Citation

Patt S, Brodhun M. Exp. Toxicol. Pathol. 1999; 51(2): 119-123.

Affiliation

Institute of Pathology (Neuropathology), Friedrich Schiller University Jena, Germany. patt@bach.med.uni-jena.de

Copyright

(Copyright © 1999, Urban und Fischer)

DOI

unavailable

PMID

10192579

Abstract

The identification and interpretation of brain damage resulting from head injury is often not easy. The most obvious structural damage, which is identified post-mortem by neuropathologists, may not be the most reliable alteration with regard to clinico-pathological correlations. For example patients with a fracture of the skull, a severe cerebral contusion or a large intracerebral hematoma that is successfully treated can lead to a complete recovery if no other types of brain damage are present. Thus more subtle forms of pathology, which are often present and some of which can only be identified microscopically, may be more important. It is therefore necessary to get deeper insights into the consequences of brain injury. Though of course not exclusively, this aim can be reached by autopsy. Primary traumatic brain lesions result immediately from mechanical injury. Secondary alterations injuries develop through intracranial and extracranial trauma sequelae, which determine the course and outcome of brain damage. Traumatic brain damage can be classified as focal or diffuse. It may sometimes be difficult to distinguish traumatic from ischemic brain injury. One difference, however, is that the initial events of trauma involve mechanical distortion of the brain. Mechanoporation as traumatic defect in the cell membrane has recently been 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 lipid peroxidation occur also very early. Increased intracellular calcium, activation of phospholipases and calpains furthermore damage the membrane and cytoskeleton and block the axoplasmatic transport, by which delayed cell death can appear. For the description of the extent of traumatically induced brain damage and the possible clinico-pathological correlations it is necessary to take these alterations into consideration as specifically as possible. Neuropathology can contribute to this aim.

Language: en