| Summary: | Contemporary biomechanical theory of traumatic brain injury has its foundation in Holbourn's thesis on shear strain and Ommaya's primate experimentation demonstrating the role of rotation in a variety of lesions including subdural hematoma (SDH) and diffuse axonal injury. Empirical human observations have since confirmed, for the most part, the early concepts. Ethical concerns regarding primate research, however, have prompted in vitro models, which in turn has led to challenges with respect to the correlation between in vitro observations and the clinical data. Despite these challenges, medicolegal proceedings may call upon biomechanical engineers to reconstruct complex injury scenarios and offer opinions on the scientific plausibility of clinical disease states, such as SDH, hemorrhagic retinopathy, and cerebral edema, associated with hypothetical or proffered action sequences during the course of an unwitnessed homicide. It is important to note, however, that in vitro models by their nature are low-evidence quality studies that attempt to advance hypotheses but do not address cause and effect. As a whole, biomechanical models, as they pertain specifically to the brain and spine, are mathematically imprecise. Often, endpoints of limited relevance are relied upon (e.g., skull fracture thresholds), which predictably overestimate the in vivo risk of significant injury. Given the increasing role of biomechanical engineering in the interpretation of fatal pediatric head trauma, a heightened awareness of the limitations warranted.
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