颅内显微血管减压术的技术改进及临床应用

目的 改进颅内显微血管减压术的材料和技术方法，提高治愈率。方法 用改进的材料、技术方法治疗三叉神经痛21例，面肌痉挛8例，舌咽神经痛1例；被减压神经的全段暴露；用Teflon片包绕神经根起始部25例、包绕血管5例，钻夹固定。结果 术后所有病例均治愈，未出现手术并发症，随访3个月-2年以上，无复发。结论 经技术材料改进的颅内显微神经血管减压术操作安全，手术并发症轻微，术后神经功能良好，效果优于传统的显微神经血管减压术。     

显微外科神经血管减压术治疗原发性三叉神经痛

报告４０６例原发性三叉神经痛经乙状窦后进路显微外科神经血管减压术治疗的手术方法。随访１－７年以上，有效率９７．８％，治愈率９６．８％，复发率４．６％。讨论了原发性三叉神经痛的病因、显微外科神经血管减压术的优点及对原发性三叉神经痛的疗效评估。     

显微血管减压术治疗舌咽神经痛

自1990年2月以来采用乙状窦后入路显微神经血管减压术治疗35例舌咽神经痛。术后治愈35例,其中1例于术后1个月经第2次手术治愈。作者认为舌咽神经痛的病因主要为血管压迫神经根。舌咽神经根显微神经血管减压术,是一种解除病因的治疗方法,治愈率高,复发率低,保留了神经功能...     

微血管减压术治疗面肌痉挛的远期效果

目的：探讨微血管减压术治疗面肌痉挛1年以上的远期疗效。方法：对1987年7月至1999年6月间329例患者的临床资料及随访结果进行回顾性分析。结果：本组患者随访1－3年97例，痉挛完全缓解92．7％，明显缓解3．1％，部分缓解2．1％，无改变2．1％；3－5年77例，完全缓解92．2％，明显缓解3．9％，部分缓解1．3％，无改变占2．6％；5－10年121例，完全缓解90．9％，明显缓解4．1％，部分缓解2．5％，无改变2．5％；10年以上34例，痉挛综合缓解91．2％，明显缓解5．9％，无改变2．95。329例中主观满意度≥80％者占82．1％，痉挛复发率5．2％，并发症发生率5．5％，。结论：采用微血管减压术治疗面肌痉挛，尽量减少对脑神经及血管损伤，不遗漏面神经根附近的责任血管，是提高远期疗效养活并发症的重要环节。     

3D-TOF-MRA 在原发性三叉神经痛微血管减压术中的应用

目的：探讨磁共振成像技术在原发性三叉神经痛微血管减压术前诊断中的应用价值。方法38例原发性三叉神经痛患者经过三维时间飞跃法磁共振血管成像序列（3D-TOF-MRA）检查。结果38例患者中术前序列图像上显示血管神经压迫症状侧阳性率89．5％（34／38）,非症状侧阳性率15．8％（6／38）,两侧阳性率差异有统计学意义（P ＜0．05）;手术中见周围血管压迫神经者36例（94．7％）,未压迫神经者2例（5．3％）,3D-TOF-MRA 诊断符合率97．1％（33／34）,术后症状消失或缓解37例（97．4％）。结论3D-TOF-MRA 可清楚地显示三叉神经与责任血管的关系,在原发性三叉神经痛微血管减压术术前诊断及术中显微定位中具有较高的临床应用价值。     

单开门并神经根管扩大术治疗脊髓型颈椎病

目的：探讨应用单开门并神经根管扩大术治疗多节段脊髓型颈椎病的手术方法与效果。方法：采用后路单开门椎管扩大成形与神经根管扩大术治疗多节段脊髓型颈椎病27例。结果：全组经3-75个月，平均26个月的随访。疗效按（JOA）17分评分标准评定：优（术后改善率＞75％）16例，良（50％-74％）6例，中（25％-49％）4例，差（≤24％）1例，平均优良率81.4％。结论：后路单开门椎管扩大成形与神经根管扩大术，在脊髓得到充分减压的同时也解除了神经根的压迫，可以提高椎管扩大成形术的手术疗效。     

脑神经血管压迫综合征的诊断与治疗

目的 探讨脑神经血管压迫综合征的术前病因诊断、手术疗效评估及术中处理要点。方法 对连续收治的45例非脑内占位引起的脑神经血管压迫综合征病例进行回顾性分析，术前采用三维稳态毁损梯度回返采集序列（3D-SPGR）序列扫描确立病因，总结脑神经血管压迫综合征的诊断依据、影像学特点、治疗方法和疗效评估。结果 45例均行改良微血管减压术（MVD），其中30例术前行3D-SPGR，显示病变侧神经与血管有接触关系25例，阳性率为83．3％。术前3D-SPGR阳性（25例）、术中处理责任血管后的手术有效率达100％，45例总有效率为86．7％。结论 3D-SPGR对脑神经血管压迫综合征患者的术前病因诊断及手术适应证选择有很大的指导作用，改良显微血管减压手术对3D—SPGR阳性的病例可以起到很好的治疗效果。     

神经内镜辅助锁孔入路微血管减压术治疗面肌痉挛34例分析

目的 针对原发性面肌痉挛的发病原因,结合神经内镜技术及锁孔技术探讨神经内镜辅助锁孔入路下微血管减压术在原发性面肌痉挛治疗中的疗效. 方法 对自2008年6月至2010年6月间收治并经神经内镜辅助锁孔入路微血管减压术治疗的34例原发性面肌痉挛患者的临床资料、影像学资料及手术资料进行总结分析. 结果 总计39条责任血管中,动脉接触25条,动脉压迫6条,静脉接触与压迫8条.2条责任血管者9例(26.5％),小脑前下动脉压迫16例,小脑后下动脉压迫10例,椎动脉压迫3例,基底动脉压迫2例,静脉压迫者8例.32例患者随访2年,2例失访,术后20例(58.8％)抽搐症状立即消失,术后1个月内抽搐逐渐停止者10例(29.4％),1例术后1年左右抽搐才逐渐停止(2.9％),1例患者随访2年仍有间断抽搐发作需继续服用药物,1例有轻度同侧听力下降,其他患者症状均有效控制,无复发. 结论 神经内镜辅助锁孔入路微血管减压术是治疗面肌痉挛非常有效的方法,术中应用微创的理念结合神经内镜的优势仔细辨别相关的责任血管,对面神经根部和远端进行全程探查和有效减压,是直接影响术后临床效果的关键.     

腰骶神经根畸形的诊断和治疗

目的：通过对11例腰骶神经根畸形患的临床报道。探讨了腰骶神经根畸形的发生率，形态学分型，发病机理，影像学诊断和手术方法。方法：在978例腰椎手术中发现11例腰骶神经根畸形患，4例术前行椎管造影，确诊3例。1例术前行冠状面MRI怀疑神经根畸形。均行全椎板或半椎板切除，上，下关节突切除。根管前彻底减压，并行椎板或横突间植骨融合。结果；全部病例术后随访0．5－8年，平均4．1年，优良率达81．8％。结论：（1）腰骶神经根畸形具有较高的发生率，多发生于L5，S1神经根，（2）腰骶神经根畸形本身并不引起症状；（3）椎管造影和冠状面MRI有助于术前获得确诊；（4）提出术中必须仔细探查神经根，充分显露，彻底减压，并行植骨融合。     

双神经卡压综合征

目的：研究双神经卡压征的病因及手术治疗方法。方法：分析了自１９８８年以来同时诊断为腕管综合征和肘管综合征２６例３４侧的临床资料。全部患者均作两处神经松解术，平均随访１７个月。疗效评定标准，根据术后症状、体征的改善程度分优、良、可和无效四级。结果：２５侧术后疗效优良，占７３．６％（２５／３４）。结论：双神经卡压征手术治疗效果较好。当双神经卡压同时合并颈部神经卡压时，建议优先考虑远端的神经减压。当远端神经减压后未能改善近端神经卡压症状时，才考虑近端神经减压     

Hemifacial spasm due to vascular compression of the distal portion of root exit zone of the facial nerve: report of two cases

It has been generally assumed that only vascular contact at the root exit zone (REZ) of the facial nerve can cause hemifacial spasm. We treated two cases of hemifacial spasm in which compression of the distal site of the REZ of the facial nerve produced symptoms. The microvascular decompression for the patients showed excellent results. Extreme care must be taken not to stretch the internal auditory artery during surgical manipulation. The ABR monitoring is useful to prevent the postoperative hearing loss. It must be kept in mind that the compression of distal portions of the facial nerve may be responsible for hemifacial spasm in cases in which neurovascular compression at the REZ is not confirmed intraoperatively.     

Neurovascular decompression for hemifacial spasm]

Thirty-six cases of hemifacial spasm were treated by neurovascular decompression. Via transposterior cranial fossa approach, a small incision was made behind the ear. After careful dissection, a piece of teflon was placed between the vessel and initial segment of the facial nerve root and fixed with silver clip after wrapping of the nerve root. The cases were free from tic immediately after operation. Follow-up of 34 cases for 1 month to 3.5 years showed no recurrence and less and mild operative complications. In this series physiological function of the facial nerve was kept well and there was no mortality. This operation is regarded as the first choice in the treatment of hemifacial spasm.     

Role of postoperative magnetic resonance imaging after microvascular decompression of the facial nerve for the treatment of hemifacial spasm

OBJECTIVE: This study was performed to investigate the role of postoperative three-dimensional short-range magnetic resonance angiography in the prediction of clinical outcomes after microvascular decompression (MVD) for the treatment of hemifacial spasm. METHODS: We examined pre- and postoperative magnetic resonance imaging scans obtained between March 1999 and May 2000 for 122 patients with hemifacial spasm, to evaluate the degree of detachment of the vascular contact and changes in the positions of offending vessels. The degree of vascular decompression of the facial nerve root was classified into three groups, i.e., contact, partial decompression, or complete decompression. Contact was defined as unresolved compression, as indicated by postoperative three-dimensional short-range magnetic resonance angiography. Partial decompression was defined as incompletely resolved compression; vascular indentation of the facial nerve was improved, but contact with the facial nerve remained. Complete decompression was defined as completely resolved compression. These findings were compared with the surgical findings and clinical outcomes. RESULTS: Of 122 patients with MVD, complete decompression of offending vessels at the root entry zone of the facial nerve was observed for 106 patients (86.9%), partial decompression was observed for 10 patients (8.2%), and contact with offending vessels was observed for 6 patients (4.9%) by using postoperative three-dimensional short-range magnetic resonance angiography. Our study demonstrated that the types of offending vessels affected neither the degree of decompression of the root entry zone of the facial nerve nor surgical outcomes (P > 0.05). Also, there was no significant relationship between the degree of decompression and improvement of symptoms (P > 0.05). Furthermore, there was no significant relationship between the degree of decompression and the timing of symptomatic improvement (P > 0.05). CONCLUSION: Our data suggest that MVD of the facial nerve alone may not be sufficient to resolve symptoms for all patients with hemifacial spasm. Therefore, unknown factors in addition to vascular compression may cause symptoms in certain cases, and it may be necessary to remove those factors, simultaneously with MVD, to obtain symptom resolution.     

Intraoperative monitoring of facial EMG responses during microvascular decompression for hemifacial spasm. Prognostic value for long-term outcome: a study in a 33-patient series

Lateral spread responses (LSR), an electrophysiological characteristic of hemifacial spasm (HFS), can be recorded during surgery. This work aims at evaluating the prognostic value of the persistence or suppression of the LSR at the end of the microvascular decompression (MVD) procedure of the facial nerve. Thirty-three patients with HFS, which had been evolving for 5.5 years, underwent MVD with intraoperative EMG. Monitoring required the placement of a needle in the frontalis and mentalis muscles. Responses were recorded after stimulation of inferior or superior branches of the facial nerve to search for abnormal ephaptic LSR. Preoperative abnormal LSRs were present in all patients. In 23 patients, LSR disappeared with vascular decompression and was not present upon closure. Among those patients, 20 were considered clinically cured and three still presented with mild/moderate spasm at 3-month follow-up. At late follow-up, 22 patients were free of spasm. One patient had recurrence of spasm at month 10. On the contrary, 10 patients had persistent abnormal LSR upon closure. Among those, seven were cured at early follow-up (3 months on average), whereas spasm disappeared at late follow-up (12 to 36 months) in the other three patients. The prognostic value of LSR monitoring is questionable; a good clinical result may be obtained in patients who presented with persistent LSR at the end of MVD. Delayed cure strongly supports the hypothesis that HFS is not only due to the mechanical pulsations of the elongated artery against the root exit zone of the facial nerve, but also to demyelination of the nerve and/or hyperactivity of the facial motornucleus generated by the neurovascular compression.     

Arteries in contact with the cisternal portion of the facial nerve in autopsy cases: microsurgical anatomy for neurovascular decompression surgery of hemifacial spasm

The cisternal portion of the facial nerve and its contact arteries were examined anatomically in relation to neurovascular decompression surgery to treat hemifacial spasm. Thirty-five sides of brains from 20 autopsied adult patients were examined under a surgical microscope (x 5-x 25). One attaching point was found on 10 facial nerves, two points on 20 nerves, and three points on four nerves. More than two thirds of the facial nerves were attached at two points: the root exit zone and the distal cisternal portion. In a case of distal attachment, the contact artery formed an arterial-nerve complex with the distal portions of the facial and acoustic nerves. The arterial attachment at the root exit zone was evident on 24 of the 35 facial nerves (69%), and most of the contact arteries were the anterior inferior cerebellar artery and its branches. In five nerves, the root exit zone was attached at two points to arteries. The anatomy of autopsied brains without hemifacial spasm is not identical to that of actual clinical cases of hemifacial spasm; nevertheless, the results do aid in intraoperative anatomical orientations.     

A case of hemifacial spasm in a juglar foramen tumor patient treated by microvascular decompression

Hemifacial spasm is a movement disorder characterized by involuntary paroxysmal chronic contractions of the facial musculature. The usual cause is simple vascular compression of the facial nerve, at its root exit zone of the brain stem. Previously only a case of hemifacial spasm associated with a juglar foramen tumor has been reported in the literature. In this article, we report a case in which hemifacial spasm accompanied an ipsilateral juglar foramen tumor in a 62-year-old woman. The sole use of arterial decompression of the facial nerve at the root exit zone resulted in complete resolution of the patient's symptoms.     

Hemifacial spasm caused by a tortuous recurrent perforating artery: A case report

IntroductionWhen the culprit vessel in hemifacial spasm (HFS) is hard to determine, this is a challenge in microvascular decompression (MVD) surgery. In such a situation, small arteries such as perforators to the brainstem might be suspected. But small arteries are omnipresent near the facial nerve root exit/entry zone (fREZ). How to decide whether a given small artery is responsible for HFS is unclear.MethodWe report a case with a previously unreported form of neurovascular impingement, in which the culprit was found to be the recurrent perforating artery (RPA) from the anterior inferior cerebellar artery (AICA). An aberrant anatomic configuration of the RPA was found intraoperatively, which we thought was responsible for generating focal pressure on the facial nerve.Case reportA 62-year-old woman presented with a 1-year history of paroxysmal but increasingly frequent twitching in her right face. MRI showed tortuosity of the vertebral artery and apparently marked neurovascular impingement on the asymptomatic left side, while only the right AICA could be implicated as the possible culprit. Hemifacial spasm was diagnosed based on the typical clinical manifestation, and MVD was performed. The pre-meatal segment of the AICA was found not to be impinging the facial nerve at any susceptible portion near the fREZ: root exit point, attached segment, or root detachment point. The real culprit was in fact the RPA. This occult culprit vessel was tortuous, forming a coil-shaped twist which was interposed between the facial nerve and the intermediate nerve near the root detachment point. Focal pressure atrophy of the nerve was clearly observed at the compressing site. The patient achieved total spasm relief immediately after surgery, and remained spasm-free at 1-year follow-up, without any postoperative complications.ConclusionMVD is the only curative treatment for hemifacial spasm, but with a failure rate of around 10%. Mistaking the real culprit has been reported to be the most likely reason for surgical failure. Therefore, intraoperative identification of atypical occult forms of vascular compression is of importance to improve surgical outcome. In the present case, the RPA formed a coil-shaped twist, which inflicted focal vascular compression causing hemifacial spasm. We recommend careful inspection of the recurrent perforating artery during MVD for HFS, and decompressing any such neurovascular impingement.     

Traitement neurochirurgical du spasme hémifacial primaire par décompression vasculaire microchirurgicale

In nearly all cases, primary hemifacial spasm is related to arterial compression of the facial nerve in the root exit zone at the brainstem. The offending arterial loops originate from the posterior inferior cerebellar, anterior inferior cerebellar, or vertebrobasilar artery. In as many as 40% of the patients, neurovascular conflicts are multiple. The cross-compression at the brainstem is almost always seen on magnetic resonance imaging combined with magnetic resonance angiography. Botulinum toxin can be useful by alleviating the symptoms, but the effects are inconstant and only transient. The definitive conservative treatment is microvascular decompression (MVD), which cures the disease in 85 to 95% of patients. In expert hands, the MVD procedure can be done with relatively low morbidity. Because cure of spasms is frequently delayed - by several months to even a few years -, we do not recommend early reoperation in patients with failure or until at least 1 year of follow-up. Delayed cure could well be explained by the slow reversal of the plastic changes in the facial nucleus that may have caused the symptoms.     

Hemifacial spasm due to tumor, aneurysm, or arteriovenous malformation.

The authors report eight cases of so-called symptomatic hemifacial spasm. They had gross pathological lesions such as a tumor (one epidermoid, one neurinoma, and two meningiomas), vascular malformation (one medullary venous malformation and two arteriovenous malformations), and aneurysm. In all four cases with a tumor, no artery compressed the facial nerve at the root exit zone. In three of the four cases, the hemifacial spasm disappeared after removal of the tumor in contact with the facial nerve. Compression or encasement of the facial nerve by the tumor was the pathogenesis of the hemifacial spasm in these three cases. The remaining case with tumor (tentorial meningioma) did not have a mass or vessel that directly compressed the facial nerve at the root exit zone. However, the hemifacial spasm disappeared after the removal of the tumor. In a case with a medullary venous malformation with arterial component, an engorged draining vein compressed the root exit zone of the facial nerve. In the remaining three vascular cases--two cases of arteriovenous malformation and a case of saccular aneurysm--enlarged feeding arteries and an aneurysm directly compressed the root exit zone of the facial nerve. Not only arterial or venous but also mass compression can cause hemifacial spasm in some symptomatic cases. Surgical decompression of the facial nerve from the causative organic lesion is the primary choice of treatment.