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UNASSIGNED: This study investigates the association between vestibular function and prognosis in patients with unilateral idiopathic sudden sensorineural hearing loss (UISSNHL).
UNASSIGNED: A retrospective analysis of 64 patients with UISSNHL was performed. Pure tone audiometry and vestibular function tests for otoliths and semicircular canals were performed to assess the influence of vestibular functional status on the outcome of patients with UISSNHL.
UNASSIGNED: Patients with abnormal cervical vestibular evoked myogenic potential (cVEMP) or ocular vestibular evoked myogenic potential (oVEMP) responded less favorably to treatment. In the ineffective group, cVEMP was normal in four patients (6.3%) and oVEMPs in three (4.7%). Meanwhile, cVEMP was abnormal in 32 patients (50.0%) and oVEMP in 33 (51.6%). Better hearing recovery occurred in those with normal cVEMP (33.76 ± 15.07 dB HL improvement) or oVEMP (32.55 ± 19.56 dB HL improvement), but this was not the case in those with normal caloric tests. Patients with abnormalities in both cVEMP and oVEMP were less responsive to treatment and had worse hearing recovery than those with normal results in only one of the two tests.
UNASSIGNED: Abnormal oVEMP and/or cVEMP results indicate poor auditory outcomes in patients with UISSNHL. Patients with impaired otolith organ function are likely to have a larger and more severe pathological change in their inner ear.

Downbeat nystagmus (DBN) observed in head-hanging positions, may be of central or peripheral origin. Central DBN in head-hanging positions is mostly due to a disorder of the vestibulo-cerebellum, whereas peripheral DBN is usually attributed to canalolithiasis of an anterior semicircular canal. Here, we describe an atypical case of a patient who, after head trauma, experienced severe and stereotypic vertigo attacks after being placed in various head-hanging positions. Vertigo lasted 10-15 s and was always associated with a robust DBN. The provocation of transient vertigo and DBN, which both showed no decrease upon repetition of maneuvers, depended on the yaw orientation relative to the trunk and the angle of backward pitch. On a motorized, multi-axis turntable, we identified the two-dimensional Helmholtz coordinates of head positions at which vertigo and DBN occurred (y-axis: horizontal, space-fixed; z-axis: vertical, and head-fixed; x-axis: torsional, head-fixed, and unchanged). This two-dimensional area of DBN-associated head positions did not change when whole-body rotations took different paths (e.g., by forwarding pitch) or were executed with different velocities. Moreover, the intensity of DBN was also independent of whole-body rotation paths and velocities. So far, therapeutic approaches with repeated liberation maneuvers and cranial vibrations were not successful. We speculate that vertigo and DBN in this patient are due to macular damage, possibly an unstable otolithic membrane that, in specific orientations relative to gravity, slips into a position causing paroxysmal stimulation or inhibition of macular hair cells.

OBJECTIVE: The vestibular evoked myogenic potential (VEMP) is associated with otolithic afferents and can be used to evaluate the function of the saccule and utricle. In this study, we compared cervical VEMP evoked by stimulation with Air-conducted sound (ACS) and bone-conducted vibration (BCV) to the forehead and investigated whether BCV can be used as a substitute for ACS.
METHODS: Data were obtained from 33 patients with vestibular schwannoma. Vestibular examinations were performed preoperatively. VEMP was obtained upon stimulation with ACS (ACS cVEMP) and BCV to the forehead using a minishaker (BCV cVEMP). Vestibular function was also analyzed using the caloric test and ocular VEMP (oVEMP) testing. oVEMP was measured using bone-conductive vibration to the forehead. The results of BCV cVEMP, ACS cVEMP, and oVEMP were compared by the caloric test.
RESULTS: Rates of patients with abnormal ACS cVEMP, BCV cVEMP, oVEMP, and caloric test results were 78.8%, 75.8%, 78.8%, and 69.7%, respectively. BCV cVEMP did not correlate with ACS cVEMP, but correlated with oVEMP and caloric test results.
CONCLUSIONS: BCV cVEMP did not correlate with ACS cVEMP. Therefore, BCV cVEMP cannot be used as a substitute for ACS cVEMP.

Differential diagnosis between peripheral and central spontaneous nystagmus can be difficult to classify (as peripheral or central) even on the basis of criteria recommended in the recent literature. The aim of this paper is to use the combination of spontaneous nystagmus and ocular tilt reaction to determine the site of origin of the disease that causes nystagmus. We propose to classify the nystagmus in: 1) \"Uphill\" nystagmus in which the nystagmus takes on an inclined plane and the direction of the fast phase is towards the hypertropic eye (this type of nystagmus is likely peripheral); 2) \"Downhill\" nystagmus when the nystagmus beats toward the hypotropic eye (this type of nystagmus is likely central); 3) \"Flat\" nystagmus when the plane on which nystagmus beats is perfectly horizontal: in this case, we cannot say anything about the site of lesion (it was only detected in 15% of cases). The spatial position of nystagmus vector has to be considered as an intrinsic characteristic of the nystagmus itself (as direction, frequency, angular velocity etc.) and must be reported in the description, possibly giving an indication of the site of damage (peripheral or central). In particular, similar results are obtained by comparing the inclination of the nystagmus with the head impulse test (HIT, considered the best bedside test now available). It seems that this sign may confirm HIT for safer diagnosis or replace it in case of doubt. In contrast, in case of \"Flat\" nystagmus (probably attributable to the fact that the utricular maculae are spared), HIT can replace observation of the plane of the nystagmus. Thus, the two signs confirm and integrate each other. The test does not require additional time and is not tedious for the patient. It is proposed that it be included in the evaluation of spontaneous nystagmus in everyday clinical practice.
Capita spesso che un paziente con vertigini sia difficilmente inquadrabile (se periferico o centrale), anche affidandosi ai criteri consigliati nella recente letteratura. In questo lavoro si propone di utilizzare la valutazione della combinazione tra nistagmo spontaneo ed “Ocular Tilt Reaction” per dare un giudizio sulla sede della patologia che provoca il nistagmo. Si propone di dividere il nistagmo in : 1) nistagmo “in salita” in cui il nistagmo batte su un piano inclinato e il verso della fase rapida è verso l’occhio ipertropico (questo tipo di nistagmo è verosimilmente periferico); 2) nistagmo “ in discesa” ” in cui il nistagmo batte verso l’occhio ipotropico (questo tipo di nistagmo è verosimilmente centrale); 3) nistagmo “in piano” ” in cui il piano su cui batte il nistagmo è perfettamente orizzontale e sul quale non si può dire nulla (è stato rilevato solo nel 15% dei casi). La posizione nello spazio del vettore del nistagmo è da considerare una caratteristica intrinseca del nistagmo stesso (come direzione, verso ,frequenza, velocità angolare ecc.) e va riportata nella descrizione del nistagmo, potendo dare un’indicazione sulla sua natura (periferico o centrale). In particolare, confrontando l’inclinazione del nistagmo con l’Head Impulse Test (HIT), si ottengono risultati simili nella valutazione topodiagnostica di un nistagmo spontaneo. Sembra dunque che questo segno possa confermare l’HIT per una diagnosi più sicura o sostituirlo in casi dubbi. Al contrario, in caso di nistagmo che batte in piano (né in salita né in discesa, attribuibile probabilmente al fatto che le macule utriculari sono risparmiate) l’HIT può sostituire l’osservazione del piano del nistagmo. In questo modo i due segni si confermano e si integrano a vicenda nei casi dubbi. Il test non richiede tempi aggiuntivi e non è in alcun modo causa di disturbo per il paziente, per cui se ne propone l’inserimento nella valutazione di ogni nistagmo spontaneo.

We present a video of our technique for resection of a large prostatic utricle (PU) in a patient who presented initially with disordered sexual development. His karyotype was 46XY, and phenotypically had penoscrotal hypospadias, bifid scrotum, and retractile right testis. An initial micturating cystourethrogram (MCUG) demonstrated the utricle but failed to cannulate the bladder. Being asymptomatic, we carried out staged repair of his hypospadias. Later, he started to have recurrent epididymo-orchitis with resistance to multiple antibiotics. Examination under anaesthesia was done and ruled out meatal or neo-urethral strictures. A subsequent MCUG demonstrated the large utricle and its relation to the bladder. We carried out a cystoscopic-assisted laparoscopic excision. There has been no consensus about the best surgical approach to resect a PU and most known procedures involved extensive pelvic dissection and carried a significant risk of damage to the pelvic nerves. The laparoscopic approach seems to be promising in this field as it provides proper view of the deep pelvis with reasonable magnification, less dissection and shorter postoperative pain and scarring. Cystoscopic assistance in this technique was a great addition to provide counter-traction movement and facilitate proper dissection.

Acute unilateral peripheral-vestibular hypofunction (UVH) shifts the subjective visual vertical (SVV) ipsilesionally, triggering central compensation that usually eliminates shifts when upright. We hypothesized that compensation is worse when roll-tilted.
We quantified SVV errors and variability in different roll-tilted positions (0°, ±45°, ±90°) in patients with chronic UVH affecting the superior branch (SVN; n=4) or the entire (CVN; n=9) vestibular nerve.
Errors in SVN and CVN were not different. When roll-tilted ipsilesionally 45° (9.6±5.4° vs. -0.2±6.4°, patients vs. controls, p<0.001) and 90° (23.5±5.7° vs. 16.8±8.8°, p=0.003), the patient\'s SVV was shifted significantly towards the lesioned ear. When upright, only a trend was noted (3.6±2.2° vs. 0.0±1.2°, p=0.099); for contralesional roll-tilts shifts were not different from controls. Variability was larger for CVN than SVN (p=0.046). With increasing disease-duration, adjustment errors decayed for ipsilesional roll-tilt and upright (p⩽0.025).
The reason verticality perception was distorted for ipsilesional roll-tilts, may be the insufficient integration of contralesional otolith-input. Similar errors in SVN and CVN suggest a dominant utricular role in verticality perception, albeit the sacculus may improve precision of SVV estimates.
With deficiencies in central compensation being roll-angle dependent, extending SVV-testing to roll-tilted positions may improve identifying patients with chronic UVH.