外伤性迟发性颅内血肿临床分析

目的：探讨外伤性迟发性颅内血肿（DTIH）的发生机制、早期诊断和治疗。方法：对36例外伤迟发性颅内血肿病人的临床资料进行回顾性分析，其中手术治疗32例、非手术治疗4例。结果：按GCS评分评定疗效，本组疗效良好18例，中残9例，重残5例，死亡4例，死亡率为13．3％。结论：多数DTIH在脑挫裂伤和填塞效应消失的基础上形成，确诊主要是依靠头颅CT复查，首选治疗方法是及时手术，对额颞叶挫伤病人保守治疗要慎重。     

外伤性迟发性颅内血肿72例临床分析

目的分析外伤性迟发性颅内血肿发生的相关因素及探讨处理方法,提高早期预防和治疗水平。方法回顾分析了我科近3年收治的72例外伤性迟发性颅内血肿病例,其中因症状加重进行复查CT52例,主动性复查20例。结果本组行手术治疗34例,死亡率12.5%,保守治疗38例,保守治疗无死亡,重残和轻残者均为手术组病人。结论外伤性迟发性颅内血肿与是否存在颅骨骨折、早期强力脱水、对冲伤损伤程度有关。对存在外伤性迟发性颅内血肿危险因素的患者,应在外伤后6~9h内复查头颅CT,一旦确诊,应予相应处理。     

15例高原外伤性迟发性颅内血肿临床分析

外伤后迟发性颅内血肿是指脑外伤后首次影像学检查无血肿,但经过一段时间后复查才发现的颅内血肿。我科自1994年～1996年1月共收治外伤性迟发性颅内血种15例,结合高原特殊环境发病特点,报告如     

外伤性迟发性颅内血肿的早期诊断

笔者对21例外伤性迟发性颅内血肿进行了回顾性分析,现报道如下: 1临床资料 本组病人男16例,女5例,年龄为15～83岁,平均47.3岁。其中15～40岁4例,40～60岁9例,60～83岁8例。受伤机制为减速伤15例,加速伤4例,对冲伤     

外伤性迟发性颅内血肿76例诊治体会

外伤性迟发颅内血肿（DTICH）在颅脑外伤中较常见，已成为颅脑损伤致死、致残的主要原因之一，但是可以通过早期诊断和治疗改善预后的继发性脑损害。我科2003年3月至2007年4月共收DTICH患者76例。现将其诊断、治疗体会分析报告如下。     

95例外伤迟发性颅内血肿的诊治分析

随着CT的普及,外伤性迟发颅内血肿的发现与报道逐渐增多,因其发展迅速,病情严重复杂,如延误治疗或处理不当,常导致不良后果.我科自2006年1月至2008年11月共收治600余例外伤性颅内血肿患者,其中迟发性颅内血肿95例,现报告如下:     

61例迟发性颅内血肿的综合治疗

随着CT的普及，外伤性迟发性颅内血肿的发现与报道逐渐增多，因其发展迅速，病情严重复杂，如延误治疗或处理不当，常导致不良后果。我科自2005年1月至2008年9月共收治600余例外伤性颅内血肿患者，其中迟发性颅内血肿61例，现报告如下：     

外伤性迟发性颅内血肿CT扫描动态观察的价值

目的 探讨外伤性迟发性颅内血肿CT多次扫描的意义.方法 多次CT扫描动态观察患者病情变化.结果 根据CT影像学的改变和临床变化.采取及时的手术治疗23例,非手术治疗14例.结论 CT多次扫描动态观察,对迟发性颅内血肿的早期诊断和治疗很有意义     

迟发性颅内血肿的治疗分析

近年来,随着人们交往的日益频繁,脑外伤的发病率有上升趋势.而CT的普及,使外伤性迟发性颅内血肿的发现与报道逐渐增多,因其发展迅速,病情严重复杂,如延误治疗或处理不当,常导致不良后果.     

小儿后颅窝迟发性血肿23例诊治体会

目的探讨小儿外伤性迟发性后颅窝血肿的临床特征、诊断和治疗。方法回顾性分析我院2002年1月至2012年01月收治的23例小儿外伤性后颅窝血肿的临床资料。结果本组小脑硬膜外血肿11例(3例血肿骑跨幕上),占47.82%,小脑硬膜下血肿6例,占26.08%.,小脑半球血肿4例,其中伴阻塞性脑积水2例,第四脑室内出血2例。6例行非手术治疗,全部治愈;18例行后颅窝血肿清除术(其中有1例为非手术治疗的中转手术),17例治愈,1例死亡,死亡率4.34%。结论小儿外伤性迟发性后颅窝血肿病情隐蔽,早期诊断、及时发现及选择恰当的治疗方案是抢救成功的关键。     

神经外科开颅术后颅内感染的临床分析

目的:分析神经外科开颅术后颅内感染的危险因素。方法:回顾性分析48例神经外科开颅手术感染的病历资料。结果:神经外科开颅术后颅内感染率3.9%。术前抗菌药物应用、手术时间,手术清洁状况,脑室外引流、引流管留置时间和脑脊液漏为神经外科开颅术后颅内感染的危险因素。结论:神经外科开颅术后颅内感染率较高,关注感染危险因素对降低感染率具有重要意义。     

Anatibant,a selective non-peptide bradykinin B2 receptor antagonist,reduces intracranial hypertension and histopathological damage after experimental traumatic brain injury

Bradykinin, the main metabolite of the kallikrein-kinin system and one of the first mediators released during inflammation, is well known to increase the permeability of the blood brain barrier (BBB) by activation of kinin B₂ receptors and hence promote brain edema formation following traumatic brain injury (TBI). Anatibant^® (LF 16-0687), a selective non-peptide bradykinin B₂ receptor antagonist, reduces brain edema after experimental TBI, however, so far no data are available if Anatibant^® reduces also the sequels of brain edema formation, i.e. morphological brain damage. Therefore, we investigated the effect of Anatibant (3.0 mg/kg b.w.) on intracranial pressure (ICP) and contusion volume after experimental TBI. Male C57/Bl6 mice (25–28 g) were subjected to Controlled Cortical Impact trauma (CCI). Anatibant^® was administrated as a subcutaneous bolus 15 min and 8 h after TBI. ICP was measured 3, 6, and 10 h after injury and contusion volume was quantified 24 h after trauma. Our data demonstrate a significant reduction of ICP (16.6 ± 1.67 mmHg vs. 24.40 ± 3.58 mmHg; n = 6; p = 0.002) and of contusion volume 24 h after trauma (28.28 ± 5.18 mm³ vs. 35.0 ± 3.32 mm³n = 7; p = 0.003) in treated mice. Therefore we conclude, that inhibition of bradykinin B₂ receptors seems to be a promising treatment option, and might therefore be investigated in clinical trails for the treatment of TBI.     

闽东地区小儿颅内感染52例临床分析

目的 探讨小儿各型颅内感染的临床表现、脑脊液及CT影像学检查在鉴别诊断中的价值。方法 本文回顾性分析了52例1996年3月-2003年5月闵东医院住院的颅内感染患儿的临床表现、脑脊液常规检查及CT影像学表现。结果 脑脊液白细胞数在各型颅内感染中无显著性差异,各组间P>0.05;蛋白含量细菌性感染组(包括化脓性脑膜炎及结核性脑膜炎)显著高于无菌性感染组(包括病毒性脑炎及流行性乙型脑炎),P<0.001;糖含量则前组显著低于后组,P<0.01;组内无显著性差异,P>0.05。氯化物含量结脑显著低于其余各组,P<0.01。结论 脑脊液生化常规对各型颅内感染具有鉴别诊断意义。白细胞计数不能作为鉴别的金标准。CT检查对结脑患儿诊断意义较大。     

Pathogenesis and biomechanics of traumatic intracranial haemorrhages

Summary Intracranial haemorrhage is frequently seen by the general pathologist in the context of neural trauma. Thus, the differential diagnosis, pathogenesis and biomechanics are of practical interest in the routine work. Extradural haematomas are produced when branches of the middle meningeal vessels are lacerated. They are commonly located in the temporal fossa, and other intracranial haematomas may be present. Skull fractures occur in a high percentage of cases and play a key role in the pathogenesis of this type of bleeding. Acute subdural haematomas commonly arise from tearing of the bridging veins. They are often located in the temporal and frontal regions, and the morbidity and mortality are related to the extent of the underlying brain damage. The visco-elastic behaviour of the bridging veins and their lack of reinforcement by arachnoid trabecula in the subdural space explains why they tear under high rates of acceleration during trauma. Subacute and chronic subdural haematomas are weakly correlated with trauma. The less striking onset of symptoms may be related to the rate of blood accumulation and the capacity of the brain to accommodate the mass effect of the bleeding. Intracerebral haematomas are probably due to the direct rupture of the intrinsic cerebral vessels. The mortality rate shows no correlation with location, but those located in the basal ganglia are compatible with a good recovery when occurring in isolation. Traumatic subarachnoid haemorrhage, when in isolation, is usually associated with evidence of injury elsewhere, such as the neck muscles or the ligamentary system of the cervical spinal column. It may be secondary to intraventricular bleeding due to tearing of the tela choroidea, or associated with contusions.     

The poor outcome of the delayed diagnosis of acute spontaneous spinal epidural hematoma: two cases report

We present two patients who had acute paraplegia with sensory loss due to spontaneous spinal epidural hematoma (SSEH). One had myocardial infraction and the other had deep vein thrombosis, and the former was treated with anticoagulants and the latter was treated with thrombolytic agent. We analyzed the neurological status of our two cases each between its preoperative and postoperative state. Postoperatively both showed no improvement of neurologic symptom, and on follow-up of 12 months, one showed no neurologic improvement and the other showed a insignificant improvement of lower extremity muscle power (trace knee extensor/ankle dorsi-flexor). We thought that this poor outcome was due to delayed operation, which was done more than 24 hr after the symptom onset. The outcome in SSEH is essentially determined by the time taken from symptom onset to operation. Therefore, early and precise diagnosis such as careful history taking and MRI evaluation is necessary.     

YL-1型颅内血肿穿刺针的临床应用

目的探讨YL-1型颅内血肿穿刺针对颅内疾病微创治疗的价值及临床应用。方法回顾性分析本院2005年3月至2007年3月应用YL-1型颅内血肿穿刺针治疗颅内疾病患者58例（高血压幕上脑出血38例;慢性硬膜下血肿12例;急性硬膜外血肿5例;脑积水2例;颅内张力性积气1例）评价YL-1型颅内血肿穿刺针其在颅内疾病的应用价值。结果经采用CT定位YL-1型颅内血肿穿刺针微创手术治疗颅内疾病患者58例,存活51例;死亡4例;术后放弃治疗3例。结论采用YL-1型颅内血肿穿刺针微创手术治疗颅内血肿、积水、积气是简单、有效的微创手术方法。     

外伤后脑血肿对颅内压分布的力学分析研究

目的　根据患者CT和颅内压数据，建立外伤性脑损伤的有限元模型，分析脑血肿对颅内压产生的压力响应。 方法　采用成人头部有限元模型（GHBMC）与气体分子动力学分析脑血肿膨胀与颅内压增高的关系，提取并折叠血肿，置入有限元模型中相对应的位置，根据CT图像和颅内压值，加入肿胀曲线，进行模拟计算，得到各个部分的脑组织压力分布云图、脑组织应变的分布云图，计算脑疝多发区域的脑组织压力差。 结果　有限元模型中的压力值、中线偏离量与临床病人脑室型探头压力、CT图像中线的吻合度较好，误差率分别为4%和2%。模拟结果显示，在左侧颞枕叶矢状位上，左侧基底节区血肿病例大脑镰下方、小脑幕切迹后部压力差不显著，分别为1400 Pa和1320 Pa。但幕上颞叶压力明显大于小脑小叶的压力，分别为2504 Pa和1360 Pa。小脑前叶与后环池的压力无明显差异。左侧脑血肿患者小脑幕比右侧脑血肿患者具有更大的等效应变。 结论　左侧患者额颞基底节区的血肿更有可能导致小脑幕切迹疝。而右侧患者的脑血肿导致的压力被小脑幕的应变代偿，脑疝风险因此下降。通过本研究计算脑疝易形成区域的压力差，可更好地理解血肿造成的颅内压分布对激发脑损伤的影响，为损伤的预后提供力学依据。     

外伤后脑血肿对颅内压分布的力学分析研究

目的　根据患者CT和颅内压数据,建立外伤性脑损伤的有限元模型,分析脑血肿对颅内压产生的压力响应。 方法　采用成人头部有限元模型（GHBMC）与气体分子动力学分析脑血肿膨胀与颅内压增高的关系,提取并折叠血肿,置入有限元模型中相对应的位置,根据CT图像和颅内压值,加入肿胀曲线,进行模拟计算,得到各个部分的脑组织压力分布云图、脑组织应变的分布云图,计算脑疝多发区域的脑组织压力差。 结果　有限元模型中的压力值、中线偏离量与临床病人脑室型探头压力、CT图像中线的吻合度较好,误差率分别为4%和2%。模拟结果显示,在左侧颞枕叶矢状位上,左侧基底节区血肿病例大脑镰下方、小脑幕切迹后部压力差不显著,分别为1400 Pa和1320 Pa。但幕上颞叶压力明显大于小脑小叶的压力,分别为2504 Pa和1360 Pa。小脑前叶与后环池的压力无明显差异。左侧脑血肿患者小脑幕比右侧脑血肿患者具有更大的等效应变。 结论　左侧患者额颞基底节区的血肿更有可能导致小脑幕切迹疝。而右侧患者的脑血肿导致的压力被小脑幕的应变代偿,脑疝风险因此下降。通过本研究计算脑疝易形成区域的压力差,可更好地理解血肿造成的颅内压分布对激发脑损伤的影响,为损伤的预后提供力学依据。     

Memory and executive functions correlates of self-awareness in traumatic brain injury

Objective: The purpose of this study was to investigate the contribution of executive functions (EF) components and episodic and working memory variables, as well as clinical and demographic factors, to awareness of cognitive ability in traumatic brain injury (TBI).

Methods: Sixty-five TBI patients (mild: n?=?26; moderate/severe: n?=?39) took part in the study. Independent stepwise regression models were calculated for EF and memory predictors, with awareness being measured by patient/informant discrepancy in the Patient Competency Rating Scale.

Results: Models with EF variables indicated that semantic verbal fluency and age are the best predictors of awareness, whereas models including mnemonic functions suggested verbal delayed episodic recall and TBI severity as predictors.

Conclusions: These results are discussed in relation to clinical implications, such as the need to focus efforts of rehabilitation in the cognitive abilities related to awareness, and theoretical models.