• Ornella Piazza, Simona Cotena, Edoardo De Robertis, Ferdinando Caranci, and Rosalba Tufano.
• Dipartimento di Scienze Chirurgiche Anestesiologiche Rianimatorie e dell'Emergenza, Università degli Studi di Napoli Federico II, via Pansini 5, 80131, Naples, Italy. orpiazza@unina.it
• Neurochem. Res. 2009 Jul 1;34(7):1289-92.

AbstractThe pathogenesis of sepsis associated encephalopathy (SAE) is not yet clear: the blood-brain barrier (BBB) disruption has been indicated among the possible causative mechanisms. S100B, a calcium binding protein, originates in the central nervous system but it can be also produced by extra-cerebral sources; it is passively released from damaged glial cells and neurons; it has limited passage through the BBB. We aimed to demonstrate BBB damage as part of the pathogenesis of SAE by cerebral spinal fluid (CSF) and serum S100B measurements and by magnetic resonance imaging (MRI). This paper describes four septic patients in whom SAE was clinically evident, who underwent MRI and S100B measurement. We have not found any evidence of CSF-S100B increase. Serum S100B increase was found in three out of four patients. MRI did not identify images attributable to BBB disruption but vasogenic edema, probably caused by an alteration of autoregulation, was diagnosed. S100B does not increase in CSF of septic patients; S100B increase in serum may be due to extracerebral sources and does not prove any injury of BBB. MRI can exclude other cerebral pathologies causing brain dysfunction but is not specific of SAE. BBB damage may be numbered among the contributors of SAE, which aetiology is certainly multifactorial: an interplay between the toxic mediators involved in sepsis and the indirect effects of hyperthermia, hypossia and hypoperfusion.

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