癫痫手术的麻醉

在皮质脑电图监测下行癫痫病灶切除术才能达到满意效果。癫痫手术时一般常用全麻,亦可选用局麻,前提是术中不影响皮质脑电图的描记。现将我院70例颞叶癫痫病灶切除术的麻醉体会报告如下。1 资料和方法 本组70例均为颞叶癫痫病人,施行前颞叶切除或杏仁核海马回切除术。男47例,女23例,年龄:11岁～55岁。局麻8例采用0,5％～1％普鲁卡因,每100毫升内含1:1000肾上腺素0.5毫升,不加任何     

伴有结构性病变颞叶癫痫的显微外科治疗

目的探讨显微外科治疗伴有结构性病变的颞叶癫痫及手术方式。方法回顾总结显微外科手术治疗伴有结构性病变颞叶癫痫临床资料。结果13例术后未再发癫痫,随访2例单纯病灶切除术后3个月发作1次。1例外伤性癫痫术后6月发作1次,药物控制。结论显微病灶 癫痫灶切除是治疗颞叶癫痫的有效方法。     

以癫痫为首发症状的颅内小型病灶手术治疗

我院自1986年2月至1993年10月对以癫痫为首发症状的46例颅内小型病灶患者,进行病灶切除术,术后近期辅以抗癫痫药物治疗,取得了好疗效。其中男32例,女14例,年龄最小8岁,最大56岁,平均年龄24岁。 临床表现:部分发作22例,部分感觉发作2例,部分发作加半身发作9例,部分发     

皮层脑电图监测下手术治疗儿童继发性癫痫的疗效探讨

目的探讨皮层脑电图监测下儿童继发性癫痫的手术治疗效果。方法124例继发性癫痫患儿,术中通过皮层脑电图定位癫痫灶,显微手术切除原发病变后,再根据癫痫发作的临床表现、病灶部位及皮层脑电图监测所提示的异常脑电图波释放决定是否进行致痫灶切除、扩大致痫灶切除、皮层热灼术、前颞叶切除术、海马杏仁核切除术及胼胝体前部切开术。术后规范应用抗癫痫药物。结果124例患儿切除病变前皮层脑电图均可记录到癫痫波,原发病变切除后即时皮层脑电图监测病变周围可记录到异常癫痫波112例,检出率为90.32%。其中38例致痫波发放区域位于非功能区者该范围内皮层予以完全切除,术后即时皮层脑电图提示癫痫波消失;74例位于或毗邻重要功能区者,采用低功率热灼该处皮层后,69例癫痫波消失,5例患者经联合胼胝体前部切开和(或)海马、杏仁核切除,术后即时皮层脑电图监测效果满意。术后随访18个月至6年,按Engle标准评定疗效:Ⅰ级87例(68.50%),Ⅱ级30例(24.19%),Ⅲ级5例(4.03%),Ⅳ级2例(1.61%);手术总有效率为94.35%。89例患者停止服用抗癫痫药物满1年且无癫痫发作;24例患者低剂量维持;11例患者停药后癫痫复发再次服用初始量,发作频率较术前明显减少。结论皮层脑电图监测下,不同术式应用可明显提高儿童继发性癫痫手术治疗的效果。     

脑部手术过程中 患者竟然意识清醒能说话

正患者躺在手术台上一边接受开颅手术,一边辨认医生手里的图案是苹果还是熊猫,并反馈术中的感受。这不是科幻,这是在首都医科大学三博脑科医院正在进行的术中唤醒手术。接受手术的是一名患难治性癫痫患者。这台术是帮助患者在清醒状态下切除脑部癫痫病灶。患者已经有6年的癫痫病史,术前的长程视频脑电监测,捕捉到患者的癫痫病灶已侵袭到了他的大脑功能区,如果直接切除病灶,一旦影响到大脑功能,可能导致瘫痪、失语等严重并发症。而术中唤醒全麻后的患     

完整结肠系膜切除术与传统根治术治疗结肠癌的临床疗效

目的:比较完整结肠系膜切除术与传统根治术治疗结肠癌的临床疗效。方法:选择某院收治的54例结肠癌患者作为本次观察对象,收治时间为2013年6月~2015年3月,将54例结肠癌患者随机分成两组,每组27例,两组结肠癌患者分别行传统根治术及完整结肠系膜切除术进行治疗,观察两组结肠癌患者治疗后的病灶复发率、术后肛门排气时间及感染率。结果:术后对照组与实验组结肠癌患者的病灶复发率、术后肛门排气时间及感染率均存在显著差异(P<0.05),统计学有意义。结论:针对结肠癌患者采用完整结肠系膜切除术的临床疗效比传统根治术的临床疗效高,能有效降低病灶复发率及感染率,改善患者预后。     

腹腔镜下子宫腺肌瘤病灶切除术治疗子宫腺肌病的临床效果评价

目的:研究子宫腺肌病采用腹腔镜下子宫腺肌瘤病灶切除术进行治疗的疗效。方法:选取2015年2月至2018年2月期间于我院进行治疗的子宫腺肌病患者100例,分为研究组和参照组,研究组行子宫腺肌瘤病灶切除术,参照组行子宫切除术,比较两组患者的临床疗效。结果:两种手术方法在手术时间、术中出血量及住院时间方面存在统计学意义(P0.05),术后并发症和治疗效果对比差异不显著,不具有统计学意义(P0.05)。结论:腹腔镜下行子宫腺肌瘤病灶切除术对子宫腺肌病的治疗效果有明显优势,可以保留患者生育能力,减少术中出血,值得推广。     

改良大脑半球切除术临床疗效分析

目的探讨改良大脑半球切除患者术后癫痫控制情况与病理基础间的关系。方法对12例行改良大脑半球切除术患者的临床资料、术后癫痫控制情况进行观察，其中6例为半侧巨脑畸形（HME），4例为梗影缺血，2例为Rasmussen脑炎。结果HME组癫痫始发年龄最小；术前各病理组癫痫发作频率差异无显著性。术后10例癫痫获得完全控制，余2例HME患者发作减少75％以上。结论改良大脑半球切除术能有效地控制各种病理基础、病变累及一侧半球的顽固性癫痫，不同病理基础的患者在术后癫痫控制方面差异不明显。     

PET辅助定位颞叶致痫灶切除术的围手术期护理

目的总结经18F-FDG-PET显像定位后行颞叶致痫灶切除术的68例顽固性癫痫患者的围手术期护理经验,探讨最佳的护理经验。方法 68例顽固性癫痫患者于术前行系统检查,确定致痫灶位于颞叶前部。术中应用皮层及深部电极证实致痫灶,予与切除。仔细分析术前及术后的护理方法,总结出最有效的护理措施。结果经过严密的监护、精心的护理和恰当的治疗,所有患者得到了顺利的康复,无严重并发症出现。结论 PET辅助定位可大大提高癫痫灶定位的准确性,可提高手术的成功率,精心的术前护理准备,严密的术后观察是减少术后并发症的发生,保证手术成功的重要环节。     

腹腔镜下多种微创保守性术式治疗子宫腺肌病的短期临床疗效分析

目的:探讨腹腔镜下多种微创保守性术式治疗子宫腺肌病的短期临床疗效。方法:回顾性分析93例子宫腺肌瘤患者的临床资料,按照不同的手术方式分为三组:A组为子宫动脉阻断术(UAB)组(n=32),B组为病灶切除术组(n=33),C组为子宫动脉阻断联合病灶切除术组(n=28)。比较三组患者手术时间、术中出血量、肛门排气时间、术后疼痛评分、并发症发生率及住院时间、月经量、子宫大小、痛经评分等指标。结果:三组间的手术时间比较,差异有统计学意义(F=2.082,P<0.05);而三组的术中出血量、肛门排气时间、术后疼痛评分、并发症发生率及住院时间比较,差异无统计学意义(P>0.05)。与术前比较,三组患者术后1,3个月的月经量均显著减少,痛经评分下降,子宫体积显著缩小;而术后1,3个月同期多组间各指标比较,差异均无统计学意义(P>0.05)。结论:腹腔镜下子宫动脉阻断术、病灶切除术及子宫动脉阻断联合病灶切除术均可安全用于子宫腺肌病患者,短期随访显示3种术式均可有效改善患者的症状。     

左乙拉西坦添加治疗儿童耐药性癫痫部分性发作的临床研究

目的观察左乙拉西坦添加治疗儿童耐药性癫痫的疗效、用药方法、剂量和副作用。方法对50例儿童耐药性癫痫部分性发作进行添加左乙拉西坦治疗,观察其疗效。结果左乙拉西坦治疗儿童耐药性癫痫部分性发作,总有效率达72%,17例患儿发作停止。结论左乙拉西坦治疗儿童难治性癫痫有良好的疗效,患儿对其有较好的耐受性,副作用轻微。     

Pharmacotherapeutic management of epilepsy in MERRF syndrome

Introduction: Epilepsy is a prominent feature of myoclonic epilepsy with ragged-red fibers (MERRF)-syndrome. The most frequent seizure type is myoclonic seizures, of which the treatment is challenging and empiric.

Areas covered: Herein, the author summarises and discusses previous and recent findings of antiepileptic drug (AED) treatment in MERRF-syndrome.

Expert opinion: MERRF-syndrome is a predominantly maternally inherited, multisystem mitochondrial disorder caused by pathogenic variants predominantly of the mitochondrial DNA (mtDNA). Canonical clinical features of MERRF include myoclonus, epilepsy, ataxia, and myopathy. Additionally, other manifestations in the CNS, peripheral nerves, eyes, ears, heart, gastrointestinal tract, and endocrine organs may occur (MERRF-plus). Today, MERRF is considered rather as myoclonic ataxia than as myoclonic epilepsy. Genotypically, MERRF is due to mutations in 13 mtDNA-located genes and 1 nDNA-located gene. According to the modified Smith-score, the strongest gene–disease relationship exists for MT-TK, MT-TL1, and POLG1. Epilepsy is the second most frequent phenotypic feature of MERRF. Seizure-types associated with MERRF include focal myoclonic, focal clonic, and focal atonic seizures, generalized myoclonic, tonic-clonic, atonic, and myoclonic-atonic seizures, or typical absences. Treatment of myoclonic epilepsy relies on expert judgments recommending levetiracetam, together with clonazepam, or topiramate, zonisamide, or piracetam in monotherapy as the first line AEDs.     

Cerebral cortex modulation of pain

Pain is a complex experience encompassing sensory-discriminative, affective-motivational and cognitiv e-emotional components mediated by different mechanisms. Contrary to the traditional view that the cerebral cortex is not involved in pain perception, an extensive cortical network associated with pain processing has been revealed using multiple methods over the past decades. This network consistently includes, at least, the anterior cingulate cortex, the agranular insular cortex, the primary （SⅠ） and secondary somatosensory （SⅡ） cortices, the ventrolateral orbital cortex and the motor cortex. These cortical structures constitute the medial and lateral pain systems, the nucleus submedius-ventrolateral orbital cortex-periaqueductal gray system and motor cortex system, respectively. Multiple neurotransmitters, including opioid, glutamate, GABA and dopamine, are involved in the modulation of pain by these cortical structures. In addition, glial cells may also be involved in cortical modulation of pain and serve as one target for pain management research. This review discusses recent studies of pain modulation by these cerebral cortical structures in animals and human.     

Allosteric activation mechanism of the cys-loop receptors

Binding of a neurotransmitter to its ionotropic receptor opens a distantly located ion channel, a process termed allosteric activation. Here we review recent advances in the molecular mechanism by which the cys-loop receptors are activated with emphasis on the best studied nicotinic acetylcholine receptors （nAChRs）. With a combination of affinity labeling, mutagenesis, electrophysiology, kinetic modeling, electron microscopy （EM）, and crystal structure analysis, the allosteric activation mechanism is emerging. Specifically, the binding domain and gating domain are interconnected by an allosteric activation network. Agonist binding induces conformational changes, resulting in the rotation of a β sheet of aminoterminal domain and outward movement of loop 2, loop F, and cys-loop, which are coupled to the M2-M3 linker to pull the channel to open. However, there are still some controversies about the movement of the channel-lining domain M2. Nine angstrom resolution EM structure of a nAChR imaged in the open state suggests that channel opening is the result of rotation of the M2 domain. In contrast, recent crystal structures of bacterial homologues of the cys-loop receptor family in apparently open state have implied an M2 tilting model with pore dilation and quaternary twist of the whole pentameric receptor. An elegant study of the nAChR using protonation scanning of M2 domain supports a similar pore dilation activation mechanism with minimal rotation of M2. This remains to be validated with other approaches including high resolution structure determination of the mammalian cys-loop receptors in the open state.     

Effects of hormone replacement therapy on magnetic resonance imaging of brain parenchyma hyperintensities in postmenopausal women

Aim： To apply 3.0 magnetic resonance imaging （MRI） to study the effects of long-term, low dose hormone replacement therapy （HRT） on the brain parenchyma of postmenopausal women.
Methods： A total of 155 postmenopausal healthy female medical staff members from Peking Union Medical College Hospital were enrolled. The HRT group was composed of 71 subjects who had been given a low dose of HRT for over 4 years, while 84 women who had never been given HRT were enrolled in the control group. The Mini-Mental State Examination （MMSE） was used to evaluate menta state, and an Enzyme-Linked ImmunoSorbent Assay （ELISA） was used to detect plasma levels of sex hormones. In addition, all participants were subjected to an MRI, including axial T2 weighted imaging （T2WI）, fluid-attenuated inversion recovery （FLAIR）, T1 weighted imaging （T1WI, oblique coronal, vertical to the hippocampus, slice thickness 3 mm without gaps）, and a 3D image of the whole brain.
Results： The ELISA showed that the plasma level of estradiol in the HRT group was significantly higher than that in the control group （P〈0.05）. No differences were observed in the MMSE between the two groups. In participants older than 70 years of age, the number of deep white matter hyperintensities （DWMHs） in the control group was significantly higher than that in the HRT group （P=0.0013）; however, in other age subgroups, no statistical differences were observed. Finally, no significant difference in periventricular hyperintensity （PVH） between the two groups was observed.
Conclusion： We found that a high plasma level of estradiol in postmenopausal women receiving long-term HRT was correlated with the survival of brain parenchyma.     

嘉定某村女性乳腺保健知识、态度、行为调查

目的：了解农村地区女性乳腺保健知识、态度和行为状况。方法：2012年12月采用问卷调查方式对华亭镇某村501名20～74岁女性进行乳腺保健知识的调查分析。结果：12道乳腺疾病知识题回答正确率最高为73.65%,最低为6.79%。26.35%被调查者曾接受乳腺保健知识培训。在过去一年里，有38.12%的被调查者曾行乳腺自查，67.47%的被调查者持积极对待乳腺自我检查。结论：采取适合农村地区健康教育形式开展乳腺健康宣教，加强指导农村妇女开展乳腺自查，促进形成健康行为。     

N-acetylcysteine infusion reduces the resistance index of renal artery in the early stage of systemic sclerosis

Aim： To evaluate resistance index （RI） changes in renal artery after N-acetylcysteine infusion in patients with systemic sclerosis. Methods： In an open-label study 40 patients with systemic sclerosis （SSc） were treated with N-acetylcysteine （NAC） iv infusion over 5 consecutive hours, at a dose of 0.015 g.kg^-1.h^-1. Renal haemodynamic effects were evaluated by color Doppler examination before and after NAC infusion. Results： NAC infusion significantly reduced RI in a group of sclerodermic patients with early/active capillaroscopic pattern, modified Rodnan Total Skin Score （mRTSS） 〈14 and mild-moderate score to the vascular domain of Medsger Scleroderma Disease Severity Scale （DSS）. RI increased after NAC infusion in patients with late capillaroscopic pattern, mTRSS〉14 and severe-end stage score to the vascular domain of DSS. In patients with reduction of RI after NAC infusion, diffusion capacity for carbon monoxide mean value was significantly higher than in those patients with an increase of RI. No significant differences in renal blood flow were found between patients with different subsets of SSc. Conclusion： In patients with low disease severity NAC ameliorates vascular renal function.     

Modulation of KATP currents in rat ventricular myocytes by hypoxia and a redox reaction

Aim： The present study investigated the possible regulatory mechanisms of redox agents and hypoxia on the KATP current （IKATP） in acutely isolated rat ventricular myocytes. Methods： Single-channel and whole-cell patch-clamp techniques were used to record the KATP current （IKATP） in acutely isolated rat ven- tricular myocytes. Results： Oxidized glutathione （GSSG, 1 mmol/L） increased the IKATP while reduced glutathione （GSH, 1 mmol/L） could reverse the increased IKATP during normoxia. To further corroborate the effect of the redox agent on the KATP channel, we employed the redox couple DTT （1 mmol/L）/H202 （0.3, 0.6, and 1 mmol/L） and repeated the previous processes, which produced results similar to the previous redox couple GSH/GSSG during normoxia. H202 increased the IKATP in a concentration dependent manner, which was reversed by DTr （1 mmol/L）. In addition, our results have shown that 15 min of hypoxia increased the IWTP, while GSH （1 mmol/L） could reverse the increased IKATP, Furthermore, in order to study the signaling pathways of the IKATP augmented by hypoxia and the redox agent, we applied a protein kinase C（PKC） inhibitor bisindolylmaleimide Vl （BIM）, a protein kinase G（PKG） inhibitor KT5823, a protein kinase A （PKA） inhibitor H-89, and Ca（2＋）/calmodulin-dependent protein kinase II （CaMKII） inhibitors KN-62 and KN-93. The results indicated that BIM, KT5823, KN-62, and KN-93, but not H-89, inhibited the IKATP augmented by hypoxia and GSSG; in addition, these results sug- gest that the effects of both GSSG and hypoxia on KATp channels involve the activation of the PKC, PKG, and CaMK II pathways, but not the PKA pathway. Conclusion： The present study provides electrophysiological evidence that hypoxia and the oxidizing reaction are closely related to the modulation of IKATP.     

Functional study of the effect of phosphatase inhibitors on KCNQ4 channels expressed in Xenopus oocytes

Aim： KCNQ4 channels play an important part in adjusting the function of cochlear outer hair cells. The aim of this study was to investigate the effects of ser/thr phosphatase inhibitors on human KCNQ4 channels expressed in Xenopus laevis oocytes. Methods： Synthetic cRNA encoding human KCNQ4 channels was injected into Xenopus oocytes. We used a two-electrode voltage clamp to measure the ion currents in the oocytes. Results： Wild-type KCNQ4 expressed in Xenopus oocytes showed the typical properties of slow activation kinetics and low threshold activation. The outward K~ current was almost completely blocked by a KCNQ4 blocker, linopirdine （0.25 mmol/L）. BIMI （a PKC inhibitor） prevented the effects of PMA （a PKC activator） on the KCNQ4 current, indicating that PKC may be involved in the regulation of KCNQ4 expressed in the Xenopus oocyte system. Treatment with the ser/thr phosphatase inhibitors, cyclosporine （2 pmol/L）, calyculin A （2 pmol/L） or okadaic acid （1 pmol/L）, caused a significant positive shift in V1/2 and a decrease in the conductance of KCNQ4 channels. The V1/2 was shifted from -14.6±0.5 to -6.4±0.4 mV by cyclosporine, -18.8±0.5 to -9.2_＋0.4 mV by calyculin A, and -14.1±0.5 to -0.7＋0.6 mV by okadaic acid. Moreover, the effects of these phosphatase inhibitors （okadaic acid or calyculin A） on the induction of a positive shift of V1/2 were augmented by further addition of PMA. Conclusion： These results indicate that ser/thr phosphatase inhibitors can induce a shift to more positive potentials of the activation curve of the KCNQ4 current. It is highly likely that the phosphatase functions to balance the phosphorylated state of substrate protein and thus has an important role in the regulation of human KCNQ4 channels expressed in Xenopus oocytes.     

The protective effect of the RAS inhibitor on diabetic patients with nephropathy in the context of VEGF suppression

Aim： The aim of the present study was to explore whether renin angiotensin system （RAS） inhibitor can reduce the production of vascular endothelium growth factor （VEGF）. Further, we sought to elucidate the correlation between VEGF level and certain clinical parameters, such as albumin excretion rate （AER）, before and after treatment with angiotensin type 1 receptor blocker. Methods： We recruited 166 type 2 diabetic patients at various stages of diabetic nephropathy （DN） and 46 healthy control subjects for a cross-sectional study. We recruited another 42 hypertensive type 2 diabetic patients with microalbuminuria for a longitudinal study involving a 6-month irbesartan treatment protocol. Urinary VEGF （uVEGF） levels were determined using ELISA. Results： In the cross-sectional study, hypertensive type 2 diabetic patients who received RAS inhibitor presented lower uVEGF levels than those who did not receive the RAS inhibitor. Statistical analysis indicated that uVEGF level was independently correlated with the AER. In the longitudinal study involving the 6-month irbesartan treatment, we demonstrated that uVEGF levels decreased significantly in patients who achieved a 50% AER reduction （remission group, n=32）. In contrast, uVEGF levels remained unchanged in patients who did not exhibit a 50% AER reduction （nonremission group, n=10）. Furthermore, the change in uVEGF was significantly correlated with the change in AER （r=0.65, P〈0.01） before and after 6 months of irbesartan treatment. This result held true even after we had adjusted for the decrease in average blood pressure. Conclusion： The protective effect of the RAS inhibitor in DN patients is associated with the suppression of VEGF. Accordingly, it may be possible to use uVEGF as a marker of DN progression. We suggest that uVEGF may be an important target for therapeutic intervention in the context of DN.