Mr. Garnett et al., Altered cellular metabolism following traumatic brain injury: A magnetic resonance spectroscopy study, J NEUROTRAU, 18(3), 2001, pp. 231-240
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.