Spinal cord compression due to metastatic disease: diagnosis with MR imaging versus myelography

To determine the efficacy of magnetic resonance (MR) imaging and myelography for the diagnosis of spinal cord compression due to metastatic disease, the authors prospectively examined 70 patients who had known or suspected spinal involvement by malignancy. Most MR examinations consisted of T1-weighted sagittal imaging of the entire spine, with additional sequences as needed for clarification. Extradural masses were found in 46 patients, 25 of whom had cord compression. For extradural masses causing cord compression, the sensitivity and specificity of MR imaging was .92 and .90, respectively, compared with .95 and .88 for myelography. For extradural masses without cord compression the sensitivity and specificity of MR imaging was .73 and .90, versus .49 and .88 for myelography. MR imaging was much more sensitive for metastases to bone (.90 vs .49), as expected. MR imaging is an acceptable alternative to myelography for diagnosing spinal cord compression and is preferable as a first study because it is noninvasive and better tolerated.     

Acute cerebral infarction in monkeys: an experimental study using MR imaging

Magnetic resonance (MR) imaging was performed in five monkeys with experimentally induced acute cerebral infarction to define the MR imaging features and correlate these with computed tomographic (CT) findings, laboratory analysis, and histopathologic studies. Acute infarct (2-4 hours after embolization) was generally visible on MR images but not on CT scans. CT at 24 and 48 hours did show the infarcts. In all cases the infarct was more clearly depicted with MR imaging and was visualized as an area of high signal intensity on T2-weighted images. Spectrometric nuclear MR measurements of the postmortem cerebral tissue confirmed prolongation of both T1 and T2 values similar to that calculated from MR images. At postmortem laboratory testing, the area of infarction detected with MR imaging had decreased specific gravity and increased water content, reflecting edema.     

Effects of platelet inhibitors on the platelet aggregation induced by plasma from patients with thrombotic thrombocytopenic purpura

Antiplatelet drugs have been used in the treatment of thrombotic thrombocytopenic purpura (TTP) but there in vivo efficacy remains controversial. It has been shown that, in vitro, the plasmas obtained from patients with TTP induced the aggregation of washed platelets from normal donors as well as patients in remission. The effects of platelet inhibitors on the TTP plasma-induced platelet aggregation were examined. It was found that aspirin, indomethacin, ibuprofen, sulfinpyrazone, 5, 8, 11, 14-eisacotetraynoic acid, prostaglandin E1, prostaglandin I2, dBcAMP, apyrase, creatine phosphate/creatine phosphokinase, antimycin, 2-deoxy-D-glucose, dipyridamole, clofibrate, dextran 40, dextran 70, dibucaine, xylocaine, methylmaleimide, and ethylenediamine tetraacetic acid had little or no effect at all. These data lead us to conclude that at least in certain cases, antiplatelet drugs probably play a limited role in the treatment of patients with TTP.