The exact cellular and molecular mechanisms of sepsis-induced encephalopathy remain elusive. The breakdown of the blood-brain barrier (BBB) is considered a focal point in the development of sepsis-induced brain damage. Contributing factors for the compromise of the BBB include cytokines and chemokines, activation of the complement cascade, phagocyte-derived toxic mediators, and bacterial products. To date, we are far from fully understanding the neuropathology that develops as a secondary remote organ injury as a consequence of sepsis. However, recent studies suggest that bacterial proteins may readily cross the functional BBB and trigger an inflammatory response in the subarachnoid space, in absence of a bacterial invasion. A better understanding of the pathophysiological events leading to septic encephalopathy appears crucial to advance the clinical care for this vulnerable patient population. © 2010 BioMed Central Ltd.
CITATION STYLE
Flierl, M. A., Rittirsch, D., Huber-Lang, M. S., & Stahel, P. F. (2010, June 16). Pathophysiology of septic encephalopathy - an unsolved puzzle. Critical Care. https://doi.org/10.1186/cc9035
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