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Departments of Neurology (Drs. Petroff, Graham, Fayad, Brass, and Prichard), Pathology (Dr. Al-Rayess). Medicine (Dr. Rothman), and Molecular Biophysics and Biochemistry (Drs. Blamire and Shulman), Yale University School of Medicine, New Haven, CT.
Previous studies of human stroke by 1H nuclear magnetic resonance spectroscopy have shown elevation of lactate lasting 3 to 6 months. Complete metabolic turnover of the elevated lactate pool has been demonstrated 5 weeks after a stroke. Its cellular localization is among the first questions requiring clarification. Information pertinent to this question came to us from a patient with a 2-week-old stroke by 1H nuclear magnetic resonance spectroscopic imaging 1 week before his death led to neuropathologic examination of the brain. 1H spectra from voxels including the infarcts showed increased lactate and decreased N-acetylaspartate. Histopathology showed sheets of foamy macrophages in the infarct, but few neurons. Macrophage density ranged from 196 cells/mm2 near the surface of the infarct to 788 near its medial margin. Glial density was 500 to 800 cells/mm2. Lactate concentration in voxels including portions of the infarct was estimated at 7 to 14 mM. Voxels showing low N-acetylaspartate and high lactate on spectroscopic imaging were associated with histopathologic sections containing foamy macrophages. Brain macrophages—which begin to appear 3 days after infarction and gradually disappear over several months—could be a major source of elevated lactate signals that persist for months after stroke.
Address correspondence and reprint requests to Dr. Ognen AC Petroff, Department of Neurology, Yale University School of Medicine, 333 Cedar Street, New Haven CT 06510.
Supported by National Institutes of Health Grants NS21708, NS27883, and DK34576.
Received August 9, 1991 Accepted for publication in final form December 23, 1991.
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