On inferring blindsight from normal vision

of the original article: Blindsight is the term commonly used to describe visually guided behaviour elicited by a stimulus falling within the scotoma (blind area) caused by a lesion of the striate cortex. Such "vision" is normally held to be unconscious and to be mediated by subcortical pathways involving the superior colliculus. Blindsight is of considerable theoretical importance since it suggests that destriate man is more like destriate monkey than had been previously believed and also because it supports the classical notion of two visual systems. It is also of potential clinical importance, since it has been claimed recently that systematic practice in blindsight can lead to the recovery of normal visual function in patients with cortical lesions. From a review of the literature it is concluded that all of the phenomena of blindsight can be attributed either to light scatter into unimpaired parts of the visual field or to residual vision resulting from spared striate cortex. The possible contribution of other factors is also considered. It is concluded that blindsight studies have generally failed to control for such nonblindsight interpretations partly because of poor methodology and partly because of difficulties in defining the term "blindsight. " Experiments were carried out to investigate the extent to which subjects can exhibit performance similar to blindsight when they are using scattered light as a cue. This was done both with hemianopic subjects (by manipulating the amount of scattered and direct light coming from a stimulus) and with normal subjects (by presenting targets within their blind spots). Good blindsight performance was observed when only scattered light was available as a cue to the subjects. It is therefore concluded that an adequate case for blindsight has not been made. It is probably impossible to demonstrate the existence of blindsight on purely behavioural grounds. What is required is the establishment of relationships between visual function and independent anatomical evidence. On inferring blindsight from normal vision L Lutzemberger, C. A. Marzi, and G. Tassinari "Istituto di Neurochirurgia, University di Pisa, Pisa, Italy, "Istituto di Psicologia, Universita di Padua, Padua, Italy, and lstituto di Fisiologia, University di Pisa, Pisa, Italy Campion, Latto & Smith (1983) have certainly done a fine job in clarifying the conceptual and methodological framework of blindsight research. Yet, their conclusion that it is impossible to demonstrate the existence of blindsight on purely behavioral grounds seems too pessimistic to us. In this commentary we would like to describe a simple method that avoids one of the major sources of artifacts correctly deemed by Campion et al. to plague blindsight research, namely, shifts in response criteria. In addition, our method employs light stimuli that can easily be shown not to be scattered into the intact field of hemianopic patients. Before briefly describing our experiments we would like to devote a few words to an important point that has perhaps been overlooked in both the target article and the first round of commentaries, namely, the site and the extent of extrastriate damage. Various theories of the neural substrates of visual perception view the primary visual cortex as providing a basis for high-resolution vision whereas attentional and high-order aspects of perception are likely to depend on extrastriate areas (see Marzi 1983). It seems reasonable, therefore, to assume lack of blindsight in a hemianopic patient suffering from concomitant damage in a putative attentional system which orients visual attention to a given portion of the visual field in and around the scotoma. Posner and his associates (see Posner 1980) have shown that visual attention can be allocated to various portions of space without overt movements of the head and eyes, and that this implicit visual orienting is very important for subsequent overt visually guided behavior. Now, part of the variability observed in blindsight experiments might stem from variations in the patient's capacity to shift attention toward his island of blindness. Such an inability might result either as a consequence of the brain lesions involving "attentional" areas or as a consequence of the paradigm used to test residual vision, for example, blocked versus randomized stimulus presentation. In patients with long-lasting field defects this might lead to a "disuse" of the hemianopic side and thus to irreversible total blindness. This might explain why some patients recover part of their vision following extensive training in which they are forced to pay attention to the damaged side (Zihl 1980). As mentioned above, in our laboratory we are trying to verify the existence of true blindsight phenomena by using stimuli and paradigms that prevent light from scattering into the normal hemifield and decisional changes in response from occurring. Subjects are tested in a simple reaction time (RT) paradigm which employs as stimuli very brief (5 msec) light flashes of low suprathreshold intensity generated by small LEDs (light-emitting diodes). Under such conditions, light scattering, as assessed by measuring the blind spot (see Schmielau & Marzi 1983) is 754 THE BEHAVIORAL AND BRAIN SCIENCES (1985) 8:4 Continuing Commentary absent. Following testing with normal subjects we were able to ascertain with great reliability (the effect shows up in every subject and usually in every session) that RTs are faster for responses to two flashes presented simultaneously than for responses to one flash alone. The stimuli were presented at 10° and 30° along the horizontal meridian in the same or in opposite hemifields. On each trial the subject was instructed to press a key as soon as possible following the onset of either one or two lights, no matter which hemifield the light or lights appeared in. The various stimulus conditions were randomly alternated, and the subject's fixation on a central point was continuously monitored through a TV system. It is important to point out that the effect of spatial summation was found not only for stimuli presented in the same hemifield but also when the two flashes appeared across the vertical meridian. There are at least two advantages in using such a paradigm to verify the presence of blindsight in hemianopic patients. First, since number and position of the stimuli are randomly alternated, on each trial there is only a one in four chance of not seeing the stimuli (i.e. when both flashes appear in the blind hemifield), and there is no reason for a change in response strategy. In fact, patients are told in advance that they may sometimes fail to see the stimuli. Second, the site of stimulation that is closer to the boundary of the intact visual field is 10°, a distance that, considering the small size and the low intensity of the flashes (not to mention their short duration) makes light scattering into the normal side quite implausible. Eleven patients with homonymous hemianopia caused by an occipital lobectomy or by vascular lesions restricted to the occipital lobe have been tested so far in the same apparatus and with the same procedure as normal individuals. The rationale is as follows: In normal individuals two flashes appearing simultaneously at different points in either the same or opposite hemifields yield faster RTs than a single flash presented in one hemifield. A hemianopic patient should provide the same result as normal individuals only for stimulation of the good hemifield, whereas, unlike what happens with normal individuals, the condition in which the two flashes are on opposite sides should yield the same RT as for single flashes. The presence of blindsight, however, should result in an increase in speed of response even for stimuli in opposite hemifields. Thus, as pointed out in Haber's (1983) commentary, a stimulus of which the patient is unaware should still be capable of influencing behavior in a measurable way. The results so far obtained with our patients show that when the two stimuli fell onto the hemianopic side no responses were obtained, whereas when the double flash appeared on the normal side, RT was faster than for a single flash. No clear-cut evidence for blindsight could be obtained, since stimuli presented to opposite hemifields yielded average RTs not significantly different from those obtained for stimulation of the intact field alone. However, eight out of 11 patients showed a trend toward faster RTs for double contralateral stimulation as opposed to stimulation of the normal field alone. It is possible that using stimuli of higher intensity and duration might be necessary to reveal across-midline spatial summation in our hemianopic patients. In conclusion, even though our efforts to demonstrate the presence of blindsight have so far been unsuccessful, we think that the above paradigm represents a simple, artifact-free approach to blindsight research. At variance with the work reviewed in the target article, which is usually aimed at testing the existence of blindsight in the damaged hemisphere directly, the main thrust of our approach is to infer the presence of blindsight by testing its influence on vision subserved by the normal hemisphere. Broadly similar to ours is the approach followed by Singer, Zihl, and Poppel (1977) and by Marcel (1982 cited by Campion et al.). Singer et al. have reported that increment thresholds in the normal field can be influenced by stimulation in a contralateral scotomatous area. Marcel has instead found semantic priming following stimulation of the hemianopic field. Finally, Pizzamiglio, Antonucci, and Francia (1984) have observed that in hemianopic patients stimulation of the entire visual field with a rotating visual background elicits a greater visual tilt effect than stimulation of the normal side only. A C K N O W L E D G M E N T S The experiments reported in this commentary have been carried out