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Damage to the primary visual cortex (V1) leads to a visual field loss (scotoma) in the retinotopically corresponding part of the visual field. Nonetheless, a small amount of residual visual sensitivity persists within the blind field. This residual capacity has been linked to activity observed in the middle temporal area complex (V5/MT+). However, it remains unknown whether the organization of hV5/MT+ changes following V1 lesions. We studied the organization of area hV5/MT+ of five patients with dense homonymous defects in a quadrant of the visual field as a result of partial V1+ or optic radiation lesions. To do so, we developed a new method, which models the boundaries of population receptive fields directly from the BOLD signal of each voxel in the visual cortex. We found responses in hV5/MT+ arising inside the scotoma for all patients and identified two possible sources of activation: 1) responses might originate from partially lesioned parts of area V1 corresponding to the scotoma, and 2) responses can also originate independent of area V1 input suggesting the existence of functional V1-bypassing pathways. Apparently, visually driven activity observed in hV5/MT+ is not sufficient to mediate conscious vision. More surprisingly, visually driven activity in corresponding regions of V1 and early extrastriate areas including hV5/MT+ did not guarantee visual perception in the group of patients with post-geniculate lesions that we examined. This suggests that the fine coordination of visual activity patterns across visual areas may be an important determinant of whether visual perception persists following visual cortical lesions.

The study of blindsight has revealed a seminal dissociation between conscious vision and visually guided behavior: some patients who are blind due to V1 lesions seem to be able to employ unconscious visual information in their behavior. The standard assumption is that these findings generalize to the neurologically healthy. We tested whether unconscious processing of motion is possible without the contribution of V1 in neurologically healthy participants by disturbing activity in V1 using transcranial magnetic stimulation (TMS). Unconscious processing was measured with redundant target effect (RTE), a phenomenon where participants respond faster to two stimuli than to one stimulus, when the task is just to respond as fast as possible when one stimulus or two simultaneous stimuli are presented. We measured the RTE caused by a motion stimulus. V1 activity was interfered with different stimulus onset asynchronies (SOA) to test whether TMS delivered in a specific time window suppresses conscious perception (participant reports seeing only one of the two stimuli) but does not affect unconscious processing (RTE). We observed that at each SOA, when TMS suppressed conscious perception of the stimulus, the RTE was also eliminated. However, when visibility of the redundant target was suppressed with a visual mask, we found unconscious processing of motion. This suggests that unconscious processing of motion depends on V1 in neurologically healthy humans. We conclude that the neural mechanisms that enable motion processing in blindsight are modulated by neuroplastic changes in connectivity between subcortical areas and the visual cortex after the V1 lesion. Neurologically healthy observers cannot process motion unconsciously without functioning of V1.

Research into visual neural activity has focused almost exclusively on onset- or change-driven responses and little is known about how information is encoded in the brain during sustained periods of visual perception. We used intracranial recordings in humans to determine the degree to which the presence of a visual stimulus is persistently encoded by neural activity. The correspondence between stimulus duration and neural response duration was strongest in early visual cortex and gradually diminished along the visual hierarchy, such that is was weakest in inferior-temporal category-selective regions. A similar posterior-anterior gradient was found within inferior temporal face-selective regions, with posterior but not anterior sites showing persistent face-selective activity. The results suggest that regions that appear uniform in terms of their category selectivity are dissociated by how they temporally represent a stimulus in support of ongoing visual perception, and delineate a large-scale organizing principle of the ventral visual stream.

The neural mechanisms underlying conscious and unconscious visual processes remain controversial. Blindsight patients may process visual stimuli unconsciously despite their V1 lesion, promoting anatomical models, which suggest that pathways bypassing the V1 support unconscious vision. On the other hand, physiological models argue that the major geniculostriate pathway via V1 is involved in both unconscious and conscious vision, but in different time windows and in different types of neural activity. According to physiological models, feedforward activity via V1 to higher areas mediates unconscious processes whereas feedback loops of recurrent activity from higher areas back to V1 support conscious vision. With transcranial magnetic stimulation (TMS) it is possible to study the causal role of a brain region during specific time points in neurologically healthy participants. In the present study, we measured unconscious processing with redundant target effect, a phenomenon where participants respond faster to two stimuli than one even when one of the stimuli is not consciously perceived. We tested the physiological feedforward-feedback model of vision by suppressing conscious vision by interfering selectively either with early or later V1 activity with TMS. Our results show that early V1 activity (60ms) is necessary for both unconscious and conscious vision. During later processing stages (90ms), V1 contributes selectively to conscious vision. These findings support the feedforward-feedback-model of consciousness.

Visual stimuli can "pop out" if they are different to their background. There has been considerable debate as to the role of primary visual cortex (V1) versus higher visual areas (esp. V4) in pop-out processing. Here we parametrically modulated the relative orientation of stimuli and their backgrounds to investigate the neural correlates of pop-out in visual cortex while subjects were performing a demanding fixation task in a scanner. Whole brain and region of interest analyses confirmed a representation of orientation contrast in extrastriate visual cortex (V4), but not in striate visual cortex (V1). Thus, although previous studies have shown that human V1 can be involved in orientation pop-out, our findings demonstrate that there are cases where V1 is "blind" and pop-out detection is restricted to higher visual areas. Pop-out processing is presumably a distributed process across multiple visual regions.

Recent psychophysics studies suggest that the behavioral impact of a visual stimulus and its conscious visual recognition underlie two functionally dissociated neuronal processes. Previous TMS studies have demonstrated that certain features of a visual stimulus can still be processed despite TMS-induced disruption of perception. Here, we tested whether symbolic action priming also remains intact despite TMS-induced masking of the prime. We applied single-pulse TMS over primary visual cortex at various temporal intervals from 20 ms to 120 ms during a supraliminal action priming paradigm. This TMS protocol enabled us to identify at what exact time point a TMS-induced activity disruption of primary visual cortex interferes with conscious visual perception of the prime versus (un)conscious behavioral priming of the visual target stimulus. We also introduced spatial uncertainty by presenting visual stimuli either above or below the fixation cross, while the TMS pulse was always targeting the prime presented below fixation. We revealed that TMS over primary visual cortex interferes with both conscious visual perception and symbolic behavioral priming in a temporarily and spatially specific manner, i.e., only when disrupting primary visual cortex at approximately the same temporal stage between 60 and 100 ms after prime onset, and only for those prime stimuli presented below fixation. These findings are in disagreement with the idea of subliminal action priming being mediated by neural pathways bypassing striate cortex, and rather suggest that symbolic action priming relies on an intact neural transmission along the retino-geniculo-striate pathway. The implications of our findings for previous reports of residual visual processing during striate TMS are discussed.

Most models of the human visual system argue that higher-order motion-processing cortical regions receive their inputs only via the primary visual cortex (striate cortex), rather than also via direct projections from the thalamus that bypass primary visual cortex. However, recent evidence in non-human primates, along with some evidence in humans with damaged primary visual cortex (e.g., "blindsight" for motion in the blind visual hemifield), have argued for the existence of a direct thalamic-to-extrastriate projection for motion processing. This evidence remains controversial. Here we tested the idea that direct thalamic input to extrastriate motion processing areas exists in humans but might be masked in scalp recordings by activity from early visual areas. To do this, we employed stimuli that induced strong refractory effects in primary visual cortex--thereby creating a brief "reversable lesion" in primary visual cortex--immediately before the presentation of a motion stimulus. Under these conditions, we then assessed whether motion areas of cortex were still able to process the motion stimuli by recording event-related potentials (ERPs) and event-related magnetic fields (ERFs/MEG). We found robust motion-related activity in extrastriate motion processing areas in the ERP and MEG signals even when primary visual cortex was heavily suppressed by our manipulation. This finding provides evidence for a direct thalamic functional pathway to extrastriate visual cortical motion processing areas in the human that bypasses primary visual cortex.

Visual field defects result from postgeniculate lesions. It is generally assumed that absolute defects are caused by total destruction or denervation of primary visual cortex (V1) and that the degraded but conscious vision that remains or returns in relative or partial defects is mediated by compromised V1 cortex that retains a sufficiently large population of functional neurons. We here report the results of three patients with long-standing postgeniculate lesions who underwent functional magnetic resonance imaging while their partial defect was stimulated with high-contrast reversing checkerboard stimuli. Although the stimulation evoked conscious visual impressions in all three, in only one patient did it activate perilesional V1. In the other two we found no evidence for perilesional activation, indicating that some conscious vision may return in the absence of functional ipsilesional V1.

Many imaging studies report activity in the prefrontal and parietal cortices when subjects are aware as opposed to unaware of visual stimuli. One possibility is that this activity simply reflects higher signal strength or the superior task performance that is associated with awareness. To find out, we studied the hemianope GY who has unilateral destruction of almost all primary visual cortices. He exhibits 'blindsight', that is, he claims to have no conscious visual phenomenology (i.e., no visual qualia), for stationary stimuli presented to his right visual field (the blind field), although he can press keys to distinguish between different stimuli presented there. We presented to him a visual discrimination task, and equated performance for stimuli presented to the left or right visual field by presenting low contrast stimuli to his normal (left) field and high contrast stimuli to his blind (right) field. Superior accuracy can be a serious confound, and our paradigm allows us to control for it and avoid this confound. Even when performance was matched, and the signal strength was lower, visual stimulation to the normal (conscious) field led to higher activity in the prefrontal and parietal cortices. These results indicate that the activity in the prefrontal and parietal areas that has been reported in previous studies of awareness is not just due to a (signal strength or performance) confounds. One possibility is that it reflects the superior 'metacognitive' capacity that is associated with awareness, because GY was better able to distinguish between his own correct and incorrect responses for stimuli presented to his normal field than to his blind field.

A "late" period of activity in striate cortex (V1) in response to extrastriate feedback has been proposed to act as a marker of visual awareness. It is not clear, however, whether such recurrent activity is associated exclusively with aware perception or whether it is necessary also for unaware visual processing. We investigated the role of the "late" V1 activity in both aware and unaware visual motion perception. Participants were asked to make a forced-choice direction discrimination judgment on a coherently moving random-dot display and additionally rate their subjective awareness of the stimulus. Transcranial magnetic stimulation (TMS) was applied over the early visual cortex (V1/V2) either 20, 40, 60, 80, or 100 ms after motion offset. Visual awareness was impaired at an "early" (20 ms) and a "late" (60 ms) stimulation time window. Participants' forced-choice direction discrimination performance on "unaware" trials was above chance in No TMS baseline condition. Importantly, this performance was impaired by TMS over V1/V2 at the "late" time window. In a second experiment we show that the critical time window of V5/MT falls between the "early" and "late" time windows of V1/V2 activity. The results indicate that recurrent extrastriate-V1 activity is necessary for both aware and unaware perception.

When a single brief visual flash is accompanied by two auditory bleeps, it is frequently perceived incorrectly as two flashes. Here, we used high field functional MRI in humans to examine the neural basis of this multisensory perceptual illusion. We show that activity in retinotopic visual cortex is increased by the presence of concurrent auditory stimulation, irrespective of any illusory perception. However, when concurrent auditory stimulation gave rise to illusory visual perception, activity in V1 was enhanced, despite auditory and visual stimulation being unchanged. These findings confirm that responses in human V1 can be altered by sound and show that they reflect subjective perception rather than the physically present visual stimulus. Moreover, as the right superior temporal sulcus and superior colliculus were also activated by illusory visual perception, together with V1, they provide a potential neural substrate for the generation of this multisensory illusion.

We examined whether consciously undetected fear signals engage a collateral brainstem pathway to the amygdala and prefrontal cortex in the intact human brain, using functional neuroimaging. 'Blindsight' lesion patients can respond to visual fear signals independently from conscious experience, suggesting that these signals reach the amygdala via a direct pathway that bypasses the primary visual cortex. Electrophysiological evidence points to concomitant involvement of prefrontal regions in automatic orienting to subliminal signals of fear, which may reflect innervation arising from brainstem arousal systems. To approximate blindsight in 22 healthy subjects, facial signals of fear were presented briefly (16.7 ms) and masked such that conscious detection was prevented. Results revealed that subliminal fear signals elicited activity in the brainstem region encompassing the superior colliculus and locus coeruleus, pulvinar and amygdala, and in fronto-temporal regions associated with orienting. These findings suggest that crude sensory input from the superior colliculo-pulvinar visual pathway to the amygdala may allow for sufficient appraisal of fear signals to innervate the locus coeruleus. The engagement of the locus coeruleus could explain the observation of diffuse fronto-temporal cortical activity, given its role in evoking collateral ascending noradrenergic efferents to the subcortical amygdala and prefrontal cortex. This network may represent an evolutionary adaptive neural 'alarm' system for rapid alerting to sources of threat, without the need for conscious appraisal.

We used functional magnetic resonance imaging (fMRI) to investigate the neural substrates mediating residual vision in the ‘‘blind’’ hemifield of hemispherectomized patients. The visual stimuli were semicircular gratings moving in opposite directions on a dynamic random-dot background. They were specifically constructed to eliminate intra- and extraocular light scatter and optimize the activation of extrastriate cortical areas and their subcortical relays. Multislice T2*weighted gradient echo (GE) echoplanar imaging (EPI) images (TR/TE 5 4 s/45 ms, flip angle 90°) were acquired during activation and baseline visual stimulation. An activation minus baseline subtraction was performed, and the acquired t statistic map transformed into the stereotaxic coordinate space of Talairach and Tournoux. In seven normal control subjects, right hemifield stimulation produced significant activation foci in contralateral V1/V2, V3/V3A, VP, and V5 (MT). Significant activation was also produced in homologous regions of the right occipital lobe with left hemifield stimulation. Stimulation of the intact hemifield in hemispherectomized patients resulted in activation of similar areas exclusively within the contralateral hemisphere. Stimulation of the anopic hemifield produced statistically significant activation in the ipsilateral occipital lobe (putative area V5 or MT) and areas V3/V3A in the only subject with blindsight. We conclude that the remaining hemisphere may contribute to residual visual functions in the blind hemifield of hemispherectomized patients, possibly through the collicular‐pulvinar route since the activated areas are known to receive their afferents from these subcortical nuclei. r 1999 Academic Press