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Pathophysiology of Head Injuries

Athletic head injuries usually result from direct impact and/or deceleration-rotational events. Classic principles of brain contusions include the concept of coup injury, in which a forceful blow to a stationary head imparts maximal brain injury directly beneath the point of impact.

On the other hand, contrecoup injuries occur when the energy of impact is transferred to the mobile brain, such that it glides against the fixed, sharp surfaces of the dural reflection or skull base ridges, thus resulting in a contusion at a site opposite that of the initial external trauma. The effect of forces on the brain parenchyma normally are buffered by the cerebrospinal fluid (CSF), which serves as a shock absorber, protecting the brain by converting focal stresses to more uniformly distributed compressive stress.

The contrecoup injury pattern occurs because, in the moving head, the floating brain lags behind the leading skull edge, diminishing the protective CSF in the trailing surface and creating a thickened layer of CSF at the leading cranial surface. In the setting of skull fractures, the depressed fragment may directly injure the adjacent parenchyma.

Three types of stresses commonly are imparted to brain tissue—compression, tensile, and shear—and these types may occur in combination. Compressive forces result in direct impact to the brain parenchyma, as in the case of depressed skull fractures. Tensile and compressive forces may occur with linear acceleration injuries, such as in the coup/contrecoup injury patterns.

Shearing injuries are often caused by rotational forces and are poorly tolerated by brain parenchyma. These injuries are thought to be related to differences in the physical properties of gray matter and axonal fibers (density differences), such that they decelerate at different velocities; thus, shearing injuries typically occur at gray matter–white matter junctions.

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