Document Detail


Altered cellular metabolism following traumatic brain injury: a magnetic resonance spectroscopy study.
MedLine Citation:
PMID:  11284544     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Experimental studies have reported early reductions in pH, phosphocreatine, and free intracellular magnesium following traumatic brain injury using phosphorus magnetic resonance spectroscopy. Paradoxically, in clinical studies there is some evidence for an increase in the pH in the subacute stage following traumatic brain injury. We therefore performed phosphorus magnetic resonance spectroscopy on seven patients in the subacute stage (mean 9 days postinjury) following traumatic brain injury to assess cellular metabolism. In areas of normal-appearing white matter, the pH was significantly alkaline (patients 7.09 +/- 0.04 [mean +/- SD], controls 7.01 +/- 0.04, p = 0.008), the phosphocreatine to inorganic phosphate ratio (PCr/Pi) was significantly increased (patients 4.03 +/- 1.18, controls 2.64 +/- 0.71, p = 0.03), the inorganic phosphate to adenosine triphosphate ratio (Pi/ATP) was significantly reduced (patients 0.37 +/- 0.10, controls 0.56 +/- 0.19, p = 0.04), and the PCr/ATP ratio was nonsignificantly increased (patients 1.53 +/- 0.29, controls 1.34 +/- 0.19, p = 0.14) in patients compared to controls. Furthermore, the calculated free intracellular magnesium was significantly increased in the patients compared to the controls (patients 0.33 +/- 0.09 mM, controls 0.22 +/- 0.09 mM, p = 0.03)). Proton spectra, acquired from similar regions showed a significant reduction in N-acetylaspartate (patients 9.64 +/- 2.49 units, controls 12.84 +/- 2.35 units, p = 0.03) and a significant increase in choline compounds (patients 7.96 +/- 1.02, controls 6.67 +/- 1.01 units, p = 0.03). No lactate was visible in any patient or control spectrum. The alterations in metabolism observed in these patients could not be explained by ongoing ischemia but might be secondary to a loss of normal cellular homeostasis or a relative alteration in the cellular population, in particular an increase in the glial cell density, in these regions.
Authors:
M R Garnett; R G Corkill; A M Blamire; B Rajagopalan; D N Manners; J D Young; P Styles; T A Cadoux-Hudson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurotrauma     Volume:  18     ISSN:  0897-7151     ISO Abbreviation:  J. Neurotrauma     Publication Date:  2001 Mar 
Date Detail:
Created Date:  2001-04-03     Completed Date:  2001-08-09     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8811626     Medline TA:  J Neurotrauma     Country:  United States    
Other Details:
Languages:  eng     Pagination:  231-40     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, University of Oxford, United Kingdom. Mg@bioch.ox.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism*
Adolescent
Adult
Aspartic Acid / analogs & derivatives,  metabolism
Brain / metabolism*,  pathology
Brain Injuries / diagnosis,  metabolism*
Choline / metabolism
Creatine / metabolism
Female
Humans
Hydrogen-Ion Concentration
Magnetic Resonance Spectroscopy / methods*
Male
Middle Aged
Phosphates / metabolism*
Phosphocreatine / metabolism*
Chemical
Reg. No./Substance:
0/Phosphates; 56-65-5/Adenosine Triphosphate; 56-84-8/Aspartic Acid; 57-00-1/Creatine; 62-49-7/Choline; 67-07-2/Phosphocreatine; 997-55-7/N-acetylaspartate

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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