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.
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.
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.
The combination of HFS-TN-GPN is extremely rare and is often associated with a looped VBA and a smaller posterior fossa. However, MVD is still a good choice for treatment. To achieve a safe and effective outcome, dissection of the caudal cranial nerves and proximal transposition of the vertebral artery before decompression of the affected nerve roots are strongly recommended.
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