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

Abstract

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.

Case Report: Could Hennebert's Sign Be Evoked Despite Global Vestibular Impairment on Video Head Impulse Test? Considerations Upon Pathomechanisms Underlying Pressure-Induced Nystagmus due to Labyrinthine Fistula

“…Although a reverse functional dissociation pattern impairing low-velocity while sparing high-velocity canal VOR has been often observed in several vestibular diseases ( 66 – 69 ), other vestibular pathologies have been related to a loss of sensitivity for high-acceleration head movements while low-acceleration behavior remains intact, likewise LF herein reported ( 70 – 72 ). In particular, SSC dehiscence represents another condition accounting for a third window mechanism that has been demonstrated to result in ocular movements aligning with the plane of the affected canal in response to loud sounds and/or pressure changes despite selectively impaired canal function on vHIT.…”

Less common forms of posterior canal benign paroxysmal positional vertigo

“…A partial canal jam might determine impaired responses for high-frequency stimuli, such as head impulses in v-HIT, whereas low-frequency stimuli, such as the cupular stimulus of the endolymph flow activated during the positional test, remain active (low-pass filter). Data reported by Castellucci et al 23 highlight the difference between APC and TPC, in which the posterior canal VOR gain is not affected 24 .…”

“…In a recent multicentre study through v-HIT, Castellucci et al 23 demonstrated a decrease of the VOR gain of the affected canal in 72.9% of 59 cases of PDN, either from APC or from AC, increasing up to 88.6% in the subgroup with persistent down beat nystagmus, either positional or spontaneous. This datum was useful to distinguish between APC and contralateral AC.…”

Possible pathomechanisms accounting for both sound/pressure-induced eye movements and video head impulse test data in superior canal dehiscence

“…Finally, we would also suggest to always warrant further investigations for patients presenting with isolated loss of SSC function on vHIT, as SCD might not be the sole underlying disorder as it has been found among 300 patients in a recently published study [7]. In fact, along with anecdotal reports implicating Meniere's disease in the acute stage [20], Castellucci et al have reported how benign positional paroxysmal vertigo (BPPV) presenting with positional downbeat nystagmus due to an involvement of a vertical canal might lead to a selective impairment of the affected canal VOR- gain, including the SSC [16,17]. Probably, the unlikelihood to examine patients either during the acute attack of Meniere's disease or with SSC-BPPV (accounting for less than 10% of overall BPPV) could represent one of the reasons for this discrepancy.…”

“…In fact, it has been reported how Tullio phenomenon does not only arise from a sustained triggering of phaselocking irregularly-discharging sensors, but also to a slowly developing but sustained activation of regularly discharging afferents [4,15]. Similarly, cases with persistent positional downbeat nystagmus, where an incomplete canal plug (also called "incomplete canalith jam") exerted by an otolith clot has been assumed as the underlying mechanism, have also been related to the same functional dissociation paradigm impairing high-velocity responses while sparing low-velocity VOR for the canal involved [16,17].…”