Discrimination of Metabolite from Lipid and Macromolecule Resonances in Cerebral Infarction in Humans Using Short Echo Proton Spectroscopy
Corresponding Author
Dawn E. Saunders Md, Mrcp
King's College Hospital, Denmark Hill, Camberwell, London SE5, United Kingdom
King's College Hospital, Denmark Hill, Camberwell, London SE5, United KingdomSearch for more papers by this authorFranklyn A. Howe DPhil
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorAad Van Den Boogaart MscEng, PhD
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorJohn R. Griffiths DPhil
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorMartin M. Brown Md, Frcp
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorCorresponding Author
Dawn E. Saunders Md, Mrcp
King's College Hospital, Denmark Hill, Camberwell, London SE5, United Kingdom
King's College Hospital, Denmark Hill, Camberwell, London SE5, United KingdomSearch for more papers by this authorFranklyn A. Howe DPhil
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorAad Van Den Boogaart MscEng, PhD
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorJohn R. Griffiths DPhil
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorMartin M. Brown Md, Frcp
St. George's Hospital Medical School, London, United Kingdom
Search for more papers by this authorAbstract
Short-echo proton spectroscopy allows the noninvasive study of metabolites, lipids, and macromolecules in stroke patients, but spectra are difficult to interpret and quantify because narrow metabolite peaks are added to a broad background of lipid and macromolecule peaks. “Metabolite nulling” was used to distinguish the lactate peak from underlying lipid and macromolecule peaks. Increases in the lipid and macromolecule peaks were initially observed within the region of infarction in all patients, and further increases in lipid peaks were seen in five of the six patients during the following 6 weeks. The initial high lactate concentration decreases during the first 2 weeks after stroke, whereas lipid and macromolecule signals show a persistent elevation during the same period. Differences in the time courses of the observed changes suggest that lipid, macromolecule, and lactate signals arise from more than one source.
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