(Stroke. 1995;26:1007-1013.)
© 1995 American Heart Association, Inc.
Articles |
Continuing Ischemic Damage After Acute Middle Cerebral Artery Infarction in Humans Demonstrated by Short-Echo Proton Spectroscopy
Presented in part at the Second Meeting of the Society of Magnetic Resonance, San Francisco, Calif, August 6-12, 1994, and published in abstract form in Proc Soc Magn Reson. 1994;1:188.
From the Divisions of Clinical Neuroscience (D.E.S., M.M.B.) and Biochemistry (F.A.H., A. van den B., M.A.M., J.R.G.), St George's Hospital Medical School, London, UK.
Correspondence to Dr Dawn E. Saunders, Division of Clinical Neuroscience, St George's Medical School, Cranmer Terr, Tooting, London SW 17 ORE, UK.
Background and Purpose Proton MR spectroscopy is a noninvasive method of monitoring in vivo metabolite concentration changes over time. The aim of this work was to study the ischemic penumbra in humans by measuring the metabolic changes that occur after a middle cerebral artery territory infarction.
Methods Diagnostic MRI and short–echo time MR spectroscopy were performed on a 1.5-T system. Localized proton MR spectroscopy was performed within the area of cerebral infarction and in a homologous area of the contralateral hemisphere. The residual water resonance in the spectra was removed with the use of the Hankel Lanczos singular value decomposition method, after which peak area estimates were obtained by means of the variable projection time domain fitting analysis. The unsuppressed water signal was used as an internal concentration standard. Ten patients with acute middle cerebral artery infarction were studied within 28 hours of stroke onset and followed up for a period of up to 3 months.
Results Significant changes were seen in the initial spectra from the infarct compared with the contralateral spectra. Lactate, a marker of anaerobic metabolism, was present within the infarct but not detected in the contralateral hemisphere. N-Acetyl aspartate, a neuronal marker, and total creatine were significantly reduced. The initial choline signal, arising from choline-containing compounds within the cell and cell membrane, remained unchanged in the infarct core compared with the contralateral hemisphere. Further reductions in N-acetyl aspartate and total creatine concentrations occurred within the first week. A fall in the lactate concentration was seen within the infarct core during the first 7 to 10 days. Similar reductions in the choline concentration were observed during this period.
Conclusions The demonstration of the continuing loss of cerebral metabolites within an infarct region suggests that further cell loss occurs up to 10 days after infarction. The continuing loss of neurons may represent continued ischemic damage after middle cerebral artery infarction.
Key Words: spectroscopy, nuclear magnetic resonance • cerebral infarction • metabolism
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