Novel patterns of visual-vestibular intersensory stimulation often result in symptoms of simulator sickness, raising health and safety concerns regarding virtual environment exposure. Two experiments investigated the effect of conflicting visual-vestibular cues on subjective reports of simulator sickness during and after a 50-min exposure to a head-coupled virtual interface. Virtual image scale factors (0.5. 1.0, 2.0 magnification, generated by varying geometric field of view angle) were investigated in Experiment 1, and additional system time delays (125, 250 ms) were investigated in Experiment 2. Simulator sickness metrics included spoken self-reports during exposure and simulator sickness questionnaires (pre-exposure, immediate postexposure, and 20 min postexposure). Head yaw angular position data were also recorded. Reports of simulator sickness symptoms were significantly greater in the minification (0.5) and magnification (2.0) image scale factor conditions than in the neutral condition (1.0). Simulator sickness did not vary with changes in time delay, however. Furthermore, a comparison across experiments suggests no appreciable increase in simulator sickness with increasing time delays above the nominal value (48 ms). Head angular position data exhibited certain systematic variations across conditions. Actual or potential applications of this research include virtual environment training, simulation, and entertainment systems.

The properties of the vestibuloocular reflex (VOR) when the axis of rotation is behind the eyes and fixation of a near target is required were studied in the monkey. The magnitude of VOR gain in each eye was found to be above 1.0 and near the ideal value for stabilizing a retinal image. Evidence that this large VOR gain was not visually mediated was provided by the observations that no reduction in gain and no phase lag were observed at high frequencies of head rotation (2 Hz), large gain was observed in the dark, and large gain was observed within 10-20 ms of the start of head rotation. The magnitude of VOR gain was found to increase with increasing radius of head rotation and also to increase with decreasing target distance. When the distances from the two eyes to the target were different the instantaneous velocities and VOR gains of the eyes were also different. The dependence on radius of rotation indicates that the VOR is mediated by a combination of otolith and canal inputs. A general model for otolith-canal interaction is proposed in which VOR gain is based on a computation of target location relative to the head. This model simplifies to the classical VOR reflex when a cyclopean eye is subjected only to angular displacement.

Sudden hearing loss is common, but unexplained in many cases. Although usually attributed to a viral infection of the inner ear in most patients, the abrupt onset of the hearing loss in many patients argues against a viral etiology. We present 13 cases of unexplained sudden hearing loss who meet the diagnostic criteria for migraine. All had the sudden onset of hearing loss and other neurologic phenomena that could be attributed to vasospasm, including vertigo, amaurosis fugax, hemiplegia, facial pain, chest pain, and visual aura. We suggest that vasospasm of the cochlear vasculature was the cause of the sudden hearing loss in these patients. A personal and family history of migraine should be sought in patients with sudden hearing loss and when found, a trial of antispasmodic agents should be considered.

Our data, in conjunction with that of others, suggest that Meniere's disease may predispose patients to intractable BPPV. Hydropically induced damage to the maculae of the utricle and saccule or partial obstruction of the membranous labyrinth may be possible mechanisms that explain the coexistence of Meniere's disease and BPPV.