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Inventis Maestro - July 2023

Inner Ear Disorders that Lie Behind a Selective Canal Impairment on the Video-HIT

Andrea Castellucci, MD

March 13, 2023
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This interview is focused on the peripheral vestibular disorders resulting in an isolated impairment of an SC at the video-HIT, with the aim to increase clinicians’ awareness of the possible pathomechanisms behind a selective lesion of an SC on video-HIT in accordance with the data collected from video-oculography (VOG) and other tests including VEMPs and audiometry.

Introduction

It is well known that vestibular sensors include three semicircular canals (SCs), i.e., horizontal (HSC), anterior (ASC), posterior (PSC), and two otolithic organs: the saccule and the utricle. The recent introduction of modern devices assessing ampullary and otolith reflexes in the high-frequency domain (video-HIT for the three ampullary afferents, cervical VEMPs, and ocular VEMPs for saccular and utricular afferents, respectively) has enabled a fast, functional analysis of all inner ear receptors. This allows for new interpretations of abnormalities involving end-organs and afferents that can be detected in patients with cochleovestibular pathologies in both acute and chronic stages. In fact, case series and investigations on study cohorts have demonstrated how vestibular disorders can result in specific lesion patterns depending on the lesion site, the underlying pathomechanism, and the related etiology.

To better understand the reasons behind a selective SC involvement, a brief recall of anatomical principles is needed. The labyrinthine afferents run through the vestibular nerve, that is composed of two branches: the superior and the inferior vestibular nerve (IVN). While the former is mainly composed of the lateral and anterior ampullary nerves and the utricular nerve (with a possible afferent coming from the anterosuperior portion of the saccule), the IVN is composed of the posterior ampullary nerve (or singular nerve) and the saccular nerve. Basically, the same dichotomy of “superior” and “inferior” labyrinth is also preserved in the arterial vascularization of the labyrinth. In fact, the inner ear is supplied by the internal auditory artery, which divides into two main terminal branches: the anterior vestibular artery and the common cochlear artery (CCA). Whereas the first mostly supplies the utricle and both HSC and ASC, the latter mainly serves the saccule, PSC, and the cochlea, with slight possible interindividual differences. In turn, the CCA divides into the vestibulocochlear artery, which serves PSC, the saccule, and the cochlear basal turn, and in the main cochlear artery supplying the rest of the cochlear neuroepithelium. Finally, the posterior vestibular artery generates from the vestibulo-cochlear artery, providing blood supply to both PSC and saccule.

figure

Figure 1. (A) Labyrinthine innervation (modified from Schuknecht HF, 1993) and (B) inner ear arterial supply (modified from Kim JS & Lee H, Semin Neurol 2009).

AudiologyOnline: Which is the most frequently involved semicircular canal on video-HIT, and which are the underlying pathomechanisms accounting for a selective canal impairment?

Andrea Castellucci: Given the aforementioned conditions, it is easy to understand how the PSC represents the most frequently involved SC in isolation on the video-HIT, as both acute and chronic diseases affecting the neural pathways, such as vestibular neuritis and vestibular schwannoma, respectively, can give an isolated SC impairment mostly when involving the IVN (resulting in PSC and saccular dysfunction) and, similarly, acute ischemic lesions of the labyrinth can result in a selective SC dysfunction mostly when the CCA or its branches represent the lesion sites (resulting in PSC and saccular involvement in association with sudden hearing loss). While in both cases, the saccular function should be damaged, resulting in cervical VEMPs impairment, acute vestibular symptoms should be associated with sudden sensorineural hearing loss (SSNHL) only in ischemic lesions, whereas the cochlear function is spared in inferior vestibular neuritis.

figure

Figure 2. (A) Inner ear structures involved in inferior vestibular neuritis (from Comacchio C & Castellucci A, Front Neurol, 2022). (B) Vestibular schwannoma growing from the IVN and related instrumental pattern (from Castellucci A et al., Otol Neurotol. 2021).

Depending on the ischemic arterial branch, cochlear lesion could result either in profound SSNHL due to an ischemia of all cochlear turns (in case of CCA infarction) or in high-frequency SSNHL likely due to an infarction in the territory supplied by the vestibulocochlear artery (basal turns). Clinicians should also be aware that the instrumental picture due to an infarction in the territory supplied by the posterior vestibular artery perfectly overlaps an inferior vestibular neuritis, as the cochlear blood supply is spared in this case. This condition likely represents the only exception to the rule that inner ear vascular lesions with PSC impairment are always associated with SSNHL.

Figure

Figure 3. Labyrinthine ischemia and related instrumental patterns due to (A) CCA occlusion and (B) vestibulocochlear artery involvement (from Castellucci A et al., Front Neurol. 2023).

Moreover, we should also consider that the PSC lies in the undermost part of the labyrinth when the patient is in both an upright and supine position, enhancing its vulnerability to chronic damages on a hydropic basis and acute dysfunctions due to dislodged otoconia. Both conditions can result in canal VOR-gain hypofunction at the video-HIT through different mechanisms.

Less commonly, the video-HIT can detect an isolated abnormal VOR gain for the other SCs. For example, in case of an acute unilateral vestibular loss (AUVL), a selective impairment either for the HSC or for the ASC could be found mostly in the recovery stage following a superior vestibular neuritis or an anterior vestibular artery ischemia (where the damaged receptors are both HSC and ASC, together with the utricle in both cases), likely due to an asynchronous/asymmetrical recovery process between the two SCs and/or to different central compensatory mechanisms.

Figure

Figure 4. video-HIT measurements in acute and post-acute stage of an AUVL on the right (A) and left side (B) where an asynchronous recovery between the HSC and ASC occur. Presenting scenario could be due either due to a superior vestibular neuritis or an anterior vestibular artery ischemia.

On the other hand, both Menière’s disease (MD) in its different stages and benign paroxysmal positional vertigo (BPPV) can result in different patterns of selective SCs involvement depending on the site of the inner ear that is mostly affected by endolymphatic hydrops (EH) and on how and where otoliths are disposed, respectively.

In fact, MD represents an idiopathic fluctuating inner ear disorder likely due to EH leading to episodic vertigo spells variably associated with tinnitus and hearing loss. Likewise, low-frequency hearing fluctuations, and rapid fluctuations of vestibular function have also been documented with video-HIT and VEMPs in MD during the attack, and different lesion patterns have been reported according to the different stages of the disease (early-stage vs. late-stage) and to the possible inner ear compartments involved by EH. Several pathomechanisms might occur in patients with MD; they include the ionic - chemical perilymphatic intoxication, the endolymphatic space collapse due to membranes rupture, both acute and chronic fluid pressure changes, and saccular/utricular herniation into the SCs. All these phenomena can variably result in either transient or persistent hair cells dysfunction and in alterations of the dynamic property of the peripheral vestibular system leading either to fluctuation of SC and otolith activity during MD attacks or progressive impairment of vestibular function. Depending on the area affected by EH and the aforementioned phenomena, it might be possible to detect a selective lesion of an SC on video-HIT, variably associated with different results at the rest of the instrumental test battery. For example, it is possible to observe in the acute stage either irritative or paretic spontaneous horizontal nystagmus associated with impaired HSC VOR-gain at the video-HIT, normal or reduced cervical VEMPs, and enhanced ocular VEMPs for the affected side. In some other cases, it is possible to observe an ictal spontaneous downbeat nystagmus with slight contralesional torsional components associated with reduced PSC function and cervical VEMPs for the affected ear.  Anecdotally, it has been reported the onset of spontaneous upbeat nystagmus with reduced ASC VOR-gain on video-HIT for the affected side during the acute stage of MD.

Usually, all these findings tend to normalize as soon as the ictal stage ceases. In chronic stages of MD, PSC tends to impair over time, as well as both cochlear and otolith function.

Figure

Figure 5. (A) Ictal stage in a patient with left-sided MD with related instrumental pattern. (B) Inter-ictal/chronic stage in a patient with right-sided MD with related instrumental pattern.

Conversely, BPPV can result in SC impairment only in selected conditions, as free-floating otoconia leading to paroxysmal nystagmus with crescendo-decrescendo course usually do not alter high-frequency responses of the affected SC, preserving video-HIT measurements. On the contrary, in case otoliths are completely or incompletely entrapped in narrow tracts of the membranous ducts, dynamic responses of the affected SC might be impaired, resulting in challenging differential diagnosis with AUVL or with central nervous system (CNS) disorders. According to the recent literature, these situations include the canalith jam and those ASC-BPPV and apogeotropic variants of PSC-BPPV with persistent positional downbeat nystagmus (DBN), where an incomplete (or positional) canalith jam could be hypothesized. In the first case, an otolith clot is thought to entirely plug the canal (either spontaneously or as a result of inappropriate repositioning procedures) and prevent endolymphatic flows resulting in a continuous positive or negative pressure between the clot itself and the cupula. This condition may likely result in a persistent deflection of the cupula, accounting for spontaneous nystagmus irrespective to head positions. Depending on the SC affected, spontaneous nystagmus might be either horizontal, mimicking an AUVL, or vertical/torsional, mimicking CNS disorders. In these situations, both high- and low-frequency responses for the affected SC should be impaired.

Figure

Figure 6. Complete canalith jam involving either the right HSC (A) (from Castellucci et al. Am J Otolaryngol. 2019), the right PSC (B) (from Castellucci et al. Neurol Sci. 2021), and the left ASC (C) (from Castellucci et al. J Audiol Otol, 2022) with related video-HIT measurements.

In the second condition, otoliths are supposed to be only partially entrapped in a stenotic tract of the ASC (ASC-BPPV) or settle in the distal portion of the non-ampullary arm of the PSC, close to the common crus (“apogeotropic variant” of PSC-BPPV), generating a persistent positional DBN in provoking positionings (straight head hanging and/or Dix Hallpike positions). In fact, whereas in ASC-BPPV, debris are thought to shift away from ASC ampulla resulting in a utriculofugal deflection of the cupula and in an excitatory discharge of the superior ampullary nerve, in apogeotropic PSC-BPPV positioning maneuvers should move debris towards the ampulla, producing an inhibition of PSC afferents. In particular, in cases with persistent positional DBN, where a partial otolith entrapment is more likely to occur than in cases with paroxysmal transient positional DBN, an “incomplete” or “positional” jam behaving as a “low-pass filter” has been hypothesized, i.e., allowing the cupula to be activated by low-frequency stimuli (otoconial shifts) while impeding the ampullary receptor to respond to high-frequency inputs (head impulses). This pathomechanism has allowed explaining how patients with persistent positional DBN due to ASC-BPPV or apogeotropic PSC-BPPV exhibited impaired VOR-gain values for the affected SC, restoring after repositioning maneuvers or after conversion in a classical ipsilateral BPPV with paroxysmal nystagmus.

Figure

Figure 7. Incomplete canalith jam resulting in left ASC-BPPV (A) and right apogeotropic PSC-BPPV (B) (from Castellucci et al. Front Neurol. 2020).

Finally, since wide-sized bony dehiscences have demonstrated to result in a functional impairment in the high-frequency domain for the involved SC, it is possible to detect a selective hypofunction of a dehiscent SC on video-HIT depending on the affected SC. According to the literature, the ASC (also known as superior SC - SSC) is the far more frequently affected structure, while the PSC has been less often reported and the HSC only anecdotally. In case of particularly wide bony defect, the content of the surrounding structures (middle fossa in case of SSC dehiscence, while posterior fossa or high-riding jugular bulb for PSC dehiscence) might herniate into the canal through the dehiscence and spontaneously plug the membranous duct, excluding the SC from labyrinthine function by impeding the flow of endolymph. Conversely, it has been recently hypothesized how particularly large dehiscence might allow a dissipation of mechanical energy through the dehiscence during high-acceleration movements. This condition could result in a reduced amount of fluid-mechanical waves efficiently pulling the SC cupula away from the utricle to excite canal afferents during head impulse, thus accounting for impaired VOR-gain values on video-HIT.

Figure

Figure 8. Left wide-sized SSCD with related instrumental assessment.

AudiologyOnline: Which are the peripheral disorders of the inner ear underlying an HSC impairment on video-HIT?

Andrea Castellucci: Below, a schematic overview of the possible diseases leading to selective impairment for the HSC on video-HIT in relation with the remaining clinical-instrumental data, including VOG findings, cervical/ocular VEMPs, caloric test, and audiometry.

Selective HSC loss on video-HIT

disease

VOG

audiometry

cervical VEMPs

ocular VEMPs

caloric test

assumed pathomechanisms

MD

(ictal stage)

spontaneous ipsilesional (“irritative”) or contralesional (“paretic”) horizontal nystagmus

normal or low-frequency hearing loss

normal or reduced +/- frequency tuning

enhanced

canal paresis / normal values

hydrops in the membranous labyrinth and/or fluid pressure changes and/or ionic - chemical perilymphatic intoxication might lead to increased mechanical resistance and/or transient hair cells dysfunction

MD

(inter-ictal / chronic stage)

spontaneous contralesional (“paretic”) or ipsilesional (“recovery”) horizontal nystagmus or

nystagmus elicited by head shakings and/or skull vibrations

normal or low-frequency hearing loss or flat hearing loss

reduced +/- frequency tuning

normal or reduced

canal paresis

hydrops in the membranous labyrinth, increased mechanical resistance, endolymphatic space collapse due to membrane rupture, and utricular herniation into the HSC might lead to chronic hair cells dysfunction

HSC BPPV (complete canalith jam)

spontaneous contralesional (“paretic”) or ipsilesional (“irritative”) horizontal nystagmus

normal

normal

normal

canal paresis

an otolith clot entrapped within the membranous duct of the HSC is thought to exert spontaneously a continuous pressure (either negative or positive) on the cupula, persistently inhibiting or exciting HSC afferents, respectively

previous AUVL (superior vestibular neuritis or labyrinthine ischemia)

contralesional “paretic” horizontal nystagmus induced by head shakings and/or skull vibrations

normal

normal

reduced or normal

canal paresis

asymmetrical and/or asynchronous recovery of peripheral afferents/sensors and/or different central compensatory mechanisms

 

AudiologyOnline: Which are the peripheral disorders of the inner ear underlying an ASC impairment on video-HIT?

Andrea Castellucci: Below, a schematic overview of the possible diseases leading to selective impairment for the ASC on video-HIT in relation with the remaining clinical-instrumental data, including VOG findings, cervical/ocular VEMPs, and audiometry.

Selective ASC loss on video-HIT

disease

VOG

audiometry

cervical VEMPs

ocular VEMPs

assumed pathomechanisms

SSC dehiscence

vertical/torsional nystagmus induced by Valsalva maneuvers and/or by, loud sounds and/or skull vibrations

normal or low-frequency conductive hearing loss with preserved acoustic reflexes

enhanced amplitudes with lowered thresholds

enhanced amplitudes with lowered thresholds

auto-plugging process due to herniation of middle fossa content into the canal

or

dissipation of mechanical energy through the dehiscence during head impulses

MD

(ictal stage)

spontaneous upbeat nystagmus with contralesional (“paretic”) torsional components or nystagmus evoked by head shakings or skull vibrations

normal or low-frequency hearing loss

reduced +/- frequency tuning

normal or enhanced

hydrops in the membranous labyrinth and/or fluid pressure changes and/or ionic - chemical perilymphatic intoxication might lead to increased mechanical resistance and/or transient hair cells dysfunction

ASC-BPPV (incomplete canalith jam)

persistent positional DBN in Dix Hallpike and/or straight head hanging positions with variable torsional components

normal

normal

normal

debris are partially entrapped in the ASC and are thought to exert a continuous negative pressure on the cupula in provoking positionings, exciting ASC afferents

ASC-BPPV (complete canalith jam)

upbeat spontaneous nystagmus with variable torsional components

normal

normal

normal

debris is completely entrapped in the membranous duct and are thought to exert spontaneously a continuous positive pressure on the cupula, persistently inhibiting ASC afferents

previous AUVL (superior vestibular neuritis or labyrinthine ischemia)

upbeat nystagmus with contralesional (“paretic”) torsional components evoked by head shakings and/or skull vibrations

normal

normal

reduced or normal

asymmetrical and/or asynchronous recovery of peripheral afferents and/or different central compensatory mechanisms

AudiologyOnline: Which are the peripheral disorders of the inner ear underlying a PSC impairment on video-HIT?

Andrea Castellucci: Below, a schematic overview of the possible diseases leading to selective impairment for the PSC on video-HIT in relation with the remaining clinical-instrumental data, including VOG findings, cervical/ocular VEMPs, and audiometry.

Selective PSC loss on video-HIT

disease

VOG

audiometry

cervical VEMPs

ocular VEMPs

assumed pathomechanisms

Labyrinthine ischemia in the CCA territory

variable spontaneous DBN with contralesional torsional components

flat / down-sloping SSNHL

reduced / absent

normal / reduced

acute damage of the inner ear sensors supplied by the CCA and its branches (i.e. cochlea, saccule, PSC)

Inferior vestibular neuritis

spontaneous DBN with contralesional torsional components

normal

reduced / absent

normal

acute loss of PSC and saccular afferent running through the IVN

Vestibular schwannoma

nystagmus induced by skull vibrations and/or head shakings and/or hyperventilation test

sensorineural hearing loss or normal hearing function

reduced / absent

normal

progressive impairment of PSC and saccular afferents running through the IVN associated with tumor compression on cochlear artery

MD

(ictal stage)

spontaneous DBN with contralesional (“paretic”) torsional components or nystagmus evoked by skull vibrations and/or head shakings

normal or low-frequency hearing loss

reduced +/- frequency tuning

enhanced or reduced

hydrops in the membranous labyrinth and/or fluid pressure changes and/or ionic - chemical perilymphatic intoxication might lead to increased mechanical resistance and/or transient hair cells dysfunction

MD

(inter-ictal stage)

DBN with contralesional (“paretic”) torsional components evoked by skull vibrations and/or head shakings

normal or low-frequency or flat hearing loss

reduced +/- frequency tuning

normal or reduced

hydrops in the membranous labyrinth, increased mechanical resistance, endolymphatic space collapse due to membrane rupture, and saccular herniation into the PSC might lead to chronic hair cells dysfunction

PSC-BPPV (incomplete canalith jam)

persistent positional DBN in Dix Hallpike and/or straight head hanging positions with variable torsional components

normal

normal

normal

debris are partially entrapped in the non-ampullary arm of the PSC and are thought to exert a continuous positive pressure on the cupula in provoking positionings, inhibiting PSC afferents

PSC-BPPV (complete canalith jam)

spontaneous DBN with contralesional (“paretic”) torsional components

normal

normal

normal

debris is completely entrapped in the membranous duct and are thought to exert spontaneously a continuous positive pressure on the cupula, persistently inhibiting PSC afferents

PSC dehiscence

vertical/torsional nystagmus induced by Valsalva maneuvers and/or by, loud sounds, and/or by skull vibrations

normal or low-frequency conductive HL with preserved acoustic reflexes

enhanced amplitudes with lowered thresholds

enhanced amplitudes with lowered thresholds

auto-plugging process due to herniation of posterior fossa content or high-riding jugular bulb into the canal

or

dissipation of mechanical energy through the dehiscence during head impulses

Resources for More Information 

For more information, visit https://www.inventis.it/en-na or view this AudiologyOnline course, Selective Canal Impairment on Video-HIT in Peripheral Vestibular Diseases.

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andrea castellucci

Andrea Castellucci, MD

Andrea grew up with the otoneurological group of the University of Bologna where he graduated as MD and specialized in ORL-HNS. He currently works as a consultant at the ENT Department of AUSL – IRCCS in Reggio Emilia (Italy), where he is involved in medical and surgical activities. As head of the otoneurological outpatient clinic, in collaboration with Neurology and Emergency Departments, he is involved in research activities in the otoneurological field with other national and international Departments and Universities. He is speaker at national and international congresses, seminars, and webinars and author of publications in national and international scientific journals.



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