Cognitive Neuropsychology of Visual Perception
There have been many proposed hypotheses as to why and how perceptual distortion after deprivation occurs. Perceptual distortion in the in the human adult somatosensory system has been well studied however; researchers still don’t fully understand the consequences of deprivation in the visual system. In a previous study the authors examined a type of visual deprivation (elongation) observed in a stroke patient. Perceptual elongation in visual studies is the apparent increase in width or height of an object due to vision deprivation. The study provided ample evidence using fMRI to show that the perceptual elongation is a result of concomitant changes in V1 where deprived upper left visual field neurons now respond to stimuli in the lower left visual field. There were several limitations in the previous study that the authors adequately overcome in this paper in order to strengthen their findings.
Building on the previous study, the authors would like to answer if they can replicate the previous study’s findings in healthy individuals and also determine how soon after deprivation elongation occurs. To do this the authors used a one-eye patch technique to deprive bottom-up input to the blind spot region of the primary visual cortex (V1). The strength of this approach is that it is noninvasive (unlike the stroke case) and is reversible. Their reasoning in patching one eye is that the blind spot region of the unpatched eye will no longer be receiving input from the patched eye since the cortical representation of the blind spot of the left eye only receives information from the right eye. This is why the authors present visual stimuli (rectangles) only around the blind spot rather than at other locations in the visual field.
Using five different experiments the authors’ results show that participants perceive rectangles adjacent to the deprived blind spot to be elongated toward the blind spot. This means that rectangles placed lateral to the blind spot appeared to widen whereas rectangles placed above and below appeared to increase in height. Using a probit analysis to determine the PSE, the magnitude of elongation was quantified. Their results show that rectangles 10% or shorter or narrower than a square would be perceived as squares rather than rectangles. Interestingly, the authors found that the magnitude of elongation increases with eccentricity meaning that elongation was greatest for the right side of the blind spot and weakest on the left side, which is closest to the fovea. In terms of the timing of perceptual elongation, these results held at both 10min and 2h of deprivation. In order to rule out the possibility that elongations are the result of reduced acuity for peripheral stimuli, the authors show that the magnitude of elongation decreases with increasing distance from the border of the deprived blind spot. To determine how quickly elongation occurs shape judgments were made at 2-min intervals, to which all time points after patching resulted in elongation especially within 2-min of first deprivation. More specifically in the next study, aspect ratio judgments were obtained and analyzed in 1-second time intervals for deprivation and nondeprivation. Again, participants perceived elongation within seconds of the onset of deprivation and showed reversal within seconds when the elongation ended.
There are two aspects of cortical representation that are important to define in order to appreciate the findings of this study. A visual stimulus in a specific visual field location causes neurons in a specific cortical region to respond but also, that neural activity in that cortical region signals throughout the brain that a visual stimulus appeared in that visual field location. This neural activity causes a person to see the stimulus regardless of whether or not a stimulus actually appeared there. There a several possible forms of cortical reorganization that can occur. For example let’s assume that cortical region A now represents visual field location Y instead of location X. One possibility is that a visual stimulus at location Y will result in a cortical response in A that signals to brain areas that something appears at X. Another is that a visual stimulus at location Y will result in a cortical response in A that signals to brain areas that something appears at Y. Lastly a visual stimulus at location X will result in a cortical response in A that signals to brain areas that something appears at Y.
The authors provide an interesting hypothesis as to how this observed rapid and reversible visual elongation occurs. They suggest that perceptual elongations are due to rapid receptive field expansion after deprivation. Their hypothesis is strongly supported by electrophysiological studies that show after minutes of deprivation, the V1 neurons will now respond to stimuli that normally would only activate adjacent cortex. Moreover, the underlying neural mechanism has to be an “unmasking” of already existing connections because the observed “referred visual sensations” are far too fast to be due to growth of new dendrites/synapses. In terms of cortical representation, it was assumed that by patching an eye loss of visual input from the patched eye (by deafferentation) means that that visual information no longer innervates the cortical region for the blind spot of the unpatched eye. Patching effectively removes this bottom-up input to a region of cortex. The synaptic connections and innervations still exist however the loss of visual information results in cortical reorganization, which is why elongation is observed. Neural activity in that blind spot cortical region is now activated by adjacent blind spot stimuli, which signal throughout the brain that the rectangle is taller or wider than in actuality.
Overall the authors provide convincing evidence for visual elongation after cortical deprivation and credible arguments as to how and why these referred visual sensations occur. However some limitations and weaknesses exist in their study. Experimentally they show occurrence of perceptual elongation around the deprived blind spots and show that these occur within seconds of deprivation. The authors significantly build on previous studies by studying the time scale for cortical reorganization to occur. Evidence of such rapid cortical reorganization was one of the most interesting findings in the study given the typical length of time needed for cortical reorganization in previous studies. Without such rapid changes in receptive field properties the authors wouldn’t have been able to assertively state that the underlying neural mechanism is an unmasking of preexisting conditions. I thought the authors’ application of their results to other contradictory cases of long-term reorganization of visual cortex was fair; they state that cortical reorganization differences in these other cases may be occurring over longer timescales or may even include some structural changes in cortex. They adequately disregard several alternate hypotheses such as the perceptual filling-in explanation. I thought their methodology in determining the blind spot in each subject was accurate since it was highly reproducible. However, there were too few available response choices in describing the rectangles. Participants could only state whether the stimulus was thinner than a square, a square, or wider than a square. Despite the simplicity, the study generated sufficient and convincing quantitative results. In future studies they should examine fMRI responses to specific areas within the blind spot, which would highly strengthen their findings.