Positional and positioning down-beating nystagmus without central nervous system findings

Ogawa, Yasuo; Suzuki, Mamoru; Otsuka, Koji; Shimizu, Shigetaka; Inagaki, Taro; Hayashi, Momoko; Hagiwara, Akira; Kitajima, Naoharu

doi:10.1016/j.anl.2009.04.001

Cited by 16 publications

(10 citation statements)

References 7 publications

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“…According to our original series of 93 patients, most pDBN recognize a peripheral origin confirming previous studies (8,9,15). Despite confirming that ASC-canalolithiasis represents a rare entity, it is actually possible to occur.…”

Section: Discussionsupporting

confidence: 85%

“…Additionally, pDBN often lacks of torsional components in both ASC-BPPV and apogeotropic PSC-BPPV. Authors advocated several explanation for this finding ( 8 , 9 , 11 , 19 , 20 , 64 ). Basically, they stated that since in the human skull, on average, ASC is closer to the sagittal plane (on average only 41°) than PSC (56°) ( 65 , 66 ), a much smaller torsional component is expected from ASC stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…Though central pDBN may also present with paroxysmal course, purely vertical direction, long duration, lack of latency, fatigability and no suppression with visual fixation represent the most prominent features of pDBN of central origin (3)(4)(5)(6)(7). Nevertheless, it has been widely demonstrated how pDBN may not rarely occur also in peripheral pathologies (1)(2)(3)8). It can be elicited when the patient is brought into the straight head hanging (SHH) position and/or by Dix Hallpike (DH) maneuvers and it has been mainly related to benign paroxysmal positional vertigo (BPPV) involving the anterior semicircular canal (ASC) (3,(9)(10)(11)(12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

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Feasibility of Using the Video-Head Impulse Test to Detect the Involved Canal in Benign Paroxysmal Positional Vertigo Presenting With Positional Downbeat Nystagmus

et al. 2020

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Positional downbeat nystagmus (pDBN) represents a relatively frequent finding. Its possible peripheral origin has been widely ascertained. Nevertheless, distinguishing features of peripheral positional nystagmus, including latency, paroxysm and torsional components, may be missing, resulting in challenging differential diagnosis with central pDBN. Moreover, in case of benign paroxysmal positional vertigo (BPPV), detection of the affected canal may be challenging as involvement of the non-ampullary arm of posterior semicircular canal (PSC) results in the same oculomotor responses generated by contralateral anterior canal (ASC)-canalolithiasis. Recent acquisitions suggest that patients with persistent pDBN due to vertical canal-BPPV may exhibit impaired vestibulo-ocular reflex (VOR) for the involved canal on video-head impulse test (vHIT). Since canal hypofunction normalizes following proper canalith repositioning procedures (CRP), an incomplete canalith jam acting as a "low-pass filter" for the affected ampullary receptor has been hypothesized. This study aims to determine the sensitivity of vHIT in detecting canal involvement in patients presenting with pDBN due to vertical canal-BPPV. We retrospectively reviewed the clinical records of 59 consecutive subjects presenting with peripheral pDBN. All patients were tested with video-Frenzel examination and vHIT at presentation and after resolution of symptoms or transformation in typical BPPV-variant. BPPV involving non-ampullary tract of PSC was diagnosed in 78%, ASC-BPPV in 11.9% whereas in 6 cases the involved canal remained unidentified. Presenting VOR-gain values for the affected canal were greatly impaired in cases with persistent pDBN compared to subjects with paroxysmal/transitory nystagmus (p < 0.001). Each patient received CRP for BPPV involving the hypoactive canal or, in case of normal VOR-gain, the assumed affected canal. Each subject exhibiting VOR-gain reduction for the involved Castellucci et al. vHIT in Positional Downbeat Nystagmus canal developed normalization of vHIT data after proper repositioning (p < 0.001), proving a close relationship with otoliths altering high-frequency cupular responses. According to our results, overall vHIT sensitivity in detecting the affected SC was 72.9%, increasing up to 88.6% when considering only cases with persistent pDBN where an incomplete canal plug is more likely to occur. vHIT should be routinely used in patients with pDBN as it may enable to localize otoconia within the labyrinth, providing further insights to the pathophysiology of peripheral pDBN.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Feasibility of Using the Video-Head Impulse Test to Detect the Involved Canal in Benign Paroxysmal Positional Vertigo Presenting With Positional Downbeat Nystagmus

et al. 2020

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“…pDBN of central origin is often associated with brainstem or cerebellar signs such as gait unsteadiness with falls, motor weakness, clumsiness of extremities, diplopia, and slurred speech 1. However, diagnosing isolated pDBN in the absence of other neurological signs remains challenging 56. It can be ascribed to benign paroxysmal positional vertigo (BPPV) involving an anterior canal (AC) 5678910.…”

Section: Introductionmentioning

confidence: 99%

“…However, diagnosing isolated pDBN in the absence of other neurological signs remains challenging 56. It can be ascribed to benign paroxysmal positional vertigo (BPPV) involving an anterior canal (AC) 5678910. In AC BPPV, the otoconial debris moves away from the cupula during straight head-hanging (SHH) or Dix-Hallpike (DH) maneuver, giving rise to an ampullofugal deflection of the cupula and excitation of the AC.…”

Section: Introductionmentioning

confidence: 99%

Incidence and Clinical Significance of Positional Downbeat Nystagmus in Posterior Canal Benign Paroxysmal Positional Vertigo

Lee

Kim

et al. 2019

J Clin Neurol

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Background and Purpose The aim of this study was to determine the incidence and clinical significance of positional downbeat nystagmus (pDBN) after treatment of posterior canal (PC) benign paroxysmal positional vertigo (BPPV). Methods We recruited 77 patients with a diagnosis of PC BPPV, and assessed the presence of pDBN during follow-up positional tests after performing the Epley maneuver. Results An immediate response to the Epley maneuver was exhibited by 57 of the 77 patients, with resolution of their positional torsional upbeat nystagmus (pT-UBN). Twenty-two (39%) of them exhibited pDBN during follow-up tests performed 1 hour later. The latency and duration of pDBN were 3.2±2.0 and 12.0±10.0 s (mean±SD), respectively. The maximum slowphase velocity of pDBN was 5.1±2.5 degrees, and ranged from 2.0 to 12.2 degrees. A torsional component was also observed in six patients. The patients with pDBN were much more likely to develop a typical form of PC BPPV again at a 1-week follow-up (5/22, 23%) compared to those without pDBN (1/31, 3%; p =0.036). pDBN disappeared in all patients within 6 months. Conclusions Our study found transient pDBN in 40% of patients with PC BPPV after the immediate resolution of positional vertigo and pT-UBN. pDBN may be attributed to residual debris in the distal portion of the PC, which can move toward the ampulla producing an ampullopetal flow of endolymph during positioning.

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Natural course of positional down-beating nystagmus of peripheral origin

et al. 2013

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The aim of this study was to assess the natural course of positional down-beating nystagmus (pDBN) and vertigo in patients with no evidence of central nervous system involvement and of presumed peripheral origin. Fifty-three patients with pDBN had a complete otoneurological examination. All subjects, apart from three (excluded from the study), showed no additional neurological signs and normal brain imaging. Patients were randomly assigned to two groups: with or without treatment with exercise. Patients were seen again after 24 h, and then weekly for up to 6 months. Forty-seven patients (94%) showed pDBN in the straight head-hanging position and in a Dix-Hallpike position. A torsional component was detected in 17 patients (34%). The mean latency and duration of pDBN was 4.7 ± 5 s and 40.1 ± 22 s, respectively. After 2 weeks, only 12 patients (24%) still had pDBN and all but one patient had recovered by 1 month. Twenty patients (40%) were diagnosed with a typical posterior canal benign paroxysmal positional vertigo (PC BPPV) before or after pDBN. This study assessed for the first time the natural course of presumed peripheral pDBN, which was characterized by a spontaneous remission in 24 patients in the first week and in 49 patients within 4 weeks. pDBN is much more common than previously suggested, with about the same frequency as lateral canal BPPV. Furthermore, the clinical characteristics of pDBN have been highlighted, as well as its possible relationship to PC BPPV.

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Positional and positioning down-beating nystagmus without central nervous system findings

Cited by 16 publications

References 7 publications

Feasibility of Using the Video-Head Impulse Test to Detect the Involved Canal in Benign Paroxysmal Positional Vertigo Presenting With Positional Downbeat Nystagmus

Feasibility of Using the Video-Head Impulse Test to Detect the Involved Canal in Benign Paroxysmal Positional Vertigo Presenting With Positional Downbeat Nystagmus

Incidence and Clinical Significance of Positional Downbeat Nystagmus in Posterior Canal Benign Paroxysmal Positional Vertigo

Natural course of positional down-beating nystagmus of peripheral origin

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