Document Detail

Assessment of mitochondrial impairment in traumatic brain injury using high-resolution proton magnetic resonance spectroscopy.
MedLine Citation:
PMID:  18173309     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: The goal of this study was to demonstrate the posttraumatic neurochemical damage in normal-appearing brain and to assess mitochondrial dysfunction by measuring N-acetylaspartate (NAA) levels in patients with severe head injuries, using proton (1H) magnetic resonance (MR) spectroscopy. METHODS: Semiquantitative analysis of NAA relative to creatine-containing compounds (Cr) and choline (Cho) was carried out from proton spectra obtained by means of chemical shift (CS) imaging and single-voxel (SV) methods in 25 patients with severe traumatic brain injuries (TBIs) (Glasgow Coma Scale scores < or = 8) using a 1.5-tesla MR unit. Proton MR spectroscopy was also performed in 5 healthy volunteers (controls). RESULTS: The SV studies in patients with diffuse TBI showed partial reduction of NAA/Cho and NAA/Cr ratios within the first 10 days after injury (means +/- standard deviations 1.59 +/- 0.46 and 1.44 +/- 0.21, respectively, in the patients compared with 2.08 +/- 0.26 and 2.04 +/- 0.31, respectively, in the controls; nonsignificant difference). The ratios gradually declined in all patients as time from injury increased (mean minimum values NAA/Cho 1.05 +/- 0.44 and NAA/Cr 1.05 +/- 0.30, p < 0.03 and p < 0.02, respectively). This reduction was greater in patients with less favorable outcomes. In patients with focal injuries, the periphery of the lesions revealed identical trends of NAA/Cho and NAA/Cr decrease. These reductions correlated with outcome at 6 months (p < 0.01). Assessment with multivoxel methods (CS imaging) demonstrated that, in diffuse injury, NAA levels declined uniformly throughout the brain. At 40 days postinjury, initially low NAA/Cho levels had recovered to near baseline in patients who had good outcomes, whereas no recovery was evident in patients with poor outcomes (p < 0.01). CONCLUSIONS: Using (1)H-MR spectroscopy, it is possible to detect the posttraumatic neurochemical damage of the injured brain when conventional neuroimaging techniques reveal no abnormality. Reduction of NAA levels is a dynamic process, evolving over time, decreasing and remaining low throughout the involved tissue in patients with poor outcomes. Recovery of NAA levels in patients with favorable outcomes suggests marginal mitochondrial impairment and possible resynthesis from vital neurons.
Stefano Signoretti; Anthony Marmarou; Gunes A Aygok; Panos P Fatouros; Gina Portella; Ross M Bullock
Related Documents :
9171929 - Heart-rate variability in chronic traumatic brain injury.
8234569 - Neuropathological basis for drawing disability (constructional apraxia) in alzheimer's ...
17457029 - Metabolic correlates of brain reserve in dementia with lewy bodies: an fdg pet study.
9341699 - 1h-mrs differentiates white matter hyperintensities in subcortical arteriosclerotic enc...
20624409 - The vertical-horizontal illusion in hemi-spatial neglect.
7940429 - Diaphragmatic movement in hemiplegic patients measured by ultrasonography.
12095599 - The role of laparoscopic cholecystectomy in the management of acute cholecystitis in pa...
1591829 - Early mortality of acute myocardial infarction in patients with and without prior coron...
2894239 - Radioiodinated meta-iodobenzylguanidine uptake in medullary thyroid cancer. a french co...
Publication Detail:
Type:  Controlled Clinical Trial; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of neurosurgery     Volume:  108     ISSN:  0022-3085     ISO Abbreviation:  J. Neurosurg.     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2008-01-04     Completed Date:  2008-02-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0253357     Medline TA:  J Neurosurg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  42-52     Citation Subset:  AIM; IM    
Department of Neurosurgery, Virginia Commonwealth University Medical Center, Richmond, Virginia, 23298-0508, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Aspartic Acid / analogs & derivatives,  metabolism
Brain Injuries / complications*,  metabolism
Choline / metabolism
Creatine / metabolism
Follow-Up Studies
Magnetic Resonance Spectroscopy*
Middle Aged
Mitochondrial Diseases / diagnosis*,  etiology*
Outcome Assessment (Health Care)
Predictive Value of Tests
Time Factors
Grant Support
Reg. No./Substance:
56-84-8/Aspartic Acid; 57-00-1/Creatine; 62-49-7/Choline; 997-55-7/N-acetylaspartate

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

Previous Document:  Preoperative depiction of cavernous sinus invasion by pituitary macroadenoma using three-dimensional...
Next Document:  Brain tissue oxygen tension response to induced hyperoxia reduced in hypoperfused brain.