Pathophysiology of traumatic brain injury

Will the secondary impacts of TBI correspond to strokes neuronal cascade of death?  And can any of their solutions be applied to stroke?
http://bja.oxfordjournals.org/content/99/1/4

1. C. Werner* and
2. K. Engelhard

+ Author Affiliations

1. Klinik für Anästhesiologie, der Johannes Gutenberg-Universität Mainz, Langenbeckstrasse 1, D-55131 Mainz, Germany

1. *Corresponding author. E-mail: werner@anaesthesie.klinik.uni-mainz.de

Abstract

The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers differentiated therapeutic options.