This article provides a concise overview, at the structural and functional level, of those changes evoked by traumatic brain injury across the spectrum of the disease. Using data derived from animals and humans, the pathogenesis of focal versus diffuse brain damage is presented for consideration of its overall implications for morbidity. Emphasis is placed on contusion and its potential expansion in concert with diffuse changes primarily assessed at the axonal level. Concomitant involvement of neuroexcitation and its role in global and focal metabolic changes is considered. Lastly, the influence of premorbid factors including age, genetics, and socioeconomic background is discussed.
Key points
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Traumatic brain injury (TBI) remains one of the most complex diseases in the most complex of all organs in the body.
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The causes of TBI are many and varied and include penetrating and nonpenetrating injuries that, based on their overall level of severity, can evoke different degrees of morbidity, typically framed within the context of the Glasgow Coma Scale (GCS) score.
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In considering the pathobiology of TBI across the spectrum of the disease ranging from mild through severe, it is common to discuss this disease within the context of focal versus diffuse change, with the inference that these events typically occur in isolation, with each following a unique footprint of pathophysiologic change.
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