BackgroundNew insights have expanded the influence of the vestibular system to the regulation of circadian rhythmicity. Indeed, hypergravity or bilateral vestibular loss (BVL) in rodents causes a disruption in their daily rhythmicity for several days. The vestibular system thus influences hypothalamic regulation of circadian rhythms on Earth, which raises the question of whether daily rhythms might be altered due to vestibular pathology in humans. The aim of this study was to evaluate human circadian rhythmicity in people presenting a total bilateral vestibular loss (BVL) in comparison with control participants.Methodology and Principal FindingsNine patients presenting a total idiopathic BVL and 8 healthy participants were compared. Their rest-activity cycle was recorded by actigraphy at home over 2 weeks. The daily rhythm of temperature was continuously recorded using a telemetric device and salivary cortisol was recorded every 3 hours from 6:00AM to 9:00PM over 24 hours. BVL patients displayed a similar rest activity cycle during the day to control participants but had higher nocturnal actigraphy, mainly during weekdays. Sleep efficiency was reduced in patients compared to control participants. Patients had a marked temperature rhythm but with a significant phase advance (73 min) and a higher variability of the acrophase (from 2:24 PM to 9:25 PM) with no correlation to rest-activity cycle, contrary to healthy participants. Salivary cortisol levels were higher in patients compared to healthy people at any time of day.ConclusionWe observed a marked circadian rhythmicity of temperature in patients with BVL, probably due to the influence of the light dark cycle. However, the lack of synchronization between the temperature and rest-activity cycle supports the hypothesis that the vestibular inputs are salient input to the circadian clock that enhance the stabilization and precision of both external and internal entrainment.

Objectives/Hypothesis Currently, it is possible to assess in vivo the morphology of each compartment of the endolymphatic spaces 4 hours after an intravenous administration of gadolinium on magnetic resonance imaging (MRI). The aim of this study was to assess the correlation between otolithic and ampullar functions (cervical vestibular evoked myogenic potential [cVEMP], ocular vestibular evoked myogenic potential [oVEMP], video head impulse test [VHIT]) and delayed inner ear MRI based on a compartmental, anatomically based classification that included the cochlea, the saccule, the utricle, and the ampullas. Study Design Retrospective case–control study. Methods In this retrospective study, we performed three‐dimensional fluid‐attenuated inversion recovery sequences with delayed acquisition in 26 healthy subjects and 31 definite Menière's disease (MD) patients. Each subject was then graded on MRI on the basis on cochlear, saccular, utricular, and ampullar hydrops in MD patients. All patients underwent pure‐tone audiometry, VHIT, cVEMP, and oVEMP testing. Results Cochlear, saccular, utricular, and ampullar hydrops were found on MRI in 88%, 91%, 50%, and 8.5% respectively. We found no significant correlation between the presence of saccular hydrops versus cVEMP, utricular hydrops versus oVEMP, and ampullar hydrops versus VHIT. However, the severity of endolymphatic hydrops on MRI was correlated to the degree of hearing loss. Conclusions We proposed a compartmental, anatomically based classification for endolymphatic hydrops on MRI, which included the whole vestibular compartment. Using this classification, we observed increasing morphological changes as the disease evolved, affecting first the saccule, then the utricle, and finally the ampullas. The severity of vestibular endolymphatic hydrops is only correlated to hearing loss severity. Level of Evidence 3 Laryngoscope, 130:E444–E452, 2020

There is a natural symbiosis between vergence and vestibular responses. Deficits in vergence can lead to vertigo, disequilibrium, and postural instability. This study examines both vergence eye movements in patients with idiopathic bilateral vestibular loss, and their standing balance in relation to vergence. Eleven patients participated in the study and 16 controls. Bilateral loss of vestibular function was objectified with many tests; only patients without significant response to caloric tests, to video head impulse tests and without vestibular evoked myogenic potentials were included in the study.Vergence testing (from 8 patients and 15 controls)A LED display with targets at 20, 40, and 100 cm along the median plane was used to elicit vergence eye movements, recorded with the IRIS device.Standing balance (11 patients and 16 controls)Four conditions were run, each lasting 1 min: fixation of a LED at 40 cm (convergence of 9°), at 150 cm (convergence of 2.3°); this last condition was repeated with eyes closed. Comparison of the eyes closed-eyes open conditions at 150 cm allowed evaluation of the Romberg Quotient. In the forth condition, two LEDS, at 20 and at 100 cm, were light on, one after the other for 1 sec, causing the eyes to converge then diverge. Standing balance was recorded with an accelerometer placed at the back near the center of mass (McRoberts, Dynaport).ResultsVergenceRelative to controls, convergence eye movements in patients showed significantly lower accuracy, lower mean velocity, and saccade intrusions of significantly higher amplitude.BalanceThe normalized 90% area of body sway was significantly higher for patients than for controls for all conditions. Yet, similarly to controls, postural stability was better while fixating at near (sustained convergence) than at far, or while making active vergence movements. We argue that vestibular loss deteriorates convergence, but even deficient, convergence can be helpful for postural control.

Introduction. To compare the efficiency of Epley (Ep) and Sémont-Toupet (ST) repositioning maneuvers and to evaluate postmaneuver restriction effect on short-term vertigo and dizziness after repositioning maneuvers by an analog visual scale (VAS) in benign positional paroxysmal vertigo (BPPV). Material and Methods. 226 consecutive adult patients with posterior canal BPPV were included. Patients were randomized into 2 different maneuver sequence groups (n = 113): 2 ST then 1 Ep or 2 Ep then 1 ST. Each group of sequence was randomized into 2 subgroups: with or without postmaneuver restrictions. Vertigo and dizziness were assessed from days 0 to 5 by VAS. Results. There was no difference between vertigo scores between Ep and ST groups. Dizziness scores were higher in Ep group during the first 3 days but became similar to those of ST group at days 4 and 5. ST maneuvers induced liberatory signs more frequently than Ep (58% versus 42% resp., P < 0.01, Fisher's test). After repositioning maneuvers, VAS scores decreased similarly in patients with and without liberatory signs. Postmaneuver restrictions did not influence VAS scores. Conclusion. Even if ST showed a higher rate of liberatory signs than Ep in this series, VAS scores were not influenced by these signs.

Patients with vestibular deficit use slow eye movements or catch-up saccades (CUS) to compensate for impaired vestibulo-ocular reflex (VOR). The purpose of CUS is to bring the eyes back to the visual target. Covert CUS occur during high-velocity head rotation and overt CUS are generated after head rotation has stopped. Dynamic visual acuity is improved with an increased rate and gain of CUS. Nevertheless, the trigger and the parametric determinants of CUS are still under debate. To clarify the underlying mechanism, especially the visual contribution, we analyzed the number, amplitude and latencies of the CUS in relation with the extent of VOR deficiency. The head and eye movements were recorded in 17 patients with bilateral vestibular loss (BVL) and in 33 subjects with normal VOR gain using the Video Head Impulse Test (vHIT) in two conditions: with visible target and in darkness with an imaginary target. Our study shows that in darkness without visible target the number of CUS is significantly reduced and the relationship between the amplitude of CUS and gaze position error is lost. Results showed that there is a correlation between the number of CUS and the drop in VOR gain. CUS occurring during the head movement and when the head remained still were not always sufficiently accurate. Up to four consecutive CUS could be required to bring eyes back to the visible target. A positive correlation was found between the amplitude of overt saccades with visible target and the gaze position error, namely the remaining eye movement to reach the target. These results suggest that the visual inputs are the main trigger and parametric determinant of the CUS or at least the presence of a visual target is necessary in most cases for a CUS to occur.