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综述
创伤性脑损伤后血管源性脑水肿的MRI研究进展
丁杏 张婧 陈芬 陈扬 周长宁 陈昆涛

Cite this article as: Ding X, Zhang J, Chen F, et al. MRI research progress of vasogenic edema after traumatic brain injury[J]. Chin J Magn Reson Imaging, 2022, 13(6): 143-146.本文引用格式:丁杏, 张婧, 陈芬, 等. 创伤性脑损伤后血管源性脑水肿的MRI研究进展[J]. 磁共振成像, 2022, 13(6): 143-146. DOI:10.12015/issn.1674-8034.2022.06.030.


[摘要] 创伤性脑损伤(traumatic brain injury,TBI)是一种常见、可危及生命的疾病,脑水肿是影响TBI病死率和其后续功能恢复的主要因素,而血管源性脑水肿是其主要的存在形式。常规磁共振在鉴别水肿类型和范围方面能力有限。随着磁共振功能序列的日益创新,各种功能磁共振成像(functional magnetic resonance imaging,fMRI)技术在研究TBI后血管源性脑水肿中各有其独特之处。相关研究应用了扩散加权成像、扩散张量成像、自由水扩散张量成像和扩散峰度成像等fMRI技术,取得了满意的效果。其他fMRI如磁化转移和磁敏感成像在这一领域也显示出应有的作用。本文对TBI后血管源性脑水肿的MRI研究进展进行总结与综述,以期为TBI后的血管源性水肿监测、治疗和预后提供更新、更全面的理论基础及检查方式。
[Abstract] Traumatic brain injury (TBI) is a common life-threatening disease, while cerebral edema is the main factor affecting the mortality and subsequent functional recovery of TBI. Different types of edema usually require different clinical treatments, and vasogenic edema is the main form. Conventional magnetic resonance sequences are limited in their ability to identify the type and extent of edema. With the increasing innovation of MRI functional sequences, various functional magnetic resonance imaging (fMRI) studies have their own unique characteristics in the study of vasogenic brain edema after TBI. Relevant studies have applied fMRI sequences such as diffusion weighted imaging, diffusion tensor imaging, free water diffusion tensor imaging and diffusion kurtosis imaging, and achieved satisfactory results. Other fMRIs, such as magnetization transfer and susceptibility imaging, have also shown their due role in this field. This article concludes and summarizes the MRI research progress of vasogenic brain edema after TBI, in order to provide an updated and more comprehensive theoretical basis and examination methods for the prevention, treatment and prognosis of vasogenic brain edema after TBI.
[关键词] 创伤性脑损伤;脑水肿;血管源性水肿;磁共振成像;功能磁共振成像
[Keywords] traumatic brain injury;cerebral edema;vasogenic edema;magnetic resonance imaging;functional magnetic resonance imaging

丁杏 1, 2   张婧 1   陈芬 1, 2   陈扬 1, 2   周长宁 1, 2   陈昆涛 1*  

1 遵义医科大学第五附属(珠海)医院医学影像科,珠海 519110

2 遵义医科大学第二临床医学院,珠海 519110

陈昆涛,E-mail:chenkunt2021@163.com

作者利益冲突声明:全体作者均声明无利益冲突。


基金项目: 贵州省卫生健康委科学技术基金项目 gzwkj2021-375 广东省医学科学技术研究基金项目 B2022144 遵义医科大学博士科研启动资金项目 BS2021-03
收稿日期:2022-03-29
接受日期:2022-05-27
中图分类号:R445.2  R742.7 
文献标识码:A
DOI: 10.12015/issn.1674-8034.2022.06.030
本文引用格式:丁杏, 张婧, 陈芬, 等. 创伤性脑损伤后血管源性脑水肿的MRI研究进展[J]. 磁共振成像, 2022, 13(6): 143-146. DOI:10.12015/issn.1674-8034.2022.06.030

       创伤性脑损伤(traumatic brain injury,TBI)是由于外力因素而导致脑功能的改变或其他脑病理的改变,具有异质性[1, 2]。目前国内外研究侧重于评估TBI的原发和继发机制及有效的治疗手段,并聚焦于MRI的无创评估[3, 4, 5, 6]。多数研究表明TBI后继发脑水肿是影响TBI病死率和预后的一个主要因素[7, 8, 9]。TBI后脑水肿包括细胞毒性水肿、离子性水肿、血管源性水肿和出血转换四个类型,具有重叠的分子机制[10, 11]。以血脑屏障破坏为特征的血管源性水肿是主要存在形式[12]。目前脑水肿的临床疗法(去骨瓣减压术和渗透疗法)有显著副作用,缺乏特定分子途径的疗法[13],其发生机制和治疗成为突破的难点。

       了解TBI继发脑水肿类型在发展过程中的相对比重有利于患者的治疗,应用无创的功能磁共振成像(functional magnetic resonance imaging,fMRI)精准、全面评估TBI后血管源性水肿的情况对治疗和改善预后有重要的意义。需要强调的是,血管源性或细胞毒性水肿通常不可单独存在,因而不能严格地区分二者。本文通过综述近年来MRI在TBI后血管源性水肿的研究进展,主要包括扩散加权成像(diffusion weighted imaging,DWI)、扩散张量成像(diffusion tensor imaging,DTI)、自由水扩散张量成像(free water diffusion tensor imaging,FWI)和扩散峰度成像(diffusion kurtosis imaging,DKI)等,以无创、定量的方式评估TBI后血管源性水肿,为临床管理提供技术和方向。

1 TBI后血管源性水肿的常规MRI评估

       既往TBI后水肿程度的评价主要依靠临床体征检查和脑脊液压力测量,前者假阴性率高,后者具有侵入性;临床其他成像方式,如超声和正电子发射断层扫描通常不用于评估TBI及其后水肿发展。目前临床常用于识别血管源性水肿的MRI序列主要有T2加权成像(T2 weighted imaging,T2WI)和液体衰减反转恢复(fluid-attenuated inversion recovery,FLAIR)序列,水肿程度通过图像显示的水肿范围和相应体积的测量来反映。两者通常在血管源性水肿发展的后期显示脑组织水含量增加。T2WI水肿区与周围脑组织区分不易,依赖于诊断医生的经验[13],并且对TBI的敏感性有限[14, 15]。动态对比增强MRI (dynamic contrast-enhanced magnetic resonance imaging,DCE-MRI)在TBI的研究主要用于评估血脑屏障破坏和脑微结构变化[16, 17],脑水肿为非强化区,肿瘤周围非强化区域在区别浸润性肿瘤和中枢神经系统转移诱导的血管源性水肿依旧有挑战性[18]。以上这些方式在一定程度上提示了TBI后血管源性水肿的发生,但存在一定的滞后性和主观性,指导临床准确评估TBI及其后血管源性水肿需要更精准、更客观的成像方式,而fMRI具有潜在的评估价值。

2 TBI后血管源性水肿的fMRI评估

2.1 DWI

       DWI在不使用外源性对比剂的情况下反映水分子的运动,表观扩散系数(apparent diffusion coefficient,ADC)可以定量分析水分子的扩散,ADC升高提示血管源性水肿[19]。Obenaus等[20]认为DWI/T2的测量为水肿形成和消退的时间过程提供了定量指标,在水肿的治疗中发挥作用。AQP4是大脑中的主要水通道,研究表明该分子在TBI损伤部位上调,而在损伤部位附近下调[21];精氨酸加压素(arginine vasopressin,AVP)是一种神经肽激素,V1a受体(V1a receptors,V1aR)作为主要的AVP受体亚型,调节AQP4的表达和功能[22]。Kulkarni等[23]探索一种V1aR拮抗剂疗效时,首次在无结构性脑损伤的大鼠创伤模型中测量到撞击后2~6 h小脑、丘脑和基底神经节区域的ADC值增高,治疗组的ADC值减低,这表明DWI可为轻微的头部撞击导致血管源性水肿提供影像学证据并验证分子疗效,但对其余神经解剖区域敏感性不足。Ren等[24]探究中度TBI大鼠的创伤半暗带区发现相对表观扩散系数(relative apparent diffusion coefficient,rADC)在创伤后1 h、48 h升高,同时IgG在1 h、12 h和48 h表达强阳性,提示血管源性水肿和血脑屏障的显著破坏,在这项研究中12 h时水肿程度是最严重的,但rADC变化不明显,可能归结于细胞毒性水肿和血管源性水肿的综合作用。Turtzo等[25]在验证轻度TBI患者早期MRI表征的与微出血相关细胞毒性水肿预后不良时,发现ADC值在损伤早期最低,亚急性期ADC值增加,表明急性期呈细胞毒性水肿,亚急性损伤后期转变为血管源性水肿,损伤早期的表现与前述学者研究结果不同。事实上,损伤早期的水肿类型尚存争议,可能与创伤的模型、损伤的程度及水肿的综合作用有关,突出了早期ADC值预测TBI结果的困难性。Mistral等[26]评估基于自动图谱的量化程序的可行性时,用DWI的异常平均扩散率(mean diffusivity,MD)值对TBI模型体积进行分类和量化,准确性可与手动描绘相匹,并可以得出脑损伤水肿的类型和体积。综上所述,DWI应用于TBI后血管源性水肿的领域广泛且成熟,具有初始识别、动态定量监测和估算体积的作用,可为未来相关临床前试验和自动程序提供技术支持[27]。但是DWI模型只考虑了水分子的扩散情况,不足以真实反映生物体内复杂的扩散过程,对大多单独的大脑区域敏感性差。

2.2 DTI

       DTI是基于多个方向上采集运动探测梯度,生成一个确定组织内水分子运动的主要方向的矩阵。各向异性分数(fractional anisotropy,FA)和ADC值分别表示水扩散的整体方向和扩散速率。MD的增加与降低可区别血管源性水肿和细胞毒性水肿[28]。Vasiukova等[29]在研究无结构性脑损伤急性小儿脑震荡的水扩散参数变化中观察到丘脑FA显著增加和ADC减少,胼胝体FA有增加的趋势,均可能是由于急性期水进入轴突间质导致轴突肿胀,并存在的微结构损伤;而多数研究报告了损伤亚急性期和慢性期的TBI患者FA值减少,MD值增加[13,30],表明轴突完整性受损和神经纤维脱髓鞘,上述DTI参量的变化受创伤后时间和两种水肿相互作用的影响。Lara等[31]前瞻性评估脑创伤周围组织中血管源性水肿的特征,发现轻中度TBI和脑肿瘤患者周围血管源性水肿区的ADC和FA值差异无统计学意义,在这项研究中脑肿瘤水肿体积更大,水肿形成的机制不一,但两组患者病灶周围区域的MRI表现却相似,这对治疗的研究方向具有提示性;另与健康对照组相比,上述两组患者的ADC值较高且FA值较低,FA降低可能是脱髓鞘或组织微结构破坏的结果,与之前的研究一致[32]。Moll等[33]研究地塞米松治疗TBI血管源性水肿的效用,发现治疗组的血管源性水肿的体积减小,ADC值减少,FA值增加,而非治疗组的体积不减反增;另外DTI主要测量细胞外空间水分子的流动性,表明地塞米松主要通过减少细胞外水含量发挥作用。总的来说,DTI可对TBI后白质完整性和预后进行评估,未来研究应将TBI的已知认知后果与扩散参数的初始变化联系起来,为各种分子机制治疗TBI后血管源性脑水肿的有效性提供支撑,是一种定量的、全脑和无创的常用和有用工具[28,34]。然而,由于大多数生物组织结构复杂且呈非高斯分布,DTI在复杂结构的观察中有局限性,DTI对扩散模型的简化不足[35],还易受细胞外游离水(free water,FW)混杂效应的影响[36]

2.3 FWI

       FWI是一种两室(即双张量)模型,通过量化FW而消除其混杂效应,估计游离水体积分数(free water volume fraction,FW-VF)图和组织隔室的常规DTI图。FWI可以定量估计水肿和脑组织萎缩的程度,多数研究证明可提高组织特异性[36, 37]。在TBI中,FW-VF可能代表细微程度的血管源性水肿、慢性神经炎症、神经胶质增生和血脑屏障破坏,具体取决于损伤的阶段。Eisenberg等[38]在中重度TBI患者静脉注射格列本脲的安全性和有效性的评估中,观察到格列本脲组未受伤的白质和病变之间的MD、FW和组织平均扩散度(tissue mean diffusivity,MDt)差异无统计学意义,表明格列本脲可能改善中重度TBI的水肿和出血进展,未来需要进一步的研究来证实这个结果。Vijayakumari等[39]首次证明中重度TBI患者3个月后大多数白质区域的FW-VF普遍增加,利用马氏距离(Mahalanobis distance,M)作为汇总度量,用3个月时的MVF预测了12个月时测量的功能和认知结果,表明FW-VF与损伤严重程度和长期预后的相关性,提供了TBI预后的影像学生物标志物,同时与多数研究共同表明FW增加与脑部疾病的不良预后相关[40, 41, 42]。FWI为TBI预后和功能恢复提供了可能的影像学标志物,但相关研究少且样本量小,未来需要更多研究来证明并将其与TBI早期损伤过程结合。

2.4 DKI

       DKI是基于水分子非高斯分布的新型扩散模型,更好地反映了生物组织中的复杂扩散,可获得DTI参量,并检测出灰质结构的各向同性[43]。TBI的平行扩散峰度(axial kurtosis,Ka)值增加是由于细胞轴断裂。熊婧彤等[44]观察兔轻度脑外伤早期DKI参量动态变化,发现6 h时MD、轴向峰度(axial kurtosis,AK)和径向峰度(radial kurtosis,RK)值较对照组增高,提示细胞毒性水肿,部分区域参量于48 h出现一过性减低的“拐点”,可能提示血管源性水肿的主导作用,其早期水肿类型亦与Turtzo关于DWI的研究相一致。Zheng等[45]评估低强度经颅超声在中度TBI大鼠模型的治疗效果时,TBI组平均峰度(mean kurtosis,MK)、Ka值在皮质早期达峰值,MK幅度更显著、更敏感,第7天丘脑MK值升高,提示丘脑可能发生继发性损伤;晚期胶质增生,MK和Ka值下降,损伤程度越重,下降程度越低,表明MK可作为对早期损伤程度和长期预后评估的特定参量;最后,治疗组MK和Ka没有显著降低,表明治疗手段有效。Karlsen等[46]证实DKI和DTI在检测轻度TBI后白质微结构改变方面具有联合效用,或许将成为TBI患者治疗及预后预测的新方向。近年来,DKI主要被用于研究各种脑肿瘤周围的血管源性水肿[47],未来或许可以提供TBI后血管源性水肿及预后的影像学生物指标。

3 其他TBI相关MRI和水肿成像

       静息态血氧水平依赖(blood oxygen level dependent,BOLD)功能连接分析在TBI对大脑功能变化方面敏感性强,表现为连接性的异常或聚集性的缺失,可在一定程度上提示预后[48]。神经突方向离散度与密度成像(neurite orientation dispersion and density imaging,NODDI)对微观结构变化的敏感性高于DTI[49];磁共振波谱(magnetic resonance spectroscopy,MRS)通过分析生物组织的代谢产物了解脑组织的变化,可评估TBI患者脑组织微结构的改变,上述技术值得未来更进一步的研究。另有一些报道较少的fMRI被用来研究水肿及其演变过程,诸多研究将磁化传递(magnetization transfer ratio,MTR)与脑肿瘤和肝性脑病所致脑水肿相联系[50, 51, 52],尚未与TBI后水肿类型相关系。磁敏感成像(magnetic sensitivity imaging,SWI)对损坏区域可能清晰可见,但不能区分水肿和正常脑组织。Badaut等[53]在使用SWI观察幼年大鼠急性TBI的出血和水肿之间关系时,认为血管外血液的程度与水肿程度有关,但尚未得到相关研究验证。MTR和SWI不是水肿成像的最佳方法,但提供的新的病理生理学信息对水肿的评估可能是有用的。Guan等[54]应用T2WI、DWI、ADC和SWI序列的多模态MRI对早期创伤性脑水肿大鼠模型探索,验证多模态MRI是评估TBI后脑水肿的有用且可靠的工具,多模态MRI将成为TBI相关的诊断和预后新方向。

4 小结与展望

       综上所述,近年来关于TBI后的血管源性脑水肿的MRI研究取得很大的进展,特别是在扩散fMRI方面,已有大量应用DWI、DTI研究该领域的成果发表。FWI和DKI能获取更多信息,多模态MRI能提供更精准的信息,均表现出一定的前景。最后,由于TBI的异质性和继发脑水肿机制的复杂性以及疗法的非特异性,获取无创的影像学生物标志物是研究的热门领域,而MRI诊断和科研水平的提高仍需更深入的探索。目前的挑战是确保这些有前景的研究结果能被重复并转化为临床实践,从而为临床监测、治疗和预后提供方向和技术。

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