Neuropathological sequelae of traumatic injury in the brain. An overview

Citation
S. Patt et M. Brodhun, Neuropathological sequelae of traumatic injury in the brain. An overview, EXP TOX PAT, 51(2), 1999, pp. 119-123
Citations number
21
Categorie Soggetti
Pharmacology & Toxicology
Journal title
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
ISSN journal
09402993 → ACNP
Volume
51
Issue
2
Year of publication
1999
Pages
119 - 123
Database
ISI
SICI code
0940-2993(199902)51:2<119:NSOTII>2.0.ZU;2-5
Abstract
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.