiple regions of the brain parenchyma, often causing impairments in cognitive, autonomic motor, and sensory function by virtue of disrupted neuronal connectivity. Areas commonly affected include axons in the brainstem, parasagittal white matter near the cerebral cortex, and corpus callosum. Though DAI is often characterized as a structural disease, where the fundamental brain architecture is irreparably disrupted on a microscopic scale, many aspects of DAI are influenced not only by physical factors but by perturbations in any number of pathways including metabolism, electrochemistry, and inflammation among others. DAI preceded by a period of relative lucidity diagnosed with imaging findings has also been described., This may correlate with animal models of DAI demonstrating direction dependence of trauma influencing coma, however, lower extremity long bone orthopedic intervention factored heavily in these clinical cases, and imaging findings in these patients’ brains may have been confounded by emboli mimicking DAI findings. DAI was first described in comatose trauma subjects who demonstrated scattered axonal injury in the cerebrum, cerebellum, and brainstem on postmortem examination. Advances in histopathology during the 1950s further revealed the extent of axonal injury associated with DAI at the cellular level. Through the 1960s additional studies would describe an early histopathological pattern of scattered axonal injury characterized by worsening swelling and distortion of normal architecture into retraction bulbs and helical structures. Extensive characterization of these histologic findings in trauma victims subject to large acceleration/deceleration forces led to the initial definitions of “diffuse axonal injury” described in 1982 by Adams and colleagues. The Adams classification is used to grade DAI from a pathology standpoint and is described (Table 3.1).

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