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.

Hemifacial spasm etiology

Although classical hemifacial spasm (HFS) has been attributed to an atraumatic pulsatile vascular compression around the root exit zone (REZ) of the facial nerve, rare tumor-related HFS associated with meningiomas, epidermoid tumors, lipomas, and schwannomas in the cerebellopontine angle have been reported. The exact mechanism and the necessity of microvascular decompression for tumor-induced HFS is not clear, especially for vestibular schwannomas.


Imaging data of 341 patients with a HFS who underwent microvascular decompression were reviewed retrospectively and compared with 360 controls. The hemodynamics of typical anatomical variations of the vertebral artery (VA) were analyzed using computational fluid dynamics (CFD) software.

Asymmetry of the left and right VAs was prevalent, and the left VA was the most dominant VA. A dominant VA was more prevalent in the HFS group than in the control group (p=0.026). A Left HFS had a significantly higher proportion of a left dominant VA, and a right HFS had a significantly higher proportion of right dominant VA (p<0.001). CFD models showed that angulation and tortuosity of vessels caused remarkable pressure difference between vascular walls of opposite sides. Dynamic clinical observations showed the mode of vessel transposition coincided with biomechanical characteristics.

Anatomical variations and hemodynamics of the vertebrobasilar arterial system are likely to contribute to vascular compression formation in a HFS1).


Liu et al. retrospectively analyzed 10 patients with vestibular schwannomas out of 5218 cases of hemifacial spasm between 2004 and 2014.

Hemifacial spasm occurred ipsilateral to the vestibular schwannoma in 9 patients and contralateral to the lesion in 1 patient. The mean follow-up period was 86 months (range, 22-140 months). All patients underwent surgery for resection of the vestibular schwannoma. Following the principle of neurovascular compression, offending vessels were found in 7 patients, no offending vessels in 2 patients, and a tumor with the displacement of brain stem contributing to contralateral facial nerve compression in 1 patient. HFS was relieved immediately postoperatively in 9 patients, whereas it improved gradually and then resolved after one month in one patient with a contralateral vestibular schwannoma.

For HFS induced by vestibular schwannomas in this study, the majority of cases are caused by a combination of tumor and vascular co-compression at the REZ. Surgical intervention resulted in resolution of symptoms. For HFS with ipsilateral vestibular schwannoma, exploration of the facial nerve root for vascular compression should be performed routinely after tumor resection. It is critical to check that no vessel is contact with the entire nerve root 2).


During the period from October 1984 to October 2008, Han et al. treated 6,910 HFS patients using a microsurgical procedure. Of these HFS patients, 55 cases were associated with cerebellopontine angle tumors. A small craniectomy was performed in order to excise the tumor. All tumors were found to compress the root exit zone (REZ) of the facial nerve to different extents, but concomitant vascular compression of the facial nerve was observed in a majority of cases, and microvascular decompression of the facial nerve at REZ was conducted in 43 of 55 patients (78.2%) by displacing the co-compressing vasculature away from the REZ and retaining it using a Teflon pad. Intraoperative findings and postoperative pathological examinations suggested that the tumors were epidermoid cysts, meningiomas, and Schwannomas. Follow-up in 48 of 55 patients for 4-230 months after surgery showed that the clinical symptoms of HFS disappeared in 43 cases, improved in two cases, and recurred in three cases. Ten patients had sequelae associated with the operation. They concluded from this study that the majority of cases of tumor-related HFS are caused by combined tumor and vascular co-compression at the REZ, and tumor removal and microvascular decompression are required in order to relieve the symptoms 3).


Kindling-like hyperactivity of the facial motor nucleus induced by constant stimulation of compressing artery is considered as the predominant mechanism underlying the pathogenesis of Hemifacial spasm (HFS).

Trigeminal neuralgia, hemifacial spasm, vestibulocochlear neuralgia and glossopharyngeal neuralgia represent the most common neurovascular compression syndromes.

In nearly all cases, primary hemifacial spasm is related to arterial compression of the facial nerve at root exit zone (REZ). The offending arterial loops originate from the posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA), or vertebrobasilar artery (VB). In as many as 40% of the patients, neurovascular conflicts are multiple. The cross-compression is almost always seen on magnetic resonance imagingcombined with magnetic resonance angiography.


Hemifacial spasm (HFS) associated with type 1 Chiari malformation is particularly uncommon and is limited to isolated case report.

Li et al retrospectively evaluated 13 patients who had simultaneously HFS and type 1 Chiari malformation among 675 HFS patients. Clinical features and radiological findings were collected from each patient and analyzed. All these 13 patients were surgically treated with MVD through retro-mastoid microsurgical approach, and postoperative outcomes were evaluated. A review of literature about this association was also provided. In this study, the frequency of type 1 Chiari malformation in HFS patients was 1.9 %. The clinical profile of this series of patients did not differ from typical form of primary HFS. MVD achieved satisfactory results in 11 patients (85 %) in short- and long-term follow-up. There was no mortality or severe complication occurred postoperatively. Although rare, clinician should be aware of the association of HFS and type 1 Chiari malformation and consider MVD as an effective surgical management 4).

References

1)

Wang QP, Yuan Y, Xiong NX, Fu P, Huang T, Yang B, Liu J, Chu X, Zhao HY. Anatomical variation and hemodynamic evolution of vertebrobasilar arterial system may contribute to the development of vascular compression in hemifacial spasm. World Neurosurg. 2018 Dec 26. pii: S1878-8750(18)32897-3. doi: 10.1016/j.wneu.2018.12.074. [Epub ahead of print] PubMed PMID: 30593967.
2)

Liu J, Liu P, Zuo Y, Xu X, Liu H, Du R, Yu Y, Yuan Y. Hemifacial Spasm as Rare Clinical Presentation of Vestibular Schwannomas. World Neurosurg. 2018 Aug;116:e889-e894. doi: 10.1016/j.wneu.2018.05.124. Epub 2018 May 28. PubMed PMID: 29852302.
3)

Han H, Chen G, Zuo H. Microsurgical treatment for 55 patients with hemifacial spasm due to cerebellopontine angle tumors. Neurosurg Rev. 2010 Jul;33(3):335-9; discussion 339-40. doi: 10.1007/s10143-010-0250-0. Epub 2010 Mar 9. PubMed PMID: 20217169.
4)

Li N, Zhao WG, Pu CH, Yang WL. Hemifacial spasm associated with type 1 Chiari malformation: a retrospective study of 13 cases. Neurosurg Rev. 2016 Jul 15. [Epub ahead of print] PubMed PMID: 27422274.

Why Me?: My 8-year treatment journey For Hemifacial Spasm (tic convulsif)

Why Me?: My 8-year treatment journey For Hemifacial Spasm (tic convulsif)


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Hemifacial spasm is a neuromuscular movement disorder characterized by brief or persistent involuntary contractions of the muscles innervated by the facial nerve. Its prevalence has been estimated at 11 cases per 100,000 individuals.
Hemifacial spasm is usually caused by an artery compressing the facial nerve at the root exit zone of the brainstem. As for treatment, many  patients obtain moderate or marked relief from local injections of botulinum toxin (Botox), which must be repeated every 3 to 4 months. Alternatively, microvascular decompression has a success rate of about 85%.

My story follows my more than 8 year struggle with this condition and is written to hopefully help those who are going through the same thing to a positive and successful treatment.

 

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