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Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience
Accepted Manuscript Title: Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience Author: Patrick W. Hitchon Mario Zanaty Toshio Moritani Ergun Uc Connie L. Pieper Wenzhuan He Jennifer Noeller PII: DOI: Reference:
S0303-8467(15)30043-3 http://dx.doi.org/doi:10.1016/j.clineuro.2015.10.012 CLINEU 4207
To appear in:
Clinical Neurology and Neurosurgery
Received date: Accepted date:
30-9-2015 9-10-2015
Please cite this article as: Hitchon PW, Zanaty M, Moritani T, Uc E, Pieper CL, He W, Noeller J, Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience, Clinical Neurology and Neurosurgery (2015), http://dx.doi.org/10.1016/j.clineuro.2015.10.012 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience.
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Patrick W. Hitchon MDa, Mario Zanaty MDa, Toshio Moritani MDb,
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Ergun Uc MD,c Connie L. Pieper MDc, Wenzhuan He MDd, Jennifer Noeller, ARNPa
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Department of Neurosurgery, University of Iowa Carver College of Medicine, Iowa City, IA Department of Radiology, University of Iowa Carver College of Medicine, Iowa City, IA
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Department of Neurology and Neurosciences, Rutgers-New Jersey Medical School, Newark, NJ
Corresponding author:
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Patrick W. Hitchon MD
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Department of Neurology, University of Iowa Carver College of Medicine, Iowa City, IA
Department of Neurosurgery
University of Iowa Hospitals and Clinics 200 Hawkins Dr, 1826 JPP Iowa City, IA 52242 USA Phone: +1 319-356-2775 Fax: +1 319-353-6605
Email: [email protected]
Disclosures: No funds were received for the preparation of this manuscript.
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Abstract Objective: For patients with medically unresponsive trigeminal neuralgia (TIC) and hemifacial
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spasm (HS), surgical microvascular decompression (MVD) is the procedure of choice. The authors of this report sought to review their outcomes with MVD in patients with TIC and HS,
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and the success of preoperative magnetic resonance imaging (MRI) in identifying the offending
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vascular compression.
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Methods: Since 2004, there were a total of 51 patients with TIC and 12 with HS with available MRI scans. All patients underwent preoperative MRI to rule out non-surgical etiologies for facial
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pain and facial spasm, and confirm vascular compression. Follow-up after surgery was 13±22
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months for the patients with TIC and 33±27 months for the patients with HS.
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Results: There were 45 responders to MVD in the TIC cohort (88%), with a Visual Analog Score (VAS) of 1±3. All patients with HS responded to MVD between 25-100%, with a mean of 75±22%. Wound complications occurred in 10% of patients with MVD for TIC, and 1 patient reported hearing loss after MVD for HS, documented by audiogram. The congruence rate between the preoperative MRI and operative findings of vascular compression was 84% in TIC and 75% in HS.
Conclusion: MVD is an effective and safe modality of treatment for TIC and HS. In addition to ruling out structural lesions, MRI can offer additional information by highlighting vascular loops associated with compressions. On conventional scans as obtained here, the resolution of MRI
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was congruent with operative findings in 84% in TIC and 75% in HS. This review emphasizes that the decision to undertake MVD in TIC or HS should be based on clinical diagnosis and not visualization of a compressing vessel by MRI. Conversely, the presence of a compressing vessel
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by MRI demands perseverance by the surgeon until the nerve is decompressed.
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Key Words: hemifacial spasm; microvascular decompression; trigeminal neuralgia
Acknowledgements: The authors wish to acknowledge the invaluable assistance provided by
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Faith Vaughn in editing and preparation of this manuscript.
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Introduction Trigeminal neuralgia (TIC) and hemifacial spasm (HS) have an incidence rate of approximately 4 and 1 per 100,000 population respectively.[1,2] Fortunately, for about 75% of patients who
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suffer TIC, the frequent lancinating pain that they suffer can be controlled with medications such as carbamazepine, oxcarbazepine, lamotrigine, or baclofen, to mention the most commonly used.
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The response to medical management is estimated at 80% initially, which declines to less than
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50% over time. When medical management is no longer effective, and the side effects from the medication overwhelming, microvascular decompression (MVD) is the most attractive option.[3-
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5] MVD is nonablative, not associated with facial numbness, and least likely to require a secondary procedure.[6,7] For those with HS, symptomatic and temporary relief can be achieved
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with botulinum toxin injection. However, this still results in a large proportion of people who continue to experience symptoms and wish to avoid repetitive facial injections. For this group of
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patients, surgical options for their disease are available and often sought. For TIC and HS, MVD
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is the procedure of choice and not associated with the numbness that can result from focused radiation or radiofrequency rhizotomy.
The authors of this report sought to review their outcomes with MVD in patients with TIC and HS, and the success of preoperative MRI in identifying the offending vascular compression of the V or VII cranial nerves.
Materials and Methods Since 2000, a total of 201 cases of TIC have been treated at our center. Thirty-five were treated with radiofrequency rhizotomy, 80 with MVD, and 86 with stereotactic focused radiation. Since
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2008, 12 patients with HS have been treated with MVD. All cases of neurovascular decompression for TIC and HS since 2004 with available MRI scans were reviewed. There were a total of 51 patients with TIC and 12 with HS. Patients without risk factors who did not wish to
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contend with facial numbness that can result from radiofrequency rhizotomy or focused radiation and were good surgical candidates underwent MVD by choice. MRI studies were obtained in all
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patients to rule out a mass lesion or demyelinating disease and to assess neurovascular anatomy.
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A high-resolution, heavily T2-weighted 3D-sequence on a 1.5 or 3T scanner was obtained. A high CSF-tissue contrast with 3D constructive interference in steady state (CISS) or its
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equivalent, 3D fast imaging employing steady-state acquisition (FIESTA), provided best resolution. (Fig. 1A and 1B) Once a mass lesion or demyelination had been ruled out, MVD was
Surgical Technique
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performed.
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This is performed in the decubitus position with facial nerve monitoring and intraoperative osmotic diuresis. The head is affixed flexed in a 3-point Mayfield head fixator with the sagittal sinus horizontal and with a fingerbreadth space between the chin and the clavicle. The torso is held in the decubitus position using 3-inch adhesive tape with an axillary roll in place. (Fig. 2A) A 3-inch-long curvilinear incision is made 15 mm medial to the mastoid process and centered on the superior nuchal line, or a line extending from the zygomatic arch to the inion. A 1-inch oval free bone flap is rotated using a 3-mm matchstick burr.[3,5] (Fig. 2B) The position of the transverse sinus is confirmed with intraoperative ultrasound. A “V”-shaped dural flap, 1 cm at its base, is rotated on the transverse sinus. The cerebellum is retracted in a downward direction with a ¼-inch self-retaining retractor. Laterally, the petrosal vein is coagulated and transected. Failing
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to secure this vein early can prove a nuisance. Ventral to the petrosal vein, the trigeminal nerve is identified and dissected free of the arachnoid. It is helpful to retain some arachnoidal bands around the trigeminal nerve to help hold the Teflon sponges in place. Medially the IV cranial
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nerve and laterally the VII-VIII complex are identified and kept covered with arachnoid for protection. Three to seven Teflon felt (Medline Industries, Mundelein, IL) sponges (1 x 5 mm
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each) are placed between the offending compressing vessel and the trigeminal nerve root entry
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zone. (Fig. 2C) In the case of HS, positioning and the craniotomy are similar. The dural flap is based laterally on the sigmoid sinus, and the cerebellum is retracted from lateral to medial with
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careful facial nerve monitoring. The VII-VIII complex is identified without sacrificing the petrosal vein. As in TIC, here too the offending vessel lies ventral. The Teflon pledgets are
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placed as they are in TIC. (Fig. 3A) The 1-inch bone flap is replaced and affixed with 3-4 titanium “I” plates, and the bony defect may be filled with hydroxyapatite cement. (Fig. 3B) The
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incision is closed in layers, the skin with 3-0 nylon, and covered with Dermabond. Patients were
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generally discharged the following day. Patients were monitored with preoperative and postoperative visual analog scores (VAS) for facial pain, preoperative and postoperative use of medications, presence or absence of facial numbness, and the need for a second procedure.
Results
Trigeminal Neuralgia
Fifty-one patients, 21 males and 30 females, with ages of 57±14 years underwent MVD for TIC (Table 1). The duration of symptoms prior to surgery was mean±SD of 7.5±6.7 years. Surgery was undertaken 20 times on the left and 31 on the right. Length of hospitalization was 2±1 day, and patients were followed for 13±22 months. Forty-five patients had an excellent outcome with
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a VAS score of 1±3, with a preop score of 10 justifying surgery. Six patients responded poorly to MVD and remained on medications such as gabapentin, pregabalin, baclofen, or oxcarbazepine. There were 2 cases of wound infection necessitating debridement, 1 case of CSF leak
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necessitating CSF drainage, 1 case of suspected meningitis requiring antibiotics, 2 cases of
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pulmonary embolism following discharge, with full recovery.
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transient diplopia that resolved spontaneously, and 1 case of deep vein thrombosis and
At surgery, the offending vessel was the superior cerebellar artery (SCA) in 31, and in
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combination with the anterior inferior cerebellar artery (AICA) in 3 (Figure 2C). The basilar artery was the offending vessel in 4, a vein in 9, a persistent trigeminal artery in 1, and no
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identifiable vessel in 5. There was agreement between the preoperative findings and the MRI interpretation in all cases with the exception of 8, for a congruence rate of 84%. In the 8 non-
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congruent findings, 3 intraoperative arterial compressions were interpreted by MRI as venous in
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1, and none in 2. Three intraoperative venous compressions were interpreted by MRI as negative in 2, and arterial in 1. In the 2 cases where no offending vessel was seen intraoperatively, the preoperative MRI was interpreted as showing a vein in 1 and an artery in 1. The offending vessel in the 6 failures who remained on medication in spite of MVD was arterial in 4, venous in 1, and no vessel in 1.
Hemifacial Spasm
Of the 12 patients undergoing MVD for HS, there were 8 women and 4 men, with (mean±SD) age of 58±11 years (Table 1). Average duration of symptoms was 7.9±6.1 years. Eight patients suffered from HS on the left, and only 4 on the right. Eight patients had tried botulinum toxin
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injection, 3 medications used for trigeminal neuralgia, and 1 no treatment. One patient had been treated for trigeminal neuralgia on the opposite side a year earlier. Length of hospitalization for neurovascular decompression was 1.8±1.5 days. The patients were followed for 33±27 months
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and a range of 1-77 months. The extent of resolution of the HS was 75±22%, with a range of 25100%. Six patients were very satisfied with their surgery, 6 were satisfied, and none of them
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regretted the operation. One patient, who reported 80% reduction of his spasms, is still receiving
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botulinum toxin injections. Only one patient reported some hearing loss, and after audiography performed one year postoperatively was found to have ipsilateral moderate to severe sensory
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neural hearing loss and hearing within normal limits on the contralateral side. Regression analysis showed that there were no significant risk factors associated with outcome, including
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duration of hemifacial spasm prior to treatment, gender, or laterality.
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At surgery, the offending artery was the vertebral artery in 6 (Fig. 3A) and a smaller artery,
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either the posterior inferior cerebellar artery (PICA) or AICA, in the remaining 6. The offending vessel was identified by MRI as the vertebral artery in 5, an artery in 4, and no vessel was identified in 3. Thus, where at surgery an artery was identified, this was not predicted by MRI in 3, for a congruence rate of 9/12 or 75%.
Discussion
Our review revealed an 88% response rate with pain relief after MVD for TIC. Review of the literature has yielded pain-free results of 80% at 1 year, 75% at 3 years, and 73% at 5 years.[2,8] We encountered 2 cases of wound infection necessitating debridement, and 1 case of CSF leakage that was treated with spinal drainage. There was 1 case of postoperative meningitis
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treated with antibiotics with full recovery, and 1 case of postoperative deep vein thrombosis with pulmonary embolism treated medically with excellent results. Our results are comparable to those reported in the literature.[1,5] In that review, 4% of patients incurred surgery-related
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complications such as leaks, infarction, or hematoma. Hearing and sensory were reported in 10%
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and 7% respectively.
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MVD for HS was associated with symptomatic improvement of varying degrees in all 12 patients. We had 1 case of reported partial hearing loss confirmed by audiogram. There was
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allusion made by the patient of preexisting hearing deficit. Our results are comparable to those in larger series with upwards of 80% good to excellent results at 10 years, and hearing loss and
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facial weakness of 3-8% and 2% respectively.[9-11] In the series of 114 cases reported by Dannebaum et al. without neurophysiological monitoring, there were 2 cases (1.7%) of facial
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palsy and 2 cases of hearing loss (1.7%). Another report of 67 patients with HS described the use
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of brainstem auditory evoked potential (BAEP) monitoring intraoperatively.[12] In that series, there was an incidence of high-frequency hearing loss in 7.4%. Thus, the benefits of BAEP monitoring for MVD in TIC and HS remain to be defined. Excellent results have been demonstrated with facial nerve monitoring alone without BAEP monitoring.
In our 51 cases of MVD for TIC, vascular compression was arterial in 37, venous in 9, and none in 5. With the exception of 8 cases, there was agreement between the preoperative MRI and intraoperative findings, for an 84% congruence rate. In the 8 non-congruent findings, 3 intraoperative arterial compressions were interpreted by MRI as venous in 1 and none in 2. Three intraoperative venous compressions were interpreted by MRI as negative in 2 and arterial in 1. In
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the 2 cases where no offending vessel was seen intraoperatively, the preoperative MRI was interpreted as showing a vein in one and an artery in the second. In the 44 responders to MVD, vascular compression was arterial in 32, venous in 8, and none in 4. The offending vessel in the 6
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failures who remained on medication in spite of MVD was arterial in 4, venous in 1, and none in 1. Our results are not dissimilar from those reported in the literature. In a review of 135 cases of
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trigeminal neuralgia [4], there was a high prevalence of neurovascular contacts on both
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symptomatic and asymptomatic sides on MRI. Neurovascular contact was more prevalent on the symptomatic (89%) compared to the asymptomatic side (78%) (p=0.014). Arterial involvement
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was present in 74% of cases, venous in 15%, and none in 11%. In the 579 cases of TIC reported by Sindou et al., the SCA alone or in association with other vessels was the compressing artery
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in 88% of patients, AICA in 25%, a vein in 5.5%, the basilar artery in 3.5%, vertebral artery in none, and no compression in 3%.[5] These were in line with other large series including Barker
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et al. involving 1,185 cases.[13] In the latter review, compression by the SCA accounted for 75%
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of cases, AICA for 10%, and vein for 13%.
In our 12 cases of HS, the offending artery at surgery was the vertebral artery in 6 and a smaller artery, either the posterior or anterior inferior cerebellar artery, in the remaining 6. In the 648 cases reported by Barker et al., compression of the facial nerve was by the posterior cerebellar artery (PICA) in 68%.[9] The AICA and the vertebral artery accounted for the majority of the remaining cases. A vein was incriminated as the main source of compression in 3%. Dannenbaum et al. in their 114 cases of HS identified AICA as the offending vessel in 43%, PICA in 9%, vertebral artery in 6%, multiple vessels in 34%, and venous compression in 8%.[10] Using 3D visualization with 3D-CISS, Naraghi et al. reviewed 25 patients with HS, 20
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of whom underwent MVD.[14] They reported AICA as the offending artery in 60%, PICA in 28%, and the vertebral artery in 12%.
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In our review, agreement between the preoperative MRI and operative findings was encountered in 43/51 cases or 84% of patients with TIC and 9/12 or 75% of cases with HS. MRI of the brain
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with and without contrast with 1-mm cuts is the gold standard test in the workup of both TIC and
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HS. MRI is mainly used to rule out structural lesions such as meningiomas, schwannomas, epidermoid tumors, cavernomas, aneurysms, and lesions that could represent migraines or
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demyelinating disease. However, with sufficient resolution and by using 3D gradient-echo (GRE) sequence, the MRI can offer additional information by highlighting vascular loops
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associated with compressions. In 146 patients with TIC, Chai et al. obtained both pre- and postoperative MR tomographic angiography (MRTA).[15] In their series, they showed a
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significant correlation between postoperative compression by MRTA and pain relief (p<0.01),
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but not between preoperative compression and relief after MVD (p=0.329). This disparity between preoperative MRI findings and outcome was attributed possibly to dislodgement or inadequacy of decompression, or even failure to identify the offending vessel(s). With the advancement in technology, perhaps high-resolution diffusion tensor imaging (HR-DTI) could allow for better visualization and outcome prediction. In fact, a study by Fujiwara et al. demonstrated alteration in the relative fractional anisotropy (FA) values of affected trigeminal nerves and a correlation with atrophic changes in patients with neurovascular compressioninduced TIC.[16] However, this study did not report any information on the operative findings or the relationship with surgical outcomes. Perhaps, in time, further improvements in imaging and
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resolution would allow improved correlation between nerve atrophy and FA on preoperative imaging and operative findings.
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For the time being, surgical intervention in medically unresponsive TIC and HS should be based on clinical grounds. Preoperative studies are not always definitively conclusive regarding
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vascular compression of the facial or trigeminal nerve, but will help with eliminating other
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causes for TIC or HS for which MVD alone would not be helpful.[1,2] Conversely, however, the presence of vascular compression by MRI should encourage the surgeon to persevere in search
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of the offending vessel when it proves elusive.
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References [1]
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Obermann M. Treatment options in trigeminal neuralgia. Ther Adv Neurol Disord
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Maarbjerg S, Wolfram F, Gozalov A, Olesen J, Bendtsen L. Significance of
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Sindou M, Howeidy T, Acevedo G. Anatomical observations during microvascular
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decompression for idiopathic trigeminal neuralgia (with correlations between topography of pain and site of the neurovascular conflict). Prospective study in a series of 579 patients. Acta Neurochir (Wien) 2002;144:1-12; discussion -3. http://dx.doi.org/10.1007/s007010200000. [6]
Holland M, Noeller J, Buatti J, He W, Shivapour ET, Hitchon PW. The cost-effectiveness of surgery for trigeminal neuralgia in surgically naive patients: A retrospective study. Clin Neurol Neurosurg 2015;137:34-7. http://dx.doi.org/10.1016/j.clineuro.2015.06.011.
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Sivakanthan S, Van Gompel JJ, Alikhani P, van Loveren H, Chen R, Agazzi S. Surgical management of trigeminal neuralgia: use and cost-effectiveness from an analysis of the
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Medicare Claims Database. Neurosurgery 2014;75:220-6; discussion 5-6. http://dx.doi.org/10.1227/NEU.0000000000000430. [8]
Miller JP, Magill ST, Acar F, Burchiel KJ. Predictors of long-term success after
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microvascular decompression for trigeminal neuralgia. J Neurosurg 2009;110:620-6. http://dx.doi.org/10.3171/2008.6.17605.
Barker FG, 2nd, Jannetta PJ, Bissonette DJ, Shields PT, Larkins MV, Jho HD.
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Microvascular decompression for hemifacial spasm. J Neurosurg 1995;82:201-10.
for hemifacial spasm: long-term results from 114 operations performed without
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decompression to treat hemifacial spasm: long-term results for a consecutive series of 143 patients. Neurosurgery 2002;50:712-8; discussion 8-9. [12]
Thirumala P, Frederickson AM, Balzer J, Crammond D, Habeych ME, Chang YF, et al. Reduction in high-frequency hearing loss following technical modifications to microvascular decompression for hemifacial spasm. J Neurosurg 2015:1-6. http://dx.doi.org/10.3171/2014.12.JNS141699.
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Barker FG, 2nd, Jannetta PJ, Bissonette DJ, Larkins MV, Jho HD. The long-term outcome of microvascular decompression for trigeminal neuralgia. N Engl J Med 1996;334:1077-83. http://dx.doi.org/10.1056/NEJM199604253341701.
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[14]
Naraghi R, Tanrikulu L, Troescher-Weber R, Bischoff B, Hecht M, Buchfelder M, et al. Classification of neurovascular compression in typical hemifacial spasm: threedimensional visualization of the facial and the vestibulocochlear nerves. J Neurosurg
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2007;107:1154-63. http://dx.doi.org/10.3171/JNS-07/12/1154. Chai Y, Chen M, Zhang W. Predicting the outcome of microvascular decompression for
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primary trigeminal neuralgia by the use of magnetic resonance tomographic angiography.
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J Craniofac Surg 2013;24:1699-702. http://dx.doi.org/10.1097/SCS.0b013e3182801b64. Fujiwara S, Sasaki M, Wada T, Kudo K, Hirooka R, Ishigaki D, et al. High-resolution
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diffusion tensor imaging for the detection of diffusion abnormalities in the trigeminal nerves of patients with trigeminal neuralgia caused by neurovascular compression. J
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Neuroimaging 2011;21:e102-8. http://dx.doi.org/10.1111/j.1552-6569.2010.00508.x.
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Figure Legends Fig. 1A. Axial T2-weighted MRI shows the superior cerebellar artery (SCA) compressing the
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trigeminal nerve on the right side in a patient with TIC.
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Fig. 1B. MRI shows the vertebral artery (VA) compressing the VII-VIII complex on the left side
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in the case of HS.
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Fig. 2A. Patient is in the lateral decubitus position with the symptomatic side uppermost. The
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dependent arm hangs over the edge of the table and is held in a sling.
Fig. 2B. A 3-mm matchstick burr is used to cut a free left-sided retroauricular bone flap. The
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course of the transverse sinus (TS) is outlined with arrow.
Fig. 2C. Intraoperative photograph of a patient with left-sided TIC. Branches of the SCA spanned by the arrow compress and indent the trigeminal nerve (TN). Arrow R spans the retractor on the cerebellum.
Fig. 3A. Intraoperative photograph of a patient with left HS. The VIII nerve (E) and facial nerve (F) are seen with the vertebral artery (VA) located ventral and medial to the root entry zone . Brain retractor (R) gently retracts cerebellum from lateral to medial.
Fig. 3B. The bone flap is affixed to the bone edges with titanium bars and screws. If large, the bone defect can be filled with hydroxyapatite cement. 16
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HS 12 58±11 4/8 4/8 7.9±6.1 12/12 (100%) 1/12 (8%) 9/12 (75%) 33±27
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TIC 51 57±14 21/30 31/20 7.5±6.7 45/51 (88%) 5/51 (10%) 43/51 (84%) 13±22
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Parameter Number Age Male/Female Right/Left Duration of symptoms (years) Symptoms controlled Complications Congruous with MRI Follow-up (months)
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Table A.1. Demographic data, complications, and MRI findings in MVD
Abbreviations: TIC=trigeminal neuralgia; HS=hemifacial spasm
Highlights 1. MVD is an effective treatment for TIC and HS, with low morbidity.
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2. Identification of the compressing vessel(s) on routine MRI is limited because of resolution. 3. MVD should be based on clinical diagnosis and not solely on visualization of offending
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Abbreviations: TIC=trigeminal neuralgia; HS=hemifacial spasm
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vessels on MRI.
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S0303-8467(15)30043-3 http://dx.doi.org/doi:10.1016/j.clineuro.2015.10.012 CLINEU 4207
To appear in:
Clinical Neurology and Neurosurgery
Received date: Accepted date:
30-9-2015 9-10-2015
Please cite this article as: Hitchon PW, Zanaty M, Moritani T, Uc E, Pieper CL, He W, Noeller J, Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience, Clinical Neurology and Neurosurgery (2015), http://dx.doi.org/10.1016/j.clineuro.2015.10.012 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience.
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Patrick W. Hitchon MDa, Mario Zanaty MDa, Toshio Moritani MDb,
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Ergun Uc MD,c Connie L. Pieper MDc, Wenzhuan He MDd, Jennifer Noeller, ARNPa
a
b
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Department of Neurosurgery, University of Iowa Carver College of Medicine, Iowa City, IA Department of Radiology, University of Iowa Carver College of Medicine, Iowa City, IA
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Department of Neurology and Neurosciences, Rutgers-New Jersey Medical School, Newark, NJ
Corresponding author:
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Patrick W. Hitchon MD
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Department of Neurology, University of Iowa Carver College of Medicine, Iowa City, IA
Department of Neurosurgery
University of Iowa Hospitals and Clinics 200 Hawkins Dr, 1826 JPP Iowa City, IA 52242 USA Phone: +1 319-356-2775 Fax: +1 319-353-6605
Email: [email protected]
Disclosures: No funds were received for the preparation of this manuscript.
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Abstract Objective: For patients with medically unresponsive trigeminal neuralgia (TIC) and hemifacial
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spasm (HS), surgical microvascular decompression (MVD) is the procedure of choice. The authors of this report sought to review their outcomes with MVD in patients with TIC and HS,
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and the success of preoperative magnetic resonance imaging (MRI) in identifying the offending
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vascular compression.
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Methods: Since 2004, there were a total of 51 patients with TIC and 12 with HS with available MRI scans. All patients underwent preoperative MRI to rule out non-surgical etiologies for facial
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pain and facial spasm, and confirm vascular compression. Follow-up after surgery was 13±22
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months for the patients with TIC and 33±27 months for the patients with HS.
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Results: There were 45 responders to MVD in the TIC cohort (88%), with a Visual Analog Score (VAS) of 1±3. All patients with HS responded to MVD between 25-100%, with a mean of 75±22%. Wound complications occurred in 10% of patients with MVD for TIC, and 1 patient reported hearing loss after MVD for HS, documented by audiogram. The congruence rate between the preoperative MRI and operative findings of vascular compression was 84% in TIC and 75% in HS.
Conclusion: MVD is an effective and safe modality of treatment for TIC and HS. In addition to ruling out structural lesions, MRI can offer additional information by highlighting vascular loops associated with compressions. On conventional scans as obtained here, the resolution of MRI
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was congruent with operative findings in 84% in TIC and 75% in HS. This review emphasizes that the decision to undertake MVD in TIC or HS should be based on clinical diagnosis and not visualization of a compressing vessel by MRI. Conversely, the presence of a compressing vessel
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by MRI demands perseverance by the surgeon until the nerve is decompressed.
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Key Words: hemifacial spasm; microvascular decompression; trigeminal neuralgia
Acknowledgements: The authors wish to acknowledge the invaluable assistance provided by
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Faith Vaughn in editing and preparation of this manuscript.
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Introduction Trigeminal neuralgia (TIC) and hemifacial spasm (HS) have an incidence rate of approximately 4 and 1 per 100,000 population respectively.[1,2] Fortunately, for about 75% of patients who
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suffer TIC, the frequent lancinating pain that they suffer can be controlled with medications such as carbamazepine, oxcarbazepine, lamotrigine, or baclofen, to mention the most commonly used.
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The response to medical management is estimated at 80% initially, which declines to less than
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50% over time. When medical management is no longer effective, and the side effects from the medication overwhelming, microvascular decompression (MVD) is the most attractive option.[3-
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5] MVD is nonablative, not associated with facial numbness, and least likely to require a secondary procedure.[6,7] For those with HS, symptomatic and temporary relief can be achieved
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with botulinum toxin injection. However, this still results in a large proportion of people who continue to experience symptoms and wish to avoid repetitive facial injections. For this group of
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patients, surgical options for their disease are available and often sought. For TIC and HS, MVD
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is the procedure of choice and not associated with the numbness that can result from focused radiation or radiofrequency rhizotomy.
The authors of this report sought to review their outcomes with MVD in patients with TIC and HS, and the success of preoperative MRI in identifying the offending vascular compression of the V or VII cranial nerves.
Materials and Methods Since 2000, a total of 201 cases of TIC have been treated at our center. Thirty-five were treated with radiofrequency rhizotomy, 80 with MVD, and 86 with stereotactic focused radiation. Since
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2008, 12 patients with HS have been treated with MVD. All cases of neurovascular decompression for TIC and HS since 2004 with available MRI scans were reviewed. There were a total of 51 patients with TIC and 12 with HS. Patients without risk factors who did not wish to
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contend with facial numbness that can result from radiofrequency rhizotomy or focused radiation and were good surgical candidates underwent MVD by choice. MRI studies were obtained in all
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patients to rule out a mass lesion or demyelinating disease and to assess neurovascular anatomy.
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A high-resolution, heavily T2-weighted 3D-sequence on a 1.5 or 3T scanner was obtained. A high CSF-tissue contrast with 3D constructive interference in steady state (CISS) or its
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equivalent, 3D fast imaging employing steady-state acquisition (FIESTA), provided best resolution. (Fig. 1A and 1B) Once a mass lesion or demyelination had been ruled out, MVD was
Surgical Technique
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performed.
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This is performed in the decubitus position with facial nerve monitoring and intraoperative osmotic diuresis. The head is affixed flexed in a 3-point Mayfield head fixator with the sagittal sinus horizontal and with a fingerbreadth space between the chin and the clavicle. The torso is held in the decubitus position using 3-inch adhesive tape with an axillary roll in place. (Fig. 2A) A 3-inch-long curvilinear incision is made 15 mm medial to the mastoid process and centered on the superior nuchal line, or a line extending from the zygomatic arch to the inion. A 1-inch oval free bone flap is rotated using a 3-mm matchstick burr.[3,5] (Fig. 2B) The position of the transverse sinus is confirmed with intraoperative ultrasound. A “V”-shaped dural flap, 1 cm at its base, is rotated on the transverse sinus. The cerebellum is retracted in a downward direction with a ¼-inch self-retaining retractor. Laterally, the petrosal vein is coagulated and transected. Failing
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to secure this vein early can prove a nuisance. Ventral to the petrosal vein, the trigeminal nerve is identified and dissected free of the arachnoid. It is helpful to retain some arachnoidal bands around the trigeminal nerve to help hold the Teflon sponges in place. Medially the IV cranial
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nerve and laterally the VII-VIII complex are identified and kept covered with arachnoid for protection. Three to seven Teflon felt (Medline Industries, Mundelein, IL) sponges (1 x 5 mm
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each) are placed between the offending compressing vessel and the trigeminal nerve root entry
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zone. (Fig. 2C) In the case of HS, positioning and the craniotomy are similar. The dural flap is based laterally on the sigmoid sinus, and the cerebellum is retracted from lateral to medial with
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careful facial nerve monitoring. The VII-VIII complex is identified without sacrificing the petrosal vein. As in TIC, here too the offending vessel lies ventral. The Teflon pledgets are
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placed as they are in TIC. (Fig. 3A) The 1-inch bone flap is replaced and affixed with 3-4 titanium “I” plates, and the bony defect may be filled with hydroxyapatite cement. (Fig. 3B) The
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incision is closed in layers, the skin with 3-0 nylon, and covered with Dermabond. Patients were
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generally discharged the following day. Patients were monitored with preoperative and postoperative visual analog scores (VAS) for facial pain, preoperative and postoperative use of medications, presence or absence of facial numbness, and the need for a second procedure.
Results
Trigeminal Neuralgia
Fifty-one patients, 21 males and 30 females, with ages of 57±14 years underwent MVD for TIC (Table 1). The duration of symptoms prior to surgery was mean±SD of 7.5±6.7 years. Surgery was undertaken 20 times on the left and 31 on the right. Length of hospitalization was 2±1 day, and patients were followed for 13±22 months. Forty-five patients had an excellent outcome with
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a VAS score of 1±3, with a preop score of 10 justifying surgery. Six patients responded poorly to MVD and remained on medications such as gabapentin, pregabalin, baclofen, or oxcarbazepine. There were 2 cases of wound infection necessitating debridement, 1 case of CSF leak
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necessitating CSF drainage, 1 case of suspected meningitis requiring antibiotics, 2 cases of
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pulmonary embolism following discharge, with full recovery.
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transient diplopia that resolved spontaneously, and 1 case of deep vein thrombosis and
At surgery, the offending vessel was the superior cerebellar artery (SCA) in 31, and in
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combination with the anterior inferior cerebellar artery (AICA) in 3 (Figure 2C). The basilar artery was the offending vessel in 4, a vein in 9, a persistent trigeminal artery in 1, and no
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identifiable vessel in 5. There was agreement between the preoperative findings and the MRI interpretation in all cases with the exception of 8, for a congruence rate of 84%. In the 8 non-
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congruent findings, 3 intraoperative arterial compressions were interpreted by MRI as venous in
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1, and none in 2. Three intraoperative venous compressions were interpreted by MRI as negative in 2, and arterial in 1. In the 2 cases where no offending vessel was seen intraoperatively, the preoperative MRI was interpreted as showing a vein in 1 and an artery in 1. The offending vessel in the 6 failures who remained on medication in spite of MVD was arterial in 4, venous in 1, and no vessel in 1.
Hemifacial Spasm
Of the 12 patients undergoing MVD for HS, there were 8 women and 4 men, with (mean±SD) age of 58±11 years (Table 1). Average duration of symptoms was 7.9±6.1 years. Eight patients suffered from HS on the left, and only 4 on the right. Eight patients had tried botulinum toxin
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injection, 3 medications used for trigeminal neuralgia, and 1 no treatment. One patient had been treated for trigeminal neuralgia on the opposite side a year earlier. Length of hospitalization for neurovascular decompression was 1.8±1.5 days. The patients were followed for 33±27 months
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and a range of 1-77 months. The extent of resolution of the HS was 75±22%, with a range of 25100%. Six patients were very satisfied with their surgery, 6 were satisfied, and none of them
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regretted the operation. One patient, who reported 80% reduction of his spasms, is still receiving
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botulinum toxin injections. Only one patient reported some hearing loss, and after audiography performed one year postoperatively was found to have ipsilateral moderate to severe sensory
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neural hearing loss and hearing within normal limits on the contralateral side. Regression analysis showed that there were no significant risk factors associated with outcome, including
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duration of hemifacial spasm prior to treatment, gender, or laterality.
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At surgery, the offending artery was the vertebral artery in 6 (Fig. 3A) and a smaller artery,
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either the posterior inferior cerebellar artery (PICA) or AICA, in the remaining 6. The offending vessel was identified by MRI as the vertebral artery in 5, an artery in 4, and no vessel was identified in 3. Thus, where at surgery an artery was identified, this was not predicted by MRI in 3, for a congruence rate of 9/12 or 75%.
Discussion
Our review revealed an 88% response rate with pain relief after MVD for TIC. Review of the literature has yielded pain-free results of 80% at 1 year, 75% at 3 years, and 73% at 5 years.[2,8] We encountered 2 cases of wound infection necessitating debridement, and 1 case of CSF leakage that was treated with spinal drainage. There was 1 case of postoperative meningitis
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treated with antibiotics with full recovery, and 1 case of postoperative deep vein thrombosis with pulmonary embolism treated medically with excellent results. Our results are comparable to those reported in the literature.[1,5] In that review, 4% of patients incurred surgery-related
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complications such as leaks, infarction, or hematoma. Hearing and sensory were reported in 10%
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and 7% respectively.
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MVD for HS was associated with symptomatic improvement of varying degrees in all 12 patients. We had 1 case of reported partial hearing loss confirmed by audiogram. There was
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allusion made by the patient of preexisting hearing deficit. Our results are comparable to those in larger series with upwards of 80% good to excellent results at 10 years, and hearing loss and
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facial weakness of 3-8% and 2% respectively.[9-11] In the series of 114 cases reported by Dannebaum et al. without neurophysiological monitoring, there were 2 cases (1.7%) of facial
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palsy and 2 cases of hearing loss (1.7%). Another report of 67 patients with HS described the use
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of brainstem auditory evoked potential (BAEP) monitoring intraoperatively.[12] In that series, there was an incidence of high-frequency hearing loss in 7.4%. Thus, the benefits of BAEP monitoring for MVD in TIC and HS remain to be defined. Excellent results have been demonstrated with facial nerve monitoring alone without BAEP monitoring.
In our 51 cases of MVD for TIC, vascular compression was arterial in 37, venous in 9, and none in 5. With the exception of 8 cases, there was agreement between the preoperative MRI and intraoperative findings, for an 84% congruence rate. In the 8 non-congruent findings, 3 intraoperative arterial compressions were interpreted by MRI as venous in 1 and none in 2. Three intraoperative venous compressions were interpreted by MRI as negative in 2 and arterial in 1. In
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the 2 cases where no offending vessel was seen intraoperatively, the preoperative MRI was interpreted as showing a vein in one and an artery in the second. In the 44 responders to MVD, vascular compression was arterial in 32, venous in 8, and none in 4. The offending vessel in the 6
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failures who remained on medication in spite of MVD was arterial in 4, venous in 1, and none in 1. Our results are not dissimilar from those reported in the literature. In a review of 135 cases of
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trigeminal neuralgia [4], there was a high prevalence of neurovascular contacts on both
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symptomatic and asymptomatic sides on MRI. Neurovascular contact was more prevalent on the symptomatic (89%) compared to the asymptomatic side (78%) (p=0.014). Arterial involvement
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was present in 74% of cases, venous in 15%, and none in 11%. In the 579 cases of TIC reported by Sindou et al., the SCA alone or in association with other vessels was the compressing artery
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in 88% of patients, AICA in 25%, a vein in 5.5%, the basilar artery in 3.5%, vertebral artery in none, and no compression in 3%.[5] These were in line with other large series including Barker
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et al. involving 1,185 cases.[13] In the latter review, compression by the SCA accounted for 75%
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of cases, AICA for 10%, and vein for 13%.
In our 12 cases of HS, the offending artery at surgery was the vertebral artery in 6 and a smaller artery, either the posterior or anterior inferior cerebellar artery, in the remaining 6. In the 648 cases reported by Barker et al., compression of the facial nerve was by the posterior cerebellar artery (PICA) in 68%.[9] The AICA and the vertebral artery accounted for the majority of the remaining cases. A vein was incriminated as the main source of compression in 3%. Dannenbaum et al. in their 114 cases of HS identified AICA as the offending vessel in 43%, PICA in 9%, vertebral artery in 6%, multiple vessels in 34%, and venous compression in 8%.[10] Using 3D visualization with 3D-CISS, Naraghi et al. reviewed 25 patients with HS, 20
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of whom underwent MVD.[14] They reported AICA as the offending artery in 60%, PICA in 28%, and the vertebral artery in 12%.
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In our review, agreement between the preoperative MRI and operative findings was encountered in 43/51 cases or 84% of patients with TIC and 9/12 or 75% of cases with HS. MRI of the brain
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with and without contrast with 1-mm cuts is the gold standard test in the workup of both TIC and
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HS. MRI is mainly used to rule out structural lesions such as meningiomas, schwannomas, epidermoid tumors, cavernomas, aneurysms, and lesions that could represent migraines or
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demyelinating disease. However, with sufficient resolution and by using 3D gradient-echo (GRE) sequence, the MRI can offer additional information by highlighting vascular loops
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associated with compressions. In 146 patients with TIC, Chai et al. obtained both pre- and postoperative MR tomographic angiography (MRTA).[15] In their series, they showed a
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significant correlation between postoperative compression by MRTA and pain relief (p<0.01),
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but not between preoperative compression and relief after MVD (p=0.329). This disparity between preoperative MRI findings and outcome was attributed possibly to dislodgement or inadequacy of decompression, or even failure to identify the offending vessel(s). With the advancement in technology, perhaps high-resolution diffusion tensor imaging (HR-DTI) could allow for better visualization and outcome prediction. In fact, a study by Fujiwara et al. demonstrated alteration in the relative fractional anisotropy (FA) values of affected trigeminal nerves and a correlation with atrophic changes in patients with neurovascular compressioninduced TIC.[16] However, this study did not report any information on the operative findings or the relationship with surgical outcomes. Perhaps, in time, further improvements in imaging and
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resolution would allow improved correlation between nerve atrophy and FA on preoperative imaging and operative findings.
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For the time being, surgical intervention in medically unresponsive TIC and HS should be based on clinical grounds. Preoperative studies are not always definitively conclusive regarding
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vascular compression of the facial or trigeminal nerve, but will help with eliminating other
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causes for TIC or HS for which MVD alone would not be helpful.[1,2] Conversely, however, the presence of vascular compression by MRI should encourage the surgeon to persevere in search
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of the offending vessel when it proves elusive.
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References [1]
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Obermann M. Treatment options in trigeminal neuralgia. Ther Adv Neurol Disord
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Jannetta PJ, McLaughlin MR, Casey KF. Technique of microvascular decompression.
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Maarbjerg S, Wolfram F, Gozalov A, Olesen J, Bendtsen L. Significance of
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Sindou M, Howeidy T, Acevedo G. Anatomical observations during microvascular
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decompression for idiopathic trigeminal neuralgia (with correlations between topography of pain and site of the neurovascular conflict). Prospective study in a series of 579 patients. Acta Neurochir (Wien) 2002;144:1-12; discussion -3. http://dx.doi.org/10.1007/s007010200000. [6]
Holland M, Noeller J, Buatti J, He W, Shivapour ET, Hitchon PW. The cost-effectiveness of surgery for trigeminal neuralgia in surgically naive patients: A retrospective study. Clin Neurol Neurosurg 2015;137:34-7. http://dx.doi.org/10.1016/j.clineuro.2015.06.011.
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Sivakanthan S, Van Gompel JJ, Alikhani P, van Loveren H, Chen R, Agazzi S. Surgical management of trigeminal neuralgia: use and cost-effectiveness from an analysis of the
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Medicare Claims Database. Neurosurgery 2014;75:220-6; discussion 5-6. http://dx.doi.org/10.1227/NEU.0000000000000430. [8]
Miller JP, Magill ST, Acar F, Burchiel KJ. Predictors of long-term success after
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microvascular decompression for trigeminal neuralgia. J Neurosurg 2009;110:620-6. http://dx.doi.org/10.3171/2008.6.17605.
Barker FG, 2nd, Jannetta PJ, Bissonette DJ, Shields PT, Larkins MV, Jho HD.
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Microvascular decompression for hemifacial spasm. J Neurosurg 1995;82:201-10.
for hemifacial spasm: long-term results from 114 operations performed without
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neurophysiological monitoring. J Neurosurg 2008;109:410-5. http://dx.doi.org/10.3171/JNS/2008/109/9/0410.
Samii M, Gunther T, Iaconetta G, Muehling M, Vorkapic P, Samii A. Microvascular
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decompression to treat hemifacial spasm: long-term results for a consecutive series of 143 patients. Neurosurgery 2002;50:712-8; discussion 8-9. [12]
Thirumala P, Frederickson AM, Balzer J, Crammond D, Habeych ME, Chang YF, et al. Reduction in high-frequency hearing loss following technical modifications to microvascular decompression for hemifacial spasm. J Neurosurg 2015:1-6. http://dx.doi.org/10.3171/2014.12.JNS141699.
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Barker FG, 2nd, Jannetta PJ, Bissonette DJ, Larkins MV, Jho HD. The long-term outcome of microvascular decompression for trigeminal neuralgia. N Engl J Med 1996;334:1077-83. http://dx.doi.org/10.1056/NEJM199604253341701.
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[14]
Naraghi R, Tanrikulu L, Troescher-Weber R, Bischoff B, Hecht M, Buchfelder M, et al. Classification of neurovascular compression in typical hemifacial spasm: threedimensional visualization of the facial and the vestibulocochlear nerves. J Neurosurg
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2007;107:1154-63. http://dx.doi.org/10.3171/JNS-07/12/1154. Chai Y, Chen M, Zhang W. Predicting the outcome of microvascular decompression for
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J Craniofac Surg 2013;24:1699-702. http://dx.doi.org/10.1097/SCS.0b013e3182801b64. Fujiwara S, Sasaki M, Wada T, Kudo K, Hirooka R, Ishigaki D, et al. High-resolution
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diffusion tensor imaging for the detection of diffusion abnormalities in the trigeminal nerves of patients with trigeminal neuralgia caused by neurovascular compression. J
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Neuroimaging 2011;21:e102-8. http://dx.doi.org/10.1111/j.1552-6569.2010.00508.x.
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Figure Legends Fig. 1A. Axial T2-weighted MRI shows the superior cerebellar artery (SCA) compressing the
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trigeminal nerve on the right side in a patient with TIC.
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Fig. 1B. MRI shows the vertebral artery (VA) compressing the VII-VIII complex on the left side
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in the case of HS.
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Fig. 2A. Patient is in the lateral decubitus position with the symptomatic side uppermost. The
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dependent arm hangs over the edge of the table and is held in a sling.
Fig. 2B. A 3-mm matchstick burr is used to cut a free left-sided retroauricular bone flap. The
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course of the transverse sinus (TS) is outlined with arrow.
Fig. 2C. Intraoperative photograph of a patient with left-sided TIC. Branches of the SCA spanned by the arrow compress and indent the trigeminal nerve (TN). Arrow R spans the retractor on the cerebellum.
Fig. 3A. Intraoperative photograph of a patient with left HS. The VIII nerve (E) and facial nerve (F) are seen with the vertebral artery (VA) located ventral and medial to the root entry zone . Brain retractor (R) gently retracts cerebellum from lateral to medial.
Fig. 3B. The bone flap is affixed to the bone edges with titanium bars and screws. If large, the bone defect can be filled with hydroxyapatite cement. 16
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HS 12 58±11 4/8 4/8 7.9±6.1 12/12 (100%) 1/12 (8%) 9/12 (75%) 33±27
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TIC 51 57±14 21/30 31/20 7.5±6.7 45/51 (88%) 5/51 (10%) 43/51 (84%) 13±22
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Parameter Number Age Male/Female Right/Left Duration of symptoms (years) Symptoms controlled Complications Congruous with MRI Follow-up (months)
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Table A.1. Demographic data, complications, and MRI findings in MVD
Abbreviations: TIC=trigeminal neuralgia; HS=hemifacial spasm
Highlights 1. MVD is an effective treatment for TIC and HS, with low morbidity.
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2. Identification of the compressing vessel(s) on routine MRI is limited because of resolution. 3. MVD should be based on clinical diagnosis and not solely on visualization of offending
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Abbreviations: TIC=trigeminal neuralgia; HS=hemifacial spasm
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vessels on MRI.
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