As people move through natural environments, they experience both visual and inertial stimuli. These can be integrated into a unified perception of self-motion (i.e. common causation) or segregated so that inertial or vestibular stimuli represents self-motion and visual represents external motion. There has been very little work on how causal inference (CI) or determination of common causation occurs for visual and inertial stimuli. Yet this is an important factor in fall risk, motion sickness, simulator sickness, concussion, dementia, and migraine. This proposal aims to develop and establish methods for studying CI in visual and inertial heading perception. This will be used to define the relevant variables in CI for these sensory systems. Common causation is likely a plastic process that occurs when stimuli occur simultaneously. The proposal will also examine this hypothesis by adapting heading perception, which may form the basis for a novel vestibular rehabilitation method.
Aim I: Causal inference (CI) for visual and inertial headings. During natural movements visual and inertial cues occur together. Inertial cues always represent self-motion, visual cues are ambiguous as they can represent motion through a fixed environment, environmental motion relative to the observer, or a combination of both. IA. Techniques for measuring CI for visual and inertial stimuli are not well established. The investigators have developed a technique to measure CI by presenting offset visual and inertial headings simultaneously using a full range of possible directions within the horizontal plane. Subjects report the perceived direction of the visual and inertial stimuli independently and whether or not they share common causation. These trial blocks can be repeated to determine reproducibility. IB. Parameters that influence perception of CI will be varied to determine their relative influences. These parameters will include stimulus timing, duration, and visual field size. It is hypothesized that full-field visual stimuli that are most consistent with the inertial stimulus will be perceived as having common causation. IC. Subjects with unilateral vestibular lesions will be tested using the techniques in IA. These individuals may have increased reliance on visual cues as well as decrease reliability and biases in inertial heading perception. As such, this may cause inertial headings to be more influenced by vision and result in a greater range of common causation.
Aim II: Visual-inertial heading adaptation. Plasticity in vestibular perception has received minimal attention, despite perception being the primary issue in common disorders such as vertigo, motion, and simulator sickness. Better understanding of how adaptation occurs could form the basis for improved therapeutic options as well as better tolerated virtual environments and simulations. IIA. Exposure to visual and inertial headings with similar characteristics, that are systematically offset, will be studied. It is hypothesized that exposure to this situation will influence subsequent visual and inertial heading perception as well as their common causation. These factors will also be measured before and after adaptation. The limits of what types of offsets can induce adaptation, and the range of headings that can be adapted will be explored. IIB. Preliminary data demonstrate that heading adaptation can also be induced by exposure to a virtual environment with an angular velocity offset in the visual stimulus. This method of adaptation will also be studied with regard to its influence on perception of rotation, visual and inertial headings and common causation of these headings. As with IIA, the potential limitations of the method will be explored.
Aim III: Heading adaptation after vestibular loss. Errors in heading perception are a clinically significant problem. Abnormal perception of rotation often quickly normalizes after vestibular lesions, but preliminary data indicate heading perception remains deviated for years afterwards. This could be due to asymmetry in the otolith system which current vestibular rehabilitation methods do not address. Abnormal heading perception may be a significant factor in other disorders including vestibular migraine, dementia, and concussion. Understanding long-term adaptation is potentially important in these populations. IIIA. Time course and etiology of perceptual pathology after acute vestibular lesions is unclear. This will be investigated by sequentially measuring bias and perceptual thresholds of yaw rotation, sway, and heading in individuals with acute loss of vestibular function. Initially subjects have a rotation bias towards the intact side which normalizes over time. The heading bias may correlate with rotational bias or may be related to otolith dysfunction, as measured with sway translation perception, or may occur as a result of adapting to the rotatory vertigo. IIIB. Study of long-term heading adaptation in subjects with chronic unilateral vestibular hypofunction (e.g. those who have had vestibular schwannomas removed, gentamicin ablative therapy for Meniere's disease). Since these subjects often have biased heading perception at baseline, they may be able to exhibit long term adaptation. Heading perception as well as visual-inertial common causation will be measured using the techniques described in Aim IC. Ability to adapt these patients to heading offsets will be measured using the methods established in normal controls (Aim II) but the adaptation will always be in a consistent direction to attempt to normalize baseline deviation in heading perception. It will be determined if durable long-term heading adaptation can be achieved. The proposal aims to understand how visual and inertial cues inform motion perception and how adaptation has the potential to improve pathological perception.
