Introduction: Standard b-value DWI (sDWI) and high b-value DWI (hDWI) and ADC calculation from each DWI have been widely used for diagnosis of (acute ischemic stroke) AIS. However, diagnosis of… Click to show full abstract
Introduction: Standard b-value DWI (sDWI) and high b-value DWI (hDWI) and ADC calculation from each DWI have been widely used for diagnosis of (acute ischemic stroke) AIS. However, diagnosis of AIS subtypes by using hDWI and ADC have not been well investigated. Hypothesis: AIS has several pathophysiological subtypes such as lacunar infarction, cardio-embolism(CE), and atherothrombotic brain infarction (ATBI), and so on, and condtion of collateral circulations differ among those subtypes. Several studies have shown that hDWI is relatively dominant in intracellular diffusion, conversely, sDWI is comparatively dominant in extracellular diffusion. Therefore, our hypothesis is that calculation of ADC from sDWI and hDWI could give valuable information for differentiation among AIS subtypes. Methods: We evaluated 130 AIS patients from medical records. Pathophysiological diagnoses were made by experienced neurologists. We acquired sDWI and hDWI at 3T MRI in all patients. 321 ADC values were obtained by calculating 200 ischemic lesions sequentially. We used relative ADC (rADC) value to adjust the difference caused by location and age. The rADC values were measured by manually placing regions of interest on the ADC maps at the ischemic lesion defined by DWI high and divided by the ADC values on the contralateral normal brain. For assessment of the AIS (within 30hrs from the onset) relationship between ATBI and CE, we subtract high b-value rADC (hrADC) from standard b-value rADC (srADC) to focus on the extracellular diffusion. To analyze the subacute phase stroke relationship between ATBI and CE, we evaluated the each rADC. And at both phase we conducted Mann-Whitney U test. Results: In superacute phase, hDWI more clearly showed hyper-intense signal than sDWI. From the onset, rADC of CE was lower than that of ATBI (median srADC-hrADC: ATBI/CE =0.0699/0.0244) (P=0.0445), this might imply the poor collateral status in CE. Contrary, for subacute phase, CE rapidly underwent necrosis in the ischemic core, rADC was higher than ATBI rADC (median ATBI/CE:0.5939/0.6480) (P=0.0011). Conclusions: We found that quantitative assessment of hrADC and srADC could give valuable information for differential diagnoses of AIS subtypes.
               
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