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Diagnostic and Therapeutic Maneuvers for Anterior Canal BPPV Canalithiasis: Three-Dimensional Simulations.

ABSTRACT: Background and Objectives: Anterior canal BPPV is a rare BPPV variant. Various diagnostic and therapeutic maneuvers have been described for its management. The aim of this study was to use three-dimensional simulation models to visualize otoconial debris movement within the anterior canal during diagnostic tests and different liberatory maneuvers. This can help to optimize existing treatment maneuvers and help in the development of better management protocols. Methods: Based on reconstructed MRI images and fluid dynamics, a 3D dynamic simulation model (as a function of time) was developed and applied. Simulations of the supine head-hanging test for diagnosis of ac-BPPV were studied. Three repositioning maneuvers were simulated: 1) the Yacovino maneuver and its modifications, 2) the reverse Epley maneuver and 3) the short canal repositioning (CRP) maneuver. Results: The simulation showed that the supine head-hanging test is a good test for diagnosis of ac-BPPV affecting both labyrinths and demonstrated why there is no inversion of nystagmus on sitting up. The Yacovino maneuver was seen to be an effective treatment option for ac-BPPV without having to determine the side involved. However, simulations showed that the classical Yacovino maneuver carried a risk of canal switch to the posterior canal. To overcome this risk, a modified Yacovino maneuver is suggested. The reverse Epley maneuver was not an effective treatment. Short CRP is useful in ac-BPPV treatment; however, it requires determination of side of involvement. Conclusion: The 3D simulator of the movement of the otoconial debris presented here can be used to test the mechanism of action and the theoretical efficacy of existing diagnostic tests and maneuvers as well as to develop new treatment maneuvers to optimize BPPV treatment.

SUBMITTER: Bhandari A

PROVIDER: S-EPMC8497794 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The functional integrity of the inferior vestibular nerve (IVN) may be evaluated by the cervical vestibular evoked myogenic potential (cVEMP) response, which requires signal transmission via the nerve. As functional integrity of the IVN innervating the posterior semicircular canal is required to produce the typical positioning vertigo and nystagmus characterizing posterior canal benign paroxysmal positional vertigo (PCBPPV), we hypothesized that normal cVEMPs would be found in most PCBPPV patients. Twenty-four PCBPPV patients participated in a prospective cohort study. All were treated by canal repositioning maneuver and had air-conduction cVEMP and videonystagmography (VNG). Follow-up evaluations including history and otoneurological bedside examination were carried out 1, 3, 6, and 12 months after the initial treatment. At the last follow-up, the patients filled the Dizziness Handicap Inventory (DHI) questionnaire. Normal cVEMPs were recorded in 19 (79%) and were absent in 5 (21%) of the subjects. The average DHI in the patients with normal cVEMP was 16.42 ± 17.99 vs. 0.4 ± 0.89 among those with pathological cVEMP (p < 0.04, Mann-Whitney test). Thirteen (54%) patients experienced recurrent PCBPPV (rPCBPPV). The average DHI score was significantly higher among patients having recurrence (22.15 ± 18.61) when compared to those with complete cure (2.36 ± 5.98; p < 0.003, Mann-Whitney test). Ten (77%) of the subjects with rPCBPPV had normal and 3 (23%) had pathological cVEMP as compared to 9 (82%) and 2 (18%) subjects in the non-recurrent (nrPCBPPV) group (Fisher's exact test-not significant). cVEMP p13 and n23 wave latencies and amplitudes, inter-aural differences in p13-n23 peak-to-peak amplitudes, and response thresholds did not differ between the groups. No differences were found between the rPCBBPV and nrPCBBPV groups in VNG caloric lateralization and directional preponderance values. We have found that in most cases, PCBPPV symptoms and signs are associated with normal cVEMP response supporting the role of IVN functional integrity. The absent cVEMPs in the minority of patients, although having similar clinical presentation, raise the possibility that the ipsilateral saccule is affected by the same pathology causing degeneration of the utricle macula. Alternatively, lacking inhibitory stimuli from the involved ipsilateral utricle or partial degeneration of the IVN and ganglion could explain the diminished cVEMP response. Clinical Trial Registration: The study was registered in ClinicalTrials.gov Internet site (study ID-NCT01004913; https://clinicaltrials.gov/ct2/show/NCT01004913?cond=BPPV&cntry=IL&draw=2&rank=3).

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Diagnostic and Therapeutic Maneuvers for Anterior Canal BPPV Canalithiasis: Three-Dimensional Simulations.

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