Article: article from journal or magazin.
Mechanisms of brain injury in bacterial meningitis: workshop summary.
Clinical Infectious Diseases
Morbidity and mortality associated with bacterial meningitis remain high, although antibiotic therapy has improved during recent decades. The major intracranial complications of bacterial meningitis are cerebrovascular arterial and venous involvement, brain edema, and hydrocephalus with a subsequent increase of intracranial pressure. Experiments in animal models and cell culture systems have focused on the pathogenesis and pathophysiology of bacterial meningitis in an attempt to identify the bacterial and/or host factors responsible for brain injury during the course of infection. An international workshop entitled "Bacterial Meningitis: Mechanisms of Brain Injury" was organized by the Department of Neurology at the University of Munich and was held in Eibsee, Germany, in June 1993. This conference provided a forum for the exchange of current information on bacterial meningitis, including data on the clinical spectrum of complications, the associated morphological alterations, the role of soluble inflammatory mediators (in particular cytokines) and of leukocyte-endothelial cell interactions in tissue injury, and the molecular mechanisms of neuronal injury, with potential mediators such as reactive oxygen species, reactive nitrogen species, and excitatory amino acids. It is hoped that a better understanding of the pathophysiological events that take place during bacterial meningitis will lead to the development of new therapeutic regimens.
Animals, Anti-Bacterial Agents/therapeutic use, Brain Diseases/complications, Brain Diseases/etiology, Cell Communication/physiology, Cerebrovascular Circulation/physiology, Cytokines/physiology, Disease Models, Animal, Endothelium/cytology, Endothelium/physiology, Forecasting, Humans, Leukocytes/physiology, Meningitis, Bacterial/complications, Meningitis, Bacterial/drug therapy, Meningitis, Bacterial/</QualifierName> <QualifierName MajorTopicYN="N">, Reactive Oxygen Species/metabolism
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