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Neuroanatomy and Physiology of Brain Dysfunction in Sepsis
Aurelien Mazeraud1, Quentin Pascal2, Franck Verdonk3
1Institut Pasteur - Unité Histopathologie Humaine et Modèles Animaux, Département Infection et Épidémiologie, Rue du docteur roux, Paris 75724 Cedex 15, France; Sorbonne Paris Cité, Paris Descartes University, Rue de l'école de médecine, Paris 75006, France; General Intensive Care, Assistance Publique Hopitaux de Paris, Raymond Poincaré Teaching Hosptal, Garches 92380, France.
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.
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