MR imaging and spectroscopy in clinical and experimental cerebral ischemia: a review.

AJR 148:579-588, March 1987 0361 -803x/87/1 483-0579 © American Roentgen Ray Society The superior sensitivity of MR imaging to changes in brain water caused by various insults is well established [1 -6]. Because detectable alteration of brainwater content may start within the first hours after an ischemic insult [7, 8], MR imaging promises to be a unique tool in the experimental and clinical approach to cerebral infarction. MR spectroscopy offers a noninvasive method for observing the fundamental metabolic processes of cell function. Phosphorus-31 (P-31) MR spectroscopy can elucidate the accumulation and depletion of molecules that act as the energy storage substrates of the cell and their breakdown products. The pH within the tissue of interest can be calculated. Hydrogen MR spectroscopy can detect lactate accumulation when ischemia forces a shift from aerobic to anaerobic glycolysis. More sophisticated metabolic pathways are also accessible to MR spectroscopy. Because MR imaging and MR spectroscopy can be done with the same instrument in a single experimental model or in a human patient, MR offers a unique methodology for investigating acute (potentially reversible) ischemia, its evolution, and the effect of various therapeutic interventions on its prognosis. The purpose ofthis review is to summarize the initial experience with MR imaging in the clinical setting of cerebral ischemia and to introduce the reader to the potential future application of combined MR imaging/spectroscopy in this disease process by discussing clinically relevant experimental models. A brief overview of the basic principles of MR spectroscopy is included. A broad understanding of the pathophysiology of ischemia is vital to the task at hand and is a good starting point for subsequent discussion.