ABSTRACT
PURPOSE: Diffusion-weighted magnetic resonance imaging (DWI) has been known to visualize hyperacute ischemic stroke. And it takes only a few minutes to do. Moreover only a small amount of time and little cost is required to add T2-weighted imaging (T2WI) to DWI. The purpose of this study is to determine the usefulness of T2WI in addition to DWI as a primary imaging modality for patients with suspected ischemic stroke. METHODS: DWI plus T2WI was performed from January to May 2001 on the patients with suspected ischemic stroke. Two emergency physicians reviewed the films and medical records. The sensitivity and the specificity of DWI and T2WI for acute ischemic stroke were calculated. The agreement between DWI and T2WI was calculated using kappa statistics. RESULTS: A total of 241 patients were enrolled. Acute ischemic stroke was confirmed in 86 (35.7%) patients. The sensitivity and the specificity of DWI for acute ischemic stroke were 94.2% and 98.7%, and those for T2WI were 60.5% and 94.2%, respectively. The kappa value was 0.721 (p<0.01). Among the 86 acute ischemic stroke patients, the number of cases who presented less than 6 hours after symptom onset was significantly lower in the T2WI positive group (31% vs. 68.7%, p<0.05). CONCLUSION: This study suggests that the addition of T2WI to DWI as a primary imaging modality for acute ischemic stroke has little benefit compared to DWI alone, especially, when the symptom duration has been less than 6 hours.
Subject(s)
Humans , Emergencies , Magnetic Resonance Imaging , Medical Records , Sensitivity and Specificity , StrokeABSTRACT
BACKGROUND: The ischemia responsive protein 94 kDa(irp94) gene belongs to the heat shock protein 110 family and was isolated in 1999 from rat brain by transiently induced forebrain ischemia. The PC12 cell is the pheochromocytoma cell line of rat, which is differentiated to a sympathetic neuron-like cell by the stimulation of a nerve growth factor. This study is to determine whether irp94 is expressed when an ischemia-like condition is induced by ATP depletion in cultured PC12 cells in vitro. METHODS: PC12 cells were maintained as monolayer cultures in RPMI-1640 medium(Sigma) supplemented with 10% horse serum, 5% fetal bovine serum, 5 mg/ml transferrin, and 1 mg/ml insulin in a humidified 5% CO2 incubator at 37degrees C. The ATP depleting agent antimycin A was added at concentrations of 1, 2.5, and 5 microM to simulate ischemia, and 10 microgram/ml of tunicamycin, which is expected to express heat shock protein maximally, was used as a positive control. The cells were harvested after a 60-minute incubation, and the total RNA was extracted. The reverse transcription polymerase chain reaction(RT-PCR) was performed to use 501 bp irp94 cDNA as a molecular probe, and the expression of irp94 mRNA was analyzed by northern blotting. RESULTS: The irp94 mRNA expression was enhanced, compared to the negative control group, as the concentration of antimycin A was increased. CONCLUSION: This study suggests that irp94 mRNA expression is enhanced as the severity of ischemia is increased. Thus, it is possible to investigate the mechanism of ischemic neuronal injury indirectly by using this in-vitro model of neuronal ischemia.