What Accounts for Blindsight: Cortical Preservation or Subcortical Routes?
Blindsight describes a phenomenon where cortically blind individuals have a residual ability to perceive stimuli unconsciously. It is attributed to the primary visual cortex (V1) lesions that hamper information flow to the cortex, causing deficient responsiveness in the ventral stream neurons (Cowey, 2010). However, despite the lesions, V1 cells still react to certain features of stimuli like motion and direction.
Explanations for Blindsight Causation
The residual visual responsiveness is hypothesized to come from either the preservation of the V1 that allows it to process visual stimuli or the existence of subcortical routes feeding the dorsal pathway areas. The cortical preservation hypothesis holds that unaffected cortical areas that make up the dorsal pathway account for the residual perceptual ability after V1 damage in an unconscious state. However, evidence from neuroimaging and behavioral studies disproves this hypothesis on grounds that the cortical preservation only occurs in a small number of blindsight patients (Silvanto, 2015). Furthermore, the integrity of the superior colliculi, a visual area near the extrastriate cortex, remains unaffected in blindsight patients with a preserved cortex (Silvanto, 2015). In contrast, it has been found that the extrastriate cortex receives important input via dorsal and ventral streams, providing a possible explanation for the capacity of patients to perceive stimuli, albeit in an unconscious state.
The debate on blindsight causation centers on the two hypotheses. Research associates the residual visual ability to the dorsal and ventral pathways that continue to feed input to the V1 and extrastriate regions after the damage (Whitwell, Striemer, Nicolle, & Goodale, 2011). Further, it is hypothesized that the ventral pathway accounts for perceptual awareness while the dorsal pathway controls unconscious tasks. In a study by Tamietto and de Gelder (2010), V1 lesions were found to affect the ventral pathway; however, the residual visual ability for mobile objects persisted in the subjects. The finding corroborates the hypothesis that mobile stimuli evoke awareness in the dorsal pathway leading to a blindsight condition.
The above model also explains the observed features of dorsal pathway stimuli. It explains why patients can perceive features of a visual stimulus such as motion, movement, and color, which is believed to be perceivable via the ventral route (Whitwell et al., 2011). An explanation provided for the residual color perception is that the “interlaminar layers of the LGN” that are normally interlinked with the color-specific areas in V1 extend “koniocellular color fibers” to the V4 cortical region (Whitwell et al., 2011, p. 918). Thus, in the case of a V1 lesion, the ventral pathway remains active, which explains the residual perceptive ability in blindsight patients.
Research evidence on residual facial recognition ability corroborates the hypothesis that subcortical routes account for the retained visual responsiveness after V1 damage. Tamietto and de Gelder (2010) found that unperceived stimuli could activate the ventral pathway. Further, in this study, the blindsight subjects could perceive facial expressions. They established that “face-selective processing” in the cortical region communicates with the amygdala to mediate the perception of facial expressions (Tamietto & de Gelder, 2010, p. 701). Alternatively, according to the researchers, the dorsal regions located in the “superior temporal sulcus” retained their activity after V1 damage, mediating the residual responsiveness towards facial expressions (Tamietto & de Gelder, 2010, p. 704). It appears, therefore, that the ventral and dorsal pathways continue to receive input via subcortical routes even after V1 occipital lesions.
Cortical Sparing vs. Subcortical Routes
Visual awareness in humans requires the synchronous activity of various cognitive and perceptual elements. Alexander and Cowey (2012) found that the quantitative measure of visual awareness in blindsight subjects with preserved superior colliculus was neither robust nor detectable due to the lack of “global long-range synchrony” between extrastriate regions and V1 (p. 151). Therefore, the preservation of cortical neurons after V1 damage does not explain how the extrastriate cortex receives input to cause the blindsight condition.
Therefore, subcortical routes must mediate any input reaching the cortical regions. Cowey (2010) establishes that a visually guided response in blindsight patients principally involves the SC/PV route, which is also present in people with normal vision. V1 lesions have a bigger effect on the ventral pathway’s responsiveness to visual stimuli than on the dorsal pathway. Cowey (2010) concludes that visual stimulation comprises the synchronous activation of the cortical and subcortical areas and ventral and dorsal streams. Because of this activation, blindsight people can perceive the basic features of a visual stimulus.
Research further shows that damage to the V1 and extrastriate regions affects visually guided response to a visual stimulus (Silvanto, 2015). The lesions inhibit synchronous activation, indicating that extrastriate responsiveness, as opposed to V1 preservation, accounts for the residual visual ability. Therefore, while the loss of awareness can be attributed to the absence of feedback processes in the V1, it does not explain the residual perceptive capacity in blindsight people. For the synchronous activation to occur, a feedback system comprising of the V1 and extrastriate cortex must exist (Cowey, 2010). The subcortical routes feed input into the V1 and extrastriate cortex, allowing blindsight people to perceive certain stimulus features despite the diminished awareness.
The V1 plays a critical role in visual perception and awareness. However, extrastriate stimulation must be received by the V1 to enable a person to perceive the stimuli consciously. In the blindsight condition, while visual awareness becomes diminished, stimuli responsiveness is retained. Empirical evidence indicates that the residual responsiveness to visual stimuli after V1 damage may come from a feedback activity between V1 and extrastriate cortex mediated by subcortical routes as opposed to the superior colliculus preservation.
Alexander, I., & Cowey, A. (2012). Isoluminant Coloured Stimuli are Undetectable in Blindsight Even When They Move. Experimental Brain Research, 225, 147–152.
Cowey, A. (2010). Visual System: How Does Blindsight Arise?. Current Biology 20(17), 1–3.
Silvanto, J. (2015). Why is “Blindsight” Blind? A New Perspective on Primary Visual Cortex, Recurrent Activity, and Visual Awareness. Conscious Cognition, 32, 15-32.
Tamietto, M., & de Gelder, B. (2010). Neural Basis of the Non-conscious Perception of Emotional Signals. Nature Reviews Neuroscience, 11, 697–709.
Whitwell, R., Striemer, C., Nicolle, D., & Goodale, M. (2011). Grasping the Non-conscious: Preserved Grip Scaling to Unseen Objects for Immediate but not Delayed Grasping Following a Unilateral Lesion to Primary Visual Cortex. Vision Research, 51(8), 908–924.