弥漫性轴索损伤(完成)

弥漫性轴索损伤 Diffuse Axonal Injury （ D A I ）,徐州医学院附属医院王永,弥漫性轴索损伤是病理诊断，而临床工作中难以取得标本综合临床表现及影像学表现（CT、MRI）得出诊断 DAI临床表现缺乏特异性，目前常规影像学检查都不能直接显示轴索损伤的存在目前对其累及范围和病变程度，预后评估等缺乏准确有效的检查方法,DAI诊断中的主要问题早期诊断困难,以往认为，伤后原发性意识障碍的发生机制与脑干的功能损伤有关，具体而言是与脑干网状结构上行激活系统的损伤有关。 然而近年来该学说受到了强有力的挑战。对严重颅脑损伤、原发性昏迷继而死亡的患者进行病理检查发现，患者大脑半球白质存在广泛的变性，这种病理变化即弥漫性轴索损伤。 大宗病例研究和动物实验结果表明，绝大多数原发性昏迷的发生原因是弥漫性轴索损伤而非单纯的脑干损伤。,DAI诊断中的主要问题-昏迷,DAI的定义,弥漫性轴索损伤(diffuse axonal injury，DAI)是指头部在加速度，尤其是减速运动时，在成角旋转的剪应力作用下，造成深部脑白质广泛神经轴索肿胀断裂而引起的脑损伤。,弥漫性轴索损伤(diffuse axonal injury，DAI)是在特定的外力机制作用下，脑内发生的以神经轴索断裂为特征的一系列病理生理变化，以意识障碍为主要临床表现。,DAI发病率,弥漫性轴索损伤在重型颅脑损伤中占20%左右，在脑外伤死亡病例中占29%43%。DAI是颅脑外伤致死致残最常见、医疗纠纷最多的一类损伤。,DAI的发生机制,1982年，Gennarelli成功地用灵长类动物复制出与人类DAI病理特征和临床表现一致的创伤性迁延性昏迷的动物模型，证明：DAI是一种原发性脑损伤，并阐明了DAI发生的生物力学机理。DAI只发生于头部成角和/或旋转加（减）速过程中。不必有任何物体打击头部或头部撞击任何物体。,DAI的发病机制,动物实验进一步证实，轴索损伤的严重程度及分布范围与加（减）速度的大小、持续时间以及头部运动的方向有密切的关系。加（减）速度小、持续时间长（1020ms）的加/减速运动容易产生DAI。不同旋转方向造成的DAI轻重不同。临床的实际情况与DAI的生物力学原理相吻合。DAI常见于交通事故伤中。在翻车、撞车时，头部将经历加速或减速和旋转运动过程，同时头部撞击到相对较软的车内钝物（如衬垫的仪表盘、有弹性的挡风玻璃、可变形的车顶棚等）时，减速运动过程也相对较长，因而特别容易发生DAI。临床和病理研究发现DAI较少合并颅骨骨折，这与脑挫裂伤多伴有颅骨骨折形成鲜明对照，说明两者的致伤机制的确不同。,DAI的发生机制,DAI发生的生物力学机理：在头部成角和/或旋转加（减）速过程中，由于脑内各组织的质量不同，因此其运动的加速度和惯性也不同，头部在成角或旋转加/减速运动中，周围脑组织与中央脑组织之间产生相对运动，将在脑组织内产生剪切力和牵张力，作用于神经纤维，即造成轴索的剪切伤或牵拉伤。在损伤时，头部不必与外界接触，如果有接触，这种接触也只对头部的运动产生影响（出现加速或减速），而与否发生DAI无关。,DAI受力模式图,多为交通事故伤少数为坠落伤、打击伤,DAI 病 因,受 伤机制,挥鞭损伤,抛鞭样损伤植物状态的主要原因（剪力，DAI弥漫性轴索损伤）,挥鞭损伤,轴突受力模式图,轴突受力模式图,牵张 撕裂 旋转 压缩,轴突断裂后，其远端渐裂解资料来源,轴突受损后，离子和细胞外液内流破坏轴膜资料来源,脑脊液冲击作用使胼胝体向外伸展资料来源: N. Beenski,(2002) Traumatic injuries imaging of head injuries EMERGENCY RADIOLOGY 12: 12371252,猪DAI模型中观察到脑组织移位(冠状位)左:静止 中: 加速 右:减速资料来源:Douglas H.(2003) Diffuse Axonal Injury in Head Trauma. J Head Trauma Rehabil Vol. 18: 307316,病理改变,病理生理,三大病理特征1.广泛的轴索损害：累及大脑、脑干和小脑的白质和大脑深部核质，包括中线旁皮质下白质、胼胝体、穹隆柱、内囊、基底节及丘脑、齿状核背侧小脑叶、皮质脊髓束、内侧丘脑系、内侧纵束等。2.胼胝体局限性出血灶：病变多位于中线一侧，常见于胼胝体下部，室间隔可受累甚至断裂。3.上脑干背外侧局限性出血灶：病变位于中脑和桥脑上部，单侧或双侧，常常累及小脑上角。,DAI大体病理,在大脑灰白质交界处、胼胝体、内囊、基底节、脑干及小脑等脑中轴部位可见组织的损伤、出血或水肿。,病理分级,级 只有广泛的轴索损害-轻型DAI。级 级胼胝体局限性出血灶-中型DAI。级 级上脑干背外侧局限性出血灶-重型DAI。,脑震荡属于弥漫性轴索损伤的轻型,病理反应过程,1.轴索球形成 传统的观点认为: 轴索在受伤瞬间即刻发生断裂，轴浆被挤出，断端形成回缩球（axonal retraction ball），这一过程被称为原发性轴索断裂（primary axotomy）。但在动物实验中很少见到原发性轴索断裂， 相反，轴索损伤后，轴索不会即刻中断，而是经历连锁的病理反应：首先是轴浆运输（axonal transport）在某些局部受阻，随后在阻塞处近端出现轴索肿胀（axonal swelling），继而在肿胀处出现轴索缩窄（axonal contriction），最后在受伤数小时后于缩窄断裂，这一过程称为继发性轴索断裂（secondary axotomy）或延迟性轴索断裂（delayed acotomy）。 尸检标本可见，轴索球一般于伤后12小时出现，2周以内数量逐日增多，持续存在最长可达64天。现在认为，只有在遭受最大负荷时，轴索才在受伤瞬间断裂，而在绝大多数情况下，轴索将发生迟发性断裂。,病理反应过程,2.神经纤维丝破坏 轴索内神经纤维丝（neurofilament,NF）结构紊乱，是引起轴索肿胀的关键始动因素，是轴索损伤最早、最主要的超微形态学改变。 DAI超早期在轴索完整时，神经纤维蛋白多种亚单位的免疫活性即已暴露。近来证实，DAI后神经纤维丝蛋白以低分子量（68kD）亚单位免疫活性暴露最早。国外学者用Western blotting技术分析及NF68免疫组化观察，认为NF68的磷酸化水解，造成了NF68免疫活性增强及其含量减少，这是导致NF结构破坏的重要原因。可见，轴索损伤不是外力直接引发，而是一种继发损伤，有其复杂的中介机制。,病理反应过程,3.钙离子超载DAI时轴索内Ca2超载则使轴索膜性结构水解、破坏，膜通透性增加，从而引起髓鞘板层分离、断裂，线粒体肿胀及空泡变，微管和微丝断裂、溶解及排列紊乱，最终形成组织水肿、软化。 Ca2超载对血管内皮细胞同样产生类似的破坏作用，导致血管屏障受损，这也是造成脑组织水肿的一个原因。钙结抗剂通过抑止Ca2大量内流，对DAI起到了一定的保护作用，这也进一步证实Ca2超载是DAI发生发展的关键环节。,病理反应过程,4.轴索反应 神经轴索受到损伤后，其神经元胞体会出现中央染色质溶解或称轴索反应。胞体的轴索反应在伤后24小时以内即可发生，并可持续十数日，它包括：神经元胞体肿大、变圆；胞浆中空泡形成，尼氏体变小，甚至消失；胞核肿胀，远离轴丘，最后固缩溶解。,病理反应过程,5.DAI晚期改变 DAI数周后，轴索断裂为多个节段，髓鞘碎片皱缩成空心或空心小球，吞噬细胞侵入吸收髓鞘分解产物，可特征性地出现小胶质神经细胞群落，但也可弥散存在非特异性的星型细胞。数月后，轴索远侧断端发生Waller变性，脑实质内胶质细胞弥散增生并演变为瘢痕收缩，脑室则被动扩张。,病 理 表 现,急性期(1周内)病变区域弥漫或成簇的小针尖样出血灶,部分成融合状态病变区域轴索扭曲、肿胀、断裂和轴索收缩球(axonal retraction ball, ARB)形成,病 理 表 现,轴索损伤时间窗伤后2h 轴索明显肿胀伤后16h 出现ARB伤后72h ARB发展到高峰轴索损伤区和小出血灶周条带样水肿,病 理 表 现,吸收期(第2周8周)弥漫的小针尖样出血灶被吸收较大的小出血灶囊性变,小疤痕形成损伤的轴索周大量小胶质细胞成簇增生,病 理 表 现,恢复期(8周后)脑白质萎缩脑室扩大髓鞘变性,胼胝体出血,DAI. Lesions of the corpus callosum. The pathology illustrates vascular rupture but the key lesion is axonal damage.,胼胝体出血,Demonstration of macroscopic alterations accompanying b-APP-reactive axons: Focal hemorrhages in the corpus callosum,脑干出血,DAI. Lesions of the brain stem.,脑干出血,Diffuse axonal injury. Section at the level of the pontomesencephalic junction showing a hemorrhagic lesion in the left dorsolateral quadrant.,晚期DAI:胼胝体萎缩,变性的白质 因陈旧性出血而变成棕色,Severe white matter degeneration and atrophy of the corpus callosum in old DAI. Brownish color of the degenerated white matter due to old hemorrhages.,DAI镜下病理,脑组织轴索断裂、肿胀、轴浆溢出，断裂处形成圆形轴索球；出血处红细胞溶解后遗留含铁血黄素。,轴缩球（ PAP染色，取自胼胝体）资料来源:Jos Eymard Homem Pittella1,(2004),The conformation of the brain plays an important role in the distribution of diffuse axonal injury in fatal road traffic accident . Arq Neuropsiquiatr 62(2-B):406-413,Diffuse axonal injury. Axonal swellings and bulbs in the corpus callosum. PAP, antineurofilament proteins and hematoxylin counterstaining, X450.,轴缩球 (取材部位:右侧内囊)资料来源: Sahuquillo J.(1988) Acute subdural hematoma and diffuse axonal injury after severe head trauma. Clinico-pathological study. J. Neurosurg. 68: 894-900,轴突病理切片取材部位（左:皮质下白质 右:脑干）资料来源: Douglas H.(2003) Diffuse Axonal Injury in Head Trauma. J Head Trauma Rehabil Vol. 18: 307316,Photomicrographs demonstrating traumatic axonal pathology revealed by immunoreactivity of accumulating neurofilament protein. Darkly stained profiles show axonal pathology in the subcortical white matter (left) and brainstem (right), represented by elongated varicose swellings and axonal bulbs that form at the terminal stump of disconnected axons.,电镜下：神经细胞胞体及轴突资料来源: R. S. Chung ,(2005), Mild Axonal Stretch Injury In Vitro Induces a Progressive Series of Neurofilament Alterations Ultimately Leading to Delayed Axotomy. JOURNAL OF NEUROTRAUMA Volume 22, Number 10:10811091,Neuronal cultures at 21 days in vitro had formed large clusters, interconnected by fasciculated bundles of axons. shown by bright-field microscopy (A), immunocytochemical neurofilament staining (B), and scanning electron microscopy (C). Bar 10 m (A,C), 20 m (B).,电镜下：无菌空气吹打轴突致轴突牵张损伤箭头示轴突原先位置资料来源: R. S. Chung ,(2005), Mild Axonal Stretch Injury In Vitro Induces a Progressive Series of Neurofilament Alterations Ultimately Leading to Delayed Axotomy. JOURNAL OF NEUROTRAUMA Volume 22, Number 10:10811091,An individual bundle of axons was targeted with a single blast of sterile air, and the resultant deflection was captured by video camera. In the selected series of frames (AD), the axon bundle is rapidly stretched, before recovering to its original position (indicated by arrowheads). For reference, frame B displays an increase in original axon length of 3%. Bar 25 m.,电镜下：伤后48h在损伤位点可见轴突逐渐裂解(C),并出现神经微丝环状结构(D); 伤后72h：轴突完全裂解，神经微丝环状结构增多(F)资料来源: R. S. Chung ,(2005), Mild Axonal Stretch Injury In Vitro Induces a Progressive Series of Neurofilament Alterations Ultimately Leading to Delayed Axotomy. JOURNAL OF NEUROTRAUMA Volume 22, Number 10:10811091,电镜下：伤后48h轴突三维重建，在损伤位点可见许多成球状的肿胀神经微丝(B箭头) 资料来源: R. S. Chung ,(2005), Mild Axonal Stretch Injury In Vitro Induces a Progressive Series of Neurofilament Alterations Ultimately Leading to Delayed Axotomy. JOURNAL OF NEUROTRAUMA Volume 22, Number 10:10811091,诊 断,诊 断,1、有确切的颅脑外伤史；2、伤后立即昏迷或无昏迷；3、可能有瞳孔、眼球位置改变。,诊 断,4、CT、MRI发现胼胝体、脑干、基底节、大脑半球皮质髓质交界区、小脑、脑室等部位有出血灶；或弥漫性脑肿胀。,诊 断,5、颅内压增高症状、体征不明 显，CT、MRI可无明显改变。6、病检发现轴缩球。,诊 断,7、病情恢复后CT、MRI出现弥漫 性脑萎缩，伴有严重的神经 系统后遗症。8、可合并其他类型的颅脑损伤。,临床表现,DAI的典型表现,1有明确外伤史，尤其是车祸伤；2伤后持续昏迷6小时；3头颅CT、MRI有DAI的影像学依据；4病情严重程度与颅内压升高程度不符；5临床状况差，而头颅CT未见明显结构异常， 或颅内病变不能解释临床症状； 6伤后晚期出现弥漫性脑萎缩； 7尸检发现弥漫性轴索损伤的证据。,临床表现,1、意识障碍： 绝大部分患者头部受伤后立即出 现昏迷， 入院时GCS 计分： 70%80% 的病人8分， 15%25% 的病人912分， 73 的病人1315分, 昏迷时间长 24小时病人占2030。 24小时病人占7080。,临床表现,2、脑干损伤 ： 34%51%的病人可有 一侧或双侧瞳孔散大， 或双瞳针尖样缩小， 对光反应消失， 眼球分离运动 或同向凝视。,临床表现,2、脑干损伤 ： 双侧锥体束征阳性 去大脑、去皮层状态等。 一般无颅内压增高,临床表现,3、生命体征： 7090病人有呼吸、心率、 血压及体温改变； 约4%32%的病人有中间清期，神志 好转后，可因继发性脑水肿很快进入 再次昏迷。易引发医疗纠纷。,临床表现,特点,颅脑外伤后长时间的原发昏迷该昏迷系DAI累及脑内广泛纵、横轴索导致上行激活系统和或皮层广泛抑制所致,特点,定位体征：可出现程度不同的偏瘫, 而CT却很少有相应部位局灶性改变颅内压：多无明显颅内压增高,辅助检查,影像学征象,（一）DAI的CT表现：1.大脑半球白质内单发或多发小出血灶，直径2mm,2.胼胝体出血，3.脑室内出血，4.第三脑室周围小出血灶，直径2mm,5.脑干出血，6.急性期合并脑肿胀，蛛网膜下腔出血，7.后期弥漫性脑萎缩，脑室代偿性扩大。需要指出CT发现与临床病情轻重相关性不高。（二）DAI的MRI表现：1.非出血灶：T2相显示大脑白质、胼胝体、小脑和脑干背侧圆形、椭圆形或线条状高信号影，T1相呈等或低信号，T2优于T1。2.出血性灶：伤后4天内，T2相显示大脑白质、胼胝体、脑干背侧低信号影，4天后在T1相上显示高信号影，T1优于T2相。 3.后期弥漫性脑萎缩，脑室代偿性扩大。,1、CT： 可见大脑皮质与髓质交界处、 胼胝体、内囊区或第三脑室周 围、脑干等有多个点状或小片 状出血灶。,辅助检查,CT资料来源:Yoshihiro Toyama,(2005), CT for acute stage of closed head injury.Radiat Med. 2005 Aug;23(5):309-16,辅助检查：CT, 可见脑室系统变小； 脑池，如外侧裂池变小，尤其 是环池变小或消失； 脑干肿胀；,CT,CT,CT,CT,CT,CT,CT,CT可以“正常”,辅助检查：CT, 晚期脑室系统扩大。,患者26岁，伤后2月CT资料来源: N. Beenski,(2002) Traumatic injuries imaging of head injuries EMERGENCY RADIOLOGY 12: 12371252,Patient, 26 years of age, with persistent vegetative state CT scan 2 months after injury shows an extensive lesion within the frontal periventricular white matter and at the gray matter/white matter junction (long arrow). A hypodense lesion in the right putamen (thin arrow). Mild dilatation,DAI晚期，脑室系统扩大,患者33岁持续性植物生存资料来源: N. Beenski,(2002) Traumatic injuries imaging of head injuries EMERGENCY RADIOLOGY 12: 12371252,Patient, 33 years of age, who suffered DAI with persistent vegetative state. Non-enhanced CT shows marked dilatation of the ventricles with diffuse brain atrophy,DAI晚期，脑室系统扩大资料来源：www.anatpat.unicamp.br,DAI晚期，脑室系统扩大资料来源：www.anatpat.unicamp.br,2、MRI： 可精确反映出早期脑组织缺血灶、 轴索损伤、脑室、脑池及脑等 结构改变的情况。,辅助检查,T1WI呈等、稍低信号，部分不均匀，少数为低信号；合并出血者有小点状高信号；T2WI均为高信号，合并出血者有等、稍低信号；可以合并脑室内出血；均无占位效应。,辅助检查：MRI,外伤后14天MRI，示胼胝体压部损伤资料来源:W. Marks,(2006) Brain Perfusion Imaging (SPECT-Tc-99m HM-PAO) in Diagnosis of Diffuse Axonal Injury Neurosurg Q 16:8991,MRI obtained 14 days after the accident. Multifocal lesions of the white matter and lesions of the posterior parts of corpus callosum.,79岁男性,伤后5天MRI资料来源: A. Uchino,(2006), Acquired lesions of the corpus callosum: MR imaging. Eur Radiol 16: 905914,Diffuse axonal injury in a 79-year-old man. a, b FLAIR axial and midsagittal images (TR/TI/TE=10,000/2,200/125, 1.5 T) obtained 5 days after head injury show lesions in the posterior half of the corpus callosum. The midbrain, cingulate gyrus and both frontal lobes are also involved,MRI:右海马旁回继发于正铁血红蛋白的异常稍高信号及中脑背侧脑桥损伤信号资料来源: N. Beenski,(2002) Traumatic injuries imaging of head injuries EMERGENCY RADIOLOGY 12: 12371252,Slightly abnormal increase of signal on T1-weighted spin echo secondary to methemoglobin in the right parahipoccampal gyrus (thick arrow) and a small lesion within the midbrain and dorsal part of the pons (thin arrow).,T2WI 示颞上回表面小脑挫伤灶,周围水肿. 右侧丘脑和胼胝体压部亦有小损伤灶资料来源: N. Beenski,(2002) Traumatic injuries imaging of head injuries EMERGENCY RADIOLOGY 12: 12371252,T2-weighted imaging shows very small cortical contusion along the superior temporal gyral surface surrounded by high-signal edema (long thin arrow). The right thalamic lesion (small thin arrow) and a small lesion within the splenium of corpus callosum (thick arrow) due to shearing injury is also seen,伤后15天 T2WI资料来源：J H M Chan;（2003）Diffuse axonal injury detection of changes in anisotropy of water diffusion. Neuroradiology; Jan 45, 1;,A midsagittal T2-weighted fast spin-echo image clearly shows high-signal lesions in the body of the corpus callosum,39岁女性,伤后8天 MR- DWI弥散加权 成像资料来源: T. Kinoshita et al. (2005) Conspicuity of diffuse axonal injury lesions on diffusion-weighted MR imaging. European Journal of Radiology 56: 511,A 39-year-old woman underwent MR imaging 8 days after a motor vehicle accident: (d) DWIGx image clearly demonstrates high-intensity lesion in the splenium of the corpus callosum; (e) DWIGz image reveals high-intensity foci in the left frontal gray/white matter interface,11岁女性,伤后3天 MR-DWI弥散加权成像资料来源: T. Kinoshita et al. (2005) Conspicuity of diffuse axonal injury lesions on diffusion-weighted MR imaging. European Journal of Radiology 56: 511,An 11-year-old girl underwent MR imaging 3 days after a motor vehicle accident: (a and b) DWIs reveal high-signal intensity lesions in the fornix and splenium of the corpus callosum,27岁男性 伤后48h内 FLAIR及T2WI成像 资料来源:K. Paterakis,(2000); Outcome of Patients with Diffuse Axonal Injury The Significance and Prognostic Value of MRI in the Acute Phase.J Trauma.Vol 49 :1071-1075,A 27-year-old man with a GOS score consistent with moderate disability. (A) Turbo FLAIR (cerebrospinal fluid 5 0) shows hemorrhagic DAI in the subcortical white matter. (B) T2-weighted turbo spin echo sequence shows edematous DAI in the posterior half corpus callosum.,左: TurboFLAIR液体衰减反转恢复序列示皮质下白质出血信号（箭头示） 右:T2WI示胼胝体后半部水肿信号,25岁男性 伤后48h内 FLAIR及T2WI成像 资料来源:K. Paterakis,(2000); Outcome of Patients with Diffuse Axonal Injury The Significance and Prognostic Value of MRI .Trauma.Vol 49 :1071-1075,A 25-year-old man with severe disability. (A) Turbo FLAIR shows hemorrhagic DAI in the right dorsolateral midbrain, cortical hemorrhagic contusion in the right temporal lobe, and subarachnoid hemorrhage. (B) T2WI shows edematous DAI in the posterior half of the corpus callosum and hemorrhagic DAI in the midbrain.,Turbo FLAIR示右颞叶皮质下、中脑背外侧出血（箭头示）,T2WI示胼胝体后部水肿及中脑出血（箭头示）,39岁女性,伤后8天 MR-FLAIR 液体衰减反转恢复序列成像资料来源: T. Kinoshita et al. (2005) Conspicuity of diffuse axonal injury lesions on diffusion-weighted MR imaging. European Journal of Radiology 56: 511,A 39-year-old woman underwent MR imaging 8 days after a motor vehicle accident: FLAIR image shows high-intensity lesions in the splenium of the corpus callosum, and in the left frontal gray/white matter interface,66岁女性,伤后4天 MR-FLAIR 液体衰减反转恢复序列成像资料来源: T. Kinoshita et al. (2005) Conspicuity of diffuse axonal injury lesions on diffusion-weighted MR imaging. European Journal of Radiology 56: 511,A 66-year-old woman underwent MR imaging 4 days after a motor vehicle accident: coronal FLAIR image shows high-intensity lesion in the body of the corpus callosum,胼胝体损伤左:T2WI 中、右：快速梯度回波序列（GRE）资料来源: N. Beenski,(2002) Traumatic injuries imaging of head injuries EMERGENCY RADIOLOGY 12: 12371252,Lesions of corpus callosum (corpus, splenium) demonstrated by a T2-weighted imaging(arrow) and b, c GRE sequences show the course of the traumatic force within splenium (b, arrow) and corpus callosum (c, arrow). Note that lesions are better seen on the GRE sequences,GRE-MR(快速梯度回波序列) 资料来源: N. Beenski,(2002) Traumatic injuries imaging of head injuries EMERGENCY RADIOLOGY 12: 12371252,Multifocal low signal on GRE T2* sequences caused by shearing injury correspond to a small foci of former hemorrhage within the periventricular white matter (arrow), basal ganglia, and b deep parasagittal subcortical hemispheric white matter (arrows),正常的纤维重构成像（可以不同颜色表示不同的纤维成分）,Reconstruction of white matter fibres of the brain superimposed over DTI b0 images. The fibres are colour-coded for direction: blue fibres are cranio-caudal, green fibres are anteroposterior and red fibres are transverse. Normal pattern of the white matter fibres inside the genu (anterior) and splenium (posterior) part of the corpus callosum, with anterior efferent forceps fibres. Note that the cortico-spinal tract appears in blue on the posterior part of the internal capsula,19岁男性,入院时GCS 7分,治疗一周出院预后良好.伤后2天 FLAIR-MR 资料来源：D. Ducreux,(2005) Brain MR diffusion tensor imaging and fibre tracking to differentiate between two diffuse axonal injuries, Neuroradiology 47: 604608,Patient 1: axial FLAIR (a) and coronal T2 (b) images centred on the corpus callosum. Hyperintense area in T2 and FLAIR on the splenium without T2 hypointense area (no magnetic susceptibility effect) that suggests the presence of oedema,脑白质纤维重构示：胼胝体压部纤维轻度弯曲并增宽(箭头示),reconstruction of brain white matter fibres superimposed over DTI b0 images. The fibres are colour-coded for direction: blue fibres are cranio-caudal, green fibres are anteroposterior and red fibres are transverse. Splenium fibres are slightly warped in the superior part and widened (arrow). There are no broken fibres,19岁男性患者入院时GCS 4分,预后差植物生存. 伤后1天 FLAIR-MR 资料来源：D. Ducreux,(2005) Brain MR diffusion tensor imaging and fibre tracking to differentiate between two diffuse axonal injuries, Neuroradiology 47: 604608,Patient 2: axial FLAIR (a) and T2* (b) images centred on the corpus callosum. The FLAIR hyperintense areas that are hypointense on T2* and FLAIR on the genu and splenium suggest the presence of magnetic susceptibility effect,脑白质纤维重构示胼胝体膝、压部左侧纤维增宽(如箭头)，右侧损坏,reconstruction of brain white matter fibres superimposed over DTI b0 images. The fibres are colour-coded for direction: blue fibres are cranio-caudal, green fibres are anteroposterior and red fibres are transverse. Splenium and genu fibres are widened and warped in the left segment and broken in the right segment,辅助检查：MRI,2月后MRI复查： 大部分较小的病灶消失、吸收、变小 较大的病灶缩小、边界较前清晰； T1WI信号更低；T2WI信号更高； 脑萎缩,伤后12天 T2WI及弥散加权成像资料来源:H Takayama,(2000), Diffusion-weighted imaging demonstrates transient cytotoxic edema involving the corpus callosum in a patient with diffuse brain injury.Clinical Neurology and Neurosurgery 102:135139,(a) Axial T2-weighted image on 12 days postinjury reveals an