Without disputing the experimental evidence that subjects have available most of the content of brief displays for a fraction of a second, or that visual stimuli Persist after their physical termination for a similar time, I argue that this evidence is irrelevant to perception. Specifically, the notion of an icon as a brief storage of information persisting after stimulus termination cannot possibly be useful in any typical visual information-processing task except reading in a lightning storm. Since the visual world that provides the stimuli for perception is continuous and not chopped up by tachistoscopes, and since our eyes and heads are rarely motionless, no realistic circumstances exist in which having a frozen iconic storage of information could be helpful. Rather, the presence of such an icon interferes with perception. This paper examines instances of normal perception, and then reviews experimental evidence on temporal integration, saccadic suppression, masking, and the photoreceptor basis of visual persistence, to further demonstrate that a storage of excitation cannot be a useful device for storing information. Finally, I note that little would have to be changed in our theories of visual perception or information processing if we simply forgot all about the icon and iconic memory as an early stage of processing.

Thresholds for psychophysically opposite stimuli—light and dark, or equiluminous red and green, or equiluminous blue and yellow—are usually nearly equal. This color threshold symmetry is sometimes violated in subjects who have optic nerve hypoplasia, a congenital loss of retinal ganglion cells. We describe a subject who has optic nerve hypoplasia, who exhibits large red-green and blue-yellow detection threshold asymmetries for equiluminous spots. Temporal and spatial integration for equiluminous red and green test spots also differed from normal; static perimetric thresholds for equiluminous green, blue, and yellow (but not red) spots lacked the normal “V” shaped minimum at the fovea. These asymmetries may relate to a developmental paucity of some ganglion cell subtypes. Optic nerve hypoplasia may allow the contributions to detection made by individual ganglion cell subtypes to be isolated psychophysically, in analogy to the study of cone spectral sensitivity in dichromats.

We examined achromatic contrast discrimination in asymptomatic carriers of 11778 Leber‘s hereditary optic neuropathy (LHON 18 controls) and 18 age-match were also tested. To evaluate magnocellular (MC) and Parvocellular (PC) contrast discrimination, we used a version of Pokorny and Smith's (1997) pulsed/steady-pedestal paradigms (PPP/SPP) thought to be detected via PC and MC pathways, respectively. A luminance pedestal (four 1° × 1° squares) was presented on a 12 cd/m2 surround. The luminance of one of the squares (trial square, TS) was randomly incremented for either 17 or 133 ms. Observers had to detect the TS, in a forced-choice task, at each duration, for three pedestal levels: 7, 12, 19 cd/m2. In the SPP, the pedestal was fixed, and the TS was modulated. For the PPP, all four pedestal squares pulsed for 17 or 133 ms, and the TS was simultaneously incremented or decremented. We found that contrast discrimination thresholds of LHON carriers were significantly higher than controls' in the condition with the highest luminance of both paradigms, implying impaired contrast processing with no evidence of differential sensitivity losses between the two systems. Carriers’ thresholds manifested significantly longer temporal integration than controls in the SPP, consistent with slowed MC responses. The SPP and PPP paradigms can identify contrast and temporal processing deficits in asymptomatic LHON carriers, and thus provide an additional tool for early detection and characterization of the disease.

The color appearance of a physically steady central region can appear to vary over time if a surrounding chromatic light varies in time. The induced temporal variation, however, is strongly attenuated at surround temporal frequencies above ∼3 Hz. At these higher temporal frequencies, the central region appears steady (De Valois et al., 1986). The posited explanation is a cortical low-pass temporal filter. Here, we investigate whether higher temporal-frequency surrounds induce color shifts in the steady appearance of the central test. Surrounds modulated in time along the l or s chromatic direction of MacLeod-Boynton color space were symmetric around equal-energy white (EEW). The temporal frequency of the surround was varied. If observers perceived the central test to be temporally modulating between two points in time, they set two separate matches to the extreme points of this modulation. If the central test appeared steady in time, then color matches were made to this steady appearance. Corroborating previous reports, measurements showed that surround temporal frequencies below ∼3 Hz induced temporal modulation. At higher temporal frequencies, however, the surround induced steady color shifts, compared to a steady surround at its time average (EEW). The measurements imply that a nonlinear neural process affects chromatic induction from time-varying context.

Amblyopia is usually considered to be a deficit in spatial vision. But there is evidence that amblyopes may also suffer specific deficits in motion sensitivity as opposed to losses that can be explained by the known deficits in spatial vision. We measured sensitivity to visual motion in random dot displays for strabismic and anisometropic amblyopic monkeys. We used a wide range of spatial and temporal offsets and compared the performance of the fellow and amblyopic eye for each monkey. The amblyopes were severely impaired at detecting motion at fine spatial and long temporal offsets, corresponding to fine spatial scale and slow speeds. This impairment was also evident for the untreated fellow eyes of strabismic but not anisometropic amblyopes. Motion sensitivity functions for amblyopic eyes were shifted toward large spatial scales for amblyopic compared to fellow eyes, to a degree that was correlated with the shift in scale of the spatial contrast sensitivity function. Amblyopic losses in motion sensitivity, however, were not correlated with losses in spatial contrast sensitivity. This, combined with the specific impairment for detecting long temporal offsets, reveals a deficit in spatiotemporal integration in amblyopia which cannot be explained by the lower spatial resolution of amblyopic vision.

At reduced luminance levels, the visual system integrates light over extended periods of time. Although the general effects of this process are known, specific changes in the visual cortex have not been identified. We have studied the physiological changes that occur during a transition from high to low luminance by measurements of single neurons in the cat's primary visual cortex. Under low-luminance conditions, we find increased latencies, expanded temporal responses, and a loss of temporal structure. This results in temporal-frequency tuning curves that are peaked at relatively low frequencies. To examine parallel perceptual changes, we compared perceived temporal frequency in human subjects under high- and low-luminance conditions. Low-luminance flickering patterns are perceived to modulate at relatively high rates. This occurs even though peak sensitivity is shifted to relatively low temporal frequencies. To explore further the perceptual component, we measured perceived temporal frequency in human subjects with unilateral optic neuritis for whom optic nerve transmission is known to be relatively slow and generally similar to the normal physiological state under low luminance. These subjects also perceive relatively high modulation rates through their affected eye. Considered together, these results demonstrate an inverse relationship between the physiological and the perceptual consequences of reduced stimulus luminance. This relationship may be accounted for by shifts of neuronal population responses between high- and low-luminance levels.