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

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.

Via-cerebellar-fissures approach for microvascular decompression of trigeminal nerve.

Although the infratentorial superior-lateral cerebellar approach has been traditionally chosen for exposure of the V cranial nerve root in the process of microvascular decompression for treatment of trigeminal neuralgia, those petrosal veins often block this surgical corridor. To detour these petrosal veins, we require a new approach. We provide a via-cerebellar-fissures approach to expose well the trigeminal nerve. With microscopy, cerebrospinal fluid was drained sufficiently to relax the cerebellum. Caudally to petrosal veins, the dissection was started from the cerebellar fissures. With the arachnoid membranes around the petrosal fissure and superior cerebellopontine fissures being opened thoroughly, the root entry zone of V nerve was visualized directly. This new approach was used in 106 patients. Among them, the block veins were encountered in 17 (16.0%). Among the 17 vein-blocked cases, 1 or 2 branches of the veins were finally cut in 2 (1.9%). The postoperative relief rate was 95.3% without complications. This via-cerebellar-fissures approach may access the root entry zone of the V cranial nerve without killing those petrosal veins, which is worth to be recommended and popularized.

Microvascular decompression of trigeminal nerve root for treatment of a patient with hemimasticatory spasm.

Hemimasticatory spasm is a rare disease; with little knowledge of the pathogenesis, it has still been intractable today. We presented a 56-year-old woman with involuntary painful spasm in her left masseter muscle for 11 years. The patient was successfully treated with microvascular decompression surgery. An offending superior cerebellar artery was found to contact with the motor branch of the trigeminal nerve root, which was then removed away and pieces of soft wadding were interposed between the nerve and the vessel to assure the separation. Postoperatively, the symptom totally disappeared and no recurrence was observed during the 7 months' follow-up. The treatment as well as the pathogenesis of the disease was reviewed, and we put forward a new hypothesis.

Treatment of hemimasticatory spasm with microvascular decompression.

Hemimasticatory spasm is a rare disorder characterized by paroxysmal involuntary contraction of the jaw-closing muscles. As the ideology and pathogenesis of the disease are still unclear, there has been no treatment that could give rise to a good outcome so far. Herein, we tried to use surgical management to cure the disease. Six patients with the disease were included in this study. These patients underwent microvascular decompression of the motor fibers of the trigeminal root. After the operation, all faces of the patients felt relaxed at varied degrees, except for 1 patient. Our study showed that microvascular decompression of the trigeminal nerve could lead to a better outcome. However, a control study with a large sample is needed before this technique is widely used.

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

Painful 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.

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.

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

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.

Microvascular decompression on patients with trigeminal neuralgia caused by ectatic vertebrobasilar artery complex: technique notes.

BACKGROUND: Due to its anatomical features, the vertebrobasilar artery complex (VBA) seldom contributes to the neurovascular conflict in patient with trigeminal neuralgia (TN). However, once it offends the trigeminal root, this large artery is really difficult to manipulate during microvascular decompression (MVD) surgery. Therefore, the surgical strategy for such cases needs to be detailed in order to obtain a satisfactory outcome. METHODS: From 2009 through 2011, 475 consecutive TN patients underwent MVDs in our department. Among them, ten were found in which an ipsilateral deviating ectatic vertebrobasilar artery complex (VBA) offended the trigeminal nerve. Those cases were focused on in this study and each operation was analyzed retrospectively. RESULTS: During the operation, the vertebral artery was regarded as the direct culprit in six (60 %) patients, while the basilar artery in four (40 %). As companions, some smaller vessels were also observed to be close to the nerve, including the superior cerebellar artery (SCA) in five, veins in two and anterior inferior cerebellar artery (AICA) in two. The neurovascular conflict was discovered in the cisternal segment of the trigeminal root in eight, while in the root entry zone (REZ) in two. In six out of the ten cases, the affected nerves were demonstrated to be squeezed towards the tentorium by the ectatic VBA. Postoperatively, the symptom of pain totally disappeared immediately in eight (80 %) patients, while it was relieved apparently in two (20 %). During the follow-up period of 3-30 months, no recurrence or complication was found, except for one patient who had numbness of the face. CONCLUSION: With a proper strategy, MVD is probably the most effective therapy for the TN cases caused by ectatic vertebrobasilar artery complex. The substance of the surgery is to withdraw the proximal vertebral artery caudally via a lateroinferior cerebellar approach.

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.