American Journal of Neuroradiology, Vol 13, Issue 5 1439-1445, Copyright © 1992 by American Society of Neuroradiology
ARTICLES |
Non-heme mechanisms for T1 shortening: pathologic, CT, and MR elucidation
OB Boyko, PC Burger, JD Shelburne and P Ingram
Department of Radiology, Duke University Medical Center, Durham, NC 27710.
PURPOSE: To further elucidate the nonparamagnetic effects of T1- relaxation mechanisms in MR imaging. PATIENTS AND METHODS: In 12 patients with lesions having hyperintense signal on T1-weighted spin- echo MR, findings were correlated with autopsy/surgical biopsy in seven cases and/or noncontrast CT scans in 10 cases. RESULTS: Eight of the 10 CT scans demonstrated hyperattenuation in the lesions, indicating mineralization, which correlated with the areas of hyperintense signal on MR. Histologic characterization of the mineralization was accomplished in three cases using four stains; hematoxylineosin, alizarin red S, von Kassa stains for calcium and Perls' iron. The areas of mineralization were homogeneously strongly positive with the calcium stains and only focally weakly positive with the Perls' iron stain. The mineralization was further characterized in all three cases as containing calcium and phosphorus using energy-dispersive x-ray analysis. Four of the 12 cases had either no correlating CT scans (two cases) or the CT showed no hyperattenuating properties to the lesions (two cases). In all four of these cases, microscopic examination showed that the gyriform configuration of the cortical hyperintense signal on T1-weighted images correlated with linear zones of nonhemorrhagic laminar necrosis (cerebral infarction). No mineralization, except for an occasional ferruginated neuron, could be demonstrated with the four histologic stains. Specimen MR imaging of formalin-fixed brain sections in one case demonstrated in vitro the gyriform hyperintense signal seen in vivo. CONCLUSION: Our studies describe and pathologically characterize two associations with T1 shortening in neuroimaging unrelated to the presence of heme: 1) calcification and 2) laminar necrosis in cerebral infarction.
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