FIGURE 3-2 Rodent models of TBI: (A) weight-drop model, (B) impact acceleration model, (C) controlled cortical impact model, and (D) fluid percussion model.

FIGURE 3-2 Rodent models of TBI: (A) weight-drop model, (B) impact acceleration model, (C) controlled cortical impact model, and (D) fluid percussion model.

SOURCE: Morales et al., 2005.

disruption of the blood-brain barrier (BBB), cortical and subcortical cell loss, and diffuse axonal injury. The weight-drop model relies on a free-falling, guided weight that strikes the exposed skull or the dura; the head may be either restrained or unrestrained. The midline fluid percussion injury model entails delivery of a brief pulse of fluid to the intact dura. The skull is exposed and after a craniectomy to expose the dura, an injury is produced by delivery of a fluid bolus, resulting from the release of a pendulum. The controlled cortical impact model utilizes a rigid impactor, controlled by pressurized air, to strike the exposed dura.

The impact acceleration model is characterized by a more diffuse injury that includes hemorrhage (typically intraparenchymal as well as subarachnoid); disruption of the BBB; cortical and subcortical damage; and widespread axonal swelling, damage, or both. This model uses a weight-drop strategy. However, a plate is secured to the skull to distribute the weight and minimize skull fractures. The head is unrestrained and positioned on a cushion with specified properties that allow a defined movement of the head after impact. Finally, it is noteworthy that a modification to the fluid percussion injury, with the insult shifted from midline to a more lateral position, results in both focal and diffuse brain injury.

Models of blast-induced brain injury, developed and characterized in both large and small animals, were reviewed by Cernak and Noble-Haeusslein in 2010. In brief, shock waves are produced by either shock tubes using compressed air or gas, or blast tubes that rely on explosive charges. There is increasing evidence that these models share pathologic and biochemical characteristics seen in the more traditional models of focal and diffuse TBI, including hemorrhage, diffuse axonal injury, cortical and subcortical cell injury, metabolic disturbances/energy failure, inflammation, and oxidative stress. What remains controversial is the extent to which blast-induced brain injuries have unique temporal and spatial profiles of pathogenic events that would distinguish them from other types of TBIs.



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