创伤性脑弥漫性轴索损伤106例

为增强对交通事故所致的创伤性脑弥漫性轴索损伤(TBDAI)的认识，提高诊治水平，现对我院1995年1月-2002年2月收治的106例TBDAI患者的临床资料进行分组回顾分析。     

弥漫性轴索损伤在重型颅脑损伤诊治中的意义

报告了２３例脑弥漫性轴索损伤（ＤＡＩ）病人。根据其临床表现详细分析了ＣＴ扫描的特征及诊断条件，讨论了ＤＡＩ的病理解剖学方面的变化，并提出了有助于ＤＡＩ与脑挫裂伤的鉴别诊断依据。ＤＡＩ的治疗主要为非手术疗法。对合并有颅内压增高的ＤＡＩ病人可进行减压手术。ＤＡＩ的预后较差，是重型颅脑外伤死亡的主要原因。     

单核吞噬细胞在创伤性非断离性轴索损伤继发断离的作用

目的 观察单核吞噬细胞在创伤性非断离轴索损伤(NDAI)继发断离的作用，探讨NDAI继发断离的机制。方法 液压冲击脑损伤SD大鼠55只，采用全鼠脑连续矢状冰冻切片去磷酸化神经丝蛋白轻链(NF68)和单核吞噬细胞标记抗原(ED1)组化双标及NF68组化电镜染色，光镜电镜观察，计数肿胀轴索及轴索球。结果 伴有血管损伤的冲击区皮质及部分胼胝体主要是断离性轴索损伤，轴索碎片呈NF68杂染，早期即有ED1阳性细胞浸润；远离冲击区的基底节区、脑干、小脑无血管损伤，主要是NDAI，伤后3～12h出现NF68阳性反应的肿胀轴索和轴索球，7～14d毛细血管周边出现ED1阳性细胞，21～28d除肿胀轴索和轴索球外，部分神经元NF68阳性反应，ED阳性细胞广泛浸润。结论 延迟的NDAI继发断离与中枢吞噬细胞免疫反应密切相关。     

重型颅脑损伤的神经轴索形态改变与病理机制研究

为探讨重型颅脑损伤的发生机制,将大鼠制成脑弥漫性轴索损伤(DAI)模型和Mamarou自由落体致伤模型.对DAI鼠脑行小鼠抗神经纤维丝(NF)蛋白NF68亚单位和HSP70免疫组化检测,延髓部分行电镜观察;对落体致伤鼠脑左顶叶皮层行HE和HSP70检测.结果发现,DAI大鼠伤后30min延髓轴索纡曲肿胀,髓鞘轻度分离,轴浆NF结构紊乱;伤后2h～24h,轴索破坏渐重并形成轴缩球;髓鞘局部断裂,线粒体空泡变,部分胞浆溶解,NF68染色强度也渐增强.两组的HSP70的变化趋势一致,均在伤后3h开始表达,24h达高峰,72h下降.该结果说明DAI可引起NF结构破坏,缺血和缺氧等因素诱发了HSP产生.     

弥漫性轴索损伤救治

回顾分析近2年来收治的6例弥漫性轴索损伤（DAI）患者的临床表现、治疗方法及效果。提高综合治疗及有效地防治并发症,仍是临床倡导的治疗方案。     

弥漫性轴索损伤影像学分析

目的探讨弥漫性轴索损伤(DAI)影像学表现及诊断价值。方法回顾性分析2010年9月~2015年9月26例DAI患者临床与CT、低场MRI资料,其中男性19例,女性7例;年龄16~65岁,平均34.6岁。患者均有创伤史,道路交通伤22例,高处坠落伤3例,重物打击伤1例。伤后均立即出现昏迷或持续昏迷,入院时格拉斯哥昏迷量化表(GCS)评分,重度(≤8分)4例,中度(9~12分)6例,轻度(13~15分)16例。结果 26例均使用CT及低场MRI诊断,主要表现为颅内不同部位单发或多发点状病变,DAI病灶分为出血灶和非出血灶,主要分布在灰白质交界区、基底节区、丘脑、深部白质、胼胝体等区域。低场MRI敏感性明显高于CT(χ2=14.567,P=0.012),各序列中GRE-T2*WI对出血灶检出数(97.59%)最高,DWI对非出血灶检出数(95.18%)最高。结论 CT及低场MRI对DAI的早期诊断很有价值,低场MRI能弥补CT检查阴性颅脑损伤而症状较重患者,能明显提高颅脑损伤的检出率、诊断率,能有效避免漏诊,提示预后。     

磁敏感成像在脑弥漫性轴索损伤中的应用价值

目的:评价磁敏感成像(SWI)在脑弥漫性轴索损伤(DAI)中的价值。方法:回顾性分析45例DAI的SWI序列影像特点,并与常规MRI序列对照分析。结果:所有序列共检出病灶413个。SWI序列检出病灶402个,其中水肿灶56个,表现为片状高(稍高)信号;水肿伴出血灶346个,表现为片状高(稍高)信号区内分布斑点状低信号。常规MRI序列共检出病灶392个,表现为单纯水肿灶316个,水肿伴出血灶76个灶。SWI检出病灶以及病灶内合并出血的敏感性明显高于常规检查序列,差异有统计学意义。结论:SWI能高效检出DAI病灶,同时可明显提高出血性病灶的检出率,有助于准确评价病变的严重程度,为DAI最有价值的检查方法。     

大鼠创伤性轴索损伤后脑代谢质子磁共振波谱分析

目的 使用质子磁共振波谱(1H-MRS)研究大鼠创伤性轴索损伤(traumatic axonal injury,TAI)后组织代谢改变及其空间分布特征.方法 使大鼠头颅发生线加速和角加速运动制作TAI模型.于伤前和伤后24 h采用多体素MRS方法检测大鼠脑内多个部位的组织代谢状态,分析伤后N-乙酰门冬氨酸(NAA)/总肌酸(Cr)、NAA/胆碱类化合物(Cho)和Cho/Cr值变化及NAA/Cr值变化的空间分布特征.采用免疫组化标记β淀粉样蛋白前体蛋白(β-APP)观察轴索损伤情况.结果 与伤前相比,伤后24 h时NAA/Cr、NAA/Cho值显著下降(P<0.05).Cho/Cr值轻度升高(P>0.05);NAA/Cr值出现较大降低幅度的部位依次为脑干、海马、内囊、胼胝体和丘脑.病理学检查示这些部位出现轴索损伤.结论 TAI后脑组织出现严重代谢紊乱,以脑干、海马等部位变化最为显著.

Abstract：

Objective To investigate the brain metabolic changes and evaluate their spatial distributions after traumatic axonal injury (TAI)in rats by using proton magnetic resonance spectroscopy(1H-MRS).Methods The TAI model was made by subjecting the head of the rats to the linear and angular accelerations.The multi-voxel MRS was employed to detect the tissue metabolic state at the levels of hippocampus-caudate and pons prior to injury and at 24 hours after injury.The alterations of NAA/Cr,NAA/Cho and Cho/Cr values as well as the spatial distribution of NAA/Cr reduction were accessed. Immunohistochemical staining for β-APP was used to observe the injured axons. Results A siguificantdecrease in NAA/Cr and NAA/Cho(P<0.05)and subtle increase in Cho/Cr(P>0.05)were observed in rats at 24 hours after TAI in comparison to the pre-injury levels.Notable decrease in NAA/Cr value was observed in the areas including the brain stem,hippocampus,internal capsule,corpus callosum and thalamus,where axonal injuries were confirmed by the histological examination. Conclusion Metabolic imbalances Occur in the brains of rats with TAI.with notable changes in the brain stem and the hippocampus.     

脑弥漫性轴索损伤76例

脑弥漫性轴索损伤（DAI）是头部伤致死和致残的重要原因，在颅脑损伤死亡患者中占29％～43％。对DAI的发病机制、损伤特点、影像学特征、分型、诊断标准和治疗措施等方面进行深人研究具有重要意义。我院于2001年1月-2006年10月共收治76例DAI患者。     

Proton MR spectroscopic imaging depicts diffuse axonal injury in children with traumatic brain injury

BACKGROUND AND PURPOSE: Diffuse axonal injury (DAI) after traumatic brain injury (TBI) is important in patient assessment and prognosis, yet they are underestimated with conventional imaging techniques. We used MR spectroscopic imaging (MRSI) to detect DAI and determine whether metabolite ratios are accurate in predicting long-term outcomes and to examine regional differences in injury between children with TBI and control subjects. METHODS: Forty children with TBI underwent transverse proton MRSI through the level of the corpus callosum within 1-16 days after injury. T2-weighted, fluid-attenuated inversion recovery, and susceptibility-weighted MR imaging was used to identify voxels as normal-appearing or as nonhemorrhagic or hemorrhagic injury. Neurologic outcome was evaluated at 6-12 months after injury. Metabolite ratios for total (all voxels), normal-appearing, and hemorrhagic brain were compared and used in a logistic regression model to predict long-term outcome. Total and regional metabolite ratios were compared with control data. RESULTS: A significant decrease in N-acetylaspartate (NAA)/creatine (Cr) and increase in choline (Cho)/Cr (evidence of DAI) was observed in normal-appearing (P < .05) and visibly injured (hemorrhagic) brain (P < .001) compared with controls. In normal-appearing brain NAA/Cr decreased more in patients with poor outcomes (1.32 +/- 0.54) than in those with good outcomes (1.61 +/- 0.50, P = .01) or control subjects (1.86 +/- 0.1, P = .00). In visibly injured brains, ratios were similarly altered in all patients. In predicting outcomes, ratios from normal-appearing and visibly-injured brain were 85% and 67% accurate, respectively. CONCLUSION: MRSI can depict injury in brain that appears normal on imaging and is useful for predicting long-term outcomes.     

镁离子对大鼠弥漫性轴索损伤超微结构的影响

目的探讨镁离子(Mg^2 )对脑弥漫性轴索损伤(diffuse axonal injury，DAI)脑干超微结构的影响。方法选健康成年雄性SD大鼠36只，体重350～450g，将其随机分为实验组、对照组、空白组，每组为12只。采用改良Marmarou模型制作DAI模型，伤后30min分别给予MgSO4 250μmol／kg、等渗盐水0．2ml，伤后24h处死。用透射电镜分别检测脑干超微结构，并行综合组织损伤评分。结果伤后24h，对照组髓鞘分离，线粒体嵴明显肿胀；实验组未见髓鞘分离，线粒体轻度肿胀。实验组脑干综合组织损伤程度评分明显轻于对照组。结论Mg^2 可在超微结构水平阻止DAI轴索的继发性损害，对DAI具有一定的保护作用。     

对抗性运动诱发慢性创伤性脑病的病理机制及其研究进展

对抗性体育运动对维持心血管系统和大脑健康有益.但体育运动与风险伴行,头颅、躯干等可能发生撞击的对抗性运动可导致严重创伤.近年来,与运动相关的创伤性脑损伤(TBI)特别是轻型TBI (mTBI)日益引起关注.反复mTBI可产生持续的认知、行为和精神障碍,导致慢性创伤性脑病(CTE),引起神经变性和神经退化.笔者围绕对抗性...     

创伤性轴索损伤患者脑结构及功能连接改变的磁共振研究进展

创伤性轴索损伤(traumatic axonal injury,TAI),也称弥漫性轴索损伤(diffuse axonal injury,DAI),是创伤性脑损伤(traumatic brain injury,TBI)常见的亚型之一。TAI 普遍存在于致命的脑外伤中,在整个大脑区域具有较特征性的分布,造成大范围脑白质破坏,易损伤胼胝体及脑干[1],常致患者严重残疾、死亡或处于植物生存状态。常规影像学检查技术对 TAI 损伤程度和范围缺乏准确判断。近年来,随着更多先进MRI 技术在 TAI 研究中的应用,特别是在脑网络的整体水平研究,为理解 TAI 患者脑结构及功能连接变化提供了更多更为深入的依据。最新研究表明,连接大脑网络节点的远程脑白质神经束的损害,导致大型脑网络中断,是引起 TAI 患者持久认知功能障碍的核心机制[2-3]。笔者通过查阅近年来国内外相关文献,对TAI 后患者脑结构及功能连接方面改变的相关研究进展进行综述。     

The latency between traumatic axonal injury and the onset of amyotrophic lateral sclerosis in young adult men

Traumatic axonal injury-induced apoptotic motor neuron cell death in neonatal rats is an established animal model used to study potential therapeutic agents in amyotrophic lateral sclerosis (ALS). In an analogous manner, trauma causing motor neuron axonal injury (which included focal neuropathy, plexopathy, and radiculopathy) preceded the onset of ALS in nine young adult men (age range, 28-43 years). The latency between the traumatic axonal injury and the onset of ALS symptoms in these patients ranged from 5 to 42 months (mean, 14.6 months).     

Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: correlation with clinical outcome after traumatic brain injury

BACKGROUND AND PURPOSE: Current imaging does not permit quantification of neural injury after traumatic brain injury (TBI) and therefore limits both the development of new treatments and the appropriate counseling of patients concerning prognosis. We evaluated the utility of magnetization transfer ratio (MTR) and proton MR spectroscopy in identifying patients with neuronal injury after TBI. METHODS: Thirty patients with TBI (21-77 years old; mean age, 42 years; admission Glasgow Coma Scale (GOS) scores 3-15; mean score, 11) were studied on a 1.5-T system with magnetization transfer imaging and MR spectroscopy of the splenium. Magnetization transfer imaging was also performed in the brain stem in all patients, and other areas of the brain were sampled in one patient. The splenium of the corpus callosum and brain stem were studied because these are often affected by diffuse axonal injury. Scans were obtained 2 to 1129 days after injury (median, 41 days). MTR was considered abnormal if it was more than 2 SD below normal. Proton MR spectroscopy was used to calculate the N-acetylaspartate (NAA)/creatine (Cr) ratio. GOS was determined at least 3 months after injury. RESULTS: In 10 patients with a GOS of 1 to 4, the mean NAA/Cr was 1.24 +/- 0.28; two of these patients had abnormal MTR in normal-appearing white matter (NAWM). In 20 patients with a GOS of 5, the mean NAA/Cr was 1.53 +/- 0.37 (P < .05); four of these patients had abnormal MTR in NAWM. MTR abnormalities in NAWM were identified in six patients, but these changes did not correlate with GOS or MR spectroscopy changes. CONCLUSION: MTR and MR spectroscopy can quantify damage after TBI, and NAA levels may be a sensitive indicator of the neuronal damage that results in a worse clinical outcome.     

Diffuse axonal injury associated with chronic traumatic brain injury: evidence from T2*-weighted gradient-echo imaging at 3 T

BACKGROUND AND PURPOSE: Diffuse axonal injury is frequently accompanied by tissue tear hemorrhages. We examined whether high field strength T2*-weighted gradient-echo imaging performed during the chronic stage of traumatic brain injury may have advantages in the evaluation of diffuse axonal injury as compared with T1- and T2-weighted MR imaging. METHODS: Prospective MR imaging of 66 patients (age range, 17-57 years) was performed using a 3-T system 3 to 292 months (median, 23.5 months) after traumatic brain injury. T1-, T2-, T2*-hypointense and T2-hyperintense foci of 1- to 15-mm diameter were registered in 10 brain regions by two readers separately. Foci that appeared hypointense both on the T1- and T2- and/or on the T2*-weighted images were defined as traumatic microbleeds. RESULTS: For 46 (69.7%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds. Hyperintense foci were observed on the T2-weighted images of only 15 (22.7%) patients. T2*-weighted imaging showed significantly more traumatic microbleeds (P =.000) than did T1- and T2-weighted imaging. Interobserver agreement was strong (kappa = 0.79, tau = 0.749, P =.000). For 14 (21.2%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds in the corpus callosum, whereas for only two (3%), hyperintense callosal lesions were seen on the T2-weighted images. Although a significant correlation existed between the total amount and callosal appearance of traumatic microbleeds and Glasgow Coma Scale scores (P =.000), no correlation existed with extended Glasgow Outcome Scale scores. CONCLUSION: T2*-weighted gradient-echo imaging at high field strength is a useful tool for the evaluation of diffuse axonal injury during the chronic stage of traumatic brain injury. Diffuse axonal injury-related brain lesions are mainly hemorrhagic. The relevance of diffuse axonal injury for long-term clinical outcome is uncertain.