经小脑脑桥裂上、下支入路全程减压治疗面肌痉挛

目的总结经小脑脑桥裂手术入路治疗面肌痉挛的初步经验。方法回顾性分析经小脑脑桥裂入路全程减压治疗123例面肌痉挛病例的临床资料。术中打开小脑脑桥裂上、下支,探查责任血管,行个体化减压。结果123例均发现责任血管压迫。术后痉挛立即消失112例,明显减轻11例。115例随访10～45个月,痉挛未完全消失仅1例;听力下降1例;术后脑脊液漏致颅内严重感染1例,遗留双侧视力下降和对侧听力下降;轻、中度复发2例;无死亡病例。结论经小脑脑桥裂上、下支入路,有利于全程显露面神经,特别是面神经出脑干区,有利于责任血管的探查、减压及减轻面、听神经的牵拉,有助于提高治愈率、减少并发症、降低复发率。     

微血管减压术治疗168例面肌痉挛临床报告

目的总结微血管减压术MVD在治疗面肌痉挛HFS中的手术疗效及并发症。方法 168例HFS患者行乙状窦后入路面神经根MVD,手术时经绒球小叶显露面神经脑干段,仔细寻找责任血管后,将其推移离开面神经,在血管与脑干之间放置Teflon棉固定。结果术中发现责任血管构成情况:小脑前下动脉94例,小脑后下动脉38例,椎基底动脉15例,椎基底动脉及其分支血管(小脑前下动脉或小脑后下动脉)共同压迫21例。术后随访半年,150例患者抽搐完全消失,10例术后抽搐频率及强度均明显减轻,但仍有抽搐。总有效率为95.2%。4例(2.4%)术后出现听力下降。2例(1.2%)患者在术后7 d以后出现迟发性面瘫。3例(1.7%)皮下积液,无脑脊液漏。1例(0.6%)死亡。结论 MVD是目前HFS最有效的治疗方法。     

神经内镜经小脑绒球下入路面神经显微血管减压术治疗面肌痉挛的临床疗效

目的初步探讨神经内镜经小脑绒球下入路面神经显微血管减压术治疗面肌痉挛的临床疗效。方法回顾性分析山东大学齐鲁医院神经外科2019年6月至2021年3月收治的97例面肌痉挛患者的临床资料。97例患者术前均行影像学检查,以明确责任血管与面神经出脑干区的关系。所有患者均采用神经内镜经小脑绒球下入路面神经显微血管减压术,术中在神经电生理监测下充分解剖后组脑神经背侧的蛛网膜,从而显露面神经出脑干区,明确责任血管,并准确置入垫片。术后疗效评估分为即刻治愈、延迟治愈、复发和未治愈。结果97例患者术中发现责任血管为小脑前下动脉59例;小脑后下动脉3例;椎-基底动脉35例,其中单纯椎-基底动脉8例,椎-基底动脉联合小脑前下动脉24例,椎-基底动脉联合小脑后下动脉3例。术后即刻治愈68例(70.1%)。术后发热13例,听力减退4例,耳鸣2例,一过性面瘫5例。97例患者的术后中位随访时间为9个月(1~19个月),末次随访显示,93例(95.9%)患者的面部抽动完全消失,其中延迟治愈者25例;未治愈者4例;无复发病例。结论神经内镜经小脑绒球下入路面神经显微血管减压术治疗面肌痉挛,不仅可以提高手术治愈率,而且可以减少术后并发症。     

神经内镜经小脑绒球下入路面神经显微血管减压术治疗面肌痉挛的临床疗效

目的初步探讨神经内镜经小脑绒球下入路面神经显微血管减压术治疗面肌痉挛的临床疗效。方法回顾性分析山东大学齐鲁医院神经外科2019年6月至2021年3月收治的97例面肌痉挛患者的临床资料。97例患者术前均行影像学检查,以明确责任血管与面神经出脑干区的关系。所有患者均采用神经内镜经小脑绒球下入路面神经显微血管减压术,术中在神经电生理监测下充分解剖后组脑神经背侧的蛛网膜,从而显露面神经出脑干区,明确责任血管,并准确置入垫片。术后疗效评估分为即刻治愈、延迟治愈、复发和未治愈。结果97例患者术中发现责任血管为小脑前下动脉59例;小脑后下动脉3例;椎-基底动脉35例,其中单纯椎-基底动脉8例,椎-基底动脉联合小脑前下动脉24例,椎-基底动脉联合小脑后下动脉3例。术后即刻治愈68例(70.1%)。术后发热13例,听力减退4例,耳鸣2例,一过性面瘫5例。97例患者的术后中位随访时间为9个月(1~19个月),末次随访显示,93例(95.9%)患者的面部抽动完全消失,其中延迟治愈者25例;未治愈者4例;无复发病例。结论神经内镜经小脑绒球下入路面神经显微血管减压术治疗面肌痉挛,不仅可以提高手术治愈率,而且可以减少术后并发症。     

小脑水平裂-小脑脑桥裂入路治疗三叉神经痛

目的 介绍一种经小脑水平裂-小脑脑桥裂治疗三叉神经痛的手术入路.方法 回顾性分析经小脑水平裂-小脑脑桥裂人路治疗的17例三叉神经痛病例.结果 所有患者均可顺利分开小脑水平裂外侧部和小脑脑桥裂上肢,均发现有责任血管压迫,术后立即止痛15例,2例疼痛分别于术后第2、3天完全消失.术后1例出现口唇疱疹,1例患侧面部轻微麻木.结论 经小脑水平裂-小脑脑桥裂入路治疗三叉神经痛,可以避免传统的枕下乙状窦后人路三叉神经感觉根人脑桥处显露不良的缺陷,减少听力下降、面瘫等并发症的发生.     

绒球下入路微血管减压术治疗面肌痉挛疗效分析

目的 探讨绒球下入路微血管减压术（MVD）治疗面肌痉挛（HFS）的安全性和有效性。方法 回顾性分析2020年7月至2021年6月采用绒球下入路MVD治疗的233例HFS的临床资料。结果 术中发现单一血管压迫166例（71.2%）,其中小脑前下动脉142例;多支血管压迫67例（28.8%）,其中椎动脉参与53例。术后1、3、6、12个月有效率分别为95.3%、94.8%、95.3%、94.8%。术后1年复发率为1.7%。术后发生并发症26例（11.2%）,其中无菌性脑膜炎10例,脑脊液鼻漏3例,迟发性面瘫6例,后组颅神经麻痹4例,听力损伤2例,小脑梗死1例。结论 绒球下入路MVD治疗HFS是一种安全的、有效的手术方法,可充分显露面神经根出脑干区,同时减少对小脑的牵拉,降低听力损伤风险。     

面神经监测显微手术切除听神经瘤(附16例报告)

目的总结面神经监测下神经内镜辅助锁孔入路切除听神经瘤的临床经验.方法采用神经内镜辅助经枕下乙状窦后锁孔入路切除听神经瘤16例,术中行面神经自发和诱发电位监测,指导手术切除.结果肿瘤全切除14例(87.5%),面神经解剖保留15例(93.8%),术后2周面神经功能保留13例(81.3%).结论面神经自发和诱发电位监测下行神经内镜辅助枕下乙状窦后锁孔入路显微手术,可以有效提高听神经瘤全切率,减少并发症.     

内镜辅助显微外科血管减压术治疗面肌痉挛的并发症及其防治

目的探讨内镜辅助微血管减压术(MVD)治疗面肌痉挛(HFS)患者出现的并发症及其预防。方法分析内镜辅助MVD治疗的43例HFS患者的临床资料。结果手术有效率为95.3%(41/43)。术后出现头痛、头晕13例,剧烈头痛3例,无菌性脑膜炎3例,眩晕耳鸣5例,听力下降3例,术后轻度面瘫5例,迟发性面瘫3例,复视1例,给予对症处理后恢复满意。所有病例随访2年,均无复发。结论内镜辅助MVD治疗HFS有效率高,复发率低,并发症较少,效果较好。     

微血管减压术治疗125例面肌痉挛临床分析

目的探讨微血管减压术（MVD）治疗面肌痉挛（HFS）的疗效及并发症。方法125例HFS患者行乙状窦后入路面神经根MVD,手术时经绒球小叶显露面神经脑干段,仔细找寻责任血管后,将其推移离开面神经,在血管与脑干之间放置Teflon棉固定。结果术中发现责任血管为小脑前下动脉63例,小脑后下动脉34例,椎基动脉6例,椎基动脉及其分支血管（小脑前下动脉或小脑后下动脉）共同压迫22例。术后随访4年,全部病例抽搐完全消失,有效率为100％。1例术后出现面瘫（0．8％）,经针灸、理疗、药物治疗后仍有轻微的面瘫（House-Brackmann评分II级）;3例出现迟发性面瘫（2．4％）,经针灸、理疗、药物治疗后均完全恢复;1例出现咽部不适（0．8％）。无脑脊液漏及死亡病例。结论MVD是HFS最有效的治疗方法。术中不遗漏责任血管,在血管与脑干间恰当的放置Teflon棉,使责任血管远离面神经是提高手术疗效的关键。     

前庭蜗神经显微血管减压术的初步报告

目的 探讨前庭蜗神经显微血管减压术(MVD)治疗耳鸣、眩晕的疗效.方法 10例耳鸣患者,5例眩晕患者,2例耳鸣伴眩晕的患者,均合并三叉神经痛(TN)或者面肌痉挛(HFS),以上患者均在实施乙状窦后入路手术治疗TN、HFS的同时行前庭蜗神经MVD治疗伴随的耳鸣或眩晕.3例单纯耳鸣患者以及1例单纯眩晕患者均接受乙状窦后入路单纯前庭蜗神经MVD,治疗耳鸣或眩晕.结果 术中均发现有动脉性血管压迫前庭蜗神经.术后即刻疗效:15例耳鸣患者中治愈7例,好转5例,无效3例;8例眩晕患者中治愈4例,好转2例,无效2例.平均随访8个月,随访疗效:15例耳鸣患者中治愈8例,好转4例,无效3例,总有效率80%;8例眩晕患者中治愈4例,好转2例,无效2例,总有效率75%.1例单纯耳鸣患者术后出现患侧听力丧失,随访期间未恢复.结论 血管压迫前庭蜗神经是顽固性耳鸣、致残性眩晕的病因之一;MVD针对有选择的耳鸣、眩晕患者是一种安全、有效的治疗方法.     

Phe(1)Psi(CH(2)-NH)Gly(2)]NC(1-13)NH(2) does not antagonize orphaninFQ/nociceptin-induced prolactin release

The specificity of the orphaninFQ (OFQ)/nociceptin (N)-induced prolactin increase was determined in male and female rats by pretreating animals with different doses of [Phe(1)Psi(CH(2)-NH)Gly(2)]NC(1-13)NH(2), a compound originally reported to be a specific OFQ/N antagonist. In addition, the effect of naloxone pretreatment on OFQ/N-induced prolactin release was examined to determine if OFQ/N's effects were mediated by opiate receptors. Furthermore, dose response studies using [Phe(1)Psi(CH(2)-NH)Gly(2)]NC(1-13)NH(2) only were performed to determine potential agonist activity of this drug. Finally, growth hormone (GH) levels were determined as an index of specificity of the prolactin response. Our results confirm previous findings that OFQ/N potently stimulates prolactin release and that a gender difference exists in the magnitude of the response, with females showing a much greater response than male rats. The endocrine response is specific because OFQ/N potently stimulated prolactin, but not GH secretion. The prolactin response is not mediated by actions at opiate receptors because naloxone did not inhibit OFQ/N's effects on prolactin release. However, [Phe(1)Psi(CH(2)-NH) Gly2]NC(1-13) NH(2) did not antagonize OFQ/N's effects on prolactin release. Indeed, this drug acted as a potent agonist. Demonstrating pharmacological specificity of OFQ/N's effects on prolactin release awaits the development of more selective, specific antagonists.     

Source localization (LORETA) of the error-related-negativity (ERN/Ne) and positivity (Pe)

We investigated error processing of 39 subjects engaging the Eriksen flanker task. In all 39 subjects a pronounced negative deflection (ERN/Ne) and a later positive component (Pe) were observed after incorrect as compared to correct responses. The neural sources of both components were analyzed using LORETA source localization. For the negative component (ERN/Ne) we found significantly higher brain electrical activity in medial prefrontal areas for incorrect responses, whereas the positive component (Pe) was localized nearby but more rostral within the anterior cingulate cortex (ACC). Thus, different neural generators were found for the ERN/Ne and the Pe, which further supports the notion that both error-related components represent different aspects of error processing.     

Allosteric regulation of alpha(IIb)beta(3) by beta(3) 95-105

The linear recognition sequences of an anti-beta(3) antibody that blocked platelet aggregation were identified using beta(3) tryptic peptides. Two of these recognition sequence-containing peptides were mapped to beta(3) 92-105, and antibodies affinity purified using these peptides blocked platelet aggregation. Examining the structure of alpha(IIb)beta(3) identified beta(3) 95-105 as the solvent accessible sequence within beta(3) 92-105. A peptide corresponding to beta(3) 95-105 was synthesized and used to affinity purify the beta(3) antibody. Anti-beta(3) 95-105 completely blocked platelet aggregation and agonist-induced fibrinogen binding to platelets, but had no effect on cyclic-RGD binding. Binding of anti-beta(3) 95-105 to alpha(IIb)beta(3) also did not alter the structure of the alpha(IIb) cap subdomain, as measured by anti-alpha(IIb) 201-217 binding. beta(3) 95-105 and peptides spanning two adjacent sequences in the structure of beta(3) did not bind fibrinogen and were ineffectual in blocking agonist-induced platelet aggregation. Structure analysis revealed that beta(3) 95-105 is adjacent to one of the two hinges in beta(3) that allows for the outward swing of the hybrid and PSI domains which is central to the conversion of alpha(IIb)beta(3) from a low into a high affinity state. Thus, the binding of an antibody to beta(3) 95-105 could serve as a fulcrum for allosteric regulation of alpha(IIb)beta(3) by regulating the movement of the hybrid-PSI domain.