Following damage to the primary visual cortex, some patients exhibit “blindsight,” where they report a loss of awareness while retaining the ability to discriminate visual stimuli above chance. Transient disruption of occipital regions with TMS can produce a similar dissociation, known as TMS-induced blindsight. The neural basis of this residual vision is controversial, with some studies attributing it to the retinotectal pathway via the superior colliculus whereas others implicate spared projections that originate predominantly from the LGN. Here we contrasted these accounts by combining TMS with visual stimuli that either activate or bypass the retinotectal and magnocellular (R/M) pathways. We found that the residual capacity of TMS-induced blindsight occurs for stimuli that bypass the R/M pathways, indicating that such pathways, which include those to the superior colliculus, are not critical. We also found that the modulation of conscious vision was time and pathway dependent. TMS applied either early (0–40 msec) or late (280–320 msec) after stimulus onset modulated detection of stimuli that did not bypass R/M pathways, whereas during an intermediate period (90–130 msec) the effect was pathway independent. Our findings thus suggest a prominent role for the R/M pathways in supporting both the preparatory and later stages of conscious vision. This may help resolve apparent conflict in previous literature by demonstrating that the roles of the retinotectal and geniculate pathways are likely to be more nuanced than simply corresponding to the unconscious/conscious dichotomy.
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