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dc.contributor.advisorMoore, Ida M. (Ki)en_US
dc.contributor.authorPasvogel, Alice Eleanor
dc.creatorPasvogel, Alice Eleanoren_US
dc.date.accessioned2013-04-25T09:51:30Zen
dc.date.available2013-04-25T09:51:30Zen
dc.date.issued1999en_US
dc.identifier.urihttp://hdl.handle.net/10150/284010en
dc.description.abstractTraumatic brain injury (TBI) is a leading cause of mortality and morbidity in young adults. With TBI, a cascade of events is initiated that leads to the degradation of the lipid bilayer of the cell membrane. The purpose of this study was to investigate central nervous system membrane damage following traumatic brain injury through biological (phospholipid and creatine kinase isoenzyme) and behavioral (Glasgow Coma Scale score and Survival Status) measures. The purpose was also to determine the relationship between the biological measures of injury and the behavioral assessment of neurological status. Ten patients participated in the study. The cerebrospinal fluid (CSF) samples from the ventricular catheter system and Glasgow Coma Scale (GCS) scores were obtained 2-3 times each day over 2 to 3 days. The phospholipids were extracted from the CSF samples with a 2 step procedure using Chloroform:Methanol. The phospholipid classes were separated using normal phase High Performance Liquid Chromatography with a Hexane:Isopropanol:Water gradient and quantified from calibration curves for each of the phospholipid classes: phosphatidylethanolamine, phosphatidylserine, phosphatidylcholine, sphingomyelin, and lysophosphatidylcholine. The creatine kinase isoenzyme (CK-BB) concentration was determined by electrophoresis. Data were analyzed using descriptive statistics, Spearman rank order correlation coefficient, and point biserial correlation. The concentration of phospholipids and CK-BB changed over time with the peak mean concentration for phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin on day 4 after injury; for phosphatidylserine on day 2 after injury, and for lysophosphatidylcholine and CK- BB on day 1 after injury. There was a significant positive relationship between phospholipids and the GCS score on day 2 after injury and a significant negative relationship between phospholipids and the GCS score on day 6 after injury. There was a significant relationship between Survival Status and phospholipids on day 1 and day 4 after injury. There was a significant relationship between Survival Status and CK-BB on day 1 and day 2 after injury. Future studies are needed to test the relationship between acute measures of membrane damage and long term physical, cognitive, emotional and behavioral outcomes.
dc.language.isoen_USen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectHealth Sciences, Medicine and Surgery.en_US
dc.subjectHealth Sciences, Nursing.en_US
dc.titleCerebrospinal fluid phospholipid and creatine kinase isoenzyme changes following traumatic brain injuryen_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.identifier.proquest9957951en_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineNursingen
thesis.degree.namePh.D.en_US
dc.description.noteThis item was digitized from a paper original and/or a microfilm copy. If you need higher-resolution images for any content in this item, please contact us at repository@u.library.arizona.edu.
dc.identifier.bibrecord.b40137715en_US
dc.description.admin-noteOriginal file replaced with corrected file September 2023.
refterms.dateFOA2018-09-05T23:37:47Z
html.description.abstractTraumatic brain injury (TBI) is a leading cause of mortality and morbidity in young adults. With TBI, a cascade of events is initiated that leads to the degradation of the lipid bilayer of the cell membrane. The purpose of this study was to investigate central nervous system membrane damage following traumatic brain injury through biological (phospholipid and creatine kinase isoenzyme) and behavioral (Glasgow Coma Scale score and Survival Status) measures. The purpose was also to determine the relationship between the biological measures of injury and the behavioral assessment of neurological status. Ten patients participated in the study. The cerebrospinal fluid (CSF) samples from the ventricular catheter system and Glasgow Coma Scale (GCS) scores were obtained 2-3 times each day over 2 to 3 days. The phospholipids were extracted from the CSF samples with a 2 step procedure using Chloroform:Methanol. The phospholipid classes were separated using normal phase High Performance Liquid Chromatography with a Hexane:Isopropanol:Water gradient and quantified from calibration curves for each of the phospholipid classes: phosphatidylethanolamine, phosphatidylserine, phosphatidylcholine, sphingomyelin, and lysophosphatidylcholine. The creatine kinase isoenzyme (CK-BB) concentration was determined by electrophoresis. Data were analyzed using descriptive statistics, Spearman rank order correlation coefficient, and point biserial correlation. The concentration of phospholipids and CK-BB changed over time with the peak mean concentration for phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin on day 4 after injury; for phosphatidylserine on day 2 after injury, and for lysophosphatidylcholine and CK- BB on day 1 after injury. There was a significant positive relationship between phospholipids and the GCS score on day 2 after injury and a significant negative relationship between phospholipids and the GCS score on day 6 after injury. There was a significant relationship between Survival Status and phospholipids on day 1 and day 4 after injury. There was a significant relationship between Survival Status and CK-BB on day 1 and day 2 after injury. Future studies are needed to test the relationship between acute measures of membrane damage and long term physical, cognitive, emotional and behavioral outcomes.


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