132例滑动性脑挫伤类型与受力机制、受力部位的探讨

目的研究脑受力后在颅腔内滑动挫伤的类型与受力机制、受力部位的关系。方法按颅骨解剖部位划定受力部位，根据案情确定受力方式后，对132例滑动性脑挫伤的脑标本，经福尔马林固定后作冠状、矢状或连续切面，肉眼、镜下观察。结果滑动性脑挫伤按发生部位不同分3型：脑顶型，65例（49．24％）；脑底型，38例（28．78％）；混合型，29例（21．96％）。脑顶型多见于额顶部的加速性受力，脑底型多见于枕部的减速性受力，混合型多见于顶枕部的减速性受力。结论3种类型与头部的受力机制、受力部位有相应关系。     

脑室系统周围脑组织损伤致死1例

某男，39岁。2005年11月，被人用脚踹击头部后在30min内死亡。尸表检验见：右顶部有片状头皮下出血；左枕部有头皮下血肿。颅脑解剖检验见：颅骨无骨折。蛛网膜下腔弥漫出血，遍布额叶、顶叶、颢叶、小脑脑表面及外侧裂、脚间池、环池，以脑底面为著。脑沟脑回轻度肿胀，双侧小脑扁桃体疝及轻度海马钩回疝形成。完整剥离Willis环，未见动脉粥样硬化斑块形成，无动脉瘤和血管畸形。冠状切面可见蛛网膜下腔出血以脑底部为著，脑室系统内出血和凝血，中脑被盖部、双侧侧脑室枕角及三脑室周围脑实质质软，呈粉红色。其余脑实质未见著变。     

39例小脑扁桃体疝性脑挫伤分析

报告39例小脑扁桃体疝性脑挫伤，其中钝器打击33例，枪弹创6例，并对其病理学改变及发生机理进行观察与探讨。认为小脑扁桃体疝性脑挫伤是由于小脑扁桃体在头部遭受暴力的瞬间，撞击枕骨大孔边缘所发生的一类远区脑挫伤。见于加速性损伤，多数与冲击性脑挫伤相伴随，常累及延髓，且以线状颅骨骨折多见，伤后死亡较为迅速。熟悉该类损伤，对分析损伤性质，确定和解释死因以及估计伤后存活时间有一定的实际意义。     

1例单纯性脑室周围系统损伤及机制分析

脑室周围系统位于脑中线部位,其损伤属于中间型脑损伤。目前多认为中间型脑损伤因减速运动伴有头部旋转时,脑组织因脑膜等结构限制而受剪切力作用所致[1]。另有观点认为中间型脑挫裂伤见于脑中线附近,是由于头部受伤后脑组织做水平旋转运动时,在大脑纵裂附近发生脑挫裂伤[2]。脑室周围系统损伤被认为主要是因暴力作用在额部或枕部时,脑组织沿前后方向猛烈运动,脑室壁发生剪力变形,进而撕破室管膜[3]。笔者遇到1例单纯性脑室周围系统损伤未发现剪切力作用的案例,报道如下。1案例资料某男,39岁,被人拽倒、脚踹头部后立即死亡。尸检见:右顶部片状头皮下出血,左枕部头皮下血肿;弥漫性蛛网膜下腔出血,以脑底面为著。脑沟脑回轻度肿胀,双侧小脑扁桃体疝及轻度海马钩回疝形成。脑动脉未见动脉粥样硬化、动脉瘤和血管畸形。冠状切面可见脑室系统内出血及血凝块,中脑被盖部、双侧侧脑室枕角及第三脑室周围脑实质质软,呈粉红色(照片1,2,3)。病理组织学检验见:中脑被盖部、双侧桥臂表层点灶状出血和组织破损,呈挫伤病变,侧脑室枕角及第三脑室周围等处的脑实质内亦可见组织疏松、新鲜出血和水肿,近脑表面的脑组织内可见多量吞噬细胞,脉络丛内未见畸形血管。脑组织水肿。检...     

外伤性蛛网膜囊肿1例

头部外伤引起外伤性蛛网膜囊肿在法医临床学鉴定中较为少见，现报道１例。１案例某男，４６岁，农民。某年１月２２日上午被他人用拳脚击伤头面部，当即昏迷，速送医院。检查见 :生命体征平稳；左颞部有一６ ０ｃｍ×７ ０ｃｍ肿胀区，右耳前有一３ ０ｃｍ×１ ０ｃｍ肿胀区，有触压痛；右眼睑肿胀、淤血，球结膜下可见片状出血，角膜有擦伤，黄斑区反射消失。当日头部ＣＴ检查：颅内诸脑室、脑池及脑组织密度未见异常。临床诊断：（１）头部外伤；（２）视网膜震荡（右）。住院治疗一个月后，出现头痛、恶心，口服索密痛可缓解；查体见两眼…     

脑肿瘤死亡尸检3例

在法医学尸检中,颅内肿瘤的检出率在0.16％～0.54％之间,有些表现为突然、意外的死亡,有些则可能在死亡发生之前有临床症状。现将临案中遇到的3例尸检报道如下。1 案 例 案例1:死者,男,42岁,农民。某日因与人发生纠纷并相互撕打,被击中头部,即感头疼,3天后头痛加剧,并于第4天出现昏迷、呕吐,送医院抢救无效于伤后第5天死亡。尸检见头顶部正中偏左有一5cm×4cm的类圆形皮下出血,右枕叶颅后窝硬脑膜下可见约15ml的凝血块。全脑重1450g,小脑右侧扁桃体疝形成,左侧脑室内可见凝血块约30ml,左     

外伤性脑梗死的形态学观察

目的 观察外伤性脑梗死的形态学特点,并探讨其与脑挫伤的鉴别。方法 从81例重型颅脑损伤中选出15例符合继发性出血坏死标准的脑标本,另选15例脑挫伤标本作对照,两者均经福尔马林固定后分别作冠状、矢状及水平切面,用肉眼与光镜观察。结果 外伤性脑梗死常见于5个部位,即基底节(3例)、扣带回(2例)、对称性枕部楔叶回(2例)、枕颞外侧回(6例,5例合并有中脑桥脑出血)和枕回(2例);梗死均不在直接受力点或其对冲点,范围明确局限,呈楔形或类楔形,且与脑疲密切相关。镜下见梗死区高度淤血、出血及坏死;水肿,并有白细胞浸润和胶质细胞反应。大脑各叶的梗死,严重者累及全皮层与蛛网膜下腔,未见软脑膜破裂;神经细胞缺氧或缺血性病变明显。脑挫伤的案例,见受力点或对冲部位的皮质及皮质下髓质处出血,挫伤处脑回顶部的软脑膜多破裂,挫伤的脑组织可有挫烂。结论 外伤性脑梗死在法医学上习惯称为继发性出血坏死;它是由于脑疝和水肿压迫颅内血管而形成。外伤性脑梗死和脑挫伤,根据其与脑疝的关系、病变部位、软脑膜是否完整,以及其它组织学改变,二者不难鉴别。     

脑干轴索肿胀的半定量研究

目的 探讨轴索肿胀在鉴定脑干损伤中的意义。方法 取明确死于原发性脑干损伤(36例)和脑外疾病(28例)者共64例，分为损伤组(36例)和对照组(其中死于心血管疾病12例、非心血管疾病16例)，并将其死后24h和48h前、后做尸体解剖分为2组，通过对中脑、脑桥和延脑切片、镀银染色，在100倍光镜下采用显微测微器测量每片9条最粗的轴索横径，对所得数据作方差分析、t检验统计学处理。结果 损伤组与对照组(不包括心血管疾病死亡者)相比，中脑、延脑部的轴索肿胀程度有明显差异(P＜0.05)；死后48h内解剖的损伤组与对照组相比无差异(P＞0.05)，但超过48h解剖两组有明显差异(P＜0.05)。结论 中脑、延脑部轴索肿胀与外伤有明显的相关性。轴索肿胀对判断脑干损伤有意义。需排除心血管疾病致死。     

中间冲击性脑挫伤22例报告

<正> 钝性暴力作用于头部时,暴力冲击的速度、强度、受力面积的大小、受力位置及有关部位颅内结构的特性,脑受力变形以及在颅腔内的异常运动,都是决定脑组织损伤类型与程度的因素。在硬脑膜不破裂情况下发生的脑组织出血坏死称为脑挫伤。     

85例成人闭合性脑挫伤组织病理学研究

目的研究大脑及脑干脑挫伤后组织病理学变化及与损伤时间的关系,并比较大脑与脑干损伤之间有无差异。方法对85例闭合性颅脑损伤死亡的脑挫伤组织进行病理学GFAP、HSP70、NF200免疫组织化学染色。结果脑损伤早期出现的胞浆嗜酸性肿胀胶质细胞(ECSG)是脑损伤后一种早期应激性反应,挫伤部位淀粉样小体(CA)的增多及噬神经细胞现象也可在脑挫伤后早期形成,而脑干挫伤ECSG发生率高于大脑。中性粒细胞浸润、泡沫细胞及胶质瘢痕形成有一定时序性。结论ECSG在判断生前脑挫伤及推断脑挫伤时间中有重要的参考价值。在ECSG较多的部位,泡沫细胞及CA也较多,三者之间可能存在联系,并提出CA是脑挫伤后反应性产物之一,可用于推断脑损伤时间。     

Quantitative immunohistochemical analysis of human brain basic fibroblast growth factor, glial fibrillary acidic protein and single-stranded DNA expressions following traumatic brain injury

Previous studies demonstrated the healing process after traumatic brain injury (TBI), usually at the site or in the area adjacent to the injury, in connection with wound timing. However, the whole brain condition after TBI has not been elucidated clearly. In the present study, we investigated immunohistochemistry of the basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) in the parietal lobe and hippocampus distant from the primary injury site in forensic autopsy cases of TBI (n=174). Characteristic findings were detected with regard to brain compression signs and survival time (ST). Peracute deaths (n=22) had a lower GFAP positivity in the parietal white matter. Fatalities without a brain compression sign (parahippocampal herniation/Duret hemorrhage; n=53) had a lower brain weight without glial loss; however, GFAP positivity in the parietal white matter was decreased during ST of <12h, and glial bFGF positivity was increased at each site in deaths after 12h to 3 days, followed by a delayed neuronal loss after 3 days. Fatalities with a brain compression sign (n=78) showed a higher brain weight, and gradual glial and neuronal losses with an early increase of glial bFGF positivity in the parietal cerebral cortex (ST <0.5h). This was followed by an increase of glial bFGF positivity in other sites (ST, 6-24h), and final decreases of glial bFGF and GFAP positivities with increased neuronal ssDNA positivity in the parietal lobe and hippocampus (ST >3 days), which were detected in earlier deaths despite decompressive craniectomy (ST, 12-60h; n=21). These observations suggest that the combined use of bFGF, GFAP and ssDNA immunohistochemistry can be used to evaluate the severity of damage and response of brain after TBI.     

脑挫裂伤后脑水肿CT表现及其与受伤时间的相关研究

分析120例脑挫裂伤后脑水肿的CT表现及其两者形成时间的关系,提出脑水肿的分级和分型,以Ⅰ-Ⅱ组脑水肿和“O”型脑水肿多见,Ⅰ级脑水肿形成时间平均17小时,Ⅱ级形成时间平均30小时,Ⅲ-Ⅳ级形成时间平均72～73／小时,受伤时间与R值呈正相关（r=0．431）,P＜0．001．回归方程Y=6658＋79．152x,受伤时间与D值也呈正相关（r=0．429）P＜0．001,回归方程Y=39．362－32．335x。并首次指出这时间变化规律可作为脑挫裂伤受伤时间的推断依据。     

171例脑干颅神经损伤

目的　观察头部受力致脑干颅神经损伤的形态学改变 ,探讨脑干颅神经损伤形成机制及其与头受力部位和方式的关系。方法　 171例脑干标本 ,于双侧第 3～ 12对颅神经的根部水平横切取组织块 ,常规固定、脱水、包埋、切片、HE染色 ,光镜检查。结果　所有标本均见颅神经损伤。有动眼神经损伤 ( 12 0例 ,70 2 % ) ,面听神经损伤( 92例 ,5 3 8% ) ,三叉神经损伤 ( 85例 ,49 7% ) ,外展神经损伤 ( 4 5例 ,2 6 3 % ) ,舌下神经损伤 ( 3 1例 ,18 1% ) ,迷走神经损伤 ( 2 7例 15 8% ) ,舌咽神经损伤 ( 2 4例 ,14 0 % )及滑车神经和副神经损伤 (各 10例 ,5 8% )。损伤可为单侧或双侧 ,累及单条或多条。病理形态学改变有出血 ( 4 2例 ,2 4 6% ) ,水肿 ( 2 6例 ,15 2 % ) ,神经根部组织结构变形 ( 71例 ,41 5 % ) ,根部撕裂 ( 3 2例 ,18 7% )等。结论　脑干颅神经损伤是脑干损伤的并存病变 ;位脑干高位的颅神经损伤比位低位的多 ,粗的神经损伤比细的多而严重 ;动眼、面、听神经损伤的发生率较高。     

人脑挫伤后波形蛋白表达的免疫组化染色观察

目的观察人脑挫伤后波形蛋白（vimentin,Vim）的动态变化,探讨星形胶质细胞Vim表达变化与脑损伤时间的关系。方法42例闭合性脑损伤死亡者,根据伤后死亡时间分为6组（〈2h,〈24h,〈3d,〈7d,〈14d,≤30d）;取大脑挫伤灶进行HE和Vim免疫组织化学染色,对Vim染色阳性细胞面积进行图像分析。结果HE染色显示,脑挫伤后2h挫伤灶内脑组织挫碎、出血,5．5h挫伤灶周出现反应性星形胶质细胞,3d脑水肿明显,7d反应性星形胶质细胞明显增多,14d胶质结节形成,30d出现大量泡沫细胞,胶质瘢痕增多。Vim染色结果显示,脑挫伤后5．5hVim开始表达,少量Vim阳性细胞出现在挫伤灶周围,7d阳性反应性最强,14d逐渐下降,30d胶质瘢痕增多,Vim阳性表达又增强。Vim阳性细胞主要为反应性星形胶质细胞。结论Vim在反应性星形胶质细胞内表达呈现一定波动性,其表达部位在脑挫伤周围,Vim免疫组化染色结合图像分析技术可作为推断脑挫伤时间及部位的参考指标。     

道路交通事故颅脑损伤的法医学鉴定

目的　研究道路交通事故中颅脑损伤的类型、特点、主要并发症及其受伤人员的伤残评定。方法　 862例道路交通事故颅脑损伤的案例资料 ,按伤者受伤的不同部位、有无并发症、并发症的类型及伤残程度进行统计分析。结果　复合性颅脑损伤 2 76例 ,脑挫伤 192例 ,颅骨骨折 79例 ,颅内出血 91例 ,头皮外伤 2 2 4例 ;主要并发症为脑积水 ( 19例 ,2 2 0 % )、癫痫 ( 16例 ,1 86% )、偏瘫 ( 14例 ,1 62 % )、植物人状态 ( 12例 ,1 3 9% )。结论　道路交通事故中颅脑损伤 ,以头部复合性损伤最多见 ,严重的脑挫伤为最常见的损伤类型 ,并发症的诊断应掌握诊断标准 ,并注意与相关疾病鉴别。     

颅脑损伤后精神障碍的相关因素分析

目的 探讨颅脑损伤后精神障碍的相关因素。方法 对42例颅脑损伤伤者的法医学鉴定资料进行回顾性分析,颅脑损伤诊断按照病史资料和颅脑CT/MRI确定;精神障碍按照CCMD-Ⅱ-R、CCMD-3及龚氏修订的韦氏智力量表(WAIS-RC)确定;伤残程度评定根据《道路交通事故受伤人员伤残评定》标准。将所获得的结果,进行统计学分析。结果 精神障碍以脑震荡后综合征居首位(26.2％),其次是遗忘综合征(21.4％)、神经症(16.6％)等。精神障碍以脑伤的低伤残等级多见(Ⅹ级52.4％,Ⅷ级14.3％,Ⅶ级19.0％),但整体差异无显著性意义(P>0.05)。精神病性精神障碍多分布于脑器质性损伤(脑挫裂伤54.8％,脑干损伤16.7％);非精神病性精神障碍多分布于脑功能性损伤,其中脑震荡占21.4％,其差异有高度显著性(P<0.01);智力缺损多见于脑器质性损伤(P<0.05),80.6％分布于脑伤的Ⅹ级、Ⅷ级和Ⅶ级(P<0.01)。结论 颅脑损伤后精神障碍及智力缺损的发生与颅脑损伤的类型、性质有关,与颅脑损伤的严重程度并不平行。     

The expression of excitatory amino acid transporter 2 in traumatic brain injury

It is well recognized that glutamate is the major excitatory neurotransmitter, which is removed from the synaptic cleft by excitatory amino acid transporter 2 (EAAT2) located on the perisynaptic astrocytes and that neuronal death has been associated with an increased extracellular glutamate concentration. In this study, we have immunohistochemically demonstrated the expression of EAAT2 protein in the human brain after traumatic brain injury (TBI). The EAAT2 expression patterns can be divided into three types: continuous and highly extensive staining (E); continuous but sporadic staining (M); and sporadic pattern staining (S). In six of the nine short survival cases studied (1 h to 1 day), continuous and highly extensive staining for EAAT2 (E type) was observed in the ipsilateral cerebral cortex. On the other hand, we were able to demonstrate weak staining (S and M types) in 5 of the 7 long survival cases (> or =1 day) and in 12 of the 14 very short survival cases (<1 h) studied. Similar findings were obtained in the contralateral cerebral cortex and also in the ipsilateral hippocampus. In addition, positive staining for glial fibrillary acidic protein was detected around the cerebral contusion, but the EAAT2-positive expression was not observed in the same region for all of the six short and long survival cases (> or =1 h) after TBI. These findings clearly showed the differences in EAAT2 expression in the cerebral cortex according to the survival time and severity of cerebral contusion after TBI. Therefore, we emphasized that EAAT2 might play an important role in contributing to extracellular glutamate concentrations and secondary brain injury after TBI.     

Axonal injury – a diagnostic tool in forensic neuropathology?: A review

We used β-amyloid precursor protein (β-APP) to investigate our own forensic neuropathological case material (n=252) in light of the current literature on the phenomenon “axonal injury” (AI) to determine the incidence, specificity and biomechanical significance of AI and its significance for determining vitality and survival time. The case material consisted of cases of fatal nonmissile closed-head injury (n=119), gunshot injury (n=30), fatal cerebral ischemia/hypoxia (n=51), brain death caused by mechanical trauma (n=14) or nonmechanical injury (n=18), and acute hemorrhagic shock (n=20). AI was observed in 65% to 100% of cases of closed-head injury, fatal cerebral ischemia/hypoxia, and brain death with a survival time of more than 3 h; AI could not be detected in the cases of acute hemorrhagic shock. A statistically significant difference between traumatically and nontraumatically induced (nondisruptive) AI was not found. There was no statistical evidence of a correlation between AI and the different types of external force, since AI could be demonstrated after both acceleration/deceleration injuries and traumatic impact. Therefore, biomechanical inferences for reconstruction purposes are not possible. On the other hand, β-APP was found to be a definite marker of vitality. In our material, cases with a posttraumatic interval of under 180 min did not express β-APP. Moreover, the literature shows that the posttraumatic interval can be determined by other methods for demonstration of AI such as by ubiquitin immunostaining (360 min), silver staining (15–18 h), hematoxylin and eosin staining (about 24 h), or by demonstration of a microglial reaction (about 4 to 10 days) or of a few remaining isolated bulbs, without accompanying fibers, which can be detected after a survival time of up to 17 months.