Abstract
- Since most vestibular disorders are controlled by medical treatments, surgical options are rarely required. However, there are several vestibular lesions in which surgery can fix the underlying pathophysiology, or should be considered when patients do not benefit from medical treatments. Those diagnoses are labyrinthine fistula, perilymphatic fistula, superior semicircular canal dehiscence syndrome, vestibular paroxysms, rotational vertebral artery syndrome, refractory benign paroxysmal positional vertigo, and intractable Ménière disease. Many surgical options may produce irreversible changes in the vestibular system as well as hearing function. So, accurate diagnosis is paramount for appropriate treatment. In addition, a thorough understanding of disease pathology and the natural course of the condition are essential, as are the experience and judgment of the surgeon, which significantly influence treatment outcomes. Also, it should be noted that surgical procedures are not always successful in controlling vertigo or dizziness. Except in cases of dizziness caused by tumors or inner ear fistula, the role of surgery in treating vestibular disorders is primarily to control symptoms rather than to eliminate the underlying disease. Therefore, most patients should be managed surgically only when medical treatments fail or when surgery is deemed more effective. Before proceeding, patients must fully understand the surgical objectives, potential outcomes, and possible complications. This review provides surgical options for vestibular disorders, emphasizing accurate diagnosis, patient-centered decision-making, and the potential risks of each surgical procedure.
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Keywords: Surgery; Vertigo; Meniere disease; Semicircular canal dehiscence; Benign paroxysmal positional vertigo
INTRODUCTION
When dizziness persists without improvement or recurring frequently, it can significantly disrupt patients’ daily lives, and in severe cases, lead them to despair with the fear that recovery may never be possible. In such instances, if nonsurgical treatments fail to promise relief, surgical treatment options are considered. Many patients who have been suffering from dizziness for an extended period are often willing to opt for surgery if it offers the possibility of complete recovery.
However, even persistent dizziness often presents nonspecific symptoms. So, it is crucial to understand why the patient complains of dizziness and whether the previous treatments were appropriate. For instance, patients who report years-long dizziness accompanied by alternating ear fullness, tinnitus that fluctuates between ears, and frequent headaches might be eager to seek surgical options for Ménière disease. In such cases, it is essential to evaluate whether the patient meets the diagnostic criteria for Ménière disease. Also, it is necessary to identify the affected ear and assess the potential for improvement with surgery. Lack of response to medication prescribed under the assumption of Ménière disease does not determine immediate surgical treatment. Instead, it is necessary to identify triggers, evaluate psychological state, assess vestibular and auditory functions, and consolidate responses to prior treatments to arrive at an accurate diagnosis. It is also important to recognize that surgical intervention might worsen the patient’s condition rather than improve it.
Treatment should first focus on resolving the cause of disease, based on accurate diagnosis and understanding the underlying pathophysiology. If the condition can be addressed with conservative medical treatment, surgery should not be considered as an option.
Dizziness and imbalance caused by vestibular paralysis, such as vestibular neuritis or labyrinthitis, usually improve gradually through proper central compensation [1]. Thus, even if central compensation is incomplete and dizziness persists to the point of hindering daily life, surgical intervention would likely exacerbate the condition.
On the other hand, diseases such as labyrinthine fistula or superior semicircular canal dehiscence syndrome often require surgical approaches to address the underlying lesion for symptomatic improvement. Additionally, in case of frequent or refractory dizziness due to Ménière disease or benign paroxysmal positional vertigo (BPPV), surgery may be considered as a secondary option. Procedures such as endolymphatic sac surgery, perilymph fistula surgery, or microvascular decompression for neurovascular cross compression are performed by many surgeons but remain controversial regarding their roles and efficacy.
Briefly, when considering surgical treatment for patients with dizziness, the following factors should be kept in mind: (1) Accurate diagnosis based on thorough evaluation is essential. (2) It must be checked whether symptoms improved with conservative treatment before surgery. (3) The patient’s general health status should be assessed to ensure they can go through for surgery. (4) Detailed explanations of expected surgical outcomes and potential side effects should be provided, and patients must actively consent and be prepared to accept the surgical results.
The most desirable surgical outcome is to alleviate dizziness while preserving the inner ear structures and auditory function. This article will summarize surgical treatment options for vestibular disorders, covering indications, surgical techniques, and postoperative considerations. Additionally, these surgical options are broadly divided into two categories based on whether vestibular function is preserved after surgery. The first involves nondestructive procedures aimed at correcting the fundamental cause of vertigo. The second involves destroying the vestibular function in the affected side to induce appropriate central compensation. Within the latter category, some procedures aim to preserve hearing while eliminating vestibular function, while others result in the loss of both hearing and vestibular function. The choice of procedure must consider the patient’s hearing ability, age, and the condition of the opposite ear. Vestibular disorders and their surgical treatment options are summarized in Table 1 [1-25], and details of some major surgical procedures are described in this manuscript.
ENDOLYMPHATIC SAC SURGERY
Indications
Endolymphatic sac decompression is performed for intractable Ménière disease in cases where hearing loss is not severe (approximately 40 dB) and the condition frequently recurs despite medical treatment [2]. Since its introduction by George Portmann in 1926, this procedure has remained a widely practiced surgical technique [26]. The theoretical basis of endolymphatic sac surgery is predicated on the assumption that endolymphatic hydrops is the underlying cause of Ménière disease. This procedure can be performed while preserving the patient’s current level of hearing.
Patients with Ménière disease often experience repeated episodes of acute rotatory vertigo, which can severely disrupt normal daily life. The unpredictability of each episode can lead to deepening anxiety and depression, which may, in turn, trigger further vertigo attacks. Alongside treatments aimed at alleviating acute symptoms, it is crucial to implement lifestyle modifications and maintenance pharmacotherapy over an adequate period to control recurrent episodes. Intractable Ménière disease is typically diagnosed when such episodes persist despite at least 6 to 12 months of medical treatment, rendering normal daily life unsustainable, and invasive treatments are then considered.
However, given the potential risks associated with invasive treatments and the irreversible loss of function they may entail, it is imperative to confirm the accuracy of the diagnosis, determine which ear is affected, and verify these findings through comprehensive diagnostic tests before proceeding. The choice of surgical procedure should consider the patient’s hearing status, the potential for bilateral disease, and the residual vestibular function.
Endolymphatic sac decompression is therefore indicated for intractable unilateral Ménière disease with mild to moderate hearing loss and secondary endolymphatic hydrops. It may also be considered for bilateral Ménière disease [27,28]. The surgical procedure can be an option for the patient whose affected side is the sole hearing ear, though there is some risk for sensorineural hearing loss, or in cases where symptoms recur after previous endolymphatic sac surgery.
Preoperative Considerations
Surgical treatment poses risks of complications and irreversible functional loss. Thus, as with any invasive treatment, it is vital to confirm the diagnosis of Ménière disease and the lesion side prior to surgery. Comprehensive diagnostic testing should ensure accurate identification of the affected ear and the triggers of vertigo attacks. The choice of surgical procedure depends on the patient’s hearing condition, bilateral involvement, and residual vestibular function.
The reported effectiveness of endolymphatic sac decompression for vertigo control in Ménière disease varies between 60% and 94% across studies [2,3]. However, persistent doubts have been raised as to whether this procedure is more effective than a placebo in controlling vertigo attacks in Ménière disease. Notably, Thomsen et al. [29,30] reported no significant difference in vertigo improvement between patients who underwent endolymphatic sac decompression and those who underwent simple mastoidectomy. Patients must be informed that vertigo may recur even after surgery. Despite these uncertainties, this procedure is still widely recognized as a primary surgical treatment for intractable Ménière disease, especially since it can preserve auditory function and, in some cases, improve hearing.
Additionally, steroids can be instilled into the opened endolymphatic sac during the procedure. This approach has been acknowledged as a viable option for managing intractable bilateral Ménière disease where medical treatments are limited [31]. Studies utilizing magnetic resonance imaging hydrops protocols to evaluate endolymphatic space changes before and after endolymphatic sac decompression surgery have shown improvements in vestibular hydrops after surgery, along with reductions in the frequency of vertigo attacks [32]. However, cochlear hydrops remained unchanged, and summating potential/action potential ratios on electrocochleography exhibited no significant differences pre- and postsurgery [32]. Although endolymphatic sac decompression is classified as a hearing-preserving procedure, approximately 2% of cases result in hearing loss. This postoperative hearing loss may stem from lymphatic fluid leakage, local inflammatory responses, infection, or inadequate control of Ménière disease postoperatively.
Technique
A retroauricular skin incision is made, exposing the cortical bone of the mastoid, followed by a simple mastoidectomy. The mastoidectomy is extended into the posterior cranial fossa, sufficiently exposing the sigmoid sinus and the posterior fossa dura bordered by the vertical segment of the facial nerve and the posterior semicircular canal. The location of the endolymphatic sac is identified below Donaldson line, an imaginary line extending from the horizontal semicircular canal. Once the endolymphatic sac is opened, a silastic sheet may be inserted to create a shunt into the mastoid or cerebrospinal fluid (CSF) space (Fig. 1). Alternatively, simple decompression without shunting can be performed. Reports indicate significant improvement in vertigo symptoms in Ménière disease with decompression alone [33], and some surgeons recommend avoiding shunts due to concerns that they may obstruct the flow within the endolymphatic sac. However, most surgeons perform a shunt between the endolymphatic sac and the mastoid cavity during surgery [4]. The use of steroids or mitomycin-C during shunting has also been reported to prevent fibrosis at the sac opening [34,35].
Recently, a modification of endolymphatic sac decompression has been studied [5]. Based on the concept that the accumulation of endolymph from the endolymphatic sac is responsible for endolymphatic hydrops, Saliba et al. [5] proposed an endolymphatic duct blockage procedure by ligating the endolymphatic duct. Surgical procedures after identification of the sac are as follows. The sac is completely skeletonized. The bone of the vestibular aqueduct operculum is dissected. The posterior fossa dura from the retrolabyrinthine bone medial to the sac around the endolymphatic duct is exposed in order to identify the duct in its superior and inferior parts in continuity from the sac, and to create a place to insert the tips of the instrument to clip the duct. At this level, care must be taken not to traumatize the thin dura. The dissected endolymphatic duct is blocked with two pieces of 2-mm titanium clips used to control an aneurysm (Fig. 2) [5].
Intraoperative Considerations
As with other mastoid surgeries, a thorough preoperative review of temporal bone computed tomography (CT) scans is crucial. The degree of mastoid pneumatization, the position of the sigmoid sinus, and its proximity to the lateral mastoid cortex should be evaluated. Additionally, atypical emissary veins, a high-riding jugular bulb, the course of the facial nerve, and the position of the vestibular aqueduct must be carefully assessed.
Before identifying the location of the endolymphatic sac, the surrounding critical structures should be noted to prevent unnecessary bleeding or facial nerve injury. For identification of the facial nerve, the mastoid antrum is exposed, followed by the horizontal semicircular canal, the incus in the epitympanic recess, and the tympanic segment of the facial nerve up to the stylomastoid foramen. The bony canal of the facial nerve, identified by its reddish tint due to underlying vasculature, should be distinguished without exposing the nerve. Once these landmarks are confirmed, the posterior fossa dura and the endolymphatic sac can be safely identified.
If exposure of the posterior cranial fossa region is limited due to an anteriorly displaced sigmoid sinus, the overlying bone of the sigmoid sinus can be carefully drilled using a diamond burr, and the sinus can be retracted posteriorly to allow sufficient exposure of the posterior fossa dura where the endolymphatic sac is located.
When opening the endolymphatic sac, care must be taken not to aspirate the sac’s contents with a suction device. Using fine instruments, the internal space of the sac can be visualized and manipulated without causing damage.
VESTIBULAR NEURECTOMY
Indications
Vestibular neurectomy selectively severs the vestibular nerve to induce unilateral functional loss, thereby preventing abnormal peripheral vestibular stimuli from being transmitted to the central nervous system. This procedure is indicated for unilateral Ménière disease patients whose vertigo attacks persist despite intratympanic gentamicin injections [36] and who retain some residual hearing, making labyrinthectomy unsuitable.
Contraindications include patients over 60 years of age or those with bilateral vestibular dysfunction. Although the surgery aims to preserve hearing [37], the possibility of hearing loss should be anticipated.
Preoperative Considerations
The surgical removal of unilateral vestibular nerve leads to functional loss on the ipsilateral side. While dizziness may persist for a significant period immediately following surgery, central compensation occurs as the spontaneous activity of bilateral vestibular nuclei balances out, eventually alleviating dizziness and eliminating recurrent episodes.
Vestibular neurectomy is typically considered only after intratympanic gentamicin injection or exploratory tympanotomy with direct gentamicin application fails to control vertigo [6,36]. Preoperative preparations include repeated audiometric and vestibular function tests to ensure that vertigo originates from the affected ear and not from incomplete central compensation following vestibular ablation [37].
Technique
Three primary surgical approaches can be used for vestibular neurectomy: the retrolabyrinthine, retrosigmoid, and middle cranial fossa approaches. Neuromonitoring systems are employed to monitor the facial nerve and assess auditory function changes using evoked potentials during surgery. For all approaches except the middle cranial fossa, lumbar drainage is preemptively performed to reduce CSF pressure and prevent postoperative CSF leakage.
The surgical procedure of retrolabyrinthine approach is as follows. A mastoidectomy is performed, and space is created between the posterior semicircular canal and the posterior fossa dura to access the cerebellopontine angle. The vestibular nerve is sectioned near its root entry zone to the brainstem. Since this approach involves the proximal portion of the 8th cranial nerve before its division into cochlear and vestibular nerves, incomplete vestibular nerve sectioning or cochlear nerve injury may occur. Adequate retraction of the sigmoid sinus is essential, and skin incisions must be made at least 2 cm posterior to the auricle for proper exposure. After the vestibular nerve is severed, the mastoid cavity is packed with abdominal fat to prevent CSF leakage.
In the retrosigmoid approach, a suboccipital craniotomy is performed to access the cerebellopontine angle and sever the vestibular nerve at the opening of the internal auditory canal. Skin incisions are made approximately 6 to 7 cm posterior to the ear, followed by subperiosteal dissection to expose the occipital bone. The craniotomy window is centered on the posterior sigmoid sinus and the inferior transverse sinus. After CSF drainage and cerebellar retraction, the vestibular nerve is carefully dissected and sectioned using fine instruments, avoiding damage to nearby structures such as the facial nerve. The dura is sealed, and the bone defect is repaired with bone wax and muscle or tissue grafts.
In the middle cranial fossa approach, a 4×4 cm craniotomy is performed to expose the middle cranial fossa floor after a temporal skin incision and reflection of the temporalis muscle. The superior semicircular canal and greater superficial petrosal nerve serve as landmarks for identifying the internal auditory canal. The vestibular nerve is severed within the internal auditory canal, where it is distinctly separated from the cochlear nerve (Fig. 3). The dura is repaired, and the craniotomy site is reconstructed with the bone flap.
Intraoperative Considerations
Key considerations include identifying critical anatomical landmarks and ensuring complete sectioning of the vestibular nerve while avoiding damage to the facial and cochlear nerves. The advantages and disadvantages of each approach are summarized in Table 2.
LABYRINTHECTOMY
Indications
Labyrinthectomy involves the surgical removal of the vestibular structures in the inner ear to eliminate vestibular function on the affected side, thereby preventing abnormal stimuli from being transmitted to the central nervous system. This procedure is considered a last resort for unilateral Ménière disease or Ménière-like syndrome with severe recurrent vertigo that does not respond to other invasive treatments.
With the widespread adoption of simpler procedures such as intratympanic gentamicin injections, the frequency of traditional surgeries like vestibular nerve section and labyrinthectomy has declined. Since this surgery results in total hearing loss, it is only considered for patients with little to no residual hearing. Age is not a contraindication for this procedure.
Preoperative Considerations
Before proceeding with surgery, repeated audiometric and vestibular function tests must confirm that the affected side has significant damage to hearing and balance functions, that the recurrent vertigo attacks are a result of this damage, and that the contralateral ear’s auditory and vestibular functions are stable and unaffected.
Although labyrinthectomy is rarely performed immediately for Ménière disease, it is typically considered after unsuccessful attempts at intratympanic gentamicin injections. In such cases, it is crucial to distinguish whether the patient’s persistent vertigo is due to inadequate vestibular ablation caused by gentamicin or whether it stems from central compensation failure following vestibular loss [38]. Detailed inquiry into the patient’s symptoms and an evaluation of vestibular function changes are essential. Failure to differentiate between vertigo caused by Ménière disease and dizziness resulting from incomplete central compensation could lead to unnecessary or ineffective surgical intervention.
If persistent vertigo after intratympanic gentamicin treatment is due to insufficient vestibular ablation, exploratory tympanotomy can be considered before proceeding with labyrinthectomy or vestibular neurectomy [6]. This involves lifting the tympanomeatal flap, checking for anatomical obstacles (e.g., scarring or bony overgrowth) around the round and oval windows, and administering gentamicin directly to induce sufficient vestibular ablation, thereby potentially avoiding more invasive procedures.
In a study tracking 780 patients with Ménière disease and secondary endolymphatic hydrops over 2 years, 95 required intratympanic gentamicin injection, but 10 of these patients experienced uncontrolled vertigo due to anatomical barriers that prevented adequate absorption of gentamicin [38]. Among seven patients who underwent exploratory tympanotomy, vertigo control was achieved in five cases without needing vestibular nerve section or labyrinthectomy.
Technique
Labyrinthectomy can be performed via the transmastoid approach or the transcanal approach.
In transmastoid labyrinthectomy, a postauricular incision is made, and mastoidectomy is performed to expose the horizontal semicircular canal. The course of the facial nerve is identified to prevent damage. Using a drill, the three semicircular canals are sequentially opened, and the neuroepithelium within the ampullae is removed. The vestibule, which houses the utricle and saccule, is also removed. The remaining bony labyrinth is irrigated with saline and sealed with bone wax and soft tissue.
In transcanal labyrinthectomy, the tympanomeatal flap is elevated, and the stapes is removed from the oval window. The vestibule is accessed, and the sensory structures are excised. Additional bone removal between the oval and round windows can widen the exposure. However, this approach is limited as it cannot fully address the posterior and superior semicircular canal ampullae or their associated sensory structures. Consequently, transcanal labyrinthectomy has a higher incidence of postoperative disequilibrium (63% vs. 23%) compared to the transmastoid approach [39].
Intraoperative Considerations
For transcanal labyrinthectomy, complete removal of the vestibular neuroepithelium may not be possible. To address this, the vestibule can be packed with aminoglycoside-soaked gelfoam to induce additional vestibular ablation.
Over time, the remaining bony labyrinth undergoes fibrosis and ossification. As such, cochlear implantation can be considered simultaneously during labyrinthectomy if hearing restoration is desired.
SURGERY FOR SUPERIOR CANAL DEHISCENCE SYNDROME
Indications
When vestibular and auditory symptoms caused by superior semicircular canal dehiscence significantly disrupt daily life, closing the dehiscent area can alleviate or resolve symptoms. The primary symptoms of superior canal dehiscence syndrome (SCDS) include ear fullness, autophony, and dizziness. Although originally recognized as a cause of Tullio phenomenon (dizziness induced by loud sounds) and Hennebert sign (dizziness and nystagmus triggered by pressure on the external auditory canal), patients often report chronic imbalance or brief episodes of nonspecific dizziness rather than these specific signs.
Auditory symptoms such as autophony, ear fullness, and tinnitus can be mistaken for other inner ear disorders or Eustachian tube dysfunction unless carefully examined. Objective tests like caloric testing, rotational chair tests, and video head impulse tests often yield normal results [40]. Consequently, SCDS diagnosis requires detailed symptom evaluation and pure-tone audiometry. If SCDS is suspected, high-resolution temporal bone CT is used to confirm the presence of dehiscence in the superior semicircular canal or other areas. However, as false positives are common, it is essential to correlate the imaging findings with the patient’s symptoms and rule out other vestibular disorders before considering surgery [41].
Preoperative Considerations
Various surgical approaches have been explored to address SCDS. In the middle cranial fossa approach, bony dehiscence can be directly identified and sealed in most cases except for SCD by the superior petrosal sinus. While effective, it is invasive and requires temporal bone exposure.
The transmastoid approach is to access the superior canal using a familiar technique through mastoidectomy. Although less invasive and more familiar to otologists, this approach could not directly visualize the dehiscent area.
Transcanal round window obliteration is a less invasive method that involves sealing the round window to mitigate the “third mobile window” effect. However, its symptom improvement is limited.
Surgical Technique
The procedures of the middle cranial fossa approach are described in the vestibular neurectomy section. The dura is carefully elevated around the dehiscent area, leaving the dura over the lesion intact until the last stage. After the defect is exposed, the semicircular canal is sealed with autologous soft tissue and bone wax to ensure a watertight seal (Fig. 4). The craniotomy site is reconstructed with the bone flap.
Several techniques have been employed to repair the dehiscence. A recent meta-analysis classifies them into three main categories [42]: (1) canal plugging: the semicircular canal is occluded internally using fascia and bone pate, followed by coverage with bone fragments. (2) Canal resurfacing: the membranous labyrinth is separated from the dura and covered with fascia and bone fragments. However, this method has lower success rates due to fragment displacement. (3) Canal capping: after covering the dehiscence with fascia, hydroxyapatite bone cement is used to secure the repair.
The meta-analysis suggests that canal plugging and canal capping yield higher success rates compared to resurfacing techniques [42]. In cases where middle cranial fossa exposure is limited, the transmastoid approach may serve as an alternative [43], although its ability to directly address the defect is constrained.
Intraoperative Considerations
Facial nerve monitoring is essential, and auditory function should be tracked intraoperatively using auditory brainstem response or electrocochleography [44]. Navigation systems can help optimize the craniotomy location and identify the dehiscence. The location and the size of the dehiscence should be studied in a preoperative temporal bone CT. It would be in the arcuate eminence facing the middle fossa dura at the highest point of the superior semicircular canal. Dehiscence would be easily visualized. When the dehiscence is located near the common crus where the superior and posterior canals merge, it is dehiscent by the superior petrosal sinus and is more difficult to access through the middle cranial fossa.
The thin bone surrounding the dehiscent area requires reinforcement with multiple layers of bone wax, fascia, and soft tissue to ensure durability. Minimal soft tissue packing of the lumen should be used to avoid disrupting the ampulla’s function.
For the transmastoid approach, since the defect cannot be visualized, a controlled opening of the canal allows occlusion, but this results in broader closure compared to direct repair.
SEMICIRCULAR CANAL OCCLUSION FOR INTRACTABLE BENIGN PAROXYSMAL POSITIONAL VERTIGO
Indications
For cases of BPPV that do not respond to appropriate canalith repositioning maneuvers, surgical intervention can be considered. The procedure involves occluding the affected semicircular canal to block the flow of endolymph and prevent abnormal stimulation caused by dislodged otoliths. This technique was first attempted for posterior semicircular canal BPPV (Parnes surgery) and requires opening the bony labyrinth to occlude the canal [45]. Due to the risk of sensorineural hearing loss, this surgery should be carefully considered and reserved for patients with persistent symptoms lasting over a year or for those experiencing frequent recurrences that significantly impact their quality of life.
Preoperative Considerations
Postoperatively, BPPV in the affected canal is completely resolved, but approximately 15% of patients may experience prolonged mild dizziness or imbalance. In a study involving 28 patients, the Dizziness Handicap Inventory score improved significantly from 70 to 13, with only one patient experiencing hearing loss [46]. A meta-analysis of 32 cases reported an average postoperative hearing loss of 6 dB, with no cases of facial nerve paralysis [47].
Technique
Following a mastoidectomy, the horizontal semicircular canal and the course of the facial nerve are identified to locate the posterior semicircular canal. Using a diamond burr, the bony wall of the posterior semicircular canal is thinned until the canal’s bluish endolymphatic space becomes visible. Approximately 2 mm of the canal is exposed, and the canal is occluded proximally and distally with soft tissue prepared in advance. Bone dust is then used to fill the canal, and the external surface is sealed with bone wax and covered with soft tissue (Fig. 5).
Intraoperative Considerations
When occluding the canal, care should be taken to avoid damaging surrounding structures, such as the facial nerve, and to prevent leakage of endolymph from the canal. After surgery, mild dizziness may persist for days, although positional vertigo diminishes. If sensorineural hearing loss develops postoperatively, the surgeon should monitor the symptom carefully by giving systemic steroid treatment, considering the possibility of labyrinthitis.
CONCLUSION
Surgical treatment is rarely required for dizziness but can significantly benefit patients with conditions such as labyrinthine fistula, perilymphatic fistula, superior semicircular canal dehiscence syndrome, disabling positional vertigo, rotational vertebral artery syndrome, refractory BPPV, or Ménière disease.
Accurate diagnosis is paramount for appropriate treatment. In Ménière disease, the most effective approach is one that preserves hearing while alleviating vertigo. Endolymphatic sac decompression is the most commonly preferred surgical treatment among clinicians, although its effectiveness remains a topic of debate [2,27,29]. Conversely, some practitioners favor vestibular neurectomy for its ability to prevent bilateral progression of Ménière disease and effectively reduce vertigo recurrence [28]. For patients with significant hearing loss, intratympanic gentamicin injections are often more effective in controlling vertigo than surgical interventions [38].
In intractable Ménière disease, as vertigo episodes recur and hearing loss progresses, the natural course of the disease often leads to eventual exhaustion of inner ear function, reducing the frequency of vertigo attacks. Despite numerous studies claiming the superiority of certain treatments over control groups, well-designed randomized double-blind studies have yet to confirm any medical treatment that can halt the progression of hearing loss [29]. Therefore, it is crucial to use treatments that are less likely to accelerate hearing loss compared to the natural progression of the disease. Accurate diagnosis, a thorough understanding of disease pathology, and the natural course of the condition are essential, as are the experience and judgment of the surgeon, which significantly influence treatment outcomes.
Except in cases of dizziness caused by tumors, the role of surgery in treating vestibular disorders is primarily to control symptoms rather than to eliminate the underlying disease. While conditions like perilymphatic and labyrinthine fistulas warrant primary surgical intervention, other cases should be managed surgically only when medical treatments fail or when surgery is deemed more effective. Before proceeding, patients must fully understand the surgical objectives, potential outcomes, and possible complications.
ARTICLE INFORMATION
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Funding/Support
This study was supported by Seoul National University Bundang Hospital Research Fund (No. 02-2023-0042).
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Conflicts of Interest
No potential conflict of interest relevant to this article was reported.
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Availability of Data and Materials
The datasets are not publicly available but are available from the corresponding author upon reasonable request.
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Authors’ Contributions
Conceptualization: Koo JW, Nam DW; Funding acquisition: Koo JW; Writing–original draft: Koo JW; Writing–review and editing: Lee JK.
All authors read and approved the final manuscript.
Fig. 1.Endolymphatic sac decompression (left ear). The endolymphatic duct is located in the posterior fossa dura, also known as Trautman triangle, which is outlined by the sigmoid sinus posteriorly, the sinodural angle superiorly, and the posterior canal anteriorly. The endolymphatic sac is located, and then the lumen is opened following L-shaped incision. FN, facial nerve; HC, horizontal semicircular canal; SC, superior semicircular canal; PC, posterior semicircular canal.
Fig. 2.Endolymphatic duct blockage. The endolymphatic duct is ligated with two pieces of small aneurysmal clips.
Fig. 3.Vestibular neurectomy via middle fossa approach (left ear). The cleavage line is identified between the facial nerve and the superior vestibular nerve. Superior and inferior vestibular nerves are identified posteriorly and ligated.
Fig. 4.Surgical plugging of superior canal dehiscence. (A) Superior canal dehiscence is exposed via the middle fossa approach. The temporal lobe dura is retracted, and the middle cranial base is carefully explored to locate the superior canal dehiscence. (B) Lumen is plugged with prepared soft tissue and then sealed with bone wax.
Fig. 5.Posterior canal occlusion. (A) First, the course of the facial nerve (FN), horizontal semicircular canal (HC), and posterior semicircular canal (PC) are clearly located (A), and then the PC is identified by blue line (arrow). (B) Dislodged otolith particles are seen in the membranous labyrinth. (C) The PC lumen is occluded using soft tissue and then sealed using bone wax. SS, sigmoid sinus.
Table 1.Surgical options for vestibular disorders
|
Vestibular disorder |
Surgical options [reference] |
|
Ménière disease and secondary endolymphatic hydrops |
Sacculotomy [7], Cochleo-sacculotomy [8] |
|
Endolymphatic sac decompression [1-4] |
|
Endolymphatic duct blockage [5] |
|
Exploratory tympanotomy and gentamicin application [6] |
|
Vestibular neurectomy [9-13] |
|
Labyrinthectomy [14] |
|
Superior canal dehiscence syndrome |
Plugging surgery [15-16] |
|
Round window obliteration [17] |
|
Benign paroxysmal positional vertigo |
Semicircular canal occlusion [18] |
|
Singular neurectomy [19] |
|
Labyrinthine fistula |
Tympanomastoidectomy and fistula repair [20] |
|
Perilymph fistula |
Exploratory tympanotomy and fistula repair [21-22] |
|
Subtotal petrosectomy [22] |
|
Vestibular paroxysmia |
Microvascular decompression [23] |
|
Vestibular neurectomy [9-13] |
|
Rotational vertebral artery syndrome |
Fusion of C1 and C2 [24] |
|
Decompressive laminectomy [25] |
Table 2.The advantages and disadvantages of each approach for vestibular neurectomy
|
Variable |
Retrolabyrinthine |
Retrosigmoid |
Middle cranial fossa |
|
Nerve section site |
Root entry zone |
Porus acousticus |
Internal auditory canal |
|
Advantage |
Low risk of facial nerve injury |
Less invasive to temporal bone, shorter operative time |
Precise nerve sectioning post-cochlear division |
|
Minimal cerebellar retraction |
|
Disadvantage |
Incomplete vestibular nerve sectioning, risk of cochlear nerve damage |
Requires cerebellar retraction, risk of postoperative headache |
Technically challenging |
|
Risk of facial nerve damage |
|
Requires temporal lobe retraction |
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