Possible pathomechanism behind the transient
hypofunction of the affected canal in BPPV. Letter to
the editor regarding "Clinical significance of video head
impulse test in benign paroxysmal positional vertigo: a
meta-analysis" by Elsherif M et al. European Archives
of Oto-Rhino-Laryngology (2021);278(12):4645-4651

Andrea Castellucci, Pasquale Malara, Salvatore Martellucci, Enrico Armato,
Luigi Califano

► To cite this version:

Andrea Castellucci, Pasquale Malara, Salvatore Martellucci, Enrico Armato, Luigi Califano. Possible pathomechanism behind the transient hypofunction of the affected canal in BPPV. Letter to the editor regarding "Clinical significance of video head impulse test in benign paroxysmal positional vertigo: a meta-analysis" by Elsherif M et al. European Archives of Oto-Rhino-Laryngology (2021);278(12):4645-4651. European Archives of Oto-Rhino-Laryngology, 2021, 10.1007/s00405-021-07202-9. http://dx.doi.org/10.1007/s00405-021-07202-9

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# Possible pathomechanism behind the transient hypofunction of the affected canal in BPPV. Letter to the editor regarding "Clinical significance of video head impulse test in benign paroxysmal positional vertigo: a meta-analysis" by Elsherif M et al. European Archives of Oto-Rhino-Laryngology (2021);278(12):4645-4651

Andrea Castellucci<fnref n="1" /> ID • Pasquale Malara<fnref n="2" /> ID • Salvatore Martellucci<fnref n="3" /> ID • Enrico Armato<fnref n="4" /> ID • Luigi Califano<fnref n="5" /> ID

Received: 21 November 2021 / Accepted: 23 November 2021

© The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2021

Dear Editors,

We read with interest the recent article by Elsherif M et al. entitled "Clinical significance of video head impulse test in benign paroxysmal positional vertigo: a meta-analysis" [1]. The Authors conducted a meta-analysis including the most relevant research published within December 30th, 2020 on the role of the video Head Impulse Test (vHIT) in Benign Paroxysmal Positional Vertigo (BPPV), aiming to assess the effect of cupular deflection due to dislodged otoconia on the vestibulo-ocular reflex (VOR) of the involved semicircular canal (SC). The Authors concluded that vHIT can be of support in the diagnosis of posterior SC (PSC) BPPV, as they found significant reduction of the VOR-gain for the affected PSC compared with controls and with contralateral PSC. Conversely, they did not find significant differences in VOR-gain values comparing the involved anterior (ASC) and lateral SC (LSC) with both contralateral healthy SCs

and controls. The Authors explained these discrepant data assuming anatomical differences among the ampullary arm of different canals that would facilitate a hypoactive PSC.

Despite this hypothesis might be possible, we would like to point out a couple of aspects.

First, since the Authors used "BPPV" and "vHIT" as keywords for literature search, we found quite surprising they did not include in the meta-analysis our free-access paper published in October, 2020 on the use of the vHIT in BPPV presenting with positional downbeat nystagmus [2]. Our study fully met the strict inclusion criteria set by the Authors, as we provided two detailed tables with VOR-gain values for all six SCs before and after repositioning procedures (Supplementary Materials) of 59 patients with BPPV involving either the ASC or the non-ampullary arm of PSC.

Second, we would like to propose a different explanation that can more likely account for VOR-gain reduction of the affected SC in certain BPPV. As demonstrated by Califano et al. in 150 patients with BPPV involving the ampullary arm of PSC [3], in cases presenting with paroxysmal positional nystagmus free-floating otoconia hardly result in impaired VOR-gain measures for the affected SC, as they are not expected to alter "per se" high-frequency cupular responses. Conversely, the involved SC function could likely be impaired in patients with BPPV presenting with persistent/long-lasting positional nystagmus, as in this condition otoconia might be partially entrapped in stenotic tracts of the membranous canal acting as an "incomplete" canalith jam [2, 4]. In fact, while in a "complete" jam an otolith clot is supposed to entirely plug the canal lumen leading to a persistent endolymphatic flow deflecting the cupula (which in turn results in spontaneous nystagmus and in highly reduced VOR-gain values for the affected SC as dynamic responses to high- and low-frequency inputs are temporarily prevented)

This comment refers to the article available online at https://doi.org/10.1007/s00405-021-06832-3.

<figure><img src="image_1.png" /></figure>

Andrea Castellucci
andrea.castellucci@ausl.re.it

<footnote n="1">¹ ENT Unit, Department of Surgery, Azienda USL—IRCCS di Reggio Emilia, Viale Risorgimento 80, 42123 Reggio Emilia, Italy</footnote>

<footnote n="2">² Audiology and Vestibology Service, Centromedico, Bellinzona, Switzerland</footnote>

<footnote n="3">³ ENT Unit, Santa Maria Goretti Hospital, Azienda USL Latina, Latina, Italy</footnote>

<footnote n="4">⁴ ENT Unit, SS Giovanni e Paolo Hospital, Venice, Italy</footnote>

<footnote n="5">⁵ Department of Audiology and Phoniatrics, San Pio Hospital, Benevento, Italy</footnote>
[4, 5], in these cases otoconia might be only partially embed-
ded in narrow canal tracts. Therefore, when the patient is
brought in the diagnostic positions, otoliths might behave as
a “positional jam” leading to a cupular bending that might
partially saturate the SC afferents, decreasing cupular sen-
sitivity to high-acceleration stimuli and resulting in a slight
VOR-gain impairment. This pathomechanism could likely
explain presenting impaired vHIT measures for the affected
SC in patients with certain BPPV subtypes and normaliza-
tion of data after symptoms resolution or conversion into
a typical paroxysmal nystagmus [2, 4, 5]. Therefore, we
suggest that vHIT data of the affected canal might change
depending on how and where otoconia are disposed within
the canal [4] rather than on the affected canal itself. We
would, therefore, encourage the use of the vHIT in atypical
BPPV variants where detection of the affected SC due to the
heterodox nystagmic features may be challenging.

**Acknowledgements** None.

**Author contributions** All authors contributed to the study conception and design. The first draft of the manuscript was written by AC and LC, and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

**Funding** None.

**Declarations**

**Disclosures** None.

**Conflict of interest** Not applicable.

**Ethics approval** Not applicable.

**Consent** Not applicable.

**Data** Not applicable.

**Materials and/or code availability** Not applicable.

**References**

1. Elsherif M, Eldeeb D, Eldeeb M (2021) Clinical significance of video head impulse test in benign paroxysmal positional vertigo: a meta-analysis. Eur Arch Otorhinolaryngol 278(12):4645–4651. https://doi.org/10.1007/s00405-021-06832-3

2. Castellucci A, Malara P, Martellucci S et al (2020) Feasibility of using the video-head impulse test to detect the involved canal in benign paroxysmal positional vertigo presenting with positional downbeat nystagmus. Front Neurol 11:578588. https://doi.org/10.3389/fneur.2020.578588

3. Califano L, Iannella R, Mazzone S, Salafia F, Melillo MG (2021) The video head impulse test in the acute stage of posterior canal benign paroxysmal positional vertigo. Acta Otorhinolaryngol Ital 41(1):69–76. https://doi.org/10.14639/0392-100X-N1033

4. Castellucci A, Malara P, Martellucci S, Delmonte S, Ghidini A (2021) Fluctuating posterior canal function in benign paroxysmal positional vertigo depending on how and where Otoconia are disposed. Otol Neurotol 42(2):e193–e198. https://doi.org/10.1097/MAO.00000000000002913

5. Castellucci A, Malara P, Brandolini C et al (2019) Isolated horizontal canal hypofunction differentiating a canalith jam from an acute peripheral vestibular loss. Am J Otolaryngol 40(2):319–322. https://doi.org/10.1016/j.amjoto.2018.12.005

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<figure><img src="image_2.png" /></figure>