颅神经血管压迫综合征微血管减压术后并发症分析

颅神经血管压迫综合征是指脑血管压迫相应的神经根所产生的一系列临床症状，根据血管压迫的神经不同，可以表现为三叉神经痛、面肌痉挛、舌咽神经痛。而针对此类疾病病因的治疗是微血管减压术。但有些病例术后出现并发症。我院行微血管减压术（MVD）术后的患者中共165例出现并发症分析如下。     

脑神经血管压迫综合征微血管减压术后并发症的观察与护理

原发性三叉神经痛、舌咽神经痛和面肌痉挛为桥小脑角区三大主要的功能性神经外科疾病,大都由于脑神经根部被血管压迫所致.由于桥小脑角区解剖结构复杂,重要血管、神经的空间结构变化较大,术中有可能损伤脑干、岩静脉及临近的脑神经.患者术后有脑干、小脑功能损害及后组脑神经损害的风险.因此,神经血管压迫综合征微血管减压术(MVD)后患者的颅高压评估与术后并发症的防护是确保患者手术安全与手术疗效的措施之一.自1967年普及以来,现已为国内外神经外科广泛接受,并成为了手术治疗三叉神经痛、面积痉挛、舌咽神经痛的首选方法,成功率大约为87.5％-99.3％[1].我科2010年1月-2011年12月,采用MVD治疗原发性三叉神经痛、舌咽神经痛、面肌痉挛共45例,现总结其术后护理措施如下.     

MRI在了解颅神经疾病患者血管神经关系上的作用

根据目前的神经血管冲突（neurovascular conflict,NVC）的发病机理,微血管减压术（microvascular decompression,MVD）是当前治疗颅内血管压迫症状的公认有效方法。本研究通过MRI观察正常人群和颅神经疾病患血管压迫神经的情况,比较健侧和患侧颅神经受压之间的差异,从而评价神经血管压迫在此类疾病发生中的作用,探讨颅神经疾病的发病机理,现报道如下。     

枕颈部畸形Chiar畸形临床分析

目的 分析枕颈部畸形Chiar畸形的临床症状,探讨有效的治疗方法.方法 回顾性分析本院自2010年8月～2012年8月收治的56例枕颈部畸形Chiar畸形患者临床资料,分析其临床特点,并采用小骨窗颅后凹减压及人工硬脑膜修补术治疗,观察其临床治疗效果.结果 枕颈部畸形Chiar畸形伴随头晕、头痛等临床症状,临床特征无特异性,易出现误诊,经过治疗.患者治疗显效26例,有效25例,死亡2例,治疗总有效率为91.1％,对患者进行随访期间发现,患者Tator评价标准下,治疗总有效率为92.9％.结论 枕颈部畸形Chiar畸形误诊率较高,通过小骨窗颅后凹减压及人工硬脑膜修补术能够有效提高患者康复率,效果显著,值得推广.     

Application of magnetic resonance imaging at 3.0-tesla and neuroendoscope in microvascular decompression

目的 探讨MRI图像结合神经内镜在微血管减压术(MVD)治疗原发性三叉神经痛的应用.方法 用3.0T MRI对16例患者行快速稳态梯度回波(True FISP)和三维时间飞跃法磁共振血管成像(3D TOF MRA)序列扫描.其中,2例并在注射对比剂后行三维快速小角度激发成像(3DFLASH)序列扫描,使用OsiriX图像软件进行图像融合三维重建来评定神经血管压迫情况.16例患者均在神经内镜辅助显微神经外科(EAM)下行MVD并术中录像,术后与影像结果进行回顾性分析.结果 患者压迫动脉或静脉及其严重程度与手术所见吻合度达100％.1例用神经内镜探查时发现并存动静脉压迫,3例内镜探查后调整隔片位置.16例患者中,13例(81.2％)疼痛立即消失,3例(18.7％)疼痛减轻,总有效率100％.随访6个月效果满意.结论 三叉神经术前3.0T MRI重建技术有利于选择病例和术中有目的探查微血管压迫,应用神经内镜协助则能提高手术效果.     

去骨瓣减压术后骨窗疝的成因及防治

目的探讨去骨瓣减压术后骨窗疝及其并发症的成因及防治措施。方法回顾性分析行去骨瓣减压术后发生切口疝患者32例临床资料。结果去骨瓣减压术后发生骨窗疝的患者中,中等大小骨瓣者、单侧去骨瓣者、术中敞开硬脑膜者和GCS评分≤8分者居多。结论合理选择骨瓣大小和尽量减张缝合修补硬脑膜可以有效减少去骨瓣减压术后骨窗疝的发生。     

枕下乙状窦后锁孔经小脑桥脑裂入路治疗面肌痉挛的临床研究

目的:评估枕下乙状窦后锁孔经小脑桥脑裂入路治疗面肌痉挛的安全性和有效性,探讨改良后的手术切口、骨瓣设计和打开桥脑裂上、下支的临床意义。方法:收集2009年2月—2016年1月采用该入路手术治疗的148例面肌痉挛患者的临床资料,进行回顾性分析。结果:148例均发现责任血管压迫,其中136例完全减压,12例未完全减压;术后痉挛消失134例,明显减轻14例;听力下降1例,面部轻瘫3例,脑脊漏1例。结论:该入路治疗面肌痉挛,有利于显露面神经全程,特别是面神经入脑干区,有利于责任血管的探查、减压及减轻面、听神经的牵拉,可提高治愈率、降低复发率。改良的手术切口、骨瓣符合手术要求,可减少并发症。     

浮动骨瓣减压术治疗颅脑外伤体会

颅脑外伤手术中,为了减轻因术后脑水肿引起的颅压增高,常使用去骨瓣减术。虽然可取得一定的减压效果,但不免遗留颅骨缺损而需要行颅骨成形术。给病人带来一定的心理负担和经济负担。近几年来,我们对14例手术中没有或仅有轻度脑膨出骨窗的病人采用浮动骨瓣减压术,收效满意,现将初浅体会报告如下。 1 方法:与一般骨瓣开颅手术相同,但锯开骨瓣时骨缘尽量形成斜面,翻开骨瓣后马蹄形剪开硬脑膜翻向静脉窦侧,清除硬脑膜下或脑内血肿后将硬脑膜回复不缝。硬脑     

神经内镜结合3.0T MRI重建技术在三叉神经痛微血管减压术中的应用

目的探讨MRI图像结合神经内镜在微血管减压术(MVD)治疗原发性三叉神经痛的应用。方法用3.0T MRI对16例患者行快速稳态梯度回波(True FISP)和三维时间飞跃法磁共振血管成像(3DTOF MRA)序列扫描。其中,2例并在注射对比剂后行三维快速小角度激发成像(3DFLASH)序列扫描,使用OsiriX图像软件进行图像融合三维重建来评定神经血管压迫情况。16例患者均在神经内镜辅助显微神经外科(EAM)下行MVD并术中录像,术后与影像结果进行回顾性分析。结果患者压迫动脉或静脉及其严重程度与手术所见吻合度达100%。1例用神经内镜探查时发现并存动静脉压迫,3例内镜探查后调整隔片位置。16例患者中,13例(81.2%)疼痛立即消失,3例(18.7%)疼痛减轻,总有效率100%。随访6个月效果满意。结论三叉神经术前3.0T MRI重建技术有利于选择病例和术中有目的探查微血管压迫,应用神经内镜协助则能提高手术效果。     

经锁孔枕下乙状窦后经内听道上人路研究岩斜区的显微解剖

目的 通过锁孔枕下乙状窦后经内听道上入路对岩斜区结构进行显微解剖.方法 用成人湿性头颅标本10例,20侧,模拟锁孔枕下乙状窦后经内听道上人路对岩斜区进行显微解剖观察.结果 该入路可以清楚暴露颞骨岩部、三叉神经、面听神经、部分后组颅神经、脑桥外侧面、岩静脉、椎动脉、小脑前下动脉、小脑后下动脉.磨除部分岩骨可以扩大内听道的暴露,切开小脑幕缘可以暴露部分滑车神经.结论 锁孔枕下乙状窦后经内听道上入路,充分利用了有效的骨窗,减少无效脑暴露;同时,手术创伤小、并发症少.对于主体位于后颅窝的岩斜区肿瘤显微切除是一种有效、安全、便捷的微创手术方法 .     

微血管减压术治疗脑神经血管压迫综合征

目的总结微血管减压术治疗脑神经血管压迫综合征的临床效果。方法采用微血管减压术治疗脑神经血管压迫综合征患者61例。其中,三叉神经痛40例,舌咽神经痛3例,面肌痉挛18例。随访5-22个月。对临床资料进行回顾性分析。结果三叉神经痛患者手术有效率为95%,舌咽神经痛手术有效率100%,面肌痉挛患者为94.5%。术后发生轻度不良反应者9例(15.5%);发生较重并发症1例(1.7%),无死亡病例。结论微血管减压术治疗因血管压迫导致的相关脑神经疾病疗效确切,不良反应少。     

The anti-migraine 5-HT(1B/1D) agonist rizatriptan inhibits neurogenic dural vasodilation in anaesthetized guinea-pigs

These studies investigated the pharmacology of neurogenic dural vasodilation in anaesthetized guinea-pigs. Following introduction of a closed cranial window the meningeal (dural) blood vessels were visualized using intravital microscopy and the diameter constantly measured using a video dimension analyser. Dural blood vessels were constricted with endothelin-1 (3 microg kg(-1), i.v.) prior to dilation of the dural blood vessels with calcitonin gene-related peptide (CGRP; 1 microg kg(-1), i.v.) or local electrical stimulation (up to 300 microA) of the dura mater. In guinea-pigs pre-treated with the CGRP receptor antagonist CGRP((8-37)) (0.3 mg kg(-1), i.v.) the dilator response to electrical stimulation was inhibited by 85% indicating an important role of CGRP in neurogenic dural vasodilation in this species. Neurogenic dural vasodilation was also blocked by the 5-HT(1B/1D) agonist rizatriptan (100 microg kg(-1)) with estimated plasma levels commensurate with concentrations required for anti-migraine efficacy in patients. Rizatriptan did not reverse the dural dilation evoked by CGRP indicating an action on presynaptic receptors located on trigeminal sensory fibres innervating dural blood vessels. In addition, neurogenic dural vasodilation was also blocked by the selective 5-HT(1D) agonist PNU-142633 (100 microg kg(-1)) but not by the 5-HT(1F) agonist LY334370 (3 mg kg(-1)) suggesting that rizatriptan blocks neurogenic vasodilation via an action on 5-HT(1D) receptors located on perivascular trigeminal nerves to inhibit CGRP release. This mechanism may underlie one of the anti-migraine actions of the triptan class exemplified by rizatriptan and suggests that the guinea-pig is an appropriate species in which to investigate the pharmacology of neurogenic dural vasodilation.     

磁共振3D FIESTA—C序列和3D TOF SPGR序列对显示后颅窝颅神经及血管的价值

目的评价MRI三维循环相位稳态采集快速成像（three—dimensional fast imaging employing steady state acquisition with cycled phases,3D FIESTA—C）和三维时间飞跃法扰相梯度回波（three—dimensional time of flight spoiled gradient recalled acquisition,3D TOF SPGR）序列对显示后颅窝颅神经及血管的价值。方法分析49例后颅窝肿块病例和29例神经血管压迫病例MRI 3D FIESTA—C和3D TOF SPGR序列图像资料。结果49例后颅窝肿块患者中,44例（90％）MRI 3D FIESTA-C序列结合MPR及MPVE图像可清晰显示受累颅神经及其与肿块的关系,3D TOF SPGR序列颅神经显示率60％（29／49）,结合MIP图像78％（38／49）可确认肿块压迫或包绕的血管来源。29例神经血管压迫病例中,MRI 3D FIESTA-C序列结合MPR图像均可清晰显示受累颅神经及其与血管的关系,结合3D TOF SPGR序列及其MIP图像可准确判断血管的来源。结论MRI 3D FIESTA—C序列结合3D TOF SPGR序列可清晰显示后颅窝肿块侵犯或压迫神经、血管情况及评价神经血管压迫、接触情况。     

Topiramate inhibits trigeminovascular activation: an intravital microscopy study

Activation, or the altered perception of activation, of trigeminal nerves that innervate the cranial vasculature is considered to be a pivotal component of the pathophysiology of acute migraine. Calcitonin gene-related peptide (CGRP) levels are increased during migraine and after trigeminal nerve stimulation in the cat. Both CGRP and nitric oxide (NO) infusion causes headache and delayed migraine in migraineurs. Neurogenic stimulation of a cranial window, CGRP and NO injection all cause meningeal artery dilation in the rat when viewed using intravital microscopy. Topiramate is an antiepileptic drug with established efficacy as a migraine preventive, and has recently been shown to inhibit neurons of the trigeminocervical complex after superior sagittal sinus stimulation. In this study, we used intravital microscopy with neurogenic dural vasodilation, and CGRP- and NO-induced dilation to examine whether intravenous topiramate has effects on the trigeminovascular system. Topiramate was able to attentuate neurogenic dural vasodilation maximally after 15 min by 52% at 30 mg kg(-1) (t(5) = 6.78, n = 6); there was no significant inhibition at 10 mg kg(-1). There was also significant attenuation of the NO-induced dilation maximally after 15 min, at both 10 and 30 mg kg(-1) by 21% (t(6) = 6.09, n = 7) and 41% (t(6) = 5.3, n = 7), respectively. CGRP-induced dilation was not inhibited at either dose of topiramate.The study demonstrates that topiramate is likely to inhibit neurogenic dural vasodilation by inhibiting the release of CGRP from prejunctional trigeminal neurons, thus attenuating the dural vasodilation. Topiramate is not able to act postsynaptically at the blood vessels themselves as the CGRP-induced dilation was not attenuated. The data are consistent with an effect of topiramate on trigeminovascular activation which may form part of its preventive antimigraine mechanisms of action.     

原发性三叉神经痛手术中出现窦性心动过缓的临床分析

目的 探讨微血管减压术及(或)感觉根选择性切断术治疗原发性三叉神经痛(idiopathic trigminal neuralgia,ITN)术中发生窦性心动过缓的相关因素、预防及治疗措施.方法 回顾性分析全麻下行微血管减压术及/或感觉根选择性切断术治疗ITN 67例术中出现窦性心动过缓的情况.结果 术中出现5例心律改变(7.46％)均为窦性心动过缓,术中给予阿托品治疗后均有效,术后随访7日至3个月,平均1.5个月,均无心律失常发现.结论 导致窦性心动过缓的相关因素有很多,与手术操作及手术方式密切相关,与可能存在的传导通路也有一定相关性,术中及时处理,常对手术影响较小.为减少其发生,应以预防为主.     

36例体枕大池成形术治疗Chiari畸形合并脊髓空洞症的体会

目的研究探讨一种小脑扁桃体切除+枕大池成形术治疗Chiari畸形合并脊髓空洞症的手术治疗方法。方法采用枕下正中入路,咬开枕骨大孔后缘下至下项线,两侧至枕骨大孔4、8点钟位置大小约2.5cm×4.0cm,咬除寰椎后弓,"T"形切开硬脑膜和蛛网膜。软脑膜下切除两侧小脑扁桃体,开放正中孔直至四脑室底并且打通两侧小脑延髓池。取肌筋膜行硬脑脊膜连同蛛网膜的扩大修补,形成新的枕大池。结果本组病例术后两年均得到随访,MRI复查示空洞腔都明显缩小,其中2例空洞消失,感觉恢复较肌力恢复良好。结论此手术方法效果满意。其要点是:①小脑扁桃体在软膜下切除并行软膜缝合。②四脑室正中孔开放并和两侧小脑延髓池相通。③枕骨大孔区蛛网膜下腔扩大修补缝合,无须行后颅窝减压术。     

微血管减压术治疗面肌痉挛的临床研究

目的探讨微血管减压术治疗面肌痉挛的临床疗效。方法回顾性分析2004年来79例面肌痉挛患者,行微血管减压术治疗,分析发病原因、术后疗效和并发症。结果面肌痉挛发病原因主要是由于血管压迫面神经出脑干区,产生的机械性搏动刺激所致。术中发现责任血管与小脑前下动脉（AreA）相关占68．4％（54例）,复合血管压迫者占36．7％（29例）,微血管减压术后总有效率为100％。术后并发症常见的有头痛、耳鸣,较严重的有患侧面肌瘫痪、听力下降,多可在6个月后逐渐恢复。结论微血管减压术治疗面肌痉挛的有效率高,并发症少,复发率低,有很好的治疗效果。     

3D-TOF-MRA结合多平面重建在血管压迫性三叉神经痛术前评估中的诊断价值

目的 探究三维时间飞跃法磁共振血管成像(3D-TOF-MRA)结合多平面重建在血管压迫性三叉神经痛术前评估中的诊断价值.方法 选择2015年2月至2016年12月本院收治的血管压迫性三叉神经痛患者194例,均行三叉神微血管加压术(MVD)治疗.所有患者术前均予以3D-TOF-MRA检查结合多平面重建,将其检查结果与MVD术中对神经血管压迫(NVC)的检查结果对比,并分析3D-TOF-MRA术前显示三叉神经责任血管性质与MVD术中判定结果的一致性.结果 3D-TOF-MRA术前结合多平面重建对神经血管压迫的检查结果与MVD术中判定结果比较,差异无统计学意义(P＞0.05);3D-TOF-MRA术前显示三叉神经责任血管性质与MVD术中判定结果具有较高的一致性(K=0.93).结论 3D-TOF-MRA结合多平面重建能清晰显示血管与三叉神经之间的关系,准确评估血管压迫性三叉神经痛患者的责任血管性质和神经血管压迫征象,能为临床制定MVD手术方案提供可靠的参考依据.     

Activation of the central pathway of the baroreceptor reflex,a possible mechanism of the hypotensive action of clonidine

Summary Arterial blood pressure, heart rate and discharges in the preganglionic splanchnic and a postganglionic renal sympathetic nerve were recorded in cats anaesthetized with urethane. Electrical stimulation of the posterior hypothalamus or the fastigial nucleus of the cerebellum elicited an immediate increase in sympathetic nerve activity and a rise in blood pressure and heart rate. The stimulation-induced discharge pattern in the sympathetic nerves was characterized by a strong initial burst followed by a phase of inhibition and a final stabilization of the discharges at a level definitely lower than the initial burst. This pattern was reversibly converted into a constant high amplitude firing during a lowering of the blood pressure by bleeding the cats and irreversibly so after cutting the buffer nerves. These findings indicate that the inhibitory phase of the sympathetic discharge pattern during central stimulation is due to the rise in blood pressure and the ensuing baroreceptor-reflex activation.Clonidine (0.03 and 0.1 mg/kg i.v.) reduced the spontaneous sympathetic nerve activity and lowered blood pressure and heart rate. The sympathetic discharges evoked by central stimulation were partially inhibited by clonidine, an effect which could be overcome by raising the voltage used for central stimulation. Independent of the strength of this stimulation an inhibitory phase in the evoked discharge pattern was not observed after clonidine, even when the low blood pressure due to the drug action was raised by a noradrenaline infusion. After clonidine, the evoked discharge pattern closely resembled that after simultaneous stimulation of both sinus nerves and the hypothalamus or the fastigial nucleus, and it was not altered by additional stimulation of the sinus nerves. These observations have led to the hypothesis that clonidine causes a long-lasting activation within an as yet unidentified part of the central pathway of the depressor baroreceptor reflex. In view of the well-known -adrenoceptor stimulating property of clonidine, and since the central effect of clonidine was antagonized by the -adrenoceptor blocking agent piperoxan, it is likely that the central part of the baroreceptor-reflex pathway is modified by or contains adrenergic neurones.