Impact of Canal-Otolith Integration on Postural Control

Roll tilt vestibular perceptual thresholds, an assay of vestibular noise, have recently been shown to be associated with suboptimal balance performance in healthy older adults. However, despite the strength of this correlation, the use of a categorical (i.e., pass/fail) balance assessment limits insight into the impacts of vestibular noise on postural sway. As a result, an explanation for this correlation has yet to be determined. We hypothesized that the correlation between roll tilt vestibular thresholds and postural control reflects a shared influence of sensory noise. To address this hypothesis, we measured roll tilt perceptual thresholds at multiple frequencies (0.2 Hz, 0.5 Hz, 1 Hz) and compared each threshold to quantitative measures of quiet stance postural control in 33 healthy young adults (mean = 24.9 years, SD = 3.67). Our data showed a significant linear association between 0.5 Hz roll tilt thresholds and the root mean square distance (RMSD) of the center of pressure in the mediolateral (ML; β = 5.31, p = 0.002, 95% CI = 2.1–8.5) but not anteroposterior (AP; β = 5.13, p = 0.016, 95% CI = 1.03–9.23) direction (Bonferroni corrected α of 0.006). In contrast, vestibular thresholds measured at 0.2 Hz and 1 Hz did not show a significant correlation with ML or AP RMSD. In a multivariable regression model, controlling for both 0.2 Hz and 1 Hz thresholds, the significant effect of 0.5 Hz roll tilt thresholds persisted (β = 5.44, p = 0.029, CI = 0.60–10.28), suggesting that the effect cannot be explained by elements shared by vestibular thresholds measured at the three frequencies. These data suggest that vestibular noise is significantly associated with the temporospatial control of quiet stance in the mediolateral plane when visual and proprioceptive cues are degraded (i.e., eyes closed, standing on foam). Furthermore, the selective association of quiet-stance sway with 0.5 Hz roll tilt thresholds, but not thresholds measured at lower (0.2 Hz) or higher (1.0 Hz) frequencies, may reflect the influence of noise that results from the temporal integration of noisy canal and otolith cues.

Characterising acetabular component orientation with pelvic motion during total hip arthroplasty

Introduction: Suboptimal acetabular component position can result in impingement, dislocation, and accelerated wear. Intraoperative pelvic motion has led to surgeon error and acetabular cup malposition. This study characterises the relationship between pelvic rotation and postoperative acetabular cup orientation. Methods: A device was constructed to allow cadaveric pelvis rotation along three axes about an acetabular cup in fixed orientation. The acetabular cup was fixed in space at 40° of radiographic inclination and 15° of anteversion relative to the anterior pelvic plane to represent consistent surgeon intraoperative placement. Active marker clusters were fixed to surgical equipment while the cadaveric pelvis was cemented with passive reflective markers, both identified with the Optotrak Certus motion capture system. The reamed cadaveric pelvis was rotated along three axes from –45° to 45° of roll, –30° to 30° of tilt, and –35° to 35° of pitch. The change in component inclination and anteversion was recorded at each 5° interval. Using computed tomography 3D reconstruction, the experimental setup was duplicated computationally to assess against a greater range of pelvis and implant sizes. Results: Radiographic anteversion and inclination showed a non-linear relationship dependent on pelvic roll, tilt, and pitch. Radiographic anteversion changed –0.59°, 0.76° and 0.01° while radiographic inclination changed 0.23°, 0.18° and 1.00° for every 1° of pelvic roll, tilt and pitch, respectively. Computationally, anteversion changed –0.61°, 0.75° and 0.00° while inclination changed 0.22°, 0.19° and 1.00° for every 1° of pelvic roll, tilt and pitch, respectively. These results were independent of cup and pelvis size. Conclusions: Intraoperative pelvic motion can significantly affect final cup position, and this should be accounted for when placing acetabular components during total hip arthroplasty. Based on this study, intraoperative adjustment of the acetabular component position based on pelvis motion may be implemented to improve postoperative component position.

Roll tilt self-motion direction discrimination training: First evidence for perceptual learning

Perceptual learning, the ability to improve the sensitivity of sensory perception through training, has been shown to exist in all sensory systems but the vestibular system. A previous study found no improvement of passive self-motion thresholds in the dark after intense direction discrimination training of either yaw rotations (stimulating semicircular canals) or y-translation (stimulating otoliths). The goal of the present study was to investigate whether perceptual learning of self-motion in the dark would occur when there is a simultaneous otolith and semicircular canal input, as is the case with roll tilt motion stimuli. Blindfolded subjects (n = 10) trained on a direction discrimination task with 0.2-Hz roll tilt motion stimuli (9 h of training, 1,800 trials). Before and after training, motion thresholds were measured in the dark for the trained motion and for three transfer conditions. We found that roll tilt sensitivity in the 0.2-Hz roll tilt condition was increased (i.e., thresholds decreased) after training but not for controls who were not exposed to training. This is the first demonstration of perceptual learning of passive self-motion direction discrimination in the dark. The results have potential therapeutic relevance as 0.2-Hz roll thresholds have been associated with poor performance on a clinical balance test that has been linked to more than a fivefold increase in falls.

The neural basis of motion sickness

Although motion of the head and body has been suspected or known as the provocative cause for the production of motion sickness for centuries, it is only within the last 20 yr that the source of the signal generating motion sickness and its neural basis has been firmly established. Here, we briefly review the source of the conflicts that cause the body to generate the autonomic signs and symptoms that constitute motion sickness and provide a summary of the experimental data that have led to an understanding of how motion sickness is generated and can be controlled. Activity and structures that produce motion sickness include vestibular input through the semicircular canals, the otolith organs, and the velocity storage integrator in the vestibular nuclei. Velocity storage is produced through activity of vestibular-only (VO) neurons under control of neural structures in the nodulus of the vestibulo-cerebellum. Separate groups of nodular neurons sense orientation to gravity, roll/tilt, and translation, which provide strong inhibitory control of the VO neurons. Additionally, there are acetylcholinergic projections from the nodulus to the stomach, which along with other serotonergic inputs from the vestibular nuclei, could induce nausea and vomiting. Major inhibition is produced by the GABAB receptors, which modulate and suppress activity in the velocity storage integrator. Ingestion of the GABAB agonist baclofen causes suppression of motion sickness. Hopefully, a better understanding of the source of sensory conflict will lead to better ways to avoid and treat the autonomic signs and symptoms that constitute the syndrome.