| Literature DB >> 27229649 |
Aurelien Mazeraud1, Quentin Pascal2, Franck Verdonk3, Nicholas Heming4, Fabrice Chrétien5, Tarek Sharshar6.
Abstract
Sepsis-associated encephalopathy (SAE), a complication of sepsis, is often complicated by acute and long-term brain dysfunction. SAE is associated with electroencephalogram pattern changes and abnormal neuroimaging findings. The major processes involved are neuroinflammation, circulatory dysfunction, and excitotoxicity. Neuroinflammation and microcirculatory alterations are diffuse, whereas excitotoxicity might occur in more specific structures involved in the response to stress and the control of vital functions. A dysfunction of the brainstem, amygdala, and hippocampus might account for the increased mortality, psychological disorders, and cognitive impairment. This review summarizes clinical and paraclinical features of SAE and describes its mechanisms at cellular and structural levels.Entities:
Keywords: Amygdala; Hippocampus; Neuroanatomy; Neuroinflammation; Sepsis; Sepsis-associated encephalopathy
Mesh:
Year: 2016 PMID: 27229649 DOI: 10.1016/j.ccm.2016.01.013
Source DB: PubMed Journal: Clin Chest Med ISSN: 0272-5231 Impact factor: 2.878