Origins of Cerebral Edema: Implications for Spaceflight-Associated Neuro-Ocular Syndrome

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Title Origins of Cerebral Edema: Implications for Spaceflight-Associated Neuro-Ocular Syndrome
Creator Laura A. Galdamez, Tyson J. Brunstetter, Andrew G. Lee, William J. Tarver
Affiliation Department of Emergency Medicine (LAG), Baylor College of Medicine, Houston, Texas; United States Navy detailed to NASA Johnson Space Center (TJB), Houston, Texas; Department of Ophthalmology (AGL), Blanton Eye Institute, Houston Methodist Hospital, Houston, Texas; Department of Ophthalmology (AGL), Baylor College of Medicine, Houston, Texas; Department of Ophthalmology, Neurology, and Neurosurgery (AGL), Weill Cornell Medicine, New York, New York; Department of Ophthalmology (AGL), University of Texas Medical Branch (UTMB), Galveston, Texas; Department of Ophthalmology (AGL), University of Iowa Hospitals and Clinics, Iowa City, Iowa; University of Texas Maryland Anderson Cancer Center (AGL), Houston, Texas; and NASA Johnson Space Center (WJT), Houston, Texas
Abstract Background: Spaceflight-associated neuro-ocular syndrome (SANS) was first described in 2011 and is associated with structural ocular changes found to occur in astronauts after long-duration missions. Despite multiple insufficient potential terrestrial models, an understanding of the etiology has yet to be described. Evidence acquisition: A systematic review was conducted on literature published about the pathophysiology of cerebral edema. Databases searched include PubMed, Scopus, and the Texas Medical Center Online Library. This information was then applied to create theories on mechanisms on SANS etiology. Results: Cerebral edema occurs through 2 general mechanisms: redistribution of ions and water intracellularly and displacement of ions and water from the vascular compartment to the brain parenchyma. These processes occur through interconnected endocrine and inflammatory pathways and involve mediators such as cytokines, matrix metalloproteases, nitric oxide, and free radicals. The pathways ultimately lead to a violation of cellular membrane ionic gradients and blood-brain barrier degradation. By applying the principles of cerebral edema pathophysiology to the optic disc edema (ODE) see in SANS, several theories regarding its etiology can be formed. Venous stasis may lead to ODE through venous and capillary distension and leak, as well as relative hypoxia and insufficient ATP substrate delivery causing axoplasmic flow stasis and local oxidative stress. Conclusions: Using the pathophysiology of cerebral edema as a model, hypotheses can be inferred as to the etiology of ODE in SANS. Further studies are needed to determine the presence and contribution of local vascular stasis and resulting inflammation and oxidative stress to the pathophysiology of SANS.
OCR Text Show
Publisher Lippincott, Williams & Wilkins
Date 2020-03
Type Text
Source Journal of Neuro-Ophthalmology, March 2020, Volume 40, Issue 1
Language eng
Rights Management © North American Neuro-Ophthalmology Society
Publication Type Journal Article
ARK ark:/87278/s60p6rd5
Setname ehsl_novel_jno
Date Created 2021-01-22
Date Modified 2021-05-06
ID 1653472
Reference URL https://collections.lib.utah.edu/ark:/87278/s60p6rd5
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