马桑内酯诱导惊厥发作海马结构内神经元损伤的观察

目的：观察国产中药制剂马桑内酯诱导惊厥发作后，海马结构内神经元损害的范围和特征。方法：采用SD大鼠，马桑内酯单次腹腔内注射诱发惊厥，在发作后不同时间点取脑，行H＆E染色和GFAP免疫组化染色观察海马结构内神经元和神经胶质细胞的改变。结果：海马结构内有显著的神经元损伤。其损伤次序表现为：齿状回、门区和CA3区、CA1区，损伤区周围有反应性星形胶质细胞增生。结论：马桑内酯致惊厥发作后海马神经元的损害与兴奋性细胞毒制剂海仁酸致惊厥具有相似的病理学改变特征，提示国产中药制剂马桑内酯致惊厥与兴奋性细胞毒有关。     

Threshold of seizure activity of the brain and higher nervous activity in the postresuscitation period for intracerebral allotransplantation of fetal neocortex tissue

The threshold of seizure activity of the brain, long-term memory, and learning ability are studied in Wistar rats for bilateral transplantation of fetal nervous tissue in area CA1 of the hippocampus. The grafts are performed on the 2nd, 7th, 14th and 30th days after clinical death caused by asphyxia. A neurotransplantation performed on the 2nd day of the postresuscitation period is found to prevent seizure activity, whereas that performed on the 7th–14th days results in a sharp decline or cessation of spontaneous and induced epileptiform convulsive seizures, prolonged preservation of the long-term memory trace, an improvement of learning ability, and a lessening of defensive and phobic behavior in a large proportion of the animals. Translated fromByulleten's Eksperimental'noi Biologii i Meditsiny, Vol. 121, N ^o 2, pp. 234–237, February, 1996 Presented by V. A. Negovskii, Member of the Russian Academy of Medical Sciences     

在戊四氮致痫大鼠早期前脑中OX-42和Fos蛋白的表达变化

研究大鼠在戊四氮导致癫痫发作早期前脑内小胶质细胞的变化及其与神经元的关系,本研究应用免疫组织化学法分别显示前脑内OX-42和Fos蛋白表达的时程变化,并用双重标记显示OX-42和Fos阳性细胞的相互关系。结果发现:在戊四氮导致大鼠癫痫发作早期(从15min到360min),前脑的小胶质细胞OX-42表达阳性,随着存活时间的变化,OX-42的阳性反应经历逐渐升高又降低的过程;Fos蛋白在神经元和小胶质细胞中有表达,也呈现逐渐升高又降低的变化;Fos在小胶质细胞表达高峰的时间早于在神经元的表达;另外OX-42阳性小胶质细胞和Fos阳性神经元在前脑分布基本相同,主要分布在大脑皮层、海马、杏仁核等部位。以上结果表明,前脑的小胶质细胞和神经元一样在戊四氮所致癫痫发作的早期表现明显的反应,但小胶质细胞反应的意义有待进一步研究。     

Maxillofacial Fractures and Dental Trauma in a High School Soccer Goalkeeper: A Case Report

Objective: To present the case of a 17-year-old male soccer goalkeeper who sustained maxillofacial fractures and dental trauma after being struck in the face by an opponent's knee.Background: Because of the nature of the sport and a lack of protective headgear, soccer players are at risk for sustaining maxillofacial trauma. Facial injuries can complicate the routine management of on-field medical emergencies often encountered by certified athletic trainers. The appropriate management of maxillofacial trauma on the playing field may help to reduce both the immediate and long-term morbidity and mortality associated with these injuries.Differential Diagnosis: Lacerated superior labial artery, lacerated upper lip, dental fractures, maxillofacial fractures, orbital blowout fracture, closed head injury, cervical spine injury, cerebrovascular accident.Treatment: The athlete received immediate on-field medical care and was subsequently transported to the hospital, where diagnostic testing was performed and further treatment was provided. Hospital inpatient management included dental and plastic surgery. After discharge from the hospital, the athlete underwent several additional dental procedures, including gingival surgery and nonsurgical endodontic treatments. The fractures were followed closely to assure that adequate healing had occurred. The athlete did not return to soccer.Uniqueness: Certified athletic trainers need to be prepared for on-field medical emergencies. Bleeding associated with maxillofacial trauma can complicate basic medical interventions such as airway maintenance. Inappropriate on-field management may result in unnecessary morbidity and mortality for the injured athlete. Therefore, immediate recognition of the severity of the injury is needed in order to institute appropriate airway-management strategies.Conclusions: It is sometimes necessary to consider nonstandard methods of airway management in order to first address heavy bleeding that may be associated with facial trauma. Achieving hemostasis is essential in order to prevent potentially life-threatening complications related to hemorrhage, such as airway obstruction and hypovolemic shock.     

基于EEG模糊相似性的癫痫发作预测

本研究提出基于EEG序列模糊相似性指数方法预测癫痫发作.首先,结合复自相关法和Cao法对EEG序列进行了相空间重构;然后,计算相关积分时用Gaussian函数代替Heavyside函数,克服了Heavyside函数的刚性边界问题,使得计算相似性指数更加准确和可靠;最后,分析大鼠癫痫EEG信号,检测癫痫发作前期状态.分析结果表明模糊相似性指数方法能够比动态相似性指数方法获得更长的预测时间和更低的错误预测率.     

听源性惊厥易感性大鼠上丘神经元构筑的研究

用石蜡切片Nissl染色方法，光镜下计数、结合计算机图象分析系统观察、测量惊厥鼠与正常鼠土丘神经元的一些指标．结果显示：（1）在吻例段和中段上丘第Ⅱ层和吻侧段上丘第Ⅲ层的神经元胞体平均直径惊厥鼠显著小于正常鼠，说明惊厥鼠上丘上述部位神经元较小；（2）在吻侧段上丘第Ⅵ层，中段上丘第Ⅰ、Ⅱ层和屋倒段上丘第Ⅴ层，神经元剖面椭圆率惊厥鼠显著地小于正常鼠，说明惊厥鼠土丘上述部位神经元胞体较细长；（3）除第Ⅲ层外，土丘各板层神经元剖面面数密度惊厥鼠都大于正常鼠．本研究结果表明，惊厥鼠的土丘有神经元的形态学变化。这种变化与惊厥鼠惊厥易感性的形成之间是否存在着某种关系，有待深入研究．     

Effect of cerebral ischemia on acute convulsions and chronic epileptogenesis

The pharmacological kindling with corazol was used as a model of chronic cerebral epileptization. In contrast to sham-operated rats or rats with unilateral occlusion of the common carotid arteries, bilateral occlusion of these vessels moderated acute seizures provoked by a single administration of the convulsant corazol and abated the enhanced cerebral seizure readiness induced by its repeated administration. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 7, pp. 30–33, July, 1998     

Partial epilepsy in neurologically normal children: clinical syndromes and prognosis

A clinical and electroencephalographic study of 107 neurologically normal children with partial seizures was undertaken to verify the existence and determine the frequency of epileptic syndromes reported in selected populations. Sixty-three children had simple partial seizures, 39 had complex partial seizures, and 5 children were unclassifiable. The syndrome of benign partial epilepsy of children with rolandic spikes (BPEC, 38 cases) was clearly identified and its uniformly benign final prognosis was confirmed even if some of these children had at times severe or poorly controlled seizures. Among the children with simple partial seizures outside the BPEC (25 cases) and complex partial seizures (39 cases), no homogeneous clinical or electroclinical subgroup could be found. Two children with benign partial epilepsy and myoclonic-astatic seizures ("atypical benign partial epilepsy of childhood") and one child with "benign epilepsy with occipital spike-waves" were identified. 74% of children with epilepsy with complex partial seizures (ECP) had a 1-year seizure-free interval, and many children with epilepsy with simple partial seizures outside the BPEC group (ESP) had no more than two seizures. A benign course is thus not limited to the BPEC but is difficult to predict. Prospective studies are necessary to confirm the existence of well-defined benign syndromes among the idiopathic partial epilepsies of childhood, which appear quite rare outside the BPEC.     

Investigation of the involvement of opioid receptors in the action of anticonvulsants

This study investigates the possible involvement of opioid receptors in the action of a variety of anticonvulsant agents. The opioid antagonist naloxone (0.3, 1 mg/kg IP) and the selective -opioid antagonist cyprodime (3 mg/kg IP) significantly inhibited the increase in electroshock seizure threshold induced by phenytoin (3 mg/kg IP) in mice. The anticonvulsant effects of ethanol (1 g/kg IP) were also significantly antagonised by naloxone (1 mg/kg IP) but not by a 0.3 mg/kg IP dose or by cyprodime (3 mg/kg IP). The results with naloxone were confirmed using higher doses of phenytoin (10 mg/kg IP) and ethanol (1.5 g/kg IP). In contrast to the above findings, naloxone (0.3, 1 mg/kg IP) had no effect on the increase in seizure threshold induced by sodium valproate (200 mg/kg IP) or dizocilpine (MK801, 0.5 mg/kg IP) and paradoxically potentiated the increase in seizure threshold produced by phenobarbitone (15 mg/kg IP); carbamazepine (10 mg/kg IP) and the benzodiazepine agonist loprazolam (1 mg/kg IP), clearly differentiating these compounds from phenytoin and ethanol. These findings suggest that the anticonvulsant effects of phenytoin and ethanol (as assessed by their ability to prevent tonic hindlimb extension in the mouse electroshock model) may be mediated, at least in part, by the release of endogenous opioids and subsequent activation of opioid receptors (, in the case of phenytoin, but non-, in the case of ethanol) although direct activity at opioid receptors cannot be precluded.