Xiaosheng Yang

A clinical analysis on microvascular decompression surgery in a series of 3000 cases.

OBJECTIVE Despite the microvascular decompression (MVD) has become a definitive treatment for trigeminal neuralgia (TN) and hemifacial spasm (HFS), not all of the patients have been cured completely so far and this sort of operation is still with risk because of the critical operative area. In order to refine this surgery, we investigated thousands MVDs. METHODS Among 3000 consecutive cases of MVDs have been performed in our department, 2601 were those with typical TN or HFS, who were then enrolled in this investigation. They were retrospectively analyzed with emphasis on the correlation between surgical findings and postoperative outcomes. The differences between TN and HFS cases were compared. The strategy of each surgical process of MVD was addressed. RESULTS Postoperatively, the pain free or spasm cease occurred immediately in 88.3%. The symptoms improved at some degree in 7.2%. The symptoms unimproved at all in 4.5%. Most of those with poor outcome underwent a redo MVD in the following days. Eventually, their symptoms were then improved in 98.7% of the reoperative patients. The majority reason of the failed surgery was that the neurovascular conflict located beyond REZ or the offending veins were missed for TN, while the exact offending artery (arteriole) was missed for HFS as it located far more medially than expected. CONCLUSION A prompt recognition of the conflict site leads to a successful MVD. To facilitate the approach, the craniotomy should be lateral enough to the sigmoid sinus. The whole intracranial nerve root should be examined and veins or arterioles should not be ignored. For TN, all the vessels contacting the nerve should be detached. For HFS, the exposure should be medial enough to the pontomedullary sulcus.

The role of autonomic nervous system in the pathophysiology of hemifacial spasm.

Abstract Objectives: Despite the vascular compression of the seventh cranial nerve has been verified by the microvascular decompression surgery as the cause of hemifacial spasm (HFS), the mechanism of the disease is still unknown. We believe that the autonomic nervous system in adventitia of the offending artery may contribute to the HFS. To prove our hypothesis, we performed an experiment in SD rats. Methods: Moller’s HFS model was adopted and the abnormal muscle response (AMR) wave was electrophysiologically monitored. With randomization, some HFS rats underwent exclusion of the offending artery or removal of the ipsilateral superior cervical ganglion. Some HFS rats with negative AMR following exclusion of the offending artery were dripped with norepinephrine onto the neurovascular conflict site. Results: With exclusion of the offending artery, AMR disappeared in 14 (70%) of the 20 HFS rats, while in three (30%) of the 10 from sham operation group (P<0·05). With ganglionectomy, AMR disappeared in 12 (75%) of the 16 HFS rats, while in two (25%) of the eight from the sham operation group (P<0·05). With norepinephrine drip, AMR reappeared in four (67%) of the six from those offending-artery-excluded HFS rats, while in zero of the six from normal-saline-dripped group (P<0·05). Discussion: The neurotransmitter releasing from the autonomic nervous endings in the worn adventitia of the offending artery may induce an ectopia action potential in those demyelinated facial nerve fibers expanding to the neuromuscular conjunction and trigger an attack of HFS.

Role of arterioles in management of microvascular decompression in patients with hemifacial spasm

Although microvascular decompression (MVD) is accepted as an effective therapy for hemifacial spasm (HFS), some operations fail. While performing MVD, many surgeons focus on the large arteries but ignore the arterioles. Failure to identify involved arterioles may account for unsuccessful MVD. We aimed to refine the MVD surgery and improve post-operative outcomes by proper management of involved arterioles. Clinical data were collected from 69 consecutive patients who underwent MVD. Intraoperative electromyography (EMG) was employed for each MVD. Each operation was reviewed with a focus on the involved arterioles. All patients were followed up for between nine and 12 months. An abnormal muscle response (AMR) wave was identified by EMG in all patients before decompression, but vanished in most patients as soon as the involved arteries were removed from the cranial nerve (CN). However, in nine of 69 patients, the AMR did not immediately disappear. Further dissection and exploration of the entire CN VII identified an arteriole in contact with, or in some patients embedded in, the nerve. Once the arteriole was isolated from the CN, the AMR disappeared. After surgery, spasms ceased in all patients and no recurrence was found up to the one-year follow-up. To achieve a positive post-operative outcome, exploration of the entire CN VII is necessary, with a focus on the small arterioles. AMR can be a good adjuvant to identify the involved arterioles.

The mechanism of hemifacial spasm: a new understanding of the offending artery

Abstract Although neurovascular confliction was believed to be the cause of hemifacial spasm (HFS), the mechanism of the disorder remains unclear to date. Current theories, merely focusing on the facial nerve, have failed to explain the clinical phenomenon of immediate relief following a successful microvascular decompression surgery (MVD). With the experience of thousands of microvascular decompression surgeries and preliminary investigations, we have learned that the offending artery may play a more important role than the effect of merely mechanical compression in the pathogenesis of the disease. We believe that the attrition of neurovascular interface is the essence of the etiology, and the substance of the disease is emersion of ectopic action potentials from the demyelinated facial nerve fibers, which were triggered by the sympathetic endings from the offending artery wall. In this paper, we put forward evidence to support this hypothesis, both logically and theoretically.

Microvascular decompression for hemifacial spasm.

Objective Although microvascular decompression (MVD) has been accepted as effective therapy for hemifacial spasm, failed surgery has been reported frequently. For a sophisticated neurosurgeon, an apparent offending artery is seldom missed. However, it is still an embarrassed situation when the neurovascular conflict site could not be approached. Methods Clinical data were collected from consecutive 211 MVDs in 2010. Intraoperative abnormal muscle response was recorded. Among them, the neurovascular conflict was not finally discovered in 3 patients, whom were then focused on. All patients were followed up for 6 to 15 months. Results In 17 of the 211 MVDs, the cerebellum was hard to be retracted because of adhesions. After careful dissection, a working space was finally created in the cerebellopontine angle. However, there still were 3 cases, whose neurovascular conflict site was unable to be discovered at last because of a branch of an artery embedded in the petrous bone and made the cerebellum unmovable. With navigation of real-time abnormal muscle response, the offending artery was moved away eventually even without exposing the conflict site. Postoperatively, all the patients were completely spasm-free immediately. No recurrence was noticed in the last follow-up period. Conclusions The most important thing for a successful MVD operation is to remove the offending artery off the nerve. However, if the conflict site failed to be approached after endeavors, a successful MVD can still be achieved by relocating the offending artery with the guidance of real-time electromyography even without visualization of the confliction. Abbreviation MVD, microvascular decompression HFS, hemifacial spasm AMR, abnormal muscle response

Analysis of therapeutic effect of microvascular decompression surgery on idiopathic hemifacial spasm.

Objective The objective of this paper is to study the therapeutic effect of microvascular decompression surgery on idiopathic hemifacial spasm with compression on different zones of facial nerve. Methods The clinical data of 348 patients with idiopathic hemifacial spasm treated by microvascular decompression surgery were retrospectively analyzed. Patients were divided into 5 groups according to compression on different zones of facial nerve by offending vessels. Root exit point was compressed in 18 patients (group A), transitional zone of brainstem was compressed in 42 patients (group B), attached segment of brainstem was compressed in 35 patients (group C), distal cisternal portion was compressed in 21 patients (group D), and 2 or more zones were compressed in 232 patients (group E). The therapeutic effect was observed, and outcome of excellent and partial good were regarded as effective. Results Patients were followed up for 0.5 to 2 years. The effective rates were 94.4%, 95.2%, 97.1%, 95.2%, and 93.9% in group A, group B, group C, group D, and group E, respectively.No death occurred during operation,and there were no severe complications such as complete facial paralysis, intracranial hematoma, and hearing loss after operation. Conclusion Microvascular decompression surgery is the first choice for treatment hemifacial spasm.Proper detection of offending vessels and complete decompression may be the key factors to increase the cure rate.

CD151 mediates netrin-1-induced angiogenesis through the Src-FAK-Paxillin pathway.

Crosstalk between the nervous and vascular systems is important during development and in response to injury, and the laminin‐like axonal guidance protein netrin‐1 has been studied for its involvement in angiogenesis and vascular remodelling. In this study, we examined the role of netrin‐1 in angiogenesis and explored the underlying mechanisms. The effect of netrin‐1 on brain tissues and endothelial cells was examined by immunohistochemistry and western blotting in a middle cerebral artery occlusion model and in human umbilical vein endothelial cells. Cell proliferation and cell cycle progression were assessed by the MTT assay and flow cytometry, and the Transwell and tube formation assays were used to examine endothelial cell motility and function. Netrin‐1 up‐regulated CD151 and VEGF concomitant with the activation of focal adhesion kinase (FAK), Src and Paxillin in vitro and in vivo and the induction of cell proliferation, migration and tube formation in vitro. Silencing of CD151 abolished the effects of netrin‐1 on promoting cell migration and tube formation mediated by the activation of FAK/Src signalling. Netrin‐1 promoted angiogenesis in vitro and in vivo by activating the FAK/Src/Paxillin signalling pathway through a mechanism dependent on the expression of the CD151 tetraspanin, suggesting the existence of a netrin‐1/FAK/Src/CD151 signalling axis involved in the modulation of angiogenesis.

Microvascular decompression for the patient with painful tic convulsif after Bell palsy.

AbstractPainful tic convulsif is referred to as the concurrent trigeminal neuralgia and hemifacial spasm. However, painful tic convulsif after ipsilateral Bell palsy has never been reported before. We report a case of a 77-year-old woman with coexistent trigeminal neuralgia and hemifacial spasm who had experienced Bell palsy half a year ago. The patient underwent microvascular decompression. Intraoperatively, the vertebrobasilar artery was found to deviate to the symptomatic side and a severe adhesion was observed in the cerebellopontine angle. Meanwhile, an ectatic anterior inferior cerebellar artery and 2 branches of the superior cerebellar artery were identified to compress the caudal root entry zone (REZ) of the VII nerve and the rostroventral cisternal portion of the V nerve, respectively. Postoperatively, the symptoms of spasm ceased immediately and the pain disappeared within 3 months. In this article, the pathogenesis of the patient’s illness was discussed and it was assumed that the adhesions developed from inflammatory reactions after Bell palsy and the anatomic features of the patient were the factors that generated the disorder. Microvascular decompression surgery is the suggested treatment of the disease, and the dissection should be started from the caudal cranial nerves while performing the operation.

Use of High-Resolution Ultrasonography in Anterior Subcutaneous Transposition of the Ulnar Nerve for Cubital Tunnel Syndrome

OBJECTIVES Cubital tunnel syndrome (CTS) is the most common form of ulnar nerve entrapment. In this study, ultrasonography (US) was used not only for diagnosis but also for operation. US findings could be used to establish the diagnosis of CTS and could demonstrate the pathological anatomy in the cubital tunnel region to guide anterior subcutaneous transposition of the ulnar nerve. METHODS Sixty-two patients with clinical and electrophysiological evidence of ulnar nerve entrapment were included. All patients received ultrasonographic examination and anterior subcutaneous transposition of the ulnar nerve. The maximal diameter of the ulnar nerve (MDU) was measured in longitudinal views and the range of the hypoechoic area around the nerve was observed. The cross-sectional area (CSA) was also measured on transverse scans. The actual MDU was measured during operation. RESULTS The actual MDU was 6.4 ± 0.4 mm, measured during operation. The preoperative MDU was 3.1 ± 0.2 mm. The MDU values recorded in CTS patients were greater than those in normal subjects. The range of the hypoechoic area observed on longitudinal US scans was 2.9-5.6 mm (mean, 4.1 ± 0.4 mm). CONCLUSIONS High-resolution US can be used not only in the diagnosis of CTS, also for providing effective preoperative evaluation for the anterior subcutaneous transposition of the ulnar nerve in CTS.