Skip to main content
NCBI home page
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2020 Apr 10.
Published in final edited form as: Otolaryngol Head Neck Surg. 2017 Sep 12;158(1):62–75. doi: 10.1177/0194599817728878

Hearing Loss following Posterior Fossa Microvascular Decompression: A Systematic Review

Matthew Bartindale 1, Matthew Kircher 1, William Adams 2, Neelam Balasubramanian 2, Jeffrey Liles 1, Jason Bell 1, John Leonetti 1
PMCID: PMC7147641  NIHMSID: NIHMS1556971  PMID: 28895459

Abstract

Objectives.

(1) Determine the prevalence of hearing loss following microvascular decompression (MVD) for trigeminal neuralgia (TN) and hemifacial spasm (HFS). (2) Demonstrate factors that affect postoperative hearing outcomes after MVD.

Data Sources.

PubMed-NCBI, Scopus, CINAHL, and PsycINFO databases from 1981 to 2016.

Review Methods.

Systematic review of prospective cohort studies and retrospective reviews in which any type of hearing loss was recorded after MVD for TN or HFS. Three researchers extracted data regarding operative indications, procedures performed, and diagnostic tests employed. Discrepancies were resolved by mutual consensus.

Results.

Sixty-nine references with 18,233 operations met inclusion criteria. There were 7093 patients treated for TN and 11,140 for HFS. The overall reported prevalence of hearing loss after MVD for TN and HFS was 5.58% and 8.25%, respectively. However, many of these studies relied on subjective measures of reporting hearing loss. In 23 studies with consistent perioperative audiograms, prevalence of hearing loss was 13.47% for TN and 13.39% for HFS, with no significant difference between indications (P = .95). Studies using intraoperative brainstem auditory evoked potential monitoring were more likely to report hearing loss for TN (relative risk [RR], 2.28; P <.001) but not with HFS (RR, 0.88; P = .056).

Conclusion.

Conductive and sensorineural hearing loss are important complications following posterior fossa MVD. Many studies have reported on hearing loss using either subjective measures and/or inconsistent audiometric testing. Routine perioperative audiogram protocols improve the detection of hearing loss and may more accurately represent the true risk of hearing loss after MVD for TN and HFS.

Keywords: microvascular decompression, cerebellopontine angle, posterior fossa, complications, hearing loss, neurotology

Dandy1 first proposed the neurovascular conflict theory in 1934 when he suggested that ectatic vessels could cause clinical syndromes. In the late 1960s, Jannetta2 developed microvascular decompression (MVD), where the offending artery is transposed away from the cranial nerve root exit zone. MVD has been found to be an effective and safe treatment for several pathologies, most commonly trigeminal neuralgia (TN) and hemifacial spasm (HFS).2–5

Trigeminal neuralgia is a clinical syndrome manifesting as a lancinating unilateral facial pain in the sensory distribution of the trigeminal nerve.6 The annual incidence of TN is 4 to 13 cases per 100,000 people per year.7,8 First-line treatments are medical, but for those patients with symptoms intractable to medical treatment or with intolerable medication side effects, MVD is an effective surgical option.3 HFS is characterized by irregular, involuntary, and recurring contractions of unilateral facial muscles.4 The annual incidence of HFS is 9.8 to 11.0 cases per 100,000 people per year.9 Medical therapy and botulinum toxin injection are less invasive treatment alternatives, but MVD has been shown to provide consistent long-lasting relief.5 Other indications for MVD surgery include glossopharyngeal neuralgia,10 occipital neuralgia,11 tinnitus,12 and vagal palsy.13 Figure 1 shows the view the neurosurgeon has when performing a microvascular decompression surgery.

Figure 1.

Figure 1.

Open in a new tab

The view the neurosurgeon has while performing a microvascular decompression in the posterior fossa. ©Jackler RK. Atlas of Skull Base Surgery and Neurotology. Stuttgart, Germany: Thieme; 2017.105

An important complication of posterior fossa MVD is hearing loss. Potential causes of sensorineural hearing loss (SNHL) previously discussed include stretching of cranial nerve (CN) VIII while retracting the cerebellum, direct trauma to CN VIII, manipulation of the labyrinthine artery or the anteroinferior cerebellar artery, neocompression of the nerve by the spacer material, and acoustic trauma from drill noise.14–16 Conductive hearing loss (CHL) is usually caused by a middle ear effusion secondary to fluid entering the mastoid air cells during craniotomy.16 Brainstem auditory evoked potential monitoring (BAEP) is used at many institutions and has previously been shown to decrease the prevalence of postoperative hearing loss.17

While numerous articles have been written regarding hearing loss as a complication of MVD, no meta-analysis or systematic review has investigated the true prevalence of hearing loss as a postoperative complication. Surprisingly, many centers report on hearing outcomes after MVD without the use of perioperative audiograms. In patients requiring MVD for TN or HFS, we aimed to determine the frequency of hearing loss as a complication and evaluate the impact of the indication for surgery, perioperative audiogram protocols, use of BAEP, and use of fully endoscopic technique by performing a systematic literature review.

Methods

Eligibility Criteria

(1) Patients must have been treated with MVD, (2) the reference had to report hearing loss, (3) the indication for included surgeries had to be either TN or HFS, (4) the complications had to be matched with the indication for MVD, and (5) the patients in the study could not be selected based on specific factors related to hearing loss (eg, intraoperative BAEP changes).

Search Strategy

To identify relevant studies, searches were performed in PubMed-NCBI, Scopus, PsycINFO, and CINAHL by an academic librarian. Search strategies are included in the appendix (available in the online version of the article). Only articles printed in English were included, and no year filter was used. The search was conducted according to PRISMA guidelines.18 An institutional review board exemption was granted because human subjects were not involved in this study.

Study Selection and Validation

Two reviewers both screened the abstracts and then evaluated the remaining full articles for eligibility. Discrepancies were resolved by a third reviewer.

Data Abstraction

Information extracted from each study included author, year of publication, number of patients who underwent MVD for each indication, number of patients with each indication with hearing loss, number of patients with transient vs permanent hearing loss, usage of a perioperative audiogram protocol, use of BAEP, whether revision surgeries were included, whether the study was retrospective or prospective, and the study’s level of evidence based on the Oxford Centre for Evidence Based Medicine 2011 criteria.19 If perioperative audiograms were performed, the type of hearing loss, laterality of hearing loss, and hearing loss threshold used were documented if recorded. If audiograms were not mentioned, it was assumed that there was no audiogram protocol in place. The data were entered into an electronic research database (REDCap).20

Assessment of Bias of Individual Studies

The National Institutes of Health’s (NIH’s) Quality Assessment of Case Series Studies21 was used to evaluate bias of individual studies. Figure 2 shows the criteria used in this assessment.

Figure 2.

Figure 2.

Open in a new tab

Criteria for the National Institutes of Health’s Quality Assessment of Case Series Studies. Source: National Heart, Lung, and Blood Institute, National Institutes of Health.21

Statistical Methods

All statistical analyses were conducted using SAS software version 9.4 (SAS Institute, Cary, North Carolina). Raw prevalence estimates for each article were first transformed using a double arcsine method to free them from their 0 to 1 range. These prevalence estimates were weighted using the inverse of the summation of their between- and within-study variances as described by Hedges and Veva.22 Cochran’s Q statistic was used as an assessment of the heterogeneity between articles, and the pooled prevalence of hearing loss was estimated using a weighted linear random-effects model with a back transformation to the original 0 to 1 raw prevalence scale as described by Barendregt et al.23

A weighted linear random-effects model was also used to evaluate moderators of hearing loss, including whether hearing loss varied by studies using BAEP, routine audios, or endoscopic procedures. In these models, the transformed estimates were weighted as described above, and random intercepts were allowed for each article. Model-derived pooled estimates were back transformed to the raw 0 to 1 prevalence scale as described by Barendregt et al,23 and the relative ratio of hearing loss among articles with and without the moderator was estimated as described by Agresti.24 Publication bias was evaluated visually using Light and Pillemer25 funnel plots.

Results

Study Selection

A total of 481 studies were identified from the 4 databases searched. There were 50 duplicate studies removed. After implementation of our selection criteria, 309 studies were excluded based on their abstracts. The remaining 122 full articles were reviewed, and 69 studies fulfilled all inclusion criteria. The reasons for exclusion of studies are listed in Figure 3.

Figure 3.

Figure 3.

Open in a new tab

Study selection process and reasons for exclusion. HL, hearing loss; MVD, microvascular decompression.

Study Characteristics

The studies that met inclusion criteria were published in English between 1981 and 2016. A total of 18,233 patients were described, with 7093 for TN and 11,140 for HFS. Twenty-two of the studies had a perioperative audiogram protocol in place (preoperative and postoperative audiograms), comprising 6530 of the patients. The threshold for what was considered hearing loss in those studies was inconsistent and often unreported (Table 1). Of these 23 studies, 8 reported whether the hearing loss was conductive or sensorineural, 9 reported whether the hearing loss was transient or permanent, and 10 reported laterality of the hearing loss. Forty-six studies had no audiogram protocol and relied on subjective complaints of hearing loss (Table 2). Intraoperative BAEP monitoring was consistently used in 21 studies. Four studies used fully endoscopic techniques for performing the surgery. Fourteen studies included some revisions surgeries, and the remaining 55 only included primary MVD. The assessment of bias for each study was recorded in Table 3.

Table 1.

Studies That Used Perioperative Audiometry and Their Hearing Loss Thresholds.

First Author PY Cases HL Threshold BAEP Rev. C/SN R/P CEBM
Lee15 2015 2027 >15 dB PTA or 20% SDS Yes No Yes R 4
Thirumala44 2015 67 >15 dB PTA Yes Yes No R 4
Shimizu45 2015 100 NR Yes No No P 4
Soriano-Baron46 2015 226 NR No Yes No R 4
Shah29 2012 151 >15 dB PTA or 20% SDS Yes No Yes R 4
Ferroli47 2010 476 NR No No No R 4
Gunther48 2009 362 NR No No No R 4
Lee49 2009 20 >10 dB PTA No No Yes P 4
Huh50 2008 1524 >25 dB PTA Yes No Yes R 4
Ramnarayan51 2006 75 >20 dB PTA Yes No Yes P 4
Moffat52 2005 15 NR No No Yes R 4
Brock53 2004 45 >20 dB PTA Yes Yes No R 4
Polo17 2004 84 >20 dB PTA Yes No No P 4
Strauss38 2000 1 >20 dB PTA Yes No No R 4
Van54 1999 6 >35 dB PTA No No Yes P 4
Rizvi55 1999 9 NR Yes No No P 4
Sindou43 1992 34 >20 dB PTA Yes No No R 4
Fukaya56 1991 963 NR No No Yes R 4
Yokota57 1991 80 >15 dB PTA Yes No No P 4
Moller42 1989 78 >10 dB PTA or 15% SDS Yes Yes No R 4
Fritz58 1988 21 >15 dB PTA or 20% SDS No No Yes R 4
Moller59 1985 143 >10 dB PTA No No No R 4
Saito60 1985 23 >10 dB PTA No No Yes R 4
Open in a new tab

Abbreviations: BAEP, brainstem auditory evoked potential monitoring; C/SN, distinguishes conductive and sensorineural hearing loss; CEBM, Centre for Evidence-Based Medicine Level of Evidence; HL, hearing loss; NR, not reported; PTA, pure-tone average; PY, publication year; Rev., revisions included; R/P, retrospective or prospective; SDS, speech discrimination score.

Table 2.

Studies That Did Not Use Perioperative Audiometry.

First Author PY Cases, No. BAEP Rev. R/P CEBM
Qi4 2016 46 No No R 4
Dou61 2016 10 No No R 4
Li62 2016 17 No No R 4
Hitchon5 2015 63 No No R 4
Li63 2015 23 No No R 4
Amagasaki64 2015 100 Yes No R 4
Bohman65 2014 47 No Yes R 4
Ma66 2014 348 No No R 4
Lee67 2014 43 Yes No R 4
Sun68 2014 356 No No R 4
Sandel69 2013 283 No No R 4
Jagannath70 2012 137 No Yes P 4
Oesman71 2011 156 No No R 4
Bond72 2010 119 Yes Yes R 4
Chang73 2010 2137 No No R 4
Li74 2010 481 No No R 4
Ma75 2010 200 No No R 4
Zhong76 2010 298 No No R 4
Sato77 2009 18 No No R 4
Huang78 2009 36 Yes No P 4
Salama79 2009 21 No No P 4
Linskey80 2008 35 Yes No P 4
Cheng81 2008 32 No No R 4
Dannenbaum82 2008 114 No No R 4
Artz83 2008 19 No No R 4
Joo84 2008 72 Yes No R 4
Ali85 2007 86 No No P 4
Sindou86 2007 362 No Yes R 4
Teo87 2006 114 No No R 4
Zakrzewska88 2005 245 No No R 4
Hitotsumatsu89 2003 300 No No R 4
Javadpour90 2003 85 Yes Yes R 4
Samii91 2002 145 No Yes R 4
Mooij92 2001 74 No Yes R 4
McLaughlin93 1999 4265 No No R 4
Ryu94 1998 7 No No R 4
Magnan95 1997 60 No No R 4
Acevedo96 1997 75 No No R 4
Illingworth97 1996 83 No No P 4
Zhang98 1995 300 No No R 4
Cutbush99 1994 109 No No R 4
Auger100 1986 54 No Yes R 4
Kolluri101 1984 71 No No R 4
Fairholm102 1983 20 No No R 4
Rushworth103 1982 26 No Yes R 4
Yeh104 1981 10 No No R 4
Open in a new tab

Abbreviations: BAEP, brainstem auditory evoked potential monitoring; CEBM, Centre for Evidence-based Medicine Level of Evidence; PY, publication year; Rev., revisions included; R/P, retrospective or prospective.

Table 3.

Standardized Risk Assessment of Individual Studies Based on the NIH Quality Assessment Tool for Case Series Studies.21,a

First Author PY 1. Objective? 2. Population Description? 3. Consecutive Cases? 4. Comparable Subjects? 5. Intervention Described? 6. Outcomes Defined? 7. Adequate Follow-up? 8. Well-Described Statistical Methods? 9. Well-Described Results?
Dou61 2016 Y Y N Y Y N Y Y Y
Li62 2016 Y Y Y Y Y N Y NA Y
Qi4 2016 Y Y CD Y Y N Y Y Y
Amagasaki64 2015 Y Y Y Y Y N CD Y Y
Hitchon5 2015 Y Y Y Y Y N Y Y Y
Lee15 2015 Y Y Y Y Y Y Y Y Y
Li63 2015 Y Y Y Y Y N Y NA Y
Shimizu45 2015 Y Y Y Y Y N CD NA Y
Soriano-
Baron46 		2015 Y Y CD Y Y N Y Y Y
Thirumala44 2015 Y Y Y Y Y Y N Y Y
Bohman65 2014 Y Y Y Y Y N Y Y Y
Lee67 2014 Y Y CD Y Y N Y Y Y
Ma66 2014 Y Y CD Y Y N Y NA Y
Sun68 2014 Y Y Y Y Y N Y Y Y
Sandel69 2013 Y Y Y Y Y N Y Y Y
Jagannath70 2012 Y Y Y Y Y N Y NA Y
Shah29 2012 Y Y CD Y Y Y N Y Y
Oesman71 2011 Y Y Y Y Y N Y Y Y
Bond72 2010 Y Y CD Y Y N Y N Y
Chang73 2010 Y Y CD Y Y N Y Y Y
Ferroli47 2010 Y Y CD Y Y N Y Y Y
Li74 2010 Y Y CD Y Y N Y NA Y
Ma75 2010 Y Y Y Y Y N Y N Y
Zhong76 2010 Y Y Y Y Y N CD Y Y
Gunther48 2009 Y N Y Y Y N Y Y Y
Huang78 2009 Y N Y Y Y N Y N Y
Lee49 2009 Y Y Y Y Y Y Y Y Y
Salama79 2009 Y Y Y Y Y N Y Y Y
Sato77 2009 Y Y N Y Y N CD Y Y
Artz83 2008 Y N CD Y Y N Y Y Y
Cheng81 2008 Y Y Y Y Y N Y NA Y
Dannenbaum82 2008 Y Y Y Y Y N Y Y Y
Huh50 2008 Y Y Y Y Y Y Y Y Y
Joo84 2008 Y Y CD Y Y N Y Y Y
Linskey80 2008 Y Y Y Y Y N Y Y Y
Ali85 2007 Y Y Y Y Y N CD NA Y
Sindou86 2007 Y Y Y Y Y N Y Y Y
Ramnarayan51 2006 Y Y CD Y Y Y Y Y Y
Teo87 2006 Y Y Y Y Y N Y NA Y
Moffat52 2005 Y Y CD Y Y N Y NA Y
Zakrzewska88 2005 Y Y N Y Y N Y Y Y
Brock53 2004 Y N Y Y Y Y Y N Y
Polo17 2004 Y Y Y Y Y Y Y Y Y
Hitotsumatsu89 2003 Y N CD CD Y N CD N Y
Javadpour90 2003 Y N Y Y Y N Y Y Y
Samii91 2002 Y Y Y Y Y N Y NA Y
Mooij92 2001 Y Y CD Y Y N Y N Y
Strauss38 2000 Y Y NA Y Y Y Y NA Y
McLaughlin93 1999 Y N Y Y Y N CD N Y
Rizvi55 1999 Y N CD Y Y N CD N Y
Van54 1999 Y N Y Y Y Y Y N Y
Ryu94 1998 Y Y N Y Y N Y NA Y
Acevedo96 1997 N Y Y Y Y N CD NA Y
Magnan95 1997 Y Y Y Y Y N Y NA Y
Illingworth97 1996 Y Y CD Y Y N Y NA Y
Zhang98 1995 N Y CD Y Y N Y NA Y
Cutbush99 1994 Y Y Y Y Y N Y N Y
Sindou43 1992 Y Y N Y Y Y Y N Y
Fukaya56 1991 Y N N Y Y N Y N Y
Yokota57 1991 Y Y CD Y Y Y Y NA Y
Moller42 1989 Y N Y Y Y Y Y N Y
Fritz58 1988 Y N N Y Y Y N NA Y
Auger100 1986 Y Y Y Y Y N Y Y Y
Moller59 1985 Y Y Y Y Y Y Y NA Y
Saito60 1985 Y N Y Y Y Y Y NA Y
Kolluri101 1984 Y Y Y Y Y N Y N Y
Fairholm102 1983 Y Y Y Y Y N Y NA Y
Rushworth103 1982 N N Y Y Y N CD NA Y
Yeh104 1981 N Y Y Y Y N Y NA Y
Open in a new tab

Abbreviations: CD, cannot determine; N, no; NA, not applicable; NIH, National Institutes of Health; PY, publication year; Y, yes.

a

Full questions are listed in Figure 2.

True Prevalence Estimates of Hearing Loss across All Studies

There was a significant amount of heterogeneity in prevalence across the sampled TN articles (Q = 262.33, P< .001) and HFS articles (Q = 388.29, P < .001). Compared with HFS articles, the risk of hearing loss was lower among TN studies (relative risk [RR], 0.67; 95% confidence interval [CI], 0.60–0.76; P < .001), and consequently, a decision was made to stratify the results by indication.

Among TN studies (κ = 35), the estimated true prevalence of hearing loss in patients who underwent MVD was 5.58% (95% CI, 3.85%–7.61%). Figure 4 displays the forest plot of individual study prevalence estimates as well as the overall pooled estimate for TN studies. Conversely, the estimated true prevalence of hearing loss among patients treated for HFS (κ = 47) is 8.25% (95% CI, 6.51%–10.18%). Figure 5 displays the forest plot for these estimates. Supplemental Tables S1 and S2 (available in the online version of the article) report the individual study sample sizes, prevalence estimates, and article weights.

Figure 4.

Figure 4.

Open in a new tab

Forest plot for hearing loss in patients who underwent microvascular decompression for trigeminal neuralgia across all studies.

Figure 5.

Figure 5.

Open in a new tab

Forest plot for hearing loss in patients who underwent microvascular decompression for hemifacial spasm across all studies

Impact of Perioperative Audiograms on Hearing Loss Detection

Studies with routine perioperative audiograms detected significantly more hearing loss. TN studies that used perioperative audiograms were 3.64 times more likely to report hearing loss compared to TN studies not using routine audiograms (95% CI, 2.98–4.44; P < .001). Similarly, HFS studies using perioperative audiograms were 2.27 times more likely to report hearing loss compared to HFS studies not using routine audiograms (95% CI, 2.01–2.57; P < .001). An Altman and Bland test for interaction26 confirmed routine audiograms had a larger impact on detection of hearing loss among patients with TN than HFS (z = 3.93, P < .001).

True Prevalence Estimates of Hearing Loss in Studies with Perioperative Audiograms

The estimated true prevalence of hearing loss in patients who underwent MVD for TN in studies with consistent perioperative audiograms (κ = 10) was 13.47% (95% CI, 7.79%–20.35%), while the estimated true prevalence for HFS (κ = 16) was 13.39% (95% CI, 9.39%–17.96%). In these studies, there was no significant difference in prevalence when comparing the 2 indications (P = .95). Of the studies that made these distinctions, 45.64% reported that hearing loss was conductive (κ = 8) and 67.12% indicated that it was transient (κ = 9). In the studies where the laterality of hearing loss was reported (κ = 10), 4.59% had a bilateral hearing loss and 1.53% had only a contralateral loss (κ = 10).

Impact of BAEP on Hearing Loss

Compared to TN articles not using BAEP, patients were 2.29 times more likely to report hearing loss when BAEP was used (95% CI, 1.70–3.08; P < .001). There was no meaningful difference between articles using or not using BAEP among HFS studies (RR, 0.88; 95% CI, 0.77–1.00; P = .056). Perioperative audiograms were performed more frequently in studies where BAEP was used. When BAEP was used, 58% of TN studies and 69% of HFS studies performed consistent audiograms. However, when BAEP was not used, consistent audiograms were only performed in 13% of TN studies and 21% of HFS studies.

Additional Findings

There was no difference in hearing loss between studies using or not using a fully endoscopic technique among TN articles (RR, 0.47; 95% CI, 0.10–2.12; P = .32) as well as among HFS articles (RR, 0.91; 95% CI, 0.45–1.84; P = .81). Studies that included revision surgeries showed a decreased prevalence of hearing loss among TN studies (RR, 0.69; 95% CI, 0.49–0.97; P = .03). However, HFS studies that included revision surgeries demonstrated a significantly higher prevalence of hearing loss compared to studies that excluded revision surgeries (RR, 1.80; 95% CI, 1.45–2.23; P < .001).

Regarding publication bias, Light and Pillemer25 funnel plots revealed a high level of publication bias for both TN and HFS (Figures 6 and 7). As such, these results should be treated as nascent estimates of hearing loss following microvascular decompression for TN and HFS.

Figure 6.

Figure 6.

Open in a new tab

Publication bias in trigeminal neuralgia studies.

Figure 7.

Figure 7.

Open in a new tab

Publication bias in hemifacial spasm studies.

Discussion

Microvascular decompression has been consistently shown to be an effective treatment option for TN and HFS. However, as examined in this study, hearing loss is a relatively common complication.3 Hearing loss can have a significant impact on quality of life,27 particularly in the auditory frequencies critical to discriminating daily speech (500–2000 Hz).28

While many studies do mention hearing loss as a complication after MVD, standards used in the testing and reporting of hearing loss vary significantly between studies. In this review, nearly two-thirds of all reviewed studies (46 of 69 articles) relied solely on subjective assessment of hearing loss. This type of reporting is obviously inadequate yet surprisingly common. We found that studies with consistent perioperative audiograms are over 3 times more likely to detect hearing loss among patients with TN and over 2 times more likely with HFS. Shah et al29 have shown that the sensitivity of patients subjectively reporting hearing loss is only 56.3% for class C or D hearing in the American Academy of Otolaryngology—Head and Neck Surgery (AAO-HNS) hearing classification system30 and 17.2% for CHL. The timing of the audiogram, type of hearing loss, and hearing loss threshold are also important factors to consider in the diagnosis and management of these patients.

The distinction between conductive and sensorineural hearing loss is critical when the audiogram is performed shortly after surgery. This is because new-onset CHL after posterior fossa surgery is almost uniformly transient, as it results from a middle ear effusion secondary to fluid entering the mastoid air cells during craniotomy.16 Timing of the audiogram then becomes important because an observation period of 2 to 3 months will allow for middle ear and mastoid fluid to resolve and conductive hearing to normalize in most patients.31 SNHL, on the other hand, is more likely permanent and can result from a number of factors as previously mentioned earlier.

Hearing loss following MVD is not necessarily specific to the ipsilateral ear. Noise level exposures ranging from 117 to 122 dB in sound pressure level have been reported from drilling the cortical and mastoid bone.32 It has been suggested that this acoustic trauma could lead to auditory threshold shifts.33–35 These shifts are more likely to occur at high frequencies due to increased susceptibility to sound stimulation of the short outer hair cells in the high-frequency cochlear region compared to the less susceptible taller receptor cells in the low-frequency regions.36,37 In animal models, this threshold shift has been found to be more likely to occur in older animals.35 Some patients will recover their hearing over a period of time; therefore, long-term follow-up audiograms would be needed to detect these changes. Other theories for the cause of contralateral hearing loss after MVD include intraoperative brainstem shift, brainstem edema, labyrinthine fluid imbalance secondary to cerebrospinal fluid release, or venous congestion at the ipsilateral inferior colliculus.38,39

There is also considerable inconsistency in what qualifies as hearing loss across studies (Table 1). Many studies either did not report auditory thresholds or used variable end points. Too small of a threshold could lead to false positives due to testing error,40 and too large of a threshold allows patients who have significant hearing loss to go unreported. It is important that speech discrimination as well as pure-tone average is involved in consideration of hearing loss. The most frequently used threshold in past studies includes a greater than 15 dB pure-tone average increase and/or 20% speech discrimination score decrease (Table 1). More detailed audiometry reporting standards are well established, including the 1995 AAO-HNS hearing classification system30 and the more recently developed scattergram plots.41

Across all studies, MVD of CN VII had a significantly higher risk of hearing loss than MVD of CN V. When only studies with consistent audiograms were included, there was no significant difference between indications. Given the facial nerve’s closer proximity to the vestibulocochlear nerve and important inner ear vasculature, a higher rate of hearing loss is not surprising. The facial nerve’s location necessitates more high-risk manipulation as well as a higher possibility of neocompression from the spacer material. However, with the discrepancy in the 2 data analyses, no conclusion can definitively be made.

Surgeons have employed BAEP in the interest of detecting and avoiding hearing loss in MVD.42,43 Interestingly, the risk of hearing loss increased when BAEP was used among TN articles, whereas it had no impact among HFS articles. It is not immediately clear why the prevalence of hearing loss was higher in TN studies using BAEP. It is possible that this is because authors who used BAEP were more likely to obtain audiograms for TN; however, that is also the case for studies focusing on HFS. It is possible that BAEP leads to overconfidence when surgeons decompress CN V, leading to less caution in cerebellar retraction. The actual cause of this observed difference is a possible topic for future study. The studies that used fully endoscopic technique showed no significant difference in rates of hearing loss compared to those that did not use fully endoscopic technique; however, this analysis was limited by the small number of these studies.

Perioperative audiograms should consist of a preoperative hearing test within 6 months of surgery and a postoperative hearing test approximately 2 to 3 months after surgery. This timing of the preoperative audiogram provides an up-to-date preoperative assessment and a baseline value to establish reasonable patient expectations. In patients with previously undetected preoperative hearing loss, a preoperative audiogram becomes an important medicolegal consideration when the patient has a postoperative hearing complaint. Appropriate timing of a postoperative audiogram allows time for a potential mastoid effusion to resolve and avoids false-positive hearing loss.

All studies have some limitations, and Light and Pillemer25 funnel plots revealed a high level of publication bias in this meta-analysis. This may be because neurosurgeons who have higher than normal rates of hearing loss are less likely to publish. Worse, when they publish, they may be less likely to publicize their complication rates. The variability in reporting standards in the body of literature may also contribute to this uncertainty. Only additional original research will help improve the reported estimates of hearing loss among patients with MVD.

It is important that all measures are taken to document and protect hearing during MVD for TN and HFS. Even the most experienced surgeon taking all necessary precautions may still be faced with some cases of hearing loss after MVD. This hearing loss in many cases is likely a multifactorial pathologic process that is more complicated than simple nerve stretching or trauma and may represent patient susceptibility to a number of surgical factors.44 Thus, it is critically important that patients are counseled regarding the risk to hearing after MVD for TN and HFS. In the 23 studies using routine perioperative audiograms, the estimated true prevalence of hearing loss was 13.47% and 13.39% among patients with TN and HFS, respectively. We believe these numbers are likely the most accurate representation of the prevalence of postoperative hearing loss and would be appropriate to quote when counseling patients regarding the risk of hearing loss following MVD.

Conclusion

Hearing loss is a potential complication following MVD for TN and HFS. In general, reporting on hearing loss after MVD has been of poor quality, with many studies relying on patient-reported subjective hearing loss and/or inadequate audiometric measures. Distinctions should be made between types of hearing loss (sensorineural or conductive), timing of audiometry, and standardizing audiometric reporting thresholds between studies. Routine perioperative audiogram protocols improve the detection of hearing loss and may better represent the true risk of hearing loss after MVD for TN and HFS.

Supplementary Material

supplementary material

Acknowledgments

Special thanks to Jeanne Sadlik, MLS, from the Loyola University Chicago Health Sciences Library for performing the literature search.

Sponsorships: Loyola University Medical Center, Department of Otolaryngology–Head and Neck Surgery. All but 2 authors are members of this department.

Footnotes

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

Disclosures

Competing interests: None.

Supplemental Material

Additional supporting information is available in the online version of the article.

References

  • 1.Dandy WE. Concerning cause of trigeminal neuralgia. Am J Surg. 1934;24:447–455. [Google Scholar]
  • 2.Jannetta PJ. Arterial compression of the trigeminal nerve atthe pons in patients with trigeminal neuralgia. J Neurosurg. 1967;26:159–162. [DOI] [PubMed] [Google Scholar]
  • 3.Sarsam Z, Garcia-Finana M, Nurmikko TJ, Varma TRK,Eldridge P. The long-term outcome of microvascular decompression for trigeminal neuralgia. Br J Neurosurg. 2010;24:18–25. [DOI] [PubMed] [Google Scholar]
  • 4.Qi H, Zhang W, Zhang X, Zhao C. Microvascular decompression surgery for hemifacial spasm. J Craniofac Surg. 2016;27: 124–127. [DOI] [PubMed] [Google Scholar]
  • 5.Hitchon PW, Zanaty M, Moritani T, et al. Microvasculardecompression and MRI findings in trigeminal neuralgia and hemifacial spasm: a single center experience. Clin Neurol Neurosurg. 2015;139:216–220. [DOI] [PubMed] [Google Scholar]
  • 6.Devor M, Amir R, Rappaport ZH. Pathophysiology of trigeminal neuralgia: the ignition hypothesis. Clin J Pain. 2002;18:4–13. [DOI] [PubMed] [Google Scholar]
  • 7.Katusic S, Williams DB, Beard CM, Bergstralh EJ, Kurland LT. Epidemiology and clinical features of idiopathic trigeminal neuralgia and glossopharyngeal neuralgia: similarities and differences. Neuroepidemiology. 1991;10:276. [DOI] [PubMed] [Google Scholar]
  • 8.MacDonald BK, Cockerell OC, Sander JW, Shorvon SD. Theincidence and lifetime prevalence of neurological disorders in a prospective community-based study in the UK. Brain. 2000; 123:665. [DOI] [PubMed] [Google Scholar]
  • 9.Chaudhry N, Srivastava A, Joshi L. Hemifacial spasm: thepast, present, and future. J Neurol Sci. 2015;356:27–31. [DOI] [PubMed] [Google Scholar]
  • 10.Gaul C, Hastreiter P, Duncker A, Naraghi R. Diagnosis and neurosurgical treatment of glossopharyngeal neuralgia: clinical findings and 3-D visualization of neurovascular compression in 19 consecutive patients. J Headache Pain. 2011;12:527–534. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.White JB, Atkinson PP, Cloft HJ, Atkinson JL. Vascular compression as a potential cause of occipital neuralgia: a case report. Cephalalgia. 2008;28:78–82. [DOI] [PubMed] [Google Scholar]
  • 12.Zhang L, Yu Y, Yuan Y, Xu J, Xu X, Zhang J. Microvascular decompression of cochleovestibular nerve in patients with tinnitus and vertigo. Neurol India. 2012;60:495–497. [DOI] [PubMed] [Google Scholar]
  • 13.Taha JM, Tew JM. Long term results of surgical treatment of idiopathic neuralgias of the glossopharyngeal and vagal nerves. Neurosurgery. 1995;36:926–930. [DOI] [PubMed] [Google Scholar]
  • 14.Park K, Hong SH, Hong SD, Cho Y-S, Chung W-H, Ryu NG. Patterns of hearing loss after microvascular decompression for hemifacial spasm. J Neurol Neurosurg Psychiatry. 2009;80: 1165–1167. [DOI] [PubMed] [Google Scholar]
  • 15.Lee MH, Lee HS, Jee TK, et al. Cerebellar retraction and hearing loss after microvascular decompression for hemifacial spasm. Acta Neurochir. 2015;157:337–343. [DOI] [PubMed] [Google Scholar]
  • 16.Ying T, Thirumala P, Gardner P, Habeych M, Crammond D,Balzer J. The incidence of early postoperative conductive hearing loss after microvascular decompression of hemifacial spasm. J Neurol Surg B. 2015;76:411–415. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Polo G, Fischer C, Sindou MP, Marneffe V. Brainstem auditory evoked potential monitoring during micorvascular decompression for hemifacial spasm: intraoperative brainstem auditory evoked potential changes and warning values to prevent hearing loss—prospective study in a consecutive series of 84 patients. Neurosurgery. 2004;54:97–106. [DOI] [PubMed] [Google Scholar]
  • 18.Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMAGroup. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. J Clin Epidemiol. 2009;62:1006–1012. [DOI] [PubMed] [Google Scholar]
  • 19.Oxford Centre for Evidence-Based Medicine. Levels of evidence (March 2009). http://www.cebm.net/oxford-centre-evidence-based-medicine-levels-evidence-march-2009/ Accessed June 8, 2017.
  • 20.Harris PA, Taylor R, Thielke R, Payne J, Gonzalez Conde JG.Research electronic data capture (REDCap)—a metadatadriven methodology and workflow process for providing translational research informatics support. J Biomed Inform. 2009; 42:377–381. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.National Institutes of Health. Quality Assessment tool for caseseries studies. https://www.nhlbi.nih.gov/health-pro/guidelines/indevelop/cardiovascular-risk-reduction/tools/case_series Accessed June 8, 2017.
  • 22.Hedges L, Veva J. Fixed- and random-effects models in meta-analysis. Psychol Methods. 1998;3:486–504. [Google Scholar]
  • 23.Barendregt JJ, Doi SA, Lee YY, Norman RE, Vos T. Metaanalysis of prevalence. J Epidemiol Community Health. 2013; 67:974–978. [DOI] [PubMed] [Google Scholar]
  • 24.Agresti A Categorical Data Analysis. 3rd ed New York, NY: John Wiley; 2013. [Google Scholar]
  • 25.Light RJ, Pillemer DB. Summing Up: The Science of Reviewing Research. Cambridge, MA: Harvard University Press; 1984. [Google Scholar]
  • 26.Altman DG, Bland JM. Interaction revisited: the differencebetween two estimates. BMJ. 2003;326:219. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Chia EM, Wang JJ, Rochtchina E, Cumming RR, Newall P,Mitchell P. Hearing impairment and health-related quality of life: the Blue Mountains Hearing Study. Ear Hear. 2007;28: 187–195. [DOI] [PubMed] [Google Scholar]
  • 28.Dobie RA, Van Hemel S. Basics of sounds, the ear, and hearingIn: Hearing Loss: Determining Eligibility for Social Security Benefits. Washington, DC: National Academies Press; 2004:42–63. [PubMed] [Google Scholar]
  • 29.Shah A, Nikonow T, Thirumala P, et al. Hearing outcomes following microvascular decompression for hemifacial spasm. Clin Neurol Neurosurg. 2012;114:673–677. [DOI] [PubMed] [Google Scholar]
  • 30.Monsell E, Balkany T, Gates G, Goldenberg RA, Meyerhoff WL, House JW. Committee on Hearing and Equilibrium guidelines for the evaluation of hearing preservation in acoustic neuroma (vestibular schwannoma). Otolaryngol Head Neck Surg. 1995;113:179–180. [DOI] [PubMed] [Google Scholar]
  • 31.Watanabe T, Saito N, Sato N, et al. High incidence and spontaneous resolution of mastoid effusion after craniotomy on early postoperative magnetic resonance images. Neuroradiology. 2003;45:482–488. [DOI] [PubMed] [Google Scholar]
  • 32.Yin X, Stromber AK, Duan M. Evaluation of the noise generated by otological electrical drills and suction during cadaver surgery. Acta Otolaryngol. 2011;131:1132–1135. [DOI] [PubMed] [Google Scholar]
  • 33.Frazanegan G, Ghasemi M, Panahi F, Raza M, Alghasi M. Doesdrill induced noise have an impact on sensorineural hearing during craniotomy procedure? Br J Neurosurg. 2010;24:40–45. [DOI] [PubMed] [Google Scholar]
  • 34.Hegewald M, Heitman R, Weiderhold ML, Cooper JC, Gates GA. High frequency electrostimulation hearing after mastoid-ddectomy. Otolaryngol Head Neck Surg. 1989;100:49–56. [DOI] [PubMed] [Google Scholar]
  • 35.Zou J, Bretlau P, Pyykko I, Starck J, Toppila E. Sensorineural hearing loss after vibration: an animal model for evaluating prevention and treatment of inner ear hearing loss. Acta Otolaryngol. 2001;121:143–148. [DOI] [PubMed] [Google Scholar]
  • 36.Chan E, Euneson A, Ulfendahl M. Acoustic trauma causes reversible stiffness changes in auditory sensory cells. Neuroscience. 1998;83:961–968. [DOI] [PubMed] [Google Scholar]
  • 37.Hamernik RP, Patterson JH, Turrentine GA, Ahroon WA. The quantitative relation between sensory cell loss and hearing thresholds. Hear Res. 1989;38:199–211. [DOI] [PubMed] [Google Scholar]
  • 38.Strauss C, Naragi R, Bischoff B, et al. Contralateral hearing loss as an effect of venous congestion after microvascular decompression: report of a case. J Neurol Neurosurg Psychiatry. 2000;69:679–682. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39.Park K, Hong SH, Hong SD, Cho YS, Chung WH, Ryu NG. Patterns of hearing loss after microvascular decompression for hemifacial spasm. J Neurol Neurosurg Psychiatry. 2009;80: 1165–1167. [DOI] [PubMed] [Google Scholar]
  • 40.Lemkens N, Vermeire K, Brokx JP, et al. Interpretation of pure-tone thresholds in sensorineural hearing loss: a review of measurement variability and age-specific references. Acta Otorhinolaryngol Belg. 2002;56:341–352. [PubMed] [Google Scholar]
  • 41.Gurgel RK, Jackler RK, Dobie RA, Popelka GR. A new standardized format for reporting hearing outcome in clinical trials. Otolaryngol Head Neck Surg. 2012;147:803–807. [DOI] [PubMed] [Google Scholar]
  • 42.Moller AR, Moller MB. Does intraoperative monitoring ofauditory evoked potentials reduce incidence of hearing loss as a complication of microvascular decompression of cranial nerves? Neurosurgery. 1989;24:257–263. [DOI] [PubMed] [Google Scholar]
  • 43.Sindou M, Fobe JL, Ciriano D, Fischer C. Hearing prognosis and intraoperative guidance of brainstem auditory evoked potential in microvascular decompression. Laryngoscope. 1992;102:678–682. [DOI] [PubMed] [Google Scholar]
  • 44.Thirumala P, Meigh K, Dasyam N, et al. The incidence of high-frequency hearing loss after microvascular decompression for trigeminal neuralgia, glossopharyngeal neuralgia, or geniculate neuralgia. J Neurosurg. 2015;123:1500–1506. [DOI] [PubMed] [Google Scholar]
  • 45.Shimizu K, Matsumoto M, Wada A, et al. Supine no-retractor method in microvascular decompression for hemifacial spasm: results of 100 consecutive operations. J Neurol Surg B Skull Base. 2015;76:202–207. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46.Soriano-Baron H, Vales-Hidalgo O, Arvizu-Saldana E, Moreno-Jimenez S, Revuelta-Gutierrez R. Hemifacial spasm: 20 year surgical experience, lessons learned. Surg Neurol Int. 2015;6:83. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 47.Ferroli P, Acerbi F, Tomei M, Tringali G, Franzini A, Broggi G. Advanced age as a contraindication to microvascular decompression for drug-resistant trigeminal neuralgia: evidence of prejudice? Neurol Sci. 2010;31:23–28. [DOI] [PubMed] [Google Scholar]
  • 48.Gunther T, Gerganov VM, Stieglitz L, Ludemann W, Samii A, Samii M. Microvascular decompression for trigeminal neuralgia in the elderly: long-term treatment outcome and comparison with younger patients. Neurosurgery. 2009;65:477–482. [DOI] [PubMed] [Google Scholar]
  • 49.Lee SH, Song DG, Kim S, Lee JH, Kang DG. Results of auditory brainstem response monitoring of microvascular decompression: a prospective study of 22 patients with hemifacial spasm. Laryngoscope. 2009;119:1887–1892. [DOI] [PubMed] [Google Scholar]
  • 50.Huh R, Han IB, Moon JY, Chang JW, Chung SS. Microvascular decompression for hemifacial spasm: analyses of operative complications in 1582 consecutive patients. Stereotact Funct Neurosurg. 2012;90:260–265. [DOI] [PubMed] [Google Scholar]
  • 51.Ramnarayan R, Mackenzie I. Brain-stem auditory evoked responses during microvascular decompression for trigeminal neuralgia: predicting post-operative hearing loss. Neurol India. 2006;54:250–254. [DOI] [PubMed] [Google Scholar]
  • 52.Moffat DA, Durvasula VS, Stevens KA, De R, Hardy DG. Outcome following retrosigmoid microvascular decompression of the facial nerve for hemifacial spasm. J Laryngol Otol. 2005;119:779–783. [DOI] [PubMed] [Google Scholar]
  • 53.Brock S, Scaioli V, Ferroli P, Broggi G. Neurovascular decompression in trigeminal neuralgia: role of intraoperative neurophysiological monitoring in the learning period. Stereotact Funct Neurosurg. 2004;82:199–206. [DOI] [PubMed] [Google Scholar]
  • 54.Van HV, Deguine O, Esteve-Fraysse MJ, Bonafe A, Fraysse B. Relationship between cochleovestibular disorders in hemifacial spasm and neurovascular compression. Laryngoscope. 1999;109:741–747. [DOI] [PubMed] [Google Scholar]
  • 55.Rizvi SS, Goyal RN, Calder HB. Hearing preservation in microvascular decompression for trigeminal neuralgia. Laryngoscope. 1999;109:591–594. [DOI] [PubMed] [Google Scholar]
  • 56.Fukaya T, Nomura Y, Fukushima T. Transient retrocochlear low-frequency sensorineural hearing loss: a new clinical entity. Laryngoscope. 1991;101:643–647. [DOI] [PubMed] [Google Scholar]
  • 57.Yokota M, Masaru A, Suzuki T, et al. Evaluation of neurotological examinations in patients with trigeminal neuralgia and hemifacial spasm. Practica Otorhinolaryngol Suppl. 1991;51:111–118. [Google Scholar]
  • 58.Fritz W, Schafer J, Klein HJ. Hearing loss after microvascular decompression for trigeminal neuralgia. J Neurosurg. 1988;69: 367–370. [DOI] [PubMed] [Google Scholar]
  • 59.Moller MB, Moller AR. Loss of auditory function in microvascular decompression for hemifacial spasm. J Neurosurg. 1985; 63:17–20. [DOI] [PubMed] [Google Scholar]
  • 60.Saito H Neurovascular decompression for hemifacial spasm. Acta Otolaryngol. 1984;419:149–154. [PubMed] [Google Scholar]
  • 61.Dou NN, Zhong J, Liu MX, et al. Management of bilateral hemifacial spasm with microvascular decompression. World Neurosurg. 2016;87:640–645. [DOI] [PubMed] [Google Scholar]
  • 62.Li X, Zheng X, Wang X, et al. Microvascular decompression treatment of post-Bell’s palsy hemifacial spasm. Neurol Res. 2013;35:187–192. [DOI] [PubMed] [Google Scholar]
  • 63.Li G, Lan Q, Zhang W. Clinical characteristics and treatment of trigeminal neuralgia following herpes zoster. J Craniofac Surg. 2015;26:448–451. [DOI] [PubMed] [Google Scholar]
  • 64.Amagasaki K, Watanabe S, Naemura K, Nakaguchi H. Microvascular decompression for hemifacial spasm: how can we protect auditory function? Br J Neurosurg. 2015;29:347–352. [DOI] [PubMed] [Google Scholar]
  • 65.Bohman LE, Pierve J, Stephen JH, Sandhu S, Lee JY. Fullyendoscopic microvascular decompression for trigeminal neuralgia: technique review and early outcomes. Neurosurg Focus. 2014;37:E18. [DOI] [PubMed] [Google Scholar]
  • 66.Ma Q, Zhang W, Li G, et al. Analysis of therapeutic effect of microvascular decompression surgery on idiopathic hemifacial spasm. J Craniofac Surg. 2014;25:1810–1813. [DOI] [PubMed] [Google Scholar]
  • 67.Lee CC, Liao CH, Lin CF, et al. Brainstem auditory evoked potential monitoring and neuro-endoscopy: two tools to ensure hearing preservation and surgical success during microvascular decompression. J Chin Med Assoc. 2014;77:308–316. [DOI] [PubMed] [Google Scholar]
  • 68.Sun H, Li ST, Zhong J, et al. The strategy of microvascular decompression for hemifacial spasm: how to decide the endpoint of an MVD surgery. Acta Neurochir. 2014;156:1155–1159. [DOI] [PubMed] [Google Scholar]
  • 69.Sandel T, Eide PK. Long-term results of microvascular decompression for trigeminal neuralgia and hemifacial spasms according to preoperative symptomatology. Acta Neurochir. 2013;155:1681–1692. [DOI] [PubMed] [Google Scholar]
  • 70.Jagannath PM, Venkataramana NK, Bansal A, Ravichandra M. Outcome of microvascular decompression for trigeminal neuralgia using autologous muscle graft: a five-year prospective study. Asian J Neurosurg. 2012;7:125–130. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 71.Oesman C, Mooij JJA. Long term follow-up of microvascular decompression for trigeminal neuralgia. Skull Base. 2011;21: 313–322. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 72.Bond AE, Zada G, Gonzalez AA, Hansen C, Giannotta SL. Operative strategies for minimizing hearing loss and other major complications associated with microvascular decompression for trigeminal neuralgia. World Neurosurg. 2010;74:172–177. [DOI] [PubMed] [Google Scholar]
  • 73.Chang WS, Kim HY, Chung SS, Chang JW. Microneurovascular decompression in patients with hemifacial spasm caused by vascular compression of facial nerve at cisternal portion. Acta Neurochir. 2010;152:2105–2111. [DOI] [PubMed] [Google Scholar]
  • 74.Li D, Wang H, Fan Z, Fan Z. Complications in retrosigmoid cranial nerve surgery. Acta Otolaryngol. 2010;130:247–252. [DOI] [PubMed] [Google Scholar]
  • 75.Ma Z, Li M, Cao Y, Chen X. Keyhole microsurgery for trigeminal neuralgia, hemifacial spasm and glossopharyngeal neuralgia. Eur Arch Otorhinolaryngol. 2010;267:449–454. [DOI] [PubMed] [Google Scholar]
  • 76.Zhong J, Li ST, Zhu J, Guan HX. Is entire nerve root decompression necessary for hemifacial spasm? Int J Surg. 2011;9: 254–257. [DOI] [PubMed] [Google Scholar]
  • 77.Sato S, Yamada M, Koizumi H, et al. Neurophysiological mechanisms of conduction impairment of the auditory nerve during cerebellopontine angle surgery. Clin Neurophysiol. 2009;120:329–335. [DOI] [PubMed] [Google Scholar]
  • 78.Huang BR, Chang CN, Hsu JC. Intraoperative electrophysiological monitoring in microvascular decompression for hemifacial spasm. J Clin Neurosci. 2009;16:209–213. [DOI] [PubMed] [Google Scholar]
  • 79.Salama H, Ben-Khayal H, Mohamed MAS. Outcome of medical and surgical management in intractable idiopathic trigeminal neuralgia. Ann Indian Neurol. 2009;12:173–178. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 80.Linskey ME, Ratanatharathorn V, Penagaricano J. A prospective cohort study of microvascular decompression and Gamma Knife surgery in patients with trigeminal neuralgia. J Neurosurg. 2008;109S:160–172. [DOI] [PubMed] [Google Scholar]
  • 81.Cheng WY, Chao SC, Shen CC. Endoscopic microvasculardecompression of the hemifacial spasm. Surg Neurol. 2008; 70(suppl 1):40–46. [DOI] [PubMed] [Google Scholar]
  • 82.Dannenbaum M, Lega BC, Suki D, Harper RL, Yoshor D. Microvascular decompression for hemifacial spasm: long-term results from 114 operations performed without neurophysiological monitoring. J Neurosurg. 2008;109:410–415. [DOI] [PubMed] [Google Scholar]
  • 83.Artz GJ, Hux FJ, Larouere MJ, Bojrab DI, Babu S, Pieper DR. Endoscopic vascular compression. Otol Neurotol. 2008;29: 995–1000. [DOI] [PubMed] [Google Scholar]
  • 84.Joo WI, Lee KJ, Park HK, Chough CK, Rha HK. Prognostic value of intraoperative lateral spread response monitoring during microvascular decompression in patients with hemifacial spasm. J Clin Neurosci. 2008;15:1335–1339. [DOI] [PubMed] [Google Scholar]
  • 85.Ali M, Khan H. Neuro-vascular conflict as causative factor inidiopathic trigeminal neuralgia. ARYA Atherosclerosis J. 2007; 3:175–177. [Google Scholar]
  • 86.Sindou M, Lesont J, Decullier E, Chapuis F. Microvascular decompression for primary trigeminal neuralgia: long term effectiveness and prognostic factors in a series of 362 consecutive patients with clear-cut neurovascular conflicts who underwent pure decompression. J Neurosurg. 2007;107:1144–1153. [DOI] [PubMed] [Google Scholar]
  • 87.Teo C, Nakaji P, Mobbs RJ. Endoscope assisted microvascular decompression for trigeminal neuralgia: technical case report. Neurosurgery. 2006;59:489–490. [DOI] [PubMed] [Google Scholar]
  • 88.Zakrzewska JM, Lopez BC, Kim SE, Coakham HB. Patientreports of satisfaction after microvascular decompression and partial sensory rhizotomy for trigeminal neuralgia. Neurosurgery. 2005;56:1304–1311. [DOI] [PubMed] [Google Scholar]
  • 89.Hitotsumatsu T, Matsushima T, Inoue T. Microvascular decompression for treatment of trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia: three surgical approach variations: technical note. Neurosurgery. 2003;53:1436–1441. [DOI] [PubMed] [Google Scholar]
  • 90.Javadpour M, Eldridge PR, Varma TR, Miles JB, NurmikkoTJ. Microvascular decompression for trigeminal neuralgia in patients over 70 years of age. Neurology. 2003;60:520. [DOI] [PubMed] [Google Scholar]
  • 91.Samii M, Gunther T, Iaconetta G, Muehling M, Vorkapic P, Samii A. Microvascular decompression to treat hemifacial spasm: long-term results for a consecutive series of 143 patients. Neurosurgery. 2002;50:712–718. [DOI] [PubMed] [Google Scholar]
  • 92.Mooij JJ, Mustafa MK, van Weerden TW. Hemifacial spasm: intraoperative electromyographic monitoring as a guide for microvascular decompression. Neurosurgery. 2001;49:1365–1370. [DOI] [PubMed] [Google Scholar]
  • 93.McLaughlin MR, Jannetta PJ, Clyde BL, Subach BR, Comey CH, Resnick DK. Microvascular decompression of cranial nerves: lessons learned after 4400 operations. J Neurosurg. 1999;90:1–8. [DOI] [PubMed] [Google Scholar]
  • 94.Ryu H, Yamamoto S, Sugiyama K, Uemera K, Miyamoto T. Hemifacial spasm caused by vascular compression of the distal portion of the facial nerve: report of seven cases. J Neurosurg. 1998;88:605–609. [DOI] [PubMed] [Google Scholar]
  • 95.Magnan J, Caces F, Locatelli P, Chays A. Hemifacial spasm: endoscopic vascular decompression. Otolaryngol Head Neck Surg. 1997;117:308–314. [DOI] [PubMed] [Google Scholar]
  • 96.Acevedo JC, Sindou M, Fischer C, Vial C. Microvascular decompression for the treatment of hemifacial spasm: retrospective study of a consecutive series of 75 operated patients—electrophysiologic and anatomical surgical analysis. Stereotact Funct Neurosurg. 1997;68:260–265. [DOI] [PubMed] [Google Scholar]
  • 97.Illingworth RD, Porter DG, Jakubowski J. Hemifacial spasm: aprospective long term follow up of 83 cases treated by microvascular decompression at two neurosurgical centres in the United Kingdom. J Neurol Neurosurg Psychiatry. 1996;60:72–77. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 98.Zhang KW, Shun ZT. Microvascular decompression by the retrosigmoid approach for idiopathic hemifacial spasm: experience with 300 cases. Ann Otol Rhinol Laryngol. 1995;104:610–612. [DOI] [PubMed] [Google Scholar]
  • 99.Cutbush K, Atkinson RL. Treatment of trigeminal neuralgia byposterior fossa microvascular decompression. Aust NZ J Surg. 1994;64:173–176. [DOI] [PubMed] [Google Scholar]
  • 100.Auger RG, Piepgras DG, Laws ER. Hemifacial spasm: resultsof microvascular decompression of the facial nerve in 54 patients. Mayo Clin Proc. 1986;61:640–644. [DOI] [PubMed] [Google Scholar]
  • 101.Kolluri S, Heros RC. Microvascular decompression for trigeminal neuralgia: a five year follow up study. Surg Neurol. 1984;22:235–240. [DOI] [PubMed] [Google Scholar]
  • 102.Firholm D, Wu JM, Liu KN. Hemifacial spasm: results of microvascular relocation. Can J Neurol Sci. 1983;10:187–191. [DOI] [PubMed] [Google Scholar]
  • 103.Rushworth RG, Smith SF. Trigeminal neuralgia and hemifacial spasm: treatment by microvascular decompression. Med J Aust. 1982;1:424–426. [DOI] [PubMed] [Google Scholar]
  • 104.Yeh HS, Tew JM, Ramirez RM. Microsurgical treatment of intractable hemifacial spasm. Neurosurgery. 1981;9:383–386. [DOI] [PubMed] [Google Scholar]
  • 105.Jackler RK. Atlas of Skull Base Surgery and Neurotology. Stuttgart, Germany: Thieme; 2017. [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

supplementary material
NIHMS1556971-supplement-supplementary_material.pdf (140.1KB, pdf)

RESOURCES