Flicker Adaptation Research Articles

Motion coherence thresholds can be elevated by flicker adaptation or red background

Purpose: Previous studies have shown that motion coherence thresholds are elevated in several disorders including dyslexia (Cornelissen et al. 1995), glaucoma (Silverman et al. 1990), Alzheimer's disease (Gilmore et al. 1994) and Parkinson's disease (Trick et al. 1994). This threshold elevation is consistent with a deficit in the functioning of the magnocellular (M) pathway. We compared two psychophysical methods of temporarily disrupting normal M-pathway functioning as indexed by elevated motion coherence thresholds. Methods: 30 normal adults participated in this study. We measured motion coherence thresholds for limited lifetime dots moving left or right at a speed of 0.935 deg/s. Dot density was 1 dot/deg2. Coherence thresholds were determined in 4 conditions: after 2 minutes of adaptation to (i) a uniform field flickering at 9 Hz (experimental 1) (ii) a uniform gray field (control 1) and with dots presented on (iii) a uniform red background (experimental 2) and (iv) a gray background (control 2). Results: Motion coherence thresholds were significantly elevated in both experimental conditions (experimental 1 M = 0.2771, control 1 M = 0.1981, experimental 2 M = 0.2198, control 2 M = 0.1873). In addition, the threshold elevation was significantly greater after flicker adaptation than in the presence of a uniform red background. Conclusions: Either flicker adaptation or a red background can be used to disrupt direction selective global motion perception. Physiological studies have shown that magnocellular layers of the LGN are inhibited by a red background (Wiesel & Hubel, 1966) and are essential for flicker perception in monkeys (Merigan, Byrne & Maunsell, 1991). Therefore our results suggest that interference with processing at this level in the M pathway disrupts global motion perception. These techniques are currently being used to study the relationship between M-pathway functioning and reading in people with dyslexia.

Visually-based temporal distortion in dyslexia

In this study, we show that invisible flicker adaptation reduces the perceived duration of a subsequently viewed stimulus in control subjects, but not in dyslexics. Dyslexics, like controls, show apparent duration compression after 20 Hz flicker and show normal shifts in apparent temporal frequency after adaptation. However a subgroup of the test group, scoring low on both a test of phonological skill (spoonerisms) and a test of literacy (NART), show an apparent temporal expansion after 5 Hz flicker adaptation, a finding not previously seen in controls. Recent studies have linked genes conferring susceptibility to a cluster of language and sensory deficits to anomalous neural migration, providing a tentative biological basis for dyslexia. However it has proved difficult to establish a clear link between sensory deficits and impaired reading. The results presented here point to an abnormal adaptation response within the early precortical stages of the magnocellular pathway, occurring in tandem with a deficit in word-level cognitive processing, providing psychophysical evidence for anomalous cortico-thalamic circuits in dyslexia.

Human visual cortex responds to invisible chromatic flicker

When two isoluminant colors alternate at frequencies of 25 Hz or higher, observers perceive only one fused color. Chromatic flicker beyond the fusion frequency induces flicker adaptation in human observers and stimulates monkey V1 neurons. Here we use functional magnetic resonance imaging (fMRI) to show that many human visual cortical areas, with the exception of VO, can distinguish between fused chromatic flicker and its matched nonflickering control. This result supports the existence of significant intracortical temporal filtering of high-frequency chromatic information. The result also suggests that a considerable difference in cortical activation in many visual cortical areas does not necessarily lead to different conscious experiences.

Modulation depth threshold in the Compensation Comparison approach

Recently, the "Compensation Comparison" method was introduced for measuring retinal straylight. In this article, basic aspects are described, in particular a generalization of the approach using the concept of "precompensation," and including flicker threshold as parameter in the psychophysical model. The model was experimentally verified in lab measurements with and without artificially increased straylight and was tested on the data from the multi-center GLARE study. The resulting flicker threshold estimates were analyzed to better understand their origin. An effect of flicker adaptation over distance was found. The new approach proved suitable to describe Compensation Comparison measurements including precompensation, and also for subjects with poor psychometric behavior.

Microsaccades Counteract Visual Fading during Fixation

Our eyes move continually, even while we fixate our gaze on an object. If fixational eye movements are counteracted, our perception of stationary objects fades completely, due to neural adaptation. Some studies have suggested that fixational microsaccades refresh retinal images, thereby preventing adaptation and fading. However, other studies disagree, and so the role of microsaccades remains unclear. Here, we correlate visibility during fixation to the occurrence of microsaccades. We asked subjects to indicate when Troxler fading of a peripheral target occurs, while simultaneously recording their eye movements with high precision. We found that before a fading period, the probability, rate, and magnitude of microsaccades decreased. Before transitions toward visibility, the probability, rate, and magnitude of microsaccades increased. These results reveal a direct link between suppression of microsaccades and fading and suggest a causal relationship between microsaccade production and target visibility during fixation.

Pattern specificity of human visual motion processing

Visual motion processing is strongly susceptible to adaptation. A variety of patterns have been used as stimuli in previous studies. Three of these, namely random dots, barcode-like gratings, and sinusoidal gratings, were compared in the present study using motion-onset visual evoked potentials (VEPs). We assessed the effects of the adaptation pattern and the test pattern to which the VEP is recorded. Furthermore, we evaluated the interaction between both, i.e. whether differences between adaptation and test pattern affect the response. Isodirectional and antidirectional adaptation were used to differentiate between the actual motion adaptation and associated flicker adaptation. Motion adaptation was almost 2.5-fold stronger ( p < 0.01) if the same rather than different pattern types were used for both adaptation and test. This implies that separate neural populations are involved, suggesting the presence of pattern-tuned motion mechanisms.

Adaptation from invisible flicker.

Human ability to resolve temporal variation, or flicker, in the luminance (brightness) or chromaticity (color) of an image declines with increasing frequency and is limited, within the central visual field, to a critical flicker frequency of approximately 50 and 25 Hz, respectively. Much remains unknown about the neural filtering that underlies this frequency-dependent attenuation of flicker sensitivity, most notably the number of filtering stages involved and their neural loci. Here we use the process of flicker adaptation, by which an observer's flicker sensitivity is attenuated after prolonged exposure to flickering lights, as a functional landmark. We show that flicker adaptation is more sensitive to high temporal frequencies than is conscious perception and that prolonged exposure to invisible flicker of either luminance or chromaticity, at frequencies above the respective critical flicker frequency, can compromise our visual sensitivity. This suggests that multiple filtering stages, distributed across retinal and cortical loci that straddle the locus for flicker adaptation, are involved in the neural filtering of high temporal frequencies by the human visual system.

An electrophysiological test of the effect of the temporal pattern of light adaptation on teleost H1 type horizontal cell plasticity

The possible importance of the temporal pattern of photon delivery in light adaptation-induced physiological plasticity in the outer retina of carp was tested by intracellular recording. Steady and flicker (3 Hz) background adaptation was applied whilst recording chromatic voltage responses of H1 type horizontal cells (HCs) to 680 and 440 nm full-field test flashes (generating response amplitudes of V r and V b, respectively). A third parameter V b/ V r ( B/ R) was calculated as an indicator of the cells’ short/long wavelength relative spectral contrast. Steady light adaptation increased V r and to a lesser extent V b, and reduced B/ R. Flicker adaptation also increased V r (by a similar amount), but, unlike steady adaptation, consistently decreased V b. The reduction in B/ R was statistically greater for flicker than for steady adaptation, although the former delivered half as many photons to the retina. These results suggest that the temporal pattern of light adaptation is indeed an important determinant of qualitative and quantitative aspects of plasticity induced in the outer retina, and complement earlier morphological findings. The effects are discussed in terms of dopamine and nitric oxide as underlying possible neurochemical control mechanisms.

Evaluation of optic nerve function by flicker adaptation in optic nerve diseases

The time required for the fading of a full-field 30-Hz flick-ering stimulus was measured in 15 patients (18 eyes) with optic nerve diseases to evaluate optic nerve function. Eleven eyes of eight patients had optic neuritis, five eyes had autosomal dominant hereditary optic nerve atrophy (DOA), and two eyes had Leber's hereditary optic neu-ropathy (LHON). The results were correlated with visual acuities and critical flicker frequencies (CFF). The fading was not complete within 50 seconds in the eyes with DOA (Group A) or in normal subjects; con-versely, complete fading was experienced in the eyes with optic neuri-tis and with LHON (Group B). No significant differences in CFF and visual acuity were found between Groups A and B. We conclude that visual fatigue in optic neuritis and LHON can be observed easily by flicker adaptation, and that flicker adaptation can be used as an addi-tional test for evaluating optic nerve function.

Flicker adaptation can be explained by probability summation between ON- and OFF-mechanisms.

This study considered whether the dynamics of flicker adaptation can be explained in terms of probability summation over time between independent ON- and OFF-processors. Foveal thresholds were measured for flickering probes, and for static ON- and OFF-probes that have durations consistent with the flicker duty cycle. Thresholds were obtained using a probe-flash stimulus onset asynchrony paradigm. The outcome of the experiment suggests that flicker thresholds are lower than the component ON- and OFF-thresholds, and that the flicker response can be predicted by assuming probability summation between the ON- and OFF-mechanisms.

Effects of flicker adaptation and temporal gain control on the flicker ERG

The flicker electroretinogram (ERG) to stimuli varying in temporal frequency and modulation depth was recorded to investigate retinal gain control. With increasing modulation of a sinusoidal flickering stimulus, the flicker ERG shows an amplitude compression and a phase retardation (of the fundamental component) at 16 Hz, an amplitude expansion and a phase advance around 40–48 Hz, and an approximately linear response at 72 Hz. With sum-of-two-sinusoids stimuli, the second stimulus enhances the fundamental response to a 40 or 48 Hz test stimulus at low modulations, and reduces the variation in phase with modulation. This interaction depends primarily on the amplitude of the response to the second stimulus, but not its frequency. With temporally alternating stimuli, a similar but smaller interaction effect is measured. The results suggest that there is an active nonlinear gain control mechanism in the outer retina and this gain control works by adjusting the phase delay of the retinal response. The phase control mechanism is set by the amplitude of the outer retinal response integrated over time.

Subsidiary influence and autonomy in international firms

We study the influence of motion on the visibility of flicker distortions in naturalistic videos. A series of human subjective studies were executed to understand how motion silences the visibility of flicker distortions as a function of object motion, flicker frequency, and video quality. We found that flicker visibility is strongly reduced when the speed of coherent motion is large, and the effect is pronounced when video quality is poor. Based on this finding, we propose a model of flicker visibility on naturalistic videos. The target-related activation levels in the excitatory layer of neurons were estimated for a displayed video using a spatiotemporal backward masking model, and then the flicker visibility is predicted based on a learned model of neural flicker adaptation processes. Experimental results show that the prediction of flicker visibility using the proposed model correlates well with human perception of flicker distortions. We believe that sufficiently fast and coherent motion silences the perception of flicker distortions on naturalistic videos in agreement with a recently observed “motion silencing” effect on synthetic stimuli. We envision that the proposed model could be applied to develop perceptual video quality assessment algorithms that can predict “silenced” temporal distortions and account for them when computing quality judgments.

Contrast adaptation and contrast masking in human vision

After a preliminary study of visual evoked potentials (VEPS) to a test grating seen in the presence of masks at different orientations, psychophysical data are presented showing the effects of adaptation and of masking on thresholds for detecting the same test grating. The test is a vertical grating of spatial frequency 2 cycles per degree; adapting and masking gratings differ from the test either in orientation or in spatial frequency. The effects of adaptation and masking are explained by a single mechanism model that assumes: (i) adaptation and masking both alter the contrast response (or transducer) function of the mechanism that detects the test; (ii) masks, but not adaptors, stimulate the mechanism that detects the test; and (iii) a test is detectable when it raises response level by a constant amount. The model incorporates two distinct tuning functions, a broad adaptive contrast function and a narrow effective contrast function. It accounts adequately for all the data, including the location and size of the facilitative dip found in some masking functions, the constant slopes of the threshold elevation segments of adaptation functions and the varying slopes of masking functions. It also predicts the sometimes surprising joint effects of adaptation followed by masking and of two masks operating simultaneously.

Flicker Adaptation in the Periphery at Constant Perceived Modulation Depth

At constant physical flicker modulation depth, the time taken to adapt to flicker in the periphery varies inversely with temporal frequency. It has recently been suggested that this effect may indicate differential susceptibility to adaptation of the underlying temporal mechanisms. Using suprathreshold gratings, temporally modulated in contrast at constant perceived, rather than physical, modulation depth, we found the opposite result: the time required to adapt increased with temporal frequency. Given some uncertainty concerning the appropriateness of employing apparent or physically constant modulation depths, we conclude that rate of adaptation does not, at present, provide clear evidence as to the nature of the underlying temporal mechanisms.

Abnormal visual adaptation to flicker in multiple sclerosis.

A visual psychophysical adaptation procedure was used on patients with Multiple Sclerosis (MS) in an attempt to induce a temporary and local exacerbation of subclinical visual impairment. Using a flicker detection task, sensitivity before and after adaptation to a flickering stimulus was measured in 9 MS patients and 9 control subjects. Although only 22% of patient eyes had abnormal flicker sensitivity prior to adaptation, visual deficit was observed in 83% of eyes studied after adaptation. Of the 7 MS eyes studied for which no other sign or symptom of visual involvement was present, 5 were found to have visual deficits after flicker adaptation. In addition, 10 of the 11 eyes affected by MS showed an abnormal response to flicker adaptation. Recovery from the effects of adaptation was complete in all patients within 2 minutes. The results suggest that partial demyelination of visual pathway neurons may exist in patients without signs or symptoms of visual involvement. The prolonged stimulation provided during adaptation may produce a temporary fatiguing or conduction blockade of such neurons which may lead to reductions in sensory sensitivity.

Flicker adaptation in the peripheral retina.

With strict fixation, a flickering light spot smaller than 3 deg presented to the peripheral retina will rapidly appear to lose contrast and stop flickering within 35 s, before fading away completely. The time required for this adaptation to occur decreases with: decreasing depth of modulation (97-9%); decreasing stimulus diameter (2 deg-7 min arc); increasing retinal eccentricity (20-50 deg); and increasing flicker frequency (1-7 Hz). Interestingly, the effect does not depend upon the regularity of the flickering stimulus, and it occurs twice as fast for stimuli presented to the temporal retina as for stimuli presented to the nasal retina. When changes in retinal eccentricity are compensated for by taking into account the cortical magnification factor, the time needed for perceived flicker to disappear remains constant at all eccentricities. With dichoptic stimulation interocular transfer is about 35%, suggesting a cortical contribution to flicker adaptation. The results indicate that the visual system adapts rather easily to peripheral flickering stimuli. Similarities as well as differences to motion adaptation are discussed.

Frequency dependence in scotopic flicker sensitivity

Sensitivity to rod-mediated (scotopic) flicker was parametrically studied in the parafoveal retina of human observers. Confirming prior studies, the present results show that sensitivity to scotopic flicker has many similarities to that at photopic levels. Specifically, our results show that the frequency response function for scotopic flicker is characterized by both low- and high-frequency cutoffs and that sensitivity to low frequencies is described by Weber's law. Overall, however, scotopic flicker sensitivity is characterized by higher increment thresholds and lower frequency tuning than photopic flicker. The influences of spatial factors and the prevailing level of illuminance on sensitivity is sufficiently different for relatively low (< 3 Hz) and relatively high (> 5 Hz) temporal frequencies to suggest that they may be mediated by different channels. This possibility is also suggested by selective adaptation experiments. These show that adaptation to flicker frequencies of 3, 5, and 7 Hz have a similar influence on sensitivity to subsequent flicker which is different from the influence on 1 Hz flicker adaptation. Results are compared with prior evidence for channeling within both the scotopic and photopic visual systems.

The effects of flicker adaptation upon temporal contrast enhancement.

Temporal contrast enhancement refers to the finding that intermediate-duration, low-spatial-frequency gratings are perceived to have a greater contrast than long-duration gratings of similar spatial frequency. Kitterle and Corwin (1979) suggested that this effect reflects primarily activity in transient channels. To test this, 30 subjects were run in one of three groups consisting of either adaptation to a steady or flickering low-spatial-frequency grating or no adaptation. Temporal contrast enhancement was found for both steady and no-adaptation conditions. Flicker adaptation abolished temporal contrast enhancement. It was suggested that flicker adaptation may decrease the contribution of transient channels to perceived contrast and may cause processing of the test gratings to be switched to sustained channels. The implications of these results for understanding the coding of brightness are discussed.

Transient tritanopia after flicker adaptation

Transient tritanopia, the rise in blue test threshold following extinction of a yellow background, is “abolished” if the adapting background is flickered rectangularly at a low rate (0.25 Hz, duty cycle 0.2), and reduced at rates below 10 Hz. By “abolition”, is meant that the threshold falls to the same extent as after extinction of a II 1-equated “opponently neutral” (494 nm) background. These results, like those of Loomis (1980), require modifications in Pugh and Mollon's (1979) dynamic model for transient tritanopia.

Psychophysical relationships among mechanisms sensitive to pattern, motion and flicker

Sensitivity to drifting gratings was measured both before and after adaptation to a uniform flickering field. In the first experiment, it was found that viewing uniform flicker with one eye impaired sensitivity for drifting gratings presented to the same or contralateral eye. Likewise, adaptation to drifting gratings increased flicker detection thresholds. In the second experiment, temporal tuning of the adaptation effect was determined by adapting observers to several different flicker frequencies and testing with gratings of different drift rate. The data suggested the existence of broadly tuned temporal channels which respond to both flicker and motion. In a third experiment, spatial tuning of uniform flicker adaptation was evaluated by employing test gratings of different spatial frequency. The threshold elevation curves were low-pass in shape and exhibited an upper cut-off at 3–4 c/deg. Moreover, the 3–4 c/deg limit was found even when observers explicitly set thresholds for detecting temporal change. The results of the three experiments are consistent with the view that the human visual system contains separate sustained and transient mechanisms. Contrary to previous suggestions that the two systems play specialized roles in perception, however, our data indicate that both transient and sustained mechanisms can signal motion.