The identification and interpretation of brain damage resulting from head i
njury is often not easy. The most obvious structural damage, which is ident
ified post-mortem by neuropathologists, may not be the most reliable altera
tion with regard to clinico-pathological correlations. For example patients
with a fracture of the skull, a severe cerebral contusion or a large intra
cerebral hematoma that is successfully treated can lead to a complete recov
ery if no other types of brain damage are present. Thus more subtle forms o
f pathology, which are often present and some of which can only be identifi
ed microscopically, may be more important. It is therefore necessary to get
deeper insights into the consequences of brain injury. Though of course no
t exclusively, this aim can be reached by autopsy. Primary traumatic brain
lesions result immediately from mechanical injury. Secondary alterations in
juries develop through intracranial and extracranial trauma sequelae, which
determine the course and outcome of brain damage. Traumatic brain damage c
an be classified as focal or diffuse. It may sometimes be difficult to dist
inguish traumatic from ischemic brain injury. One difference, however, is t
hat the initial events of trauma involve mechanical distorsion of the brain
. Mechanoporation as traumatic defect in the cell membrane has recently bee
n found to be one of the first steps which leads via ionic influxes to the
activation of immediate early genes. Oxygen radicals and cell membrane lipi
d peroxidation occur also very early. Increased intracellular calcium, acti
vation of phospholipases and calpains furthermore damage the membrane and c
ytoskeleton and block the axoplasmatic transport, by which delayed cell dea
th can appear. For the description of the extent of traumatically induced b
rain damage and the possible clinico-pathological correlations it is necess
ary to take these alterations into consideration as specifically as possibl
e. Neuropathology can contribute to this aim.