The workshop was held on behalf of the Society of Magnetic Resonance in Medicine, the Society for Magn e t ~~ Resonance Imaging, and the European Society for Magnetic Resonance in Medicine and Biology, and attracted 160 participants from 18 countries. There were 27 oral presentations and 37 poster presentations together with vigorous discussion led by enthusiastic session chairmen.
An important aim of the workshop was to provide an assessment not just of the research applications of 'H MRS, but also of the extent to which it could become a more routine clinical method, forming one part of an integrated imaging/spectroscopy examination. In fact, the chairmen of the clinical sessions were chosen with a view to provoking discussion on the clinical utility of 'H MRS.
The first session was concerned with studies of model systems and their role in aiding interpretation of spectra obt<dned in vivo. As might be anticipated, these studies have generated at least as many questions as answers; they also serve to emphasize an interesting point, namely that we still remain uncertain about the roles of many of the metabolites (including N-acetylaspartate, cholinecontaining compounds, and myoinositol) that can make malor contributions to the spectra. However, even if the roles of these compounds remain unclear, their signals can nevertheless be exploited if their cellular distribution is known. For example, much interest has focused on the possible use of the N-acetylaspartate (NAA) signal as a neuronal marker. Dr. Williams (London) discussed recent data confirming a largely neuronal location for NAA. However, he pointed out that NAA is also expressed in an oligodendrocyte precursor cell (the 02-A progenitor). Caution is therefore necessary in using NAA as a neuronal marker under those conditions ( e g , perinatally) where these cells may be present at relatively high concentrations. As an aside, the presence of NAA metabolism in 02-A progenitors may explain why patients with Canavan's disease (which involves a disorder of NAA metabolism) myelinate so poorly; this may be a reflection not so much of neuronal metabolism but of abnormal metabolism in the precursors of the myelin-forming cells. Along similar lines, Dr. Leibfritz (Bremen) suggested that myoinositol may be a marker for glial cells. This needs to MRll 3O:l-3 (1993) 0740-31 94/93 $3.00 Copvright 0 1993 by Williams & Wilkins All rights of reproduction in any form resewed.