重度颅脑损伤：应该预防癫痫吗？

重度颅脑损伤患者有较高概率发生癫痫,是否需要抗癫痫药物预防癫痫发作存在争议。文章认为,重度颅脑损 伤患者早期（7 d内）在应用镇痛镇静治疗基础上无需加用抗癫痫药物,晚期无预防性应用抗癫痫药物的必要。而确 诊为癫痫者则需应用抗癫痫药物规范治疗。     

颅骨成形术后癫痫发作的临床研究

目的分析颅骨成形术后癫痫发作的发生率、相关因素和预防性应用抗癫痫药物(AED)的临床效果。方法选择行颅骨成形术患者107例,分析术后癫痫发作、AED预防性使用及术后早期癫痫发作者术后住院日及晚期癫痫发作情况。结果术后早期癫痫发作17例(15.9%),晚期癫痫发作19例(17.8%)。自体颅骨成形术后早期癫痫发作发生率低于钛网成形术(P<0.05)。术后未使用AED患者早期癫痫发作发生率为23.5%,术后使用AED发生率为2.6%(P<0.01)。术后出现早期癫痫发作患者术后平均住院日和晚期癫痫发作发生率明显高于术后未出现早期癫痫发作患者(P<0.01)。结论颅骨修补术后早期和晚期癫痫发作发生率高,早期癫痫发作可导致平均住院日延长,并增加晚期癫痫发作的风险。预防使用AED可以显著减少术后早期癫痫发作的发生。     

脑卒中后癫痫76例临床分析

对840例脑卒中患者的临床资料进行回顾性分析，其中76例继发癫痫，卒中后癫痫发生率为9．05％，早期癫痫发作5．88％，晚期癫痫发作3．28％，以全身强直一阵挛性发作最常见（47．86％）。卒中后癫痫的发生率与病灶部位有关，与卒中类型无关。卒中早期癫痫发作的主要致病因素为脑水肿，晚期为胶质疤痕所致。对卒中发作癫痫患者进行系统治疗可取得良好疗效。     

脑卒中后癫痫86例临床分析

目的分析脑卒中后癫痫的临床特点。方法回顾性分析86例脑卒中后癫痫患者的临床资料。结果早发型癫痫47例,其中出血性脑卒中（33例）,缺血血性脑卒中（14例）;迟发型癫痫39例,缺血血性脑卒中（21例）,出血性脑卒中（18例）。早发型癫痫患者中19例长期服用抗癫痫药,14例（73．6％）无发作;24例未给予抗癫痫治疗,18例（75％）无发作。迟发型癫痫患者中28例长期服用抗癫痫药,24例（85．7％）无发作;11例未给正规应用抗癫痫药物,6例（54．5％）无发作。结论出血性卒中发生早发型癫痫的可能性大,缺血性卒中更倾向于发生迟发型癫痫。服用抗癫痫药物对早发型癫痫预后并无明显影响,但可明显改善迟发型癫痫的预后。     

老年脑膜瘤术后早期癫痫临床相关因素分析

目的探讨老年患者脑膜瘤术后早期癫痫与临床各相关因素的关系,以及临床特点及主要危险因素和保护因素。方法收集我院老年脑膜瘤手术患者86例的临床资料,通过χ2检验、计算C值及OR值观察各临床相关因素与术后早期癫痫的关联程度。结果各相关因素中术前癫痫、术后预防用药、肿瘤位置等因素有统计学意义(P0.05),其C值依次增强(P0.05);术前癫痫发作OR1;术后预防应用抗癫痫药物OR1;位于幕下深部、幕下浅部、幕上深部、幕上浅部的脑膜瘤患者术后早期癫痫的发生率依次增高。结论术前癫痫发作为脑膜瘤术后并发早期癫痫的危险因素;术后预防应用抗癫痫药物为脑膜瘤术后并发早期癫痫的保护因素;肿瘤位于小脑幕上时,更易并发术后早期癫痫。     

急性脑卒中后的早期癫痫发作:迟发性癫痫的危险因素

急性脑卒中后的早期癫痫发作与迟发性癫痫发作间的关系尚有争论。作者选择31例住院的急性脑卒中(19例皮层梗寒,8例为脑叶出血或广泛性出血,4例蛛网膜下腔出血)病例,在住院的2周内均有癫痫发作(称早期发作):16例为单纯部分性发作,4例为单纯部分性伴继发性全身性发作,11例为强直阵挛性发作。在平均26个月的随访中,10例(32%)出现了迟发性发作,其中9例的发作类型与早期发作类型相同。这31例具有早期癫痫发作的病例中,21例接受了抗痈药物治疗,但仍有7例(7/21)出现迟发性发作,未接受抗痫药物治疗的10例中,3例     

脑出血后继发性癫痫患者脑电图动态监测结果分析

目的探讨脑电图动态监测对脑出血后继发性癫痫的诊断价值。方法选取2016年3月至2019年2月我院收治的脑出血后继发性癫痫患者60例(观察组)和同期收治的脑出血后未发生癫痫的患者60例(对照组)为研究对象。比较两组患者脑电图异常情况;比较观察组患者中继发性癫痫早期发作患者(早期发作组)和晚期发作患者(晚期发作组)的脑电图异常情况。结果对照组患者的脑电图异常率(43.3%)显著低于观察组患者(65.0%),差异有统计学意义(P0.05)。观察组患者中癫痫晚期发作组患者的脑电图轻度异常率、中度异常率、重度异常率、癫痫样放电发生率与早期发作组患者相比较,差异均无统计学意义(P0.05)。结论对脑出血后患者进行脑电图动态监测,对继发性癫痫的诊治具有重要的意义,但对判断患者继发性癫痫发作的早晚情况作用不大。     

癫痫持续状态32例诊治体会

癫痫持续状态（SE）或称癫痫状态,是指癫痫连续发作之间意识尚未完全恢复又频繁再发,或癫痫发作时间持续30 min以上不能自行停止者。癫痫持续状态是神经内科常见急症,若不及时处理可因高热、循环衰竭或神经元兴奋性损伤导致永久性脑损害,致残率和死亡率很高。临床上在持续状态患者抢救过程中,快速控制发作、综合观察病情变化、有效预防并发症的发生,是抢救成功的关键。     

高血压脑出血术后死亡原因分析

目的探讨高血压脑出血（HICH）术后的死亡原因。方法回顾性分析1998—2008年我科手术后死亡的HICH病例124例。结果中枢衰竭死亡者58例,肺部感染、多脏器功能衰竭（MOF）死亡者各22例,其他并发症死亡者为22例。结论中枢衰竭是术后患者早期（≤7d）死亡的最主要原因。术前的意识状态、出血量是影响HICH患者术后死亡的最重要因素。手术后并发症是术后患者晚期（〉7d）死亡的最主要原因,主要是肺部感染和MOF。     

癫痫大鼠海马线粒体COXⅠ和COXⅣ表达的变化

目的探讨癫痫对大鼠海马线粒体细胞色素氧化酶（COX）的mtDNA和nDNA编码亚基Ⅰ、Ⅳ表达的影响。方法成年雄性Wistar大鼠随机分为生理盐水对照组、癫痫持续状态（SE）后急性期（3h）、静止期（7d）、慢性期（45d）组和注射匹鲁卡品（PILO）但未出现SE组。免疫组化并荧光实时定量PCR检测海马线粒体COXⅠ、Ⅳ阳性染色及其mRNA的表达。结果COXⅠ阳性细胞数在SE后3h明显增加,7d降到对照组水平,45d显著降低;COXⅣ阳性细胞数SE后3h稍有增加,但较对照组无显著性差异,7和45d时COXⅣ染色变化与对照组相似;注射PILO但未出现SE组COXⅠ、Ⅳ的表达与对照组类似。COXⅠmRNA在SE后3h表达明显升高（P〈0.001）,7d时降到对照水平,45d显著降低（P〈0.001）;COXⅣmRNA在3h时表达较对照组升高,但差异无显著性,7和45d时下降至对照组水平。注射PILO但无SE组与对照组结果类似。结论颞叶癫痫海马COX功能紊乱与痫性发作相关,线粒体编码的基因更易受痫性发作的影响。     

左乙拉西坦对外伤性癫痫预防作用的实验研究

目的建立外伤性癫痫模型,观察左乙拉西坦(LEV)干预对大鼠行为学以及海马苔藓纤维出芽的影响,探讨LEV对外伤性癫痫的预防作用。方法 (1)外伤性癫痫模型建立:除正常对照组外,其余大鼠均立体定向注射5μl浓度为0.2 mol/L的氯化铁于右侧运动皮层,癫痫发作分级采用Racine(1972)评分标准,除死亡外发作至4级以及4级以上的随机分为3组,每组7只。(2)实验分组:正常对照组,等体积生理盐水连续灌胃7 d;模型对照组,右侧运动皮层注射氯化铁,而后给予等体积生理盐水连续灌胃7 d;低剂量预防组,右侧运动皮层注射氯化铁,造模清醒后立即给予LEV150 mg/kg,1次/d,连续灌胃7 d;高剂量预防组,右侧运动皮层注射氯化铁,造模清醒后立即给予LEV300 mg/kg,1次/d,连续灌胃7 d。(3)行为学观察:视频监控24 h大鼠行为学变化,采用Racine(1972)评分标准对癫痫发作进行观测和记录,记录大鼠造模后7 d内癫痫发作次数。(4)海马苔藓纤维出芽Timm染色:大鼠造模后15 d,海马冰冻切片做Timm染色,观察右侧海马CA3区苔藓纤维出芽情况,并选用Cavazos的标准对其进行评分。(5)统计学分析:用SPSS 17.0统计软件进行单因素方差分析及LSD-t组间比较,评价LEV对外伤性癫痫的预防作用。以P0.05为差异有统计学意义。结果 LEV低、高剂量预防组与模型组相比明显减少癫痫发作次数及苔藓纤维出芽程度,差异有统计学意义(t值分别为11.36、5.88、18.39、8.12,均P0.05),低剂量预防组与高剂量预防组相比,差异有统计学意义(t值分别为8.22、3.58,均P0.05)。结论 LEV在外伤性癫痫模型中可以减少癫痫发作次数,抑制苔藓纤维出芽,提示LEV有预防外伤性癫痫的作用。     

Poststroke seizures in the elderly

Strokes are the most common cause of epilepsy in the elderly. Seizures after an acute stroke have been estimated to occur in 5% to 10% of cases. A distinction between early and late seizures should be made. Early seizures are more common, occur very early in the evolution of the stroke, and tend to be focal motor, brief, and isolated. They are likely to be the result of an acute local brain metabolic alteration induced by the cerebrovascular event, and once these derangements are reversed, seizures disappear. Epilepsy usually does not follow early seizures, but the risk is probably increased. Late seizures occur months to years after the stroke and are probably due to structural brain abnormalities leading to the development of an epileptic focus. The majority of these cases develop epilepsy. The risk of seizures is markedly increased when the cerebrovascular event involves the cerebral cortex. Deep-seated hemispheric or infratentorial lesions rarely produce seizures or epilepsy. It is possible that hemorrhagic stroke carries a higher incidence of seizures, but the issue remains controversial. It has also been suggested that embolic infarction has a higher incidence of seizures that does thrombotic infarction, but definitive evidence is lacking. The presence of seizures in an acute stroke does not seem to correlate with the size of the lesion, functional outcome, or mortality. Prophylactic treatment with antiepileptic drugs is probably not indicated in most types of strokes, except for subarachnoid hemorrhage after a ruptured intracranial aneurysm. When early seizures develop, treatment is indicated but may not be necessary for a prolonged period of time. If late seizures develop, chronic anticonvulsant therapy is recommended.     

以癫痫为主要表现的儿童遗传代谢性疾病

目的提高对遗传代谢性疾病所致儿童癫痫的认识。方法采用回顾性方法,对我院以癫痫发作为主诉就诊,经血氨、乳酸、血同型半胱氨酸、尿有机酸气相色谱质谱联用分析、骨髓涂片、脑脊液检查、溶酶体酶活性分析、线粒体基因检测、线粒体酶活性分析确诊的先天代谢性缺陷病26例患儿的临床表现、生化特点以及诊疗情况进行回顾和分析。结果所有患儿均有癫痫发作,以部分性发作、痉挛发作为最常见发作形式,少数患者可有肌阵挛发作。患者多有不同程度的体格或智力运动发育迟滞,年长儿发病的线粒体脑肌病患者发病前智力正常,发病后出现智力运动倒退。脑电图表现以多灶独立性棘波、高度失律、背景慢波为主要表现。患者癫痫发作多难以控制,部分患者对因治疗后癫痫发作明显好转。结论先天代谢性疾病是儿童癫痫的病因之一;临床上应根据患儿发病急缓、生长发育、智力行为等,选择适宜的检查,以早期诊断。除了抗癫痫治疗以外,应根据不同的病因给予病因治疗。     

卒中后癫痫发作及其发病机制的研究进展

卒中是成人尤其是老年癫痫及癫痫发作的重要病因。随着卒中患者的增加和治疗手段的进步,卒中后癫痫发作及其诊治受到越来越多的关注,对于癫痫发作和癫痫的发病机制进行了大量研究。作者就卒中后癫痫发作及其发病机制的研究进展进行综述。     

Endocrine changes after pediatric traumatic brain injury

Traumatic brain injury (TBI) is a very common occurrence in childhood, and can lead to devastating long term consequences. Recent research has focused on the potential endocrine consequences of TBI in adults. The research in children is less robust. This paper reviews current literature regarding TBI and possible hypothalamic and pituitary deficiencies in childhood. Acute endocrine changes are commonly found after TBI in pediatric patients, which can include changes in hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release. In the long term, both temporary and permanent alterations in pituitary function have been found. About 30% of children have hypopituitarism up to 5 years after injury. Growth hormone deficiency and disturbances in puberty are the most common, but children can also experience ACTH deficiency, diabetes insipidus, central hypothyroidism, and elevated prolactin. Every hormonal axis can be affected after TBI in children, although growth hormone deficiency and alterations in puberty are the most common. Because transient and permanent hypopituitarism is common after TBI, survivors should be screened serially for possible endocrine disturbances. These children should undergo routine surveillance at least 1 year after injury to ensure early detection of deficiencies in hormonal production in order to permit normal growth and development.     

Up-regulation of intestinal nuclear factor kappa B and intercellular adhesion molecule-1 following traumatic brain injury in rats

AIM: Nuclear factor kappa B (NF-κB) regulates a large number of genes involved in the inflammatory response to critical illnesses, but it is not known if and how NF-KB is activated and intercellular adhesion molecule-1 (ICAM-1) expressed in the gut following traumatic brain injury (TBI). The aim of current study was to investigate the temporal pattern of intestinal NF-κB activation and ICAM-1 expression following TBI. METHODS: Male Wistar rats were randomly divided into six groups (6 rats in each group) including controls with sham operation and TBI groups at hours 3, 12, 24, and 72, and on d 7. Parietal brain contusion was adopted using weight-dropping method. All rats were decapitated at corresponding time point and mid-jejunum samples were taken. NF-KB binding activity in jejunal tissue was measured using EMSA. Immunohistochemistry was used for detection of ICAM-1 expression in jejunal samples. RESULTS: There was a very low NF-κB binding activity and little ICAM-1 expression in the gut of control rats after sham surgery. NF-KB binding activity in jejunum significantly increased by 160% at 3 h following TBI (P<0.05 vs control), peaked at 72 h (500% increase) and remained elevated on d 7 post-injury by 390% increase. Compared to controls, ICAM-1 was significantly up-regulated on the endothelia of microvessels in villous interstitium and lamina propria by 24 h following TBI and maximally expressed at 72 h post-injury (P<0.001). The endothelial ICAM-1 immunoreactivity in jejunal mucosa still remained strong on d 7 post-injury. The peak of NF-κB activation and endothelial ICAM-1 expression coincided in time with the period during which secondary mucosal injury of the gut was also at their culmination following TBI. CONCLUSION: TBI could induce an immediate and persistent up-regulation of NF-κB activity and subsequent up-regulation of ICAM-1 expression in the intestine. Inflammatory response mediated by increased NF-κB activation and ICAM-1 expression may play an important role in the pathogenesis of acute gut mucosal injury following TBI.     

Sudden unexpected death in epilepsy

Sudden unexpected death in epilepsy (SUDEP) refers to the sudden death of a seemingly healthy individual with epilepsy, usually occurring during, or immediately after, a tonic-clonic seizure. The frequency of SUDEP varies depending on the severity of the epilepsy, but overall the risk of sudden death is more than 20 times higher than that in the general population. Several different mechanisms probably exist, and most research has focused on seizure-related respiratory depression, cardiac arrhythmia, cerebral depression, and autonomic dysfunction. Data from a pooled analysis of risk factors indicate that the higher the frequency of tonic-clonic seizures, the higher the risk of SUDEP; furthermore, risk of SUDEP is also elevated in male patients, patients with long-duration epilepsy, and those on antiepileptic polytherapy. SUDEP usually occurs when the seizures are not witnessed and often at night. In this Seminar, we provide advice to clinicians on ways to minimise the risk of SUDEP, information to pass on to patients, and medicolegal aspects of these deaths.     

外伤性癫痫79例临床分析

目的探讨外伤性癫痫的危险因素、临床特征及防治措施。方法79例外伤性癫痫患者均常规给予抗癫痫药物治疗,其中35例难治性癫痫患者接受手术治疗,术中行皮质脑电图监测。术式包括致痫灶切除、前颞叶切除、选择性杏仁核-海马切除、胼胝体前部切开、多处软膜下横纤维切断术等。结果随访6—48个月,44例保守治疗者中,18例在癫痫控制2年后逐步减量停药,未见发作;其余患者仍继续口服药物治疗,2例仍时有发作。35例手术患者,按照Engel分级,I级18例,Ⅱ级12例,Ⅲ级5例,无Ⅳ级患者,有效率85．7％（30／35）。结论消除外伤性癫痫的危险因素以降低其发生率、正规抗癫痫药物治疗、选择合适的患者手术治疗是获得外伤性癫痫理想治疗效果的重要措施。     

Antiphospholipid and antinuclear antibodies in patients with epilepsy or new-onset seizure disorders

PURPOSE: The increased prevalence of autoantibodies in patients with epilepsy has been traditionally regarded to be a consequence of antiepileptic drugs. The purpose of this study was to measure autoantibodies in well-defined groups of patients with seizures to determine the effects of epilepsy and antiepileptic medications on the presence of autoantibodies. PATIENTS AND METHODS: We studied the frequency of antinuclear antibodies, anti-beta2-glycoprotein I antibodies, and anticardiolipin antibodies in 50 patients with therapy-resistant localization-related epilepsy, 50 patients with generalized epilepsy syndromes, 52 patients with a newly diagnosed seizure disorder but no antiepileptic medication, and 83 healthy controls. RESULTS: Compared with controls, newly diagnosed patients had a significantly greater prevalence of immunoglobulin (Ig) G class anticardiolipin antibodies (21% versus 7%); the prevalence was 14% in patients with localization-related epilepsy and 8% in patients with generalized epilepsy. The prevalence of IgM class anticardiolipin antibodies was significantly greater in all seizure groups (60% in localization-related epilepsy, 42% in generalized epilepsies, and 33% in newly diagnosed patients) compared with controls (7%). Antinuclear antibodies were significantly more common in newly diagnosed patients (21%) and localization-related epilepsy (24%) compared with controls (12%). When patients with generalized epilepsy (8%) were used as the reference group, antinuclear antibodies were also significantly more frequent in localization-related epilepsy (relative risk [RR] = 2.9, 95% confidence interval [CI]: 1.1 to 8.2) and newly diagnosed seizures (RR = 3.4, 95% CI: 1.2 to 9.3). There were no consistent associations between autoantibodies and specific antiepileptic medications. CONCLUSIONS: The prevalence of autoantibodies is greater in patients with epilepsy, including newly diagnosed seizure disorder. The increased prevalence of autoantibodies is more strongly associated with epilepsy than with antiepileptic drugs, perhaps indicating that immune dysregulation may be commonly associated with epilepsy.     

EEG activation with bemegride in epilepsy diagnosis. 1: Literature review

In patients with suspected epilepsy, an EEG "activation" with bemegride can be performed as last link of the diagnostic chain. The administration of bemegride intends the activation of epileptiform discharges in the EEG of patients with a disposition for epilepsy. This activation is not supposed to occur in healthy subjects at the same dosage. The occurrence of generalized and focal epileptiform discharges during the intravenous administration of bemegride is regarded as a positive test result by most investigators. Changes like a slowing of the background activity, dysrhythmias, parenrhythmias, and focal changes are not reliable. The provocation of seizures should be avoided. Dosage and injection rate must be chosen in such a way that false negative results are more probable than false positive. The result of the bemegride test is influenced by sex, type of seizures, age and alcohol intake. Slight side effects of the intravenous administration of bemegride are relatively common, severe side effects rather uncommon when the test is carefully performed. According to the literature and personal experience, the activation of typical epileptiform discharges in the EEG by bemegride in adults with doubtful episodes of unconsciousness indicates the possible presence of epilepsy (epileptic seizures respectively), but does not confirm this. In our opinion, the bemegride test is contraindicated in patients with established epilepsy (epileptic seizures respectively) or in cases in whom the occurrence of epileptic seizures is probable.