Hearing loss after microvascular decompression for hemifacial spasm

Hearing loss after microvascular decompression for hemifacial spasm

Risk factors

The cochlear nerve function is at risk during microvascular decompression for hemifacial spasm.

Cause and risk factors are highly variable.

A study strongly suggested a correlation between the cerebellar retraction factors, especially retraction depth and duration, and possibility of hearing loss following MVD for HFS 1).

Intradural compression due to overinfusion of saline may lead to postoperative hearing loss, although the incidence is low, and immediate decompression by drainage may be required 2).

Prevention

Intraoperative monitoring of brainstem auditory evoked potentials (BAEPs) can be a useful tool to decrease the danger of hearing loss 3) 4) 5).

It is important to emphasize the need for clean exposure of the lower cranial nerves (except for cranial nerve VIII) to obtain enough working space, sharp arachnoid dissection, minimal cerebellar retraction, and proper responses to changes identified during intraoperative monitoring 6).

Diagnosis

Prolongation of the inter-peak latency of waves I-III seems to be associated with the occurrence of delayed hearing loss. It is possible that BAEP changes may predict delayed hearing loss, but confirmatory evidence is not available as yet. Analysis of more cases is necessary to determine the utility of BAEP monitoring to predict delayed hearing loss after MVD and to identify its exact cause 7).

Case series

Lee et al., from the Samsung Medical Center in a study aimed to analyze cases of delayed hearing loss after microvascular decompression (MVD) for hemifacial spasm and identify the characteristic features of these patients.

They retrospectively reviewed the medical records of 3462 patients who underwent MVD for hemifacial spasm between January 1998 and August 2017.

Among these, there were 5 cases in which hearing was normal immediately postoperatively but delayed hearing loss occurred. None of the 5 patients reported any hearing disturbance immediately after the operation. However, they developed hearing problems suddenly after some time (median, 22 days; range 10-45 days). On examination, sensorineural hearing loss was confirmed. High-dose corticosteroid treatment was prescribed. Preoperative hearing levels were restored after several months (median duration from the time of the operation, 45 days; range 22-118 days). Interestingly, the inter-peak latency of waves I-III in the brainstem auditory evoked potentials (BAEP) was prolonged during the surgery, but recovered within a short time.

Delayed hearing loss may occur after MVD for HFS. Prolongation of the inter-peak latency of waves I-III seems to be associated with the occurrence of delayed hearing loss. It is possible that BAEP changes may predict delayed hearing loss, but confirmatory evidence is not available as yet. Analysis of more cases is necessary to determine the utility of BAEP monitoring to predict delayed hearing loss after MVD and to identify its exact cause 8).


Nine hundred and thirty-two patients with HFS who underwent MVD with intraoperative monitoring (IOM) of BAEP were analyzed. Park et al., used a 43.9 Hz/s stimulation rate and 400 averaging trials to obtain BAEP. To evaluate HL, pure-tone audiometry and speech discrimination scoring were performed before and one week after surgery. We analyzed the incidence for postoperative HL according to BAEP changes and calculated the diagnostic accuracy of significant warning criteria.

Only 11 (1.2%) patients experienced postoperative HL. The group showing permanent loss of wave V showed the largest percentage of postoperative HL (p < 0.001). No patient who experienced only latency prolongation (≥1 ms) had postoperative HL. Loss of wave V and latency prolongation (≥1 ms) with amplitude decrement (≥50%) were highly associated with postoperative HL.

Loss of wave V and latency prolongation of 1 ms with amplitude decrement ≥50% were the critical warning signs of BAEP for predicting postoperative HL 9).


Jung et al., retrospectively analyzed the medical records of patients with HFS who underwent MVD with the same surgeon from March 2003 to October 2016, and reviewed the pertinent literature. Patients who were followed up for more than 6 months were selected, resulting in the analysis of 1434 total patients. Postoperative hearing complications were evaluated audiometrically and subjectively (patient-reported symptoms). Clinical factors such as the intraoperative findings were reviewed to identify their correlation with auditory function.

Symptoms in 1333/1434 patients (93.0%) resolved more than 90% from their preoperative state. Among them, 16 patients (1.1%) complained of hearing impairment after surgery. Most impairment was transient, although 6/1333 patients (0.4%) required additional interventions for persistent hearing deficits (one surgical intervention and five hearing aids). A >50% decrease in the amplitude of brainstem auditory evoked potentials during the operation was significantly associated with postoperative hearing deficits.

Few auditory complications, mostly transient, result from MVD. Although MVD is a commonplace surgical technique, to reduce complications it is important to emphasize the need for clean exposure of the lower cranial nerves (except for cranial nerve VIII) to obtain enough working space, sharp arachnoid dissection, minimal cerebellar retraction, and proper responses to changes identified during intraoperative monitoring 10)


Three hundred thirty-one patients with HFS underwent MVD from March 2009 to October 2010.

Brain stem auditory evoked potential (BAEP) was monitored during the surgery. Before completion of the dural closure, the surgical field was routinely filled with warm saline to avoid postoperative pneumocephalus and epidural hematoma.

Seven patients experienced a change in wave V amplitude and latency after the dural closure. In 2 patients, the amplitudes decreased by less than 50%, and latencies were delayed by less than 1.0 ms, ipsilaterally in 1 patient and contralaterally in the other. In 1 patient, decreased amplitude and delayed latency appeared bilaterally with more severity on the operated side, accompanied by delayed ipsilateral permanent hearing loss. In 4 of the 7 patients, an ipsilateral response of BAEP was completely absent. Of these 4 patients, 2 experienced permanent hearing loss, and another 2 patients who underwent dural reopening and saline drainage had restoration of their normal hearing.

Intradural compression due to overinfusion of saline may lead to postoperative hearing loss, although the incidence is low, and immediate decompression by drainage may be required 11).


668 patients (95.7%) had no hearing loss immediately after surgery (group 1). 17 patients (2.4%) had a postoperative decrease in PTA exceeding 15 dB and a decrease in SDS which was proportional to the postoperative PTA thresholds (group 2). Eight patients (1.2%) had poor SDS that appeared to be out of proportion to the degree of hearing loss depicted by the postoperative PTA thresholds, suggesting retrocochlear or cochlear nerve pathology (group 3). Five patients (0.7%) had total deafness after surgery (group 4). In group 2, 12 patients (70.6%) returned to their preoperative hearing capacity. However, among the eight patients in group 3 and five in group 4, only two (25%) and none (0%) have returned to their preoperative hearing status, respectively.

In this large study, permanent hearing loss occurred in 16 patients (2.2%). Patients with a mild hearing loss with a good SDS (cochlear type) demonstrated much better prognosis than those with poor SDS (retrocochlear type) or total deafness. In addition, total deafness after surgery had no chance of recovery to preoperative hearing capacity 12).


Auditory function was studied before and after surgery in 143 consecutive patients who were operated on for hemifacial spasm by microvascular decompression of the intracranial portion of the facial nerve. The acoustic reflex was abnormal preoperatively in 41% of the patients, indicating that the vascular abnormalities that caused the hemifacial spasm also affected the auditory nerve. Three patients suffered a profound hearing loss in the ear on the operated side, and one lost hearing function totally. In addition, 24 patients had a moderate elevation in the pure-tone threshold at one or more octave frequencies. Of these, 16 patients experienced a hearing loss at only one frequency (8000 Hz), while eight had a threshold evaluation of no more than 20 dB in the speech frequency range (500, 1000, and 2000 Hz). Two patients were deaf on the side of the spasm before the operation. Three patients were not tested postoperatively, and one patient was tested only after surgery. Thus, in this series of 143 patients, only 2.8% suffered a significant hearing loss as a complication of facial nerve decompression to relieve hemifacial spasm 13).

Case reports

Onoda et al., reported two unusual cases of delayed hearing loss after microvascular decompression (MVD) for hemifacial spasm. In the first case, A 59-year-old female noted left hearing loss one week after receiving MVD for left hemifacial spasm. In the second case, A 39-year-old male also noticed ipsilateral hearing loss on the 7th day after MVD for right hemifacial spasm. Both cases were treated by steroid. Two months after the onset, their hearing function improved dramatically. These cases indicated that the delayed hearing loss after MVD for hemifacial spasm can occur, even when gentle microsurgical technique is used, but the prognosis for this condition is fairly good 14).

References

1)

Li N, Zhao WG, Pu CH, Yang WL. Quantitative study of the correlation between cerebellar retraction factors and hearing loss following microvascular decompression for hemifacial spasm. Acta Neurochir (Wien). 2018 Jan;160(1):145-150. doi: 10.1007/s00701-017-3368-9. Epub 2017 Oct 26. PubMed PMID: 29075904.
2) , 11)

Jo KW, Lee JA, Park K, Cho YS. A new possible mechanism of hearing loss after microvascular decompression for hemifacial spasm. Otol Neurotol. 2013 Sep;34(7):1247-52. doi: 10.1097/MAO.0b013e31829b5786. PubMed PMID: 23942352.
3) , 7) , 8)

Lee MH, Lee S, Park SK, Lee JA, Park K. Delayed hearing loss after microvascular decompression for hemifacial spasm. Acta Neurochir (Wien). 2019 Mar;161(3):503-508. doi: 10.1007/s00701-018-3774-7. Epub 2018 Dec 19. PubMed PMID: 30569226.
4) , 9)

Park SK, Joo BE, Lee S, Lee JA, Hwang JH, Kong DS, Seo DW, Park K, Lee HT. The critical warning sign of real-time brainstem auditory evoked potentials during microvascular decompression for hemifacial spasm. Clin Neurophysiol. 2018 May;129(5):1097-1102. doi: 10.1016/j.clinph.2017.12.032. Epub 2018 Jan 4. PubMed PMID: 29342440.
5)

El Damaty A, Rosenstengel C, Matthes M, Baldauf J, Dziemba O, Hosemann W, Schroeder HWS. A New Score to Predict the Risk of Hearing Impairment After Microvascular Decompression for Hemifacial Spasm. Neurosurgery. 2017 Nov 1;81(5):834-843. doi: 10.1093/neuros/nyx111. PubMed PMID: 28973677.
6) , 10)

Jung NY, Lee SW, Park CK, Chang WS, Jung HH, Chang JW. Hearing Outcome Following Microvascular Decompression for Hemifacial Spasm: Series of 1434 Cases. World Neurosurg. 2017 Dec;108:566-571. doi: 10.1016/j.wneu.2017.09.053. Epub 2017 Sep 18. PubMed PMID: 28927910.
12)

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 Oct;80(10):1165-7. doi: 10.1136/jnnp.2007.136713. PubMed PMID: 19762909.
13)

Møller MB, Møller AR. Loss of auditory function in microvascular decompression for hemifacial spasm. Results in 143 consecutive cases. J Neurosurg. 1985 Jul;63(1):17-20. PubMed PMID: 4009269.
14)

Onoda K, Ono S, Miyoshi Y, Tokunaga K, Date I. [Delayed hearing loss after microvascular decompression for hemifacial spasm: report of two cases]. No Shinkei Geka. 2006 Oct;34(10):1045-9. Review. Japanese. PubMed PMID: 17052017.

Update: Microvascular decompression for glossopharyngeal neuralgia

Microvascular decompression for glossopharyngeal neuralgia

For glossopharyngeal neuralgia treatment, should pharmacologic management be ineffective, surgical intervention is indicated. The first-choice treatment is typically microvascular decompression (MVD), as it has the highest initial and long-term success rates.
In 1932, Walter Edward Dandy 1) thought that the operative approach of GPN was the same with trigeminal neuralgia or Meniere’s disease.
Laha and Jannetta 2) proposed that GPN could be treated by surgically relieving the pressure that offending vascular structures imposed on the glossopharyngeal nerves.
Resnick et al. 3) reporteded excellent postoperative surgical results for 79%.
Patel et al. reported in 217 a immediate success rate of 90% 4).
There are three types of neurovascular compression (NVC): type I – NVC at the root entry zone (REZ) of the IX CN within the retro-olivary sulcus; type II – the vertebral artery causes NVC at the IX CN REZ by the shoulder of the artery, and the type III – a “sandwich-like” compression where the vertebral artery and the PICA perform a combination of NVC 5).

Technique

Once the anesthetic induction and intubation have been performed, the patient should be positioned in lateral decubitus fashion, fixing the head with a Mayfield head clamp, followed by the placement of an axillary roll. The neck should be narrowed with slight flexion and rotated approximately 10 degrees to the affected side. The vertex is tilted 15 degrees toward the floor. The shoulder is pulled out of the way and finally the patient is accommodated in such a way that the table can be rotated laterally or adjusted for a Trendelenburg position or reverse Trendelenburg position. For the incision, the mastoid eminence is initially demarcated, then a line is drawn from the external auditory canal to the inion to mark the transverse sinus. Then, a 3-4 cm arcuate or linear incision is performed, with the concave side toward the ear. Half of the incision should be above the mastoid notch or even more posteriorly in large, muscular or dolichocephalic patients. Subsequently, a retractor is placed and the bone is opened with a perforator, making sure to use bone wax in case of bleeding and filling the mastoid cells.
Ordónez-Rubiano et al. propose to target the opening of the bone depending on the CN affected. Three different approaches could be performed. The superior for the V CN (mini extreme-lateral or microasterional), the middle for VII and VIII CNs (usual for the cerebellopontine angle), and the inferior for the IX to XII CNs (mini far-lateral).
Once the dura is exposed, it is incised and stretched. The form in which the dura is opened includes the L or reverse L shape, 3-5 mm parallel to the sigmoid sinus and to the floor of the posterior fossa, after which they are secured with sutures for a wider exposure. A retractor is placed under the cerebellum and raised from its inferolateral margin, after which the microscope is introduced, and the retractor is advanced anteriorly until the spinal part of the XI CN is observed, the arachnoid is dissected, which allows to elevate the cerebellum and expose the remaining CNs within the jugular foramen. Once the rootlets of the IX CN are identified, they are separated from the rootlets of the X and XI CNs. The involved vessel is identified and dissected before the decompression and finally, the Teflon is placed between the two structures 6).
If there is no NVC, the glossopharyngeal nerve and the upper bundle of the X CN can be sectioned 7).

Case series

2018

Between 2006 and 2016, 228 idiopathic GPN patients underwent MVD in our department. Those cases were retrospectively reviewed with emphasis on intraoperative findings and long-term postoperative outcomes. The average period of follow-up was 54.3 ± 6.2 months.
Intraoperatively, the culprit was identified as the posterior inferior cerebellar artery (PICA) in 165 cases (72.3%), the vertebral artery (VA) in 14 (6.1%), vein in 10 (4.4%), and a combination of multiple arteries or venous offending vessels in 39 (17.2%). The immediately postoperative outcome was excellent in 204 cases (89.5%), good in 12 (5.3%), fair in 6 (2.6%) and poor in 6 (2.6%). More than 5-year follow-up was obtained in 107 cases (46.9%), which presented as excellent in 93 (86.9%), good in 6 (5.6%), fair in 3 (2.8%) and poor in 5 (4.7%). Thirty-seven (16.2%) of the patients experienced some postoperative neurological deficits immediately, such as dysphagia, hoarseness and facial paralysis, which has been improved at the last follow-up in most cases, except 2.
This investigation demonstrated that MVD is a safe and effective remedy for treatment of GPN 8).

2017

30 patients with intractable primary typical GPN who underwent MVD without rhizotomy and were followed for more than 2 years were included in the analysis. Each MVD was performed using one of four different surgical techniques: interposition of Teflon pieces, transposition of offending vessels using Teflon pieces, transposition of offending vessels using a fibrin-glue-coated Teflon sling, and removal of offending veins.
The posterior inferior cerebellar artery was responsible for neurovascular compression in 27 of 30 (90%) patients, either by itself or in combination with other vessels. The location of compression on the glossopharyngeal nerve varied; the root entry zone (REZ) only (63.3%) was most common, followed by both the REZ and distal portion (26.7%) and the distal portion alone (10.0%). In terms of detailed surgical techniques during MVD, the offending vessels were transposed in 24 (80%) patients, either using additional insulation, offered by Teflon pieces (15 patients), or using a fibrin glue-coated Teflon sling (9 patients). Simple insertion of Teflon pieces and removal of a small vein were also performed in five and one patient, respectively. During the 2 years following MVD, 29 of 30 (96.7%) patients were asymptomatic or experienced only occasional pain that did not require medication. Temporary hemodynamic instability occurred in two patients during MVD, and seven patients experienced transient postoperative complications. Neither persistent morbidity nor mortality was reported.
This study demonstrates that MVD without rhizotomy is a safe and effective treatment option for GPN 9).


From January 2004 to June 2006, 35 consecutive patients were diagnosed with GPN. All of them underwent MVD. Demographic data, clinical presentation, operative findings, clinical results, operative complications were reviewed.
A total of 33 patients (94.3%) experienced complete pain relief immediately after MVD. Long-term follow-up was available for 30 of these 35 patients, and 28 of these 30 patients continued to be pain-free. There was no long-term operative morbidity in all cases. One patient had a cerebrospinal fluid leak and 1 case presented with delayed facial palsy.
Classic GPN is usually caused by pulsatile neurovascular compression of the glossopharyngeal and vagus rootlets. MVD is a safe, effective, and durable operation for GPN 10).

2015

A retrospective review of the case notes of patients who had undergone surgery for GPN in the authors’ department between 2008 and 2013 was performed to investigate baseline characteristics and immediate outcomes during the hospitalization. For the long-term results, a telephone survey was performed, and information on pain recurrence and permanent complications was collected. Pain relief meant no pain or medication, any pain persisting after surgery was considered to be treatment failure, and any pain returning during the follow-up period was considered to be pain recurrence. For comparative study, the patients were divided into 2 cohorts, that is, patients treated with GPNR alone and those treated with GPNR+VNR.
One hundred three procedures, consisting of GPNR alone in 38 cases and GPNR+VNR in 65 cases, were performed in 103 consecutive patients with GPN. Seventy-nine of the 103 patients could be contacted for the follow-up study, with a mean follow-up duration of 2.73 years (range 1 month-5.75 years). While there were similar results (GPNR vs GPNR+VNR) in immediate pain relief rates (94.7% vs 93.8%), immediate complication rates (7.9% vs 4.6%), and long-term pain relief rates (92.3% vs 94.3%) between the 2 cohorts, a great difference was seen in long-term complications (3.8% vs 35.8%). The long-term complication rate for the combined GPNR+VNR cohort was 9.4 times higher than that in the GPNR cohort. There was no operative or perioperative mortality. Immediate complications occurred in 6 cases, consisting of poor wound healing in 3 cases, and CSF leakage, hoarseness, and dystaxia in 1 case each. Permanent complications occurred in 20 patients (25.3%) and included cough while drinking in 10 patients, pharyngeal discomfort in 8 patients, and hoarseness and dysphagia in 1 case each.
In general, this study indicates that GPNR alone or in combination with VNR is a safe, simple, and effective treatment option for GPN. It may be especially valuable for patients who are not suitable for the microvascular decompression (MVD) procedure and for surgeons who have little experience with MVD. Of note, this study renews the significance of GPNR alone, which, the authors believe, is at least valuable for a subgroup of GPN patients, with significantly fewer long-term complications than those for rhizotomy for both glossopharyngeal nerve and rootlets of the vagus nerve 11).

2002

Patel et al. present the experience with more than 200 patients and conducted a retrospective review of the database and identified patients who presented for treatment of presumed GPN. When possible, patients were contacted by telephone for collection of follow-up information regarding symptom relief, complications, functional outcomes, and patient satisfaction. Univariate and multivariate analyses were performed to identify predictors of good outcomes after MVD. Subgroup analyses were performed with quartiles of approximately 50 patients each, for assessment of the effects of improvements in techniques and anesthesia during this 20-year period.
They observed GPN to be more common among female (66.8%) than male (33.2%) patients, with an overall mean patient age of 50.2 years (standard deviation, 14.4 yr). The most common presenting symptoms were throat and ear pain and throat pain alone, and the mean duration of symptoms was 5.7 years (standard deviation, 5.8 yr; range, 1-32 yr). Symptoms appeared almost equally on the left side (54.8%) and the right side (45.2%). The overall immediate success rate exceeded 90%, and long-term patient outcomes and satisfaction were best for the typical GPN group (with pain restricted to the throat and palate). Complication rates decreased across quartiles for all categories evaluated.
MVD is a safe, effective form of therapy for GPN. It may be most beneficial for patients with typical GPN, especially when symptoms are restricted to deep throat pain only 12).

1995

Since 1971, 40 patients have undergone microvascular decompression of the glossopharyngeal and vagus nerves for treatment of typical glossopharyngeal neuralgia. This procedure provided excellent immediate results (complete or > 95% relief of pain) in 79%, with an additional 10% having a substantial (> 50%) reduction in pain. Long-term follow-up (mean, 48 mo; range, 6-170 mo) reveals excellent results (complete or > 95% reduction in pain without any medication) in 76% of the patients and substantial improvement in an additional 16%. There were two deaths at surgery (5%) both occurring early in the series as the result of hemodynamic lability causing intracranial hemorrhage. Three patients (8%) suffered permanent 9th nerve palsy 13).

1986

20 patients who had undergone microvascular decompression for the treatment of “idiopathic” trigeminal neuralgia (9 cases), hemifacial spasm (7 cases), glossopharyngeal neuralgia (3 cases) and paroxysmal vertigo and tinnitus (1 case) were followed up for 25 months on average. Permanent relief of symptoms was observed in 19 (95%), with sparing of cranial nerve function. Analysis of the clinical data shows that the patients described in the present series did not differ from those considered to suffer from “idiopathic” cranial nerve dysfunction syndromes. The importance of vascular cross compression as etiological factor in such conditions is stressed and the pathophysiology discussed. The term “cryptogenic” applied to trigeminal neuralgia or hemifacial spasm thus needs revising. Lastly, the indications of microvascular decompression in the treatment of “cryptogenic” cranial nerve dysfunction syndromes are defined 14).

1977

Microsurgical observations werw made of the cranial nerve root entry or exit zones 117 patients operated upon for the treatment of hyperactive-hypoactive dysfunction syndromes (trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction, and glossopharyngeal neuralgia). Cross-compression or distortion of the appropriate nerve root at its entry or exit zone was noted in all patients. This compression or distortion was usually caused by normal or arteriosclerotic, elongated arterial loops, it was usually relieved by decompressive microsurgical techniques. A small percentage of patients were found to have compression of the nerve root at the entry-exit zone by a tumor, a vein, or some other structural abnormality; they were relieved by tumor excision or other measures as described. Relief was gradual postoperatively if the treated nerve was not stroked or manipulated at operation but it was immediate if the nerve was manipulated. Preoperative evidence of decreased nerve function improved postoperatively 15).

Case reports

A case of coexistent glossopharyngeal neuralgia and hemifacial spasm was treated by transposition of the vertebral artery. A 60-year-old man was referred to our hospital due to pain in the left posterior part of the tongue that was difficult to control with oral medication at a local hospital. The diagnosis was left glossopharyngeal neuralgia based on the symptoms, imaging findings, and lidocaine test results. Moreover, the patient had left hemifacial spasm. Microvascular decompression was performed, which confirmed that the vertebral artery was compressing the lower cranial nerve and the posterior inferior cerebellar artery was compressing the root exit zone of the facial nerve. The vertebral artery and posterior inferior cerebellar artery were transposed using TachoSil. After the surgery, both glossopharyngeal neuralgia and hemifacial spasm disappeared, and the patient was discharged 16).

1985

A case of combined trigeminal and glossopharyngeal neuralgia is described. The superior cerebellar artery and normal choroid plexus compressed and indented the root entry zones of the trigeminal and glossopharyngeal nerves, respectively. Complete relief was obtained after microvascular decompression and resection of the choroid plexus 17).


A case of glossopharyngeal neuralgia associated with episodic cardiac arrest and syncope is presented. Posterior fossa exploration showed that the left glossopharyngeal and vagus nerves were compressed by the posterior inferior cerebellar artery. Microvascular decompression resulted in complete relief of glossopharyngeal neuralgia, cardiac syncope, and seizure. The mechanism of glossopharyngeal neuralgia associated with cardiac syncope is discussed 18).


Murasawa A, Yamada K, Hayakawa T, Aragaki Y, Yoshimine T. Glossopharyngeal neuralgia treated by microvascular decompression–case report. Neurol Med Chir (Tokyo). 1985 Jul;25(7):551-3. PubMed PMID: 2415848 19).
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Dandy WE (1932) The treatment of trigeminal neuralgia by the cerebellar route. Ann Surg 96:787–795
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Laha RK, Jannetta PJ (1977) Glossopharyngeal neuralgia. J Neurosurg 47:316–320
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Resnick DK, Jannetta PJ, Bissonnette D, Jho HD, Lanzino G. Microvascular decompression for glossopharyngeal neuralgia. Neurosurgery. 1995 Jan;36(1):64-8; discussion 68-9. PubMed PMID: 7708170.
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Patel A, Kassam A, Horowitz M, Chang YF. Microvascular decompression in the management of glossopharyngeal neuralgia: analysis of 217 cases. Neurosurgery. 2002 Apr;50(4):705-10; discussion 710-1. PubMed PMID: 11904019.
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Tanrikulu L, Hastreiter P, Dörfler A, Buchfelder M, Naraghi R. Classification of neurovascular compression in glossopharyngeal neuralgia: Three-dimensional visualization of the glossopharyngeal nerve. Surg Neurol Int. 2015 Dec 24;6:189. doi: 10.4103/2152-7806.172534. eCollection 2015. PubMed PMID: 26759734; PubMed Central PMCID: PMC4697202.
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Ordónez-Rubiano EG, García-Chingaté CC, Rodríguez-Vargas S, Cifuentes-Lobelo HA, Perilla-Cepeda TA. Microvascular Decompression for a Patient with a Glossopharyngeal Neuralgia: A Technical Note. Cureus. 2017 Jul 20;9(7):e1494. doi: 10.7759/cureus.1494. PubMed PMID: 28948114; PubMed Central PMCID: PMC5606712.
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Rey-Dios R, Cohen-Gadol AA. Current neurosurgical management of glossopharyngeal neuralgia and technical nuances for microvascular decompression surgery. Neurosurg Focus. 2013 Mar;34(3):E8. doi: 10.3171/2012.12.FOCUS12391. Review. PubMed PMID: 23451790.
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Xia L, Li YS, Liu MX, Zhong J, Dou NN, Li B, Li ST. Microvascular decompression for glossopharyngeal neuralgia: a retrospective analysis of 228 cases. Acta Neurochir (Wien). 2018 Jan;160(1):117-123. doi: 10.1007/s00701-017-3347-1. Epub 2017 Nov 4. PubMed PMID: 29103137.
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Kim MK, Park JS, Ahn YH. Microvascular Decompression for Glossopharyngeal Neuralgia: Clinical Analyses of 30 Cases. J Korean Neurosurg Soc. 2017 Nov;60(6):738-748. doi: 10.3340/jkns.2017.0506.010. Epub 2017 Oct 25. PubMed PMID: 29142635; PubMed Central PMCID: PMC5678068.
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Zhao H, Zhang X, Zhu J, Tang YD, Li ST. Microvascular Decompression for Glossopharyngeal Neuralgia: Long-Term Follow-Up. World Neurosurg. 2017 Jun;102:151-156. doi: 10.1016/j.wneu.2017.02.106. Epub 2017 Mar 2. PubMed PMID: 28263933.
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Ma Y, Li YF, Wang QC, Wang B, Huang HT. Neurosurgical treatment of glossopharyngeal neuralgia: analysis of 103 cases. J Neurosurg. 2015 Sep 4:1-5. [Epub ahead of print] PubMed PMID: 26339847.
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Michelucci R, Tassinari CA, Samoggia G, Tognetti F, Calbucci F. Intracranial microvascular decompression for “cryptogenic” hemifacial spasm, trigeminal and glossopharyngeal neuralgia, paroxysmal vertigo and tinnitus: II. Clinical study and long-term follow up. Ital J Neurol Sci. 1986 Jun;7(3):367-74. PubMed PMID: 3733417.
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Jannetta PJ. Observations on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction and glossopharyngeal neuralgia. Definitive microsurgical treatment and results in 117 patients. Neurochirurgia (Stuttg). 1977 Sep;20(5):145-54. PubMed PMID: 198692.
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Fujii T, Otani N, Otsuka Y, Matsumoto T, Tanoue S, Ueno H, Tomura S, Tomiyama A, Toyooka T, Wada K, Mori K. [A Case of Coexistent Glossopharyngeal Neuralgia and Hemifacial Spasm Successfully Treated with Transposition of the Vertebral Artery]. No Shinkei Geka. 2017 Jun;45(6):503-508. doi: 10.11477/mf.1436203540. Review. Japanese. PubMed PMID: 28634310.
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Tsuboi M, Suzuki K, Nagao S, Nishimoto A. Glossopharyngeal neuralgia with cardiac syncope. A case successfully treated by microvascular decompression. Surg Neurol. 1985 Sep;24(3):279-83. PubMed PMID: 4023909.
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Murasawa A, Yamada K, Hayakawa T, Aragaki Y, Yoshimine T. Glossopharyngeal neuralgia treated by microvascular decompression–case report. Neurol Med Chir (Tokyo). 1985 Jul;25(7):551-3. PubMed PMID: 2415848.

Hydrocephalus after posterior fossa decompression for Chiari type 1 deformity

Hydrocephalus after posterior fossa decompression for Chiari type 1 deformity

Hydrocephalus may be seen in association with Chiari type 1 deformity, likely because of disruptions in normal CSF flow. Although patients sometimes demonstrate evidence of hydrocephalus during their initial presentation for CM-I, a subset of patients appear to develop hydrocephalus only after posterior fossa decompression. These patients may present with evidence of raised intracranial pressure, ventricular dilation on imaging, or persistent cerebrospinal fluid leakage postoperatively. To date, there are no reports in the literature investigating what factors are associated with the need for CSF diversion after PFD is performed to treat CM-I.
Guan et al. performed a retrospective clinical chart review of all patients who underwent PFD surgery and duraplasty for CM-I at the Primary Children’s Hospital in Utah from June 1, 2005, through May 31, 2015. Patients were dichotomized based on the need for long-term CSF diversion after PFD. Analysis included both univariate and multivariable logistic regression analyses.
The authors identified 297 decompressive surgeries over the period of the study, 22 of which required long-term postoperative CSF diversion. On multivariable analysis, age < 6 years old (OR 3.342, 95% CI 1.282-8.713), higher intraoperative blood loss (OR 1.003, 95% CI 1.001-1.006), and the presence of a fourth ventricular web (OR 3.752, 95% CI 1.306-10.783) were significantly associated with the need for long-term CSF diversion after decompressive surgery.
Younger patients, those with extensive intraoperative blood loss, and those found during surgery to have a fourth ventricular web were at higher risk for the development of CRH. Clinicians should be alert to evidence of CRH in this patient population after PFD surgery. 1) 2).
Elton et al. present three patients who developed infratentorial supracerebellar hygromas causing acute hydrocephalus after posterior cranial fossa decompression 3).
A 34-year-old woman presented with strain-related suboccipital headache and myelopathy for 6 months. Imaging revealed tonsillar herniation up to C2 level and cervical syringomyelia. A standard FMD, C1 posterior arch removal, and tonsillar reduction was performed. After an initial uneventful postoperative course, she had 2 readmissions with headache, vomiting, and ataxia. Imaging showed a tense pseudomeningocele and concomitant supratentorial and infratentorial (initially right-sided, followed by left-sided) SDHs with ventriculomegaly. She was conservatively managed with antiedema measures and had excellent relief of symptoms. For the literature review, only cases with concomitant supratentorial and infratentorial SDHs with hydrocephalus were searched online and analyzed.
Including this, 10 cases have been reported. Mean age was 25.3 years. The male-to-female ratio was 1:2.3. Symptoms appeared an average of 12.6 days postoperatively. Treatment was with conservative management in 3 cases, and 3 cases required permanent cerebrospinal fluid diversions. Mean follow-up duration was 9.4 months (range, 1-27 months).
Coexistent supratentorial and infratentorial SDHs with hydrocephalus after Chiari decompression is a very rare occurrence. Treatment needs to be individualized based on the predominant symptomatic lesion, and surgical options need to be judiciously considered. Good prognosis is the rule in most cases 4).


A 2-year-old girl with the Chiari 1 malformation underwent FMD, including suboccipital craniotomy, C1 laminectomy and durotomy without opening the arachnoid.
After initial postoperative improvement, the patient deteriorated, developing subdural hygromas and hydrocephalus. These were treated successfully with observation and acetazolamide.
Subdural hygromas may complicate FMD. A slit valve opening in the arachnoid might be part of the pathophysiology. While surgical intervention may be necessary in some circumstances, non-operative measures may be effective as well 5).
1)

Guan J, Riva-Cambrin J, Brockmeyer DL. Chiari-related hydrocephalus: assessment of clinical risk factors in a cohort of 297 consecutive patients. Neurosurg Focus. 2016 Nov;41(5):E2. PubMed PMID: 27798986.
2)

Pereira EA, Magdum SA. Foramen magnum decompression – from hygromas to hydrocephalus. Br J Neurosurg. 2016 Jun;30(3):355. doi: 10.3109/02688697.2016.1173198. Epub 2016 Apr 21. PubMed PMID: 27100816.
3)

Elton S, Tubbs RS, Wellons JC 3rd, Blount JP, Grabb PA, Oakes WJ. Acute hydrocephalus following a Chiari I decompression. Pediatr Neurosurg. 2002 Feb;36(2):101-4. PubMed PMID: 11893893.
4)

Prasad GL, Menon GR. Coexistent Supratentorial and Infratentorial Subdural Hygromas with Hydrocephalus After Chiari Decompression Surgery: Review of Literature. World Neurosurg. 2016 Sep;93:208-14. doi: 10.1016/j.wneu.2016.06.025. Epub 2016 Jun 16. Review. PubMed PMID: 27319314.
5)

Filis AK, Moon K, Cohen AR. Symptomatic Subdural Hygroma and Hydrocephalus following Chiari I Decompression. Pediatr Neurosurg. 2009;45(6):425-8. doi: 10.1159/000270159. Epub 2009 Dec 24. PubMed PMID: 20051703.
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