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Astroglia and Acute Hepatic Encephalopathy: The Mechanisms of Cytotoxic Brain Edema
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Author(s): Omar El Hiba (Faculty of Sciences, Chouaib Doukkali University, Morocco), Bilal El-Mansoury (Faculty of Sciences, Chouaib Doukkali University, Morocco), Michael Norenberg (Miller School of Medicine, University of Miami, USA)and Arumugam Radhakrishnan Jayakumar (Miller School of Medicine, University of Miami, USA)
Copyright: 2024
Pages: 18
Source title:
Physiology and Function of Glial Cells in Health and Disease
Source Author(s)/Editor(s): Bilal El-Mansoury (Faculty of Sciences, Chouaib Doukkali University, Morocco), Omar El Hiba (Chouaib Doukkali University, Morocco)and Arumugam Radhakrishnan Jayakumar (University of Miami, USA)
DOI: 10.4018/978-1-6684-9675-6.ch013
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Abstract
Acute hepatic encephalopathy (AHE) is a fatal neuro-psychological complication associated with acute liver failure (ALF). While different etiologies were established, over dosage of acetaminophen consumption is still the most frequent. The neuropathological basis of AHE induced death is still not fully understood; however, a body line of evidence sustains the role of rapid onset and progress of brain edema leading to intracranial hypertension, and finally brain herniation and death. The role of astrocytes in the pathogenesis of HE, in general, is well sustained through their role as a detoxifying component of the central nervous system, especially from peripheral generated ammonia, leading to astrocyte swelling, generally associated to brain edema onset. The current chapter will describe the pathomechanisms underlying astrocyte swelling in AHE, with the eventual evolution into macroscopic brain edema and the deathly herniation in humans as well as animal models of AHE.
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