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Traumatic Brain Injury (TBI) is the leading cause of death and disability in young people under 45,affecting nearly 70 Million people worldwide every year. As the leading cause of disability-adjusted lifeyears lost, TBI holds enormous financial and societal implications globally. Defined as any injury to thebrain caused by external mechanical forces, TBI is characterized by an elongated pathophysiologicalcascade that induces molecular and cellular degenerations through focal and diffuse patterns of secondaryinsults that cause substantial necrosis, cortical atrophy and diffuse axonal injuries. Clinical cases of TBIfrequently display cerebral oedema, intracranial haemorrhage, altered neuronal function, and diminishedCerebral Blood Flow (CBF) regulation. Although substantial progress has been made in understanding thepathogenesis of intracranial injuries and the clinical presentation of TBI, there are currently nodisease-modifying therapeutic interventions or predictive models for treating TBI. Contemporary animalmodels of TBI, particularly controlled cortical impact (CCI) injury and fluid percussion injury (FPI)models have yielded substantial success in reproducing key pathophysiological, cognitive andneurobehavioral cascades characteristic of secondary insults in human TBI. These models not onlyrecapitulate clinically relevant features of the disease but also serve as highly promising preclinicalwindows into developing patient-stratified therapies for treating clinical TBI. The current paper reviewsthe basic pathophysiology, clinical presentation, treatment strategies and contemporary experimentalmodels of TBI. Lastly, the paper aims to elucidate the role of emergent FPI and CCI animal models thatcombine secondary insults as highly promising ventures into developing prediction models andpatient-stratified strategies for treating moderate-to-severe TBI.
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Matthew A Abikenari (2024) studied this question.
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