Visual Motion Stimulation Research Articles

Vection Induced by Illusory Motion in a Stationary Image

Ilusory self-motion (vection) can be induced by large areas of visual motion stimulation. Here we demonstrate for the first time that illusory expansion can induce vection in the absence of any physical display motion.

Neuronal Variability of MSTd Neurons Changes Differentially With Eye Movement and Visually Related Variables

Neurons in macaque cortical area MSTd are driven by visual motion and eye movement related signals. This multimodal characteristic makes MSTd an ideal system for studying the dependence of neuronal activity on different variables. Here, we analyzed the temporal structure of spiking patterns during visual motion stimulation using 2 distinct behavioral paradigms: fixation (FIX) and optokinetic response. For the FIX condition, inter- and intra-trial variability of spiking activity decreased with increasing stimulus strength, complying with a recent neurophysiological study reporting stimulus-related decline of neuronal variability. In contrast, for the optokinetic condition variability increased together with increasing eye velocity while retinal image velocity remained low. Analysis of stimulus signal variability revealed a correlation between the normalized variance of image velocity and neuronal variability, but no correlation with normalized eye velocity variance. We further show that the observed difference in neuronal variability allows classifying spike trains according to the paradigm used, even when mean firing rates (FRs) were similar. The stimulus-dependence of neuronal variability may result from the local network structure and/or the variability characteristics of the input signals, but may also reflect additional timing-based mechanisms independent of the neuron's mean FR and related to the modality driving the neuron.

Role of latency jittering correction in motion-onset VEP amplitude decay during prolonged visual stimulation

Visual evoked potentials to motion-onset stimulation (M-VEPs) gradually attenuate in amplitude during examination. The observed decline in averaged responses can be caused by decreases in single response magnitudes and/or increased variability in a response delays, that is, latency jittering. To illuminate the origins of the suppression of M-VEPs during stimuli repetition, we used correlation technique to estimate an upper bound of possible latency jittering of single sweeps and we evaluated the effect of its correction on the amplitudes of three M-VEP dominant peaks P1, N2 and P3. During prolonged visual motion stimulation, the variability of corrective latency shifts in the occipital region increased (r = 0.35: 0.44) and the number of single responses corresponding to the average curve declined in occipital and parietal derivations (r = -0.48: -0.62). While the P1 peak amplitude did not exhibit any time-specific behaviour, the N2 amplitude exhibited a significant decay of 29.4% that was partially reduced to 16.6% in the central occipital derivation by the latency jitter and non-correspondence corrections. The strongest attenuation (32.7%) was observed in the P3 amplitude and was less sensitive to the corrections, dropping only to 27.9%. The main part of the response suppression to repeated motion stimulation was caused by amplitude drop and represents non-stationary process that likely correspond to a fatigue model. The rise of variability in latency jitter correction and the reduction in single responses correlated with the M-VEP were significant factors associated with prolonged motion stimulation. The relation of these parameters to a hypothetical veridical response is ambiguous and can be caused by a time shift of the response or by a change of signal-to-noise ratio. Using selective averaging and latency jitter correction, the effect of response suppression was partially removed.

9. Origins of VEP response suppression during prolonged visual motion stimulation

9. Origins of VEP response suppression during prolonged visual motion stimulation

Visual dependence and BPPV

The increased visual dependence noted in some vestibular patients may be secondary to their vertigo. We examine whether a single, brief vertigo attack, such as in benign paroxysmal positional vertigo (BPPV), modifies visual dependency. Visual dependency was measured before and after the Hallpike manoeuvre with (a) the Rod and Frame and the Rod and Disc techniques whilst seated and (b) the postural sway induced by visual roll-motion stimulation. Three subject groups were studied: 20 patients with BPPV (history and positive Hallpike manoeuvre; PosH group), 20 control patients (history of BPPV but negative Hallpike manoeuvre; NegH group) and 20 normal controls. Our findings show that while both patient groups showed enhanced visual dependency, the PosH and the normal control group decreased visual dependency on repetition of the visual tasks after the Hallpike manoeuvre. NegH patients differed from PosH patients in that their high visual dependency did not diminish on repetition of the visual stimuli; they scored higher on the situational characteristic questionnaire ('visual vertigo' symptoms) and showed higher incidence of migraine. We conclude that long term vestibular symptoms increase visual dependence but a single BPPV attack does not increase it further. Repetitive visual motion stimulation induces adaptation in visual dependence in peripheral vestibular disorders such as BPPV. A positional form of vestibular migraine may underlie the symptoms of some patients with a history of BPPV but negative Hallpike manoeuvre. The finding that they have non adaptable increased visual dependency may explain visuo-vestibular symptoms in this group and, perhaps more widely, in patients with migraine.

The influence of dual task on gait during galvanic vestibular or visual motion stimulation

The influence of dual task on gait during galvanic vestibular or visual motion stimulation

Cerebellar and visual gray matter brain volume increases in congenital nystagmus

Structural brain abnormalities associated with congenital nystagmus (CN) are still unknown. In some patients with CN additional sensory, metabolic, or gross structural alterations can be detected. In the present study voxel-based morphometry was used to compare the gray matter (GM) brain volumes of 14 individuals with CN without associated sensory, metabolic, or obvious structural alterations (i.e., idiopathic CN) to those of a group of controls. Further, GM brain volumes were correlated with nystagmus severity as measured by sway path. Intergroup comparison exhibited significant volume increases in the human motion sensitive complex V5/MT+, the fusiform gyrus, and the middle occipital gyrus bilaterally in CN. These volume increases may be associated with excess visual motion stimulation due to involuntary retinal slip of the visual scene. A positive correlation (linear model) of nystagmus sway path with cerebellar GM volume was seen in the following areas: vermal parts VIII-X as well as hemisphere lobule II, hemisphere VI, crus I, crus II, and lobule VII-IX bilaterally. There is evidence that the reported GM volume changes in the vestibulo-cerebellum, which correlated with nystagmus sway path, might be related to the subjects‘ attempt to maintain fixation, rather than be due to the generation of nystagmus.

Effects of Long-Term Adaptation to Sway-Yoked Visual Motion and Galvanic Vestibular Stimulation on Visual and Vestibular Control of Posture

Human postural control is a multimodal process involving visual and vestibular information. The aim of the present study was to measure individual differences in the contributions of vision and vestibular senses to postural control, and to investigate if the individual weights could be modulated by long-term adaptation to visual motion or galvanic vestibular stimulation (GVS). Since GVS is a less expensive technique than a motion platform and can be wearable, it is a promising virtual reality (VR) technology. We measured the postural sway of observers induced by a visual motion or GVS before and after a 7-day adaptation task. We divided participants into four groups. In visual adaptation groups, visual motions were presented to either enhance voluntary body movement (enhancing vision group) or inhibit voluntary body movement (inhibiting vision group). In GVS adaptation groups, GVS was applied to enhance voluntary body movement (enhancing GVS group) or inhibit voluntary body movement (inhibiting GVS group). The adaptation to enhancing body-movement-yoked visual motion decreased the GVS-induced postural sway at a low motion frequency. The adaptation to the enhancing GVS slightly increased the GVS-induced postural sway and decreased the visually-induced sway at a low motion frequency. The adaptation to the inhibiting GVS increased the GVS-induced postural sway and decreased the visually-induced sway at a high motion frequency. These data suggest that long-term adaptation can modify weights of vision and vestibular senses to control posture. These findings can be applied to training or rehabilitation systems of postural control and also to adaptive virtual-reality systems.

Frequency-phase analysis of postural sway induced by visual motion and galvanic vestibular stimulation

Frequency-phase analysis of postural sway induced by visual motion and galvanic vestibular stimulation

Cerebellar and Visual Gray Matter Brain Volume Increases in Congenital Nystagmus

Structural brain abnormalities associated with congenital nystagmus (CN) are still unknown. In some patients with CN additional sensory, metabolic, or gross structural alterations can be detected. In the present study voxel-based morphometry was used to compare the gray matter (GM) brain volumes of 14 individuals with CN without associated sensory, metabolic, or obvious structural alterations (i.e., idiopathic CN) to those of a group of controls. Further, GM brain volumes were correlated with nystagmus severity as measured by sway path. Intergroup comparison exhibited significant volume increases in the human motion sensitive complex V5/MT+, the fusiform gyrus, and the middle occipital gyrus bilaterally in CN. These volume increases may be associated with excess visual motion stimulation due to involuntary retinal slip of the visual scene. A positive correlation (linear model) of nystagmus sway path with cerebellar GM volume was seen in the following areas: vermal parts VIII-X as well as hemisphere lobule II, hemisphere VI, crus I, crus II, and lobule VII-IX bilaterally. There is evidence that the reported GM volume changes in the vestibulo-cerebellum, which correlated with nystagmus sway path, might be related to the subjects‘ attempt to maintain fixation, rather than be due to the generation of nystagmus.

Gait Deviations Induced by Visual Motion Stimulation in Roll Depend on Head Orientation

Locomotion control uses proprioceptive, visual, and vestibular signals. Previously, we analyzed the visual contribution with visual motion stimulation in roll while participants kept their heads in a normal upright orientation. In this study we applied the same visual disturbance in a head-upright and a nose-down condition. Random dot patterns were constantly rotated in roll at +/-15 degrees/sec on a computer-driven binocular head-mounted display, while the participants walked a distance of 6 m. The stimulation effect was more pronounced in the nose-down condition. These results are similar to the results of previous galvanic vestibular stimulation (GVS) studies, suggesting that in terms of the direction of action visual motion stimulation in the roll plane is similar to GVS.

Novel, continuous visual motion induces c-fos expression in the avian optokinetic nuclei and optic tectum

We studied the stimulus characteristics necessary for the expression of c- fos protein in optokinetic system neurons using immunocytochemistry. Using whole-field visual motion as a stimulus, we found substantial c- fos expression in the optic tectum (TeO), the nucleus of the basal optic root (nBOR) and the pretectal nucleus lentiformis mesencephali (LM); in all cases immunostaining was seen only on the side contralateral to the eye viewing whole-field unidirectional motion; the side of the brain contralateral to the eye wearing a diffuser showed no staining. In the nBOR and the LM, different regions showed a remarkable specificity of c- fos expression depending on the direction of visual motion stimulation. Neurons were stained primarily in regions known from previous electrophysiological recordings to be maximally responsive to that direction of motion; little staining was seen after motion orthogonal to the preferred motion direction. Novel, continuous visual motion stimuli, lasting more than 30 min, was required for maximal c- fos expression, suggesting that brief periods of unidirectional optic flow, as would be experienced during normal life, do not stimulate the expression of c- fos. The largest number of neurons was labeled when birds raised from hatching with one eye covered by a diffuser were exposed to full-field visual motion immediately after the diffuser was switched from one eye to the other, so that only the previously naive eye was visually stimulated. We conclude that the expression of c- fos in the optokinetic nuclei is linked to near peak firing rates on the one hand, and the novelty and duration of the visual signals, on the other, supporting the assumption that this expression is mainly related to stimulus contexts leading to neuronal plastic changes.

Adaptation of Velocity Encoding in Synaptically Coupled Neurons in the Fly Visual System

Although many adaptation-induced effects on neuronal response properties have been described, it is often unknown at what processing stages in the nervous system they are generated. We focused on fly visual motion-sensitive neurons to identify changes in response characteristics during prolonged visual motion stimulation. By simultaneous recordings of synaptically coupled neurons, we were able to directly compare adaptation-induced effects at two consecutive processing stages in the fly visual motion pathway. This allowed us to narrow the potential sites of adaptation effects within the visual system and to relate them to the properties of signal transfer between neurons. Motion adaptation was accompanied by a response reduction, which was somewhat stronger in postsynaptic than in presynaptic cells. We found that the linear representation of motion velocity degrades during adaptation to a white-noise velocity-modulated stimulus. This effect is caused by an increasingly nonlinear velocity representation rather than by an increase of noise and is similarly strong in presynaptic and postsynaptic neurons. In accordance with this similarity, the dynamics and the reliability of interneuronal signal transfer remained nearly constant. Thus, adaptation is mainly based on processes located in the presynaptic neuron or in more peripheral processing stages. In contrast, changes of transfer properties at the analyzed synapse or in postsynaptic spike generation contribute little to changes in velocity coding during motion adaptation.

Unilateral vestibular failure suppresses cortical visual motion processing

Patients with unilateral vestibular failure (UVF) experience oscillopsia (apparent motion of the visual scene) during rapid head movements due to increased retinal slip caused by vestibulo-ocular reflex impairment. Oscillopsia is always smaller than the net retinal slip and decreases over time in patients with acquired vestibular loss; this correlates with increased thresholds for visual motion detection and increased tolerance to retinal slip. We investigated the underlying cortical adaptive processes using visual motion stimulation during blood oxygen level-dependent (BOLD) fMRI. Optokinetic nystagmus was elicited in seven patients with right-sided and seven patients with left-sided unilateral vestibular neurectomy and in seven age- and gender-matched healthy controls. Patients showed diminished activation of bilateral visual cortex areas (including the motion-sensitive area MT/V5, cuneus, middle occipital, fusiform and lingual areas) and ocular motor regions compared to their controls during visual motion stimulation. Concurrent BOLD signal decreases of temporo-parietal and insular multisensory cortical areas occurred in controls and patients. The diminished activation of visual motion processing areas plausibly reflects an adaptive mechanism that suppresses distressing oscillopsia in patients with UVF and thereby stabilizes the perceived visual surroundings. This study provides for the first time neuroimaging evidence of suppressed cortical visual motion processing in patients with vestibulopathy.

Chronic subjective dizziness

Conclusion. Chronic subjective dizziness (CSD) is frequent and affects twice as many women as men. Anxiety is a strong predisposing factor. The pathophysiologic concept of this disorder assumes that balance function and emotion share common neurologic pathways, which might explain that the balance disorder can provoke fear and vice versa, giving rise to a problem in perception of space and motion. In anxious patients this can turn into a space and motion phobia, with avoidance behaviour. Objective. CSD is a diagnosis based on the hypothesis of an interaction between the vestibular system and the psychiatric sphere. Patients complain of chronic imbalance, worsened by visual motion stimulation, and frequently suffer from anxiety. Vestibular examination reveals no anomalies. We evaluated the incidence and characteristics of CSD in patients referred to our neuro-otology centre (tertiary hospital outpatient clinic). Subjects and methods. This was a retrospective study of 1552 consecutive patients presenting with vertigo. CSD was diagnosed in 164 patients (female:male=111:53). Results. CSD represents 10.6% of the dizzy patients in our clinic. Psychiatric disorder, mainly anxiety, was found in 79.3% of the cases. Other frequently associated factors were fear of heights and former vestibular lesion (healed). In all, 79.0% of the patients with CSD had poor balance performance on dynamic posturography testing.

Gait deviations induced by visual stimulation in roll

Locomotion control uses proprioceptive, visual, and vestibular signals. The vestibular contribution has been analyzed previously with galvanic vestibular stimulation (GVS), which constitutes mainly a virtual head-fixed rotation in the roll plane that causes polarity-specific deviations of gait. In this study we examined whether a visual disturbance has similar effects on gait when it acts in the same direction as GVS, i.e., when roll vection is induced by head-fixed visual roll motion stimulation. Random dot patterns were constantly rotated in roll at +/-15 degrees /s on a computer-driven binocular head-mounted display that was worn by eight healthy participants. Their gait trajectories were tracked while they walked a distance of 6 m. A stimulation effect was observed only for the first three to four steps, but not for the whole walking distance. These results are similar to the results of previous GVS studies, suggesting that in terms of the direction of action visual motion stimulations in the roll plane are similar to GVS. Both kinds of stimulation cause only initial balance responses in the roll plane but do not contribute to the steering of gait in the yaw plane.

Fixation suppression of optokinetic nystagmus modulates cortical visual???vestibular interaction

Water activation positron emission tomography and statistical group analysis were used to evaluate differences in activation-deactivation patterns during small-field visual motion stimulation, eliciting rightward optokinetic nystagmus and its fixation suppression in 12 healthy volunteers. Bilateral patterns of activation in the visual cortex, including the motion-sensitive area MT/V5, and deactivations in an assembly of vestibular areas (posterior insula, thalamus, anterior cingulate gyrus) during optokinetic nystagmus was markedly diminished or totally absent during its fixation suppression. This finding agrees with the concept of a reciprocal inhibitory interaction between the visual-optokinetic and the vestibular systems, which takes place at a lower level during fixation suppression, because the potential mismatch between the two sensory inputs, visual and vestibular, is then reduced.

Expectation of Sensory Stimulation Modulates Brain Activation during Visual Motion Stimulation

The differential effects of visual hemifield motion stimulation during fixation of a stationary target were compared under two conditions: fixation straight ahead without any further instructions and fixation straight ahead with attention shifted to the "dark hemifield." Data from nine right-handed volunteers revealed that striate and extrastriate right hemispheric visual areas exhibited larger activations during left hemifield motion stimulation when attention was shifted to the right dark hemifield. Montreal Neurological Institute (MNI) coordinates (26, -98, -4) of the additional clusters activated in the latter condition corresponded best to the kinetic occipital region, which is known to process both shape and motion information, and to parts of area V3 posterior to V3A, which has been shown repeatedly to mediate motion perception. A simple computational model of transhemispheric visuovisual interaction is proposed. The basic mechanism of this model is a central predictor formed by a feedback loop that detects a mismatch between input to the two hemispheres. Predicted stimulation is then compared with the actual input. If the sensed motion of a visual hemifield is larger than the predicted net motion in the model, activation of the respective neural population is increased; conversely, a smaller actual motion causes less activation.

Cerebral Correlates of the Activation of the Cardiovascular Autonomic Nervous System – An FDG-PET Study

Background: Visual self-motion perception is induced by large-field visual motion stimulation (circular vection, CV). The stationary observer perceives the surroundings as being stable and himself as being moved. This stimulus provides profound activation, in particular, of the sympathetic nervous system (arousal reaction) Our fluorodeoxyglucose (FDG)-PET study focused on those brain areas that are involved in the processing of autonomic changes during CV. Correlation analyses were performed between metabolic effects and autonomic parameters during visual motion stimulation. Methods: FDG-PET (Siemens, Germany) was performed in 14 healthy subjects (8 male, 7 female; mean age 29.5 years) during CV induced by a computer-animated coherent dot pattern moving clockwise, or a random dot pattern of the same size. Correlation analyses with different parameters for autonomic cardiovascular control (blood pressure, heart rate variability, blood pressure and plasma catecholamines) were performed with the SPM99b software (threshold for significant activation was set at p<0.001, uncorrected). Results: Significant positive correlations were found between the high frequency spectrum of heart rate variability and activations in the anterior cingulate gyrus (BA 6) and nucleus caudatus.. Low frequency heart rate variability correlates either with activations in the anterior cingulate and the amygdala bilaterally. Deactivation in the caudate nucleus significantly correlated to frequency changes of heart rate and levels of plasma catecholamines. Conclusion: Our study showed that arousal reaction activates and deactivates a network of „autonomic“ brain areas. Obviously the limbic cortex and the basal ganglia are the most important to control cardiovascular function.

Preparatory deployment of attention to motion activates higher-order motion-processing brain regions

We used event-related fMRI to test the hypothesis that preparatory attention modulations occur in higher-order motion-processing regions when subjects deploy attention to internally driven representations in a complex motion-processing task. Using a cued attention-to-motion task, we found preparatory increases in fMRI activity in visual motion regions in the absence of visual motion stimulation. The cue, a brief enlargement of the fixation cross, directed subjects to prepare for a complex motion discrimination task. This preparation activated higher-order and lower-order motion regions. The motion regions activated included temporal regions consistent with V5/MT+, occipital regions consistent with V3+, parietal-occipital junction regions, ventral and dorsal intraparietal sulcus, superior temporal sulcus (STS), posterior insular cortex (PIC), and a region of BA 39/40 superior to V5/MT+ involving the angular gyrus and supramarginal gyrus (A-SM). Consistent with our hypothesis that these motion sensory activations are under top-down control, we also found activation of an extensive frontal network during the cue period, including anterior cingulate and multiple prefrontal regions. These results support the hypothesis that anticipatory deployment of attention to internally driven representations is achieved via top-down modulation of activity in task-relevant processing areas.