scholarly journals Apogeotropic variant of horizontal semicircular canal benign paroxysmal positional vertigo: Where are the particles?

2019 ◽  
Vol 9 (2) ◽  
Author(s):  
Bernardo Faria Ramos ◽  
Renato Cal ◽  
Camila Martins Brock ◽  
Pedro Luiz Mangabeira Albernaz ◽  
Francisco Zuma e Maia

The apogeotropic variant of horizontal semicircular canal benign paroxysmal positional vertigo (HC-BPPV) is attributed to free floating particles in the anterior arm of the lateral semicircular canal – particles attached to the cupula facing the canal or particles attached to the cupula facing the utricle. Zuma e Maia described a new treatment for both canalithiasis of the anterior arm of the horizontal semicircular canal (HC) and cupulolithiasis of the HC. Seventeen patients with apogeotropic HC-BPPV were enrolled and treated with Zuma’s Maneuver. During the repositioning of the particles to the utricule, we observed the direction of the nystagmus evoked in each step of this maneuver in order to know where the otoliths were probably located. Eight patients were diagnosed with canalithiasis of the anterior arm, six patients with cupulolithiasis with the particles facing the canal and three patients with cupulolithiasis with the particles facing the utricle. Our data suggest that we can assume where the otoliths are probably located by observing the pattern of the nystagmus evoked in each step of the Zuma’s Maneuver in patients with apogeotropic HC-BPPV.

2016 ◽  
Vol 6 (2) ◽  
Author(s):  
Francisco Zuma e Maia

The apogeotropic variant of horizontal semicircular canal benign paroxysmal positional vertigo (HC-BPPV) is attributed to canalithiasis of the anterior arm or cupulolithiasis. Despite some therapeutic maneuvers, I propose a new treatment strategy for apogeotropic HCBPPV that is designed to detach both the otoconial debris from the anterior arm of the semicircular canal and the debris that is attached to the utricular side of the cupula using inertia and gravity and based on simulations with a 3D biomechanical model.


Author(s):  
Bernardo Faria Ramos ◽  
Renato Cal ◽  
Camila Martins Brock ◽  
Pedro Luiz Mangabeira Albernaz ◽  
Francisco Zuma e Maia

Abstract Introduction Benign Paroxysmal Positional Vertigo (BPPV) is the most common vestibular disorder, resulting from detached otoliths that migrate to one of the semicircular canals – canalolithiasis – or one of the cupulas – cupulolithiasis. The present study is related to lateral canal BPPVs, which may be either geotropic or apogeotropic. The geotropic variant of lateral semicircular canal benign paroxysmal positional vertigo (LC-BPPV) is attributed to free floating particles in the posterior arm of the lateral semicircular canal. Objectives To verify the possibility of employing the Zuma repositioning maneuver, with a brief modification, as an alternative treatment for geotropic LC-BPPV. Methods Seven patients with geotropic LC-BPPV were enrolled and treated with the Zuma modified maneuver. Patients were reevaluated 1 hour after a single maneuver, to confirm the resolution of vertigo and positional nystagmus. Results All seven patients achieved immediate resolution of vertigo and positional nystagmus as measured 1 hour after the application of the maneuver. Conclusion The Zuma modified maneuver was effective for geotropic LC-BPPV after a single application. The use of the Zuma maneuver for both apogeotropic and geotropic LC-BPPV may simplify the treatment of these patients.


2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Jing Li ◽  
Rui Wu ◽  
Bin Xia ◽  
Xinhua Wang ◽  
Mengzhou Xue

Abstract Objective: To investigate the possible role of superoxide dismutases (SODs) in the development of benign paroxysmal positional vertigo (BPPV) and recurrence events in a 1-year follow-up study. Methods: This was a prospective one-center study. A total of 204 patients with BPPV and 120 age-and sex matched healthy subjects were included. The levels of SOD between patients and control cases were compared. The levels of SOD between posterior semicircular canal (PSC) and horizontal semicircular canal (HSC) were also compared. In the 1-year follow-up, recurrence events were confirmed. The influence of SOD levels on BPPV and recurrent BPPV were performed by binary logistic regression analysis. Results: The serum levels of SOD in patients with BPPV were lower than in those control cases (P<0.001). Levels of SOD did not differ in patients with PSC and HSC (P=0.42). As a categorical variable, for per interquartile range (IQR) increment of serum level of SOD, the unadjusted and adjusted risks of BPPV would be decreased by 72% (with the odds ratio [OR] of 0.28 [95% confidence interval (CI): 0.21–0.37], P<0.001) and 43% (0.57 [0.42–0.69], P<0.001), respectively. Recurrent attacks of BPPV were reported in 50 patients (24.5%). Patients with recurrent BPPV had lower levels of SOD than in patients without (P<0.001). For per IQR increment of serum level of SOD, the unadjusted and adjusted risks of BPPV would be decreased by 51% (with the OR of 0.49 [95% CI: 0.36–0.68], P<0.001) and 24% (0.76 [0.60–0.83], P<0.001), respectively. Conclusion: Reduced serum levels of SOD were associated with higher risk of BPPV and BPPV recurrence events.


PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242580
Author(s):  
Hyun-Jin Lee ◽  
Seong Ki Ahn ◽  
Chae Dong Yim ◽  
Dae Hwan Kim ◽  
Dong Gu Hur

Objectives We investigated the incidence and characteristics of pseudo-spontaneous nystagmus (PSN) in benign paroxysmal positional vertigo involving the lateral semicircular canal (LC-BPPV) and evaluated the correlation between PSN and the bow and lean test. Methods We examined nystagmus in the sitting position using video-oculography goggles in 131 LC-BPPV patients. The positioning test and bow and lean test were also performed. Patients were divided into canalolithiasis and cupulolithiasis groups according to the character of nystagmus. In each group, the incidence and direction of PSN, correlation with the bow and lean test, and treatment outcome were analyzed. Results PSN was observed in 25 cases (19.1%) in LC-BPPV patients, 7 of which were canalolithiasis and 18 of which were cupulolithiasis (p = 0.098). Of the 25 patients with PSN, 21 (84%) exhibited nystagmus consistent with the lean test whereas 4 (16%) exhibited nystagmus consistent with the bow test. In patients with PSN, nystagmus was observed in the bow and lean test in all cases (23/23), but in patients without PSN, no nystagmus was observed in 13 cases (13/87) in the bow and lean test (p = 0.048). The number of barbecue maneuvers performed until the end of treatment was 1.4 ± 0.7 in patients with PSN and 1.4 ± 0.9 in those without PSN (p = 0.976). Conclusion We identified PSN in patients with LC-BPPV irrelevant of subtype. Moreover, all patients with PSN showed nystagmus in the bow and lean test. The direction of PSN was mostly consistent with that of the lean test (21/25, 84%). The presence of PSN was not related to the treatment outcome in this study.


2020 ◽  
Vol 5 (4) ◽  
pp. 917-939
Author(s):  
Richard A. Clendaniel

Purpose The purposes of this article are (a) to describe the different test procedures for benign paroxysmal positional vertigo (BPPV) and (b) to provide guidance for the treatment of the various forms of BPPV and to discuss the efficacy of the different interventions. Conclusions While BPPV primarily occurs in the posterior semicircular canal, it is also seen in the anterior and horizontal semicircular canals. There are distinctive patterns of nystagmus that help identify the affected semicircular canal and to differentiate between cupulolithiasis and canalithiasis forms of BPPV. There is reasonable evidence to support the different treatments for both posterior and horizontal semicircular canal BPPV. Anterior semicircular canal BPPV is rare, and as a consequence, there is little evidence to support the various treatment techniques. Finally, while BPPV is generally easy to identify, there are central causes of positional nystagmus with and without vertigo, which can complicate the diagnosis of BPPV. The signs and symptoms of BPPV are contrasted with those of the central causes of positional nystagmus.


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