Journal
REVISTA BRASILEIRA DE PSIQUIATRIA
Volume 36, Issue 3, Pages 251-258Publisher
ASSOC BRASILEIRA PSIQUIATRIA
DOI: 10.1590/1516-4446-2013-1233
Keywords
Sepsis-associated encephalopathy; acetylcholine; amines; GABA; inflammation
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Funding
- Center of Excellence in Applied Neurosciences of Santa Catarina (NENASC)
- Program of Support to Centers of Excellence (PRONEX)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Fundacao de Amparo a Pesquisa e Inovacao do Estado de Santa Catarina (FAPESC)
- National Science and Technology Institute for Translational Medicine (INCT-TM)
- Programa de Cooperacao Academica (PROCAD) - Sepse
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Sepsis and the multiorgan dysfunction syndrome are among the most common reasons for admission to an intensive care unit, and are a leading cause of death. During sepsis, the central nervous system (CNS) is one of the first organs affected, and this is clinically manifested as sepsis-associated encephalopathy (SAE). It is postulated that the common final pathway that leads to SAE symptoms is the deregulation of neurotransmitters, mainly acetylcholine. Thus, it is supposed that inflammation can affect neurotransmitters, which is associated with SAE development. In this review, we will cover the current evidence (or lack thereof) for the mechanisms by which systemic inflammation interferes with the metabolism of major CNS neurotransmitters, trying to explain how systemic inflammation drives the brain crazy.
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