颅脑损伤患者继发外伤性癫痫的危险因素分析

目的探讨外伤性癫痫发病的危险因素,为预防和控制外伤性癫痫提供依据。方法回顾性分析我院神经外科2012年1月~2015年12月收治的358例颅脑损伤患者的临床资料,对继发外伤性癫痫的相关因素进行单因素分析和多因素Logistics回归分析。结果单因素分析发现,年龄、硬膜破裂、颅脑损伤程度、皮层挫裂伤、凹陷性颅骨骨折、颅脑受损部位、颅内血肿与外伤性癫痫的发生有关。Logistics回归分析发现年龄、硬膜破裂、颅脑损伤程度、凹陷性颅骨骨折、颅脑受损部位、颅内出血是外伤性癫痫的危险因素。结论低龄、硬脑膜破裂、脑外伤严重、颅骨凹陷性骨折、顶叶受损、颅内有血肿的患者发生外伤性癫痫的风险更高。     

重型颅脑损伤继发外伤性癫103例临床分析

目的分析重型颅脑损伤继发外伤性癫形成的原因、发病机制,以及外伤性癫的预防措施。方法对重型颅脑损伤患者救治过程中继发外伤性癫的临床特点和治疗结果进行回顾分析。结果 946例重型颅脑损伤病人继发性癫103例,发生率10.9%。其中颅骨凹陷粉碎性骨折39例(37.9%),开放性颅脑损伤28例(27.2%),颅内血肿25例(24.3%),单纯脑挫裂伤11例(10.7%)。结论重型颅脑损伤继发外伤性癫是局部严重的脑神经细胞结构损伤和神经抑制、负反馈系统破坏,导致神经细胞异常过度放电和异常放电进一步扩展形成的。     

颅脑损伤患者开颅术后血肿的原因分析

目的分析颅脑损伤患者开颅术后发生术后血肿的主要原因。方法回顾性分析863例颅脑损伤患者开颅术后发生术后血肿的38例患者的临床资料。结果脑挫裂伤伴颅内血肿的患者和凝血功能障碍的颅脑损伤患者术后颅内血肿的发生率分别明显高于硬膜外(或硬膜下)血肿的患者和凝血功能正常的颅脑损伤患者。血压高于160/110mmHg的颅脑损伤患者术后颅内血肿的发生率明显高于血压为140-160/90-110mmHg者(P0.05),而后者术后颅内血肿的发生率又明显高于血压低于140/90mmHg者(P0.01)。不同性别、年龄和入院时GCS评分的颅脑损伤患者术后颅内血肿的发生率无明显差异(P0.05)。结论脑挫裂伤并脑内血肿、高血压、凝血机制异常、止血不彻底等是导致颅脑损伤患者开颅术后血肿的主要原因,完全可靠的止血技术、细致耐心的手术操作及周密的防范措施是预防其开颅术后血肿的关键。     

小儿重型颅脑损伤特点与救治经验：附366例总结

本文报告366例小儿重型颅脑损伤的临床特征及诊治结果,Glasgow 昏迷计分均在8分以下。男271例,女95例。年龄1.1月～15岁。闭合性颅脑损伤274例(74.9%);开放性颅脑损伤92例(25.1%)。108例(29.5%)合并颅内血肿。全组均有不同程度意识障碍及局灶神经征,癫痫发生率为21.3%。对有广泛脑挫裂伤、脑肿胀和颅内血肿及颅骨凹陷骨折的288例采用手术治疗,余78例脑损伤较局限,行保守治疗。300例(81.96%)恢复良好;3例重残;63例(17.22%)死亡。     

创伤性颅脑损伤后血钠紊乱的危险因素与预后

目的探讨创伤性颅脑损伤发生血钠紊乱的危险因素以及对预后的影响。方法回顾性分析80例中、重型颅脑损伤病例资料。分析血钠紊乱的发生率,外伤性脑损伤后首次CT扫描时的伤情表现和意识状态。结果 36例发生血钠紊乱,20例表现为高钠血症,16例表现为低钠血症。血钠紊乱在硬膜下血肿、脑内血肿和弥散性轴索损伤的病例中发生率更高。弥漫性脑损伤的病例血钠紊乱的发生率比局限性脑挫裂伤组高。结论弥漫性脑损伤病例血钠紊乱的发生率比较高。局限性脑损伤与血钠紊乱的比例并没有相关性。     

外伤性癫痫的手术

前言外伤性癫痫的发生率约占闭合性颅脑损伤的1—5%,开放性颅脑损伤的发生率更高。如果说开放性颅脑损伤的清创术、异物摘除、予防感染、凹陷骨折整复、硬脑膜修补及颅骨成形等处理的主要目的是为了予防外伤性癫痫,也不过份。     

病情明显恶化的轻中型颅脑损伤治疗体会

目的探讨病情明显恶化的轻、中型颅脑损伤的临床特点、原因和机制。方法对手术救治的326例轻中型颅脑损伤患者的临床资料和动态头颅CT扫描结果进行回顾性分析。结果①引起病情恶化的原因主要有迟发性血肿、外伤后脑水肿和脑肿胀,其中硬膜外血肿134例,硬膜下血肿95例,外伤性脑挫裂伤血肿32例,脑水肿和脑肿胀65例;②硬膜外血肿常出现于颅骨骨折的年轻患者,外伤性脑挫裂伤血肿常见于枕部减速伤的老年患者;③恶化距受伤时间:6h内54例,6~24h225例,24~72h33例,>72h14例。④临床表现:所有患者均有意识改变,剧烈头痛和频繁呕吐,尿失禁以及躁动等。术前瞳孔一侧略大于对侧35例,双侧散大12例。⑤GOS评分:良好278例(85.3%),中残32例(9.8%),重残7例(2.2%),植物生存3例(0.9%),死亡6例(1.8%)。结论意识变化是轻、中型颅脑损伤病情恶化的特征性临床表现,应加强早期重症监护,及时复查头颅CT和手术,提高救治率。     

颅脑损伤手术中急性脑膨出的形成原因初步探讨

目的探究颅脑损伤手术中急性脑膨出的形成原因及影响因素,提出有效防治措施。方法选取2014年1月至2016年1月我院神经外科实施开颅手术的颅脑损伤患者130例,根据术中是否发生急性脑膨出分为观察组(发生急性脑膨出)和对照组(未发生急性脑膨出)。收集患者的临床资料,通过单因素卡方检验和多因素Logistic回归分析总结颅脑损伤患者术中发生急性脑膨出的影响因素。结果 40例患者术中发生急性脑膨出,发生率为30.8%。经单因素卡方检验,两组患者性别比、年龄、致伤原因、有无脑脊液漏以及合并多发伤情况差异均无统计学意义(P0.05);观察组入院后首次格拉斯哥昏迷评分(glasgow coma scale,GCS)8分、受伤至手术时间3 h、合并手术远隔部位颅骨骨折、合并迟发性外伤性颅内血肿(delayed traumatic intracranial hematoma,DTIH)以及合并外伤性弥漫性脑肿胀(post-traumatic acute diffuse brain swelling,PADBS)的比例均高于对照组,差异均有统计学意义(P0.05)。经多因素Logistic回归分析,入院后首次GCS评分低、受伤至手术时间短以及合并手术远隔部位颅骨骨折、DTIH和PADBS均为颅脑损伤患者术中发生急性脑膨出的危险因素。结论颅脑损伤患者手术过程中发生急性脑膨出的几率较高,且与入院后首次GCS评分、受伤至手术时间以及合并手术远隔部位颅骨骨折、DTIH和PADBS情况相关,术前应对患者发生急性脑膨出的风险进行综合评估。     

CT与MRI在脑弥漫性轴索损伤诊断中的应用

目的探讨CT与MRI对弥漫性轴索损伤的诊断意义。方法选择40例弥漫性轴索损伤患者为研究对象,均接受颅脑CT及MRI检查,比较两种检查方法对弥漫性轴索损伤病灶的显示情况。结果 40例患者中,颅内异常表现包括弥漫性脑肿胀、蛛网膜下腔出血、脑室出血、硬膜下(外)血肿、脑内出血性病灶及脑内非出血性病灶,MRI对上述异常表现显示总体情况优于CT。MRI对弥漫性轴索损伤病灶显示明显优于CT,差异有统计学意义(P0.05)。磁共振各序列间比较,DWI显示弥漫性轴索损伤病灶数量最多,其次为T2FLAIR,T1WI最少。结论与CT比较,MRI对弥漫性轴索损伤病灶显示具有优势。     

重型颅脑损伤去骨瓣减压术后脑膨出的临床特征

目的总结重型颅脑损伤去骨瓣减压术后并发脑膨出的临床特征,为减少或避免脑膨出的发生提供临床依据。方法对60例重型颅脑损伤去骨瓣减压术后患者进行回顾性探讨分析。结果颅脑损伤去骨瓣减压术后,脑膨出发生率67.7%,术前广泛脑挫裂伤及弥漫性脑肿胀,术后新发颅内血肿和(或)脑挫裂伤灶扩大、脑积水、大面积脑梗死、张力性硬膜下积液、颅内感染是导致术后脑膨出的重要原因。术后脑膨出的发生率与预后有相关性(Spearman=0.990,双侧P=0.000).结论颅脑损伤去骨瓣减压术后脑膨出的发生率高,需要严格把握去骨瓣减压术的手术指征,预防或及时处理术后各种导致术后颅高压的并发症。     

开放性颅脑创伤早期癫痫发作危险因素分析

目的探讨开放性颅脑创伤后早期癫痫发作危险因素,并提出初步预防措施。方法对2006年9月-2009年9月诊断与治疗的91例开放性颅脑创伤患者的临床资料进行单因素及多因素Logistic逐步回归分析,筛选颅脑创伤后早期癫痫发作之危险因素。结果单因素分析显示,年龄（X^2=5．131,P=0．023）、颅脑创伤分型（X^2=6．302,P=0．043）、损伤部位（X^2=12．800,P=0．046）,以及伴发脑挫裂伤（X^2=7．187,P=0．007）、外伤性蛛网膜下隙出血（X^2=11．092,P=0．001）、颅内血肿（X^2=6．555,P=0．010）和凹陷性骨折（X^2=8．463,P=0．043）等项因素与开放性颅脑创伤后早期癫痼发作显著相关。进一步Logistie逐步回归分析,仅年龄（OR=7．719,95％CI=1．129。52．777;P=0．037）、脑挫裂伤（OR=28．590,95％CI=2．241．364．734;P=0．010）、外伤性蛛网膜下隙出血（OR=8．244,95％CI=1．259。53．706;P=O．028）和颅内血肿（OR=24．344,95％CI=2．415．345．395;P=0．007）为危险因素,且以脑挫裂伤危险度相对较高;而与颅脑创伤分型、损伤部位及凹陷性骨折无关。结论开放性颅脑创伤后早期癫痼发作应及时治疗,对合并危险因素的患者应早期给予预防性抗癫痫药物治疗。     

Predictors and dynamics of posttraumatic epilepsy

Objectives - The goal of our study was to identify clinical, neurophysiological and neuroradiological variables in severe head trauma (SHT) with predictive value for posttraumatic epilepsy (PTE) and to evaluate the influence of each risk factor for the dynamics of epilepsy. Material and methods - We systematically compared 57 PTE patients with 50 age and sex-matched control patients with SHT and no PTE. Mean follow-up was 8 years.
Results - Of all PTE-patients 68.5% had their first seizure within 2 years after the trauma. Significant risk factors for PTE were focal signs in the first examination ( P <0.01), missile injuries ( P <0.01), frontal lesions ( P <0.01), intracerebral hemorrhage ( P <0.01), diffuse contusion ( P <0.01), prolonged posttraumatic amnesia ( P <0.001), depression fracture ( P <0.01) and cortical-subcortical lesions ( P <0.001). The combination of the last 3 variables conferred a particularly high risk for PTE (logistic regression analysis). Combined seizure pattern, high seizure frequency, AED-non-compliance and alcohol abuse predicted poor seizure control.
Conclusion -The risk for PTE is clearly determined by those variables which correlate with the severity, the extent of tissue loss and the penetrating nature of the brain trauma.     

外伤后急性半球脑肿胀的手术治疗

目的 探讨外伤后急性大脑半球肿胀（ACHS）的治疗效果以及影响疗效的主要因素.方法 对38例外伤后急性半球脑肿胀病人的资料进行回顾性分析.所有患者均接受了去骨瓣减压手术.结果 大骨瓣减压术后,CT影像显示脑中线结构无明显移位、环池结构清晰.术后6个月按GOS评分标准评估：良好14例（占36.8%）、中残9例（占23.7%）、重残5例（占13.2%）、植物生存4例（占10.5%）、死亡6例（占15.8%）.结论 早期去骨瓣减压手术可改善患者预后,而脑肿胀合并急性硬膜下血肿、手术后出血性脑挫伤处血肿量明显增加以及出现创伤后大面积脑梗死的患者预后较差.     

超薄多层螺旋CT与脑灌注成像在颅脑损伤早期诊断中的对比研究

目的探讨超薄多层螺旋CT和脑灌注成像在急性颅脑外伤(TBI)早期诊断中的临床应用价值。方法收集2010年12月~2012年10月我院收治的200例急性颅脑外伤患者检查资料,均于伤后6 h内行超薄多层螺旋CT(MSCT)和CT脑灌注成像(CTP)检查,全部病例于伤后2~3 d动态复查MSCT明确诊断,将数据进行回顾性分析,采用卡方检验评价。结果在MSCT与CTP这两种检测方法中,CTP在脑挫裂伤、硬膜下血肿和脑内血肿的诊断中优于超薄MSCT(P0.05),并且病灶周围低灌注区域大于超薄MSCT。结论 CTP对于急性颅脑外伤早期和微小损伤的诊断优于超薄MSCT,同时可以反映脑组织的灌注情况,具有可靠的临床价值。     

纳络酮早期干预对大鼠弥漫性轴索损伤的影响

目的观察纳络酮早期干预对大鼠实验性弥漫性轴索损伤(DAI)的治疗效果。方法采用改良Marmarou的方法制作大鼠颅脑DAI模型。将Wister雄性大鼠99只随机分为对照(假损伤)组、损伤组和干预组,干预组用纳络酮2mg/kg于伤后45min腹腔一次性注射给药,于伤后2、6、24、72h观察动物行为、脑组织含水量及组织病理学变化。结果损伤组大鼠伤后2、6、24、72h,行为学评分(满分为21.00±0.00分)分别为(9.05±1.52)、(12.12±1.41)、(17.23±1.34)和(19.36±0.92)分;干预组各时间点分别为(9.32±1.23)、(14.48±1.54)、(18.68±1.09)和(20.18±0.75)分;其中干预组伤后6和24h与损伤组比较差异显著(P0.05)。对照组24h脑组织含水量测定结果为(78.19±0.35)%;伤后2、6、24、72h脑组织含水量,损伤组分别为(79.91±0.18)%、(80.70±0.49)%、(81.69±0.40)%和(80.32±0.42)%;干预组分别为(79.22±0.33)%、(79.59±0.46)%、(80.44±0.49)%和(79.50±0.44)%。同损伤组比较,干预组致伤6h后脑含水量均明显减轻(P0.01)。干预组光镜下病理损害明显减轻。结论纳络酮伤后早期干预,有助于减轻大鼠DAI后继发性脑损害。     

The pathobiology of moderate diffuse traumatic brain injury as identified using a new experimental model of injury in rats

Experimental models of traumatic brain injury have been developed to replicate selected aspects of human head injury, such as contusion, concussion, and/or diffuse axonal injury. Although diffuse axonal injury is a major feature of clinical head injury, relatively few experimental models of diffuse traumatic brain injury (TBI) have been developed, particularly in smaller animals such as rodents. Here, we describe the pathophysiological consequences of moderate diffuse TBI in rats generated by a newly developed, highly controlled, and reproducible model. This model of TBI caused brain edema beginning 20 min after injury and peaking at 24 h post-trauma, as shown by wet weight/dry weight ratios and diffusion-weighted magnetic resonance imaging. Increased permeability of the blood-brain barrier was present up to 4 h post-injury as evaluated using Evans blue dye. Phosphorus magnetic resonance spectroscopy showed significant declines in brain-free magnesium concentration and reduced cytosolic phosphorylation potential at 4 h post-injury. Diffuse axonal damage was demonstrated using manganese-enhanced magnetic resonance imaging, and intracerebral injection of a fluorescent vital dye (Fluoro-Ruby) at 24-h and 7-day post-injury. Morphological evidence of apoptosis and caspase-3 activation were also found in the cerebral hemisphere and brainstem at 24 h after trauma. These results show that this model is capable of reproducing major biochemical and neurological changes of diffuse clinical TBI.     

Hemostatic and neuroprotective effects of human recombinant activated factor VII therapy after traumatic brain injury in pigs

Human recombinant activated factor-VII (rFVIIa) has been used successfully in the treatment of spontaneous intracerebral hemorrhage. In addition, there is increasing interest in its use to treat uncontrolled bleeding of other origins, including trauma. The aim of this study was to evaluate the safety and potential effectiveness of rFVIIa to mitigate bleeding using a clinically relevant model of traumatic brain injury (TBI) in the pig. A double injury model was chosen consisting of (1) an expanding cerebral contusion induced by the application of negative pressure to the exposed cortical surface and (2) a rapid rotational acceleration of the head to induce diffuse axonal injury (DAI). Injuries were performed on 10 anesthetized pigs. Five minutes after injury, 720 microg/kg rFVIIa (n=5) or vehicle control (n=5) was administered intravenously. Magnetic resonance imaging (MRI) studies were performed within 30 min and at 3 days post-TBI to determine the temporal expansion of the cerebral contusion. Euthanasia and histopathologic analysis were performed at day 3. This included observations for hippocampal neuronal degeneration, axonal pathology and microclot formation. The expansion of contusion volume over the 3 days post-injury period was reduced significantly in animals treated with rFVIIa compared to vehicle controls. Surprisingly, immunohistochemical analysis demonstrated that the number of dead/dying hippocampal neurons and axonal pathology was reduced substantially by rFVIIa treatment compared to vehicle. In addition, there was no difference in the extent of microthrombi between groups. rFVIIa treatment after TBI in the pig reduced expansion of hemorrhagic cerebral contusion volume without exacerbating the severity of microclot formation. Finally, rFVIIa treatment provided a surprising neuroprotective effect by reducing hippocampal neuron degeneration as well as the extent of DAI.     

外伤后颅内进展性出血性损伤106例分析

目的探讨颅脑损伤后进展性出血性损伤（PHI）的发生及影响预后的相关因素。方法对2007年颅脑损伤后出现PHI的106例患者的临床资料进行回顾性分析,并与同期无PHI患者进行对照研究。结果颅脑损伤后是否出现PHI与患者的年龄是否超过50岁（P〈0．05）、血浆纤维蛋白原水平是否低于2g／L（P〈0．01）及有无蛛网膜下腔出血（SAH）（P〈0．05）密切相关。PHI患者的预后与年龄是否超过50岁（P〈0．01）、血浆纤维蛋白原水平是否低于2g／L（P〈0．01）、有无SAH（P〈0．01）及入院时的GCS评分（P〈0．01）密切相关。结论PHI最常出现于颅脑伤后12h内,好发于着力点的对冲部位,以额颞部为主,与患者的年龄、血浆纤维蛋白原水平及是否伴有SAH等因素密切相关;其预后与患者的年龄是否超过50岁、入院时GCS评分、血浆纤维蛋白原水平是否低于正常及是否伴有SAH密切相关。