Microstructure And Microvascular Alterations In Subacute Stroke Using IVIM

PurposeThe purpose was to assess the changes of microstructure and microvascular of the stroke lesions using introvoxel incoherent motion(I VIM),and observe the correlation between IVIM and clinical deficits.MethodsTwenty-five stroke patients without thrombolytic therapy in middle cerebral artery territory were enrolled between 3and 7 days after stroke onset,whom signed a informed consent to received diffusion-weighted imaging(DWI)and IVIM sequence.Baseline National Institute of Health stroke scale(NIHSS)on admission were obtained,and clinical outcome was classified as unfavorable,if the modified Rankin score(mRS)was greater than 2.We got regions of interest(ROI)masks by apparent diffusion coefficient(ADC),including the infarct core(?0.55×10-3 mm2/s)and the peri-core(>0.55×10-3 mm2/s).ADC,IVIM and volume were used to quantify ROIs.IVIM includes slow diffusion coefficient(D),fast diffusion coefficient(D*)and perfusion fraction(f).The relative ADC(rADC)was calculated by dividing the lesion ADC by the contralateral ADC.A paired t-test and pearson correlation were used to analyze the differences and relationships in ROIs.Further,the relationship of IVIM with NIHSS score on admission and mRS after 3months were evaluated.ResultsThe ADC,D,and f values in the ipsilateral regions were overall decreased(P<0.05)than these in normal contralateral regions.The rADC,rD and rf of the peri-core were significantly higher(P<0.001)than the infarct core.There were negative correlations between rADC and rD(P=0.004)in infarct core,between rADC and rD(P=0.01)and rADC and rf(P=0.029)in peri-core.The rD was negatively associated with NIHSS score and 3-month mRS score in the infarct core.ConclusionCompared to the infarct core,there were increased D and f values in the peri-core,which inferring the compensatory pathophysiology mechanism of microstructure and microvascular perfusion in the subacute stage.The diffusion-related D values was useful to evaluate the stroke deficits and clinical neurological outcome.