Yong-Nan Wang

Microvascular decompression surgery: surgical principles and technical nuances based on 4000 cases

Abstract Background: As an etiological treatment of trigeminal neuralgia (TN) and hemifacial spasm (HFS), microvascular decompression (MVD) has been popularized around the world. However, as a functional operation in the cerebellopontine angle (CPA), this process can be risky and the postoperative outcomes might not be good enough sometimes. Objective: In order to obtain a better result with less complication, this surgery should be further addressed. Methods: With experience of more than 4000 MVDs, we have gained knowledge about the operative technique. Through abundant intraoperative photos, each step of the procedure was demonstrated in detail and the surgical strategy was focused. Results: The principle of MVD is to separate the nerve-vessel confliction rather than isolate it with prostheses. A prompt identification of the conflict site is important, which hinges on a good exposure. A satisfactory working space can be established by an appropriate positioning of the patients head and a proper craniectomy as well as a rational approach. A sharp dissection of arachnoids leads to a maximal visualization of the entire intracranial course of the nerve root. All the vessels contacting the trigeminal or facial nerve should be treated. Intraoperative electrophysiological mentoring is helpful to distinguish the offending artery for hemifacial cases. Conclusion: MVD is an effective treatment for the patient with TN or HFS. Immediate relief can be achieved by an experienced neurosurgeon with good knowledge of regional anatomy. A safe surgery is the tenet of MVD, and accordingly, no single step of the procedure should be ignored.

Effectiveness and safety of microvascular decompression surgery for treatment of trigeminal neuralgia: a systematic review.

Abstract Microvascular decompression has been now accepted worldwide as a reasonable treatment for trigeminal neuralgia, yet, as a functional operation in the cerebellopontine angle, this process may be risky and the postoperative outcomes might not be good enough sometimes. To assess the effectiveness and safety of microvascular decompression for treatment of trigeminal neuralgia, we conducted a systematic review. Using the keywords “trigeminal neuralgia”, “microvascular decompression”, or “neurovascular conflict”, manuscripts published in English-language journals and indexed in PubMed between January 1, 2000 and June 1, 2013 on the treatment of trigeminal neuralgia (TN) with microvascular decompression were considered for this study. The success and complications were analyzed. The success in this investigation was defined as complete pain free. Continuous outcomes were summarized using means or medians, and dichotomous outcomes were presented as percentage associated with 95% confidence interval. Twenty-six papers with 6,847 patients were finally enrolled in this review. Among them, the male-to-female ratio was 1:1.4, the left-to-right ratio was 1:1.6, and the pain was located in the innervation of V3 and/or V2 in most of the cases with only 2.3% (0.1–4.7) of V1 exclusively. The average age at surgery was 60.9 years (52.5–64.1) with TN symptoms duration of 24.7 months (6.1–42.1) before microvascular decompression (MVD). Operative findings confirmed the superior cerebellar artery, anterior inferior cerebellar artery, posterior inferior cerebellar artery, and multiple vascular contacts (including veins) as the most common sources of nerve compression. The average follow-up duration was 35.8 months (26.2–56.6). The success rate was 83.5% (79.6–89.1). Complications included incisional infection in 1.3% (0.1–2.5), facial palsy 2.9% (0.5–6.2), facial numbness 9.1% (1.3–19.6), cerebrospinal fluid leak 1.6% (0.7–2.5), and hearing deficit 1.9% (0.2–3.9). The postoperative mortality was 0.1% (0.02–0.2). Accordingly, MVD is the most effective treatment for patients with trigeminal neuralgia. An immediate pain free can be achieved by an experienced neurosurgeon with good knowledge of the regional anatomy. To avoid complications, each single step of the process cannot be overemphasized.

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.

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.

Treatment of Hemimasticatory Spasm With Microvascular Decompression

Abstract 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.

Upregulation of Nav1.8 in Demyelinated Facial Nerves Might be Relevant to the Generation of Hemifacial Spasm

Abstract Our previous studies demonstrated that the abnormal muscle response could vanish when the ipsilateral superior cervical ganglion was removed and reappear when norepinephrine was dripped at the neurovascular conflict site. Evidentially, we believed that the mechanism of hemifacial spasm should involve emersion of ectopical action potential in the compressed facial nerve fibers. As the action potential is ignited by ion channel opening, we focused on Nav1.8 that has been found overexpressed in peripheral nerve while damaged. In this study, Moller model was adopted, 20 Sprague-Dawley rats underwent drip of norepinephrine, and the abnormal muscle response wave was monitored in 14 rats. Antibodies against unique epitopes of the &agr; subunit of sodium channel isoforms were used to detect the Nav1.8 neuronal isoforms, and the immunohistochemistry showed strong staining in 13 rats, which were all in the abnormal muscle response positive group (P < 0.05). Accordingly, we concluded that the substance of hemifacial spasm is an ectopic action potential that emerged on the damaged facial nerve, which might be coupled by Nav1.8.

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

Abstract 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.

AbstractHemimasticatory 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.

Cholesteatoma of cerebellopontine angle presented as trigeminal neuralgia.

Abstract Cholesteatoma in the cerebellopontine angle presented as trigeminal neuralgia are not common. Between 2010 and 2013, 12 such patients were operated on in our department. Those patients included 8 females and 4 males with an average age of 47.8 years. One patient was combined with the ipsilateral hemifacial spasm. Five patients had hypesthesia in the ipsilateral side of the face. During the surgery, a pearly sheen mass with boundary was found in the cerebellopontine angle, and the trigeminal root was buried in the tumor. The tumor was removed totally in all the cases. Afterwards, the trigeminal root was observed distorted in 5 and the offending vessel was finally distinguished in 9. Postoperatively, the symptoms were relieved in all the cases and no recurrence was found up to the 36-month period of follow-up. We believed that the etiology of secondary trigeminal neuralgia caused by cholesteatoma is still the neurovascular confliction; the only difference is that the offending vessel was pushed by the tumor instead of idiopathically. Sometimes, the offending artery may not be found after the tumor resection for it may have been transposed off while the tumor is being removed.