联合应用钕：钇和二氧化碳激光切除颅内脑膜瘤

目的：研究临床联合应用钕：钇(Nd：YAG)激光和二氧化碳(CO2)激光切除颅内脑膜瘤的优点。方法：应用国产Nd：YAG激光-CO2激光切除23例颅内脑膜瘤，其中位于幕上16例，后颅窝7例。肿瘤直径3～12cm，其中直径>8cm的巨大肿瘤8例。所用Nd：YAG激光功率10～45W，平均25W；CO2激光功率10～60W，平均45W。结果：19例全切，全切率82.5％．无一例死亡。手术安全快捷，出血明显减少．去除肿瘤较彻底．术后反应轻，优于常规手术切除。结论：联合应用Nd：YAG激光-CO2激光切除颅内脑膜瘤．效果满意．是目前最佳的激光手术刀的组合。     

接触式Nd:YAG激光辅助显微手术切除脑室内脑膜瘤

自1991年1月至2003年12月,我院共收治脑膜瘤213例,其中脑室内脑膜瘤13例,占6.1%.采用接触式Nd:YAG激光辅助显微手术切除肿瘤,取得了良好的效果,报告如下.     

钬激光在颅底脑膜瘤手术中的应用

目的　探讨钬激光在辅助颅底脑膜瘤手术中的作用。　　方法　在 1 2例颅底脑膜瘤常规手术中应用纤维光导脉冲式钬激光气化肿瘤 ,处理肿瘤附着处辅助肿瘤切除。　　结果　 1例Smpson 1级切除 ,1 0例 2级切除 ,另 1例 4级切除 ,术后 2周Karnofsky评分 90分 5例 ,80分 2例 ,60分 2例 ,40分 1例 ,死亡 2例 ,平均随访 2 5 1个月无肿瘤复发。　　结论　钬激光辅助颅底脑膜瘤手术能够减少出血、手术时间和并发症 ,提高术后生存质量。     

二氧化碳激光焊接周围神经的实验研究

目的:试图借助二氧化碳(CO_2)激光作用来焊接周围神经,并与外膜缝合为对照,研究CO_2激光焊接神经的效果,期望为小脑桥脑角肿瘤手术时为顿神经断裂的焊接,特别是面神经断裂的焊接打下基础。方法:实验动物用雄性大白鼠20只,取双侧同体配对,吻合坐骨神经采用激光焊接和神经外膜缝合法。结果:研究结果表明:电生理研究、腓肠肌重测定、组织学研究、超微结构观察虽均显示无差异,但证明激光的优点在于:①焊接快;②神经纤维损伤少;③修复较好,水肿反应较轻;④神经功能恢复满意等。结论:本法可望应用于周围神经离断的焊接。     

无水乙醇在颅内巨大高血运脑膜瘤中的应用

目的 评估无水乙醇在颅内巨大高血运脑膜瘤手术中的止血作用及脑膜瘤的切除效果. 方法 四川省肿瘤医院颅脑外科自2004年9月至2008年10月对12例颅内巨大高血运脑膜瘤患者采用术中无水乙醇(8.5～27 mL,平均11.2 mL)注射止血后,显微镜下行肿瘤全切术. 结果 脑膜瘤注射区不同程度变白.瘤体变硬,表面及切面出血明显减少甚至停止.本组病例术中出血约48～154mL,平均67mL;手术全切11例,次全切1例,全切率91.6%;术后无任何手术并发症发生. 结论 高血运脑膜瘤手术中注射无水乙醇止血,简便易行,效果良好,值得推广.     

CTA检查对脑膜瘤手术切除的应用价值

目的探讨术前CTA检查对脑膜瘤手术方案的参考价值。方法回顾性分析31例脑膜瘤资料,均在CT血管成像后进行手术治疗。根据CTA所见进行手术入路的个性化设计和调整。切口设计需考虑在术中能充分暴露CTA所见的重要供血动脉或引流静脉。结果脑膜瘤达SimpsonⅠ级切除10例,Ⅱ级切除12例,Ⅲ级切除6例,Ⅳ级切除3例。随访12~26个月,未见肿瘤复发29例,残留肿瘤增生2例。结论通过CTA评估脑膜瘤与周围重要血管的关系、侵蚀情况,有利于术中肿瘤相关的血管显露、控制出血和保护重要血管。     

超声吸引器在脑膜瘤手术切除中的应用

目的 探讨超声吸引器在脑膜瘤手术中的应用价值。方法 对2012年6月至2014年6月收住我科行超声吸引手术治疗的45例脑膜患者的资料进行回顾性分析。结果 肿瘤全切除30例,次全切除12例,大部分切除3例。使用超声吸引器进行切除,平均操作时间为28.5 min,平均出血量约195.6 ml。所有患者均未出现与超声吸引手术直接相关的并发症。结论 运用超声吸引器辅助显微手术切除脑膜瘤,脑组织损伤小,手术出血少,术野清晰,能提高切除率,缩短手术时间,减少并发症的发生率。     

颅内外沟通型嗅沟脑膜瘤切除及骨水泥颅底重建

1病历摘要男,68岁;因癫疒间发作于2008年3月17日急诊入院。头部CT检查示(图1A):颅前窝底中线处3.5 cm×4.0 cm×6.0 cm类圆形占位,颅前窝底筛板     

Nd：YAG接触式激光的实验研究及临床癫痫手术的应用

应用１０只家兔，分为激光组和对照组，每组５只，用Ｎｄ：ＹＡＧ接触式激光和传统神经外科手段对兔脑进行切割研究，激光组切割力与对照组没有差别（ｐ＞０．０５），但止血作用强（ｐ＜０．０５），对脑组织损伤小。对２８例病人随机平均分为激光组和对照组，每组１４人，分别对致痫灶手术切除，激光组出血少，解剖分明，术后无菌性脑膜炎和功能障碍发生率较对照组明显低（ｐ＜０．０５），抗癫痫的效果明显优于对照组（ｐ＜０．０５）。     

Calpain‐dependent proteolysis of NF2 protein: Involvement in schwannomas and meningiomas

The neurofibromatosis type 2 (NF2) protein, known as merlin or schwannomin, is a tumor suppressor, and the NF2 gene has been found to be mutated in the majority of schwannomas and meningiomas, including both sporadically occurring and familial NF2 cases. Although the development of these tumors depends on the loss of merlin, the presence of tumors lacking detectable NF2 mutations suggests different mechanisms for inactivating merlin. Recent studies have demonstrated cleavage of merlin by calpain, a calcium‐dependent neutral cysteine protease, and marked activation of the calpain system resulting in the degradation of merlin in these tumors. Increased turnover of merlin by calpain in some schwannomas and meningiomas exemplifies tumorigenesis linked to the calpain‐mediated proteolytic pathway.     

Immunohistochemical analysis of cyclooxygenase‐2 and brain fatty acid binding protein expression in grades I‐II meningiomas: Correlation with tumor grade and clinical outcome after radiotherapy

This study was done to evaluate the association of cyclooxygenase 2 (COX‐2) and brain fatty acid binding protein (BFABP) with tumor grade and outcome of grades I‐II meningiomas treated with radiotherapy. From 1996 to 2008, 40 patients with intracranial grades I‐II meningiomas were treated with radiotherapy. Immunohistochemical staining for COX‐2 and BFABP were performed on formalin‐fixed paraffin‐embedded tissues. COX‐2 expression was significantly associated with BFABP status and both COX‐2 (P < 0.01) and BFABP (P = 0.01) expression were stronger in the grade II meningiomas than in grade I tumors. Among the clinicopathologic factors, age and COX‐2 status were prognostic in progression‐free survival. Patients with moderate or strong COX‐2 expression had worse outcome than those with negative or weak COX‐2 expression (P = 0.03) after controlling for potential confounders. Our results suggest that the molecular biomarker COX‐2 has prognostic significance in intracranial grades I‐II meningiomas following radiotherapy.     

The activation of unmyelinated or myelinated afferent fibers by brief infrared laser pulses varies with skin type

Brief infrared laser pulses were applied to 3 different skin areas in man. Reaction times indicated that A delta-fibers were activated in the dorsal and volar skin of the finger whereas only C-fibers were activated in the hairy skin of the forearm. The qualitative sensations were in line with this interpretation. We conclude that the activation of unmyelinated or myelinated afferent fiber populations with brief laser pulses varies with skin type.     

Mg2+对神经元保护机制的研究-Mg2+对培养的大鼠海马神经元GABAA受体介导电流的影响

目的 研究镁离子（Mg^2 ）对神经元保护的机制。方法 采用全细胞膜片钳技术，研究Mg^2 对培养的大鼠海马神经元GABAA受体介导电流的作用。结果 （1）在钳制电压为－40mV时，GABA可通过GABAA受体介导产生内向电流；（2）当GABA和Mg^2 同时作用时，该电流峰值增高；（3）在Mg^2 存在的情况下，GABA的浓度－效应曲线平行左移。结论 Mg^2 通过正性变构调节机制影响GABAA受体的功能，达到保护神经元的作用。     

The expression of MHC antigens on oligodendrocytes: Induction of polymorphic H-2 expression by lymphokines

Neither class I nor class II major histocompatibility complex (MHC) antigen has been demonstrated in native oligodendrocytes, the possible target of viral or immune damage in multiple sclerosis (MS). In this report, we show that H-2, but not Ia, antigen expression is induced on isolated mouse oligodendrocytes in vitro by crude supernatant from lectin-activated spleen cells, lectin-free interleukin 2, and cloned gamma-interferon. This induction of H-2 expression is not accompanied by proliferation of oligodendrocytes, whereas MHC induction in spleen cells is highly related to their proliferation, or blastoid transformation. Oligodendrocytes as well as other brain cells are probably isolated from these lymphokines by the blood-brain barrier (BBB). However, it is possible that oligodendrocytes express MHC class I antigen as a consequence of impairment of the BBB, or in the presence of activated T-cells which have been demonstrated in active MS lesions. This activation then renders oligodendrocytes possible target cells for MHC-restricted cytotoxic T-cells.     

The role of cyclo-oxygenase 1 and 2 activity in prostaglandin E(2) secretion by cultured human adult microglia: implications for Alzheimer's disease

Microglial cyclo-oxygenase (COX) expression is considered to be important in the pathogenesis of Alzheimer's disease (AD) and, therefore, constitutes a key target for therapeutic intervention. We investigated the influence of AD plaque associated factors on COX-1 and COX-2 expression and activity in adult human microglial cells in vitro. COX-2 immunoreactivity and mRNA were induced by lipopolysaccharide (LPS), not by AD plaque associated cytokines interleukin (IL)-1alpha, IL-1beta, IL-6, tumor necrosis factor (TNF)-alpha, or amyloid (A)beta(1-42). To assess functional COX activity, the release of PGE(2) into the culture medium was determined. LPS and also arachidonic acid (AA) dose-dependently stimulated PGE(2) release. The effects of AA are independent from induction of COX mRNA expression, or of de novo protein synthesis. No effects of either plaque-associated cytokines or Abeta(1-42) on PGE(2) secretion were seen, even when cells were co-stimulated with AA, to provide enough substrate. COX isotype selective inhibitors were used to discern relative contributions of COX-1 and COX-2 activities to microglial PGE(2) secretion. COX-2 and in part COX-1-selective inhibitors inhibited LPS-induced PGE(2) secretion, whereas the AA-induced PGE(2) secretion was reduced by COX-1-selective inhibitors only. Apparently, adult human microglia in vitro (1) constitutively express COX-1, and (2) do not express COX-2 upon exposure to either Abeta or plaque associated cytokines. In the light of microglial COX activity as a potential therapeutical target in AD, the data presented in this study suggest that classical NSAIDs, rather than selective COX-2 inhibitors, are more potent in reducing microglial prostaglandin secretion.     

Cortical modulation of nociception by galvanic vestibular stimulation: A potential clinical tool?

ObjectiveVestibular afferents converge with nociceptive ones within the posterior insula, and can therefore modulate nociception. Consistent with this hypothesis, caloric vestibular stimulation (CVS) has been shown to reduce experimental and clinical pain. Since CVS can induce undesirable effects in a proportion of patients, here we explored an alternative means to activate non-invasively the vestibular pathways using innocuous bi-mastoid galvanic stimulation (GVS), and assessed its effects on experimental pain.MethodsSixteen healthy volunteers participated in this study. Experimental pain was induced by noxious laser-heat stimuli to the left hand while recording pain ratings and related brain potentials (LEPs). We evaluated changes of these indices during left- or right-anodal GVS (cathode on contralateral mastoid), and contrasted them with those during sham GVS, optokinetic vestibular stimulation (OKS) using virtual reality, and attentional distraction to ascertain the vestibular-specific analgesic effects of GVS.ResultsGVS elicited brief sensations of head/trunk deviation, inoffensive to all participants. Both active GVS conditions showed analgesic effects, greater for the right anodal stimulation. OKS was helpful to attain significant LEP reductions during the left-anodal stimulation. Neither sham-GVS nor the distraction task were able to modulate significantly pain ratings or LEPs.ConclusionsGVS appeared as a well-tolerated and powerful procedure for the relief of experimental pain, probably through physiological interaction within insular nociceptive networks. Either isolated or in combination with other types of vestibular activation (e.g., optokinetic stimuli), GVS deserves being tested in clinical settings.