Trigeminal Neuralgia - MVD

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Microvascular Decompression for Trigeminal Neuralgia

Microvascular decompression (MVD) is a neurosurgical procedure whose goal is the separation of the trigeminal nerve from an adjacent artery (typically the superior cerebellar artery) near the brainstem. The procedure is predicated on the presence of a compression of the nerve by the artery causing injury to the nerve fibers and abnormal transmission of impulses in the nerve related to this compression. Described by Walter Dandy and popularized by Peter Jannetta, MVD has proven to be extremely effective in alleviating TN pain for long periods of time. It is considered by many as the definitive therapy for TN. However, its results in cases where no compression is seen are considerably less favorable. In addition, MVD represents a relatively invasive procedure for TN, and entails a small likelihood (<1%) of mortality. The decision to proceed with MVD should therefore be carefully examined with respect to age, risk factors, expectations, and disease severity.

Operative Technique

After induction of general anesthesia, the patient may be positioned in the prone, lateral decubitus, sitting, or supine position depending on the surgeon’s preference. Brainstem auditory-evoked potentials and facial nerve monitoring are typically utilized. A retromastoid suboccipital craniectomy is then performed, and the cerebellopontine angle is explored (Figures 1, 2, 3). Complete decompression of the trigeminal nerve is achieved with Teflon®, Ivalon®, autologous tissue, or tentorial sling.

Figure 1

Surgical approach

Figure 2

Vessel loop compressing the nerve

Figure 3

Microsurgical view

Outcomes after MVD

The majority of the scientific literature regarding MVD is based on large retrospective analyses from select institutions. While these speak to the efficacy of MVD as a legitimate treatment modality for TN, they are subject to both recall and referral bias. The largest contemporary series published is Jannetta’s cohort from the University of Pittsburgh (1). These investigators followed 1,185 patients over a median of 6.2 years after MVD for TN. Eighty-two percent of patients reported an initial complete response rate, with 16% having partial response. At 10 years, 70% of patients were completely pain-free and off medication. Another 4% suffered from occasional facial pain. The vast majority of patients who failed MVD did so within the first 2 years postoperatively. Beyond five years post-op, the rate of recurrence was 1%/year. For patients who underwent a second MVD (N=132), 47% had good or excellent results at 10 years follow-up. Lack of immediate postoperative relief (Hazard Ratio [HR] = 2.8, P<.001), female gender (HR=1.3, P=.006), and duration of preoperative symptoms greater than 8 years (HR=1.3, P=.03), were found to be independent risk factors for recurrence after MVD.

The postoperative complication rates observed by Jannetta’s group were low. The overall mortality was 0.2%. Chemical meningitis, defined as a self-limited, non-infectious meningismus, was observed in 17% of the cohort. Other complications including facial numbness (1.6%), cerebrospinal fluid (CSF) leak (1.5%), anacusis (1.1%), transient trochlear nerve palsy (0.8%), and transient facial weakness (0.7%), were less common.

Theodosopoulos and colleagues reported their series and observed similar results as the Pittsburgh group (2). Immediate relief of pain was seen in 98% of their 420 patients. Complete resolution of symptoms was observed in 87%. At a 57-month mean follow-up, 76% of patients reported no symptoms. Predictors of recurrence included female gender (HR=3.9, P=.02), age less than 53 years (HR=2.8, P<.001), and duration of symptoms greater than 11 years (HR=2.8, P=.04). In this series, there was no perioperative mortality. Aseptic meningitis was reported in 8.3% of patients. Nearly 6% of patients suffered a major medical complication such as pneumonia, pulmonary embolism, deep venous thrombosis, or myocardial infarction. The long-term sequelae of complications were not reported. Other complications included eighth cranial nerve dysfunction (3.1%), CSF leak (1.9%), and infection (1.2%).


1. Barker, F.G., 2nd, et al., The long-term outcome of microvascular decompression for trigeminal neuralgia. N Engl J Med, 1996. 334(17): p. 1077-83.

2. Theodosopoulos, P.V., et al., Predictive model for pain recurrence after posterior fossa surgery for trigeminal neuralgia. Arch Neurol, 2002. 59(8): p. 1297-302.

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