Altered cellular metabolism following traumatic brain injury: A magnetic resonance spectroscopy study

Citation
Mr. Garnett et al., Altered cellular metabolism following traumatic brain injury: A magnetic resonance spectroscopy study, J NEUROTRAU, 18(3), 2001, pp. 231-240
Citations number
59
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROTRAUMA
ISSN journal
08977151 → ACNP
Volume
18
Issue
3
Year of publication
2001
Pages
231 - 240
Database
ISI
SICI code
0897-7151(200103)18:3<231:ACMFTB>2.0.ZU;2-H
Abstract
Experimental studies have reported early reductions in pH, phosphocreatine, and free intracellular magnesium following traumatic brain injury using ph osphorus magnetic resonance spectroscopy. Paradoxically, in clinical studie s there is some evidence for an increase in the pH in the subacute stage fo llowing 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 alkal ine (patients 7.09 +/- 0.04 [mean +/- SD], controls 7.01 +/- 0.04, p = 0.00 8), the phosphocreatine to inorganic phosphate ratio (PCr/Pi) was significa ntly increased (patients 4.03 +/- 1.18, controls 2.64 +/- 0.71, p = 0.03), the inorganic phosphate to adenosine triphosphate ratio (Pi/ATP) was signif icantly 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. Fur thermore, the calculated free intracellular magnesium was significantly inc reased 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 simila r regions showed a significant reduction in N-acetylaspartate (patients 9.6 4 +/- 2.49 units, controls 12.84 +/- 2.35 units, p = 0.03) and a significan t 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 spe ctrum. The alterations in metabolism observed in these patients could not b e explained by ongoing ischemia but might be secondary to a loss of normal cellular homeostasis or a relative alteration in the cellular population, i n particular an increase in the glial cell density, in these regions.