Human TBI can be caused by an enormous heterogeneity of forces which impact the head. Several
experimental models have been established to replicate the different pathogenetic characteristics of
TBI. Depending on the nature of forces which act on the head as well as the amount of mechanical
energy being transmitted, two major forms of TBI have been classified in humans: closed and penetrating
TBI.134 Closed TBI is further sub-classified into static and dynamic loading, depending on the
velocity of the force transmission process.134 Dynamic loading is the more common mechanism to
cause TBI. It is further categorized into impulsive or impact loading.134 The main objective of categorizing
TBI in this way is to isolate a distinct pattern of pathophysiological events that occur after brain
trauma and that contribute to brain injury.
With respect to the mechanisms leading to damage of brain tissue secondary to TBI, a distinction is
made between primary and secondary injury mechanisms. Primary damage refers to the direct effects
of the mechanical energy on the brain tissue. A primary injury can incur focal and/or diffuse damage to
the brain. Focal injuries are, for example, epidural, subdural, or intracerebral hematomas, or brain
contusions. Diffuse changes are so-called diffuse axonal injuries (DAI). Secondary injuries need
a latency of hours to days to occur and include events which subsequently result, for example, in brain
swelling and ischaemic and/or hypoxic brain injury. Not surprisingly, the mechanisms which lead to
these injuries share to some extent the same pathophysiological cascades as those which proceed after
ischaemic brain injury. In the following, the specific aspects of pathophysiological events which occur
following TBI are reviewed.