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.
Objective: Though fluctuations in vestibular function represent a common finding in Menière's disease, we describe how benign paroxysmal positional vertigo (BPPV) may result in fluctuations of vestibulo-ocular reflex for the involved canal depending on the disposition of otoliths. Patient: A 54-year-old woman suffering from refractory posterior canal (PC)-BPPV resulting in fluctuating PC function. Interventions: Diagnostic evaluation and rehabilitative treatment for BPPV involving the affected PC. Main Outcome Measures: Video-Frenzel and video-head impulse test (vHIT) findings before and after canalith repositioning procedures for PC-BPPV. Results: BPPV involving the nonampullary arm of right PC was diagnosed based on presenting positional downbeat nystagmus and selective right PC hypofunction at the vHIT. During physical treatment, nystagmus first became positional paroxysmal upbeat likely due to a shift of debris into the ampullary arm of the canal, then turned to spontaneous downbeat nystagmus consistently with a plug effect exerted by particles entrapped within the nonampullary arm of PC and finally receded proving an otoliths fall within the utriculus. Simultaneously, vHIT documented fluctuations for right PC vestibulo-ocular reflex gain as it first increased to normal values, then severely declined and finally normalized, respectively. High-resolution computed tomography scan detected ipsilateral superior canal dehiscence. Conclusions: In accordance with recently reported vHIT findings in different types of BPPV, fluctuation of PC function could be likely explained by the effect of particles on cupular dynamic responses depending on the portion of the canal gradually involved. Superior canal dehiscence may have played a role facilitating otoliths mobilization by reducing labyrinthine impedance.
We describe a rare case of posterior semicircular canal (PSC) fibrosis following acute labyrinthine ischemia in the territory supplied by the common cochlear artery (CCA) and review the relevant literature. A 71-year-old man with multiple vascular risk factors presented 12 days after the onset of acute vertigo and profound left-sided hearing loss. Right-beating spontaneous nystagmus with downbeat components elicited by mastoid vibrations and headshaking was detected. The video head impulse test (vHIT) revealed an isolated hypofunction of the left PSC, whereas vestibular evoked myogenic potentials (VEMPs) showed ipsilateral saccular loss. The clinical presentation and instrumental picture were consistent with acute ischemia in the territory supplied by left CCA. Compared to previous imaging, a new MRI of the brain with 3D-FIESTA sequences highlighted a filling defect in the left PSC, consistent with fibrosis. Hearing function exhibited mild improvement after steroid therapy and hyperbaric oxygen sessions, whereas vHIT abnormalities persisted over time. To the best of our knowledge, this is the only case in the literature reporting a filling defect on MRI, consistent with semicircular canal fibrosis following acute labyrinthine ischemia. Moreover, PSC fibrosis was related with poor functional outcome. We therefore suggest using balanced steady-state gradient-echo sequences a few weeks following an acute lesion of inner ear sensors to detect signal loss within membranous labyrinth consistent with post-ischemic fibrosis. Besides addressing the underlying etiology, signal loss might also offer clues on the functional behavior of the involved sensor over time. In cases of acute loss of inner ear function, a careful bedside examination supplemented by instrumental assessments, including vHIT and VEMPs, of vestibular receptors and afferents may be completed by MRI with balanced steady-state gradient-echo sequences at a later time to confirm the diagnosis and address both etiology and functional outcome.
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