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 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.

Background:The diagnosis of benign paroxysmal positional vertigo (BPPV) involving the lateral semicircular canal (LSC) is traditionally entrusted to the supine head roll test, also known as supine head yaw test (SHYT), which usually allows identification of the pathologic side and BPPV form (geotropic vs. apogeotropic). Nevertheless, SHYT may not always allow easy detection of the affected canal, resulting in similar responses on both sides and intense autonomic symptoms in patients with recent onset of vertigo. The newly introduced upright head roll test (UHRT) represents a diagnostic maneuver for LSC-BPPV, supplementing the already-known head pitch test (HPT) in the sitting position. The combination of these two tests should enable clinicians to determine the precise location of debris within LSC, avoiding disturbing symptoms related to supine positionings. Therefore, we proposed the upright BPPV protocol (UBP), a test battery exclusively performed in the upright position, including the evaluation of pseudo-spontaneous nystagmus (PSN), HPT and UHRT. The purpose of this multicenter study is to determine the feasibility of UBP in the diagnosis of LSC-BPPV.Methods:We retrospectively reviewed the clinical data of 134 consecutive patients diagnosed with LSC-BPPV. All of them received both UBP and the complete diagnostic protocol (CDP), including the evaluation of PSN and data resulting from HPT, UHRT, seated-supine positioning test (SSPT), and SHYT.Results:A correct diagnosis for LSC-BPPV was achieved in 95.5% of cases using exclusively the UBP, with a highly significant concordance with the CDP (p< 0.000, Cohen's kappa = 0.94), regardless of the time elapsed from symptom onset to diagnosis. The concordance between UBP and CDP was not impaired even when cases in which HPT and/or UHRT provided incomplete results were included (p< 0.000). Correct diagnosis using the supine diagnostic protocol (SDP, including SSPT + SHYT) or the sole SHYT was achieved in 85.1% of cases, with similar statistical concordance (p< 0.000) and weaker strength of relationship (Cohen's kappa = 0.80).Conclusion:UBP allows correct diagnosis in LSC-BPPV from the sitting position in most cases, sparing the patient supine positionings and related symptoms. UBP could also allow clinicians to proceed directly with repositioning maneuvers from the upright position.

Introduction: Predicting hearing outcome in sudden sensorineural hearing loss (SSNHL) is challenging, as well as detecting the underlying pathomechanisms. SSNHL could be associated with vestibular damage since cochleo-vestibular structures share the same vascularization, along with being in close anatomical proximity. Whereas viral inflammations and autoimmune/vascular disorders most likely represent the involved aetiologies, early-stage Menière's disease (MD) can also present with SSNHL. Since an early treatment could beneficially influence hearing outcome, understanding the possible etiology plays a pivotal role in orienting the most appropriate treatment. We aimed to evaluate the extent of vestibular damage in patients presenting with SSNHL with or without vertigo, investigate the prognostic role of vestibular dysfunctions on hearing recovery and detect specific lesion patterns related to the underlying pathomechanisms.Methods: We prospectively evaluated 86 patients with SSNHL. Audio-vestibular investigation included pure-tone/speech/impedance audiometry, cervical/ocular-VEMPs, vHIT and video-Frenzel examination. White matter lesions (WML) were evaluated on brain-MRI. Patients were followed-up and divided into “SSNHL-no-vertigo,” “SSNHL+vertigo” and “MD” subgroups.Results: Hearing was more impaired in “SSNHL+vertigo” patients who exhibited either down-sloping or flat-type audiograms, and was less impaired in “MD” where low frequencies were mostly impaired (p < 0.001). Otolith receptors were more frequently involved than semicircular canals (SCs). Although the “SSNHL-no-vertigo” subgroup exhibited the lowest vestibular impairment (p < 0.001), 52% of patients developed otolith dysfunctions and 72% developed nystagmus. Only “MD” subjects showed anterior SC impairment and upbeating spontaneous/positional nystagmus. They more frequently exhibited cervical-VEMPs frequency tuning (p = 0.036) and ipsilesional spontaneous nystagmus (p < 0.001). “SSNHL+vertigo” subjects presented with more frequently impaired cervical-VEMPs and posterior SC and with higher number of impaired receptors (p < 0.001). They mainly exhibited contralesional spontaneous and vibration-induced nystagmus (p < 0.05) and only they showed the highest WML score and “vascular” lesion patterns (p < 0.001). Concerning the outcomes, hearing was better in “MD” and worse in “SSNHL+vertigo” (p < 0.001). Hearing recovery was mostly affected by cervical-VEMPs impairment and the number of involved receptors (p < 0.05). Patients with “vascular” lesion patterns presented with the highest HL degree and WML score (p ≤ 0.001), while none of them exhibited a complete hearing recovery (p = 0.026).Conclusions: Our data suggest that vestibular evaluation in SSNHL can provide useful information on hearing recovery and underlying aetiologies.