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Review
Peer-Review Record

Atypical Positional Vertigo: Definition, Causes, and Mechanisms

by Sergio Carmona 1,2,*, Guillermo Javier Zalazar 1,3, Martin Fernández 1, Gabriela Grinstein 2 and João Lemos 4
Reviewer 1:
Reviewer 2: Anonymous
Submission received: 31 January 2022 / Revised: 4 March 2022 / Accepted: 7 March 2022 / Published: 14 March 2022
(This article belongs to the Special Issue Advances in Positional Vertigo)

Round 1

Reviewer 1 Report

Good review and analysis. Several points , mostly editing

 

In the Introduction from lines 23 to 31, I like to suggest the following editorial version to make it more readable:

 

Based on what patients report, though the report short the duration of symptoms lasting seconds, however, many overestimate the duration of the vertiginous sensation. The trigger effect of positional changes is a key question to ascertain. The great variability of autonomic symptoms with nausea and vomiting can possibly accompany BPPV.  Gait instability, headache, and additional neurologic complaints are potential read flags in the differential diagnosis. With a defined posiiton trigger effect, it is the neurotologist job to perform an examination to confirm the diagnosis of paroxysmal positional vertigo, and by virtue of the vertigo duration and nystagmus characteristic to determine lesion localization peripheral versus central, and to design a management plan.

 

In line 46 of the Introduction, you have Downbeat nystagmus as a phrase; you probably meant it to be “atypical direction nystagmus, especially downbeating nystagmus

 

Page 3, line 96 you probably mean subsequent transformation, rather than posterior transformation

Page 4. Line 160 when describing the nystagmus observed in the light cupula syndrome, I suggest to indicate that” it is horizontal, geotropic , direction changing with head roll  without latency and a constant slow phase velocity that does not fatigue, a mimic of positional alcohol nystagmus, phase 1”

Page 5 line 191 this reviewer cannot tell the difference between independent pathology versus a pathologic condition or stage of an inner ear pathology

 

Page 6 line 97: You may want to accept the following edit:  “’the role of the nodulus /uvula integration of inertial otolith signals normally modifies the translational VOR”. In addition, lesions of the nodulus/uvula result in activation of rotational canal efferent (abnormal central perception processing)  in response to otolith activation (tilt or pitch) resulting in downbeat positional nystagmus, or horizontal apogeotropic nystagmus variants, or both.

In the vestibular paroxysmia patients, could you report how many had an acute vertigo attack, and what was their nystagmus type?  Then, how which cases had an interictal positional nystagmus?

 

In the proposed definition of APV

#1 is accompanied by neurological disease signs or symptoms (Need to add that this does not apply to posterior canal BPPV), in many instances a posterior canal BPPV occur in patients with CNS disorders, it is unrelated to them and improve with an Epley maneuver )May want to add references:  Bertholon, Frohman Elliott, De-Schutter , Kattah among some).

Page 8 Lesions of the nodulus causes positional downbeat nystagmus as well, in fact, also associated with h-apogeotropic nystagmus (De Schutter-Kattah). Also robust positional DBN with prone position(not reported) but in agreement with the Kim, Zee hypothesis of abnormal canal activation in response to tilt).

IN Tumor of the VIII nerve, it is reasonable to add the eponym: Brun’s nystagmus

Author Response

Please see the attachment

Author Response File: Author Response.docx

Reviewer 2 Report

This article is a well written and rather comprehensive review of the recent literature about challenging forms of BPPV. I believe it can be a useful clinical guide for neurotologists. However,however, the Authors do not mention canalith jam, a condition first described by Epley in which otoconia block the involved canal mimicking its deficit.

Some of the more significant references are listed below:

. Ko KM, Song MH, Kim JH, Shim DB. Persistent spontaneous nystagmus following a canalith repositioning procedure in horizontal semicircular canal benign paroxysmal positional vertigo. JAMA Otolaryngol Head Neck Surg 2014;140:250–2.

.Castellucci A, Malara P, Brandolini C, Del Vecchio V, Giordano D, Ghidini A, et al. Isolated horizontal canal hypofunction differentiating a canalith jam from an acute peripheral vestibular loss. Am J Otolaryngol 2019;40:319–22.

. Schubert MC, Helminski J, Zee DS, Cristiano E, Giannone A, Tortoriello G, et al. Horizontal semicircular canal jam: two new cases and possible mechanisms. Laryngoscope Investig Otolaryngol 2020;5:163–7.

. Martellucci S, Castellucci A, Malara P, Pagliuca G, Clemenzi V, Stolfa A, et al. Spontaneous jamming of horizontal semicircular canal combined with canalolithiasis of contralateral posterior semicircular canal. J Audiol Otol 2021;Feb 15 [Epub] https://0-doi-org.brum.beds.ac.uk/10.7874/jao.2020.00507.

. Castellucci A, Malara P, Ghidini A. Spontaneous downbeat nystagmus in posterior semicircular canal benign paroxysmal positional vertigo: a canalith jam? Neurol Sci 2021;42:313–5.

. Castellucci A, Malara P, Martellucci S, Delmonte S, Ghidini A. Fluctuating posterior canal function in benign paroxysmal positional vertigo depending on how and where otoconia are disposed. Otol Neurotol 2021;42:e193–8.

I believe that a brief discussion of the subject and a reference to at least some of the articles above can make your review more complete.

 

Author Response

Please see the attachment

Author Response File: Author Response.docx

Round 2

Reviewer 1 Report

Good ,helpful review

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