脑弥漫性轴索损伤的临床表现及CT诊断

目的探讨脑弥漫性轴索损伤(DAI)的临床表现、CT诊断。方法分析32例脑弥漫性轴索损伤的临床资料及cT图像资料。同时对所有病例进行GCS评分。结果DAI的CT征象主要为：a)弥漫性双侧脑白质水肿、脑肿胀、灰白质界限不清；b)脑室、脑池、脑沟及蛛网膜下腔变窄、消失，无中线移位；c)脑弥漫性肿胀，白质内点、片状出血，但未形成血肿，无占位效应；d)脑弥漫性肿胀伴硬脑膜下薄层出血。患者伤后昏迷时间越长，临床表现越重，GCS评分越低，cT显示脑室系统受压程度越重则预后越差。结论DAI根据临床表现及影像学检查可作出临床诊断?但DAI病情与CT表现不一致时需行CT薄层扫描或MRI检查。     

重型颅脑损伤患者自主神经功能障碍的临床分析

目的 探讨重型颅脑损伤患者自主神经功能紊乱综合征发生率、临床症状、发病危险因素及预后.方法回顾性分析2008年1月-2010年3月收治的142例重型颅脑损伤患者,比较自主神经功能障碍组和对照组(无自主神经功能障碍患者)的临床特征;采用Logistic回归分析自主神经功能障碍发病的危险因素;伤后6个月采用GOS评分分析其预后.结果142例患者中生存并成功随访94例,自主神经功能障碍患者16例(17%),且其在GCS评分、昏迷时间、ICU时间、平均住院时间等方面较对照组差异有统计学意义(P<0.05);自主神经功能障碍患者预后较差(P<0.05),与弥漫性轴索损伤(DAI)密切相关(OR=11.25,95%CI 7.65～16.54).结论 自主神经功能障碍在严重颅脑损伤患者中发生率较高,临床表现重,DAI增加其发作风险,此类患者多预后不良.

Abstract：

Objective To investigate the incidence, clinical symptoms, correlative risk factors and prognosis of dysautonomia in patients with severe traumatic brain injury. Methods A total of 142patients with severe traumatic brain injury treated from January 2008 to March 2010 were retrospectively surveyed to compare the clinical features of dysautonomia group and control group. Logistic regression was used to analyze the risk factors for dysautonomia. At 6 months post-trauma, the Glasgow Outcome Score (GOS) was used to measure the outcome. Results Of all the patients, 94 patients survived and were followed up. There were 16 patients ( 17% ) diagnosed as dysautonomia depended on clinical symptoms,with statistical difference in aspects of GCS, coma duration, ICU time and average length of stay (ALOS)(P < 0.05). The patients with dysautonomia tended to have poorer outcome ( P < 0.05 ) and showed a positive association with diffuse axonal injury (DAI) ( OR = 11. 25, CI 7.65-16.54 ). Conclusion Dysautonomia has high incidence and is usually severe in patients with severe traumatic brain injury,when DAI may contribute to its occurrence and result in poor prognosis.     

Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain damage

Experimental studies have shown that diffuse axonal injury is usually induced by positive or negative acceleration mechanisms. In order to determine the reliability of axonal injury (AI) as a marker of this type of traumatic insult, we compared cases of trauma-induced focal cortical hemorrhage without dural involvement (n = 67) with cases of trauma-induced subdural bleeding without cortical hemorrhage (n = 26). Both groups exhibited a wide range of post-traumatic survival times. The injuries in the first group were caused mainly by direct impact to the head, those in the second by acceleration/deceleration mechanisms. The investigations were based primarily on immunohistochemical demonstration of antibodies targeted to β-amyloid precursor protein (β-APP) in the pons as a marker of AI and the results were assessed semiquantitatively. No significant differences were found between the two groups. In both groups AI was detected in 80–100% of cases with survival times of more than 3 h and two thirds of all positive cases showed pronounced positivity. Additional comparison of cases of brain death due to mechanical trauma (n = 14) with cases of brain death due to non-mechanical trauma (n = 18) also disclosed no significant intergroup differences. Finally, investigations of the pons in cases of non-traumatic death due to cerebral hypoxia/ischemia (n = 51) demonstrated AI with the same frequency as in the other groups, although the expression tended to be less pronounced. Our results confirm that β-APP expression in the pons is a reliable indicator of AI but does not discriminate between injuries caused by traumatic strain or shearing mechanisms and secondary damage due to cerebral hypoxia/ ischemia or edema. In the large majority of cases with prolonged post-traumatic survival, it can therefore be assumed that AI in the pons is the consequence of primary and/or secondary events or a combination of both, as is common in non-missile head injury survived for more than 90–120 min. Therefore, positive differentiation of the type of biomechanical event based on this criterion alone is not possible. Received: 19 December 1997 / Received in revised form: 1 April 1998     

Axonal recovery after severe traumatic brain injury demonstrated in vivo by 1H MR spectroscopy

Proton magnetic resonance spectroscopy (MRS) suggested almost complete axonal recovery 21 months after trauma in a patient with severe diffuse axonal injury. MRS while the patient was comatose showed evidence of severe diffuse axonal injury in occipitoparietal white matter, but occipital grey matter was relatively spared. At 21 months N-acetylaspartate was normal. At 33 months examination showed a Functional Independence Measure of 83 and a Rancho Los Amigos Scale of Cognitive Function of 7–8, a remarkable improvement considering all the initial findings, except those of MRS.     

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.     

联合检测血清S-100B蛋白、神经元特异性烯醇化酶、神经胶质纤维酸性蛋白对严重颅脑损伤诊断及预后的意义

目的探讨严重颅脑损伤后血清S-100B蛋白、神经元特异性烯醇化酶(NSE)、神经胶质纤维酸性蛋白(GFAP)水平变化及其临床意义。方法采用酶联免疫吸附法(ELISA)检测46例严重颅脑损伤患者伤后12、24h、3、7、14d血清S-100B蛋白、NSE、GFAP水平,其中12h～3d的平均值作为初期值结合格拉斯哥昏迷评分(GCS)分析;7～14d平均值作为后期值结合格拉斯哥预后评分(GOS)分析,并与峰值及平均值比较。结果 (1)严重颅脑损伤后血清S-100B蛋白、NSE、GFAP水平较对照组明显升高;(2)重型(GCS6～8分)与特重型颅脑损伤组(GCS 3～5分)相比,3种标记物均无显著性差异(P>0.05);(3)预后不良组(GOS 1～3分)标记物峰值、平均值及后期值均明显高于预后良好组(GOS 4～5分)(P<0.005),3个值均与预后呈负相关,后期值与预后的相关性最大。3种标记物中GFAP后期值差异尤为显著(P<0.001)。结论严重颅脑损伤后血清S-100B蛋白、NSE、GFAP水平升高,但不能作为评判重型颅脑损伤或特重型颅脑损伤的依据。3种标记物水平对评估重型颅脑损伤预后具有较高的特异性和敏感性,其中GFAP后期值是评估严重颅脑损伤预后的较好的指标。     

Course of glial immunoreactivity for vimentin, tenascin and alpha1-antichymotrypsin after traumatic injury to human brain

In a total of 104 individuals who had sustained traumatic brain injury (TBI), the course of glial immunoreactivity was investigated at the injured cortical area during the first 30 weeks after the trauma, in order to provide data for a forensic wound age estimation. Glial cells were stained with antibodies against the intermediate filament protein vimentin, the extracellular matrix protein tenascin and the serine protease inhibitor α1-antichymotrypsin (α1-ACT). Injury-induced glial staining reactions could be observed, at the earliest, after a post-infliction interval of 3.1 h for α1-ACT, 22 h for vimentin and 7 days for tenascin. Received: 21 August 2000 / Accepted: 21 November 2000