The virtual retinal display as a low-vision computer interface: a pilot study.

This pilot study examined the performance of an alternative computer visual interface, the Virtual Retinal Display (VRD), for low-vision use. The VRD scans laser light directly onto the retina, creating a virtual image. Since visually impaired individuals can have difficulty using computer displays, a matched comparison study was done between the VRD and the standard cathode ray tube (CRT) monitor. Reading speed and acuity tests were collected from 13 low-vision volunteers selected to represent the broad range of partially sighted individuals actively involved in the work force. Forty-six percent of subjects had highest visual acuity while viewing the VRD; 30% of subjects had highest acuity viewing the CRT; and 24% of subjects had equal acuity across the two displays. Although mean reading speed across all 13 subjects indicated no significant difference between displays, individual subjects with predominantly optical causes of low vision exhibited clinically important increases in reading speed versus the CRT. However, most subjects with predominantly retinal damage showed a slight disadvantage using the VRD. We give theoretical explanation to the bifurcated results and conclude that for a subset of low-vision users, the VRD technology is very promising as a basis for future low-vision aids.

Intractable benign paroxysmal positional vertigo in patients with Meniere's disease.

OBJECTIVE: To provide a detailed description of the coexistence of benign paroxysmal positional vertigo (BPPV) and Meniere's disease in individuals and to offer a possible mechanism that explains the findings in these patients. STUDY DESIGN: Retrospective. METHODS: Chart review. RESULTS: Of 162 patients diagnosed with Meniere's disease between January 1998 and January 1999, 9 were found to have both "definite" Meniere's disease and "certain" BPPV. Meniere's symptoms preceded the onset of BPPV in all of our patients. Seven of the 9 patients were female. Except for one patient who experienced BPPV bilaterally, BPPV was limited to the same ear as the Meniere's disease. All patients presented with intractable BPPV that did not respond completely to otolith repositioning procedures. A detailed description of five patients is presented. CONCLUSION: 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.

The human horizontal vestibulo-ocular reflex during combined linear and angular acceleration.

We employed binocular magnetic search coils to study the vestibulo-ocular reflex (VOR) and visually enhanced vestibulo-ocular reflex (VVOR) of 15 human subjects undergoing passive, whole-body rotations about a vertical (yaw) axis delivered as a series of pseudorandom transients and sinusoidal oscillations at frequencies from 0.8 to 2.0 Hz. Rotations were about a series of five axes ranging from 20 cm posterior to the eyes to 10 cm anterior to the eyes. Subjects were asked to regard visible or remembered targets 10 cm, 25 cm, and 600 cm distant from the right eye. During sinusoidal rotations, the gain and phase of the VOR and VVOR were found to be highly dependent on target distance and eccentricity of the rotational axis. For axes midway between or anterior to the eyes, sinusoidal gain decreased progressively with increasing target proximity, while, for axes posterior to the otolith organs, gain increased progressively with target proximity. These effects were large and highly significant. When targets were remote, rotational axis eccentricity nevertheless had a small but significant effect on sinusoidal gain. For sinusoidal rotational axes midway between or anterior to the eyes, a phase lead was present that increased with rotational frequency, while for axes posterior to the otolith organs phase lag increased with rotational frequency. Transient trials were analyzed during the first 25 ms and from 25 to 80 ms after the onset of the head rotation. During the initial 25 ms of transient head rotations, VOR and VVOR gains were not significantly influenced by rotational eccentricity or target distance. Later in the transient responses, 25-80 ms from movement onset, both target distance and eccentricity significantly influenced gain in a manner similar to the behavior during sinusoidal rotation. Vergence angle generally remained near the theoretically ideal value during illuminated test conditions (VVOR), while in darkness vergence often varied modestly from the ideal value. Regression analysis of instantaneous VOR gain as a function of vergence demonstrated only a weak correlation, indicating that instantaneous gain is not likely to be directly dependent on vergence. A model was proposed in which linear acceleration as sensed by the otoliths is scaled by target distance and summed with angular acceleration as sensed by the semicircular canals to control eye movements. The model was fit to the sinusoidal VOR data collected in darkness and was found to describe the major trends observed in the data. The results of the model suggest that a linear interaction exists between the canal and otolithic inputs to the VOR.

The human vertical vestibulo-ocular reflex during combined linear and angular acceleration with near-target fixation.

The purpose of this study was to examine the effect of fixation target distance on the human vestibuloocular reflex (VOR) during eccentric rotation in pitch. Such rotation induces both angular and linear acceleration. Eight normal subjects viewed earth-fixed targets that were either remote or near to the eyes during whole-body rotation about an earth-horizontal axis that was either oculocentric or 15 cm posterior (eccentric) to the eyes. Eye and head movements were recorded using magnetic search coils. Using a servomotor-driven chair, passive whole-body rotations were delivered as trains of single-frequency sinusoids at frequencies from 0.8 to 2.0 Hz and as pseudorandom impulses of acceleration. In the light, the visually enhanced VOR (VVOR) was recorded while subjects were asked to fixate targets at one of several distances. In darkness, subjects were asked to remember targets that had been viewed immediately prior to the rotation. In order to eliminate slip of the retinal image of a near target when the axis of rotation of the head is posterior to the eyes, the ideal gain (compensatory eye velocity divided by head velocity) of the VVOR and VOR must exceed 1.0. Both the VOR and VVOR were found to have significantly enhanced gains during sinusoidal and pseudorandom impulses of rotation (P < 0.05). Enhancement of VVOR gain was greatest at low frequencies of head rotation and decreased with increasing frequency. However, enhanced VOR gain only slightly exceeded 1.0, and VVOR gain enhancement was significantly lower than the expected ideal values for the stimulus conditions employed (P < 0.05). During oculocentric rotations with near targets, both the VOR and VVOR tended to exhibit small phase leads that increased with rotational frequency. In contrast, during eccentric rotations with near targets, there were small phase lags that increased with frequency. Visual tracking contributes during ocular compensatory responses to sustained head rotation, although the latency of visual tracking reflexes exceeds 100 ms. In order to study initial vestibular responses prior to modification by visual tracking, we presented impulses of head acceleration in pseudorandom sequence of initial positions and directions, and evaluated the ocular response in the epoch from 25 to 80 ms after movement onset. As with sinusoidal rotations, pseudorandom eccentric head rotation in the presence of a near, earth-fixed target was associated with enhancement of VVOR and VOR gains in the interval from 25 to 80 ms from movement onset. Despite the inability of visual tracking to contribute to these responses, VVOR gain significantly exceeded VOR gain for pseudorandom accelerations. This gain enhancement indicates that target distance and linear motion of the head are considered by the human ocular motor system in adjustment of performance of the early VOR, prior to a contribution by visual following reflexes. Vergence was appropriate to target distance during all VVOR rotations, but varied during VOR rotations with remembered targets. For the 3-m target distance, vergence during the VOR was stable over each entire trial but slightly exceeded the ideal value. For the 0.1-m near target, instantaneous vergence during the VOR typically declined gradually in a manner not corresponding to the time course of instantaneous VOR gain change; mean vergence over entire trials ranged from 60 to 90% of ideal, corresponding to target distances for which ideal gain would be much higher than actually observed. These findings suggest a dissociation between vergence and VOR gain during eccentric rotation with near targets in the frequency range from 0.8 to 2.0 Hz.

Visual-vestibular interaction during standing, walking, and running.

In artificial laboratory situations where subjects undergo repetitive self-generated or externally imposed head rotations, visual-vestibular interaction during the wearing of telescopic spectacles can markedly augment gain of the vestibulo-ocular reflex (VOR). The present study was conducted to determine whether the wearing of these aids for the visually impaired is associated with similar visual-vestibular interaction during more natural activities. Angular eye and head movements of unrestrained normal volunteers were measured using magnetic search coils. In some subjects, head translations and rotations were also monitored by a flux gate magnetometer array. Measurements were performed of the VOR in darkness, and of the visually enhanced VOR (VVOR) in lit conditions, during three natural activities: 1) standing quietly; 2) walking in place; 3) running in place. These data were compared with similar measurements during repetitive voluntary head oscillations at 0.8 Hz in pitch or yaw. During VVOR, subjects viewed a target placed 6 to 10 m away and remembered this target during VOR trials in darkness. To assess the effects of altering visual-vestibular interactions, VVOR testing during normal vision was augmented by wearing of binocular telescopic spectacles of 2X, 4X, and 6X powers. Dorsoventral and mediolateral head translations were consistently phase-locked with pitch and yaw head rotations, respectively, such that head translation at least partially compensated for rotational disturbances of gaze. Angular velocity of the head was greater during walking than during standing, and was greater still during running, with a greater increase in each case for pitch as compared with yaw. Eye movements were phase compensatory for head movements. VOR gain (eye velocity divided by head velocity) was near 1.0 in both pitch and yaw during standing and during actively generated head rotation. During walking and running there was a significant decrease in angular VOR gain in pitch to approximately 0.75 (P < 0.0005). During ambulatory activities, normal and magnified vision were associated with VVOR gain enhancement in pitch and yaw that was statistically significant, but substantially less than was telescope magnification and markedly lower than was the corresponding VVOR gain measured during active head rotation. Measurements of unmagnified VOR and VVOR during walking and running showed that gain was lower than the "ideal" value of 1.0. However, since translational head perturbations during these activities partially offset the visual effects of angular disturbances, lower gains may nevertheless be associated with retinal image stability at typical indoor target distances. In contrast with performance during repetitive, uniplanar motion, vision has very limited influence on VOR gain during natural activities.

Migraine as a cause of sudden hearing loss.

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.