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E. R. Anson and Y. Gimmon

Chapter 15
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Vestibular Implants
E.Loos, N.Verhaert, E.Devocht, N.Guinand, A.Perez-Fornos,
C.Desloovere, andR.van de Berg
Introduction
During the last few decades, much research has been performed to develop an implantable vestibular prosthesis to articially restore vestibular function. The concept is similar to a cochlear implant (CI), which has already been used for many years for treating
severe sensorineural hearing loss. The vestibular implant (VI) aims to provide the
E. Loos (*)
Department of Neurosciences, Research Group ExpORL, KU Leuven, University of Leuven,
Leuven, Belgium
Department of Otorhinolaryngology-Head and Neck Surgery, University Hospitals Leuven,
Leuven, Belgium
Department of ENT/Audiology, School for Mental Health and Neuroscience (MHENS),
Maastricht University Medical Center, Maastricht, The Netherlands
e-mail: elke.loos@kuleuven.be
N. Verhaert · C. Desloovere
Department of Neurosciences, Research Group ExpORL, KU Leuven, University of Leuven,
Leuven, Belgium
Department of Otorhinolaryngology-Head and Neck Surgery, University Hospitals Leuven,
Leuven, Belgium
e-mail: elke.loos@kuleuven.be; Nicolas.verhaert@kuleuven.be; christian.desloovere@
uzleuven.be
E. Devocht · R. van de Berg
Department of ENT/Audiology, School for Mental Health and Neuroscience (MHENS),
Maastricht University Medical Center, Maastricht, The Netherlands
e-mail: Elke.devocht@mumc.nl; raymond.vande.berg@mumc.nl
N. Guinand · A. Perez-Fornos
Division of Otorhinolaryngology and Head-and-Neck Surgery, Department of Clinical
Neurosciences, Geneva University Hospitals, Geneva, Switzerland
e-mail: Nils.Guinand@hcuge.ch; Angelica.PerezFornos@hcuge.ch
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
B. T. Crane et al. (eds.), Disorders of the Vestibular System,
https://doi.org/10.1007/978-3-031-40524-2_15
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central nervous system with information about head spatial orientation and movement.
The pioneering work of Bernard Cohen and Jun-Ichi Suzuki in the 1960s, who rst
described eye movements originating from electrically stimulating the ampullary
nerves of rabbits, pigeons, cats, and monkeys [1], inspired Gong and Merfeld, who
described the rst vestibular prosthesis that was tested in guinea pigs [2]. Those animal
experiments paved the way for human research. In 2004, the rst human patients underwent vestibular stimulation before undergoing surgery for cochlear implantation or surgical labyrinthectomy [3]. In these trials, it was conrmed that electrical stimulation of
the ampullary nerves could produce a nystagmic response aligned with the plane of the
stimulated canal. After this proof of concept, Guyot etal. performed the rst vestibular
implantation in humans in 2007 [4]. This implant was a modied CI (MED-EL,
Innsbruck, Austria), in which one electrode was removed from the cochlear array and
implanted in the vicinity of the posterior ampullary nerve. It was demonstrated that a
patient could adapt to electrical stimulation of the vestibular system without too much
discomfort and that, once the adaptation was completed, the electrical stimulation could
be modulated to articially evoke smooth eye movements [5]. As these prerequisites for
developing a VI were fullled, the implant was modied into a multichannel prosthesis
and implanted for the rst time in 2012 by the Geneva-Maastricht Group [6]. At the
moment, two main types of VIs exist: the semicircular canal implants and the otolith
implants. There are two subtypes of semicircular canal (SCC) implants: pure VIs and
cochleovestibular implants, which combine a CI with a VI.
In this chapter, we provide an overview of current knowledge concerning VI
candidacy, operative techniques, device programming, clinical outcomes, possible
complications, and a future outlook.
E. Loos et al.
Candidacy
To date, VIs are only available in a research setting, and therefore no reimbursement
criteria exist. They are mainly developed to treat patients with bilateral vestibulopathy (BV). This is a very debilitating disorder that can lead to a broad spectrum of
symptoms like, for example, postural instability, impairment of spatial orientation,
and distorted vision in dynamic conditions (i.e., while walking), commonly known
as oscillopsia. It has been conservatively estimated that more than 1.8 million people worldwide have severe bilateral vestibular loss, but this is probably an underestimation [7]. To date, BV has a poor prognosis, as more than 80% of the patients
experience no signicant improvement despite vestibular rehabilitation [8].
Vestibular implantation could be the solution for treating this debilitating condition.
To facilitate comparison of results from different studies, VI-implantation criteria
were proposed by van de Berg etal. [9] (Table15.1) in cooperation with all current
research groups. The diagnostic criteria for BV, according to the Bárány Society, were
modied and extended because they are solely based on the horizontal vestibularocular reex (VOR) function. As vestibular implantation is practically irreversible and
can cause a deterioration of residual vestibular functions, it was important to include

15 Vestibular Implants
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303
Table 15.1
VI implantation criteria for BV as described by van de Berg etal. [9]
A.Chronic vestibular syndrome with the following disablinga symptoms:
• Unsteadiness when walking or standing plus at least one of the following:
– Movement-induced blurred vision or oscillopsia during walking or quick head/body
movements, and/or
– Worsening of unsteadiness in darkness and/or on uneven ground
B.Symptoms greatest during head movement
C.Bilaterally reduced or absent angular VOR function documented by at least one of the
following major criteria:
• Bilaterally pathological horizontal angular VOR gain ≤0.6 and at least bilaterally one
vertical angular VOR gain <0.7, documented by the vHIT or scleral-coil technique
• Reduced caloric response (sum of bithermal max. peak slow-phase velocity on each side
≤6°/s for 30-s water stimuli or <10°/s for 60-s water or air stimuli)
• Decreased horizontal angular VOR gain ≤0.1 upon sinusoidal stimulation on a rotatory
chair (0.1Hz, V
=50°/s) and a phase lead >68° (time constant <5s)
max
C′. Obligatory only in case of implantation of otolith structures: Bilaterally absent cVEMP and
oVEMP responses
D.In case only one or two criteria from C are met (and also criterion C′ is met in case of otolith
stimulation), the remaining test(s) should comply with the following minor criteria:
• Bilaterally pathological VOR gains of at least two SSCs <0.7, measured by the vHIT or
scleral-coil technique
• Reduced caloric response (sum of bithermal max. peak slow phase velocity on each side
<10°/s for water and air stimuli of ≥30s)
• Reduced horizontal angular VOR gain <0.2 upon sinusoidal stimulation on a rotatory chair
(0.1Hz, V
=50°/s)
max
E.Symptoms are not better accounted for by another disease
F.Fitting the additional requirements relevant to initial preclinical trials
• Age 18years and above
• BV results most likely from a peripheral origin
• Vestibular function and symptoms are unlikely to signicantly improve, according to the
duration of symptoms and clinicians’ estimations
• Patent vestibular end-organ and intact vestibular nerve
b
c
d
• Ability to use the device and follow a personalized rehabilitation program
• Ability to undergo the surgery
e
G.No current psychological or psychiatric disorder that could signicantly interfere with the
use or evaluation of the VI
a
Disabling is dened as “interfering with activities of daily living”. It is up to the patient and clinician to determine whether symptoms are disabling. A Dizziness Handicap Inventory total score of
>30 can be considered
b
A disorder of peripheral origin means the etiology is localized to the inner ear (e.g., hair cell loss
or dysfunction due to gentamicin ototoxicity, a genetic abnormality, infection, ischemia, trauma,
or other labyrinthine injuries). Patients with obvious central vestibular involvement (e.g., tumors
of the vestibular nerve, brainstem lesions, and cerebellar ataxia) should be excluded. An idiopathic
BV patient with a normal MRI of the brain and internal auditory canals and without any central
vestibular signs on physical examination including ocular motor testing can be regarded as “most
likely from a peripheral origin”
c
If possible, we advise waiting at least 6months before implantation
(continued)

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Table 15.1 (continued)
d
We recommend performing a CT scan for evaluation of the anatomy. In conditions with an
increased risk of a nonpatent labyrinth, for example, meningitis with concern for developing labyrinthitis ossicans, patency should be checked with MRI and/or CT.There should be no clear signs
of structural nerve pathology
e
No allergy to the material of the prosthesis, no anesthetic contraindication
E. Loos et al.
the function of all three SSCs. For the otolith implants, cervical and ocular vestibular
myogenic potentials (cVEMP and oVEMP) were included in the criteria as well.
Possibly, more extensive criteria, including patients with uctuating vestibular
disorders, elderly patients with presbyvestibulopathy, pediatric patients, or chronically uncompensated unilateral vestibulopathy, might be considered in the future.
Additionally, bilateral VIs could also be considered. Interestingly, research has
already demonstrated that VI information is able to overrule residual natural vestibular information [10, 11]. This could lead to using a VI as a “vestibular pacemaker” in cases of a uctuation of the vestibular function and vertigo attacks in
disorders like Meniere’s disease [10]. Former research, however, demonstrated a
loss of residual vestibular function as a consequence of the implantation surgery
[11]. Therefore, at the moment, the use of the VI as a pacemaker should be considered only in patients with no “useful” vestibular function.
SSC Implants
To date, most research has been done on SSC implants. Each research group has a
specic subtype. The group of Geneva-Maastricht uses a vestibulocochlear implant
manufactured by the company MED-EL (Innsbruck, Austria) (Fig.15.1).
The system comprises 12 stimulation contacts. The three most basal electrodes
from the cochlear array were taken out and replaced by three individual electrode
branches. These three individual branches were designed to be inserted into the
SSCs to allow for stimulation of the vestibular ampullary nerves. The remaining
nine stimulation contacts make up the cochlear array, designed to be inserted into
the cochlea like a CI [12]. At the moment, the Geneva-Maastricht Group only uses
the VI on patients with severe hearing loss, as the chances of hearing loss from
implanting the vestibular organs are high. All patients were candidates for CI surgery, which reduced the surgical risks and increased the benet for the patients.
The Baltimore group uses a VI without a CI, also manufactured by the company
MED-EL (Innsbruck, Austria) [13, 14]. This implant consists of three electrode
arrays (each for one SSC) with three stimulating contacts per array and one reference electrode.
The implant of the Washington group is similar to the vestibulocochlear implant
of the Geneva-Maastricht Group but consists of a combined 16-channel cochlear and
six-channel vestibular prosthesis (two stimulating contacts in each vestibular branch)
(Cochlear Ltd., Sydney, Australia) [15, 16]. The initial design did not include a
cochlear array [11], which was added to the second generation of the implant.

15 Vestibular Implants
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Fig. 15.1 The
cochleovestibular implant
of the Maastricht-Geneva
Group
Fig. 15.2 Right ear.
Cortical mastoidectomy
and posterior tympanotomy
have been performed. Blue
lining of all SSCs. sSSC
superior semicircular
canal, lSCC lateral
semicircular canal, pSCC
posterior semicircular
canal. *=posterior
tympanotomy
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*
sSCC
lSCC
Surgical Techniques
Two surgical techniques were developed over the past years: the extralabyrinthine
and the intralabyrinthine approaches [6].
The Intralabyrinthine Approach
The rst step of the intralabyrinthine approach is a cortical mastoidectomy and
posterior tympanotomy. Subsequently, the anterior ends of the anterior and lateral
canals are blue-lined by drilling cranially at the dome of the lateral canal and following it until a V-shape appears.
Then, the SCCs are carefully fenestrated [12, 13], and the electrodes are inserted
as close as possible to the ampullary nerves (Figs.15.2, 15.3 and 15.4).
The posterior canal is located medially to the facial nerve, at an imaginary horizontal line through the stapes footplate, between the sigmoid sinus and the facial
pSCC
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