液体衰减反转恢复预脉冲序列在缺血性脑梗死表观扩散系数值定量研究中的价值

目的 探讨液体衰减反转恢复(FLAIR)序列预脉冲对缺血性脑梗死ADC值的影响及其临床应用价值.方法 回顾性分析139例次脑梗死的常规DWI和FLAIR-DWI资料,采用配对t检验的方法分别比较不同发病时间段的梗死病灶的常规ADC值(ADCCON)和FLAIR ADC值(ADCFLAIR).再根据梗死病灶是否累及大脑皮层将所有病灶分为皮层梗死组、皮层下梗死组,同样的方法比较皮层梗死组、皮层下梗死组以及对侧正常脑组织(对照组)ADCCON和ADCFLAIR值.结果 梗死病灶的平均ADCCON和ADCFLAIR值在发病0～6 h、7～12 h、13～24 h、2 d、3～4 d,5～7 d及8～14 dADCCON值分别为(0.55±0.07)、(0.50±0.09)、(0.50±0.13)、(0.50±0.13)、(0.62±0.14)、(0.60±0.12)、(0.72±0.20)×10-3mm2/s;ADCFLAIR值分别为(0.53±0.09)、(0.49±0.06)、(0.49±0.10)、(0.48±0.08)、(0.58±0.14)、(0.60±0.09)、(0.73±0.15)×10-3mm2/s]各个阶段差异均无统计学意义(P值均>0.05),发病15～30 d和31 d以上的病灶其ADCFLAIR值均低于ADCCON15～30 d组ADCFLAIR和ADCCON分别为(0.95±0.21)、(1.02±0.27)×10-3mm2/s,31 d以上组分别为(1.10±0.30)、(1.36±0.41)×10-3 mm2/s],差异均有统计学意义(P值均<0.01);14 d以内的皮层梗死组和皮层下梗死组的ADCCON值分别为(0.55±0.16)、(0.61±0.14)×10-3 mm2/s]与ADCFLAIR值分别为(0.53±0.14)、(0.60±0.13)×10-3mm2/s]差异均无统计学意义(P值均>0.05);14 d以后ADCCON值则高于ADCFLAIR皮层梗死组ADCCON和ADCFLAIR分别为(1.35±0.48)、(1.16±0.36)×10-3mm2/s,皮层下梗死组分别为(1.15±0.33)、(0.97±0.19)×10-3mm2/s],差异均有统计学意义(P值均<0.01);病灶对侧正常对照脑组织的ADCFLAIR值(0.76±0.05)×10-3 mm2/s]低于ADCCON(0.82±0.11)×10-3 mm2/s],差异具有统计学意义(P<0.01).结论 FLAIR预脉冲序列显著减低发病14 d后的脑梗死组织ADC值,这对于个体患者的脑梗死期龄的判断有帮助;同时FLAIR预脉冲能够通过减少自由水对正常脑组织ADC值的影响,从而增强相对ADC值检测细微缺血损伤的能力.

Clinical application of fluid attenuated inversion recovery in apparent diffusion coefficient quantitative measurements of ischemic brain infarction

Objective To quantitatively evaluate the influence of fluid attenuated inversion prepared recovery (FLAIR) on apparent diffusion coefficient (ADC) and its clinical application value. Methods The data of DWI and FLAIR-DWI of 139 stroke were retrospectively reviewed. Paired t-test was used to analyze DWI (ADCCON ) and FLAIR-DWI (ADCFLAIR) values at varying time points from hyperacute to chronic stage. All of the lesions were further divided into cortex involved infarction and subcortical infarction. The ADCCON and ADCFLAIR values in the lesion sides and the contralateral sides were compared separately. Results The mean ADCCON values for lesions less than 6 hours, 7--12 hours, 13--24 hours, within 2 days, 3-4 days, 5-7 days and 8--14 days were not significantly different from those of the ADCFLAIR values(P >0.05) ADCCON were (0.55±0.07), (0.50±0.09), (0.50±0. 13), (0.50 ± 0. 13), (0.62 ± 0. 14), ( 0. 60 ± 0. 12), (0. 72 ± 0. 20) × 10-3 mm2/s; ADCFLAIR were ( 0. 53 ± 0. 09 ), (0.49±0.06),(0.49±0.10),(0.48±0.08),(0.58±0. 14), (0.60±0.09),(0.73±0.15) × 10-3 mm2/s]. Lesions of 15 to 30 days (0. 95±0. 21 ) × 10-3 mm2/s and ( 1.02±0. 27) × 10-3 mm2/s for ADCFLAIR and ADCCON ] and the chronic stage ( >31 days) ADCFLAIR and ADCCON were (1.10 ± 0. 30) × 10-3 mm2/s and (1.36±0. 41 ) × 10-3 mm2/s respectively], had a significantly lower ADCFLAIR than those of the ADCCON (P <0. 01 ). For patients with a symptom duration of less than 14 days, the mean ADCFLAIR values of the cortex involved and subcortical lesions were all not significantly different from the mean ADCCON (P > 0. 05 ) ADCCON were ( 0. 55 ± 0. 16 ), ( 0. 61 ± 0. 14 ) × 10-3 mm2/s ; ADCFLAIR were (0.53±0. 14), (0.60±0. 13) × 10-3 mm2/s]. For patients with a symptom duration of longer than 14 days, the mean ADCFLAIR values of the cortex involved and subeortical lesions were all significantly lower than those of the mean ADCCON values ( 1.16±0. 36) × 10-3 mm2/s vs. ( 1.35±0. 48) × 10-3 mm2/s for cortex involved lesions and (0. 97±0. 19) × 10-3 mm2/s vs. ( 1.15±0. 33) × 10-3 mm2/s for subcortical lesions ] (P < 0. 01 ). The ADC values of the normal contralateral sides were significantly decreased after the fluid inversion prepared pulse was conducted ADCFLAIR, ( 0. 76 ± 0. 05 ) × 10-3 mm2/s and ADCCON, (0. 82 ± 0. 11 ) × 10-3 mm2/s ] ( p < 0. 01 ). Conclusions The FLAIR significantly decrease the absolute ADC values of the ischemic lesions 14 days later after the stroke onset, which may be helpful in determining individual lesion age. Meanwhile, the application of FLAIR can have a more accurate relative ADC value by reducing the free fluid partial volume effect of the normal contralateral side, and hence enhance the ability of detecting the subtle ischemic pathophysiological changes.