Absence Of Primary Visual Cortex Research Articles

On the “blindness” of blindsight: What is the evidence for phenomenal awareness in the absence of primary visual cortex (V1)?

Blindsight has been central to theories of phenomenal awareness; that a lesion to primary visual cortex (V1) abolishes all phenomenal awareness while unconscious visual functions can remain has led to the view that this region plays a crucial role in generating visual consciousness. However, since the early 20th century, there have been reports, many of which controversial, of phenomenal awareness in patients with V1 lesions. These reports include selective sparing of motion awareness, hemianopic completion and visual aftereffects. More recently, there have been successful attempts of inducing visual qualia with noninvasive brain stimulation. Here we critically review this evidence and discuss their implications to theoretical understanding of phenomenal awareness.

Audiovisual Association Learning in the Absence of Primary Visual Cortex.

Learning audiovisual associations is mediated by the primary cortical areas; however, recent animal studies suggest that such learning can take place even in the absence of the primary visual cortex. Other studies have demonstrated the involvement of extra-geniculate pathways and especially the superior colliculus (SC) in audiovisual association learning. Here, we investigated such learning in a rare human patient with complete loss of the bilateral striate cortex. We carried out an implicit audiovisual association learning task with two different colors of red and purple (the latter color known to minimally activate the extra-genicular pathway). Interestingly, the patient learned the association between an auditory cue and a visual stimulus only when the unseen visual stimulus was red, but not when it was purple. The current study presents the first evidence showing the possibility of audiovisual association learning in humans with lesioned striate cortex. Furthermore, in line with animal studies, it supports an important role for the SC in audiovisual associative learning.

Motion-Sensitive Responses in Visual Area V4 in the Absence of Primary Visual Cortex

Neurons in cortical ventral-stream area V4 are thought to contribute to important aspects of visual processing by integrating information from primary visual cortex (V1). However, how V4 neurons respond to visual stimulation after V1 injury remains unclear: While electrophysiological investigation of V4 neurons during reversible V1 inactivation suggests that virtually all responses are eliminated (Girard et al., 1991), fMRI in humans and monkeys with permanent lesions shows reliable V1-independent activity (Baseler et al., 1999; Goebel et al., 2001; Schmid et al., 2010). To resolve this apparent discrepancy, we longitudinally assessed neuronal functions of macaque area V4 using chronically implanted electrode arrays before and after creating a permanent aspiration lesion in V1. During the month after lesioning, we observed weak yet significant spiking activity in response to stimuli presented to the lesion-affected part of the visual field. These V1-independent responses showed sensitivity for motion and likely reflect the effect of V1-bypassing geniculate input into extrastriate areas.

Evidence That Primary Visual Cortex Is Required for Image, Orientation, and Motion Discrimination by Rats

The pigmented Long-Evans rat has proven to be an excellent subject for studying visually guided behavior including quantitative visual psychophysics. This observation, together with its experimental accessibility and its close homology to the mouse, has made it an attractive model system in which to dissect the thalamic and cortical circuits underlying visual perception. Given that visually guided behavior in the absence of primary visual cortex has been described in the literature, however, it is an empirical question whether specific visual behaviors will depend on primary visual cortex in the rat. Here we tested the effects of cortical lesions on performance of two-alternative forced-choice visual discriminations by Long-Evans rats. We present data from one highly informative subject that learned several visual tasks and then received a bilateral lesion ablating >90% of primary visual cortex. After the lesion, this subject had a profound and persistent deficit in complex image discrimination, orientation discrimination, and full-field optic flow motion discrimination, compared with both pre-lesion performance and sham-lesion controls. Performance was intact, however, on another visual two-alternative forced-choice task that required approaching a salient visual target. A second highly informative subject learned several visual tasks prior to receiving a lesion ablating >90% of medial extrastriate cortex. This subject showed no impairment on any of the four task categories. Taken together, our data provide evidence that these image, orientation, and motion discrimination tasks require primary visual cortex in the Long-Evans rat, whereas approaching a salient visual target does not.

“Real-time” obstacle avoidance in the absence of primary visual cortex

When we reach toward objects, we easily avoid potential obstacles located in the workspace. Previous studies suggest that obstacle avoidance relies on mechanisms in the dorsal visual stream in the posterior parietal cortex. One fundamental question that remains unanswered is where the visual inputs to these dorsal-stream mechanisms are coming from. Here, we provide compelling evidence that these mechanisms can operate in "real-time" without direct input from primary visual cortex (V1). In our first experiment, we used a reaching task to demonstrate that an individual with a dense left visual field hemianopia after damage to V1 remained strikingly sensitive to the position of unseen static obstacles placed in his blind field. Importantly, in a second experiment, we showed that his sensitivity to the same obstacles in his blind field was abolished when a short 2-s delay (without vision) was introduced before reach onset. These findings have far-reaching implications, not only for our understanding of the time constraints under which different visual pathways operate, but also in relation to how these seemingly "primitive" subcortical visual pathways can control complex everyday behavior without recourse to conscious vision.

Callosal agenesis and absence of primary visual cortex induced by prenatal X rays impair navigation's strategy and learning in tasks involving visuo-spatial working but not reference memory in mice

This study was designed for the identification of possible and distinct abilities for behavioral recovery after prenatal cerebral damage. We adopted an interesting tool for promotion of cell's death. Due to the fact that neuroblastic cells and early postmitotic neurons on the beginning of differentiation are particularly sensible for the promotion of apoptosis, we used a low whole-body dose of X radiation on pregnant female mice on E16 (sixteenth gestational day) to promote damage on specific cerebral areas of the progeny, given that the pattern of cerebral neurogenesis is not homogeneous. The morphological results were previously described by our team. Here we noticed that the recovery of behavioral functions after prenatal damage seems to be related to specific factors of local cortical circuitry organization. The deficits found on visual navigation and working memory contrast with the recovery of primary visual functions and also with reference memory, where the mice have a delay on acquisition of learning but get it. As a conclusion we reasoning that changes on laminar organization on frontal cortex as well as the inter hemispheric cortical integration through the corpus callosum could promote relatively fixed cognitive dysfunctions, as those observed on performances that require strategies for navigation (decision making) and working memory, with consequences also observed on the subsequent learning.

The unseen color aftereffect of an unseen stimulus: insight from blindsight into mechanisms of color afterimages.

We show here that, in the absence of a direct geniculostriate input in human subjects, causing loss of sight in the visual half-field contralateral to the damage, the pupil responds selectively to chromatic modulation toward the long-wavelength (red) region of the spectrum locus even when the stimulus is isoluminant for both rods and cones and entirely restricted to the subjects' "blind" hemifields. We also show that other colors are less or wholly ineffective. Nevertheless, red afterimages, generated by chromatic modulation toward the green region of the spectrum locus, also cause constrictions of the pupil even when green stimuli are themselves completely ineffective in the blind hemifield. Moreover, human subjects with damage to or loss of V1 are typically completely unaware of the stimulus that generates the aftereffect or of the aftereffect itself, both of which can be seen clearly in normal vision. The results show that pupillary responses can reveal the processing of color afterimages in the absence of primary visual cortex and in the absence of acknowledged awareness. This phenomenon is therefore a striking example of "blindsight" and makes possible the formulation of a model that predicts well the observed properties of color afterimages.