外伤性癫痫的法医学鉴定21例分析

为了探讨颅脑损伤后癫痫的法医学鉴定要点,对 21例颅脑损伤后癫痫出现发作者进行了现病史、既往史调查,并结合临床脑电图（ EEG）及 X线片、 CT片、 MRI片等影像学资料。结果发现外伤后癫痫常继发于严重的颅脑损伤,多以晚期发作为主,其发作性质决定于颅脑损伤的部位和程度,头皮 EEG和 24小时动态 EEG证实有异常癫痫样波存在,影像学检查有助于定性分析。结果提示：外伤性癫痫法医学鉴定必须以掌握外伤史及既往史为基础,结合 EEG、 CT、 MRI等检查方可作出正确鉴定。     

外伤性癫痫法医学评定100例分析

目的探讨颅脑外伤后癫痫的法医学评定要点,提出外伤性癫痫的法医学评定依据。方法对100例颅脑损伤后癫痫患者门诊及住院病历,结合临床脑电图（EEG）结果、CT片、MRI片等影像学资料,进行了回顾性分析。结果依据GBl8667-2002《道路交通事故受伤人员伤残评定》标准有关颅脑损伤后癫痫发作类型、发作频率的相关条款规定,Ⅲ级伤残8人,Ⅴ级伤残10人,Ⅶ级伤残22人,Ⅸ级伤残40人,Ⅹ级伤残20人。误工期限、营养期限和护理期限评定结论时间长短差异较大,具有个体化特征。结论外伤后癫痫常继发于严重的颅脑损伤,其发作特点决定于颅脑外伤的部位和程度,外伤性癫痫法医学鉴定必须以外伤史及既往史为基础,结合电生理及影像学检查,综合癫痫发作类型、频率及药物控制情况作出正确的伤残等级及误工期限、护理期限、营养期限的鉴定结论。     

颅脑外伤后癫痫的法医学鉴定

外伤后癫痫系指颅脑外伤后 ,由于脑急性或慢性病理改变而在脑的局部产生一个产痫灶 ,从而引起癫痫的发作。本文通过外伤后癫痫案例的统计分析 ,就其发生率、发作类型及法医学鉴定等作进一步的探讨     

外伤性癫痫及其法医学评定进展

外伤性癫痫(post traumatic epilepsy,PTE)是指颅脑损伤后的癫痫性发作,影像学检查可见器质性病变,脑电图检查可见异常脑电波与颅脑损伤部位一致。外伤后癫痫发生率低,案例报道较少,患者易夸大病情,给法医学鉴定增加难度。本文就外伤性癫痫流行病学、发病机制、临床治疗、法医学鉴定等方面的现状进行综述。     

78例交通事故致颅脑外伤后癫痫的法医学鉴定分析

外伤后癫痫是颅脑损伤,尤其是重型颅脑损伤后严重的并发症.外伤后癫痫可由颅内出血、凹陷性骨折刺激、脑损伤愈合和继发脑损伤等导致,在交通事故伤残等级鉴定中,是一个较复杂的问题.本文收集本鉴定所2009-2010年8150例交通事故中78例颅脑损伤后涉及癫痫的鉴定案例,并对颅脑损伤的严重程度、发生部位与癫痫的相关性及鉴定的注意要点进行初步分析.     

外伤后大脑癫痫灶中SLIT-2的表达变化

目的通过测定人体大脑外伤后癫痫灶中轴突再生调控因子SLIT-2的表达情况,探讨其在外伤后癫痫鉴定中的应用意义。方法 75例人大脑皮质样本分为3组:①实验组:为脑外伤后癫痫患者(30例),②对照组1:为非外伤性癫痫患者(30例),③对照组2:为车祸致颅脑损伤死亡者(15例)。实验组和对照组1样本来源于癫痫手术所切除的脑皮质(患者或其近亲属知情,自愿提供);对照组2样本来源于尸体解剖的大脑皮质。通过HE染色、免疫组化染色、westernblot和图像分析技术,观察、检测上述样本SLIT-2的表达情况,所得数据经统计学处理分析。结果 SLIT-2在实验组与对照组1癫痫灶皮质的神经细胞膜上呈阳性表达,在对照组2中仅有微量表达。实验组SLIT-2的表达高于对照组1,两组间的差异具有显著性意义(P0.05);显著高于对照组2,两组间的差异具有显著性意义(P0.05)。结论 SLIT-2有望作为区别外伤后癫痫与非外伤性癫痫的病理指标之一,通过进一步研究,逐步运用到法医学的鉴定实践之中,为外伤后癫痫的法医病理学鉴定提供客观依据。     

外伤性癫痫灶中泛素与泛素激活酶的定量分析

目的 定量测定人体外伤性癫痫灶中泛素(ubiquitin,Ub)和泛素激活酶(ubiquitin-activating enzyme,UbE1)的表达,研究泛素蛋白酶体系在外伤性癫痫(post-traumatic epilepsy,PTE)发病机制中所起的作用,探索其在PTE鉴定中的应用价值. 方法 分别收集颅脑外伤致癫痫患者脑癫痫灶组织(外伤性癫痫组)、非颅脑外伤性癫痫灶组织(非外伤性癫痫组)和交通事故死亡者正常脑组织(非癫痫组)各15例,应用RT-PCR、Western印迹技术检测3组中Ub和UbE1的含量,并对所得数据进行统计学分析. 结果 RTPCR、Western印迹技术测定显示Ub和UbE1的mRNA和蛋白质在3组中含量为外伤性癫痫组>非外伤性癫痫组>非癫痫组,两两比较,组间差异具有统计学意义(P<0.05).结论 Ub和UbE1在癫痫灶组织中表达增加,且在外伤性癫痫灶组织中增加最为明显.推断泛素蛋白酶体系的活化是PTE神经元病理改变的重要机制之一.     

司法鉴定中见到的癫痫性意识障碍

癫痫与犯罪的关系十分密切,但並非指癫痫本身而言。Roth(1968)指出:“癫痫病人的暴力行为並非由于癫痫发作本身所致,而多是由于癫痫性精神障碍所造成者。”这就是癫痫犯罪並不是癫痫本身发作所致,而是癫痫发作伴发的精神障碍而造成的违法行为。我们在鉴定实践中,遇到数例较少见的癫痫性精神障碍的违法行为与值得注意的问题,在此给于讨论。     

拳击后继发癫痫一例

<正> 拳击头部可造成颅脑损伤。部分颅脑损伤的案例可继发外伤性癫痫。成人闭合性颅脑损伤后癫痫发病率约为5%。其发病机理为颅脑损伤后形成的疤痕组织刺激神经细胞使之产生突然和过度重复地放电,大脑功能呈现短暂的阵发性失调,临床表现出间歇性、短暂性和刻板性发作。脑电图描记有特异性变化,结合临     

ECT在外伤性癫痫法医学鉴定中的应用探讨

外伤性癫痫系颅脑损伤后发生的大脑神经元的异位过度放电,表现为暂时性的中枢神经系统功能失常。在法医学鉴定中,鉴别外伤性癫痫与原发性癫痫常较为困难。笔者发现,在外伤性癫痫的法医学鉴定中利用放射性核素发射型计算机断层(emissoncom鄄putertomography,ECT)作为辅助手段,可     

外伤性脑梗塞法医学鉴定55例分析

通过对近5年来55例外伤性脑梗塞法医学鉴定案例资料的收集整理,并就其临床表现、影像学表现特点、发病机制、以及法医学损伤程度鉴定等问题进行分析,探讨颅脑外伤与梗塞的关系。     

Cerebral tissue pulmonary embolization due to head trauma: a case report with immunohistochemical confirmation

Pulmonary embolization of cerebral tissue as the result of severe head trauma is an uncommon, if not rare, phenomenon, and few cases have been reported in the literature. The authors discuss the case of a 51-year-old male who died six days after suffering extensive head trauma in a motor vehicle collision. At autopsy, white-gray emboli were found in several subsegmental pulmonary arteries. The results of histologic examination with the hematoxylineosin stain gave the impression that the emboli were necrotic cerebral tissue; however, routine special stains for neural tissue produced inconclusive results. Immunohistochemical staining of the emboli with monoclonal mouse anti-human neurofilament protein (Dako Corp., Carpinteria, California) confirmed the cerebral nature of the emboli. To the authors' knowledge, this is the first reported case of pulmonary embolization of cerebral tissue confirmed by immunohistochemistry.     

Massive pulmonary embolization by cerebral tissue after head trauma in an adult male

We report a case of an adult man who was run over by a car, suffering severe head trauma. After 3 hours in the hospital, he experienced sudden and severe hemodynamic deterioration, dying immediately. The autopsy showed massive cerebral tissue pulmonary embolization (CTPE), confirmed by immunohistochemistry. Multiple fractures of the skull, tear of the transverse sinus, and brain laceration of the occipital lobe were present. CTPE is very infrequent. In children and adults, it occurs as a complication of severe closed or penetrating head trauma. Although laceration of a large cerebral venous sinus is not always essential, in some cases (like in the present one) this laceration is the mechanism of entry of the cerebral tissue to the blood circulation. The clinical repercussion of CTPE is variable. In some cases, it could be an incidental finding of autopsy. In other cases, coagulation abnormalities and disseminated intravascular coagulation have been reported. Finally, such as in the present case, the immediate cause of death is the sudden hemodynamic failure due to the massive CTPE.     

Further investigations into the speed of cerebral swelling following blunt cranial trauma

An anesthetized sheep model of traumatic brain injury (TBI) has been developed to assess early changes in intracranial pressure (ICP) following closed head injury. Immediately after TBI, a transient (<10 min) hypertensive response occurred, followed by significant and prolonged systemic hypotension. ICP demonstrated a biphasic response, being seven times baseline values of 8 ± 2 mm Hg 10 min after injury, decreasing to 25 ± 2 mm Hg by 30 min, and then increasing to values exceeding 30 mm Hg by 4 h postinjury. ICP was always significantly higher than baseline values, which combined with hypotension, reduced cerebral perfusion pressure to less than 60% of normal. This early and sustained increase in ICP after craniocerebral trauma acutely alters cerebral perfusion pressure and brain oxygenation and provides a potential pathophysiological explanation for immediate clinical manifestations in humans following significant TBI.     

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。     

A clinico-morphological analysis of the traumatic substrates to cerebral injuries in different inertial loads on the brain]

The relationships between the inert tension of the head and the morphologic substrates of brain injuries were under study. A comparative clinical and morphologic analysis of lethal contusion and axonal injuries underlie this investigation. Differences in the neurologic semeiotics and CT data in such injuries are presented. The authors discuss the mechanisms of the physical processes in the skull, resulting in focal and diffuse injuries of the brain. Quantitative assessment of the traumatic cerebral substrates is given and relations of these parameters to the conditions of the head trauma (the direction of the external injurious factor action) and the clinical picture are shown. The results of this study may be useful in establishing some circumstances of craniocerebral injuries.     

颅脑损伤部位与智力评估分析

目的探讨颅脑损伤部位与智力损伤的关系。方法315例颅脑外伤者根据疾病诊断分成8组：蛛网膜下腔出血组、脑震荡组、硬膜外血肿组、硬膜下血肿组、颞叶损伤组、额叶损伤组、顶叶损伤组、枕叶损伤组、广泛性损伤组和其他组，按中国修订韦氏成人智力量表进行测试，分析性别、年龄、文化程度、损伤部位与智商水平的关系。结果颅脑外伤后的平均总智商（FIQ）为64．45±16．09。性别对颅脑外伤后的智商水平影响不明显（P=0．578）；老年颅脑外伤后的智商水平较青年和中年高（P〈0．01）；文盲者颅脑外伤后的智商水平较文化程度高者低（P〈0．01）。各组智商水平高低为：其他组〉蛛网膜下腔出血组、脑震荡组〉硬膜外血肿组、硬膜下血肿组〉颞叶损伤组、额叶损伤组、顶叶损伤组、枕叶损伤纽〉广泛性损伤组。同时左额叶损伤组的智商水平较右额叶损伤组低；右颞叶损伤组的操作智商（PIQ）明显比左颞叶损伤组低，而言语智商（VIQ）则反之（P〈0．01）。结论颅脑外伤后的智力损伤与损伤部位密切相关。     

Death due to positional asphyxia under severe alcoholisation: pathophysiologic and forensic considerations

In contrary to "physical restraint", describing a fixed body position due to external devices, "positional restraint" is defined as an abnormal body position, resulting from accidental fixation under unfortunate circumstances. We report on a remarkable case of positional asphyxia of an alcoholised young man after a fall down a staircase. On external examination, the body showed petechiae of the conjunctivae and oral mucosa, abrasions on the left zygomatic region and scratch marks, respectively. Neither broken fingernails, etc. nor signs of external violence against the neck were found. Autopsy revealed haemorrhages in the praevertebral cervical musculature and Simon's sign. Haemorrhagic pulmonary edema and cerebral edema were observed; blood alcohol concentration: 2.60 g/l, urine alcohol concentration: 3.26 g/l. As cause of death, positional asphyxia after blunt head trauma has to be considered as well as lethal ethanol intoxication. To us, alcoholisation attributed to the fall and together with unconsciousness following blunt head trauma circumvented self-rescue efforts, and therefore, aggravated the potentially lethal impact of positional restraint.     

3D reconstruction of emergency cranial computed tomography scans as a tool in clinical forensic radiology after survived blunt head trauma--report of two cases

When requested to evaluate surviving victims of blunt head trauma the forensic expert has to draw mainly on medical documentation from the time of hospital admission. In many cases these consist of written clinical records, radiographs and in some cases photographic documentation of the injuries. We report two cases of survived severe blunt head trauma where CT images, which had primarily been obtained for clinical diagnostic purposes, were used for forensic assessment. 3D reconstructions of the clinical CT-images yielded valuable information regarding the sequence, number and direction of the impacts to the head, their gross morphology and the inflicting weapon. We conclude that computed tomography and related imaging methods, along with their 3D reconstruction capabilities, provide a useful tool to approach questions in clinical forensic casework.     

浅析外伤性脑梗塞

通过十四例外伤后脑梗塞案例分析,对外伤与脑梗塞的关系进行阐述,认为外伤性脑梗塞的主要原因是脑动脉血栓形成和栓塞。动脉内膜损伤致血栓形成多在四小时后;颅内出血致血管痉挛造成脑血栓多在1至3周之间;外伤致动脉粥样硬化斑块脱落造成栓塞即刻发生,结合年龄大小、有无心血管疾患以及脑梗塞的部位,便可弄清损伤与脑梗塞的关系。